PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
34799378-1	2022	More people with newly diagnosed BRAFV600-mutant metastatic melanoma survive at least 2 years when they begin treatment with a combination of immunotherapies-the PD-1 inhibitor nivolumab and the CTLA4 inhibitor ipilimumab-instead of a combination of targeted therapies-the BRAF inhibitor dabrafenib and the MEK inhibitor trametinib.	dabrafenib	288-298	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	273-277
25589619-0	2015	The BRAF and MEK Inhibitors Dabrafenib and Trametinib: Effects on Immune Function and in Combination with Immunomodulatory Antibodies Targeting PD-1, PD-L1, and CTLA-4.	dabrafenib	28-38	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-8
25589619-0	2015	The BRAF and MEK Inhibitors Dabrafenib and Trametinib: Effects on Immune Function and in Combination with Immunomodulatory Antibodies Targeting PD-1, PD-L1, and CTLA-4.	dabrafenib	28-38	mitogen-activated protein kinase kinase 7	Homo sapiens	13-16
25589619-0	2015	The BRAF and MEK Inhibitors Dabrafenib and Trametinib: Effects on Immune Function and in Combination with Immunomodulatory Antibodies Targeting PD-1, PD-L1, and CTLA-4.	dabrafenib	28-38	CD274 molecule	Homo sapiens	150-155
25589619-0	2015	The BRAF and MEK Inhibitors Dabrafenib and Trametinib: Effects on Immune Function and in Combination with Immunomodulatory Antibodies Targeting PD-1, PD-L1, and CTLA-4.	dabrafenib	28-38	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	161-167
25589619-3	2015	RESULTS: Dabrafenib enhanced pERK expression levels and did not suppress human CD4(+) or CD8(+) T-cell function.	dabrafenib	9-19	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	29-33
25589619-6	2015	Dabrafenib and trametinib in BRAF V600E/K, and trametinib in BRAF wild-type tumor cells induced apoptosis markers, upregulated HLA molecule expression, and downregulated certain immunosuppressive factors such as PD-L1, IL1, IL8, NT5E, and VEGFA.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	29-33
25589619-6	2015	Dabrafenib and trametinib in BRAF V600E/K, and trametinib in BRAF wild-type tumor cells induced apoptosis markers, upregulated HLA molecule expression, and downregulated certain immunosuppressive factors such as PD-L1, IL1, IL8, NT5E, and VEGFA.	dabrafenib	0-10	CD274 molecule	Homo sapiens	212-217
25589619-6	2015	Dabrafenib and trametinib in BRAF V600E/K, and trametinib in BRAF wild-type tumor cells induced apoptosis markers, upregulated HLA molecule expression, and downregulated certain immunosuppressive factors such as PD-L1, IL1, IL8, NT5E, and VEGFA.	dabrafenib	0-10	interleukin 1 alpha	Homo sapiens	219-222
25589619-6	2015	Dabrafenib and trametinib in BRAF V600E/K, and trametinib in BRAF wild-type tumor cells induced apoptosis markers, upregulated HLA molecule expression, and downregulated certain immunosuppressive factors such as PD-L1, IL1, IL8, NT5E, and VEGFA.	dabrafenib	0-10	C-X-C motif chemokine ligand 8	Homo sapiens	224-227
25589619-6	2015	Dabrafenib and trametinib in BRAF V600E/K, and trametinib in BRAF wild-type tumor cells induced apoptosis markers, upregulated HLA molecule expression, and downregulated certain immunosuppressive factors such as PD-L1, IL1, IL8, NT5E, and VEGFA.	dabrafenib	0-10	5'-nucleotidase ecto	Homo sapiens	229-233
34958586-2	2022	However, dabrafenib was recently shown to potently activate the human nuclear receptor pregnane X receptor (PXR).	dabrafenib	9-19	nuclear receptor subfamily 1 group I member 2	Homo sapiens	108-111
34958586-3	2022	PXR activation increases the clearance of various chemicals and drugs, including dabrafenib itself.	dabrafenib	81-91	nuclear receptor subfamily 1 group I member 2	Homo sapiens	0-3
34958586-6	2022	By determining the crystal structure of dabrafenib bound to PXR and analyzing its mode of binding to both PXR and its primary target, B-Raf-V600E, we were able to derive new compounds with nanomolar activity against B-Raf and no detectable affinity for PXR.	dabrafenib	40-50	nuclear receptor subfamily 1 group I member 2	Homo sapiens	60-63
34958586-6	2022	By determining the crystal structure of dabrafenib bound to PXR and analyzing its mode of binding to both PXR and its primary target, B-Raf-V600E, we were able to derive new compounds with nanomolar activity against B-Raf and no detectable affinity for PXR.	dabrafenib	40-50	nuclear receptor subfamily 1 group I member 2	Homo sapiens	106-109
34958586-6	2022	By determining the crystal structure of dabrafenib bound to PXR and analyzing its mode of binding to both PXR and its primary target, B-Raf-V600E, we were able to derive new compounds with nanomolar activity against B-Raf and no detectable affinity for PXR.	dabrafenib	40-50	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	134-139
34958586-6	2022	By determining the crystal structure of dabrafenib bound to PXR and analyzing its mode of binding to both PXR and its primary target, B-Raf-V600E, we were able to derive new compounds with nanomolar activity against B-Raf and no detectable affinity for PXR.	dabrafenib	40-50	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	216-221
33794577-6	2021	As the patient was BRAF-mutated, she was started on dabrafenib/trametinib.	dabrafenib	52-62	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	19-23
25589619-6	2015	Dabrafenib and trametinib in BRAF V600E/K, and trametinib in BRAF wild-type tumor cells induced apoptosis markers, upregulated HLA molecule expression, and downregulated certain immunosuppressive factors such as PD-L1, IL1, IL8, NT5E, and VEGFA.	dabrafenib	0-10	vascular endothelial growth factor A	Homo sapiens	239-244
34780725-0	2022	Dabrafenib inhibits ABCG2 and cytochrome P450 isoenzymes; potential implications for combination anticancer therapy.	dabrafenib	0-10	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	20-25
34838156-16	2022	INTERPRETATION: Dabrafenib plus trametinib showed clinically meaningful activity in patients with BRAFV600E mutation-positive recurrent or refractory high-grade glioma and low-grade glioma, with a safety profile consistent with that in other indications.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	98-102
34780725-0	2022	Dabrafenib inhibits ABCG2 and cytochrome P450 isoenzymes; potential implications for combination anticancer therapy.	dabrafenib	0-10	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	30-45
34780725-1	2022	Dabrafenib is a BRAF inhibitor used in combination treatment of malignant melanoma and non-small cell lung carcinoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	16-20
34780725-3	2022	Using accumulation assays, we showed that dabrafenib inhibited ABCG2 and, less potently, ABCB1 transporter.	dabrafenib	42-52	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	63-68
34780725-3	2022	Using accumulation assays, we showed that dabrafenib inhibited ABCG2 and, less potently, ABCB1 transporter.	dabrafenib	42-52	ATP binding cassette subfamily B member 1	Homo sapiens	89-94
34780725-4	2022	We also confirmed dabrafenib as a CYP2C8, CYP2C9, CYP3A4, and CYP3A5 inhibitor.	dabrafenib	18-28	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	34-40
34780725-4	2022	We also confirmed dabrafenib as a CYP2C8, CYP2C9, CYP3A4, and CYP3A5 inhibitor.	dabrafenib	18-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
34780725-4	2022	We also confirmed dabrafenib as a CYP2C8, CYP2C9, CYP3A4, and CYP3A5 inhibitor.	dabrafenib	18-28	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	50-56
34780725-4	2022	We also confirmed dabrafenib as a CYP2C8, CYP2C9, CYP3A4, and CYP3A5 inhibitor.	dabrafenib	18-28	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	62-68
34780725-5	2022	Importantly, inhibition of ABCG2 and CYP3A4 by dabrafenib led to the potentiation of cytotoxic effects of mitoxantrone and docetaxel toward respective resistant cell lines in drug combination studies.	dabrafenib	47-57	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	27-32
34780725-5	2022	Importantly, inhibition of ABCG2 and CYP3A4 by dabrafenib led to the potentiation of cytotoxic effects of mitoxantrone and docetaxel toward respective resistant cell lines in drug combination studies.	dabrafenib	47-57	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	37-43
34780725-7	2022	We further demonstrated that mRNA levels of ABCB1, ABCG2, ABCC1, and CYP3A4 were increased after 24 h and 48 h exposure to dabrafenib.	dabrafenib	123-133	ATP binding cassette subfamily B member 1	Homo sapiens	44-49
34780725-7	2022	We further demonstrated that mRNA levels of ABCB1, ABCG2, ABCC1, and CYP3A4 were increased after 24 h and 48 h exposure to dabrafenib.	dabrafenib	123-133	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	51-56
34780725-7	2022	We further demonstrated that mRNA levels of ABCB1, ABCG2, ABCC1, and CYP3A4 were increased after 24 h and 48 h exposure to dabrafenib.	dabrafenib	123-133	ATP binding cassette subfamily C member 1	Homo sapiens	58-63
34780725-7	2022	We further demonstrated that mRNA levels of ABCB1, ABCG2, ABCC1, and CYP3A4 were increased after 24 h and 48 h exposure to dabrafenib.	dabrafenib	123-133	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	69-75
34780725-8	2022	Overall, our data confirm dabrafenib as a drug frequently and potently interacting with ABC transporters and CYP isoenzymes.	dabrafenib	26-36	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	88-91
34780725-8	2022	Overall, our data confirm dabrafenib as a drug frequently and potently interacting with ABC transporters and CYP isoenzymes.	dabrafenib	26-36	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	109-112
34949515-0	2022	Re: Pyrexia in patients treated with dabrafenib plus trametinib across clinical trials in BRAF-mutant cancers.	dabrafenib	37-47	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	90-94
34876300-0	2022	Reply to: Letter comments on: Pyrexia in patients treated with dabrafenib plus trametinib across clinical trials in BRAF-mutant cancers.	dabrafenib	63-73	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	116-120
34518309-5	2021	We developed an in vitro model of dabrafenib-resistance using genetically homogeneous single-cell clones from two cell lines with established BRAF mutations (U266, DP6).	dabrafenib	34-44	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	142-146
34482192-0	2021	Preparation and evaluation of dabrafenib-loaded, CD47-conjugated human serum albumin-based nanoconstructs for chemoimmunomodulation.	dabrafenib	30-40	albumin	Mus musculus	71-84
34418561-7	2021	Dabrafenib (ROR 2.24, 99% CI: 1.86-2.70) and trametinib (ROR 2.44, 99% CI: 2.03-2.92) had higher odds of heart failure than other targeted therapies.	dabrafenib	0-10	receptor tyrosine kinase like orphan receptor 2	Homo sapiens	12-17
34709074-3	2021	Results: Eight patients treated with rituximab (anti-CD20), nivolumab (anti-PD-1), ipilimumab (anti-CTLA-4), vemurafenib and dabrafenib (anti-BRAF), trametinib (anti-MEK) and ibritunib showed uveitis with hypopion (one patient), macular edema (five patients) and choroiditis (two patients).	dabrafenib	125-135	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	142-146
34433200-1	2021	We present two patients with stage IV melanoma, the first with BRAF wild-type melanoma with multiple visceral metastases treated with immunotherapy (pembrolizumab) and the second with BRAFV600E melanoma with subcutaneous and lymph nodes metastasis treated with BRAF and MEK-inhibitors (dabrafenib/trametinib).	dabrafenib	286-296	mitogen-activated protein kinase kinase 7	Homo sapiens	270-273
34620756-1	2021	The combination of BRAF and MEK inhibitors, such as dabrafenib and trametinib, respectively, is an established treatment option for patients with advanced BRAFV600-mutated melanoma.	dabrafenib	52-62	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	19-23
34524222-3	2021	Since adjuvant dabrafenib plus trametinib (D+T) combined therapy and anti-PD1 antibody (Ab) therapy reduce the risk of recurrence in patients with resected stage III BRAF-mutated melanoma, selecting the adjuvant therapy for BRAF-mutated melanoma is controversial.	dabrafenib	15-25	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	166-170
34620756-1	2021	The combination of BRAF and MEK inhibitors, such as dabrafenib and trametinib, respectively, is an established treatment option for patients with advanced BRAFV600-mutated melanoma.	dabrafenib	52-62	mitogen-activated protein kinase kinase 7	Homo sapiens	28-31
34509659-1	2021	Dabrafenib (Tafinlar) is used for the treatment of patients with BRAF V600 mutation positive unresectable or metastatic melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	65-69
34516041-0	2021	BRAF V600E Mediates Crizotinib Resistance and Responds to Dabrafenib and Trametinib in a ROS1-rearranged NSCLC: a Case Report.	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
34516041-7	2021	Our study revealed that BRAF V600E can confer the crizotinib resistance in ROS1 fusion-positive NSCLC and presented the first case showing that the treatment with dabrafenib and trametinib can serve as an effective option for later-line treatment for this molecular-defined subgroup.	dabrafenib	163-173	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	24-28
34516041-11	2021	This is the first case reporting the treatment with dabrafenib and trametinib may serve as an effective option for later-line treatment for patients harboring resistant BRAF V600E.	dabrafenib	52-62	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	169-173
34509659-1	2021	Dabrafenib (Tafinlar) is used for the treatment of patients with BRAF V600 mutation positive unresectable or metastatic melanoma.	dabrafenib	12-20	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	65-69
34761911-7	2021	Primary screening with further experiments has identified microtubule stabilizer taxanes, CDK4/6 inhibitor abemaciclib and Raf inhibitor dabrafenib being effective in inhibiting ciliary disassembly induced experimentally but also under physiological conditions.	dabrafenib	137-147	zinc fingers and homeoboxes 2	Homo sapiens	123-126
34938683-1	2021	Background Combination of dabrafenib-trametinib is one of the standard treatments in patients with BRAF-mutated advanced malignant melanoma (MM).	dabrafenib	26-36	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	99-103
34938683-11	2021	Conclusion Combination of dabrafenib-trametinib is effective in patients with BRAF-mutated MM with good tolerability.	dabrafenib	26-36	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	78-82
34192355-6	2021	RESULTS: Our data indicated that dabrafenib had a broad inhibitory effect on 4-MU glucuronidation by inhibiting the activities of UGTs, especially on UGT1A1, UGT1A7, UGT1A8, and UGT1A9, and dabrafenib can increase the area under curve (AUC) of co-administered drug.	dabrafenib	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	150-156
34192355-6	2021	RESULTS: Our data indicated that dabrafenib had a broad inhibitory effect on 4-MU glucuronidation by inhibiting the activities of UGTs, especially on UGT1A1, UGT1A7, UGT1A8, and UGT1A9, and dabrafenib can increase the area under curve (AUC) of co-administered drug.	dabrafenib	33-43	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	158-164
34192355-6	2021	RESULTS: Our data indicated that dabrafenib had a broad inhibitory effect on 4-MU glucuronidation by inhibiting the activities of UGTs, especially on UGT1A1, UGT1A7, UGT1A8, and UGT1A9, and dabrafenib can increase the area under curve (AUC) of co-administered drug.	dabrafenib	33-43	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	166-172
34192355-6	2021	RESULTS: Our data indicated that dabrafenib had a broad inhibitory effect on 4-MU glucuronidation by inhibiting the activities of UGTs, especially on UGT1A1, UGT1A7, UGT1A8, and UGT1A9, and dabrafenib can increase the area under curve (AUC) of co-administered drug.	dabrafenib	33-43	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	178-184
34192355-7	2021	CONCLUSIONS: Dabrafenib is a strong inhibitor of several UGTs and the co-administration of dabrafenib with drugs primarily metabolized by UGT1A1, 1A7, 1A8, or 1A9 may induce potential DDIs.	dabrafenib	13-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
34192355-7	2021	CONCLUSIONS: Dabrafenib is a strong inhibitor of several UGTs and the co-administration of dabrafenib with drugs primarily metabolized by UGT1A1, 1A7, 1A8, or 1A9 may induce potential DDIs.	dabrafenib	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
34621046-3	2021	METHODS: We develop a mechanistic mathematical model that describes how the mutant BRAF inhibitor, dabrafenib, and the MEK inhibitor, trametinib, affect BRAFV600E-MEK-ERK signalling.	dabrafenib	99-109	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	83-87
34621046-3	2021	METHODS: We develop a mechanistic mathematical model that describes how the mutant BRAF inhibitor, dabrafenib, and the MEK inhibitor, trametinib, affect BRAFV600E-MEK-ERK signalling.	dabrafenib	99-109	mitogen-activated protein kinase kinase 7	Homo sapiens	163-166
34621046-3	2021	METHODS: We develop a mechanistic mathematical model that describes how the mutant BRAF inhibitor, dabrafenib, and the MEK inhibitor, trametinib, affect BRAFV600E-MEK-ERK signalling.	dabrafenib	99-109	mitogen-activated protein kinase 1	Homo sapiens	167-170
34621046-6	2021	RESULTS: The model provides a quantitative method to compute how dabrafenib and trametinib can be used in combination to synergistically inhibit ERK activity in BRAFV600E-mutant melanoma cells.	dabrafenib	65-75	mitogen-activated protein kinase 1	Homo sapiens	145-148
34621046-7	2021	The model elucidates molecular mechanisms of vertical inhibition of the BRAFV600E-MEK-ERK cascade and delineates how elevated BRAF concentrations generate drug resistance to dabrafenib and trametinib.	dabrafenib	174-184	mitogen-activated protein kinase kinase 7	Homo sapiens	82-85
34621046-7	2021	The model elucidates molecular mechanisms of vertical inhibition of the BRAFV600E-MEK-ERK cascade and delineates how elevated BRAF concentrations generate drug resistance to dabrafenib and trametinib.	dabrafenib	174-184	mitogen-activated protein kinase 1	Homo sapiens	86-89
34621046-7	2021	The model elucidates molecular mechanisms of vertical inhibition of the BRAFV600E-MEK-ERK cascade and delineates how elevated BRAF concentrations generate drug resistance to dabrafenib and trametinib.	dabrafenib	174-184	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	126-130
34956922-0	2021	Therapeutic Effect of Combined Dabrafenib and Trametinib Treatment of BRAF V600E-Mutated Primary Squamous Cell Carcinoma of the Thyroid: A Case Report.	dabrafenib	31-41	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	70-74
34956922-3	2021	Here, we describe a case of a male patient who presented with a BRAF V600E-mutated PSCC of the thyroid gland showing response to combined dabrafenib and trametinib therapy over a period of >12 months.	dabrafenib	138-148	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	64-68
34956922-10	2021	As an individualized treatment concept, we decided to advocate combined BRAF V600E targeting by the multikinase inhibitors dabrafenib and trametinib.	dabrafenib	123-133	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	72-76
34897056-12	2021	Currently, the targeted therapy with low molecular weight selective inhibitors of mutant BRAF (vemurafenib, dabrafenib) and immune checkpoint blockers (nivolumab, pembrolizumab) is generally recommended for unresectable skin melanoma patients bearing BRAF mutations.	dabrafenib	108-118	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	89-93
34831014-2	2021	We generated trametinib and dabrafenib resistant melanoma (TDR) cell lines to the MEK and BRAF inhibitors, respectively.	dabrafenib	28-38	mitogen-activated protein kinase kinase 7	Homo sapiens	82-85
34831014-2	2021	We generated trametinib and dabrafenib resistant melanoma (TDR) cell lines to the MEK and BRAF inhibitors, respectively.	dabrafenib	28-38	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	90-94
34702278-17	2021	PPARGC1A was related to drug sensitivity of dabrafenib, vemurafenib, and trametinib.	dabrafenib	44-54	PPARG coactivator 1 alpha	Homo sapiens	0-8
34733469-6	2021	A major landmark in anaplastic thyroid cancer management history was recently reached with the approval of BRAF and MEK inhibitor combination, specifically dabrafenib and trametinib for BRAF-mutated anaplastic thyroid cancer; this treatment has improved survival and outcomes in this population.	dabrafenib	156-166	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	107-111
34595070-0	2021	Redifferentiation of BRAF V600E-Mutated Radioiodine Refractory Metastatic Papillary Thyroid Cancer After Treatment With Dabrafenib and Trametinib.	dabrafenib	120-130	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	21-25
34754579-0	2021	Treatment of BRAF V600E mutated ganglioglioma of the third ventricle with dabrafenib.	dabrafenib	74-84	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	13-17
34754579-5	2021	After an endoscopic biopsy and insertion of a ventriculoperitoneal shunt, the patient was started on the BRAF inhibitor dabrafenib, as an alternative to surgery or radiation.	dabrafenib	120-130	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	105-109
34722270-4	2021	Herein, we present the first case of anti-MUSK (+) MG in a woman with metastatic BRAF-mutant melanoma after long-term treatment with dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor).	dabrafenib	133-143	muscle associated receptor tyrosine kinase	Homo sapiens	42-46
34722270-4	2021	Herein, we present the first case of anti-MUSK (+) MG in a woman with metastatic BRAF-mutant melanoma after long-term treatment with dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor).	dabrafenib	133-143	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	81-85
34722270-4	2021	Herein, we present the first case of anti-MUSK (+) MG in a woman with metastatic BRAF-mutant melanoma after long-term treatment with dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor).	dabrafenib	133-143	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	145-149
34132762-6	2021	Moreover, treatment of patients with the BRAF inhibitor Dabrafenib resulted in MAPK cascade inhibition, inflammation prevention, and regulation of cellular metabolism within mononuclear phagocytes.	dabrafenib	56-66	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	41-45
34625515-2	2021	Although first-line dabrafenib-trametinib and ipilimumab-nivolumab have similar intracranial response rates (50%-55%), central nervous system (CNS) resistance to BRAF-MEK inhibitors (BRAF-MEKi) usually occurs around 6 months, and durable responses are only seen with combination immunotherapy.	dabrafenib	20-30	mitogen-activated protein kinase kinase 7	Homo sapiens	167-170
34625515-2	2021	Although first-line dabrafenib-trametinib and ipilimumab-nivolumab have similar intracranial response rates (50%-55%), central nervous system (CNS) resistance to BRAF-MEK inhibitors (BRAF-MEKi) usually occurs around 6 months, and durable responses are only seen with combination immunotherapy.	dabrafenib	20-30	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	183-187
34590600-1	2021	The combination of dabrafenib and trametinib is a well-established treatment for BRAF-mutated melanoma.	dabrafenib	19-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	81-85
34288281-2	2021	To identify microRNAs (miRNAs) that can improve the efficacy of the BRAF inhibitor dabrafenib (DAB) and the MEK inhibitor trametinib (TRA), we screened 240 miRNA in BRAF-mutated CRC cells and identified five candidate miRNAs.	dabrafenib	83-93	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	68-72
34288281-2	2021	To identify microRNAs (miRNAs) that can improve the efficacy of the BRAF inhibitor dabrafenib (DAB) and the MEK inhibitor trametinib (TRA), we screened 240 miRNA in BRAF-mutated CRC cells and identified five candidate miRNAs.	dabrafenib	83-93	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	165-169
34288281-2	2021	To identify microRNAs (miRNAs) that can improve the efficacy of the BRAF inhibitor dabrafenib (DAB) and the MEK inhibitor trametinib (TRA), we screened 240 miRNA in BRAF-mutated CRC cells and identified five candidate miRNAs.	dabrafenib	95-98	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	68-72
34288281-2	2021	To identify microRNAs (miRNAs) that can improve the efficacy of the BRAF inhibitor dabrafenib (DAB) and the MEK inhibitor trametinib (TRA), we screened 240 miRNA in BRAF-mutated CRC cells and identified five candidate miRNAs.	dabrafenib	95-98	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	165-169
34288281-5	2021	Furthermore, overexpression of miR-193a-3p in BRAF-mutated cells enhanced the efficacy of DAB and TRA through inhibiting reactivation of MAPK signaling and inducing inhibition of Mcl1.	dabrafenib	90-93	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	46-50
34288281-5	2021	Furthermore, overexpression of miR-193a-3p in BRAF-mutated cells enhanced the efficacy of DAB and TRA through inhibiting reactivation of MAPK signaling and inducing inhibition of Mcl1.	dabrafenib	90-93	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	179-183
34288281-6	2021	Inhibition of Mcl1 by siRNA or by Mcl1 inhibitor increased the anti-proliferative effect of combination therapy with DAB, TRA, and anti-EGFR antibody cetuximab.	dabrafenib	117-120	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	14-18
34288281-6	2021	Inhibition of Mcl1 by siRNA or by Mcl1 inhibitor increased the anti-proliferative effect of combination therapy with DAB, TRA, and anti-EGFR antibody cetuximab.	dabrafenib	117-120	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	34-38
34626563-7	2021	Early phase trials of dabrafenib plus trametinib (BRAF and MEK inhibition) and zanidatamab (a bispecific HER2-antibody) have yielded encouraging response rates.	dabrafenib	22-32	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	50-54
34626563-7	2021	Early phase trials of dabrafenib plus trametinib (BRAF and MEK inhibition) and zanidatamab (a bispecific HER2-antibody) have yielded encouraging response rates.	dabrafenib	22-32	mitogen-activated protein kinase kinase 7	Homo sapiens	59-62
34638434-0	2021	RAC1 Alterations Induce Acquired Dabrafenib Resistance in Association with Anaplastic Transformation in a Papillary Thyroid Cancer Patient.	dabrafenib	33-43	Rac family small GTPase 1	Homo sapiens	0-4
34638434-2	2021	Targeted inhibitors such as dabrafenib have been used in advanced BRAF-mutated PTC; however, acquired resistance to the drug is common and little is known about other effectors that may play integral roles in this resistance.	dabrafenib	28-38	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	66-70
34638434-4	2021	We detected a novel RAC1 (P34R) mutation acquired during dabrafenib treatment in a progressive metastatic lesion with ATC phenotype.	dabrafenib	57-67	Rac family small GTPase 1	Homo sapiens	20-24
34638434-9	2021	Copy number amplification and overexpression of other genes located on this chromosome, such as TWIST1, EGFR, and MET were also detected, which might also lead to dabrafenib resistance.	dabrafenib	163-173	twist family bHLH transcription factor 1	Homo sapiens	96-102
34638434-9	2021	Copy number amplification and overexpression of other genes located on this chromosome, such as TWIST1, EGFR, and MET were also detected, which might also lead to dabrafenib resistance.	dabrafenib	163-173	epidermal growth factor receptor	Homo sapiens	104-108
34638434-9	2021	Copy number amplification and overexpression of other genes located on this chromosome, such as TWIST1, EGFR, and MET were also detected, which might also lead to dabrafenib resistance.	dabrafenib	163-173	SAFB like transcription modulator	Homo sapiens	114-117
34506566-0	2021	Dabrafenib, idelalisib and nintedanib act as significant allosteric modulator for dengue NS3 protease.	dabrafenib	0-10	KRAS proto-oncogene, GTPase	Homo sapiens	89-92
34243078-1	2021	BACKGROUND: BRAF and MEK inhibitors combination, including dabrafenib (D) and trametinib (T) have transformed the treatment of BRAF V600-mutant advanced melanoma patients, including patients with brain metastasis (BM).	dabrafenib	59-69	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	127-131
34504796-13	2021	Conclusion: Dabrafenib combined with trametinib confer long-term survival in Chinese patients with BRAF V600-mutant, unresectable or metastatic acral/cutaneous melanoma.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	99-103
34733624-0	2021	Cyclin-dependent kinase 4 upregulation mediates acquired resistance of dabrafenib plus trametinib in BRAF V600E-mutated lung cancer.	dabrafenib	71-81	cyclin dependent kinase 4	Homo sapiens	0-25
34733624-0	2021	Cyclin-dependent kinase 4 upregulation mediates acquired resistance of dabrafenib plus trametinib in BRAF V600E-mutated lung cancer.	dabrafenib	71-81	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	101-105
34733624-1	2021	Background: Combination therapy with the B-Raf inhibitor, dabrafenib, and the MEK inhibitor, trametinib (DT) is commonly used to treat patients with B-Raf proto-oncogene, serine/threonine kinase V600E (BRAF V600E)-mutated non-small cell lung cancer (NSCLC).	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	149-154
34733624-1	2021	Background: Combination therapy with the B-Raf inhibitor, dabrafenib, and the MEK inhibitor, trametinib (DT) is commonly used to treat patients with B-Raf proto-oncogene, serine/threonine kinase V600E (BRAF V600E)-mutated non-small cell lung cancer (NSCLC).	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	202-206
34733624-8	2021	Induction of CDK4 expression in a cell line derived from a patient with the BRAF V600E mutation resulted in partial resistance to dabrafenib.	dabrafenib	130-140	cyclin dependent kinase 4	Homo sapiens	13-17
34733624-8	2021	Induction of CDK4 expression in a cell line derived from a patient with the BRAF V600E mutation resulted in partial resistance to dabrafenib.	dabrafenib	130-140	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	76-80
34350734-1	2021	BACKGROUND: Combination molecular targeted therapy with dabrafenib plus trametinib has been shown to improve progression-free survival and overall survival in patients with BRAF V600 mutated unresectable or metastatic melanoma.	dabrafenib	56-66	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	173-177
34350734-5	2021	CASE: A 37-year-old man diagnosed with metastatic melanoma (BRAF V600E mutation) who developed acute interstitial nephritis 5 years into his treatment with combination dabrafenib plus trametinib therapy.	dabrafenib	168-178	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	60-64
34484797-3	2021	Combination of BRAF-specific inhibitor dabrafenib and mitogen-activated protein kinase kinase (MEK) inhibitor trametinib is the standard treatment for BRAF V600E-mutated lung cancer.	dabrafenib	39-49	Braf transforming gene	Mus musculus	15-19
34484797-3	2021	Combination of BRAF-specific inhibitor dabrafenib and mitogen-activated protein kinase kinase (MEK) inhibitor trametinib is the standard treatment for BRAF V600E-mutated lung cancer.	dabrafenib	39-49	Braf transforming gene	Mus musculus	151-155
34504796-0	2021	Overall Survival of Patients With Unresectable or Metastatic BRAF V600-Mutant Acral/Cutaneous Melanoma Administered Dabrafenib Plus Trametinib: Long-Term Follow-Up of a Multicenter, Single-Arm Phase IIa Trial.	dabrafenib	116-126	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	61-65
34504796-1	2021	Objectives: To examine the long-term survival outcome of dabrafenib in combination with trametinib in Chinese patients with unresectable or metastatic acral/cutaneous melanoma with BRAF-V600 mutation and to explore potential predictors of effectiveness.	dabrafenib	57-67	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	181-185
34504796-2	2021	Methods: This was a long-term follow-up of Chinese patients with unresectable or metastatic BRAF V600-mutant acral/cutaneous melanoma administered dabrafenib (150 mg twice daily) plus trametinib (2 mg once daily) in an open-label, multicenter, single-arm, phase IIa study (NCT02083354).	dabrafenib	147-157	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	92-96
34193805-2	2021	We present a case where a 72-year-old woman with recurrent, metastatic BRAF-mutated melanoma developed a type I HSR to dabrafenib.	dabrafenib	119-129	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	71-75
34296750-2	2021	Since activating mutations in BRAF (B-Raf proto-oncogene, serine/threonine kinase) are highly oncogenic, BRAF inhibitors including dabrafenib have been developed for cancer.	dabrafenib	131-141	Braf transforming gene	Mus musculus	36-56
34296750-7	2021	In experiments with cardiomyocytes, cardiac fibroblasts and perfused rat hearts, dabrafenib inhibited ERK1/2 signalling.	dabrafenib	81-91	mitogen activated protein kinase 3	Rattus norvegicus	102-108
34296750-10	2021	In mice treated with 0.8 mg/kg/d angiotensin II (AngII) to induce hypertension, dabrafenib inhibited ERK1/2 signalling and suppressed cardiac hypertrophy in both acute (up to 7 d) and chronic (28 d) settings, preserving ejection fraction.	dabrafenib	80-90	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	33-47
34296750-10	2021	In mice treated with 0.8 mg/kg/d angiotensin II (AngII) to induce hypertension, dabrafenib inhibited ERK1/2 signalling and suppressed cardiac hypertrophy in both acute (up to 7 d) and chronic (28 d) settings, preserving ejection fraction.	dabrafenib	80-90	mitogen-activated protein kinase 3	Mus musculus	101-107
34296750-11	2021	At the cellular level, dabrafenib inhibited AngII-induced cardiomyocyte hypertrophy, reduced expression of hypertrophic gene markers and almost completely eliminated the increase in cardiac fibrosis both in interstitial and perivascular regions.	dabrafenib	23-33	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	44-49
34296750-14	2021	Thus, Raf is a potential therapeutic target for hypertensive heart disease and drugs such as dabrafenib, developed for cancer, may be used for this purpose.	dabrafenib	93-103	zinc fingers and homeoboxes 2	Mus musculus	6-9
34298852-6	2021	We showed that stable expression of PXR in 22Rv1 prostate cancer cells conferred a resistance to dasatinib and a higher sensitivity to erlotinib, dabrafenib, and afatinib.	dabrafenib	146-156	nuclear receptor subfamily 1 group I member 2	Homo sapiens	36-39
34278963-0	2021	Polymorphisms at site 469 of B-RAF protein associated with skin melanoma may be correlated with dabrafenib resistance: An in silico study.	dabrafenib	96-106	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	29-34
34466299-2	2021	BRAF inhibitor (dabrafenib) and MEK inhibitor (trametinib) are currently approved to treat NSCLC harboring the BRAF V600E mutation.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
34466299-2	2021	BRAF inhibitor (dabrafenib) and MEK inhibitor (trametinib) are currently approved to treat NSCLC harboring the BRAF V600E mutation.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	111-115
34466299-16	2021	Also, in the phase 2 clinical trial (BRF113928) of dabrafenib plus trametinib in patients with previously untreated BRAF V600E-mutant metastatic NSCLC, 3.2% of subjects developed a grade III or IV hemorrhage.	dabrafenib	51-61	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	116-120
34590045-0	2021	Durable Response to Combined Dabrafenib and Trametinib in a Patient With BRAF K601E Mutation-Positive Lung Adenocarcinoma: A Case Report.	dabrafenib	29-39	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	73-77
34225229-1	2021	BACKGROUND: Dabrafenib plus trametinib has demonstrated clinical benefit across multiple BRAF-mutant tumours, leading to approval for resected stage III and metastatic melanoma, non-small-cell lung cancer (NSCLC) and anaplastic thyroid cancer.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	89-93
34132225-2	2021	We present a case where a 72-year-old woman with recurrent, metastatic BRAF-mutated melanoma developed a type I HSR to dabrafenib.	dabrafenib	119-129	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	71-75
34178685-1	2021	BRAF mutations, primarily sensitizing mutations, such as BRAFV600E , have been proven to response to the BRAF inhibitor, Dabrafenib combined with trametinib therapy, but there have been no data demonstrating that it has activity against NSCLC-related brain metastases (BM).	dabrafenib	121-131	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
34178685-1	2021	BRAF mutations, primarily sensitizing mutations, such as BRAFV600E , have been proven to response to the BRAF inhibitor, Dabrafenib combined with trametinib therapy, but there have been no data demonstrating that it has activity against NSCLC-related brain metastases (BM).	dabrafenib	121-131	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	105-109
34178685-3	2021	Vemurafenib, another BRAF inhibitor, can reverse the resistance that develops with the BRAFS365L mutation following dabrafenib combined with trametentinib treatment in melanoma, but none has been reported in NSCLC.	dabrafenib	116-126	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	21-25
34201096-0	2021	Cost-Effectiveness Analysis of Dabrafenib Plus Trametinib and Vemurafenib as First-Line Treatment in Patients with BRAF V600 Mutation-Positive Unresectable or Metastatic Melanoma in China.	dabrafenib	31-41	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	115-119
34201096-1	2021	Objective: To evaluate the cost-effectiveness of dabrafenib plus trametinib combination therapy versus vemurafenib as first-line treatment in patients with BRAF V600 mutation-positive unresectable or metastatic melanoma from a healthcare system perspective in China.	dabrafenib	49-59	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	156-160
34092233-8	2021	Treatment with either dabrafenib and trametinib or with RGS, increased CD40+SOX10+ melanoma cells in the tumors of melanoma patients and patient-derived xenografts.	dabrafenib	22-32	CD40 molecule	Homo sapiens	71-75
34092233-8	2021	Treatment with either dabrafenib and trametinib or with RGS, increased CD40+SOX10+ melanoma cells in the tumors of melanoma patients and patient-derived xenografts.	dabrafenib	22-32	SRY-box transcription factor 10	Homo sapiens	76-81
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).	dabrafenib	145-155	zinc finger CCCH-type containing 13	Homo sapiens	56-62
34070224-1	2021	The dabrafenib plus trametinib (dab + tram) combination has demonstrated durable long-term efficacy in patients with BRAF V600-mutant metastatic melanoma.	dabrafenib	4-14	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	117-121
34308699-3	2021	In this article, we present the case of a patient with prior multiple sclerosis (MS) and who later developed metastatic malignant melanoma, had a marked increase of magnetic resonance imaging (MRI) findings after treatment with the combination of trametinib (MEK) and dabrafenib (BRAF), diagnostic question of metastatic disease versus new MS lesions without brain biopsy is discussed.	dabrafenib	268-278	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	280-284
34083237-11	2021	YUO-071 harboring an EGFR exon 19 deletion and a BRAF G464A mutation and the matching patient responded to dabrafenib/trametinib combination therapy.	dabrafenib	107-117	epidermal growth factor receptor	Homo sapiens	21-25
34072194-5	2021	In this study, we investigated in BRAFV600E mutated TC cell lines the effects of Vemurafenib and Dabrafenib, two BRAF inhibitors currently used in a clinical setting.	dabrafenib	97-107	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	113-117
34072194-9	2021	Our results suggest a possible mechanism of drug response to the BRAF inhibitors Vemurafenib or Dabrafenib, supporting very recent findings in TC patients treated with targeted therapies.	dabrafenib	96-106	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	65-69
34590045-1	2021	Targeted therapy with combined dabrafenib and trametinib has been proven to provide clinical benefits in patients with NSCLC with a BRAF V600E mutation.	dabrafenib	31-41	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	132-136
34590045-3	2021	Here, we present a patient with NSCLC with a BRAF K601E mutation, a class II BRAF mutation, who had a durable response to targeted therapy with combined dabrafenib and trametinib.	dabrafenib	153-163	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	45-49
34590045-3	2021	Here, we present a patient with NSCLC with a BRAF K601E mutation, a class II BRAF mutation, who had a durable response to targeted therapy with combined dabrafenib and trametinib.	dabrafenib	153-163	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	77-81
35436675-9	2022	Anti-BRAF was encorafenib for 21 patients, dabrafenib for 4 patients, with cetuximab for 24 patients and panitumumab for 1 patient.	dabrafenib	43-53	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	5-9
35377866-3	2022	This clinical trial investigated the use of combined BRAF-/MEK-inhibition with dabrafenib and trametinib plus hydroxychloroquine in patients with advanced BRAFV600 mutant melanoma who previously progressed on prior treatment with BRAF-/MEK-inhibitors and immune checkpoint inhibitors.	dabrafenib	79-89	mitogen-activated protein kinase kinase 7	Homo sapiens	59-62
35635528-3	2022	A 48-year-old man started dabrafenib/trametinib for stage IV BRAF-V600E mutated cutaneous melanoma.	dabrafenib	26-36	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	61-65
35594174-4	2022	EXPERIMENTAL DESIGN: In this prospective single-center two-arm phase-II study, patients received trametinib (BRAF-WT) or trametinib+dabrafenib (BRAF-MUT) for 21{plus minus}3 days.	dabrafenib	132-142	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	144-148
35598548-5	2022	CONCLUSIONS: The combination of a genetic analysis and computational simulation model may help predict the sensitivity for dabrafenib in cases with a rare BRAF compound mutation.	dabrafenib	123-133	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	155-159
35343921-1	2022	Dabrafenib is a BRAFkinase inhibitor approved for treatment of BRAF-mutated anaplastic thyroid carcinoma (ATC) in combination with trametinib.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	63-67
35343921-7	2022	First, we detected EGFR activation in dabrafenib resistant SW1736 cells using a phospho-receptor tyrosine kinase array.	dabrafenib	38-48	epidermal growth factor receptor	Homo sapiens	19-23
35343921-10	2022	The dabrafenib and erlotinib combination effectively inhibited phosphorylated (p)- MEK, p-ERK, and p-EGFR expressions compared with dabrafenib or erlotinib alone, while the dabrafenib and trametinib combination only inhibited p-MEK and p-ERK expressions.	dabrafenib	4-14	mitogen-activated protein kinase kinase 7	Homo sapiens	83-86
35343921-10	2022	The dabrafenib and erlotinib combination effectively inhibited phosphorylated (p)- MEK, p-ERK, and p-EGFR expressions compared with dabrafenib or erlotinib alone, while the dabrafenib and trametinib combination only inhibited p-MEK and p-ERK expressions.	dabrafenib	4-14	mitogen-activated protein kinase 1	Homo sapiens	90-93
35343921-10	2022	The dabrafenib and erlotinib combination effectively inhibited phosphorylated (p)- MEK, p-ERK, and p-EGFR expressions compared with dabrafenib or erlotinib alone, while the dabrafenib and trametinib combination only inhibited p-MEK and p-ERK expressions.	dabrafenib	4-14	epidermal growth factor receptor	Homo sapiens	101-105
35343921-10	2022	The dabrafenib and erlotinib combination effectively inhibited phosphorylated (p)- MEK, p-ERK, and p-EGFR expressions compared with dabrafenib or erlotinib alone, while the dabrafenib and trametinib combination only inhibited p-MEK and p-ERK expressions.	dabrafenib	4-14	mitogen-activated protein kinase kinase 7	Homo sapiens	228-231
35343921-10	2022	The dabrafenib and erlotinib combination effectively inhibited phosphorylated (p)- MEK, p-ERK, and p-EGFR expressions compared with dabrafenib or erlotinib alone, while the dabrafenib and trametinib combination only inhibited p-MEK and p-ERK expressions.	dabrafenib	4-14	mitogen-activated protein kinase 1	Homo sapiens	238-241
35343921-10	2022	The dabrafenib and erlotinib combination effectively inhibited phosphorylated (p)- MEK, p-ERK, and p-EGFR expressions compared with dabrafenib or erlotinib alone, while the dabrafenib and trametinib combination only inhibited p-MEK and p-ERK expressions.	dabrafenib	132-142	mitogen-activated protein kinase kinase 7	Homo sapiens	83-86
35343921-10	2022	The dabrafenib and erlotinib combination effectively inhibited phosphorylated (p)- MEK, p-ERK, and p-EGFR expressions compared with dabrafenib or erlotinib alone, while the dabrafenib and trametinib combination only inhibited p-MEK and p-ERK expressions.	dabrafenib	132-142	mitogen-activated protein kinase 1	Homo sapiens	90-93
35343921-10	2022	The dabrafenib and erlotinib combination effectively inhibited phosphorylated (p)- MEK, p-ERK, and p-EGFR expressions compared with dabrafenib or erlotinib alone, while the dabrafenib and trametinib combination only inhibited p-MEK and p-ERK expressions.	dabrafenib	132-142	epidermal growth factor receptor	Homo sapiens	101-105
35343921-10	2022	The dabrafenib and erlotinib combination effectively inhibited phosphorylated (p)- MEK, p-ERK, and p-EGFR expressions compared with dabrafenib or erlotinib alone, while the dabrafenib and trametinib combination only inhibited p-MEK and p-ERK expressions.	dabrafenib	173-183	epidermal growth factor receptor	Homo sapiens	101-105
35343921-10	2022	The dabrafenib and erlotinib combination effectively inhibited phosphorylated (p)- MEK, p-ERK, and p-EGFR expressions compared with dabrafenib or erlotinib alone, while the dabrafenib and trametinib combination only inhibited p-MEK and p-ERK expressions.	dabrafenib	173-183	mitogen-activated protein kinase kinase 7	Homo sapiens	228-231
35343921-10	2022	The dabrafenib and erlotinib combination effectively inhibited phosphorylated (p)- MEK, p-ERK, and p-EGFR expressions compared with dabrafenib or erlotinib alone, while the dabrafenib and trametinib combination only inhibited p-MEK and p-ERK expressions.	dabrafenib	173-183	mitogen-activated protein kinase 1	Homo sapiens	238-241
35343921-12	2022	The dabrafenib and erlotinib combination could be a potential novel treatment regimen to overcome drug resistance to dabrafenib alone in patients with BRAF-mutated ATC.	dabrafenib	4-14	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	151-155
35436118-0	2022	Binding of the B-Raf Inhibitors Dabrafenib and Vemurafenib to Human Serum Albumin: A Biophysical and Molecular Simulation Study.	dabrafenib	32-42	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	15-20
35067961-6	2022	MEASUREMENTS: Genetic work-up was completed, which prompted a recommendation for dual BRAF/MEK inhibition with dabrafenib and trametinib for tumors with BRAF V600E mutation.	dabrafenib	111-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	86-90
35067961-6	2022	MEASUREMENTS: Genetic work-up was completed, which prompted a recommendation for dual BRAF/MEK inhibition with dabrafenib and trametinib for tumors with BRAF V600E mutation.	dabrafenib	111-121	mitogen-activated protein kinase kinase 7	Homo sapiens	91-94
35067961-10	2022	Among patients that were BRAF V600E positive, both patients initiated urgent dabrafenib and trametinib dual tyrosine kinase inhibitor (TKI) therapy; with one patient demonstrating near complete clinical response allowing for post-treatment surgery, while the other demonstrated decreased tumor burden.	dabrafenib	77-87	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	25-29
35504360-2	2022	Patients with B-Raf proto-oncogene (BRAF) v600e mutated ATC who receive neoadjuvant Dabrafenib/Trametinib have improved rates of microscopically margin negative resection and durable locoregional control.	dabrafenib	84-94	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-34
35504360-2	2022	Patients with B-Raf proto-oncogene (BRAF) v600e mutated ATC who receive neoadjuvant Dabrafenib/Trametinib have improved rates of microscopically margin negative resection and durable locoregional control.	dabrafenib	84-94	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	36-40
35486732-4	2022	Results indicated that drug lipophilicity, plasma clearance, faster target dissociation, and, in particular, high albumin binding could limit dabrafenib action in visceral metastases compared to other KIs.	dabrafenib	142-152	albumin	Mus musculus	114-121
35486732-6	2022	Computational modeling identified a timed strategy for combining dabrafenib and encorafenib to better sustain BRAF inhibition, which showed enhanced efficacy in mice.	dabrafenib	65-75	Braf transforming gene	Mus musculus	110-114
35440004-8	2022	In BRAF-mut melanoma cells, SEMA6A coordinates actin cytoskeleton remodeling by the RhoA-dependent activation of YAP and dual BRAF/MEK inhibition by dabrafenib+trametinib induces SEMA6A/RhoA/YAP axis.	dabrafenib	149-159	semaphorin 6A	Homo sapiens	28-34
35440004-8	2022	In BRAF-mut melanoma cells, SEMA6A coordinates actin cytoskeleton remodeling by the RhoA-dependent activation of YAP and dual BRAF/MEK inhibition by dabrafenib+trametinib induces SEMA6A/RhoA/YAP axis.	dabrafenib	149-159	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	126-130
35440004-8	2022	In BRAF-mut melanoma cells, SEMA6A coordinates actin cytoskeleton remodeling by the RhoA-dependent activation of YAP and dual BRAF/MEK inhibition by dabrafenib+trametinib induces SEMA6A/RhoA/YAP axis.	dabrafenib	149-159	mitogen-activated protein kinase kinase 7	Homo sapiens	131-134
35440004-8	2022	In BRAF-mut melanoma cells, SEMA6A coordinates actin cytoskeleton remodeling by the RhoA-dependent activation of YAP and dual BRAF/MEK inhibition by dabrafenib+trametinib induces SEMA6A/RhoA/YAP axis.	dabrafenib	149-159	semaphorin 6A	Homo sapiens	179-185
35440004-8	2022	In BRAF-mut melanoma cells, SEMA6A coordinates actin cytoskeleton remodeling by the RhoA-dependent activation of YAP and dual BRAF/MEK inhibition by dabrafenib+trametinib induces SEMA6A/RhoA/YAP axis.	dabrafenib	149-159	ras homolog family member A	Homo sapiens	186-190
35440004-8	2022	In BRAF-mut melanoma cells, SEMA6A coordinates actin cytoskeleton remodeling by the RhoA-dependent activation of YAP and dual BRAF/MEK inhibition by dabrafenib+trametinib induces SEMA6A/RhoA/YAP axis.	dabrafenib	149-159	Yes1 associated transcriptional regulator	Homo sapiens	191-194
35440004-10	2022	Finally, in BRAF-mut melanoma patients treated with dabrafenib+trametinib, high SEMA6A predicts shorter recurrence-free interval.	dabrafenib	52-62	semaphorin 6A	Homo sapiens	80-86
35396243-4	2022	Here we describe a very good partial response and possible mechanisms of resistance to a combination of the BRAF inhibitor dabrafenib and the MEK inhibitor trametinib in a patient with BRAF V600E-mutant refractory MM.	dabrafenib	123-133	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	108-112
35147853-0	2022	Prediction of Drug-Drug Interaction Between Dabrafenib and Irinotecan via UGT1A1-Mediated Glucuronidation.	dabrafenib	44-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
35147853-6	2022	RESULTS: Dabrafenib noncompetitively inhibited SN-38 glucuronidation in pooled HLMs and recombinant UGT1A1 with unbound inhibitor constant (Ki,u) values of 12.43 +- 0.28 and 3.89 +- 0.40 muM, respectively.	dabrafenib	9-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
35147853-8	2022	However, the ratios of intra-enterocyte concentration of dabrafenib to Ki,u ((I)gut/Ki,u) are 2.73 and 8.72 in HLMs and recombinant UGT1A1, respectively, indicating a high risk of intestinal DDI when dabrafenib was used in combination with irinotecan.	dabrafenib	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	132-138
35147853-9	2022	CONCLUSION: Dabrafenib is a potent noncompetitive inhibitor of UGT1A1 and may bring potential risk of DDI when combined with irinotecan.	dabrafenib	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
35143639-4	2022	Furthermore, blockade of the mutant BRAF-V600E kinase (the pathogenetic hallmark of HCL) through orally available specific inhibitors (vemurafenib or dabrafenib) effaces the peculiar morphologic, phenotypic and molecular identity of this disease as well as its typical anti-apoptotic behaviour, and is emerging as an attractive chemotherapy-free strategy in various clinical scenarios.	dabrafenib	150-160	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	36-40
35143639-6	2022	Other treatments explored in clinical trials are BTK inhibition with ibrutinib and co-inhibition of BRAF (through dabrafenib or vemurafenib) and its downstream target MEK (through trametinib or cobimetinib).	dabrafenib	114-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	100-104
35379272-4	2022	We further analyzed the difference in treatment outcomes between second-line chemotherapy (cytarabine and cladribine) and targeted therapy (dabrafenib) for BRAF-V600E-positive patients.	dabrafenib	140-150	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	156-160
35379272-8	2022	BRAF-V600E-mutant patients treated with dabrafenib had prompt resolution of MAS-HLH signs and symptoms with less toxicity than second-line chemotherapy.	dabrafenib	40-50	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
35379272-11	2022	The BRAF inhibitor dabrafenib provides a promising treatment option for LCH with MAS-HLH.	dabrafenib	19-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-8
35454350-1	2022	Dabrafenib and trametinib are two available molecules that have been approved for the treatment of metastatic melanoma with BRAF-V600E or V600K mutations.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	124-128
35454350-4	2022	We report the case of a 71-year-old female patient with metastatic melanoma harboring a BRAF-V600E mutation undergoing targeted therapy with dabrafenib and trametinib.	dabrafenib	141-151	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	88-92
35372088-0	2022	Durable Response of Dabrafenib, Trametinib, and Capmatinib in an NSCLC Patient With Co-Existing BRAF-KIAA1549 Fusion and MET Amplification: A Case Report.	dabrafenib	20-30	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	96-100
35372088-0	2022	Durable Response of Dabrafenib, Trametinib, and Capmatinib in an NSCLC Patient With Co-Existing BRAF-KIAA1549 Fusion and MET Amplification: A Case Report.	dabrafenib	20-30	KIAA1549	Homo sapiens	101-109
35022320-0	2022	BAMM (BRAF Autophagy and MEK inhibition in Melanoma): A phase I/II trial of dabrafenib, trametinib and hydroxychloroquine in advanced BRAFV600-mutant melanoma.	dabrafenib	76-86	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	6-10
35022320-0	2022	BAMM (BRAF Autophagy and MEK inhibition in Melanoma): A phase I/II trial of dabrafenib, trametinib and hydroxychloroquine in advanced BRAFV600-mutant melanoma.	dabrafenib	76-86	mitogen-activated protein kinase kinase 7	Homo sapiens	25-28
35436118-0	2022	Binding of the B-Raf Inhibitors Dabrafenib and Vemurafenib to Human Serum Albumin: A Biophysical and Molecular Simulation Study.	dabrafenib	32-42	albumin	Homo sapiens	68-81
35171900-6	2022	Another BRAF inhibitor, dabrafenib, has been used in some cases as a single agent and was associated with a lower toxicity profile.	dabrafenib	24-34	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	8-12
35242981-0	2022	Impressive and durable clinical responses obtained with dabrafenib and trametinib in low-grade serous ovarian cancer harbouring a BRAF V600E mutation.	dabrafenib	56-66	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	130-134
35242981-4	2022	Here we present a case report of two patients with a BRAF V600E mutation that achieved sustained clinical responses with combination treatment with dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor).	dabrafenib	148-158	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	53-57
35242981-4	2022	Here we present a case report of two patients with a BRAF V600E mutation that achieved sustained clinical responses with combination treatment with dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor).	dabrafenib	148-158	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	160-164
35156519-3	2022	Here we highlight the results of a recently published single-arm phase I/II multi-institution trial of dabrafenib, trametinib, and the autophagy inhibitor HCQ (the BAMM trial) that established the safety and activity of this regimen in BRAF V600-mutant melanoma patients.	dabrafenib	103-113	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	236-240
35224961-1	2022	BACKGROUND: Dabrafenib+Trametinib/Dabrafenib targeted therapy has been approved for V-RAF murine sarcoma viral oncogene homolog B1 with amino acid substitution for valine at position 600 (BRAF V600E) in lung cancer patients, however, the targeted therapy strategy for lung cancer patients with BRAF non-V600E mutations has not been determined yet.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	84-130
35224961-1	2022	BACKGROUND: Dabrafenib+Trametinib/Dabrafenib targeted therapy has been approved for V-RAF murine sarcoma viral oncogene homolog B1 with amino acid substitution for valine at position 600 (BRAF V600E) in lung cancer patients, however, the targeted therapy strategy for lung cancer patients with BRAF non-V600E mutations has not been determined yet.	dabrafenib	34-44	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	84-130
35224961-1	2022	BACKGROUND: Dabrafenib+Trametinib/Dabrafenib targeted therapy has been approved for V-RAF murine sarcoma viral oncogene homolog B1 with amino acid substitution for valine at position 600 (BRAF V600E) in lung cancer patients, however, the targeted therapy strategy for lung cancer patients with BRAF non-V600E mutations has not been determined yet.	dabrafenib	34-44	Braf transforming gene	Mus musculus	188-192
35224961-1	2022	BACKGROUND: Dabrafenib+Trametinib/Dabrafenib targeted therapy has been approved for V-RAF murine sarcoma viral oncogene homolog B1 with amino acid substitution for valine at position 600 (BRAF V600E) in lung cancer patients, however, the targeted therapy strategy for lung cancer patients with BRAF non-V600E mutations has not been determined yet.	dabrafenib	34-44	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	294-298
34619701-2	2022	BRAF inhibitor-targeted therapies are also indicated in stage IV BRAF-mutant melanoma, especially dabrafenib and trametinib in combination.	dabrafenib	98-108	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
35214043-1	2022	Dabrafenib inhibits the cell proliferation of metastatic melanoma with the oncogenic BRAF(V600)-mutation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	85-89
35214043-2	2022	However, dabrafenib monotherapy is associated with pERK reactivation, drug resistance, and consequential relapse.	dabrafenib	9-19	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	51-55
35214043-3	2022	A clinical drug-dose determination study shows increased pERK levels upon daily administration of more than 300 mg dabrafenib.	dabrafenib	115-125	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	57-61
35155453-3	2021	Case Presentation: A 49-year-old man with recurrent craniopharyngioma, harboring BRAF V600E mutation, has been treated with targeted therapy based on a combination of a BRAF-inhibitor, dabrafenib (150 mg, orally two times daily), and a MEK-inhibitor, trametinib (2 mg, orally two times daily).	dabrafenib	185-195	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	81-85
35155453-8	2021	The discovery of the BRAF V600E mutation in patients with PCP is very rare, resulting in a lack of data on the efficacy of the combination of dabrafenib and trametinib.	dabrafenib	142-152	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	21-25
35072623-9	2022	We hypothesized that dual-targeted therapy with a BRAF inhibitor, dabrafenib, and a MEK inhibitor, trametinib, might prevent the regeneration and proliferation of fibrotic epithelium in lung disease by blocking downstream proliferative signals.	dabrafenib	66-76	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	50-54
33932130-1	2021	Dabrafenib is an oral BRAF kinase inhibitor approved for the treatment of various BRAF V600 mutation-positive solid tumors.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	22-26
34986718-5	2022	Other tested B-Raf inhibitors, both type-I (dabrafenib and encorafenib) and type-II (RAF265 and AZ628), also exhibited potent therapeutic effects on SM-exposed HaCaT cells.	dabrafenib	44-54	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	13-18
35169097-6	2022	Several case reports have illustrated dramatic response of the residual or recurrent papillary craniopharyngioma to molecularly targeted therapy with a BRAF inhibitor(vemurafenib or dabrafenib)and a MEK inhibitor(trametinib), which are currently approved for melanoma and non-small cell lung carcinoma.	dabrafenib	182-192	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	152-156
33866515-9	2021	If the BRAF mutation status is positive, the combination of dabrafenib and trametinib could be an option to consider.	dabrafenib	60-70	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	7-11
34018641-8	2021	Immunohistochemical examination showed higher expression of EphA2, p-EphA2, and EGFR in the melanoma cells after dabrafenib plus trametinib therapy as compared with that before therapy.	dabrafenib	113-123	EPH receptor A2	Homo sapiens	60-65
34018641-8	2021	Immunohistochemical examination showed higher expression of EphA2, p-EphA2, and EGFR in the melanoma cells after dabrafenib plus trametinib therapy as compared with that before therapy.	dabrafenib	113-123	EPH receptor A2	Homo sapiens	69-74
34018641-8	2021	Immunohistochemical examination showed higher expression of EphA2, p-EphA2, and EGFR in the melanoma cells after dabrafenib plus trametinib therapy as compared with that before therapy.	dabrafenib	113-123	epidermal growth factor receptor	Homo sapiens	80-84
34636352-7	2022	The combination of the BRAF inhibitor dabrafenib and the mitogen-activated protein kinase kinase inhibitor trametinib has shown remarkable results in clinical trials of patients with BRAF-mutated ATCs.	dabrafenib	38-48	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	23-27
34636352-7	2022	The combination of the BRAF inhibitor dabrafenib and the mitogen-activated protein kinase kinase inhibitor trametinib has shown remarkable results in clinical trials of patients with BRAF-mutated ATCs.	dabrafenib	38-48	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	183-187
34023984-0	2021	Gastrointestinal perforation following dabrafenib and trametinib administration in non-small cell lung carcinoma with BRAF V600E mutation: a case report and literature review.	dabrafenib	39-49	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	118-122
34023984-3	2021	A 62-year-old man with non-small cell lung cancer harboring BRAF V600E mutation was treated with dabrafenib and trametinib.	dabrafenib	97-107	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	60-64
34009099-1	2021	Purpose: To report a case of BRAF/MEK inhibitor-associated multifocal choroiditis that recurred after medication re-exposure and resolved after discontinuing BRAF/MEK inhibition and administering local steroid therapy.Case Report: A 32-year-old woman with metastatic cutaneous melanoma on dabrafenib/trametinib presented with bilateral anterior uveitis and new bilateral multifocal chorioretinal scars.	dabrafenib	289-299	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	29-33
34009099-1	2021	Purpose: To report a case of BRAF/MEK inhibitor-associated multifocal choroiditis that recurred after medication re-exposure and resolved after discontinuing BRAF/MEK inhibition and administering local steroid therapy.Case Report: A 32-year-old woman with metastatic cutaneous melanoma on dabrafenib/trametinib presented with bilateral anterior uveitis and new bilateral multifocal chorioretinal scars.	dabrafenib	289-299	mitogen-activated protein kinase kinase 7	Homo sapiens	34-37
34009099-1	2021	Purpose: To report a case of BRAF/MEK inhibitor-associated multifocal choroiditis that recurred after medication re-exposure and resolved after discontinuing BRAF/MEK inhibition and administering local steroid therapy.Case Report: A 32-year-old woman with metastatic cutaneous melanoma on dabrafenib/trametinib presented with bilateral anterior uveitis and new bilateral multifocal chorioretinal scars.	dabrafenib	289-299	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	158-162
34009099-1	2021	Purpose: To report a case of BRAF/MEK inhibitor-associated multifocal choroiditis that recurred after medication re-exposure and resolved after discontinuing BRAF/MEK inhibition and administering local steroid therapy.Case Report: A 32-year-old woman with metastatic cutaneous melanoma on dabrafenib/trametinib presented with bilateral anterior uveitis and new bilateral multifocal chorioretinal scars.	dabrafenib	289-299	mitogen-activated protein kinase kinase 7	Homo sapiens	163-166
33932130-6	2021	Exposure of drugs that are CYP3A4 substrates is likely to decrease when coadministered with dabrafenib.	dabrafenib	92-102	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	27-33
33159968-1	2021	Targeted BRAF(V600E) suppression by selective BRAF inhibitors (BRAFi"s, e.g. vemurafenib and dabrafenib) has led to a sea change in the treatment of metastatic melanoma (Long et al.	dabrafenib	93-103	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-14
33159968-1	2021	Targeted BRAF(V600E) suppression by selective BRAF inhibitors (BRAFi"s, e.g. vemurafenib and dabrafenib) has led to a sea change in the treatment of metastatic melanoma (Long et al.	dabrafenib	93-103	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
33883692-2	2021	In this study, we reported the identification of LIM domain kinase 1 (LIMK1) as a promoter of gastric cancer peritoneal metastasis, and its potential to be a therapeutic target of dabrafenib (DAB).	dabrafenib	180-190	LIM domain kinase 1	Homo sapiens	49-68
33883692-2	2021	In this study, we reported the identification of LIM domain kinase 1 (LIMK1) as a promoter of gastric cancer peritoneal metastasis, and its potential to be a therapeutic target of dabrafenib (DAB).	dabrafenib	180-190	LIM domain kinase 1	Homo sapiens	70-75
33883692-2	2021	In this study, we reported the identification of LIM domain kinase 1 (LIMK1) as a promoter of gastric cancer peritoneal metastasis, and its potential to be a therapeutic target of dabrafenib (DAB).	dabrafenib	192-195	LIM domain kinase 1	Homo sapiens	49-68
33883692-2	2021	In this study, we reported the identification of LIM domain kinase 1 (LIMK1) as a promoter of gastric cancer peritoneal metastasis, and its potential to be a therapeutic target of dabrafenib (DAB).	dabrafenib	192-195	LIM domain kinase 1	Homo sapiens	70-75
33883692-7	2021	Dabrafenib, a small molecule targeting LIMK1, was found to decrease cell migration and invasion of gastric cancer cells in vitro and abolish peritoneal and liver metastasis formation in vivo.	dabrafenib	0-10	LIM-domain containing, protein kinase	Mus musculus	39-44
33883692-8	2021	Mechanistically, either LIMK1 knockout or Dabrafenib inhibited LIMK1 expression and phosphorylation of its downstream target cofilin.	dabrafenib	42-52	LIM-domain containing, protein kinase	Mus musculus	63-68
33883692-8	2021	Mechanistically, either LIMK1 knockout or Dabrafenib inhibited LIMK1 expression and phosphorylation of its downstream target cofilin.	dabrafenib	42-52	cofilin 1	Homo sapiens	125-132
33883692-9	2021	Taken together, our results demonstrated that LIMK1 functions as a metastasis promoter in gastric cancer by inhibiting LIMK1-p-cofilin and that Dabrafenib has the potential to serve as a novel treatment for gastric cancer peritoneal metastasis.	dabrafenib	144-154	cofilin 1	Homo sapiens	127-134
33932130-1	2021	Dabrafenib is an oral BRAF kinase inhibitor approved for the treatment of various BRAF V600 mutation-positive solid tumors.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	82-86
33921947-0	2021	A Phase 2 Clinical Trial of Trametinib and Low-Dose Dabrafenib in Patients with Advanced Pretreated NRASQ61R/K/L Mutant Melanoma (TraMel-WT).	dabrafenib	52-62	NRAS proto-oncogene, GTPase	Homo sapiens	100-104
33921947-13	2021	CONCLUSIONS: Combining full-dose trametinib with low-dose dabrafenib can mitigate MEK-inhibitor-related skin toxicity but was insufficiently active in this patient population.	dabrafenib	58-68	mitogen-activated protein kinase kinase 7	Homo sapiens	82-85
33637608-0	2021	Clinical response to dabrafenib plus trametinib in a pediatric ganglioglioma with BRAF p.T599dup mutation.	dabrafenib	21-31	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	82-86
33637608-3	2021	This patient, based on our initial finding, is receiving combination targeted therapy with a selective BRAF inhibitor (dabrafenib) plus MEK inhibitor (trametinib).	dabrafenib	119-129	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	103-107
33637608-6	2021	Although combinatorial therapy targeting BRAF and MEK using dabrafenib and trametinib, respectively, is indicated for tumors harboring a BRAF p.V600E/K mutation, our report demonstrates efficacy of this combination in a non-V600E BRAF-mutated tumor.	dabrafenib	60-70	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	41-45
33637608-6	2021	Although combinatorial therapy targeting BRAF and MEK using dabrafenib and trametinib, respectively, is indicated for tumors harboring a BRAF p.V600E/K mutation, our report demonstrates efficacy of this combination in a non-V600E BRAF-mutated tumor.	dabrafenib	60-70	mitogen-activated protein kinase kinase 7	Homo sapiens	50-53
33637608-6	2021	Although combinatorial therapy targeting BRAF and MEK using dabrafenib and trametinib, respectively, is indicated for tumors harboring a BRAF p.V600E/K mutation, our report demonstrates efficacy of this combination in a non-V600E BRAF-mutated tumor.	dabrafenib	60-70	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	137-141
33637608-6	2021	Although combinatorial therapy targeting BRAF and MEK using dabrafenib and trametinib, respectively, is indicated for tumors harboring a BRAF p.V600E/K mutation, our report demonstrates efficacy of this combination in a non-V600E BRAF-mutated tumor.	dabrafenib	60-70	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	137-141
33898322-1	2021	We defined the lethal interaction between the novel therapeutic GZ17-6.02 and the standard of care combination of the MEK1/2 inhibitor trametinib and the B-RAF inhibitor dabrafenib in PDX isolates of cutaneous melanoma expressing a mutant B-RAF V600E protein.	dabrafenib	170-180	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	154-159
33917810-4	2021	The results indicated that dabrafenib inhibited ERK phosphorylation and enhanced ErbB2 autophosphorylation and Akt phosphorylation, and the effects of dabrafenib on ErbB2 and Akt phosphorylation were phenocopied by pharmacological inhibition of the MEK-ERK signaling pathway.	dabrafenib	151-161	erb-b2 receptor tyrosine kinase 2	Homo sapiens	165-170
33917810-0	2021	Dabrafenib Promotes Schwann Cell Differentiation by Inhibition of the MEK-ERK Pathway.	dabrafenib	0-10	mitogen-activated protein kinase kinase 7	Homo sapiens	70-73
33917810-0	2021	Dabrafenib Promotes Schwann Cell Differentiation by Inhibition of the MEK-ERK Pathway.	dabrafenib	0-10	mitogen-activated protein kinase 1	Homo sapiens	74-77
33917810-4	2021	The results indicated that dabrafenib inhibited ERK phosphorylation and enhanced ErbB2 autophosphorylation and Akt phosphorylation, and the effects of dabrafenib on ErbB2 and Akt phosphorylation were phenocopied by pharmacological inhibition of the MEK-ERK signaling pathway.	dabrafenib	27-37	mitogen-activated protein kinase 1	Homo sapiens	48-51
33917810-4	2021	The results indicated that dabrafenib inhibited ERK phosphorylation and enhanced ErbB2 autophosphorylation and Akt phosphorylation, and the effects of dabrafenib on ErbB2 and Akt phosphorylation were phenocopied by pharmacological inhibition of the MEK-ERK signaling pathway.	dabrafenib	27-37	erb-b2 receptor tyrosine kinase 2	Homo sapiens	81-86
33917810-4	2021	The results indicated that dabrafenib inhibited ERK phosphorylation and enhanced ErbB2 autophosphorylation and Akt phosphorylation, and the effects of dabrafenib on ErbB2 and Akt phosphorylation were phenocopied by pharmacological inhibition of the MEK-ERK signaling pathway.	dabrafenib	27-37	AKT serine/threonine kinase 1	Homo sapiens	111-114
33917810-4	2021	The results indicated that dabrafenib inhibited ERK phosphorylation and enhanced ErbB2 autophosphorylation and Akt phosphorylation, and the effects of dabrafenib on ErbB2 and Akt phosphorylation were phenocopied by pharmacological inhibition of the MEK-ERK signaling pathway.	dabrafenib	27-37	mitogen-activated protein kinase kinase 7	Homo sapiens	249-252
33917810-4	2021	The results indicated that dabrafenib inhibited ERK phosphorylation and enhanced ErbB2 autophosphorylation and Akt phosphorylation, and the effects of dabrafenib on ErbB2 and Akt phosphorylation were phenocopied by pharmacological inhibition of the MEK-ERK signaling pathway.	dabrafenib	27-37	mitogen-activated protein kinase 1	Homo sapiens	253-256
33872566-6	2021	Per American Joint Commission Cancer staging, BRAF mutant targeted therapy (dabrafenib) was initiated.	dabrafenib	76-86	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	46-50
34009754-5	2021	In particular, targeted therapy with dabrafenib and trametinib is indicated as first-line therapy for BRAF V600E-mutated ATC.	dabrafenib	37-47	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	102-106
33127167-5	2021	CASE PRESENTATION: We herein report the rechallenge of a 52-year-old ATC patient with BRAF V600E mutation with dabrafenib plus trametinib.	dabrafenib	111-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	86-90
33127167-9	2021	We want to emphasize that combination of dabrafenib and trametinib might be a good choice for resistant locoregional and metastatic ATC patients with BRAF V600E mutation, particularly in whom rapid clinical response is urgently needed.	dabrafenib	41-51	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	150-154
33211390-0	2021	Comment on: Response to the BRAF/MEK inhibitors dabrafenib/trametinib in an adolescent with a BRAF V600E mutated anaplastic ganglioglioma intolerant to vemurafenib.	dabrafenib	48-58	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	28-32
33211390-0	2021	Comment on: Response to the BRAF/MEK inhibitors dabrafenib/trametinib in an adolescent with a BRAF V600E mutated anaplastic ganglioglioma intolerant to vemurafenib.	dabrafenib	48-58	mitogen-activated protein kinase kinase 7	Homo sapiens	33-36
33211390-0	2021	Comment on: Response to the BRAF/MEK inhibitors dabrafenib/trametinib in an adolescent with a BRAF V600E mutated anaplastic ganglioglioma intolerant to vemurafenib.	dabrafenib	48-58	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	94-98
33731847-0	2021	Safety and efficacy of the BRAF inhibitor dabrafenib in relapsed or refractory hairy cell leukemia: a pilot phase-2 clinical trial.	dabrafenib	42-52	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	27-31
33917810-4	2021	The results indicated that dabrafenib inhibited ERK phosphorylation and enhanced ErbB2 autophosphorylation and Akt phosphorylation, and the effects of dabrafenib on ErbB2 and Akt phosphorylation were phenocopied by pharmacological inhibition of the MEK-ERK signaling pathway.	dabrafenib	151-161	AKT serine/threonine kinase 1	Homo sapiens	175-178
33917810-7	2021	These results suggest that the ErbB2-PI3K-Akt axis is required for the induction of Schwann cell differentiation by dabrafenib in vitro.	dabrafenib	116-126	erb-b2 receptor tyrosine kinase 2	Homo sapiens	31-36
33917810-7	2021	These results suggest that the ErbB2-PI3K-Akt axis is required for the induction of Schwann cell differentiation by dabrafenib in vitro.	dabrafenib	116-126	AKT serine/threonine kinase 1	Homo sapiens	42-45
33936664-2	2021	The patient was treated with a BRAF/MEK inhibitor combination therapy (dabrafenib/trametinib), which was demonstrated to be effective and well-tolerated.	dabrafenib	71-81	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	31-35
33936664-2	2021	The patient was treated with a BRAF/MEK inhibitor combination therapy (dabrafenib/trametinib), which was demonstrated to be effective and well-tolerated.	dabrafenib	71-81	mitogen-activated protein kinase kinase 7	Homo sapiens	36-39
33788730-1	2021	BACKGROUND/AIM: Despite clinical benefit from treatment with dabrafenib and trametinib in melanoma patients with BRAF mutations, half relapse within months and one-third are unresponsive to treatment.	dabrafenib	61-71	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	113-117
33399314-4	2021	RECENT FINDINGS: Vemurafenib, dabrafenib and encorafenib are designed to block mutated forms of BRAF, which cause abnormal signalling inside cancer cells leading to tumour growth.	dabrafenib	30-40	Braf transforming gene	Mus musculus	96-100
33641072-2	2021	Specific BRAF-targeted therapies, such as vemurafenib, dabrafenib, and encorafenib, have transformed treatment of many BRAF-mutated cancers, producing meaningful clinical benefit with more tolerable safety profiles compared to prior standard-of-care treatments.	dabrafenib	55-65	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
33641072-2	2021	Specific BRAF-targeted therapies, such as vemurafenib, dabrafenib, and encorafenib, have transformed treatment of many BRAF-mutated cancers, producing meaningful clinical benefit with more tolerable safety profiles compared to prior standard-of-care treatments.	dabrafenib	55-65	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	119-123
33669326-6	2021	In this setting the dual BRAF and MEK inhibition resulted in improved progression-free survival and quality of life; Case 2: The second case shows aBRAF G466A mutated Bellini duct carcinoma (BDC), treated with dabrafenib and trametinib in second line therapy.	dabrafenib	210-220	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	25-29
32971203-2	2021	In this study, PD-L1 inhibition therapy and BRAF-targeted therapy, which showed clinical benefit, were combined in a CXCR4-targeted nanoparticle co-delivering dabrafenib (Dab), a BRAF inhibitor, and miR-200c which can down-regulate PD-L1 expression.	dabrafenib	159-169	C-X-C motif chemokine receptor 4	Homo sapiens	117-122
32971203-2	2021	In this study, PD-L1 inhibition therapy and BRAF-targeted therapy, which showed clinical benefit, were combined in a CXCR4-targeted nanoparticle co-delivering dabrafenib (Dab), a BRAF inhibitor, and miR-200c which can down-regulate PD-L1 expression.	dabrafenib	159-169	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	179-183
32971203-2	2021	In this study, PD-L1 inhibition therapy and BRAF-targeted therapy, which showed clinical benefit, were combined in a CXCR4-targeted nanoparticle co-delivering dabrafenib (Dab), a BRAF inhibitor, and miR-200c which can down-regulate PD-L1 expression.	dabrafenib	171-174	C-X-C motif chemokine receptor 4	Homo sapiens	117-122
32971203-5	2021	In addition, the presence of LY2510924 peptide would enhance the binding affinity of miR@PCL-PEI/Dab@PGA-pep NPs to cancer cells, leading to improved cellular uptake, cytotoxicity, and in vivo accumulation into tumor area.	dabrafenib	97-100	membrane associated ring-CH-type finger 8	Homo sapiens	85-88
33580193-0	2021	Impressive response to dabrafenib, trametinib, and osimertinib in a metastatic EGFR-mutant/BRAF V600E lung adenocarcinoma patient.	dabrafenib	23-33	epidermal growth factor receptor	Homo sapiens	79-83
33580193-0	2021	Impressive response to dabrafenib, trametinib, and osimertinib in a metastatic EGFR-mutant/BRAF V600E lung adenocarcinoma patient.	dabrafenib	23-33	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	91-95
33580193-4	2021	We report a case of impressive radiological and ctDNA response under dabrafenib, trametinib, and osimertinib in an advanced EGFR-mutant lung adenocarcinoma patient who developed BRAF V600E as one of the acquired resistance mechanisms to second-line osimertinib.	dabrafenib	69-79	epidermal growth factor receptor	Homo sapiens	124-128
33580193-4	2021	We report a case of impressive radiological and ctDNA response under dabrafenib, trametinib, and osimertinib in an advanced EGFR-mutant lung adenocarcinoma patient who developed BRAF V600E as one of the acquired resistance mechanisms to second-line osimertinib.	dabrafenib	69-79	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	178-182
33670365-5	2021	Re-establishment of miR-181a/b expression reverses the resistance of melanoma cells to the BRAF inhibitor dabrafenib.	dabrafenib	106-116	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	91-95
33670365-8	2021	Collectively, our study demonstrated that miR-181a/b could reverse the resistance to BRAF inhibitors in dabrafenib resistant melanoma cell lines.	dabrafenib	104-114	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	85-89
33557011-11	2021	BRAF inhibitors (Dabrafenib and Vemurafenib), however, show higher overall survival and tumour response in BRAF V600E mutated pLGGs than conventional therapies in some studies.	dabrafenib	17-27	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
33557011-11	2021	BRAF inhibitors (Dabrafenib and Vemurafenib), however, show higher overall survival and tumour response in BRAF V600E mutated pLGGs than conventional therapies in some studies.	dabrafenib	17-27	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	107-111
33759774-4	2021	More recently, the standard of care has changed in favor of nivolumab and pembrolizumab and BRAF-MEK inhibitors dabrafenib plus trametinib (for BRAF mutated melanoma), based on significant RFS benefits and more favorable toxicity profiles.	dabrafenib	112-122	mitogen-activated protein kinase kinase 7	Homo sapiens	97-100
33461766-3	2021	Here we present the case of a young female with BRAF V600E-mutant eGBM who had a prolonged response to targeted therapy with the BRAF and MEK1/2 inhibitors dabrafenib and trametinib.	dabrafenib	156-166	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	48-52
33461766-3	2021	Here we present the case of a young female with BRAF V600E-mutant eGBM who had a prolonged response to targeted therapy with the BRAF and MEK1/2 inhibitors dabrafenib and trametinib.	dabrafenib	156-166	mitogen-activated protein kinase kinase 1	Homo sapiens	138-144
33669326-6	2021	In this setting the dual BRAF and MEK inhibition resulted in improved progression-free survival and quality of life; Case 2: The second case shows aBRAF G466A mutated Bellini duct carcinoma (BDC), treated with dabrafenib and trametinib in second line therapy.	dabrafenib	210-220	mitogen-activated protein kinase kinase 7	Homo sapiens	34-37
33669326-9	2021	The VE-BASKET and ROAR basket trials explored the efficacy of vemurafenib and the combination of dabrafenib/trametinib, respectively, in BRAF V600 mutation-positive cancers other than melanoma, papillary thyroid cancer, colorectal cancer and non small cell lung cancer.	dabrafenib	97-107	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	137-141
33190370-0	2021	Serum soluble CD163 and proinflammatory chemokines may be biomarkers of the onset of adverse events in dabrafenib plus trametinib combination therapy for advanced melanoma.	dabrafenib	103-113	CD163 molecule	Homo sapiens	14-19
33193858-2	2020	Although the selective B-Raf oncogene serine/threonine-kinase (BRAF) inhibitors, dabrafenib and vemurafenib, have been approved for the treatment of BRAF-mutant metastatic melanoma, the 5-year survival rate remains unfavorable due to acquired therapy resistance.	dabrafenib	81-91	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	149-153
33456727-2	2020	Two recent studies led to the registration of dabrafenib and trametinib as targeted therapies for BRAF-mutated melanoma, and of immunotherapy with nivolumab irrespective of BRAF-mutation status.	dabrafenib	46-56	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	98-102
33334695-0	2021	Combination therapy of dabrafenib plus trametinib in patients with BRAFV600E-mutated biliary tract cancer.	dabrafenib	23-33	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	67-71
33276639-0	2020	Efficacy of Dabrafenib Plus Trametinib Combination in Patients with BRAF V600E-Mutant NSCLC in Real-World Setting: GFPC 01-2019.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	68-72
33276639-1	2020	Dabrafenib plus trametinib combination is approved in Europe for BRAF V600E-mutant metastatic non-small-cell lung cancer (NSCLC).	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	65-69
33276639-7	2020	In conclusion, these results suggest that efficacy and safety of dabrafenib plus trametinib combination in patients with BRAF V600E metastatic NSCLC are comparable in a real-world setting and in clinical trials for both previously untreated and treated patients.	dabrafenib	65-75	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	121-125
33285519-7	2020	We report the successful use of dabrafenib (BRAF inhibitor) and trametinib (mitogen-activated protein kinase kinase inhibitor) in the neoadjuvant setting followed by definitive stereotactic radiosurgery.	dabrafenib	32-42	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	44-48
33268358-3	2020	Dabrafenib and six additional kinase inhibitors in the BRAF/MEK/ERK cellular pathway mitigated cisplatin-induced hair cell death in the cell line and mouse cochlear explants.	dabrafenib	0-10	Braf transforming gene	Mus musculus	55-59
33268358-3	2020	Dabrafenib and six additional kinase inhibitors in the BRAF/MEK/ERK cellular pathway mitigated cisplatin-induced hair cell death in the cell line and mouse cochlear explants.	dabrafenib	0-10	midkine	Mus musculus	60-63
33268358-3	2020	Dabrafenib and six additional kinase inhibitors in the BRAF/MEK/ERK cellular pathway mitigated cisplatin-induced hair cell death in the cell line and mouse cochlear explants.	dabrafenib	0-10	mitogen-activated protein kinase 1	Mus musculus	64-67
33268358-4	2020	In adult mice, oral delivery of dabrafenib repressed ERK phosphorylation in cochlear cells, and protected from cisplatin- and noise-induced hearing loss.	dabrafenib	32-42	mitogen-activated protein kinase 1	Mus musculus	53-56
33254249-5	2020	Recently, the PD-1 inhibitor Nivolumab and Pembrolizumab as well as the BRAF/MEK inhibitor Dabrafenib and Trametinib were approved for the adjuvant therapy of stage III malignant melanoma.	dabrafenib	91-101	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	72-76
33254249-5	2020	Recently, the PD-1 inhibitor Nivolumab and Pembrolizumab as well as the BRAF/MEK inhibitor Dabrafenib and Trametinib were approved for the adjuvant therapy of stage III malignant melanoma.	dabrafenib	91-101	mitogen-activated protein kinase kinase 7	Homo sapiens	77-80
33493146-10	2021	In patients with a BRAF mutation, a combination of dabrafenib and trametinib led to an overall response rate of 51% and disease stability in another 40% of patients.	dabrafenib	51-61	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	19-23
33215864-0	2021	Dabrafenib and trametinib therapy in an elderly patient with non-small cell lung cancer harboring the BRAF V600E mutation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	102-106
33215864-3	2021	An 86-year-old male patient, who had been diagnosed with lung adenocarcinoma with the BRAF V600E mutation, received dabrafenib and trametinib combination chemotherapy.	dabrafenib	116-126	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	86-90
33293828-4	2020	In this study, we reported three children with BRAF-mutated LCH with pituitary involvement who improved after targeted therapy (dabrafenib and trametinib).	dabrafenib	128-138	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	47-51
33205710-10	2021	Dabrafenib, a BRAF inhibitor, decreased CCL17 production in the cell line with BRAFV595E mutation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Canis lupus familiaris	14-18
33205710-10	2021	Dabrafenib, a BRAF inhibitor, decreased CCL17 production in the cell line with BRAFV595E mutation.	dabrafenib	0-10	C-C motif chemokine ligand 17	Canis lupus familiaris	40-45
33204897-3	2020	Both patients were positive for the BRAF V600E mutation on genetic testing and were treated with the BRAF inhibitors Vemurafenib and Dabrafenib respectively.	dabrafenib	133-143	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	36-40
33204897-3	2020	Both patients were positive for the BRAF V600E mutation on genetic testing and were treated with the BRAF inhibitors Vemurafenib and Dabrafenib respectively.	dabrafenib	133-143	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	101-105
33844777-2	2020	MEK- and BRAF-inhibitors trametinib and dabrafenib are successfully used for BRAF-mutated, metastasizing melanoma, but these compounds may induce side effects.	dabrafenib	40-50	mitogen-activated protein kinase kinase 7	Homo sapiens	0-3
32869334-0	2020	Dabrafenib-induced neutrophilic panniculitis in a child undergoing dual BRAF-MEK inhibitor therapy for glioblastoma multiforme.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	72-76
32869334-0	2020	Dabrafenib-induced neutrophilic panniculitis in a child undergoing dual BRAF-MEK inhibitor therapy for glioblastoma multiforme.	dabrafenib	0-10	mitogen-activated protein kinase kinase 7	Homo sapiens	77-80
32869334-3	2020	We report a case of dabrafenib-induced neutrophilic panniculitis in a 9-year-old girl that manifested within several weeks of initiating dual BRAF-MEK inhibitor therapy for glioblastoma multiforme.	dabrafenib	20-30	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	142-146
32869334-3	2020	We report a case of dabrafenib-induced neutrophilic panniculitis in a 9-year-old girl that manifested within several weeks of initiating dual BRAF-MEK inhibitor therapy for glioblastoma multiforme.	dabrafenib	20-30	mitogen-activated protein kinase kinase 7	Homo sapiens	147-150
32869334-4	2020	This case highlights neutrophilic panniculitis as a side effect of dabrafenib in children and serves as a reminder to consider cutaneous side effects of BRAF inhibitors as they are increasingly used to treat children with primary brain tumors.	dabrafenib	67-77	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	153-157
33844777-2	2020	MEK- and BRAF-inhibitors trametinib and dabrafenib are successfully used for BRAF-mutated, metastasizing melanoma, but these compounds may induce side effects.	dabrafenib	40-50	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
33844777-2	2020	MEK- and BRAF-inhibitors trametinib and dabrafenib are successfully used for BRAF-mutated, metastasizing melanoma, but these compounds may induce side effects.	dabrafenib	40-50	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	77-81
33844777-3	2020	We report a 50 years old female with BRAF-mutated metastasizing melanoma who received trametinib (2 mg/d) and dabrafenib (200 mg/d) after using interferon without benefit.	dabrafenib	110-120	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	37-41
33037234-3	2020	A combination of BRAF inhibitor (dabrafenib) and MEK inhibitor (trametinib) has recently been approved and significantly improved the survival of patients with advanced NSCLC harboring BRAF V600E/K mutation.	dabrafenib	33-43	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	17-21
32781217-2	2020	Based on structural features of dabrafenib (potent FDA approved B-Raf inhibitor), the design of new NH2-based imidazothiazole derivatives was carried out affording new highly potent derivatives of imidazothiazole-based scaffold with amino substitution on the terminal phenyl ring as well as side chain with sulfonamide group and terminal substituted phenyl ring.	dabrafenib	32-42	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	64-69
32781217-8	2020	Molecular docking study revealed that the new designed derivatives preserved the same binding mode of dabrafenib with V600E B-Raf active site.	dabrafenib	102-112	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	124-129
33037234-3	2020	A combination of BRAF inhibitor (dabrafenib) and MEK inhibitor (trametinib) has recently been approved and significantly improved the survival of patients with advanced NSCLC harboring BRAF V600E/K mutation.	dabrafenib	33-43	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	185-189
32981611-0	2020	Durable Response to Dabrafenib Combined With Trametinib in a Patient With NSCLC Harboring a BRAF G469A Mutation.	dabrafenib	20-30	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	92-96
32801082-3	2020	To present, only three BRAF small inhibitors are approved by the FDA for the treatment of patients with metastatic melanoma: Vemurafenib, Dabrafenib and Encorafenib.	dabrafenib	138-148	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	23-27
32893700-4	2020	AREAS COVERED: Anti-CD22 recombinant immunotoxin Moxetumomab Pasudotox (Moxe), CD20 Mabs rituximab and obinutuzumab, BRAF/MEK inhibitors vemurafenib and dabrafenib-trametinib, and Bruton"s tyrosine kinase (BTK) inhibitor ibrutinib have been tested for HCL.	dabrafenib	153-163	CD22 molecule	Homo sapiens	20-24
32699976-0	2020	Interim analysis for post-marketing surveillance of dabrafenib and trametinib combination therapy in Japanese patients with unresectable and metastatic melanoma with BRAF V600 mutation.	dabrafenib	52-62	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	166-170
32699976-1	2020	PURPOSE: To investigate the safety and efficacy of dabrafenib and trametinib combination therapy for BRAF V600 mutation-positive unresectable and metastatic melanoma in over 100 Japanese patients of a real-world clinical setting.	dabrafenib	51-61	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	101-105
32935463-0	2020	Melatonin synergizes BRAF-targeting agent dabrafenib for the treatment of anaplastic thyroid cancer by inhibiting AKT/hTERT signalling.	dabrafenib	42-52	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	21-25
32935463-0	2020	Melatonin synergizes BRAF-targeting agent dabrafenib for the treatment of anaplastic thyroid cancer by inhibiting AKT/hTERT signalling.	dabrafenib	42-52	AKT serine/threonine kinase 1	Homo sapiens	114-117
32935463-0	2020	Melatonin synergizes BRAF-targeting agent dabrafenib for the treatment of anaplastic thyroid cancer by inhibiting AKT/hTERT signalling.	dabrafenib	42-52	telomerase reverse transcriptase	Homo sapiens	118-123
32935463-1	2020	As a selective inhibitor of BRAF kinase, dabrafenib has shown potent anti-tumour activities in patients with BRAFV600E mutant anaplastic thyroid cancer.	dabrafenib	41-51	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	28-32
32935463-6	2020	Molecular mechanistic studies further uncovered that melatonin synergized with dabrafenib to inhibit AKT and EMT signalling pathways.	dabrafenib	79-89	AKT serine/threonine kinase 1	Homo sapiens	101-104
32935463-7	2020	Furthermore, melatonin and dabrafenib synergistically inhibited the expression of hTERT, and the inhibition of cell viability and the induction of cell cycle arrest mediated by the combination of these two drugs were reversed by hTERT overexpression.	dabrafenib	27-37	telomerase reverse transcriptase	Homo sapiens	82-87
32935463-7	2020	Furthermore, melatonin and dabrafenib synergistically inhibited the expression of hTERT, and the inhibition of cell viability and the induction of cell cycle arrest mediated by the combination of these two drugs were reversed by hTERT overexpression.	dabrafenib	27-37	telomerase reverse transcriptase	Homo sapiens	229-234
32558291-10	2020	Other BRAF inhibitors, such as dabrafenib and encorafenib, are associated with significantly lower photosensitivity.	dabrafenib	31-41	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	6-10
32540409-13	2020	Trametinib+/-dabrafenib, LXH254, and lifirafenib showed more potent inhibition of BRAF non-V600 mutant NSCLC cell lines compared to other MEK, BRAF, and ERK inhibitors, and comparable to inhibition of BRAF V600E cell line.	dabrafenib	13-23	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	82-86
32540409-13	2020	Trametinib+/-dabrafenib, LXH254, and lifirafenib showed more potent inhibition of BRAF non-V600 mutant NSCLC cell lines compared to other MEK, BRAF, and ERK inhibitors, and comparable to inhibition of BRAF V600E cell line.	dabrafenib	13-23	mitogen-activated protein kinase kinase 7	Homo sapiens	138-141
32540409-13	2020	Trametinib+/-dabrafenib, LXH254, and lifirafenib showed more potent inhibition of BRAF non-V600 mutant NSCLC cell lines compared to other MEK, BRAF, and ERK inhibitors, and comparable to inhibition of BRAF V600E cell line.	dabrafenib	13-23	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	143-147
32540409-13	2020	Trametinib+/-dabrafenib, LXH254, and lifirafenib showed more potent inhibition of BRAF non-V600 mutant NSCLC cell lines compared to other MEK, BRAF, and ERK inhibitors, and comparable to inhibition of BRAF V600E cell line.	dabrafenib	13-23	mitogen-activated protein kinase 1	Homo sapiens	153-156
32540409-13	2020	Trametinib+/-dabrafenib, LXH254, and lifirafenib showed more potent inhibition of BRAF non-V600 mutant NSCLC cell lines compared to other MEK, BRAF, and ERK inhibitors, and comparable to inhibition of BRAF V600E cell line.	dabrafenib	13-23	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	143-147
33020646-2	2020	We conducted S1320, a randomized, open-label, phase 2 clinical trial (NCT02196181) evaluating whether intermittent dosing of the BRAF inhibitor dabrafenib and the MEK inhibitor trametinib improves progression-free survival in patients with metastatic and unresectable BRAFV600 melanoma.	dabrafenib	144-154	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	129-133
32877599-1	2020	BACKGROUND: In the previously reported primary analysis of this phase 3 trial, 12 months of adjuvant dabrafenib plus trametinib resulted in significantly longer relapse-free survival than placebo in patients with resected stage III melanoma with BRAF V600E or V600K mutations.	dabrafenib	101-111	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	246-250
32883694-1	2021	OBJECTIVE: Dabrafenib, an inhibitor of mutated BRAF, has significant clinical activity in melanoma patients but is linked to a spectrum of cutaneous toxicities.	dabrafenib	11-21	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	47-51
33082744-0	2020	Durable Complete Response of a Recurrent Mesencephalic Glioblastoma Treated with Trametinib and Low-Dose Dabrafenib in a Patient with Neurofibromatosis Type 1.	dabrafenib	105-115	neurofibromin 1	Homo sapiens	134-158
33082744-7	2020	Based on interim results of a phase 2 trial in advanced BRAF V600 wild-type melanoma indicating that a low dose of the BRAF-inhibitor dabrafenib is able to counter trametinib-related cutaneous toxicity, dabrafenib 50 mg twice daily was added.	dabrafenib	134-144	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	56-60
33082744-7	2020	Based on interim results of a phase 2 trial in advanced BRAF V600 wild-type melanoma indicating that a low dose of the BRAF-inhibitor dabrafenib is able to counter trametinib-related cutaneous toxicity, dabrafenib 50 mg twice daily was added.	dabrafenib	134-144	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	119-123
33082744-7	2020	Based on interim results of a phase 2 trial in advanced BRAF V600 wild-type melanoma indicating that a low dose of the BRAF-inhibitor dabrafenib is able to counter trametinib-related cutaneous toxicity, dabrafenib 50 mg twice daily was added.	dabrafenib	203-213	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	119-123
32216548-2	2020	This mutation is considered actionable and, for BRAFV600E-mutated ATC, a BRAF inhibitor (dabrafenib) in combination with a MEK inhibitor (trametinib) is FDA approved.	dabrafenib	89-99	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	48-52
32877390-4	2020	We report the case of a 55-year-old man with a diagnosis of stage IV BRAF<sup>V600E</sup>-mutated metastatic cutaneous melanoma undergoing treatment with dabrafenib/trametinib, who consulted due to the development of erythematous nodular lesions in the upper and lower limbs associated with febrile sensation during the course of treatment.	dabrafenib	154-164	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	69-73
32811569-7	2020	The BRAF inhibitor dabrafenib moderately suppressed cell viability in PLNTY.	dabrafenib	19-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-8
32875153-2	2020	Observations: An 18-year old man with neurodegenerative Langerhans cell histiocytosis (LCH), recently started on the BRAF inhibitor dabrafenib, presented with right eye pain.	dabrafenib	132-142	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	117-121
32848419-9	2020	This case showed that the combination treatment of osimertinib and dabrafenib plus trametinib might be a great treatment option for NSCLC patients with triple mutations (EGFR-19del/T790M/BRAFV600E).	dabrafenib	67-77	epidermal growth factor receptor	Homo sapiens	170-174
32761749-0	2020	Efficacy and safety of dabrafenib-trametinib in the treatment of unresectable or metastatic melanoma with BRAF V600 mutation: a systematic review and network meta-analysis.	dabrafenib	23-33	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	106-110
32761749-1	2020	The current systematic review aimed to evaluate the efficacy and safety of dabrafenib plus trametinib (dabrafenib-trametinib) with those of other therapeutic alternatives in the treatment of patients with BRAF V600 mutation unresectable or metastatic melanoma.	dabrafenib	75-85	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	205-209
32534795-0	2020	Combined osimertinib, dabrafenib and trametinib treatment for advanced non-small-cell lung cancer patients with an osimertinib-induced BRAF V600E mutation.	dabrafenib	22-32	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	135-139
32534795-11	2020	Combined treatment using dabrafenib/trametinib concurrently with osimertinib needs to be explored for osimertinib-induced BRAF V600E mutation.	dabrafenib	25-35	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	122-126
32553555-0	2020	Acquired BRAF N581S mutation mediated resistance to gefitinib and responded to dabrafenib plus trametinib.	dabrafenib	79-89	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
32765066-9	2020	The majority of patients with BRAF mutant advanced/metastatic melanoma were treated in the first-line with BRAF-targeted therapy (61.3% USA, 71.9% WE), and few patients received conventional chemotherapy or cytokine-based treatments (11.9% USA, 12.4% WE); the most commonly used BRAF-targeted therapy was the combination of dabrafenib plus trametinib.	dabrafenib	324-334	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	30-34
32650447-0	2020	The Anti-Cancer Drug Dabrafenib Is a Potent Activator of the Human Pregnane X Receptor.	dabrafenib	21-31	nuclear receptor subfamily 1 group I member 2	Homo sapiens	67-86
32650447-4	2020	In that context, the potential of the anticancer BRAF inhibitor dabrafenib suspected to activate hPXR and the human constitutive androstane receptor (hCAR) has not been thoroughly investigated yet.	dabrafenib	64-74	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	49-53
32650447-4	2020	In that context, the potential of the anticancer BRAF inhibitor dabrafenib suspected to activate hPXR and the human constitutive androstane receptor (hCAR) has not been thoroughly investigated yet.	dabrafenib	64-74	nuclear receptor subfamily 1 group I member 2	Homo sapiens	97-101
32650447-5	2020	Using different reporter cellular assays, we demonstrate that dabrafenib can activate hPXR as efficiently as its reference agonist SR12813, whereas it does not activate mouse or zebrafish PXR nor hCAR.	dabrafenib	62-72	nuclear receptor subfamily 1 group I member 2	Homo sapiens	86-90
32650447-5	2020	Using different reporter cellular assays, we demonstrate that dabrafenib can activate hPXR as efficiently as its reference agonist SR12813, whereas it does not activate mouse or zebrafish PXR nor hCAR.	dabrafenib	62-72	nuclear receptor subfamily 1, group I, member 2	Danio rerio	87-90
32650447-6	2020	We also showed that dabrafenib binds to recombinant hPXR, induces the expression of hPXR responsive genes in colon LS174T-hPXR cancer cells and human hepatocytes and finally increases the proliferation in LS174T-hPXR cells.	dabrafenib	20-30	nuclear receptor subfamily 1 group I member 2	Homo sapiens	52-56
32650447-6	2020	We also showed that dabrafenib binds to recombinant hPXR, induces the expression of hPXR responsive genes in colon LS174T-hPXR cancer cells and human hepatocytes and finally increases the proliferation in LS174T-hPXR cells.	dabrafenib	20-30	nuclear receptor subfamily 1 group I member 2	Homo sapiens	84-88
32650447-6	2020	We also showed that dabrafenib binds to recombinant hPXR, induces the expression of hPXR responsive genes in colon LS174T-hPXR cancer cells and human hepatocytes and finally increases the proliferation in LS174T-hPXR cells.	dabrafenib	20-30	nuclear receptor subfamily 1 group I member 2	Homo sapiens	84-88
32650447-6	2020	We also showed that dabrafenib binds to recombinant hPXR, induces the expression of hPXR responsive genes in colon LS174T-hPXR cancer cells and human hepatocytes and finally increases the proliferation in LS174T-hPXR cells.	dabrafenib	20-30	nuclear receptor subfamily 1 group I member 2	Homo sapiens	84-88
32561648-1	2020	Combination use of BRAF V600E inhibitor dabrafenib and MEK inhibitor trametinib has become a standard treatment for human cancers harboring BRAF V600E.	dabrafenib	40-50	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	19-23
32561648-1	2020	Combination use of BRAF V600E inhibitor dabrafenib and MEK inhibitor trametinib has become a standard treatment for human cancers harboring BRAF V600E.	dabrafenib	40-50	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	140-144
32561648-3	2020	Using thyroid cancer, melanoma, and colon cancer cell models, we showed that dabrafenib and trametinib induced robust apoptosis of cancer cells harboring both BRAF V600E and TERT promoter mutations but had little proapoptotic effect in cells harboring only BRAF V600E.	dabrafenib	77-87	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	159-163
32561648-3	2020	Using thyroid cancer, melanoma, and colon cancer cell models, we showed that dabrafenib and trametinib induced robust apoptosis of cancer cells harboring both BRAF V600E and TERT promoter mutations but had little proapoptotic effect in cells harboring only BRAF V600E.	dabrafenib	77-87	telomerase reverse transcriptase	Homo sapiens	174-178
32561648-3	2020	Using thyroid cancer, melanoma, and colon cancer cell models, we showed that dabrafenib and trametinib induced robust apoptosis of cancer cells harboring both BRAF V600E and TERT promoter mutations but had little proapoptotic effect in cells harboring only BRAF V600E.	dabrafenib	77-87	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	257-261
32664789-3	2020	Data from The Genomics of Drug Sensitivity in Cancer database showed that three drugs: (5Z)-7-oxozeaenol, dabrafenib and nutlin-3a (-), have shown more resistance in patients with TP53 mutation.	dabrafenib	106-116	tumor protein p53	Homo sapiens	180-184
32534242-0	2020	Open-label, phase IIa study of dabrafenib plus trametinib in East Asian patients with advanced BRAF V600-mutant cutaneous melanoma.	dabrafenib	31-41	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	95-99
32534242-1	2020	PURPOSE: This study (NCT02083354) assessed the efficacy and safety of dabrafenib plus trametinib in East Asian patients with advanced BRAF V600-mutant cutaneous melanoma.	dabrafenib	70-80	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	134-138
32534242-17	2020	CONCLUSION: These results support the efficacy and tolerability of dabrafenib in combination with trametinib in East Asian patients with unresectable or metastatic BRAF V600-mutant cutaneous melanoma.	dabrafenib	67-77	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	164-168
32542792-9	2020	Dabrafenib, as an inhibitor of RIPK3, may be an effective treatment to limit the progression of the tubulointerstitial fibrosis.	dabrafenib	0-10	receptor-interacting serine-threonine kinase 3	Mus musculus	31-36
32751138-10	2020	The FDA-approved BRAF/MEK inhibitor combination of dabrafenib and trametinib has revolutionized treatment of BRAFV600E mutation positive anaplastic thyroid cancer.	dabrafenib	51-61	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	17-21
32751138-10	2020	The FDA-approved BRAF/MEK inhibitor combination of dabrafenib and trametinib has revolutionized treatment of BRAFV600E mutation positive anaplastic thyroid cancer.	dabrafenib	51-61	mitogen-activated protein kinase kinase 7	Homo sapiens	22-25
32793120-10	2020	Due to the persistence of the disease and the evidence of a BRAF V600E mutation, in February 2019, the patient underwent a combined treatment with dabrafenib (a BRAF inhibitor) and trametinib (mitogen-activated extracellular signal-regulate kinase inhibitor).	dabrafenib	147-157	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	161-165
32793120-16	2020	This is the first case of a pituitary melanoma metastasis with BRAF mutation, successfully treated with the combination of dabrafenib and trametinib after incomplete surgical removal.	dabrafenib	123-133	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	63-67
32409797-6	2020	In vitro experimental results demonstrate that the Dabrafenib sensitivity is 15.2 pm (mug mL-1)-1 (R2 = 0.993) with a limit of detection (LoD) of 74.4 mug mL-1 in serum solution.	dabrafenib	51-61	L1 cell adhesion molecule	Mus musculus	90-94
32409797-6	2020	In vitro experimental results demonstrate that the Dabrafenib sensitivity is 15.2 pm (mug mL-1)-1 (R2 = 0.993) with a limit of detection (LoD) of 74.4 mug mL-1 in serum solution.	dabrafenib	51-61	L1 cell adhesion molecule	Mus musculus	155-159
32645969-1	2020	The BRAF inhibitors vemurafenib, dabrafenib and encorafenib are used in the treatment of patients with BRAF-mutant melanoma.	dabrafenib	33-43	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-8
32645969-1	2020	The BRAF inhibitors vemurafenib, dabrafenib and encorafenib are used in the treatment of patients with BRAF-mutant melanoma.	dabrafenib	33-43	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	103-107
32487991-8	2020	In addition, we experimentally validated predicted synergy of the BRAF/insulin receptor combination (Dabrafenib/BMS-754807) in 48 colorectal cancer cell lines.	dabrafenib	101-111	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	66-70
32585852-6	2020	We observed BRAF mutant melanoma cells treated with the combination of a MEK inhibitor (trametinib) and a BRAF inhibitor (dabrafenib), exhibited elevated ROS levels, both in in vitro and in vivo melanoma models.	dabrafenib	122-132	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	12-16
32585852-6	2020	We observed BRAF mutant melanoma cells treated with the combination of a MEK inhibitor (trametinib) and a BRAF inhibitor (dabrafenib), exhibited elevated ROS levels, both in in vitro and in vivo melanoma models.	dabrafenib	122-132	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	106-110
32487991-8	2020	In addition, we experimentally validated predicted synergy of the BRAF/insulin receptor combination (Dabrafenib/BMS-754807) in 48 colorectal cancer cell lines.	dabrafenib	101-111	insulin receptor	Homo sapiens	71-87
32047001-0	2020	BRAF-mutant Transcriptional Subtypes Predict Outcome of Combined BRAF, MEK, and EGFR Blockade with Dabrafenib, Trametinib, and Panitumumab in Patients with Colorectal Cancer.	dabrafenib	99-109	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
32047001-0	2020	BRAF-mutant Transcriptional Subtypes Predict Outcome of Combined BRAF, MEK, and EGFR Blockade with Dabrafenib, Trametinib, and Panitumumab in Patients with Colorectal Cancer.	dabrafenib	99-109	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	65-69
32047001-0	2020	BRAF-mutant Transcriptional Subtypes Predict Outcome of Combined BRAF, MEK, and EGFR Blockade with Dabrafenib, Trametinib, and Panitumumab in Patients with Colorectal Cancer.	dabrafenib	99-109	epidermal growth factor receptor	Homo sapiens	80-84
32197228-3	2020	In two types of mast cells (RBL-2H3 and mouse bone marrow-derived mast cells), dabrafenib (0.01, 0.1, 1 muM) pretreatment significantly decreased IgE-induced degranulation, intracellular calcium influx, and the activity of intracellular signaling molecules, such as Lyn, Syk, Akt, and PLCgamma.	dabrafenib	79-89	LYN proto-oncogene, Src family tyrosine kinase	Mus musculus	266-269
31555967-1	2020	BACKGROUD: Synergistic combinations between BRAF and MEK inhibitors, such as dabrafenib plus trametinib, vemurafenib plus cobimetinib or encorafenib plus binimetinib, represent the current standard of care in metastatic or locally advanced BRAF V600 mutated malignant melanomas (MM).	dabrafenib	77-87	mitogen-activated protein kinase kinase 7	Homo sapiens	53-56
32197228-3	2020	In two types of mast cells (RBL-2H3 and mouse bone marrow-derived mast cells), dabrafenib (0.01, 0.1, 1 muM) pretreatment significantly decreased IgE-induced degranulation, intracellular calcium influx, and the activity of intracellular signaling molecules, such as Lyn, Syk, Akt, and PLCgamma.	dabrafenib	79-89	spleen tyrosine kinase	Mus musculus	271-274
32197228-3	2020	In two types of mast cells (RBL-2H3 and mouse bone marrow-derived mast cells), dabrafenib (0.01, 0.1, 1 muM) pretreatment significantly decreased IgE-induced degranulation, intracellular calcium influx, and the activity of intracellular signaling molecules, such as Lyn, Syk, Akt, and PLCgamma.	dabrafenib	79-89	thymoma viral proto-oncogene 1	Mus musculus	276-279
32197228-4	2020	Dabrafenib ameliorated mRNA and protein expression levels of interleukin-4 and tumor necrosis factor-alpha by the reduction of nuclear localization of nuclear factor-kappaB and nuclear factor of activated T-cells.	dabrafenib	0-10	interleukin 4	Mus musculus	61-106
32293049-2	2020	Pyrexia or a spike of fever are well-known AE of BRAF inhibitors, with or without MEK inhibitors, and have been reported to have a high incidence after dabrafenib/trametinib, but not after encorafenib/binimetinib.	dabrafenib	152-162	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	49-53
31425480-0	2020	Validation of dabrafenib-trametinib prognostic groups in patients treated with vemurafenib and cobimetinib for advanced BRAF-mutated melanoma.	dabrafenib	14-24	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	120-124
31895752-0	2020	Dabrafenib plus trametinib is effective in the treatment of BRAF V600-mutated metastatic melanoma patients: analysis of patients from the dabrafenib plus trametinib Named Patient Program (DESCRIBE II).	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	60-64
32591618-8	2020	Renoprotection was also observed using the RIPK3 inhibitor dabrafenib in eNOS-/- diabetic mice as demonstrated by reduced collagen deposition and myofibroblast activation.	dabrafenib	59-69	receptor-interacting serine-threonine kinase 3	Mus musculus	43-48
32591618-8	2020	Renoprotection was also observed using the RIPK3 inhibitor dabrafenib in eNOS-/- diabetic mice as demonstrated by reduced collagen deposition and myofibroblast activation.	dabrafenib	59-69	nitric oxide synthase 3, endothelial cell	Mus musculus	73-77
31895752-1	2020	In clinical trials, dabrafenib plus trametinib improved overall survival (OS) compared with single-agent BRAF inhibitors (BRAFi) in patients with BRAF V600-mutant unresectable or metastatic melanoma.	dabrafenib	20-30	Moloney sarcoma oncogene	Mus musculus	74-76
31895752-12	2020	Dabrafenib plus trametinib showed substantial clinical activity in NPP patients with BRAF V600-mutated unresectable or metastatic melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	85-89
32194039-2	2020	BRAF kinase inhibitors (BRAFi), including vemurafenib and dabrafenib, were discovered and used in the clinical treatment of BRAF-mutant metastatic melanoma.	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
31970865-3	2020	However, treatment with dabrafenib plus trametinib targets the BRAF V600E mutation exclusively.	dabrafenib	24-34	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	63-67
32388065-1	2020	INTRODUCTION: BRAF is a confirmed therapeutic target in non-small cell lung cancer (NSCLC), as the BRAF inhibitor dabrafenib, in combination with the MEK inhibitor trametinib, is approved for the treatment of NSCLC harbouring BRAF V600E mutation.	dabrafenib	114-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
32388065-1	2020	INTRODUCTION: BRAF is a confirmed therapeutic target in non-small cell lung cancer (NSCLC), as the BRAF inhibitor dabrafenib, in combination with the MEK inhibitor trametinib, is approved for the treatment of NSCLC harbouring BRAF V600E mutation.	dabrafenib	114-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	99-103
32388065-1	2020	INTRODUCTION: BRAF is a confirmed therapeutic target in non-small cell lung cancer (NSCLC), as the BRAF inhibitor dabrafenib, in combination with the MEK inhibitor trametinib, is approved for the treatment of NSCLC harbouring BRAF V600E mutation.	dabrafenib	114-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	99-103
32388065-7	2020	Among these eight patients, acquired molecular events potentially responsible for resistance were detected in three who progressed on dabrafenib-trametinib combination, that is, MEK1 K57N, RAS viral (v-ras) oncogene homolog (NRAS) Q61R and rat sarcoma viral oncogene homolog (KRAS) Q61R mutations.	dabrafenib	134-144	mitogen-activated protein kinase kinase 1	Homo sapiens	178-182
32388065-7	2020	Among these eight patients, acquired molecular events potentially responsible for resistance were detected in three who progressed on dabrafenib-trametinib combination, that is, MEK1 K57N, RAS viral (v-ras) oncogene homolog (NRAS) Q61R and rat sarcoma viral oncogene homolog (KRAS) Q61R mutations.	dabrafenib	134-144	NRAS proto-oncogene, GTPase	Homo sapiens	225-229
32388065-7	2020	Among these eight patients, acquired molecular events potentially responsible for resistance were detected in three who progressed on dabrafenib-trametinib combination, that is, MEK1 K57N, RAS viral (v-ras) oncogene homolog (NRAS) Q61R and rat sarcoma viral oncogene homolog (KRAS) Q61R mutations.	dabrafenib	134-144	KRAS proto-oncogene, GTPase	Rattus norvegicus	276-280
32388065-8	2020	One patient progressing on dabrafenib monotherapy developed a PTEN frameshift mutation.	dabrafenib	27-37	phosphatase and tensin homolog	Homo sapiens	62-66
32269299-2	2020	The development of first-generation RAF inhibitors, including vemurafenib (VEM) and dabrafenib led to initial excitement due to high response rates and profound regression of malignant melanomas carrying BRAFV600E mutations.	dabrafenib	84-94	zinc fingers and homeoboxes 2	Homo sapiens	36-39
32053122-4	2020	We conducted a monocentric retrospective observational study among patients treated with dabrafenib and trametinib for BRAF-mutant advanced melanoma from January 2015 to March 2019.	dabrafenib	89-99	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	119-123
32368388-4	2020	Several targeted therapy agents such as vemurafenib, dabrafenib and encorafenib have been approved by the FDA as BRAF inhibitors, as well as other immunotherapies such as anti-CTLA-4 (ipilimumab).	dabrafenib	53-63	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	113-117
32368388-6	2020	Resistance to current BRAF inhibitors is a clinical challenge and one of the strategies to overcome this phenomenon is combination treatment, with the most recently approved combination being BRAF/MEK inhibitors (dabrafenib and trametinib) and BRAF or MEK inhibitors with immunocheckpoint blockers.	dabrafenib	213-223	mitogen-activated protein kinase kinase 7	Homo sapiens	197-200
32266211-9	2020	DAB activity was proven by the decreased ERK phosphorylation in primary melanoma cells (SKmel28 BRAFV600E cell line), while TSA effect was evidenced by acetylated histones accumulation in cell"s nuclei (SKmel23 BRAF WT cell line).	dabrafenib	0-3	mitogen-activated protein kinase 1	Homo sapiens	41-44
32266211-9	2020	DAB activity was proven by the decreased ERK phosphorylation in primary melanoma cells (SKmel28 BRAFV600E cell line), while TSA effect was evidenced by acetylated histones accumulation in cell"s nuclei (SKmel23 BRAF WT cell line).	dabrafenib	0-3	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	96-100
32206360-0	2020	Response to Dabrafenib and Trametinib of a Patient with Metaplastic Breast Carcinoma Harboring a BRAF V600E Mutation.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	97-101
32206360-14	2020	Conclusion: To the best of our knowledge, this is the first report of BRAF mutation breast cancer treated with dabrafenib and trametinib and it heralds the possibility of targeted therapy for rare breast cancers.	dabrafenib	111-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	70-74
32211316-5	2020	Here we report the different fertility outcome in two cases of MM patients, harboring BRAF V600E mutation, that received vemurafenib and dabrafenib respectively.	dabrafenib	137-147	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	86-90
32131760-0	2020	Granulomatosis with polyangiitis in a patient treated with dabrafenib and trametinib for BRAF V600E positive lung adenocarcinoma.	dabrafenib	59-69	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	89-93
32131760-1	2020	BACKGROUND: Dabrafenib and trametinib combination therapy is approved for the treatment of patients with BRAF V600E positive tumors including melanoma and lung cancer.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	105-109
32131760-5	2020	A BRAF V600E mutation was identified at the time of recurrence and she received combination dabrafenib and trametinib therapy.	dabrafenib	92-102	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	2-6
32009180-0	2020	Trametinib and Dabrafenib in histiocytic sarcoma transdifferentiated from chronic lymphocytic leukemia with a K-RAS and a unique BRAF mutation.	dabrafenib	15-25	KRAS proto-oncogene, GTPase	Homo sapiens	110-115
32092141-5	2020	Four infants with LCH (range, 7-11 months at diagnosis) and secondary hemophagocytic lymphohistiocytosis were referred to our institution and subsequently treated with the BRAF V600E-specific inhibitor dabrafenib.	dabrafenib	202-212	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	172-176
32093631-0	2020	Reduced doses of dabrafenib and trametinib combination therapy for BRAF V600E-mutant non-small cell lung cancer prevent rhabdomyolysis and maintain tumor shrinkage: a case report.	dabrafenib	17-27	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	67-71
32093631-4	2020	The BRAF V600E mutation was detected by next generation sequencing, and the patient was subjected to treatment with dabrafenib and trametinib in combination.	dabrafenib	116-126	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-8
32093631-7	2020	CONCLUSION: The reduction of the doses of dabrafenib and trametinib was effective in the treatment of BRAF V600E-mutant NSCLC, and also prevented the incidence of rhabdomyolysis.	dabrafenib	42-52	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	102-106
32098410-8	2020	In tissue lysates, concentration-dependent ex vivo inhibition of STK and PTK activities with dabrafenib was stronger in responders than in non-responders.	dabrafenib	93-103	protein tyrosine kinase 2 beta	Homo sapiens	73-76
31876308-0	2020	Real-world efficacy and safety data for dabrafenib and trametinib combination therapy in Japanese patients with BRAF V600 mutation-positive advanced melanoma.	dabrafenib	40-50	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	112-116
31876308-1	2020	We conducted a retrospective investigation of the efficacy and safety of dabrafenib and trametinib combination therapy in Japanese patients with BRAF V600 mutation-positive advanced melanoma in real-world clinical practise.	dabrafenib	73-83	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	145-149
31876308-2	2020	The study analyzed 50 patients who received dabrafenib and trametinib combination therapy for BRAF V600 mutation-positive advanced melanoma in our hospital (26 men and 24 women, aged 21-86 years, inclusive; median age, 53 years).	dabrafenib	44-54	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	94-98
32098410-12	2020	While dabrafenib alone showed an inhibition of STK and PTK activities in both tissues and cell lines, the combination of dabrafenib and trametinib showed an antagonism on the STK activities and a synergism on PTK activities, resulting in stronger inhibitions of overall tyrosine kinase activities.	dabrafenib	121-131	protein tyrosine kinase 2 beta	Homo sapiens	209-212
32092958-6	2020	Current combinations of BRAF and MEK inhibitors that have demonstrated improved patient outcomes include dabrafenib with trametinib, vemurafenib with cobimetinib or encorafenib with binimetinib.	dabrafenib	105-115	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	24-28
32092958-6	2020	Current combinations of BRAF and MEK inhibitors that have demonstrated improved patient outcomes include dabrafenib with trametinib, vemurafenib with cobimetinib or encorafenib with binimetinib.	dabrafenib	105-115	mitogen-activated protein kinase kinase 7	Homo sapiens	33-36
31771879-11	2020	In HK-2 cells, DAB significantly decreased the levels of NGAL and KIM-1, inflammatory cytokines, cell death, and necroptosis-related proteins.	dabrafenib	15-18	hepatitis A virus cellular receptor 1	Mus musculus	66-71
31974262-10	2020	V600E and V600K mutations in exon 15 of the BRAF gene were codetected, and the patient was treated with dabrafenib and trametinib.	dabrafenib	104-114	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	44-48
31804972-6	2020	Using this approach, we found that spheroids from K1 and TPC1 cells demonstrate significant differences in their sensitivities to dabrafenib treatment, that closely model expected patient drug response.	dabrafenib	130-140	two pore segment channel 1	Homo sapiens	57-61
32043788-8	2020	Here we not only describe the first patient with an extramedullary CNS relapse responding to targeted dabrafenib and trametinib treatment, we furthermore provide evidence that a point mutation within the capicua transcriptional repressor (CIC) gene mediated the acquired resistance in this patient.	dabrafenib	102-112	capicua transcriptional repressor	Homo sapiens	204-237
32043788-8	2020	Here we not only describe the first patient with an extramedullary CNS relapse responding to targeted dabrafenib and trametinib treatment, we furthermore provide evidence that a point mutation within the capicua transcriptional repressor (CIC) gene mediated the acquired resistance in this patient.	dabrafenib	102-112	capicua transcriptional repressor	Homo sapiens	239-242
31519698-0	2019	Identification of targetable BRAF DeltaN486_P490 variant by whole genome sequencing leading to dabrafenib-induced remission of a BRAF-mutant pancreatic adenocarcinoma.	dabrafenib	95-105	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	29-33
31640894-0	2020	Response to the combination of dabrafenib, trametinib and osimertinib in a patient with EGFR-mutant NSCLC harboring an acquired BRAFV600E mutation.	dabrafenib	31-41	epidermal growth factor receptor	Homo sapiens	88-92
31661699-1	2020	The mitogen-activated protein kinase (MAPK) pathway consists of the Ras/Raf/MEK/ERK signaling cascade, and its upregulation plays a major role in the pathogenesis of pediatric astrocytomas and molecular inhibitors of this pathway including trametinib and dabrafenib have been tested in early-phase clinical trials and used by pediatric oncologists in children with BRAF-mutated gliomas.	dabrafenib	255-265	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	72-75
31661699-1	2020	The mitogen-activated protein kinase (MAPK) pathway consists of the Ras/Raf/MEK/ERK signaling cascade, and its upregulation plays a major role in the pathogenesis of pediatric astrocytomas and molecular inhibitors of this pathway including trametinib and dabrafenib have been tested in early-phase clinical trials and used by pediatric oncologists in children with BRAF-mutated gliomas.	dabrafenib	255-265	mitogen-activated protein kinase kinase 7	Homo sapiens	76-79
31661699-1	2020	The mitogen-activated protein kinase (MAPK) pathway consists of the Ras/Raf/MEK/ERK signaling cascade, and its upregulation plays a major role in the pathogenesis of pediatric astrocytomas and molecular inhibitors of this pathway including trametinib and dabrafenib have been tested in early-phase clinical trials and used by pediatric oncologists in children with BRAF-mutated gliomas.	dabrafenib	255-265	mitogen-activated protein kinase 1	Homo sapiens	80-83
31504796-0	2019	Dabrafenib treatment in a patient with BRAF V600E ganglioglioma: circulating exosome-derived cancer RNA supports treatment choice and clinical monitoring.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	39-43
31506385-0	2019	A Phase I and Pharmacokinetic Study of Oral Dabrafenib in Children and Adolescent Patients with Recurrent or Refractory BRAF V600 Mutation-Positive Solid Tumors.	dabrafenib	44-54	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	120-124
31506385-8	2019	CONCLUSIONS: In this first clinical trial in pediatric patients with pretreated BRAF V600-mutant tumors, dabrafenib was well tolerated while achieving target exposure levels; the average treatment duration was >1 year with many patients still on treatment.	dabrafenib	105-115	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	80-84
32155032-1	2020	The combination of dabrafenib and trametinib is an important immunotherapy option for patients with BRAF V600 mutation-positive melanoma.	dabrafenib	19-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	100-104
31864178-0	2020	Long-term outcomes in patients with BRAF V600-mutant metastatic melanoma receiving dabrafenib monotherapy: Analysis from phase 2 and 3 clinical trials.	dabrafenib	83-93	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	36-40
31864178-1	2020	BACKGROUND: Previous analyses of BREAK-2 and BREAK-3 showed that durable outcomes lasting >=3 years are achievable with dabrafenib in some patients with BRAF V600-mutant metastatic melanoma (MM); however, additional follow-up is needed to fully characterise the long-term impact of dabrafenib in these patients.	dabrafenib	120-130	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	153-157
32055496-9	2020	The results of clinical trials with dabrafenib and trametinib led to the approval from FDA of this combination for patients with BRAF V600E mutated ATC with locally advanced, unresectable, or metastatic ATC.	dabrafenib	36-46	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	129-133
33685196-0	2020	Dabrafenib monotherapy in BRAF+ non-small cell lung cancer - our experience.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	26-30
33685196-3	2020	CASE: We present two case reports of BRAF+ NSCLC patients, treated with 3rd line dabrafenib monotherapy on our department, and also brief review of available information about dabrafenib and its use in monotherapy of BRAF+ NSCLC.	dabrafenib	81-91	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	37-41
33685196-3	2020	CASE: We present two case reports of BRAF+ NSCLC patients, treated with 3rd line dabrafenib monotherapy on our department, and also brief review of available information about dabrafenib and its use in monotherapy of BRAF+ NSCLC.	dabrafenib	176-186	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	217-221
31882684-10	2019	Combination of dabrafenib and trametinib was potent against a rare BRAF K601E mutation.	dabrafenib	15-25	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	67-71
31519698-0	2019	Identification of targetable BRAF DeltaN486_P490 variant by whole genome sequencing leading to dabrafenib-induced remission of a BRAF-mutant pancreatic adenocarcinoma.	dabrafenib	95-105	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	129-133
31519698-4	2019	Working with the Novartis patient assistance program allowed us to treat the patient with the BRAF-inhibitor, dabrafenib.	dabrafenib	110-120	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	94-98
31817643-0	2019	B-RAFV600E Inhibitor Dabrafenib Attenuates RIPK3-Mediated Necroptosis and Promotes Functional Recovery after Spinal Cord Injury.	dabrafenib	21-31	receptor interacting serine/threonine kinase 3	Homo sapiens	43-48
31817643-3	2019	Interestingly, recent studies have shown that the B-RAFV600E inhibitor dabrafenib has a function to selectively inhibit RIPK3 and prevents necroptosis in various disease models.	dabrafenib	71-81	receptor interacting serine/threonine kinase 3	Homo sapiens	120-125
31817643-4	2019	In the present study, using a mouse model of thoracic spinal cord contusion injury, we demonstrate that dabrafenib administration in the acute phase significantly inhibites RIPK3-mediated necroptosis in the injured spinal cord.	dabrafenib	104-114	receptor-interacting serine-threonine kinase 3	Mus musculus	173-178
31817643-8	2019	These findings suggest that the B-RAFV600E inhibitor dabrafenib attenuates RIPK3-mediated necroptosis to provide a neuroprotective effect and promotes functional recovery after SCI.	dabrafenib	53-63	receptor interacting serine/threonine kinase 3	Homo sapiens	75-80
30950075-0	2019	BRAF-mutated, acral verrucous melanoma successfully treated by dabrafenib plus trametinib combination therapy.	dabrafenib	63-73	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
31754297-0	2019	miR- 26a Sensitizes Melanoma Cells To Dabrafenib Via Targeting HMGB1-Dependent Autophagy Pathways.	dabrafenib	38-48	microRNA 26a-1	Homo sapiens	0-8
31811016-0	2019	Efficacy and Safety of Dabrafenib in Pediatric Patients with BRAF V600 Mutation-Positive Relapsed or Refractory Low-Grade Glioma: Results from a Phase I/IIa Study.	dabrafenib	23-33	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	61-65
31811016-2	2019	Patients with BRAF V600 mutation-positive pLGG may benefit from treatment with dabrafenib.	dabrafenib	79-89	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
31811016-13	2019	CONCLUSIONS: Dabrafenib demonstrated meaningful clinical activity and acceptable tolerability in patients with BRAF V600-mutant pLGG.	dabrafenib	13-23	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	111-115
31369091-6	2019	BRAF inhibitors, such as dabrafenib or vemurafenib, either alone or in combination with the MEK inhibitors trametinib and cobimetinib, have been administered to patients with PCPs producing clinically useful and, in some cases, sustained responses.	dabrafenib	25-35	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
31223037-0	2019	Cost-effectiveness of dabrafenib and trametinib in combination as adjuvant treatment of BRAF V600E/K mutation-positive melanoma from a US healthcare payer perspective.	dabrafenib	22-32	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	88-92
31223037-1	2019	Objective: The COMBI-AD trial demonstrated the efficacy and safety of dabrafenib and trametinib in combination vs placebo as adjuvant treatment of patients with BRAF V600E/K mutation-positive resected Stage IIIA (lymph node metastasis &gt;1 mm), IIIB, or IIIC melanoma.	dabrafenib	70-80	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	161-165
31223037-13	2019	Conclusions: Given generally-accepted cost-effectiveness threshold values in the US, dabrafenib plus trametinib is likely to be a cost-effective adjuvant therapy for patients with BRAF mutation positive melanoma.	dabrafenib	85-95	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	180-184
31918469-7	2019	Since the patient"s tumor was positive for BRAF and MEK, targeted therapy with dabrafenib and trametinib was initiated.	dabrafenib	79-89	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	43-47
31918469-7	2019	Since the patient"s tumor was positive for BRAF and MEK, targeted therapy with dabrafenib and trametinib was initiated.	dabrafenib	79-89	mitogen-activated protein kinase kinase 7	Homo sapiens	52-55
31783660-4	2019	To do so, an A375 dabrafenib-resistant (A375DR) melanoma cell subpopulation was selected and its behavior compared with that of parental (A375P) cells by crystal violet, 5-Bromo-2"-deoxyuridine incorporation, and cleaved poly(ADP-ribose) polymerase 1 (PARP1) western blot measurements.	dabrafenib	18-28	poly(ADP-ribose) polymerase 1	Homo sapiens	221-250
31783660-4	2019	To do so, an A375 dabrafenib-resistant (A375DR) melanoma cell subpopulation was selected and its behavior compared with that of parental (A375P) cells by crystal violet, 5-Bromo-2"-deoxyuridine incorporation, and cleaved poly(ADP-ribose) polymerase 1 (PARP1) western blot measurements.	dabrafenib	18-28	poly(ADP-ribose) polymerase 1	Homo sapiens	252-257
31748352-5	2019	There is rapidly growing evidence that BRAF inhibitors such as vemurafenib or dabrafenib are effective in treating CNS-spread disease.	dabrafenib	78-88	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	39-43
31685033-9	2019	Treatment options varied, including surgical resection, chemotherapy, and targeted therapy with BRAF-inhibitor dabrafenib in one mutated case.	dabrafenib	111-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	96-100
31406976-0	2019	Dabrafenib plus trametinib versus dabrafenib monotherapy in patients with metastatic BRAF V600E/K-mutant melanoma: long-term survival and safety analysis of a phase 3 study.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	85-89
31445021-0	2019	Inhibition of human UDP-glucuronosyltransferase (UGT) enzymes by kinase inhibitors: Effects of dabrafenib, ibrutinib, nintedanib, trametinib and BIBF 1202.	dabrafenib	95-105	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	49-52
31445021-2	2019	The present study characterised the effects of four additional drugs in this class, dabrafenib, ibrutinib, nintedanib and trametinib, on human UGT enzyme activities in vitro.	dabrafenib	84-94	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	143-146
31445021-3	2019	Dabrafenib, ibrutinib, nintedanib and trametinib were potent inhibitors of human liver microsomal UGT1A1; Ki,u values ranged from 1.1 to 7.5 microM.	dabrafenib	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
31647501-13	2019	A patient with a large tumor and BRAF V600E mutation was treated with combined systemic BRAF (dabrafenib) and MEK (trametinib) inhibitors.	dabrafenib	94-104	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	33-37
31647501-13	2019	A patient with a large tumor and BRAF V600E mutation was treated with combined systemic BRAF (dabrafenib) and MEK (trametinib) inhibitors.	dabrafenib	94-104	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	88-92
31663466-0	2019	Budget Impact of Dabrafenib and Trametinib in Combination as Adjuvant Treatment of BRAF V600E/K Mutation-Positive Melanoma from a U.S. Commercial Payer Perspective.	dabrafenib	17-27	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	83-87
31663466-2	2019	OBJECTIVE: To evaluate the budget impact of dabrafenib and trametinib in combination for adjuvant treatment of patients with BRAF V600 mutation-positive resected Stage IIIA, IIIB, or IIIC melanoma from a U.S. commercial payer perspective using data from the COMBI-AD trial, as well as other sources.	dabrafenib	44-54	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	125-129
31663466-3	2019	METHODS: The budget impact of dabrafenib and trametinib in combination for patients with BRAF V600E/K mutation-positive, resected Stage IIIA, IIIB, or IIIC melanoma was evaluated from the perspective of a hypothetical population of 1 million members with demographic characteristics consistent with those of a commercially insured U.S. insurance plan (i.e., adults aged less than 65 years) using an economic model developed in Microsoft Excel.	dabrafenib	30-40	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	89-93
31754297-0	2019	miR- 26a Sensitizes Melanoma Cells To Dabrafenib Via Targeting HMGB1-Dependent Autophagy Pathways.	dabrafenib	38-48	high mobility group box 1	Homo sapiens	63-68
31754297-2	2019	Methods: In our study, we conducted a variety of studies, including quantitative PCR, Western blot, and autophagy and apoptosis assays to investigate the involvement of miR-26a and HMGB1 in modulation of dabrafenib sensitivity in human melanoma cell lines.	dabrafenib	204-214	microRNA 26a-1	Homo sapiens	169-176
31754297-2	2019	Methods: In our study, we conducted a variety of studies, including quantitative PCR, Western blot, and autophagy and apoptosis assays to investigate the involvement of miR-26a and HMGB1 in modulation of dabrafenib sensitivity in human melanoma cell lines.	dabrafenib	204-214	high mobility group box 1	Homo sapiens	181-186
31754297-3	2019	Results: Our studies revealed that the expressions of miR-26a and HMGB1 were altered in two melanoma cell lines after dabrafenib treatment.	dabrafenib	118-128	microRNA 26a-1	Homo sapiens	54-61
31754297-3	2019	Results: Our studies revealed that the expressions of miR-26a and HMGB1 were altered in two melanoma cell lines after dabrafenib treatment.	dabrafenib	118-128	high mobility group box 1	Homo sapiens	66-71
31754297-4	2019	Additionally, dabrafenib caused autophagy in melanoma and this autophagic process was regulated by miR-26a via modifying HMGB1 expression.	dabrafenib	14-24	microRNA 26a-1	Homo sapiens	99-106
31754297-4	2019	Additionally, dabrafenib caused autophagy in melanoma and this autophagic process was regulated by miR-26a via modifying HMGB1 expression.	dabrafenib	14-24	high mobility group box 1	Homo sapiens	121-126
31754297-5	2019	Furthermore, silencing HMGB1-inhibited autophagy induced by dabrafenib in melanoma cells.	dabrafenib	60-70	high mobility group box 1	Homo sapiens	23-28
31754297-6	2019	Last, we verified that treatment with a miR-26a mimic and HMGB1 shRNA could increase the efficacy of dabrafenib in melanoma cells.	dabrafenib	101-111	microRNA 26a-1	Homo sapiens	40-47
31754297-6	2019	Last, we verified that treatment with a miR-26a mimic and HMGB1 shRNA could increase the efficacy of dabrafenib in melanoma cells.	dabrafenib	101-111	high mobility group box 1	Homo sapiens	58-63
31754297-7	2019	Conclusion: Taken together, we showed that miR-26a is involved in the regulation of dabrafenib efficacy via a HMGB1-dependent autophagy pathway in melanoma cells.	dabrafenib	84-94	microRNA 26a-1	Homo sapiens	43-50
31754297-7	2019	Conclusion: Taken together, we showed that miR-26a is involved in the regulation of dabrafenib efficacy via a HMGB1-dependent autophagy pathway in melanoma cells.	dabrafenib	84-94	high mobility group box 1	Homo sapiens	110-115
31666933-0	2019	Newly diagnosed papillary craniopharyngioma with BRAF V600E mutation treated with single-agent selective BRAF inhibitor dabrafenib: a case report.	dabrafenib	120-130	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	49-53
31666933-0	2019	Newly diagnosed papillary craniopharyngioma with BRAF V600E mutation treated with single-agent selective BRAF inhibitor dabrafenib: a case report.	dabrafenib	120-130	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	105-109
31666933-5	2019	NGS sequencing demonstrated BRAF V600E mutation, and the patient was prescribed dual agent Dabrafenib and Trametinib.	dabrafenib	91-101	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	28-32
31666933-9	2019	The patient continues on Dabrafenib (150 mg BID) with a steady reduction in tumor size, and improvement in cognitive function leading to independent living.	dabrafenib	25-35	BH3 interacting domain death agonist	Homo sapiens	44-47
31250402-0	2019	Dabrafenib Plus Trametinib for BRAF V600E-Mutant Non-small Cell Lung Cancer: A Patient Case Report.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	31-35
31250402-1	2019	Dabrafenib plus trametinib is US Food and Drug Administration approved combination therapy for use in patients with BRAF V600E-mutant non-small cell lung cancer, but information on use outside of clinical trials is limited.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	116-120
31082388-3	2019	Here, we describe a patient with BRAF-V600E-positive metastatic melanoma who was sequentially treated with BRAF/MEK inhibitors (dabrafenib/trametinib) and checkpoint inhibitor immunotherapy (nivolumab, followed by pembrolizumab).	dabrafenib	128-138	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	33-37
31082388-3	2019	Here, we describe a patient with BRAF-V600E-positive metastatic melanoma who was sequentially treated with BRAF/MEK inhibitors (dabrafenib/trametinib) and checkpoint inhibitor immunotherapy (nivolumab, followed by pembrolizumab).	dabrafenib	128-138	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	107-111
31082388-3	2019	Here, we describe a patient with BRAF-V600E-positive metastatic melanoma who was sequentially treated with BRAF/MEK inhibitors (dabrafenib/trametinib) and checkpoint inhibitor immunotherapy (nivolumab, followed by pembrolizumab).	dabrafenib	128-138	mitogen-activated protein kinase kinase 7	Homo sapiens	112-115
31558239-0	2019	Acquired BRAF V600E Mutation Mediated Resistance to Osimertinib and Responded to Osimertinib, Dabrafenib, and Trametinib Combination Therapy.	dabrafenib	94-104	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
31095039-0	2019	Effectiveness of dabrafenib in the treatment of patients with BRAF V600-mutated metastatic melanoma in a Named Patient Program.	dabrafenib	17-27	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	62-66
31675726-2	2019	Dual inhibitor therapy using dabrafenib (a selective oral inhibitor of several mutated forms of BRAF kinase) and trametinib (a reversible inhibitor of MEK1 and MEK2) has been used successfully for treatment of metastatic melanoma, anaplastic thyroid cancer, and other tumor types, but has been reported in only a few patients with primary brain tumors and none with pleomorphic xanthoastrocytoma.	dabrafenib	29-39	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	96-100
31095039-1	2019	Given the approval of dabrafenib in patients with BRAF-mutant metastatic melanoma, a better understanding of treatment patterns and clinical outcomes with dabrafenib in a clinical setting is warranted.	dabrafenib	22-32	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	50-54
31095039-1	2019	Given the approval of dabrafenib in patients with BRAF-mutant metastatic melanoma, a better understanding of treatment patterns and clinical outcomes with dabrafenib in a clinical setting is warranted.	dabrafenib	155-165	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	50-54
31533235-1	2019	BRAF V600 mutations have been found in 1-2% of non-small-cell lung cancer (NSCLC) patients, with Food and Drug Administration (FDA) approved treatment of dabrafenib plus trametinib and progression free survival (PFS) of 10.9 months.	dabrafenib	154-164	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
31277524-8	2019	In the setting of BRAF V600E mutated ATC, dabrafenib/trametinib combination therapy and vemurafenib monotherapy have both demonstrated efficacy.	dabrafenib	42-52	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	18-22
31217294-1	2019	The BRAF/MEK inhibitor combination dabrafenib/trametinib is effective in a wide array of rare BRAF-mutant cancers, according to findings from the NCI-MATCH trial presented at the 2019 American Society of Clinical Oncology Annual Meeting in Chicago, IL.	dabrafenib	35-45	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-8
31217294-1	2019	The BRAF/MEK inhibitor combination dabrafenib/trametinib is effective in a wide array of rare BRAF-mutant cancers, according to findings from the NCI-MATCH trial presented at the 2019 American Society of Clinical Oncology Annual Meeting in Chicago, IL.	dabrafenib	35-45	mitogen-activated protein kinase kinase 7	Homo sapiens	9-12
31217294-1	2019	The BRAF/MEK inhibitor combination dabrafenib/trametinib is effective in a wide array of rare BRAF-mutant cancers, according to findings from the NCI-MATCH trial presented at the 2019 American Society of Clinical Oncology Annual Meeting in Chicago, IL.	dabrafenib	35-45	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	94-98
30868471-2	2019	Dual mitogen-activated protein kinase (MAPK) pathway inhibition of BRAF V600E/K and MEK 1/2 kinases with BRAF-MEK inhibitors using dabrafenib-trametinib, vemurafenib-cobimetinib and encorafenib-binimetinib is now the standard of care for BRAF V600E/K tumours.	dabrafenib	131-141	B-Raf proto-oncogene, serine/threonine kinase	Sus scrofa	67-71
30868471-2	2019	Dual mitogen-activated protein kinase (MAPK) pathway inhibition of BRAF V600E/K and MEK 1/2 kinases with BRAF-MEK inhibitors using dabrafenib-trametinib, vemurafenib-cobimetinib and encorafenib-binimetinib is now the standard of care for BRAF V600E/K tumours.	dabrafenib	131-141	B-Raf proto-oncogene, serine/threonine kinase	Sus scrofa	105-109
30868471-2	2019	Dual mitogen-activated protein kinase (MAPK) pathway inhibition of BRAF V600E/K and MEK 1/2 kinases with BRAF-MEK inhibitors using dabrafenib-trametinib, vemurafenib-cobimetinib and encorafenib-binimetinib is now the standard of care for BRAF V600E/K tumours.	dabrafenib	131-141	B-Raf proto-oncogene, serine/threonine kinase	Sus scrofa	105-109
31180164-0	2019	Dynamics of neutrophil and C-reactive protein reflect the clinical course of pyrexia during combination therapy with dabrafenib and trametinib.	dabrafenib	117-127	C-reactive protein	Homo sapiens	27-45
31260421-8	2019	Treatment was switched to dabrafenib (a BRAF inhibitor) with no recurrence of drug pneumonitis.	dabrafenib	26-36	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	40-44
31440061-11	2019	Moreover, a 47-year-old female with a recurrent adenocarcinoma and a BRAF V600E mutation exhibited tumor regression after a fourth line therapy with dabrafenib and trametinib, targeting agents against BRAF mutations.	dabrafenib	149-159	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	69-73
31440061-11	2019	Moreover, a 47-year-old female with a recurrent adenocarcinoma and a BRAF V600E mutation exhibited tumor regression after a fourth line therapy with dabrafenib and trametinib, targeting agents against BRAF mutations.	dabrafenib	149-159	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	201-205
31063355-9	2019	JNK-IN-8 significantly enhanced the response to dabrafenib in resistant cells overexpressing JNK1WT, JNK2WT, and JNK1C116S but had no effect on cells expressing JNK2C116S, suggesting that JNK2 signaling is also crucial for BRAFi resistance in a subset of melanomas.	dabrafenib	48-58	mitogen-activated protein kinase 8	Homo sapiens	0-3
31063355-9	2019	JNK-IN-8 significantly enhanced the response to dabrafenib in resistant cells overexpressing JNK1WT, JNK2WT, and JNK1C116S but had no effect on cells expressing JNK2C116S, suggesting that JNK2 signaling is also crucial for BRAFi resistance in a subset of melanomas.	dabrafenib	48-58	mitogen-activated protein kinase 8	Homo sapiens	93-99
31063355-9	2019	JNK-IN-8 significantly enhanced the response to dabrafenib in resistant cells overexpressing JNK1WT, JNK2WT, and JNK1C116S but had no effect on cells expressing JNK2C116S, suggesting that JNK2 signaling is also crucial for BRAFi resistance in a subset of melanomas.	dabrafenib	48-58	mitogen-activated protein kinase 9	Homo sapiens	101-105
31379943-1	2019	FDA-approved kinase inhibitors are now used for melanoma, including combinations of the MEK inhibitor trametinib, and BRAF inhibitor dabrafenib for BRAFV600 mutations.	dabrafenib	133-143	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	118-122
29152725-5	2019	The second patient had stage III BRAF V600R mutant melanoma that was treated with pembrolizumab and dabrafenib, and also developed a regressed melanocytic nevus.	dabrafenib	100-110	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	33-37
30060710-0	2019	Acute encephalopathy secondary to dabrafenib and trametinib in BRAF-positive metastatic adenocarcinoma of the lung.	dabrafenib	34-44	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	63-67
30060710-6	2019	We report a case of acute encephalopathy in a patient with BRAF mutated metastatic lung cancer due to dabrafenib and trametinib treatment.	dabrafenib	102-112	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	59-63
31467489-0	2019	Dabrafenib and Trametinib prolong coagulation through the inhibition of tissue factor in BRAFv600e mutated melanoma cells in vitro.	dabrafenib	0-10	coagulation factor III, tissue factor	Homo sapiens	72-85
31467489-4	2019	Methods: The expression of tissue factor was investigated after the treatment with the BRAF inhibitor Dabrafenib and the MEK inhibitor Trametinib in the BRAFv600e mutated melanoma cell lines A-375 and SK-MEL-28, together with its ability to activate the coagulation cascade.	dabrafenib	102-112	coagulation factor III, tissue factor	Homo sapiens	27-40
31166680-12	2019	CONCLUSIONS: First-line treatment with dabrafenib plus trametinib led to long-term benefit in approximately one third of the patients who had unresectable or metastatic melanoma with a BRAF V600E or V600K mutation.	dabrafenib	39-49	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	185-189
30598499-0	2019	Adverse Event Management in Patients with BRAF V600E-Mutant Non-Small Cell Lung Cancer Treated with Dabrafenib plus Trametinib.	dabrafenib	100-110	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	42-46
30598499-3	2019	Dabrafenib plus trametinib combination therapy was first approved for the treatment of metastatic melanoma harboring the BRAF V600-mutation in 2014.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	121-125
30598499-10	2019	IMPLICATIONS FOR PRACTICE: The combination of dabrafenib plus trametinib has demonstrated substantial clinical activity in patients with BRAF V600E-mutant non-small cell lung cancer, leading to U.S. Food and Drug Administration approval.	dabrafenib	46-56	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	137-141
29161237-0	2019	BILATERAL VISUAL FIELD DEFECTS IN A PATIENT TREATED WITH THE MEK AND BRAF INHIBITORS TRAMETINIB AND DABRAFENIB FOR MELANOMA OF UNKNOWN ORIGIN.	dabrafenib	100-110	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	69-73
31236710-9	2019	If the BRAF mutation status is positive, the combination of dabrafenib and trametinib is a plausible option.	dabrafenib	60-70	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	7-11
31171878-0	2019	Dabrafenib, trametinib and pembrolizumab or placebo in BRAF-mutant melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	55-59
31227006-0	2019	miR-126-3p down-regulation contributes to dabrafenib acquired resistance in melanoma by up-regulating ADAM9 and VEGF-A.	dabrafenib	42-52	microRNA 1263	Homo sapiens	0-10
31227006-0	2019	miR-126-3p down-regulation contributes to dabrafenib acquired resistance in melanoma by up-regulating ADAM9 and VEGF-A.	dabrafenib	42-52	ADAM metallopeptidase domain 9	Homo sapiens	102-107
31227006-0	2019	miR-126-3p down-regulation contributes to dabrafenib acquired resistance in melanoma by up-regulating ADAM9 and VEGF-A.	dabrafenib	42-52	vascular endothelial growth factor A	Homo sapiens	112-118
31227006-9	2019	RESULTS: miR-126-3p was significantly down-regulated in the dabrafenib-resistant sublines as compared with their parental counterparts.	dabrafenib	60-70	microRNA 1263	Homo sapiens	9-19
31227006-10	2019	miR-126-3p replacement in the drug-resistant cells inhibited proliferation, cell cycle progression, phosphorylation of ERK1/2 and/or AKT, invasiveness, VEGF-A and ADAM9 expression, and increased dabrafenib sensitivity.	dabrafenib	195-205	microRNA 1263	Homo sapiens	0-10
31227006-12	2019	ADAM9 knock-down in the resistant cells increased dabrafenib sensitivity, whereas miR-126-3p enforced expression or ADAM9 silencing in the drug-sensitive cells delayed the development of resistance.	dabrafenib	50-60	ADAM metallopeptidase domain 9	Homo sapiens	0-5
31227006-15	2019	CONCLUSIONS: Strategies restoring miR-126-3p expression or targeting VEGF-A or ADAM9 could restrain growth and metastasis of dabrafenib-resistant melanomas and increase their drug sensitivity.	dabrafenib	125-135	vascular endothelial growth factor A	Homo sapiens	69-75
31227006-15	2019	CONCLUSIONS: Strategies restoring miR-126-3p expression or targeting VEGF-A or ADAM9 could restrain growth and metastasis of dabrafenib-resistant melanomas and increase their drug sensitivity.	dabrafenib	125-135	ADAM metallopeptidase domain 9	Homo sapiens	79-84
30994353-2	2019	In this study, we employed two targeted quantitative proteomics approaches for monitoring separately the alterations in protein expression and ATP binding affinities of kinases in cultured human melanoma cells elicited by two FDA-approved small-molecule BRAF inhibitors, dabrafenib and vemurafenib.	dabrafenib	271-281	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	254-258
31312411-1	2019	One effective means to achieve inhibitor specificity for RAF kinases, an important family of cancer drug targets, has been to target the monomeric inactive state conformation of the kinase domain, which, unlike most other kinases, can accommodate sulfonamide-containing drugs such as vemurafenib and dabrafenib because of the presence of a unique pocket specific to inactive RAF kinases.	dabrafenib	300-310	zinc fingers and homeoboxes 2	Homo sapiens	57-60
31158244-8	2019	BRAF K601E demonstrated reduced sensitivity to dabrafenib compared to BRAF V600E, but the combination of RAF plus MEK inhibition was effective in cells expressing this mutation.	dabrafenib	47-57	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
31158244-8	2019	BRAF K601E demonstrated reduced sensitivity to dabrafenib compared to BRAF V600E, but the combination of RAF plus MEK inhibition was effective in cells expressing this mutation.	dabrafenib	47-57	zinc fingers and homeoboxes 2	Homo sapiens	1-4
31187521-4	2019	Identification of the BRAF-V600E kinase mutation as the genetic cause of HCL has opened the way, in the relapsed/refractory experimental setting, to targeted and non-myelotoxic effective strategies that are based on inhibition of BRAF with vemurafenib, co-inhibition of BRAF and its target MEK with dabrafenib and trametinib, and BRAF inhibition with vemurafenib combined with anti-CD20 immunotherapy.	dabrafenib	299-309	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	22-26
31187521-4	2019	Identification of the BRAF-V600E kinase mutation as the genetic cause of HCL has opened the way, in the relapsed/refractory experimental setting, to targeted and non-myelotoxic effective strategies that are based on inhibition of BRAF with vemurafenib, co-inhibition of BRAF and its target MEK with dabrafenib and trametinib, and BRAF inhibition with vemurafenib combined with anti-CD20 immunotherapy.	dabrafenib	299-309	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	230-234
31187521-4	2019	Identification of the BRAF-V600E kinase mutation as the genetic cause of HCL has opened the way, in the relapsed/refractory experimental setting, to targeted and non-myelotoxic effective strategies that are based on inhibition of BRAF with vemurafenib, co-inhibition of BRAF and its target MEK with dabrafenib and trametinib, and BRAF inhibition with vemurafenib combined with anti-CD20 immunotherapy.	dabrafenib	299-309	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	230-234
31187521-4	2019	Identification of the BRAF-V600E kinase mutation as the genetic cause of HCL has opened the way, in the relapsed/refractory experimental setting, to targeted and non-myelotoxic effective strategies that are based on inhibition of BRAF with vemurafenib, co-inhibition of BRAF and its target MEK with dabrafenib and trametinib, and BRAF inhibition with vemurafenib combined with anti-CD20 immunotherapy.	dabrafenib	299-309	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	230-234
30094711-1	2019	Dabrafenib is a potent and selective inhibitor of BRAF-mutant kinase that is approved, as monotherapy or in combination with trametinib (mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor), for unresectable or metastatic BRAF-mutated melanoma, advanced non-small cell lung cancer and anaplastic thyroid cancer harbouring the BRAFV600E mutation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	50-54
31024839-6	2019	Herein, we report a case of a 70-years old patient with a metastatic conjunctival melanoma harboring V600E BRAF mutation successfully treated with dabrafenib and trametinib.	dabrafenib	147-157	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	107-111
30852924-1	2019	AIM: Comparison of clinical outcomes of nivolumab + ipilimumab versus BRAF + MEK inhibitors (dabrafenib + trametinib or vemurafenib + cobimetinib) in BRAF-mutant advanced melanoma.	dabrafenib	93-103	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	150-154
30785650-4	2019	The protein expression of Raf or ERK1/2 was clearly decreased by Raf inhibitor GSK2118436 or ERK1/2 inhibitor SCH772984, respectively (p &lt; 0.05).	dabrafenib	79-89	mitogen-activated protein kinase 3	Bos taurus	33-39
30094711-1	2019	Dabrafenib is a potent and selective inhibitor of BRAF-mutant kinase that is approved, as monotherapy or in combination with trametinib (mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor), for unresectable or metastatic BRAF-mutated melanoma, advanced non-small cell lung cancer and anaplastic thyroid cancer harbouring the BRAFV600E mutation.	dabrafenib	0-10	mitogen-activated protein kinase kinase 7	Homo sapiens	185-188
30094711-1	2019	Dabrafenib is a potent and selective inhibitor of BRAF-mutant kinase that is approved, as monotherapy or in combination with trametinib (mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor), for unresectable or metastatic BRAF-mutated melanoma, advanced non-small cell lung cancer and anaplastic thyroid cancer harbouring the BRAFV600E mutation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	233-237
30094711-7	2019	The main elimination route of dabrafenib is the oxidative metabolism via CYP3A4/2C8 and biliary excretion.	dabrafenib	30-40	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	73-83
30094711-11	2019	Considering that dabrafenib is a substrate of CYP3A4/2C8 and is a CYP3A4/2B6/2C inducer, drug-drug interactions are expected with dabrafenib.	dabrafenib	17-27	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	46-56
30094711-11	2019	Considering that dabrafenib is a substrate of CYP3A4/2C8 and is a CYP3A4/2B6/2C inducer, drug-drug interactions are expected with dabrafenib.	dabrafenib	130-140	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	46-56
30719722-1	2019	The combination therapy of dabrafenib and trametinib revolutionized the treatment for BRAF V600-mutated melanoma.	dabrafenib	27-37	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	86-90
30144031-9	2019	BRAF inhibitor dabrafenib and MEK inhibitor trametinib prevented growth of BRAFV600E positive NEC xenografts.	dabrafenib	15-25	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
30802229-1	2019	Targeted therapy with the BRAF inhibitors vemurafenib and dabrafenib is an effective treatment regimen in patients with advanced melanoma carrying the BRAF V600E mutation.	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	151-155
30661097-1	2019	PURPOSE: The combination of a BRAF inhibitor dabrafenib and a MEK inhibitor trametinib (CombiDT) has improved outcomes compared with chemotherapy or BRAF inhibitor monotherapy in advanced BRAF V600E/K melanoma.	dabrafenib	45-55	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	30-34
30802229-1	2019	Targeted therapy with the BRAF inhibitors vemurafenib and dabrafenib is an effective treatment regimen in patients with advanced melanoma carrying the BRAF V600E mutation.	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	26-30
30793515-9	2019	Magnolol-induced a synergistic effect in combination with either BRAF/MEK inhibitors dabrafenib/trametinib or docetaxel at a lower concentration than usually applied in melanoma patients.	dabrafenib	85-95	mitogen-activated protein kinase kinase 7	Homo sapiens	70-73
31747798-9	2019	He began to take daily oral dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor), leading to no abnormal uptake on PET in half a year.	dabrafenib	28-38	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	40-44
30679688-1	2019	The BRAF inhibitors dabrafenib and vemurafenib induce remarkable clinical responses in patients with BRAF-mutated melanomas.	dabrafenib	20-30	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-8
30679688-1	2019	The BRAF inhibitors dabrafenib and vemurafenib induce remarkable clinical responses in patients with BRAF-mutated melanomas.	dabrafenib	20-30	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	101-105
30513023-5	2019	The combination of trametinib and dabrafenib has been approved for this population of BRAF mutant NSCLC patients.	dabrafenib	34-44	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	86-90
30794926-14	2019	The best treatments include the combination of B-Raf and MEK inhibitors (dabrafenib and trametinib, encorafenib and binimetinib, vemurafenib and cobimetanib).	dabrafenib	73-83	mitogen-activated protein kinase kinase 7	Homo sapiens	57-60
30630714-2	2019	Much effort has been made to suppress BRAF V600E through small molecules like vemurafenib and dabrafenib, but the MAPK pathway remains active through paradoxical activation, where CRAF transmits the signal of the MAPK pathway either alone or along with BRAF V600E.	dabrafenib	94-104	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	38-42
30847387-5	2019	However, MAPKi (dabrafenib or selumetinib) induced these effects only in BRAF V600E-mutant cells.	dabrafenib	16-26	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.	dabrafenib	48-58	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	99-103
29777202-2	2019	In this study, we found that the human melanoma cell clones, A375-DR and A375-TR, with acquired resistance to BRAF inhibitor dabrafenib and MEK inhibitor trametinib, were cross resistant to other MAPK pathway inhibitors.	dabrafenib	125-135	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	110-114
30248172-0	2019	Dabrafenib plus trametinib in BRAF K601E-mutant melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	30-34
30225883-0	2019	Resistance mechanism of the oncogenic beta3-alphaC deletion mutation in BRAF kinase to dabrafenib and vemurafenib revealed by molecular dynamics simulations and binding free energy calculations.	dabrafenib	87-97	T cell immune regulator 1, ATPase H+ transporting V0 subunit a3	Homo sapiens	38-43
30225883-0	2019	Resistance mechanism of the oncogenic beta3-alphaC deletion mutation in BRAF kinase to dabrafenib and vemurafenib revealed by molecular dynamics simulations and binding free energy calculations.	dabrafenib	87-97	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	72-76
30225883-2	2019	Emergence of the beta3-alphaC loop deletion mutation (DeltaNVTAP) in BRAF kinase frequently occurred in human cancers seriously compromises the therapeutic efficacy of some BRAF kinase inhibitors, such as dabrafenib and vemurafenib.	dabrafenib	205-215	T cell immune regulator 1, ATPase H+ transporting V0 subunit a3	Homo sapiens	17-22
30225883-2	2019	Emergence of the beta3-alphaC loop deletion mutation (DeltaNVTAP) in BRAF kinase frequently occurred in human cancers seriously compromises the therapeutic efficacy of some BRAF kinase inhibitors, such as dabrafenib and vemurafenib.	dabrafenib	205-215	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	69-73
30225883-4	2019	In this study, the influence of the beta3-alphaC deletion mutation on the binding profiles of three BRAF kinase inhibitors (AZ628, dabrafenib, and vemurafenib) with BRAFV600E or BRAFDeltaNVTAP was explored by conventional molecular dynamics (MD) simulations and binding free energy calculations.	dabrafenib	131-141	T cell immune regulator 1, ATPase H+ transporting V0 subunit a3	Homo sapiens	36-41
30225883-4	2019	In this study, the influence of the beta3-alphaC deletion mutation on the binding profiles of three BRAF kinase inhibitors (AZ628, dabrafenib, and vemurafenib) with BRAFV600E or BRAFDeltaNVTAP was explored by conventional molecular dynamics (MD) simulations and binding free energy calculations.	dabrafenib	131-141	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	100-104
30225883-4	2019	In this study, the influence of the beta3-alphaC deletion mutation on the binding profiles of three BRAF kinase inhibitors (AZ628, dabrafenib, and vemurafenib) with BRAFV600E or BRAFDeltaNVTAP was explored by conventional molecular dynamics (MD) simulations and binding free energy calculations.	dabrafenib	131-141	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	178-192
30383722-0	2019	Anaphylaxis-like reaction to anti-BRAF inhibitor dabrafenib confirmed by drug provocation test.	dabrafenib	49-59	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	34-38
30383722-5	2019	We report a case of anaphylactic reaction to the BRAF inhibitor dabrafenib administered as a first-line treatment.	dabrafenib	64-74	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	49-53
31709422-12	2019	The FDA recently approved Dabrafenib plus trametinib for BRAF V600E mutated ATC.	dabrafenib	26-36	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	57-61
31766881-3	2019	Recently, in BRAF V600E mutated ATCs, new targeted therapy using a combination of a BRAF inhibitor, dabrafenib (Dab), with a mitogen-activated extracellular protein kinase (MEK) inhibitor, trametinib (Tram), has shown significant promise.	dabrafenib	100-110	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	13-17
31766881-3	2019	Recently, in BRAF V600E mutated ATCs, new targeted therapy using a combination of a BRAF inhibitor, dabrafenib (Dab), with a mitogen-activated extracellular protein kinase (MEK) inhibitor, trametinib (Tram), has shown significant promise.	dabrafenib	100-110	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	84-88
30198802-3	2018	Areas covered: Dabrafenib is a potent adenosine-triphosphate-competitive inhibitor of BRAF kinase and is selective for the BRAFV600E mutation in kinase panel screening, cell lines, and xenografts.	dabrafenib	15-25	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	86-90
30343620-0	2018	Longer Follow-Up Confirms Relapse-Free Survival Benefit With Adjuvant Dabrafenib Plus Trametinib in Patients With Resected BRAF V600-Mutant Stage III Melanoma.	dabrafenib	70-80	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	123-127
30343620-1	2018	PURPOSE: Dabrafenib plus trametinib improved relapse-free survival (RFS) versus placebo (hazard ratio [HR], 0.47; P < .001) in patients with resected BRAF V600-mutant stage III melanoma (BRF115532; COMBI-AD; ClinicalTrials.gov identifier: NCT01682083).	dabrafenib	9-19	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	150-154
30422663-0	2018	Investigation on the Interaction of Dabrafenib with Human Serum Albumin Using Combined Experiment and Molecular Dynamics Simulation: Exploring the Binding Mechanism, Esterase-like Activity, and Antioxidant Activity.	dabrafenib	36-46	albumin	Homo sapiens	58-71
30422663-2	2018	The present work explored the binding mechanism of dabrafenib-human serum albumin (HSA) and the effect on the esterase-like activity and antioxidant activity of HSA by using 19F NMR, spectroscopy methods, and molecular dynamics simulation.	dabrafenib	51-61	albumin	Homo sapiens	68-81
30196713-1	2019	AIM: A survival benefit was demonstrated by dabrafenib + trametinib for metastatic BRAF-mutated melanoma patients.	dabrafenib	44-54	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	83-87
29574693-6	2018	Multivariable analysis indicated that consideration of baseline weight, body mass index, and CYP2C8, CYP3A4, and P-gp abundance strongly predicts steady-state dabrafenib trough concentration above 48 ng/mL (ROC AUC = 0.94; accuracy = 86%).	dabrafenib	159-169	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	93-99
29574693-6	2018	Multivariable analysis indicated that consideration of baseline weight, body mass index, and CYP2C8, CYP3A4, and P-gp abundance strongly predicts steady-state dabrafenib trough concentration above 48 ng/mL (ROC AUC = 0.94; accuracy = 86%).	dabrafenib	159-169	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	101-107
29574693-6	2018	Multivariable analysis indicated that consideration of baseline weight, body mass index, and CYP2C8, CYP3A4, and P-gp abundance strongly predicts steady-state dabrafenib trough concentration above 48 ng/mL (ROC AUC = 0.94; accuracy = 86%).	dabrafenib	159-169	phosphoglycolate phosphatase	Homo sapiens	113-117
30588251-7	2018	In this study, the BRAF inhibitor dabrafenib was used to generate resistant cell lines (A375DR, SK-MEL-24DR and WM-115DR).	dabrafenib	34-44	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	19-23
30559933-8	2018	BRAFV600E-expressing TCC-NECT-2 cells were sensitive to BRAF inhibitor vemurafenib, and especially dabrafenib, in vitro, and were strongly inhibited in a dose-dependent manner.	dabrafenib	99-109	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
30137437-6	2018	Among them, dabrafenib, which is known as a B-Raf kinase inhibitor and is approved for the treatment of malignant melanoma, showed remarkable cytoprotective effects in neurotoxin-treated SH-SY5Y cells and mice.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	44-49
30137437-7	2018	Dabrafenib was found to inhibit apoptosis, and to enhance the phosphorylation of extracellular signal-regulated kinase (ERK), and inhibit the phosphorylation of c-Jun NH2-terminal kinase.	dabrafenib	0-10	mitogen-activated protein kinase 1	Homo sapiens	81-118
30137437-7	2018	Dabrafenib was found to inhibit apoptosis, and to enhance the phosphorylation of extracellular signal-regulated kinase (ERK), and inhibit the phosphorylation of c-Jun NH2-terminal kinase.	dabrafenib	0-10	mitogen-activated protein kinase 1	Homo sapiens	120-123
30137437-8	2018	Dabrafenib targets B-Raf, and we confirmed a protein-protein interaction between B-Raf and Rit2, which is coded by RIT2, a PD risk gene in Asians and Caucasians.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	19-24
30137437-8	2018	Dabrafenib targets B-Raf, and we confirmed a protein-protein interaction between B-Raf and Rit2, which is coded by RIT2, a PD risk gene in Asians and Caucasians.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	81-86
30137437-8	2018	Dabrafenib targets B-Raf, and we confirmed a protein-protein interaction between B-Raf and Rit2, which is coded by RIT2, a PD risk gene in Asians and Caucasians.	dabrafenib	0-10	Ras like without CAAX 2	Homo sapiens	91-95
30137437-8	2018	Dabrafenib targets B-Raf, and we confirmed a protein-protein interaction between B-Raf and Rit2, which is coded by RIT2, a PD risk gene in Asians and Caucasians.	dabrafenib	0-10	Ras like without CAAX 2	Homo sapiens	115-119
30137437-9	2018	In RIT2-knockout cells, the phosphorylation of ERK was reduced, and dabrafenib treatment improved the ERK phosphorylation.	dabrafenib	68-78	Ras like without CAAX 2	Homo sapiens	3-7
30137437-9	2018	In RIT2-knockout cells, the phosphorylation of ERK was reduced, and dabrafenib treatment improved the ERK phosphorylation.	dabrafenib	68-78	mitogen-activated protein kinase 1	Homo sapiens	102-105
30198802-4	2018	The efficacy and safety of dabrafenib alone or in combination with the MEK inhibitor trametinib has been demonstrated in a number of clinical trials and herein, we discuss this data and outline the current and future role of BRAF/MEK inhibition in the management of advanced lung cancer.	dabrafenib	27-37	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	225-229
30198802-4	2018	The efficacy and safety of dabrafenib alone or in combination with the MEK inhibitor trametinib has been demonstrated in a number of clinical trials and herein, we discuss this data and outline the current and future role of BRAF/MEK inhibition in the management of advanced lung cancer.	dabrafenib	27-37	mitogen-activated protein kinase kinase 7	Homo sapiens	230-233
31249721-1	2018	Trametinib is a MEK inhibitor approved both as a single agent and in combination with dabrafenib for the treatment of BRAF V600E or V600K mutated melanoma.	dabrafenib	86-96	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	118-122
30383630-4	2018	PATIENT CONCERNS: A 52 year old man presented with clinical stage II unresectable melanoma with BRAF mutation, was initiated on treatement with Dabrafenib and Trametinib.	dabrafenib	144-154	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	96-100
30320090-8	2018	Systemic treatment with the combination of a BRAF-inhibitor (dabrafenib) and MEK-inhibitor (trametinib) was started and followed by a switch to an anti-PD-1 antibody (pembrolizumab).	dabrafenib	61-71	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	45-49
30410366-2	2018	Combined BRAF and MEK inhibitors such as dabrafenib and trametinib, vemurafenib and cobimetinib, and encorafenib and binimetinib are US Food and Drug Administration (FDA)-approved to treat patients with BRAF V600-mutated advanced melanoma.	dabrafenib	41-51	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
30410366-2	2018	Combined BRAF and MEK inhibitors such as dabrafenib and trametinib, vemurafenib and cobimetinib, and encorafenib and binimetinib are US Food and Drug Administration (FDA)-approved to treat patients with BRAF V600-mutated advanced melanoma.	dabrafenib	41-51	mitogen-activated protein kinase kinase 7	Homo sapiens	18-21
30320196-0	2018	Tumoral melanosis associated with combined BRAF/MEK inhibition (dabrafenib/trametinib) in metastatic melanoma.	dabrafenib	64-74	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	43-47
30320196-0	2018	Tumoral melanosis associated with combined BRAF/MEK inhibition (dabrafenib/trametinib) in metastatic melanoma.	dabrafenib	64-74	mitogen-activated protein kinase kinase 7	Homo sapiens	48-51
30541319-7	2018	On the other hand, for patients with disseminated BRAF mutant malignant melanoma or lung cancer, selective treatments with RAF and MEK inhibitors (vemurafenib, dabrafenib, and trametinib) are available.	dabrafenib	160-170	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	50-54
30541319-7	2018	On the other hand, for patients with disseminated BRAF mutant malignant melanoma or lung cancer, selective treatments with RAF and MEK inhibitors (vemurafenib, dabrafenib, and trametinib) are available.	dabrafenib	160-170	zinc fingers and homeoboxes 2	Homo sapiens	51-54
30541319-7	2018	On the other hand, for patients with disseminated BRAF mutant malignant melanoma or lung cancer, selective treatments with RAF and MEK inhibitors (vemurafenib, dabrafenib, and trametinib) are available.	dabrafenib	160-170	mitogen-activated protein kinase kinase 7	Homo sapiens	131-134
29992710-6	2018	Full-length BRAF analysis with small-molecule BRAF inhibitors shows that two drugs, dabrafenib and vemurafenib, can modestly enhance kinase activity of BRAF at low concentration.	dabrafenib	84-94	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	12-16
29992710-6	2018	Full-length BRAF analysis with small-molecule BRAF inhibitors shows that two drugs, dabrafenib and vemurafenib, can modestly enhance kinase activity of BRAF at low concentration.	dabrafenib	84-94	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	46-50
29992710-6	2018	Full-length BRAF analysis with small-molecule BRAF inhibitors shows that two drugs, dabrafenib and vemurafenib, can modestly enhance kinase activity of BRAF at low concentration.	dabrafenib	84-94	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	46-50
30255823-3	2018	Dabrafenib, a BRAF inhibitor and Trametinib, a MEK inhibitor are two molecularly targeted agents recently approved for treatment of advanced, unresectable melanomas.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
30246138-0	2018	Dramatic clinical response following dabrafenib and trametinib therapy in a heavily pretreated low grade serous ovarian carcinoma patient with a BRAF V600E mutation.	dabrafenib	37-47	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	145-149
30246138-3	2018	Thereafter, she underwent molecular profiling, which revealed a BRAF V600E mutation; accordingly, the patient was administered dabrafenib and trametinib combination therapy, a regimen that resulted in a precipitous decline of her CA-125 to 35 U/mL following the 6th cycle.	dabrafenib	127-137	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	64-68
29880583-3	2018	Here, we report a complete response followed by clinical progression in a patient with a BRAFV600E-mutant brain tumor treated with dabrafenib.	dabrafenib	131-141	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	89-93
29880583-5	2018	Expressing BRAFV600E/L514V induces ERK signaling, promotes RAF dimer formation, and is sufficient to confer resistance to dabrafenib.	dabrafenib	122-132	zinc fingers and homeoboxes 2	Homo sapiens	12-15
29880583-8	2018	We demonstrate a secondary mutation in BRAF (V600E/L514V) following progression on dabrafenib and confirm functionally that this mutation is responsible for resistance.	dabrafenib	83-93	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	39-43
30036245-3	2018	Early after the beginning of BRAF-MEK therapy (dabrafenib and trametinib), impressive improvement in PET/CT imaging was achieved.	dabrafenib	47-57	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	29-33
30036245-3	2018	Early after the beginning of BRAF-MEK therapy (dabrafenib and trametinib), impressive improvement in PET/CT imaging was achieved.	dabrafenib	47-57	mitogen-activated protein kinase kinase 7	Homo sapiens	34-37
30118796-13	2018	Vemurafenib and dabrafenib produce the paradoxical activation of the MAP kinase pathway in wild type BRAF cells.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	101-105
30118796-17	2018	Vemurafenib and dabrafenib bind to an inactive form of B-Raf (alphaC-helixout and DFG-Din) and are classified as type I1/2 inhibitors.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	55-60
30143629-5	2018	Using matched melanoma samples derived from patients receiving dabrafenib + trametinib, we identify IGFBP2 as a potential biomarker for MAPKi resistance.	dabrafenib	63-73	insulin like growth factor binding protein 2	Homo sapiens	100-106
30154717-4	2018	In this study, MMP-9 was evaluated in melanoma cells after treatment with dabrafenib.	dabrafenib	74-84	matrix metallopeptidase 9	Homo sapiens	15-20
30154717-7	2018	The performed analyses showed that MMP-9 and pEKR1-2 were statistically down-regulated in melanoma cells after treatment with dabrafenib.	dabrafenib	126-136	matrix metallopeptidase 9	Homo sapiens	35-40
29983861-6	2018	Both splenic and bone marrow-derived (BM) mouse dendritic cells (DC) up-regulated costimulator expression (CD80, CD86) in response to DAB but not VEM treatment.	dabrafenib	134-137	CD80 antigen	Mus musculus	107-111
29631033-0	2018	An Acquired NRAS Q61K Mutation in BRAF V600E-Mutant Lung Adenocarcinoma Resistant to Dabrafenib Plus Trametinib.	dabrafenib	85-95	NRAS proto-oncogene, GTPase	Homo sapiens	12-16
29631033-0	2018	An Acquired NRAS Q61K Mutation in BRAF V600E-Mutant Lung Adenocarcinoma Resistant to Dabrafenib Plus Trametinib.	dabrafenib	85-95	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	34-38
30053879-10	2018	Yet significant improvements have expanded the therapeutic options for treating brain metastases from melanoma, by combining potent BRAF inhibitors such as dabrafenib with checkpoint inhibitors or stereotactic surgery.	dabrafenib	156-166	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	132-136
29968772-6	2018	Inhibition of the MAPK pathway with dabrafenib, a B-Raf inhibitor, or trametinib, a MEK1/2 inhibitor, suppressed both the positively regulated phosphorylation of MAPKs and the negatively regulated phosphorylation of MEK1.	dabrafenib	36-46	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	50-55
29968772-7	2018	Interestingly, the combinations of dabrafenib and rigosertib or trametinib and rigosertib permitted the suppression of positively regulated MAPK phosphorylation together with the promotion of negatively regulated MEK1 phosphorylation.	dabrafenib	35-45	mitogen-activated protein kinase kinase 1	Homo sapiens	213-217
29655274-0	2018	Granulocyte colony-stimulating factor-producing melanoma treated with the combination of dabrafenib and trametinib.	dabrafenib	89-99	colony stimulating factor 3	Homo sapiens	0-37
29962848-1	2018	We report on a patient with an adenocarcinoma of the lung harbouring a BRAF V600E mutation who benefited from combination therapy with dabrafenib-trametinib after developing resistance to vemurafenib.	dabrafenib	135-145	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	71-75
29962848-2	2018	To our knowledge, our report shows, for the first time, that combination therapy with dabrafenib-trametinib can overcome vemurafenib resistance in a BRAF V600E-mutated adenocarcinoma of the lung.	dabrafenib	86-96	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	149-153
29983861-6	2018	Both splenic and bone marrow-derived (BM) mouse dendritic cells (DC) up-regulated costimulator expression (CD80, CD86) in response to DAB but not VEM treatment.	dabrafenib	134-137	CD86 antigen	Mus musculus	113-117
29983861-7	2018	Moreover, DAB and to lesser extent VEM enhanced IL-1beta (interleukin 1 beta) release by splenic DC, and by LPS-stimulated BMDC.	dabrafenib	10-13	interleukin 1 beta	Homo sapiens	48-56
29983861-7	2018	Moreover, DAB and to lesser extent VEM enhanced IL-1beta (interleukin 1 beta) release by splenic DC, and by LPS-stimulated BMDC.	dabrafenib	10-13	interleukin 1 beta	Homo sapiens	58-76
29983861-8	2018	We demonstrate that DAB and VEM activated the NLRC4/Caspase-1 inflammasome.	dabrafenib	20-23	NLR family CARD domain containing 4	Homo sapiens	46-51
29983861-8	2018	We demonstrate that DAB and VEM activated the NLRC4/Caspase-1 inflammasome.	dabrafenib	20-23	caspase 1	Homo sapiens	52-61
29983861-11	2018	Immunomodulatory activity of DAB and VEM was also observed in human monocyte-derived DC, and DAB induced IL-1beta in human primary DC.	dabrafenib	93-96	interleukin 1 beta	Homo sapiens	105-113
29438093-1	2018	On June 22, 2017, the Food and Drug Administration expanded indications for dabrafenib and trametinib to include treatment of patients with metastatic non-small cell lung cancer (NSCLC) harboring BRAF V600E mutations.	dabrafenib	76-86	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	196-200
29438093-7	2018	The treatment effect of dabrafenib 150 mg twice daily was evaluated in 78 patients with previously treated BRAF mutant NSCLC, yielding an ORR of 27% (95% CI 18%-38%), establishing that dabrafenib alone is active, but that the addition of trametinib is necessary to achieve an ORR of &gt;40%.	dabrafenib	24-34	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	107-111
29438093-9	2018	IMPLICATIONS FOR PRACTICE: The approvals of dabrafenib and trametinib, administered concurrently, provide a new regimen for the treatment of a rare subset of non-small cell lung cancer (NSCLC) and demonstrate how drugs active for treatment of BRAF-mutant tumors in one setting predict efficacy and can provide supportive evidence for approval in another setting.	dabrafenib	44-54	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	243-247
29438093-11	2018	The test was shown to accurately and reliably select patients with NSCLC with the BRAF V600E mutation for whom treatment with dabrafenib and trametinib is the optimal treatment.	dabrafenib	126-136	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	82-86
29881714-17	2018	Novel targeted and immunotherapeutic agents have also revolutionized the systemic management of melanoma (ipilimumab, nivolumab, pembrolizumab, and BRAF inhibitors dabrafenib and vemurafenib).	dabrafenib	164-174	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	148-152
29729495-4	2018	Clinical trials evaluating the efficacy of the BRAF inhibitor dabrafenib in combination with the downstream MEK inhibitor trametinib in metastatic BRAFV600E-mutated NSCLC guaranteed FDA and EMA rapid approval of the combination regimen in this clinical setting.	dabrafenib	62-72	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	47-51
30231333-8	2018	The combination dabrafenib plus trametinib for BRAF-mutant melanoma was approved in 2014, with similar success for other BRAF plus MEK inhibitor combinations.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	47-51
29380516-0	2018	Response to the BRAF/MEK inhibitors dabrafenib/trametinib in an adolescent with a BRAF V600E mutated anaplastic ganglioglioma intolerant to vemurafenib.	dabrafenib	36-46	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	16-20
29650281-6	2018	The molecules (Dabrafenib-BRAF inhibitor and Trametinib-MEK inhibitor) have proved their credentials alone and in combination as well.	dabrafenib	15-25	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	26-30
29380516-0	2018	Response to the BRAF/MEK inhibitors dabrafenib/trametinib in an adolescent with a BRAF V600E mutated anaplastic ganglioglioma intolerant to vemurafenib.	dabrafenib	36-46	mitogen-activated protein kinase kinase 7	Homo sapiens	21-24
29380516-0	2018	Response to the BRAF/MEK inhibitors dabrafenib/trametinib in an adolescent with a BRAF V600E mutated anaplastic ganglioglioma intolerant to vemurafenib.	dabrafenib	36-46	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	82-86
29380516-3	2018	Here we describe an adolescent female with anaplastic ganglioglioma and significant skin reaction to vemurafenib with subsequent tumor response and tolerance to the BRAF/MEK inhibitor combination of dabrafenib and trametinib without recurrence of previous reaction.	dabrafenib	199-209	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	165-169
29380516-3	2018	Here we describe an adolescent female with anaplastic ganglioglioma and significant skin reaction to vemurafenib with subsequent tumor response and tolerance to the BRAF/MEK inhibitor combination of dabrafenib and trametinib without recurrence of previous reaction.	dabrafenib	199-209	mitogen-activated protein kinase kinase 7	Homo sapiens	170-173
28567600-1	2018	Dabrafenib is a potent BRAF inhibitor, which showed intracranial tumor activity.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	23-27
29399853-0	2018	Phase 1/2 study assessing the safety and efficacy of dabrafenib and trametinib combination therapy in Japanese patients with BRAF V600 mutation-positive advanced cutaneous melanoma.	dabrafenib	53-63	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	125-129
29399853-1	2018	The combination of dabrafenib and trametinib demonstrated encouraging antitumor activity and tolerability, at initial analysis, in Japanese patients with BRAF V600 mutant advanced melanoma warranting further investigation.	dabrafenib	19-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	154-158
29356790-13	2018	Median OS in patients with BM from BRAF-mutated melanoma treated with dabrafenib+trametinib was significantly longer than for vemurafenib.	dabrafenib	70-80	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	35-39
29356791-4	2018	BRAF inhibitor (dabrafenib or vemurafenib) and MEK inhibitor (trametinib or cobimetinib) combination therapies are effective for BRAF-mutant advanced melanomas.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
29356791-4	2018	BRAF inhibitor (dabrafenib or vemurafenib) and MEK inhibitor (trametinib or cobimetinib) combination therapies are effective for BRAF-mutant advanced melanomas.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	129-133
29488243-0	2018	HLA-DRB1*04:05 in two cases of Vogt-Koyanagi-Harada disease-like uveitis developing from an advanced melanoma patient treated by sequential administration of nivolumab and dabrafenib/trametinib therapy.	dabrafenib	172-182	major histocompatibility complex, class II, DR beta 1	Homo sapiens	0-8
32913992-1	2018	Purpose: Dabrafenib and trametinib are approved for the management of advanced non-small-cell lung cancers (NSCLCs) that harbor BRAF V600E mutations.	dabrafenib	9-19	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	128-132
29621181-0	2018	Dabrafenib Treatment in a Patient with an Epithelioid Glioblastoma and BRAF V600E Mutation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	71-75
29662327-5	2018	This paper summarizes the clinical evidence that lead to the recent approval of the combination of dabrafenib and trametinib to treat patients with advanced NSCLC who harbor a BRAF V600E mutation.	dabrafenib	99-109	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	176-180
29534162-3	2018	In this study, we explored the effect of combined use of dabrafenib, a BRAF inhibitor, and cetuximab, an EGFR inhibitor, on BRAF(V600E)-mutant CRC stem cells and its possible mechanisms.	dabrafenib	57-67	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	124-129
29534162-4	2018	Through cell viability analysis, flow cytometry, sphere forming, and western blot analysis, we found that the dabrafenib can synergize with cetuximab to reduce cell viability, induce enhanced apoptotic rates and cell cycle arrest in BRAF(V600E)-mutant HT-29 cells and inhibits stem cell capacities.	dabrafenib	110-120	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	233-237
29534162-5	2018	Further, western blot analysis revealed that PTEN/Src/c-Myc pathway is possibly involved in the synergism between dabrafenib and cetuximab.	dabrafenib	114-124	phosphatase and tensin homolog	Homo sapiens	45-49
29534162-5	2018	Further, western blot analysis revealed that PTEN/Src/c-Myc pathway is possibly involved in the synergism between dabrafenib and cetuximab.	dabrafenib	114-124	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	50-53
29534162-5	2018	Further, western blot analysis revealed that PTEN/Src/c-Myc pathway is possibly involved in the synergism between dabrafenib and cetuximab.	dabrafenib	114-124	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	54-59
29534162-6	2018	Overall, our study shows that the combination of dabrafenib and cetuximab results in increased antitumor activity and decreased stem cell capacities in BRAF(V600E)-mutant CRC cells.	dabrafenib	49-59	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	152-156
29243287-1	2018	AIMS: The effect of repeat oral supratherapeutic dosing of the BRAF inhibitor dabrafenib on QTc interval was assessed in patients with BRAF V600-mutant tumours.	dabrafenib	78-88	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	63-67
29243287-1	2018	AIMS: The effect of repeat oral supratherapeutic dosing of the BRAF inhibitor dabrafenib on QTc interval was assessed in patients with BRAF V600-mutant tumours.	dabrafenib	78-88	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	135-139
29632053-4	2018	This report presents 2 cases of malignant brain tumors with BRAF V600E mutations that were resistant to radiation and temozolomide, and reports on their response to targeted treatment with the BRAF and MEK inhibitors dabrafenib and trametinib.	dabrafenib	217-227	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	60-64
29632053-4	2018	This report presents 2 cases of malignant brain tumors with BRAF V600E mutations that were resistant to radiation and temozolomide, and reports on their response to targeted treatment with the BRAF and MEK inhibitors dabrafenib and trametinib.	dabrafenib	217-227	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	193-197
29632053-4	2018	This report presents 2 cases of malignant brain tumors with BRAF V600E mutations that were resistant to radiation and temozolomide, and reports on their response to targeted treatment with the BRAF and MEK inhibitors dabrafenib and trametinib.	dabrafenib	217-227	mitogen-activated protein kinase kinase 7	Homo sapiens	202-205
29701552-0	2018	Recurrent papillary craniopharyngioma with BRAF V600E mutation treated with dabrafenib: case report.	dabrafenib	76-86	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	43-47
29701552-3	2018	With his most recent recurrence following previous surgery and radiotherapy, at 52 years of age, the decision was made to initiate treatment with the BRAF V600E inhibitor dabrafenib.	dabrafenib	171-181	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	150-154
28567600-3	2018	We studied 30 BRAF mutant melanoma patients with BM, who received dabrafenib after local control of the brain between 2014 and 2017.	dabrafenib	66-76	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
29491057-3	2018	MATERIALS AND METHODS: To test whether the BRAF inhibitors dabrafenib and vemurafenib together with ionizing radiation more effectively inhibit melanoma cells, primary human melanoma tumor cell lines expressing wild-type (WT) or mutant V600E BRAF were analyzed by cell survival, cell death, and cell-cycle testing.	dabrafenib	59-69	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	43-47
29363351-3	2018	The revealing of mutations in the BRAF/MEK/ERK pathway has led to the development of BRAF inhibitors such as vemurafenib and dabrafenib for the treatment of cutaneous MM.	dabrafenib	125-135	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	34-38
29363351-3	2018	The revealing of mutations in the BRAF/MEK/ERK pathway has led to the development of BRAF inhibitors such as vemurafenib and dabrafenib for the treatment of cutaneous MM.	dabrafenib	125-135	mitogen-activated protein kinase kinase 7	Homo sapiens	39-42
29363351-3	2018	The revealing of mutations in the BRAF/MEK/ERK pathway has led to the development of BRAF inhibitors such as vemurafenib and dabrafenib for the treatment of cutaneous MM.	dabrafenib	125-135	mitogen-activated protein kinase 1	Homo sapiens	43-46
29363351-3	2018	The revealing of mutations in the BRAF/MEK/ERK pathway has led to the development of BRAF inhibitors such as vemurafenib and dabrafenib for the treatment of cutaneous MM.	dabrafenib	125-135	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	85-89
29363351-7	2018	Expert opinion: Two combined treatments (i.e. trametinib plus dabrafenib and vemurafenib plus cobimetinib) target two different kinases in the BRAF/MEK/ERK pathway.	dabrafenib	62-72	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	143-147
29467863-2	2018	Other drugs target different driver mutants, including the serine/threonine-protein kinase B-raf (BRAF) inhibitor dabrafenib, which has exhibited promising efficacy for treating patients with metastatic BRAF-mutated NSCLC.	dabrafenib	114-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	91-96
28991513-0	2018	Long-Term Outcomes in Patients With BRAF V600-Mutant Metastatic Melanoma Who Received Dabrafenib Combined With Trametinib.	dabrafenib	86-96	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	36-40
29467863-2	2018	Other drugs target different driver mutants, including the serine/threonine-protein kinase B-raf (BRAF) inhibitor dabrafenib, which has exhibited promising efficacy for treating patients with metastatic BRAF-mutated NSCLC.	dabrafenib	114-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	98-102
29467863-2	2018	Other drugs target different driver mutants, including the serine/threonine-protein kinase B-raf (BRAF) inhibitor dabrafenib, which has exhibited promising efficacy for treating patients with metastatic BRAF-mutated NSCLC.	dabrafenib	114-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	203-207
29520339-8	2018	At follow-up, case #1 was a 55-year-old man who received targeted BRAF inhibitor and MEK inhibitor therapy with dabrafenib and trametinib.	dabrafenib	112-122	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	66-70
29662630-2	2018	Non-V600 BRAF mutations predict sensitivity to combination of a type I RAF inhibitor, Dabrafenib, and a MEK inhibitor, Trametinib.	dabrafenib	86-96	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
29662630-2	2018	Non-V600 BRAF mutations predict sensitivity to combination of a type I RAF inhibitor, Dabrafenib, and a MEK inhibitor, Trametinib.	dabrafenib	86-96	zinc fingers and homeoboxes 2	Homo sapiens	10-13
29662630-3	2018	Singly, Dabrafenib only weakly suppresses mutant BRAF-induced ERK signaling and can induce ERK paradoxical activation in CRAF-overexpressing cells.	dabrafenib	8-18	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	49-53
29662630-3	2018	Singly, Dabrafenib only weakly suppresses mutant BRAF-induced ERK signaling and can induce ERK paradoxical activation in CRAF-overexpressing cells.	dabrafenib	8-18	mitogen-activated protein kinase 1	Homo sapiens	62-65
29662630-3	2018	Singly, Dabrafenib only weakly suppresses mutant BRAF-induced ERK signaling and can induce ERK paradoxical activation in CRAF-overexpressing cells.	dabrafenib	8-18	mitogen-activated protein kinase 1	Homo sapiens	91-94
29662630-3	2018	Singly, Dabrafenib only weakly suppresses mutant BRAF-induced ERK signaling and can induce ERK paradoxical activation in CRAF-overexpressing cells.	dabrafenib	8-18	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	121-125
29662630-4	2018	The present study compared the effects of Dabrafenib and a type II RAF inhibitor, AZ628, on ERK activity in HEK293T cells expressing several tumor-derived BRAF mutants, and in a non-V600 and impaired-kinase BRAF-mutant lung cancer cell line (H1666).	dabrafenib	42-52	mitogen-activated protein kinase 1	Homo sapiens	92-95
29520339-8	2018	At follow-up, case #1 was a 55-year-old man who received targeted BRAF inhibitor and MEK inhibitor therapy with dabrafenib and trametinib.	dabrafenib	112-122	mitogen-activated protein kinase kinase 7	Homo sapiens	85-88
29050517-2	2018	The combination of BRAF inhibitor dabrafenib with MEK inhibitor trametinib has shown its superiority to single agent therapy and is characterized by a tolerable spectrum of adverse events which shows a decrease in incidence over time on treatment.	dabrafenib	34-44	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	19-23
29361468-3	2018	Neoadjuvant targeted therapy with BRAF and MEK inhibitors (such as dabrafenib and trametinib) might provide clinical benefit in this high-risk p opulation.	dabrafenib	67-77	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	34-38
29361468-3	2018	Neoadjuvant targeted therapy with BRAF and MEK inhibitors (such as dabrafenib and trametinib) might provide clinical benefit in this high-risk p opulation.	dabrafenib	67-77	mitogen-activated protein kinase kinase 7	Homo sapiens	43-46
29557374-0	2018	Dabrafenib, an inhibitor of RIP3 kinase-dependent necroptosis, reduces ischemic brain injury.	dabrafenib	0-10	receptor-interacting serine-threonine kinase 3	Mus musculus	28-32
29557374-3	2018	Dabrafenib, originally identified as a B-raf inhibitor that is currently used to treat melanoma, was later revealed to be a potent RIPK3 inhibitor at micromolar concentrations.	dabrafenib	0-10	Braf transforming gene	Mus musculus	39-44
29557374-3	2018	Dabrafenib, originally identified as a B-raf inhibitor that is currently used to treat melanoma, was later revealed to be a potent RIPK3 inhibitor at micromolar concentrations.	dabrafenib	0-10	receptor-interacting serine-threonine kinase 3	Mus musculus	131-136
29557374-5	2018	Dabrafenib administered intraperitoneally at 10 mg/kg one hour after photothrombosis-induced focal ischemic injury significantly reduced infarct lesion size in C57BL6 mice the following day, accompanied by a markedly attenuated upregulation of TNF-alpha.	dabrafenib	0-10	tumor necrosis factor	Mus musculus	244-253
29557374-7	2018	Dabrafenib blocked lipopolysaccharides-induced activation of TNF-alpha in bone marrow-derived macrophages, suggesting that Dabrafenib may attenuate TNF-alpha-induced necroptotic pathway after ischemic brain injury.	dabrafenib	0-10	tumor necrosis factor	Mus musculus	61-70
29557374-7	2018	Dabrafenib blocked lipopolysaccharides-induced activation of TNF-alpha in bone marrow-derived macrophages, suggesting that Dabrafenib may attenuate TNF-alpha-induced necroptotic pathway after ischemic brain injury.	dabrafenib	0-10	tumor necrosis factor	Mus musculus	148-157
29557374-7	2018	Dabrafenib blocked lipopolysaccharides-induced activation of TNF-alpha in bone marrow-derived macrophages, suggesting that Dabrafenib may attenuate TNF-alpha-induced necroptotic pathway after ischemic brain injury.	dabrafenib	123-133	tumor necrosis factor	Mus musculus	61-70
29557374-7	2018	Dabrafenib blocked lipopolysaccharides-induced activation of TNF-alpha in bone marrow-derived macrophages, suggesting that Dabrafenib may attenuate TNF-alpha-induced necroptotic pathway after ischemic brain injury.	dabrafenib	123-133	tumor necrosis factor	Mus musculus	148-157
29568360-0	2018	Methotrexate sensitizes drug-resistant metastatic melanoma cells to BRAF V600E inhibitors dabrafenib and encorafenib.	dabrafenib	90-100	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	68-72
29216787-5	2018	EXPERT OPINION: Trametinib in combination with the BRAF inhibitor dabrafenib represents the first MEK1/2 inhibitor containing regimen that is approved for advanced BRAFV600E-mutant NSCLC.	dabrafenib	66-76	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	51-55
29216787-5	2018	EXPERT OPINION: Trametinib in combination with the BRAF inhibitor dabrafenib represents the first MEK1/2 inhibitor containing regimen that is approved for advanced BRAFV600E-mutant NSCLC.	dabrafenib	66-76	mitogen-activated protein kinase kinase 1	Homo sapiens	98-104
29072975-1	2018	Purpose We report the efficacy and safety of dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor) combination therapy in BRAF V600E-mutated anaplastic thyroid cancer, a rare, aggressive, and highly lethal malignancy with poor patient outcomes and no systemic therapies with clinical benefit.	dabrafenib	45-55	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	57-61
29072975-1	2018	Purpose We report the efficacy and safety of dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor) combination therapy in BRAF V600E-mutated anaplastic thyroid cancer, a rare, aggressive, and highly lethal malignancy with poor patient outcomes and no systemic therapies with clinical benefit.	dabrafenib	45-55	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	127-131
29072975-12	2018	Conclusion Dabrafenib plus trametinib is the first regimen demonstrated to have robust clinical activity in BRAF V600E-mutated anaplastic thyroid cancer and was well tolerated.	dabrafenib	11-21	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	108-112
29295876-0	2018	Rapid Clinical and Radiographic Response With Combined Dabrafenib and Trametinib in Adults With BRAF-Mutated High-Grade Glioma.	dabrafenib	55-65	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	96-100
29295876-4	2018	Herein, we report dramatic clinical and radiographic responses to combination dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor) in 2 adults with high-grade gliomas (HGGs), with 1 patient treated in the first-line setting.	dabrafenib	78-88	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	90-94
29112787-0	2018	Dabrafenib inhibits the growth of BRAF-WT cancers through CDK16 and NEK9 inhibition.	dabrafenib	0-10	cyclin dependent kinase 16	Homo sapiens	58-63
29112787-0	2018	Dabrafenib inhibits the growth of BRAF-WT cancers through CDK16 and NEK9 inhibition.	dabrafenib	0-10	NIMA related kinase 9	Homo sapiens	68-72
29112787-1	2018	Although the BRAF inhibitors dabrafenib and vemurafenib have both proven successful against BRAF-mutant melanoma, there seem to be differences in their mechanisms of action.	dabrafenib	29-39	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	13-17
29112787-1	2018	Although the BRAF inhibitors dabrafenib and vemurafenib have both proven successful against BRAF-mutant melanoma, there seem to be differences in their mechanisms of action.	dabrafenib	29-39	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	92-96
29112787-2	2018	Here, we show that dabrafenib is more effective at inhibiting the growth of NRAS-mutant and KRAS-mutant cancer cell lines than vemurafenib.	dabrafenib	19-29	NRAS proto-oncogene, GTPase	Homo sapiens	76-80
29112787-2	2018	Here, we show that dabrafenib is more effective at inhibiting the growth of NRAS-mutant and KRAS-mutant cancer cell lines than vemurafenib.	dabrafenib	19-29	KRAS proto-oncogene, GTPase	Homo sapiens	92-96
29112787-3	2018	Using mass spectrometry-based chemical proteomics, we identified NEK9 and CDK16 as unique targets of dabrafenib.	dabrafenib	101-111	NIMA related kinase 9	Homo sapiens	65-69
29112787-3	2018	Using mass spectrometry-based chemical proteomics, we identified NEK9 and CDK16 as unique targets of dabrafenib.	dabrafenib	101-111	cyclin dependent kinase 16	Homo sapiens	74-79
29112787-8	2018	Both of these effects were phenocopied in NRAS- and KRAS-mutant cancer cells by dabrafenib, but not vemurafenib.	dabrafenib	80-90	NRAS proto-oncogene, GTPase	Homo sapiens	42-46
29112787-8	2018	Both of these effects were phenocopied in NRAS- and KRAS-mutant cancer cells by dabrafenib, but not vemurafenib.	dabrafenib	80-90	KRAS proto-oncogene, GTPase	Homo sapiens	52-56
29112787-10	2018	In summary, we have identified dabrafenib as a potent inhibitor of NEK9 and CDK16, and our studies suggest that inhibition of these kinases may have activity against cancers that do not harbor BRAF mutations.	dabrafenib	31-41	NIMA related kinase 9	Homo sapiens	67-71
29112787-10	2018	In summary, we have identified dabrafenib as a potent inhibitor of NEK9 and CDK16, and our studies suggest that inhibition of these kinases may have activity against cancers that do not harbor BRAF mutations.	dabrafenib	31-41	cyclin dependent kinase 16	Homo sapiens	76-81
29595366-0	2018	Dabrafenib in combination with trametinib in the treatment of patients with BRAF V600-positive advanced or metastatic non-small cell lung cancer: clinical evidence and experience.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	76-80
27892777-1	2018	PURPOSE: To report the diagnosis of acute VKH-like syndrome as a complication from dabrafenib (a serine/threonine inhibitor of BRAF V600) and trametinib (a MEK inhibitor).	dabrafenib	83-93	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	127-131
27892777-1	2018	PURPOSE: To report the diagnosis of acute VKH-like syndrome as a complication from dabrafenib (a serine/threonine inhibitor of BRAF V600) and trametinib (a MEK inhibitor).	dabrafenib	83-93	mitogen-activated protein kinase kinase 7	Homo sapiens	156-159
29042256-0	2017	Antiseptic effects of dabrafenib on TGFBIp-induced septic responses.	dabrafenib	22-32	transforming growth factor beta induced	Homo sapiens	36-42
29042256-5	2017	The present study determined whether DAB modulated TGFBIp-mediated septic responses in HUVECs and in mice.	dabrafenib	37-40	transforming growth factor, beta induced	Mus musculus	51-57
29042256-6	2017	Antiseptic functions of DAB were examined by measuring permeability, leukocyte adhesion and migration, and proinflammatory protein activation in TGFBIp-stimulated HUVECs and mice.	dabrafenib	24-27	transforming growth factor, beta induced	Mus musculus	145-151
29042256-8	2017	We found that DAB inhibited TGFBIp-induced vascular barrier disruption, cell adhesion molecule (CAM) expression, and neutrophil adhesion/transendothelial migration toward human endothelial cells.	dabrafenib	14-17	transforming growth factor beta induced	Homo sapiens	28-34
29042256-9	2017	DAB also suppressed TGFBIp-induced hyperpermeability and leukocyte migration in vivo.	dabrafenib	0-3	transforming growth factor beta induced	Homo sapiens	20-26
29595366-5	2018	BRAF-MEK combination therapy (dabrafenib plus trametinib) demonstrated tolerability and efficacy in a recent phase II clinical trial and was approved by the European Medicines Agency and United States Food and Drug Administration for patients with stage IV NSCLC harboring BRAF V600E mutation.	dabrafenib	30-40	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
29595366-5	2018	BRAF-MEK combination therapy (dabrafenib plus trametinib) demonstrated tolerability and efficacy in a recent phase II clinical trial and was approved by the European Medicines Agency and United States Food and Drug Administration for patients with stage IV NSCLC harboring BRAF V600E mutation.	dabrafenib	30-40	mitogen-activated protein kinase kinase 7	Homo sapiens	5-8
29595366-5	2018	BRAF-MEK combination therapy (dabrafenib plus trametinib) demonstrated tolerability and efficacy in a recent phase II clinical trial and was approved by the European Medicines Agency and United States Food and Drug Administration for patients with stage IV NSCLC harboring BRAF V600E mutation.	dabrafenib	30-40	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	273-277
28891408-1	2017	BACKGROUND: Combination therapy with the BRAF inhibitor dabrafenib plus the MEK inhibitor trametinib improved survival in patients with advanced melanoma with BRAF V600 mutations.	dabrafenib	56-66	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	41-45
29371923-5	2017	Dabrafenib abrogated PTTG1 expression and impaired invasion of the extracellular matrix (ECM) in A375 and SK-Mel28 cells.	dabrafenib	0-10	PTTG1 regulator of sister chromatid separation, securin	Homo sapiens	21-26
29371923-8	2017	PTTG1-silencing also impaired proliferation and invasiveness of A375R and SK-Mel28R cells, and counteracted dabrafenib-induced stimulation of ECM invasion in A375R cells.	dabrafenib	108-118	PTTG1 regulator of sister chromatid separation, securin	Homo sapiens	0-5
28744830-7	2017	Treatment with dabrafenib (a type of BRAF inhibitor) achieved the regression of the intraocular metastasis in the right eye.	dabrafenib	15-25	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	37-41
29235562-3	2018	First-generation Raf inhibitors, such as vemurafenib and dabrafenib, have yielded dramatic responses in malignant melanomas containing B-Raf mutations; however, their overall usefulness has been limited by both intrinsic and acquired drug resistance.	dabrafenib	57-67	zinc fingers and homeoboxes 2	Homo sapiens	17-20
29235562-3	2018	First-generation Raf inhibitors, such as vemurafenib and dabrafenib, have yielded dramatic responses in malignant melanomas containing B-Raf mutations; however, their overall usefulness has been limited by both intrinsic and acquired drug resistance.	dabrafenib	57-67	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	135-140
28891408-1	2017	BACKGROUND: Combination therapy with the BRAF inhibitor dabrafenib plus the MEK inhibitor trametinib improved survival in patients with advanced melanoma with BRAF V600 mutations.	dabrafenib	56-66	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	159-163
28891408-2	2017	We sought to determine whether adjuvant dabrafenib plus trametinib would improve outcomes in patients with resected, stage III melanoma with BRAF V600 mutations.	dabrafenib	40-50	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	141-145
28891408-10	2017	CONCLUSIONS: Adjuvant use of combination therapy with dabrafenib plus trametinib resulted in a significantly lower risk of recurrence in patients with stage III melanoma with BRAF V600E or V600K mutations than the adjuvant use of placebo and was not associated with new toxic effects.	dabrafenib	54-64	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	175-179
28974625-0	2017	Retraction: EGFR-Mediated Reactivation of MAPK Signaling Induces Acquired Resistance to GSK2118436 in BRAF V600E-Mutant NSCLC Cell Lines.	dabrafenib	88-98	epidermal growth factor receptor	Homo sapiens	12-16
29371923-0	2017	Targeting the PTTG1 oncogene impairs proliferation and invasiveness of melanoma cells sensitive or with acquired resistance to the BRAF inhibitor dabrafenib.	dabrafenib	146-156	PTTG1 regulator of sister chromatid separation, securin	Homo sapiens	14-19
29371923-0	2017	Targeting the PTTG1 oncogene impairs proliferation and invasiveness of melanoma cells sensitive or with acquired resistance to the BRAF inhibitor dabrafenib.	dabrafenib	146-156	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	131-135
29371923-4	2017	Dabrafenib-resistant cell lines (A375R and SK-Mel28R) were more invasive than their drug-sensitive counterparts (A375 and SK-Mel28), but expressed comparable PTTG1 levels.	dabrafenib	0-10	PTTG1 regulator of sister chromatid separation, securin	Homo sapiens	158-163
29142786-3	2017	In light of recent FDA approval of dabrafenib and trametinib combination for metastatic NSCLCs with BRAF V600E mutation, one question arises due to insufficient clinical data is if the targeted therapy should be used before immunotherapy in patients with both BRAF V600E and PD-L1 expression.	dabrafenib	35-45	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	100-104
29142786-7	2017	The patient was then treated with dabrafenib due to the presence of the BRAF V600E mutation and intolerance to cytotoxic chemotherapy.	dabrafenib	34-44	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	72-76
28918496-4	2017	Recently, a dramatic tumor reduction has been reported in a patient with BRAFV600E mutated, multiply recurrent papillary craniopharyngioma using a combination therapy of BRAF inhibitor dabrafenib and MEK inhibitor trametinib.	dabrafenib	185-195	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	73-77
28984291-2	2017	The US Food and Drug Administration (FDA)-approved second-generation RAF inhibitors vemurafenib and dabrafenib have elicited remarkable responses and improved survival of patients with BRAF-V600E/K melanoma, but their effectiveness is limited by resistance.	dabrafenib	100-110	zinc fingers and homeoboxes 2	Homo sapiens	69-72
28984291-2	2017	The US Food and Drug Administration (FDA)-approved second-generation RAF inhibitors vemurafenib and dabrafenib have elicited remarkable responses and improved survival of patients with BRAF-V600E/K melanoma, but their effectiveness is limited by resistance.	dabrafenib	100-110	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	185-189
29048639-1	2017	In the present study, the phenotype of melanoma cells resistant to dabrafenib (a B-RAF inhibitor) was investigated, to shed more light on melanoma resistance to B-RAF inhibition.	dabrafenib	67-77	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	81-86
29048639-3	2017	All dabrafenib-resistant cells showed, in addition to a re-activation of MAPK signaling, morphological changes compared to their sensitive counterparts, accompanied by an increase in CD90 (mesenchymal marker) expression and a decrease in E-cadherin (epithelial marker) expression, suggesting an epithelial-to-mesenchymal-like phenotypic transition.	dabrafenib	4-14	Thy-1 cell surface antigen	Homo sapiens	183-187
29048639-3	2017	All dabrafenib-resistant cells showed, in addition to a re-activation of MAPK signaling, morphological changes compared to their sensitive counterparts, accompanied by an increase in CD90 (mesenchymal marker) expression and a decrease in E-cadherin (epithelial marker) expression, suggesting an epithelial-to-mesenchymal-like phenotypic transition.	dabrafenib	4-14	cadherin 1	Homo sapiens	238-248
29048639-4	2017	However, melanoma cells with TGF-beta1-induced epithelial-to-mesenchymal transition (EMT) were more sensitive to dabrafenib treatment compared to the sensitivity noted in the non-TGF-beta1-induced EMT melanoma cells, suggesting that TGF-beta1-induced EMT was not associated with dabrafenib resistance.	dabrafenib	113-123	transforming growth factor beta 1	Homo sapiens	29-38
29048639-4	2017	However, melanoma cells with TGF-beta1-induced epithelial-to-mesenchymal transition (EMT) were more sensitive to dabrafenib treatment compared to the sensitivity noted in the non-TGF-beta1-induced EMT melanoma cells, suggesting that TGF-beta1-induced EMT was not associated with dabrafenib resistance.	dabrafenib	113-123	transforming growth factor beta 1	Homo sapiens	179-188
29048639-4	2017	However, melanoma cells with TGF-beta1-induced epithelial-to-mesenchymal transition (EMT) were more sensitive to dabrafenib treatment compared to the sensitivity noted in the non-TGF-beta1-induced EMT melanoma cells, suggesting that TGF-beta1-induced EMT was not associated with dabrafenib resistance.	dabrafenib	113-123	transforming growth factor beta 1	Homo sapiens	179-188
29048639-4	2017	However, melanoma cells with TGF-beta1-induced epithelial-to-mesenchymal transition (EMT) were more sensitive to dabrafenib treatment compared to the sensitivity noted in the non-TGF-beta1-induced EMT melanoma cells, suggesting that TGF-beta1-induced EMT was not associated with dabrafenib resistance.	dabrafenib	279-289	transforming growth factor beta 1	Homo sapiens	29-38
29048639-5	2017	Although dabrafenib-resistant cells exhibited increased cell motility and E-cadherin/vimentin reorganization, as expected in EMT, all of them showed unvaried E-cadherin mRNA and unchanged Snail protein levels, while Twist1 protein expression was decreased with the exception of A375 dabrafenib-resistant melanoma cells, where it was unaffected.	dabrafenib	9-19	cadherin 1	Homo sapiens	74-84
29048639-5	2017	Although dabrafenib-resistant cells exhibited increased cell motility and E-cadherin/vimentin reorganization, as expected in EMT, all of them showed unvaried E-cadherin mRNA and unchanged Snail protein levels, while Twist1 protein expression was decreased with the exception of A375 dabrafenib-resistant melanoma cells, where it was unaffected.	dabrafenib	9-19	vimentin	Homo sapiens	85-93
29048639-5	2017	Although dabrafenib-resistant cells exhibited increased cell motility and E-cadherin/vimentin reorganization, as expected in EMT, all of them showed unvaried E-cadherin mRNA and unchanged Snail protein levels, while Twist1 protein expression was decreased with the exception of A375 dabrafenib-resistant melanoma cells, where it was unaffected.	dabrafenib	9-19	twist family bHLH transcription factor 1	Homo sapiens	216-222
29048639-7	2017	Furthermore, dabrafenib-resistant cells exhibited stem cell-like features, with Oct4 translocation from the cytoplasm to peri-nuclear sites and nuclei, and increased CD20 expression.	dabrafenib	13-23	POU class 5 homeobox 1	Homo sapiens	80-84
29048639-7	2017	Furthermore, dabrafenib-resistant cells exhibited stem cell-like features, with Oct4 translocation from the cytoplasm to peri-nuclear sites and nuclei, and increased CD20 expression.	dabrafenib	13-23	keratin 20	Homo sapiens	166-170
28861837-7	2017	Combination treatment with trametinib and the BRAF inhibitor, dabrafenib, was initiated.	dabrafenib	62-72	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	46-50
28984141-4	2017	Here we report successful treatment of two patients with BRAFV600E mutant pleomorphic xanthoastrocytoma using the BRAF inhibitor dabrafenib in combination with the MEK inhibitor trametinib.	dabrafenib	129-139	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	57-61
29057672-3	2017	A BRAF-V600E-mutated melanoma leptomeningeal metastases patient, treated by dabrafenib and liposomal cytarabine, presented after the first injection of liposomal cytarabine with hyperthermia and headaches.	dabrafenib	76-86	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	2-6
29039591-0	2017	Dabrafenib in patients with recurrent, BRAF V600E mutated malignant glioma and leptomeningeal disease.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	39-43
29039591-10	2017	Treatment of this cell culture with dabrafenib resulted in reduced cell density and inhibition of ERK phosphorylation in vitro.	dabrafenib	36-46	mitogen-activated protein kinase 1	Homo sapiens	98-101
29039591-11	2017	To date, this is the first series on adult patients with BRAF-mutated malignant glioma and leptomeningeal dissemination treated with dabrafenib monotherapy.	dabrafenib	133-143	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	57-61
29285228-1	2017	Background: We tested the hypothesis that a 4-month course of adjuvant dabrafenib in stage IIIC BRAF-mutated melanoma would improve 2 year RFS from 24% to 51%, and that tumor-derived cell free DNA (cfDNA) in plasma would correlate with and predict recurrence.	dabrafenib	71-81	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	96-100
28974625-0	2017	Retraction: EGFR-Mediated Reactivation of MAPK Signaling Induces Acquired Resistance to GSK2118436 in BRAF V600E-Mutant NSCLC Cell Lines.	dabrafenib	88-98	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	102-106
28784858-3	2017	The 2 patients with BRAF-mutated tumors were treated with dabrafenib or a combination of dabrafenib plus trametinib.	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	20-24
28652244-4	2017	In addition, dabrafenib and trametinib treatment of CD73+ BRAFV600E-mutant melanomas caused profound CD73 downregulation in tumor cells.	dabrafenib	13-23	5'-nucleotidase ecto	Homo sapiens	52-56
28652244-4	2017	In addition, dabrafenib and trametinib treatment of CD73+ BRAFV600E-mutant melanomas caused profound CD73 downregulation in tumor cells.	dabrafenib	13-23	5'-nucleotidase ecto	Homo sapiens	101-105
28809523-0	2012	Dabrafenib Therapy and BRAF and G6PD Genotype Dabrafenib is a kinase inhibitor used in the treatment of patients with unresectable or metastatic melanoma with specific BRAF variants.	dabrafenib	46-56	glucose-6-phosphate dehydrogenase	Homo sapiens	32-36
28809523-0	2012	Dabrafenib Therapy and BRAF and G6PD Genotype Dabrafenib is a kinase inhibitor used in the treatment of patients with unresectable or metastatic melanoma with specific BRAF variants.	dabrafenib	46-56	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	168-172
28809523-1	2012	Dabrafenib can be used as a single agent to treat melanoma with the BRAF V600E variant, or in combination with the MEK inhibitor trametinib to treat melanoma with BRAF V600E or V600K variants.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	68-72
28809523-1	2012	Dabrafenib can be used as a single agent to treat melanoma with the BRAF V600E variant, or in combination with the MEK inhibitor trametinib to treat melanoma with BRAF V600E or V600K variants.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	163-167
28809523-8	2012	The FDA-approved label for dabrafenib states that the presence of BRAF mutation in tumor specimens (V600E for dabrafenib monotherapy; V600E or V600K for dabrafenib plus trametinib) should be confirmed, using an FDA-approved test, before starting treatment with dabrafenib.	dabrafenib	27-37	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	66-70
28809523-8	2012	The FDA-approved label for dabrafenib states that the presence of BRAF mutation in tumor specimens (V600E for dabrafenib monotherapy; V600E or V600K for dabrafenib plus trametinib) should be confirmed, using an FDA-approved test, before starting treatment with dabrafenib.	dabrafenib	110-120	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	66-70
28809523-8	2012	The FDA-approved label for dabrafenib states that the presence of BRAF mutation in tumor specimens (V600E for dabrafenib monotherapy; V600E or V600K for dabrafenib plus trametinib) should be confirmed, using an FDA-approved test, before starting treatment with dabrafenib.	dabrafenib	110-120	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	66-70
28809523-8	2012	The FDA-approved label for dabrafenib states that the presence of BRAF mutation in tumor specimens (V600E for dabrafenib monotherapy; V600E or V600K for dabrafenib plus trametinib) should be confirmed, using an FDA-approved test, before starting treatment with dabrafenib.	dabrafenib	110-120	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	66-70
28784858-3	2017	The 2 patients with BRAF-mutated tumors were treated with dabrafenib or a combination of dabrafenib plus trametinib.	dabrafenib	89-99	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	20-24
28684402-1	2017	The BRAF inhibitors vemurafenib and dabrafenib can be used to treat patients with metastatic melanomas harboring BRAFV600 mutations.	dabrafenib	36-46	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-8
28536078-0	2017	AKT is critically involved in the antagonism of BRAF inhibitor sorafenib against dabrafenib in colorectal cancer cells harboring both wild-type and mutant (V600E) BRAF genes.	dabrafenib	81-91	AKT serine/threonine kinase 1	Homo sapiens	0-3
28536078-0	2017	AKT is critically involved in the antagonism of BRAF inhibitor sorafenib against dabrafenib in colorectal cancer cells harboring both wild-type and mutant (V600E) BRAF genes.	dabrafenib	81-91	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	48-52
28536078-3	2017	Dabrafenib, a type I inhibitor of BRAF interrupting RAF/MEK interaction, has been approved by FDA as a single agent or combined with MEK inhibitor trametinib for the treatment of patients with BRAF V600E mutation-positive advanced melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	34-38
28536078-3	2017	Dabrafenib, a type I inhibitor of BRAF interrupting RAF/MEK interaction, has been approved by FDA as a single agent or combined with MEK inhibitor trametinib for the treatment of patients with BRAF V600E mutation-positive advanced melanoma.	dabrafenib	0-10	zinc fingers and homeoboxes 2	Homo sapiens	35-38
28536078-3	2017	Dabrafenib, a type I inhibitor of BRAF interrupting RAF/MEK interaction, has been approved by FDA as a single agent or combined with MEK inhibitor trametinib for the treatment of patients with BRAF V600E mutation-positive advanced melanoma.	dabrafenib	0-10	mitogen-activated protein kinase kinase 7	Homo sapiens	56-59
28536078-3	2017	Dabrafenib, a type I inhibitor of BRAF interrupting RAF/MEK interaction, has been approved by FDA as a single agent or combined with MEK inhibitor trametinib for the treatment of patients with BRAF V600E mutation-positive advanced melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	193-197
28536078-4	2017	In the present study, we investigated the feasibility of combined treatment with dabrafenib and sorafenib, type I and type II BRAF inhibitor respectively, on colorectal cancer cells with BRAF V600E mutation.	dabrafenib	81-91	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	187-191
28536078-8	2017	Moreover, we found that sorafenib reversed dabrafenib inhibition of AKT in HT-29 cells, and phosphatidylinositol-3-kinase (PI3K) inhibitor GDC0941 significantly restored this antagonistic effect when combined with dabrafenib and sorafenib, indicating that AKT is critically involved in this antagonism.	dabrafenib	43-53	AKT serine/threonine kinase 1	Homo sapiens	68-71
28536078-9	2017	Collectively, we found that significant antagonism was observed when dabrafenib was combined with sorafenib in colorectal cancer cells harboring heterozygous genotype of BRAF and AKT is critically involved in this antagonism.	dabrafenib	69-79	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	170-174
28536078-9	2017	Collectively, we found that significant antagonism was observed when dabrafenib was combined with sorafenib in colorectal cancer cells harboring heterozygous genotype of BRAF and AKT is critically involved in this antagonism.	dabrafenib	69-79	AKT serine/threonine kinase 1	Homo sapiens	179-182
28536078-10	2017	We suggest that BRAF inhibitor dabrafenib and sorafenib should not be combined in clinic.	dabrafenib	31-41	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	16-20
28005274-3	2017	We report the first two cases of NEH in patients treated with a BRAF inhibitor (BRAFi), either dabrafenib or vemurafenib, for a stage IV metastatic melanoma.	dabrafenib	95-105	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	64-68
28412197-0	2017	An UPLC-MS/MS method for the quantification of BRAF inhibitors (vemurafenib, dabrafenib) and MEK inhibitors (cobimetinib, trametinib, binimetinib) in human plasma.	dabrafenib	77-87	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	47-51
28659148-3	2017	We previously reported a patient with synchronous BRAF-mutated metastatic melanoma and BRAF wt /KRAS G12D-metastatic colorectal cancer (CRC), whose CRC relapsed and progressed when treated with the BRAF inhibitor dabrafenib (GSK2118436).	dabrafenib	213-223	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	50-54
28659148-3	2017	We previously reported a patient with synchronous BRAF-mutated metastatic melanoma and BRAF wt /KRAS G12D-metastatic colorectal cancer (CRC), whose CRC relapsed and progressed when treated with the BRAF inhibitor dabrafenib (GSK2118436).	dabrafenib	213-223	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	87-91
28659148-3	2017	We previously reported a patient with synchronous BRAF-mutated metastatic melanoma and BRAF wt /KRAS G12D-metastatic colorectal cancer (CRC), whose CRC relapsed and progressed when treated with the BRAF inhibitor dabrafenib (GSK2118436).	dabrafenib	213-223	KRAS proto-oncogene, GTPase	Homo sapiens	96-100
28659148-3	2017	We previously reported a patient with synchronous BRAF-mutated metastatic melanoma and BRAF wt /KRAS G12D-metastatic colorectal cancer (CRC), whose CRC relapsed and progressed when treated with the BRAF inhibitor dabrafenib (GSK2118436).	dabrafenib	213-223	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	87-91
28659148-3	2017	We previously reported a patient with synchronous BRAF-mutated metastatic melanoma and BRAF wt /KRAS G12D-metastatic colorectal cancer (CRC), whose CRC relapsed and progressed when treated with the BRAF inhibitor dabrafenib (GSK2118436).	dabrafenib	225-235	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	50-54
28659148-3	2017	We previously reported a patient with synchronous BRAF-mutated metastatic melanoma and BRAF wt /KRAS G12D-metastatic colorectal cancer (CRC), whose CRC relapsed and progressed when treated with the BRAF inhibitor dabrafenib (GSK2118436).	dabrafenib	225-235	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	87-91
28659148-3	2017	We previously reported a patient with synchronous BRAF-mutated metastatic melanoma and BRAF wt /KRAS G12D-metastatic colorectal cancer (CRC), whose CRC relapsed and progressed when treated with the BRAF inhibitor dabrafenib (GSK2118436).	dabrafenib	225-235	KRAS proto-oncogene, GTPase	Homo sapiens	96-100
28659148-3	2017	We previously reported a patient with synchronous BRAF-mutated metastatic melanoma and BRAF wt /KRAS G12D-metastatic colorectal cancer (CRC), whose CRC relapsed and progressed when treated with the BRAF inhibitor dabrafenib (GSK2118436).	dabrafenib	225-235	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	87-91
28429064-1	2017	Dabrafenib is an inhibitor of BRAF V600E used for treating metastatic melanoma but a majority of patients experience adverse effects.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	30-34
28475671-0	2017	Dabrafenib plus trametinib versus dabrafenib monotherapy in patients with metastatic BRAF V600E/K-mutant melanoma: long-term survival and safety analysis of a phase 3 study.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	85-89
28475671-1	2017	Background: Previous analysis of COMBI-d (NCT01584648) demonstrated improved progression-free survival (PFS) and overall survival (OS) with combination dabrafenib and trametinib versus dabrafenib monotherapy in BRAF V600E/K-mutant metastatic melanoma.	dabrafenib	152-162	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	211-215
28475671-12	2017	Conclusions: These data demonstrate that durable (&gt;=3 years) survival is achievable with dabrafenib plus trametinib in patients with BRAF V600-mutant metastatic melanoma and support long-term first-line use of the combination in this setting.	dabrafenib	92-102	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	136-140
28526719-3	2017	Combination therapy with BRAF and MEK inhibitors (dabrafenib plus trametinib or vemurafenib plus cobimetinib, respectively) has become standard of care.	dabrafenib	50-60	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	25-29
28526719-3	2017	Combination therapy with BRAF and MEK inhibitors (dabrafenib plus trametinib or vemurafenib plus cobimetinib, respectively) has become standard of care.	dabrafenib	50-60	mitogen-activated protein kinase kinase 7	Homo sapiens	34-37
28320730-1	2017	The BRAF inhibitor dabrafenib was recently approved for the treatment of certain BRAF V600 mutation-positive tumors, either alone or in combination therapy with the mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 inhibitor, trametinib.	dabrafenib	19-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-8
28177661-3	2017	Dabrafenib (DAB) is a B-Raf inhibitor and initially used for the treatment of metastatic melanoma therapy.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	22-27
28177661-3	2017	Dabrafenib (DAB) is a B-Raf inhibitor and initially used for the treatment of metastatic melanoma therapy.	dabrafenib	12-15	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	22-27
28177661-8	2017	Furthermore, DAB suppressed the production of tumor necrosis factor-alpha (TNF-alpha) or interleukin (IL)-6 and the activation of nuclear factor-kappaB (NF-kappaB) or extracellular regulated kinases (ERK) 1/2 by LPS.	dabrafenib	13-16	tumor necrosis factor	Homo sapiens	46-73
28177661-8	2017	Furthermore, DAB suppressed the production of tumor necrosis factor-alpha (TNF-alpha) or interleukin (IL)-6 and the activation of nuclear factor-kappaB (NF-kappaB) or extracellular regulated kinases (ERK) 1/2 by LPS.	dabrafenib	13-16	tumor necrosis factor	Homo sapiens	75-84
28177661-8	2017	Furthermore, DAB suppressed the production of tumor necrosis factor-alpha (TNF-alpha) or interleukin (IL)-6 and the activation of nuclear factor-kappaB (NF-kappaB) or extracellular regulated kinases (ERK) 1/2 by LPS.	dabrafenib	13-16	interleukin 6	Homo sapiens	89-107
28320730-1	2017	The BRAF inhibitor dabrafenib was recently approved for the treatment of certain BRAF V600 mutation-positive tumors, either alone or in combination therapy with the mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 inhibitor, trametinib.	dabrafenib	19-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	81-85
28320730-1	2017	The BRAF inhibitor dabrafenib was recently approved for the treatment of certain BRAF V600 mutation-positive tumors, either alone or in combination therapy with the mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 inhibitor, trametinib.	dabrafenib	19-29	mitogen-activated protein kinase 3	Homo sapiens	183-222
28320730-1	2017	The BRAF inhibitor dabrafenib was recently approved for the treatment of certain BRAF V600 mutation-positive tumors, either alone or in combination therapy with the mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 inhibitor, trametinib.	dabrafenib	19-29	mitogen-activated protein kinase kinase 1	Homo sapiens	224-228
26946529-0	2017	Late-onset robust curly hair growth in a patient with BRAF-mutated metastatic melanoma responding to dabrafenib.	dabrafenib	101-111	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	54-58
26988245-3	2017	While dabrafenib is an effective anti-tumor agent with acceptable tolerability in patients with BRAF-mutated melanoma, we report the development (and outcome) of a previously unpublished acute toxic reaction observed in a patient receiving the drug.	dabrafenib	6-16	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	96-100
28024926-0	2017	Durable Response to Combination of Dabrafenib and Trametinib in BRAF V600E-Mutated Non-small-cell Lung Cancer.	dabrafenib	35-45	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	64-68
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.	dabrafenib	197-207	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	51-55
28078189-0	2017	Dabrafenib and trametinib activity in a patient with BRAF V600E mutated and microsatellite instability high (MSI-H) metastatic endometrial cancer.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	53-57
28320730-1	2017	The BRAF inhibitor dabrafenib was recently approved for the treatment of certain BRAF V600 mutation-positive tumors, either alone or in combination therapy with the mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 inhibitor, trametinib.	dabrafenib	19-29	mitogen-activated protein kinase kinase 2	Homo sapiens	234-238
28320730-3	2017	Dabrafenib and its major circulating metabolites (hydroxy-, carboxy-, and desmethyl-dabrafenib) were investigated as inhibitors of the clinically relevant transporters P-gp, BCRP, OATP1B1, OATP1B3, OCT2, OAT1, and OAT3.	dabrafenib	0-10	phosphoglycolate phosphatase	Homo sapiens	168-172
28320730-8	2017	Dabrafenib, hydroxy-, and desmethyl-dabrafenib were substrates of P-gp and BCRP, whereas carboxy-dabrafenib was not.	dabrafenib	0-10	phosphoglycolate phosphatase	Homo sapiens	66-70
28320730-8	2017	Dabrafenib, hydroxy-, and desmethyl-dabrafenib were substrates of P-gp and BCRP, whereas carboxy-dabrafenib was not.	dabrafenib	0-10	BCR pseudogene 1	Homo sapiens	75-79
28425764-1	2017	We present a patient with BRAF-V600E mutant papillary craniopharyngioma successfully treated with combination BRAF (dabrafenib 150 mg twice daily) and MEK (trametinib 2 mg daily) inhibitors after her unresectable tumor proved refractory to radiation.	dabrafenib	116-126	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	26-30
28425764-1	2017	We present a patient with BRAF-V600E mutant papillary craniopharyngioma successfully treated with combination BRAF (dabrafenib 150 mg twice daily) and MEK (trametinib 2 mg daily) inhibitors after her unresectable tumor proved refractory to radiation.	dabrafenib	116-126	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	110-114
28480077-0	2017	Combined dabrafenib and trametinib treatment in a case of chemotherapy-refractory extrahepatic BRAF V600E mutant cholangiocarcinoma: dramatic clinical and radiological response with a confusing synchronic new liver lesion.	dabrafenib	9-19	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	95-99
28268064-17	2017	INTERPRETATION: Rechallenge with dabrafenib plus trametinib showed anti-tumour activity in patients who had previously progressed on BRAF inhibitors and as such, rechallenge represents a potential new treatment option for these patients.	dabrafenib	33-43	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	133-137
28252478-1	2017	Vemurafenib and dabrafenib, two Food and Drug Administration-approved selective BRAF kinase inhibitors (BRAFi), have revolutionized the targeted therapy of cutaneous melanoma.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	80-84
28252479-4	2017	We retrospectively analyzed four patients with BRAF-mutant stage IV cutaneous melanoma who were treated with dabrafenib plus trametinib and rechallenged with the same combination after previously experiencing progression.	dabrafenib	109-119	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	47-51
28611627-1	2017	The combination of MEK inhibitor (cobimetinib, trametinib) and BRAF inhibitor (vemurafenib, dabrafenib) is now the first-line treatment in patients with BRAF V600-mutated metastatic melanoma.	dabrafenib	92-102	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	63-67
28611627-1	2017	The combination of MEK inhibitor (cobimetinib, trametinib) and BRAF inhibitor (vemurafenib, dabrafenib) is now the first-line treatment in patients with BRAF V600-mutated metastatic melanoma.	dabrafenib	92-102	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	153-157
28057719-5	2017	The most potent CDK16 inhibitors revealed by cell-free and cell-based assays were the multitargeted cancer drugs dabrafenib and rebastinib.	dabrafenib	113-123	cyclin dependent kinase 16	Homo sapiens	16-21
27940476-0	2017	Trametinib after disease reactivation under dabrafenib in Erdheim-Chester disease with both BRAF and KRAS mutations.	dabrafenib	44-54	KRAS proto-oncogene, GTPase	Homo sapiens	101-105
27909955-0	2017	Suppressive effects of dabrafenib on endothelial protein C receptor shedding.	dabrafenib	23-33	protein C receptor, endothelial	Mus musculus	37-67
27909955-3	2017	Dabrafenib (DAB) is a B-Raf inhibitor and initially used for the treatment of metastatic melanoma therapy.	dabrafenib	0-10	Braf transforming gene	Mus musculus	22-27
27909955-3	2017	Dabrafenib (DAB) is a B-Raf inhibitor and initially used for the treatment of metastatic melanoma therapy.	dabrafenib	12-15	Braf transforming gene	Mus musculus	22-27
27909955-4	2017	However, little is known about the effects of DAB on EPCR shedding.	dabrafenib	46-49	protein C receptor, endothelial	Mus musculus	53-57
27909955-5	2017	We investigated this issue by monitoring the effects of DAB on phorbol-12-myristate 13-acetate (PMA)-, tumor necrosis factor (TNF)-alpha-, interleukin (IL)-1beta-induced EPCR shedding in human umbilical vein endothelial cells (HUVECs), and cecal ligation and puncture (CLP)-mediated EPCR shedding in mice and underlying mechanism.	dabrafenib	56-59	tumor necrosis factor	Homo sapiens	103-136
27909955-5	2017	We investigated this issue by monitoring the effects of DAB on phorbol-12-myristate 13-acetate (PMA)-, tumor necrosis factor (TNF)-alpha-, interleukin (IL)-1beta-induced EPCR shedding in human umbilical vein endothelial cells (HUVECs), and cecal ligation and puncture (CLP)-mediated EPCR shedding in mice and underlying mechanism.	dabrafenib	56-59	interleukin 1 beta	Homo sapiens	139-161
27909955-6	2017	Data demonstrate that DAB induced potent inhibition of PMA-, TNF-alpha-, IL-1beta- (in HUVECs), and CLP-induced EPCR shedding (in mice) via inhibition of phosphorylation of mitogen-activated protein kinases (MAPKs) such as p38, janus kinase (JNK), and extracellular signal-regulated kinase (ERK) 1/2.	dabrafenib	22-25	tumor necrosis factor	Mus musculus	61-70
27909955-6	2017	Data demonstrate that DAB induced potent inhibition of PMA-, TNF-alpha-, IL-1beta- (in HUVECs), and CLP-induced EPCR shedding (in mice) via inhibition of phosphorylation of mitogen-activated protein kinases (MAPKs) such as p38, janus kinase (JNK), and extracellular signal-regulated kinase (ERK) 1/2.	dabrafenib	22-25	interleukin 1 beta	Mus musculus	73-81
27909955-6	2017	Data demonstrate that DAB induced potent inhibition of PMA-, TNF-alpha-, IL-1beta- (in HUVECs), and CLP-induced EPCR shedding (in mice) via inhibition of phosphorylation of mitogen-activated protein kinases (MAPKs) such as p38, janus kinase (JNK), and extracellular signal-regulated kinase (ERK) 1/2.	dabrafenib	22-25	protein C receptor, endothelial	Mus musculus	112-116
27909955-6	2017	Data demonstrate that DAB induced potent inhibition of PMA-, TNF-alpha-, IL-1beta- (in HUVECs), and CLP-induced EPCR shedding (in mice) via inhibition of phosphorylation of mitogen-activated protein kinases (MAPKs) such as p38, janus kinase (JNK), and extracellular signal-regulated kinase (ERK) 1/2.	dabrafenib	22-25	mitogen-activated protein kinase 14	Mus musculus	223-226
27909955-6	2017	Data demonstrate that DAB induced potent inhibition of PMA-, TNF-alpha-, IL-1beta- (in HUVECs), and CLP-induced EPCR shedding (in mice) via inhibition of phosphorylation of mitogen-activated protein kinases (MAPKs) such as p38, janus kinase (JNK), and extracellular signal-regulated kinase (ERK) 1/2.	dabrafenib	22-25	mitogen-activated protein kinase 8	Mus musculus	228-240
27909955-6	2017	Data demonstrate that DAB induced potent inhibition of PMA-, TNF-alpha-, IL-1beta- (in HUVECs), and CLP-induced EPCR shedding (in mice) via inhibition of phosphorylation of mitogen-activated protein kinases (MAPKs) such as p38, janus kinase (JNK), and extracellular signal-regulated kinase (ERK) 1/2.	dabrafenib	22-25	mitogen-activated protein kinase 8	Mus musculus	242-245
27909955-6	2017	Data demonstrate that DAB induced potent inhibition of PMA-, TNF-alpha-, IL-1beta- (in HUVECs), and CLP-induced EPCR shedding (in mice) via inhibition of phosphorylation of mitogen-activated protein kinases (MAPKs) such as p38, janus kinase (JNK), and extracellular signal-regulated kinase (ERK) 1/2.	dabrafenib	22-25	mitogen-activated protein kinase 3	Mus musculus	252-299
27909955-7	2017	DAB also inhibited the expression and activity of PMA-induced TACE in HUVECs suggesting that p38, ERK1/2, and JNK could be molecular targets of DAB.	dabrafenib	0-3	a disintegrin and metallopeptidase domain 17	Mus musculus	62-66
27909955-7	2017	DAB also inhibited the expression and activity of PMA-induced TACE in HUVECs suggesting that p38, ERK1/2, and JNK could be molecular targets of DAB.	dabrafenib	0-3	mitogen-activated protein kinase 14	Mus musculus	93-96
27909955-7	2017	DAB also inhibited the expression and activity of PMA-induced TACE in HUVECs suggesting that p38, ERK1/2, and JNK could be molecular targets of DAB.	dabrafenib	0-3	mitogen-activated protein kinase 3	Mus musculus	98-104
27909955-7	2017	DAB also inhibited the expression and activity of PMA-induced TACE in HUVECs suggesting that p38, ERK1/2, and JNK could be molecular targets of DAB.	dabrafenib	0-3	mitogen-activated protein kinase 8	Mus musculus	110-113
27909955-7	2017	DAB also inhibited the expression and activity of PMA-induced TACE in HUVECs suggesting that p38, ERK1/2, and JNK could be molecular targets of DAB.	dabrafenib	144-147	a disintegrin and metallopeptidase domain 17	Mus musculus	62-66
27909955-7	2017	DAB also inhibited the expression and activity of PMA-induced TACE in HUVECs suggesting that p38, ERK1/2, and JNK could be molecular targets of DAB.	dabrafenib	144-147	mitogen-activated protein kinase 14	Mus musculus	93-96
27909955-7	2017	DAB also inhibited the expression and activity of PMA-induced TACE in HUVECs suggesting that p38, ERK1/2, and JNK could be molecular targets of DAB.	dabrafenib	144-147	mitogen-activated protein kinase 3	Mus musculus	98-104
27909955-7	2017	DAB also inhibited the expression and activity of PMA-induced TACE in HUVECs suggesting that p38, ERK1/2, and JNK could be molecular targets of DAB.	dabrafenib	144-147	mitogen-activated protein kinase 8	Mus musculus	110-113
27909955-8	2017	These results demonstrate the potential of DAB as an anti-EPCR shedding reagent against PMA-mediated and CLP-mediated EPCR shedding.	dabrafenib	43-46	protein C receptor, endothelial	Mus musculus	58-62
27909955-8	2017	These results demonstrate the potential of DAB as an anti-EPCR shedding reagent against PMA-mediated and CLP-mediated EPCR shedding.	dabrafenib	43-46	protein C receptor, endothelial	Mus musculus	118-122
28058658-1	2017	Raf-mitogen-activated protein kinase (Raf-MAPK) pathway inhibition with the BRAF inhibitors vemurafenib and dabrafenib, alone or in combination with a MEK inhibitor, has become a standard therapeutic approach in patients with BRAF-mutated metastatic melanoma.	dabrafenib	108-118	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	226-230
28058658-5	2017	Combinations of BRAF inhibitors and MEK inhibitors (dabrafenib plus trametinib and vemurafenib plus cobimetinib) have been approved for the treatment of BRAF-mutant metastatic melanoma and may become a new standard of care.	dabrafenib	52-62	mitogen-activated protein kinase kinase 7	Homo sapiens	36-39
28058658-5	2017	Combinations of BRAF inhibitors and MEK inhibitors (dabrafenib plus trametinib and vemurafenib plus cobimetinib) have been approved for the treatment of BRAF-mutant metastatic melanoma and may become a new standard of care.	dabrafenib	52-62	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	153-157
27759578-1	2017	BRAF inhibitors (vemurafenib and dabrafenib) are commonly prescribed in BRAF-mutant metastatic melanoma and allow improvement of the overall survival and progression-free survival.	dabrafenib	33-43	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
27759578-1	2017	BRAF inhibitors (vemurafenib and dabrafenib) are commonly prescribed in BRAF-mutant metastatic melanoma and allow improvement of the overall survival and progression-free survival.	dabrafenib	33-43	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	72-76
28062673-1	2017	A phase I/II clinical trial suggests that dabrafenib shrinks or stabilizes low-grade gliomas in children with the BRAF V600E mutation.	dabrafenib	42-52	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	114-118
28062673-3	2017	The researchers have started a second trial for patients with glioma and other BRAF-mutant tumor types, this time evaluating dabrafenib combined with trametinib.	dabrafenib	125-135	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	79-83
27775948-4	2017	Dabrafenib (a BRAF inhibitor) and trametinib (a MEK inhibitor) combined therapy was started with a complete metabolic response established by 2 consecutive PET/CT scans.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
28078189-4	2017	CASE PRESENTATION: We report herein the case of a heavily pre-treated patient with recurrent microsatellite instability high (MSI-H) BRAF V600E mutated endometrial adenocarcinoma, which was successfully treated with the V600E targeting agent dabrafenib.	dabrafenib	242-252	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	133-137
27956260-5	2017	This has led to the development of the combination of dabrafenib and trametinib or vemurafenib and cobimetanib for the treatment of BRAF V600E mutant melanomas.	dabrafenib	54-64	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	132-136
27956260-6	2017	Dabrafenib and vemurafenib target V600E/K BRAF mutants while trametinib and cobimetanib target MEK1/2.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	42-46
28078189-5	2017	After developing resistance to this agent, the MEK targeting agent trametinib was added to dabrafenib achieving again a therapeutic response.	dabrafenib	91-101	mitogen-activated protein kinase kinase 7	Homo sapiens	47-50
28078189-6	2017	CONCLUSIONS: This case shows that dabrafenib both as monotherapy and when combined with trametinib may exert significant therapeutic activity in heavily pretreated BRAF V600E mutated endometrial adenocarcinoma, and highlight potential benefits of personalized treatment in this disease.	dabrafenib	34-44	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	164-168
27797970-2	2016	Responses to the BRAF inhibitors vemurafenib and dabrafenib and the MEK inhibitors trametinib and cobimetinib are, however, transient, and complete remission is rarely observed; rather, outgrowth of resistant clones within progressed tumors appears inevitable.	dabrafenib	49-59	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	17-21
27781490-6	2017	We report the second published case of successful treatment with the BRAF inhibitor dabrafenib in a female patient with relapsed anaplastic PXA with a BRAFV600 mutation, and the first published case of dabrafinib treatment following intolerance to vemurafenib.	dabrafenib	84-94	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	69-73
27624900-1	2017	BACKGROUND: Dabrafenib, a novel selective small-molecule inhibitor of BRAF, has been shown to increase overall survival in patients with unresectable metastatic melanoma harboring the BRAF V600E mutation.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	70-74
27624900-1	2017	BACKGROUND: Dabrafenib, a novel selective small-molecule inhibitor of BRAF, has been shown to increase overall survival in patients with unresectable metastatic melanoma harboring the BRAF V600E mutation.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	184-188
27624900-3	2017	Compared with vemurafenib, dabrafenib is a more recent BRAF inhibitor approved by the Food and Drug Administration in May 2013 for metastatic melanoma; fewer data are available in the current literature regarding cutaneous toxicity.	dabrafenib	27-37	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	55-59
27624900-13	2017	CONCLUSION: Selective BRAF inhibitor dabrafenib and MEK inhibitor trametinib are associated with multiple skin adverse effects.	dabrafenib	37-47	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	22-26
27863085-1	2017	The combination of dabrafenib and trametinib is a standard of care for the management of BRAF mutant metastatic melanoma.	dabrafenib	19-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	89-93
27934295-1	2016	Patients with BRAF V600E mutant melanoma are typically treated with targeted BRAF kinase inhibitors, such as vemurafenib and dabrafenib.	dabrafenib	125-135	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
27934295-1	2016	Patients with BRAF V600E mutant melanoma are typically treated with targeted BRAF kinase inhibitors, such as vemurafenib and dabrafenib.	dabrafenib	125-135	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	77-81
27748799-8	2016	Dabrafenib strongly inhibited the viability in BRAF mutated cells by demonstrating G0/G1-arrest via the downregulation of MEK/ERK phosphorylation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	47-51
27748799-8	2016	Dabrafenib strongly inhibited the viability in BRAF mutated cells by demonstrating G0/G1-arrest via the downregulation of MEK/ERK phosphorylation.	dabrafenib	0-10	mitogen-activated protein kinase kinase 7	Homo sapiens	122-125
27748799-8	2016	Dabrafenib strongly inhibited the viability in BRAF mutated cells by demonstrating G0/G1-arrest via the downregulation of MEK/ERK phosphorylation.	dabrafenib	0-10	mitogen-activated protein kinase 1	Homo sapiens	126-129
27748799-9	2016	Upregulated phosphorylation of MEK was observed in RAS mutated cells after dabrafenib treatment and caused VEGF upregulation, but was not related to the cellular proliferation.	dabrafenib	75-85	mitogen-activated protein kinase kinase 7	Homo sapiens	31-34
27748799-9	2016	Upregulated phosphorylation of MEK was observed in RAS mutated cells after dabrafenib treatment and caused VEGF upregulation, but was not related to the cellular proliferation.	dabrafenib	75-85	vascular endothelial growth factor A	Homo sapiens	107-111
28078132-4	2016	Hereby we report 2 cases of BRAF V600E refractory ICC treated with dual BRAF and MEK inhibitors (dabrafenib and trametinib) with excellent clinical and radiological response to therapy and with protracted duration of disease control.	dabrafenib	97-107	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	28-32
27864013-3	2016	We aimed to identify clinical factors associated with long-term response and survival using pooled data from randomised trials of dabrafenib plus trametinib in patients with metastatic BRAF-mutant melanoma.	dabrafenib	130-140	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	185-189
30758923-13	2016	In practice, when a patient with metastatic or inoperable BRAF V600-positive melanoma is willing to accept the significant toxicity of trametinib in the hope of gaining several extra months of life, the trametinib + dabrafenib combination is a first-line option.	dabrafenib	216-226	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	58-62
30758924-2	2016	The first-line treatment of choice for patients with BRAF V600-positive melanoma is a combination of dabrafenib (a BRAF inhibitor) and trametinib.	dabrafenib	101-111	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	53-57
27883956-1	2016	BACKGROUND: The BRAF inhibitors vemurafenib and dabrafenib are currently the standard treatment for metastatic melanoma with BRAF V600 mutations.	dabrafenib	48-58	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	16-20
27883956-1	2016	BACKGROUND: The BRAF inhibitors vemurafenib and dabrafenib are currently the standard treatment for metastatic melanoma with BRAF V600 mutations.	dabrafenib	48-58	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	125-129
26350195-4	2016	She was treated, off label, with BRAF inhibitor (dabrafenib) + MEK inhibitor (trametinib) and radiotherapy.	dabrafenib	49-59	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	33-37
27613168-3	2016	RECENT FINDINGS: Clinical trials involving combined BRAF/MEK inhibition with either vemurafenib plus cobimetinib or dabrafenib plus trametinib have shown improved overall survival compared to monotherapy with BRAF inhibitors alone.	dabrafenib	116-126	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	209-213
27799506-0	2016	Personalized Treatment for a Patient With a BRAF V600E Mutation Using Dabrafenib and a Tumor Treatment Fields Device in a High-Grade Glioma Arising From Ganglioglioma.	dabrafenib	70-80	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	44-48
27799506-7	2016	Temozolomide was discontinued and he was offered dabrafenib, an oral selective inhibitor of BRAF V600E, with continued use of NovoTTF.	dabrafenib	49-59	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	92-96
28078132-4	2016	Hereby we report 2 cases of BRAF V600E refractory ICC treated with dual BRAF and MEK inhibitors (dabrafenib and trametinib) with excellent clinical and radiological response to therapy and with protracted duration of disease control.	dabrafenib	97-107	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	72-76
28078132-4	2016	Hereby we report 2 cases of BRAF V600E refractory ICC treated with dual BRAF and MEK inhibitors (dabrafenib and trametinib) with excellent clinical and radiological response to therapy and with protracted duration of disease control.	dabrafenib	97-107	mitogen-activated protein kinase kinase 7	Homo sapiens	81-84
27470608-0	2016	Combined therapy with dabrafenib and trametinib in BRAF-mutated metastatic melanoma in a real-life setting: the INT Milan experience.	dabrafenib	22-32	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	51-55
27464255-9	2016	Melanocyte-specific mouse models confirmed that heterozygous (but not homozygous) deletion of Atg5 enhanced melanoma metastasis and compromised the response to targeted therapy (exemplified by dabrafenib, a BRAF inhibitor in clinical use).	dabrafenib	193-203	autophagy related 5	Mus musculus	94-98
26873702-3	2016	The aim of this trial was to examine the effectiveness and tolerability of a combination of the BRAF inhibitor dabrafenib and the MAPK kinase (MEK) inhibitor trametinib compared with a monotherapy with dabrafenib (plus placebo).	dabrafenib	111-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	96-100
26796877-6	2016	One patient treated with RT alone for an unresectable ameloblastoma developed a local recurrence and metastases in both the cervical lymph nodes and lungs, but had excellent response to dual BRAF/MEK inhibition with dabrafenib and trametinib.	dabrafenib	216-226	mitogen-activated protein kinase kinase 7	Homo sapiens	196-199
27399255-3	2016	Dabrafenib is an inhibitor of BRAF, approved as a first-line treatment of metastatic or unresectable stage 3 or 4 melanoma with the BRAF mutation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	30-34
27399255-3	2016	Dabrafenib is an inhibitor of BRAF, approved as a first-line treatment of metastatic or unresectable stage 3 or 4 melanoma with the BRAF mutation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	132-136
27080364-0	2016	Pustular psoriasis eruption with dabrafenib, a BRAF inhibitor.	dabrafenib	33-43	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	47-51
27080364-1	2016	Targeted BRAF inhibition with vemurafenib and dabrafenib has dramatically improved the survival rate in metastatic melanoma.	dabrafenib	46-56	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
27697975-7	2016	She was found to have a BRAF V600E mutation on CGP, and was started on targeted therapy with the BRAF inhibitor dabrafenib and the MEK inhibitor trametinib.	dabrafenib	112-122	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	24-28
27697975-7	2016	She was found to have a BRAF V600E mutation on CGP, and was started on targeted therapy with the BRAF inhibitor dabrafenib and the MEK inhibitor trametinib.	dabrafenib	112-122	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	97-101
27572607-0	2016	Targeting the PI3K/AKT/mTOR pathway overcomes the stimulating effect of dabrafenib on the invasive behavior of melanoma cells with acquired resistance to the BRAF inhibitor.	dabrafenib	72-82	AKT serine/threonine kinase 1	Homo sapiens	19-22
27572607-0	2016	Targeting the PI3K/AKT/mTOR pathway overcomes the stimulating effect of dabrafenib on the invasive behavior of melanoma cells with acquired resistance to the BRAF inhibitor.	dabrafenib	72-82	mechanistic target of rapamycin kinase	Homo sapiens	23-27
27572607-0	2016	Targeting the PI3K/AKT/mTOR pathway overcomes the stimulating effect of dabrafenib on the invasive behavior of melanoma cells with acquired resistance to the BRAF inhibitor.	dabrafenib	72-82	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	158-162
27572607-8	2016	Dabrafenib reduced invasiveness, VEGFR-2 expression and VEGF-A secretion in A375 cells, whereas it increased invasiveness, VEGF-A and MMP-9 release in A375R cells.	dabrafenib	0-10	kinase insert domain receptor	Homo sapiens	33-40
27572607-8	2016	Dabrafenib reduced invasiveness, VEGFR-2 expression and VEGF-A secretion in A375 cells, whereas it increased invasiveness, VEGF-A and MMP-9 release in A375R cells.	dabrafenib	0-10	vascular endothelial growth factor A	Homo sapiens	56-62
27572607-8	2016	Dabrafenib reduced invasiveness, VEGFR-2 expression and VEGF-A secretion in A375 cells, whereas it increased invasiveness, VEGF-A and MMP-9 release in A375R cells.	dabrafenib	0-10	matrix metallopeptidase 9	Homo sapiens	134-139
27572607-9	2016	In these latter cells, the stimulating effects of dabrafenib on the invasive capacity were markedly impaired by the anti-VEGF-A antibody bevacizumab, or by AKT1 silencing.	dabrafenib	50-60	vascular endothelial growth factor A	Homo sapiens	121-127
27572607-9	2016	In these latter cells, the stimulating effects of dabrafenib on the invasive capacity were markedly impaired by the anti-VEGF-A antibody bevacizumab, or by AKT1 silencing.	dabrafenib	50-60	AKT serine/threonine kinase 1	Homo sapiens	156-160
27572607-11	2016	Moreover, this inhibitor given in combination with dabrafenib efficiently counteracted the stimulating effects of the BRAFi on invasiveness and VEGF-A and MMP-9 secretion.	dabrafenib	51-61	vascular endothelial growth factor A	Homo sapiens	144-150
27572607-11	2016	Moreover, this inhibitor given in combination with dabrafenib efficiently counteracted the stimulating effects of the BRAFi on invasiveness and VEGF-A and MMP-9 secretion.	dabrafenib	51-61	matrix metallopeptidase 9	Homo sapiens	155-160
27572939-1	2016	MEK kinase inhibitors (trametinib and selumetinib) or kinase inhibitors directed against mutated BRAF(V600E) (vemurafenib and dabrafenib) have initial encouraging effects in the treatment of melanoma but acquired resistance appears almost invariably after some months.	dabrafenib	126-136	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	97-102
27080216-0	2016	Dabrafenib in patients with BRAF(V600E)-positive advanced non-small-cell lung cancer: a single-arm, multicentre, open-label, phase 2 trial.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	28-32
27699043-1	2016	A retrospective observational study was conducted on patients diagnosed with serine/threonine-protein kinase B-Raf (BRAF)-mutated metastatic melanoma, who underwent first-line therapy with BRAF and mitogen-activated protein kinase kinase (MEK) inhibitors (vemurafenib, dabrafenib or a combination of dabrafenib and trametinib) at the Miguel Servet University Hospital (Zaragoza, Spain) between November, 2011 and August, 2015.	dabrafenib	300-310	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	116-120
27367293-12	2016	BRAF inhibitors like dabrafenib and vemurafenib in combination with the MEK inhibitors trametinib and cobimetinib for BRAF mutated patients should be offered as first or second line treatment.	dabrafenib	21-31	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
27124486-0	2016	Clinical, Molecular, and Immune Analysis of Dabrafenib-Trametinib Combination Treatment for BRAF Inhibitor-Refractory Metastatic Melanoma: A Phase 2 Clinical Trial.	dabrafenib	44-54	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	92-96
27124486-1	2016	IMPORTANCE: Combined treatment with dabrafenib and trametinib (CombiDT) achieves clinical responses in only about 15% of patients with BRAF inhibitor (BRAFi)-refractory metastatic melanoma in contrast to the higher response rate observed in BRAFi-naive patients.	dabrafenib	36-46	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	135-139
27207893-1	2016	Results from a phase II trial show that the BRAF inhibitor dabrafenib has significant single-agent activity in patients with advanced non-small cell lung cancer harboring the BRAF V600E mutation.	dabrafenib	59-69	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	44-48
27207893-1	2016	Results from a phase II trial show that the BRAF inhibitor dabrafenib has significant single-agent activity in patients with advanced non-small cell lung cancer harboring the BRAF V600E mutation.	dabrafenib	59-69	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	175-179
27206449-7	2016	In patients with asymptomatic BRAF V600E-mutant brain metastases, the BRAF inhibitors dabrafenib, vemurafenib, and immunotherapy with ipilimumab are used.	dabrafenib	86-96	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	30-34
27206449-7	2016	In patients with asymptomatic BRAF V600E-mutant brain metastases, the BRAF inhibitors dabrafenib, vemurafenib, and immunotherapy with ipilimumab are used.	dabrafenib	86-96	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	70-74
25917403-0	2016	Effective treatment with Dabrafenib and Trametinib for a BRAF-mutated metastatic dedifferentiated malignant spindle cell neoplasm.	dabrafenib	25-35	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	57-61
27283860-0	2016	Dabrafenib plus trametinib in patients with previously treated BRAF(V600E)-mutant metastatic non-small cell lung cancer: an open-label, multicentre phase 2 trial.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	63-67
27283860-4	2016	We aimed to assess the antitumour activity and safety of dabrafenib plus trametinib in patients with BRAF(V600E)-mutant NSCLC.	dabrafenib	57-67	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	101-105
27283860-18	2016	INTERPRETATION: Dabrafenib plus trametinib could represent a new targeted therapy with robust antitumour activity and a manageable safety profile in patients with BRAF(V600E)-mutant NSCLC.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	163-167
27196768-0	2016	EGFR-Mediated Reactivation of MAPK Signaling Induces Acquired Resistance to GSK2118436 in BRAF V600E-Mutant NSCLC Cell Lines.	dabrafenib	76-86	epidermal growth factor receptor	Homo sapiens	0-4
27196768-0	2016	EGFR-Mediated Reactivation of MAPK Signaling Induces Acquired Resistance to GSK2118436 in BRAF V600E-Mutant NSCLC Cell Lines.	dabrafenib	76-86	mitogen-activated protein kinase 3	Homo sapiens	30-34
27196768-0	2016	EGFR-Mediated Reactivation of MAPK Signaling Induces Acquired Resistance to GSK2118436 in BRAF V600E-Mutant NSCLC Cell Lines.	dabrafenib	76-86	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	90-94
27196768-1	2016	Although treatment of BRAF V600E-mutant non-small cell lung cancer (NSCLC(V600E)) with GSK2118436 has shown an encouraging efficacy, most patients develop resistance.	dabrafenib	87-97	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	22-26
27196768-4	2016	Treatment of GSR cells with GSK2118436 enhanced EGFR-mediated RAS activity, leading to the formation of BRAF-CRAF dimers and transactivation of CRAF.	dabrafenib	28-38	epidermal growth factor receptor	Homo sapiens	48-52
27196768-4	2016	Treatment of GSR cells with GSK2118436 enhanced EGFR-mediated RAS activity, leading to the formation of BRAF-CRAF dimers and transactivation of CRAF.	dabrafenib	28-38	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	104-108
27196768-4	2016	Treatment of GSR cells with GSK2118436 enhanced EGFR-mediated RAS activity, leading to the formation of BRAF-CRAF dimers and transactivation of CRAF.	dabrafenib	28-38	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	109-113
27196768-4	2016	Treatment of GSR cells with GSK2118436 enhanced EGFR-mediated RAS activity, leading to the formation of BRAF-CRAF dimers and transactivation of CRAF.	dabrafenib	28-38	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	144-148
27209484-3	2016	METHODS: A neoadjuvant treatment regime of dabrafenib was given to a patient with recurrent BRAF-mutant mandibular ameloblastoma.	dabrafenib	43-53	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	92-96
27058232-1	2016	Dabrafenib (Tafinlar( )) and trametinib (Mekinist( )) are registered for the treatment of patients with BRAF V600 mutation positive unresectable or metastatic melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	104-108
27058232-1	2016	Dabrafenib (Tafinlar( )) and trametinib (Mekinist( )) are registered for the treatment of patients with BRAF V600 mutation positive unresectable or metastatic melanoma.	dabrafenib	12-20	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	104-108
27255157-0	2016	Dabrafenib in an elderly patient with metastatic melanoma and BRAF V600R mutation: a case report.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	62-66
27255157-3	2016	Specific BRAF inhibitors such as dabrafenib and vemurafenib are the mainstays of treatment in patients with metastatic BRAF-mutant malignant melanomas.	dabrafenib	33-43	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
27255157-3	2016	Specific BRAF inhibitors such as dabrafenib and vemurafenib are the mainstays of treatment in patients with metastatic BRAF-mutant malignant melanomas.	dabrafenib	33-43	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	119-123
27255157-5	2016	Although evidence exists about the activity of dabrafenib and vemurafenib in patients with the BRAF (V600R) mutation, these patients have been systematically excluded from recent trials with targeted therapies.	dabrafenib	47-57	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	95-99
27255157-6	2016	CASE PRESENTATION: Here, we report the positive results in terms of survival and quality of life obtained with dabrafenib in an 80-year-old Caucasian male patient with a Charlson Comorbidity Index of 8 diagnosed with metastatic malignant melanoma harboring the BRAF (V600R) mutation.	dabrafenib	111-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	261-265
27126828-5	2016	Four oral targeted therapies are used in the treatment of melanoma associated with the B-Raf proto-oncogene, BRAF: cobimetinib, dabrafenib, trametinib, and vemurafenib.	dabrafenib	128-138	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	109-113
26922422-2	2016	We illustrate an unexpected diagnosis of extensive bilateral pedal Kaposi sarcoma masquerading as BRAF inhibitor-related toxicity in a patient treated with dabrafenib for metastatic melanoma.	dabrafenib	156-166	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	98-102
26922422-4	2016	The rash progressed in the context of acute-on-chronic immunosuppression and was initially thought due to commencement of the BRAF inhibitor (BRAFi) dabrafenib.	dabrafenib	149-159	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	126-130
26974967-1	2016	Targeted therapies such as the BRAF inhibitors vemurafenib and dabrafenib are highly effective in the treatment of systemic metastatic melanoma and have been shown to be effective in controlling solid brain metastases; however, limited data exist on their activity in leptomeningeal spread.	dabrafenib	63-73	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	31-35
26364606-8	2016	Second generation inhibitors such as Vemurafenib (Zelboraf) and Dabrafenib (Tafinlar) targeting BRAF(V600E), Trametinib (Mekinist) targeting MEK1/2 and the first generation pan-RAF inhibitor Sorafenib (Nexavar) have already been approved for treating renal, hepatocellular, thyroid cancers and BRAF(V600E/K) harboring metastatic melanoma.	dabrafenib	64-74	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	96-101
26364606-8	2016	Second generation inhibitors such as Vemurafenib (Zelboraf) and Dabrafenib (Tafinlar) targeting BRAF(V600E), Trametinib (Mekinist) targeting MEK1/2 and the first generation pan-RAF inhibitor Sorafenib (Nexavar) have already been approved for treating renal, hepatocellular, thyroid cancers and BRAF(V600E/K) harboring metastatic melanoma.	dabrafenib	64-74	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	96-100
27699043-1	2016	A retrospective observational study was conducted on patients diagnosed with serine/threonine-protein kinase B-Raf (BRAF)-mutated metastatic melanoma, who underwent first-line therapy with BRAF and mitogen-activated protein kinase kinase (MEK) inhibitors (vemurafenib, dabrafenib or a combination of dabrafenib and trametinib) at the Miguel Servet University Hospital (Zaragoza, Spain) between November, 2011 and August, 2015.	dabrafenib	269-279	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	109-114
27699043-1	2016	A retrospective observational study was conducted on patients diagnosed with serine/threonine-protein kinase B-Raf (BRAF)-mutated metastatic melanoma, who underwent first-line therapy with BRAF and mitogen-activated protein kinase kinase (MEK) inhibitors (vemurafenib, dabrafenib or a combination of dabrafenib and trametinib) at the Miguel Servet University Hospital (Zaragoza, Spain) between November, 2011 and August, 2015.	dabrafenib	269-279	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	116-120
27699043-1	2016	A retrospective observational study was conducted on patients diagnosed with serine/threonine-protein kinase B-Raf (BRAF)-mutated metastatic melanoma, who underwent first-line therapy with BRAF and mitogen-activated protein kinase kinase (MEK) inhibitors (vemurafenib, dabrafenib or a combination of dabrafenib and trametinib) at the Miguel Servet University Hospital (Zaragoza, Spain) between November, 2011 and August, 2015.	dabrafenib	300-310	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	109-114
27447748-4	2016	Herein, we report the case of a melanoma patient treated with sequential BRAF/MEKi (dabrafenib plus trametinib) followed by the anti CTLA-4 antibody ipilimumab who achieved a pathological complete response.	dabrafenib	84-94	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	73-77
27621653-6	2016	Based on this molecular feature, the patient was successfully treated with the BRAF inhibitor dabrafenib after the failure of treatment with standard regimen.	dabrafenib	94-104	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	79-83
28947956-0	2017	Non-V600 BRAF mutations recurrently found in lung cancer predict sensitivity to the combination of Trametinib and Dabrafenib.	dabrafenib	114-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
28947956-2	2017	Recent studies have revealed the benefits of combined targeted therapy with a RAF-inhibitor (Dabrafenib) and a MEK-inhibitor (Trametinib) in treating V600 BRAF mutant cancers, including NSCLC.	dabrafenib	93-103	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	155-159
28947956-6	2017	Herein, beyond describing a cohort of BRAF mutant NSCLC patients and functionally analyzing 13 tumor-derived BRAF mutations, we demonstrate that both types of non-V600 BRAF mutations can be sensitive to clinically relevant doses of Dabrafenib and Trametinib in HEK293T cells, in lung epithelial cellular model (BEAS-2B) and in human cancer cell lines harboring non-V600 BRAF mutations.	dabrafenib	232-242	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	38-42
28947956-6	2017	Herein, beyond describing a cohort of BRAF mutant NSCLC patients and functionally analyzing 13 tumor-derived BRAF mutations, we demonstrate that both types of non-V600 BRAF mutations can be sensitive to clinically relevant doses of Dabrafenib and Trametinib in HEK293T cells, in lung epithelial cellular model (BEAS-2B) and in human cancer cell lines harboring non-V600 BRAF mutations.	dabrafenib	232-242	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	109-113
28947956-6	2017	Herein, beyond describing a cohort of BRAF mutant NSCLC patients and functionally analyzing 13 tumor-derived BRAF mutations, we demonstrate that both types of non-V600 BRAF mutations can be sensitive to clinically relevant doses of Dabrafenib and Trametinib in HEK293T cells, in lung epithelial cellular model (BEAS-2B) and in human cancer cell lines harboring non-V600 BRAF mutations.	dabrafenib	232-242	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	109-113
28947956-6	2017	Herein, beyond describing a cohort of BRAF mutant NSCLC patients and functionally analyzing 13 tumor-derived BRAF mutations, we demonstrate that both types of non-V600 BRAF mutations can be sensitive to clinically relevant doses of Dabrafenib and Trametinib in HEK293T cells, in lung epithelial cellular model (BEAS-2B) and in human cancer cell lines harboring non-V600 BRAF mutations.	dabrafenib	232-242	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	109-113
28947956-9	2017	This study provides a basis for the clinical exploration of non-V600 BRAF mutant lung cancers upon treatment with Trametinib and Dabrafenib.	dabrafenib	129-139	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	69-73
27458080-3	2016	Dabrafenib is a B-Raf inhibitor and initially used for the treatment of metastatic melanoma therapy.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	16-21
27458080-6	2016	Dabrafenib suppressed the PolyP-mediated vascular barrier permeability, upregulation of inflammatory biomarkers, adhesion/migration of leukocytes, and activation and/or production of nuclear factor-kappaB, tumor necrosis factor-alpha, and interleukin-6.	dabrafenib	0-10	tumor necrosis factor	Homo sapiens	191-233
27458080-6	2016	Dabrafenib suppressed the PolyP-mediated vascular barrier permeability, upregulation of inflammatory biomarkers, adhesion/migration of leukocytes, and activation and/or production of nuclear factor-kappaB, tumor necrosis factor-alpha, and interleukin-6.	dabrafenib	0-10	interleukin 6	Homo sapiens	239-252
27226552-5	2016	In BRAF mutant melanoma cells, ectopic CK2alpha decreased sensitivity to vemurafenib (BRAF inhibitor), dabrafenib (BRAF inhibitor), and trametinib (MEK inhibitor) by a mechanism distinct from that of mutant NRAS.	dabrafenib	103-113	casein kinase 2 alpha 2	Homo sapiens	39-47
26926151-1	2016	The combined use of the BRAF inhibitor dabrafenib and MEK inhibitor trametinib has been found to improve survival over dabrafenib alone.	dabrafenib	39-49	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	24-28
26926151-1	2016	The combined use of the BRAF inhibitor dabrafenib and MEK inhibitor trametinib has been found to improve survival over dabrafenib alone.	dabrafenib	119-129	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	24-28
26926151-1	2016	The combined use of the BRAF inhibitor dabrafenib and MEK inhibitor trametinib has been found to improve survival over dabrafenib alone.	dabrafenib	119-129	mitogen-activated protein kinase kinase 7	Homo sapiens	54-57
26857260-1	2016	The selective BRAF inhibitors vemurafenib and dabrafenib yield high response rates and improved overall survival in patients with BRAF V600E-mutant metastatic melanoma.	dabrafenib	46-56	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
26857260-1	2016	The selective BRAF inhibitors vemurafenib and dabrafenib yield high response rates and improved overall survival in patients with BRAF V600E-mutant metastatic melanoma.	dabrafenib	46-56	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	130-134
27429963-5	2016	BRAF inhibitors (vemurafenib, dabrafenib) have shown benefit in terms of overall survival (OS) compared to chemotherapy, and their combination with MEK inhibitors has recently been shown to improve progression-free survival (PFS), compared with monotherapy with BRAF inhibitors.	dabrafenib	30-40	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
27246822-0	2016	Dabrafenib plus Trametinib: a Review in Advanced Melanoma with a BRAF (V600) Mutation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	65-75
27246822-1	2016	The BRAF inhibitor dabrafenib (Tafinlar( )) and the MEK inhibitor trametinib (Mekinist( )) are indicated, as monotherapy or in combination with each other, for the treatment of patients with unresectable or metastatic melanoma with a BRAF (V600) mutation.	dabrafenib	19-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-8
27246822-3	2016	Dabrafenib plus trametinib significantly prolonged progression-free survival (PFS) and overall survival (OS), improved objective response rates (ORRs) and preserved health-related quality of life (HR-QOL) to a greater extent than dabrafenib (in the double-blind COMBI-d study) and vemurafenib (in the open-label COMBI-v study) in two large, randomized, phase III studies in treatment-naive patients with unresectable or metastatic melanoma with BRAF (V600E/K) mutation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	445-449
27246822-7	2016	Thus, dabrafenib plus trametinib provides an important treatment option for patients with BRAF (V600) mutation-positive unresectable or metastatic melanoma.	dabrafenib	6-16	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	90-94
27028853-4	2016	To explore this mechanistically, we profiled paradoxical ERK activation by vemurafenib, dabrafenib, encorafenib (LGX818), and PLX8394, demonstrating that vemurafenib induces ERK activation the greatest, while dabrafenib and encorafenib have higher "paradox indices", defined as the pERK activation EC80 divided by the IC80 against A375, corresponding to wider therapeutic windows for achieving tumor inhibition without paradoxical ERK activation.	dabrafenib	88-98	mitogen-activated protein kinase 1	Homo sapiens	57-60
27028853-4	2016	To explore this mechanistically, we profiled paradoxical ERK activation by vemurafenib, dabrafenib, encorafenib (LGX818), and PLX8394, demonstrating that vemurafenib induces ERK activation the greatest, while dabrafenib and encorafenib have higher "paradox indices", defined as the pERK activation EC80 divided by the IC80 against A375, corresponding to wider therapeutic windows for achieving tumor inhibition without paradoxical ERK activation.	dabrafenib	209-219	mitogen-activated protein kinase 1	Homo sapiens	57-60
27226731-4	2016	The discovery of mutations in BRAF, a part of the mitogen-activated protein kinase, allowed the development of two BRAF inhibitors, vemurafenib and dabrafenib, which significantly improved the outcome of metastatic melanoma treatment.	dabrafenib	148-158	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	30-34
27226731-4	2016	The discovery of mutations in BRAF, a part of the mitogen-activated protein kinase, allowed the development of two BRAF inhibitors, vemurafenib and dabrafenib, which significantly improved the outcome of metastatic melanoma treatment.	dabrafenib	148-158	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	115-119
25902737-4	2016	BRAF mutation is very rare in patients with NSCLC, and its presence is associated with sensitivity of tumor cells to BRAF inhibitors (vemurafenib, dabrafenib).	dabrafenib	147-157	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
25902737-4	2016	BRAF mutation is very rare in patients with NSCLC, and its presence is associated with sensitivity of tumor cells to BRAF inhibitors (vemurafenib, dabrafenib).	dabrafenib	147-157	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	117-121
27080216-2	2016	Dabrafenib is an oral selective inhibitor of BRAF kinase.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	45-49
27080216-3	2016	We did a trial to assess the clinical activity of dabrafenib in patients with advanced non-small-cell lung cancer (NSCLC) positive for the BRAF(V600E) mutation.	dabrafenib	50-60	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	139-144
27080216-15	2016	INTERPRETATION: Dabrafenib showed clinical activity in BRAF(V600E)-positive NSCLC.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	55-60
27095081-3	2016	METHODS: Allele-specific quantitative PCR analysis for BRAF V600 E/E2/D/K/R/M mutations was performed on DNA extracted from plasma of patients with known BRAF V600 mutant melanoma who were treated with dabrafenib and trametinib.	dabrafenib	202-212	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	55-59
27069772-11	2015	Based on the Weibull model, the extrapolated total life-months gained for BRAF inhibitors were 26.5 months for dabrafenib, 21.3 months for trametinib, 14.3 months for vemurafenib, and 24.6 months for dabrafenib + trametinib.	dabrafenib	111-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	74-78
27069772-11	2015	Based on the Weibull model, the extrapolated total life-months gained for BRAF inhibitors were 26.5 months for dabrafenib, 21.3 months for trametinib, 14.3 months for vemurafenib, and 24.6 months for dabrafenib + trametinib.	dabrafenib	200-210	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	74-78
26592934-0	2016	Anti-septic effects of dabrafenib on HMGB1-mediated inflammatory responses.	dabrafenib	23-33	high mobility group box 1	Homo sapiens	37-42
26592934-2	2016	Dabrafenib is a B-Raf inhibitor and initially used for the treatment of metastatic melanoma therapy.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	16-21
26592934-4	2016	Here, we examined the effects of dabrafenib (DAB) on the modulation of HMGB1-mediated septic responses.	dabrafenib	33-43	high mobility group box 1	Homo sapiens	71-76
26592934-4	2016	Here, we examined the effects of dabrafenib (DAB) on the modulation of HMGB1-mediated septic responses.	dabrafenib	45-48	high mobility group box 1	Homo sapiens	71-76
26592934-5	2016	DAB inhibited the release of HMGB1 and downregulated HMGB1-dependent inflammatory responses by enhancing the expressions of cell adhesion molecules (CAMs) in human endothelial cells.	dabrafenib	0-3	high mobility group box 1	Homo sapiens	29-34
26592934-5	2016	DAB inhibited the release of HMGB1 and downregulated HMGB1-dependent inflammatory responses by enhancing the expressions of cell adhesion molecules (CAMs) in human endothelial cells.	dabrafenib	0-3	high mobility group box 1	Homo sapiens	53-58
26592934-6	2016	In addition, treatment with DAB inhibited the HMGB1 secretion by CLP and sepsis-related mortality and pulmonary injury.	dabrafenib	28-31	high mobility group box 1	Homo sapiens	46-51
26592934-7	2016	This study demonstrated that DAB could be alternative therapeutic options for sepsis or septic shock via the inhibition of the HMGB1 signaling pathway.	dabrafenib	29-32	high mobility group box 1	Homo sapiens	127-132
27220786-4	2016	Dabrafenib plus panitumumab in combination with trametinib and encorafenib plus cetuximab in combination with alpelisib, are very promising combination treatments and are currently being developed in clinical trials for patients with BRAF mutant-type tumors.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	234-238
27025703-3	2016	Vemurafenib and dabrafenib are two clinically approved inhibitors for BRAF that efficiently suppress the kinase activity of oncogenic BRAF (V600E).	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	70-74
27025703-3	2016	Vemurafenib and dabrafenib are two clinically approved inhibitors for BRAF that efficiently suppress the kinase activity of oncogenic BRAF (V600E).	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	134-138
27025703-6	2016	Dabrafenib enhanced activity of light-stimulated CRAF at low dose and inhibited CRAF signaling at high dose.	dabrafenib	0-10	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	49-53
27025703-6	2016	Dabrafenib enhanced activity of light-stimulated CRAF at low dose and inhibited CRAF signaling at high dose.	dabrafenib	0-10	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	80-84
27025703-7	2016	Moreover, dabrafenib increased the protein level of CRAF proteins but not of BRAF proteins.	dabrafenib	10-20	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	52-56
27025703-8	2016	Increased CRAF levels correlate with elevated RAF signaling in a dabrafenib-dependent manner, independent of light activation.	dabrafenib	65-75	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	10-14
27025703-8	2016	Increased CRAF levels correlate with elevated RAF signaling in a dabrafenib-dependent manner, independent of light activation.	dabrafenib	65-75	zinc fingers and homeoboxes 2	Homo sapiens	11-14
26811525-0	2016	Overall Survival and Durable Responses in Patients With BRAF V600-Mutant Metastatic Melanoma Receiving Dabrafenib Combined With Trametinib.	dabrafenib	103-113	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	56-60
26811525-1	2016	PURPOSE: To report the overall survival (OS) and clinical characteristics of BRAF inhibitor-naive long-term responders and survivors treated with dabrafenib plus trametinib in a phase I and II study of patients with BRAF V600 mutation-positive metastatic melanoma.	dabrafenib	146-156	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	77-81
26811525-1	2016	PURPOSE: To report the overall survival (OS) and clinical characteristics of BRAF inhibitor-naive long-term responders and survivors treated with dabrafenib plus trametinib in a phase I and II study of patients with BRAF V600 mutation-positive metastatic melanoma.	dabrafenib	146-156	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	216-220
26811525-7	2016	CONCLUSION: Dabrafenib plus trametinib results in a median OS of more than 2 years in BRAF inhibitor-naive patients with BRAF V600 mutation-positive metastatic melanoma, and approximately 20% were progression free at 3 years.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	86-90
26811525-7	2016	CONCLUSION: Dabrafenib plus trametinib results in a median OS of more than 2 years in BRAF inhibitor-naive patients with BRAF V600 mutation-positive metastatic melanoma, and approximately 20% were progression free at 3 years.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	121-125
26412570-4	2016	Dabrafenib, another selective BRAF inhibitor, has been licensed recently as an alternative drug with the same indications.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	30-34
26513168-7	2016	A better understanding of the BRAF/MEK/ERK pathway and the B-cell signaling pathway has allowed further exploration into the novel drugs vemurafenib, dabrafenib, trametinib, and ibrutinib.	dabrafenib	150-160	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	30-34
26419469-2	2016	Accordingly, two BRAF inhibitors (BRAFi), vemurafenib and dabrafenib are utilized to treat melanoma and resulted in an excellent clinical outcome.	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	17-21
27264268-7	2016	Currently, vemurafenib and dabrafenib are USFDA approved drugs used as B-Raf inhibitors.	dabrafenib	27-37	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	71-76
26601866-1	2016	Vemurafenib and dabrafenib, two potent tyrosine kinase inhibitors (TKIs) of the BRAF(V600E) kinase, are highly effective in the treatment of a BRAF (V600) -mutant metastatic melanoma.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	80-85
26601866-1	2016	Vemurafenib and dabrafenib, two potent tyrosine kinase inhibitors (TKIs) of the BRAF(V600E) kinase, are highly effective in the treatment of a BRAF (V600) -mutant metastatic melanoma.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	80-84
27535394-6	2016	Crizotinib has also demonstrated activity on patients with ROS1 rearrangements, and BRAF inhibitors (dabrafenib, vemurafenib) have demonstrated activity in patients with NSCLC with BRAF V600E mutation.	dabrafenib	101-111	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	84-88
27535394-6	2016	Crizotinib has also demonstrated activity on patients with ROS1 rearrangements, and BRAF inhibitors (dabrafenib, vemurafenib) have demonstrated activity in patients with NSCLC with BRAF V600E mutation.	dabrafenib	101-111	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	181-185
26680369-2	2016	Three (23%) were found positive for the presence of the BRAF mutation and were treated with the BRAF inhibitor dabrafenib.	dabrafenib	111-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	56-60
26680369-2	2016	Three (23%) were found positive for the presence of the BRAF mutation and were treated with the BRAF inhibitor dabrafenib.	dabrafenib	111-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	96-100
27042173-5	2016	Vemurafenib and dabrafenib are two selective BRAF inhibitors approved by the Food and Drug Administration (FDA).	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	45-49
26447389-1	2016	BRAF inhibitors vemurafenib and dabrafenib have become the standard of care for treatment of stage IV metastatic melanoma harboring a BRAF mutation.	dabrafenib	32-42	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	134-138
26446943-8	2016	Patients negative for BRAF mutation-positive cfDNA in plasma had higher response rates to dabrafenib and trametinib.	dabrafenib	90-100	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	22-26
27027150-1	2016	INTRODUCTION: In the 40-50% of advanced melanoma patients with tumors harboring BRAF V600E and V600 K mutations, BRAF inhibitors such as dabrafenib are a highly effective treatment.	dabrafenib	137-147	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	80-84
27027150-1	2016	INTRODUCTION: In the 40-50% of advanced melanoma patients with tumors harboring BRAF V600E and V600 K mutations, BRAF inhibitors such as dabrafenib are a highly effective treatment.	dabrafenib	137-147	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	113-117
26513168-7	2016	A better understanding of the BRAF/MEK/ERK pathway and the B-cell signaling pathway has allowed further exploration into the novel drugs vemurafenib, dabrafenib, trametinib, and ibrutinib.	dabrafenib	150-160	mitogen-activated protein kinase kinase 7	Homo sapiens	35-38
26513168-7	2016	A better understanding of the BRAF/MEK/ERK pathway and the B-cell signaling pathway has allowed further exploration into the novel drugs vemurafenib, dabrafenib, trametinib, and ibrutinib.	dabrafenib	150-160	mitogen-activated protein kinase 1	Homo sapiens	39-42
26753005-1	2016	Treatment with BRAF inhibitors such as vemurafenib or dabrafenib in patients with advanced BRAFV600 mutated melanoma has shown objective tumor responses in approximately half of the patients.	dabrafenib	54-64	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	15-19
28261653-7	2016	CONCLUSION: This analysis demonstrates improved PFS and OS with dabrafenib + trametinib versus dabrafenib, trametinib, vemurafenib, ipilimumab plus DTIC, and DTIC as first-line treatment for patients with BRAF mutation-positive metastatic melanoma.	dabrafenib	64-74	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	205-209
26730180-4	2016	Herein, we review the extensive pathways of BRAF inhibitor (vemurafenib and dabrafenib) resistance.	dabrafenib	76-86	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	44-48
26672086-0	2015	Redifferentiation of Iodine-Refractory BRAF V600E-Mutant Metastatic Papillary Thyroid Cancer with Dabrafenib-Letter.	dabrafenib	98-108	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	39-43
26672087-0	2015	Redifferentiation of Iodine-Refractory BRAF V600E-Mutant Metastatic Papillary Thyroid Cancer with Dabrafenib-Response.	dabrafenib	98-108	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	39-43
30363424-5	2016	Treatment was initiated with targeted therapy using the BRAF inhibitor Dabrafenib.	dabrafenib	71-81	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	56-60
26414886-4	2016	Based on this, we tested in vitro the efficacy of the BRAF inhibitors PLX4720 and dabrafenib in the presence of cerebrospinal fluid (CSF).	dabrafenib	82-92	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	54-58
26468227-0	2015	Dramatic transient improvement of metastatic BRAF(V600E)-mutated Langerhans cell sarcoma under treatment with dabrafenib.	dabrafenib	110-120	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	45-50
26626128-0	2015	Early Vaginal Opening in Juvenile Female Rats Given BRAF-Inhibitor Dabrafenib Is Not Associated with Early Physiologic Sexual Maturation.	dabrafenib	67-77	B-Raf proto-oncogene, serine/threonine kinase	Rattus norvegicus	52-56
26626128-1	2015	Dabrafenib (DAB), an inhibitor of BRAF kinase activity, is approved for metastatic melanoma with a BRAF V600E mutation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Rattus norvegicus	34-38
26626128-1	2015	Dabrafenib (DAB), an inhibitor of BRAF kinase activity, is approved for metastatic melanoma with a BRAF V600E mutation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Rattus norvegicus	99-103
26626128-1	2015	Dabrafenib (DAB), an inhibitor of BRAF kinase activity, is approved for metastatic melanoma with a BRAF V600E mutation.	dabrafenib	12-15	B-Raf proto-oncogene, serine/threonine kinase	Rattus norvegicus	34-38
26626128-1	2015	Dabrafenib (DAB), an inhibitor of BRAF kinase activity, is approved for metastatic melanoma with a BRAF V600E mutation.	dabrafenib	12-15	B-Raf proto-oncogene, serine/threonine kinase	Rattus norvegicus	99-103
26426764-7	2015	Since 2011, ipilimumab, an immuno-oncology therapy, and vemurafenib and dabrafenib, targeted agents that inhibit mutant BRAF, have been approved by the European Medicines Agency for the treatment of advanced melanoma.	dabrafenib	72-82	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	120-124
26202951-6	2015	A model cell line system was used to examine the effects of dabrafenib and trametinib on MAPK and BCR-ABL1 signaling.	dabrafenib	60-70	BCR activator of RhoGEF and GTPase	Homo sapiens	98-106
26392102-0	2015	Combined BRAF and MEK Inhibition With Dabrafenib and Trametinib in BRAF V600-Mutant Colorectal Cancer.	dabrafenib	38-48	mitogen-activated protein kinase kinase 7	Homo sapiens	18-21
26392102-1	2015	PURPOSE: To evaluate dabrafenib, a selective BRAF inhibitor, combined with trametinib, a selective MEK inhibitor, in patients with BRAF V600-mutant metastatic colorectal cancer (mCRC).	dabrafenib	21-31	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	45-49
26392102-1	2015	PURPOSE: To evaluate dabrafenib, a selective BRAF inhibitor, combined with trametinib, a selective MEK inhibitor, in patients with BRAF V600-mutant metastatic colorectal cancer (mCRC).	dabrafenib	21-31	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	131-135
26392102-11	2015	CONCLUSION: The combination of dabrafenib plus trametinib has activity in a subset of patients with BRAF V600-mutant mCRC.	dabrafenib	31-41	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	100-104
26612791-2	2015	The BRAF inhibitors vemurafenib and dabrafenib are characterized by rapid tumor control and high response rates.	dabrafenib	36-46	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-8
26503563-1	2015	A middle-aged female with metastatic melanoma was found to have hemoperitoneum after starting systemic therapy with the BRAF and MEK inhibitors dabrafenib and trametinib.	dabrafenib	144-154	mitogen-activated protein kinase kinase 7	Homo sapiens	129-132
26512791-0	2015	Granulomatous nephritis and dermatitis in a patient with BRAF V600E mutant metastatic melanoma treated with dabrafenib and trametinib.	dabrafenib	108-118	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	57-61
26497853-3	2015	Single treatment of BRAF mutant melanoma cell lines with vemurafenib or dabrafenib (BRAF inhibitors) alone or in combination with trametinib (MEK1/2 inhibitor) resulted in overexpression of Mcl-1.	dabrafenib	72-82	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	20-24
26340744-0	2015	Adjusting for confounding effects of treatment switching in a randomized phase II study of dabrafenib plus trametinib in BRAF V600+ metastatic melanoma.	dabrafenib	91-101	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	121-125
26340744-1	2015	Patients with BRAF V600E mutation-positive melanoma who were assigned to 150 mg dabrafenib twice daily combined with 2 mg trametinib once daily in a phase I/II study showed a median overall survival (OS) of 23.8 months, compared with 20.2 months for patients assigned to dabrafenib alone [hazard ratio (HR)=0.73, 95% confidence interval (CI) 0.43-1.24; data cutoff March 2013], on the basis of an intention-to-treat analysis.	dabrafenib	80-90	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
26340744-1	2015	Patients with BRAF V600E mutation-positive melanoma who were assigned to 150 mg dabrafenib twice daily combined with 2 mg trametinib once daily in a phase I/II study showed a median overall survival (OS) of 23.8 months, compared with 20.2 months for patients assigned to dabrafenib alone [hazard ratio (HR)=0.73, 95% confidence interval (CI) 0.43-1.24; data cutoff March 2013], on the basis of an intention-to-treat analysis.	dabrafenib	271-281	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
26497853-3	2015	Single treatment of BRAF mutant melanoma cell lines with vemurafenib or dabrafenib (BRAF inhibitors) alone or in combination with trametinib (MEK1/2 inhibitor) resulted in overexpression of Mcl-1.	dabrafenib	72-82	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	84-88
26497853-3	2015	Single treatment of BRAF mutant melanoma cell lines with vemurafenib or dabrafenib (BRAF inhibitors) alone or in combination with trametinib (MEK1/2 inhibitor) resulted in overexpression of Mcl-1.	dabrafenib	72-82	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	190-195
26619946-9	2015	For example, combination of BRAF/MEK inhibitors (e.g., dabrafenib/trametinib) have been demonstrated to improve survival compared to monotherapy.	dabrafenib	55-65	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	28-32
26664139-0	2015	A metastatic colon adenocarcinoma harboring BRAF V600E has a durable major response to dabrafenib/trametinib and chemotherapy.	dabrafenib	87-97	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	44-48
26619946-9	2015	For example, combination of BRAF/MEK inhibitors (e.g., dabrafenib/trametinib) have been demonstrated to improve survival compared to monotherapy.	dabrafenib	55-65	mitogen-activated protein kinase kinase 7	Homo sapiens	33-36
26182194-0	2015	Nephrotoxicity of the BRAF Inhibitors Vemurafenib and Dabrafenib.	dabrafenib	54-64	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	22-26
26665198-3	2015	Dabrafenib is the second registered BRAF kinase inhibitor.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	36-40
26182194-1	2015	IMPORTANCE: The selective BRAF inhibitors vemurafenib and dabrafenib have shown significant improvement in patient survival compared with standard therapy in BRAF V600-mutant metastatic melanoma.	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	26-30
26182194-1	2015	IMPORTANCE: The selective BRAF inhibitors vemurafenib and dabrafenib have shown significant improvement in patient survival compared with standard therapy in BRAF V600-mutant metastatic melanoma.	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	158-162
26498373-2	2016	Here, we describe our treatment of a man age 39 years with multiply recurrent BRAF V600E craniopharyngioma using dabrafenib (150mg, orally twice daily) and trametinib (2mg, orally twice daily).	dabrafenib	113-123	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	78-82
26048310-6	2015	Moreover, AE treatment significantly enhanced dabrafenib (a BRAF inhibitor) antiproliferative activity in BRAF mutant cell lines.	dabrafenib	46-56	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	60-64
26286452-4	2015	Literature data on the use of vemurafenib and dabrafenib in non-melanoma BRAF-mutated tumors are reviewed.	dabrafenib	46-56	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	73-77
24733801-0	2015	Complete Cytologic Remission of V600E BRAF-Mutant Melanoma-Associated Leptomeningeal Carcinomatosis Upon Treatment With Dabrafenib.	dabrafenib	120-130	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	38-42
26352988-0	2015	Primary Meningeal Pleomorphic Xanthoastrocytoma With Anaplastic Features: A Report of 2 Cases, One With BRAF(V600E) Mutation and Clinical Response to the BRAF Inhibitor Dabrafenib.	dabrafenib	169-179	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	104-109
26352988-0	2015	Primary Meningeal Pleomorphic Xanthoastrocytoma With Anaplastic Features: A Report of 2 Cases, One With BRAF(V600E) Mutation and Clinical Response to the BRAF Inhibitor Dabrafenib.	dabrafenib	169-179	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	104-108
26352988-6	2015	One case harboring a BRAF mutation disseminated to the thecal sac and showed a clinical response to the targeted BRAF inhibitor dabrafenib.	dabrafenib	128-138	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	21-25
26352988-6	2015	One case harboring a BRAF mutation disseminated to the thecal sac and showed a clinical response to the targeted BRAF inhibitor dabrafenib.	dabrafenib	128-138	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	113-117
26301799-5	2015	Combination of BRAF and MEK inhibitors using dabrafenib and trametinib is under evaluation.	dabrafenib	45-55	B-Raf proto-oncogene, serine/threonine kinase	Rattus norvegicus	15-19
26200476-3	2015	The combination of dabrafenib with the MEK inhibitor trametinib dimethyl sulfoxide (CombiDT therapy) increases response rate and survival compared with a BRAF inhibitor alone.	dabrafenib	19-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	154-158
26208524-2	2015	Despite the remarkable clinical activities achieved by vemurafenib and dabrafenib in treating BRAF(V600E) metastatic melanoma, their clinical efficacy in BRAF(V600E) colorectal cancer is far less impressive.	dabrafenib	71-81	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	94-98
26355347-8	2015	Furthermore, the inhibitor of mutant BRAF Dabrafenib, but not Vemurafenib, inhibited necroptosis in melanoma cells whenever RIPK3 is present.	dabrafenib	42-52	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	37-41
26355347-8	2015	Furthermore, the inhibitor of mutant BRAF Dabrafenib, but not Vemurafenib, inhibited necroptosis in melanoma cells whenever RIPK3 is present.	dabrafenib	42-52	receptor interacting serine/threonine kinase 3	Homo sapiens	124-129
26355347-9	2015	Our data suggest that loss of RIPK3 in melanoma and selective inhibition of the RIPK3/MLKL axis by BRAF inhibitor Dabrafenib, but not Vemurafenib, is critical to protect from necroptosis.	dabrafenib	114-124	receptor interacting serine/threonine kinase 3	Homo sapiens	80-85
26355347-9	2015	Our data suggest that loss of RIPK3 in melanoma and selective inhibition of the RIPK3/MLKL axis by BRAF inhibitor Dabrafenib, but not Vemurafenib, is critical to protect from necroptosis.	dabrafenib	114-124	mixed lineage kinase domain like pseudokinase	Homo sapiens	86-90
26355347-9	2015	Our data suggest that loss of RIPK3 in melanoma and selective inhibition of the RIPK3/MLKL axis by BRAF inhibitor Dabrafenib, but not Vemurafenib, is critical to protect from necroptosis.	dabrafenib	114-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	99-103
26710785-6	2015	Most of melanomas containing BRAF mutations, V600E (92%) and V600K (6.0%) were potentially sensitive to inhibitors vemurafenib and dabrafenib.	dabrafenib	131-141	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	29-33
26048310-6	2015	Moreover, AE treatment significantly enhanced dabrafenib (a BRAF inhibitor) antiproliferative activity in BRAF mutant cell lines.	dabrafenib	46-56	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	106-110
26387031-4	2015	The drugs vemurafenib, trametinib, and dabrafenib, which inhibit the commonly mutated BRAF pathway, have been approved based on improvements in survival outcomes.	dabrafenib	39-49	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	86-90
26347206-2	2015	The pharmacological, safety, and efficacy data come from the Phase I, II, and III studies of trametinib monotherapy, as well as those in combination with the BRAF inhibitor dabrafenib.	dabrafenib	173-183	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	158-162
26056325-1	2015	Vemurafenib and dabrafenib are both orally bioavailable small molecule agents that block mitogen activated protein kinase signalling in patients with melanoma and BRAF(V600E) mutation.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	163-168
26056325-3	2015	Continuing vemurafenib or dabrafenib therapy despite hypersensitivity reaction is especially important in patients with melanoma and BRAF(V600E) mutation, in whom this mutation plays a critical role in tumour growth.	dabrafenib	26-36	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	133-138
26347206-7	2015	The second step in developing trametinib was to use the combination of trametinib with the BRAF inhibitor, eg, dabrafenib, to postpone the progression on MEK or BRAF inhibitors.	dabrafenib	111-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	91-95
26347206-7	2015	The second step in developing trametinib was to use the combination of trametinib with the BRAF inhibitor, eg, dabrafenib, to postpone the progression on MEK or BRAF inhibitors.	dabrafenib	111-121	mitogen-activated protein kinase kinase 7	Homo sapiens	154-157
26347206-7	2015	The second step in developing trametinib was to use the combination of trametinib with the BRAF inhibitor, eg, dabrafenib, to postpone the progression on MEK or BRAF inhibitors.	dabrafenib	111-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	161-165
27622011-0	2016	Combined treatment with dabrafenib and trametinib with immune-stimulating antibodies for BRAF mutant melanoma.	dabrafenib	24-34	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	89-93
27622011-5	2016	An upregulation of PD-L1 was observed in the combination of dabrafenib, trametinib and anti-PD-1 therapy.	dabrafenib	60-70	CD274 molecule	Homo sapiens	19-24
27622011-7	2016	In conclusion, the combination of dabrafenib, trametinib, anti-PD1 or anti-PD-L1 therapy results in robust antitumor activity, which is further improved by adding the immune-stimulating Ab anti-CD137 or anti-CD134.	dabrafenib	34-44	TNF receptor superfamily member 4	Homo sapiens	208-213
25839886-0	2015	Panniculitis With Necrotizing Granulomata in a Patient on BRAF Inhibitor (Dabrafenib) Therapy for Metastatic Melanoma.	dabrafenib	74-84	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	58-62
25839886-4	2015	We describe a 50-year-old Hispanic woman with BRAF V600E mutant metastatic melanoma who was treated with surgery, radiation therapy, interleukin-2, and was enrolled on a BRAFi (dabrafenib) trial.	dabrafenib	177-187	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	46-50
26072431-1	2015	The introduction of BRAF inhibitors (BRAFi), vemurafenib and dabrafenib, revolutionized BRAFV600-mutated metastatic melanoma treatment with improved response rate and overall survival compared to standard chemotherapy.	dabrafenib	61-71	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	20-24
25748555-7	2015	Importantly, in an in vitro model of TEN, dabrafenib, an inhibitor of RIP3, prevented RIP3-mediated MLKL phosphorylation and decreased cell death.	dabrafenib	42-52	receptor interacting serine/threonine kinase 3	Homo sapiens	70-74
25748555-7	2015	Importantly, in an in vitro model of TEN, dabrafenib, an inhibitor of RIP3, prevented RIP3-mediated MLKL phosphorylation and decreased cell death.	dabrafenib	42-52	receptor interacting serine/threonine kinase 3	Homo sapiens	86-90
25748555-7	2015	Importantly, in an in vitro model of TEN, dabrafenib, an inhibitor of RIP3, prevented RIP3-mediated MLKL phosphorylation and decreased cell death.	dabrafenib	42-52	mixed lineage kinase domain like pseudokinase	Homo sapiens	100-104
24664475-2	2015	A common side effect associated with the BRAF inhibitor dabrafenib is severe fever symptoms such as pyrexia and rigors/chills; however, treatment options are limited.	dabrafenib	56-66	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	41-45
26037941-1	2015	BACKGROUND: Previously, a study of ours showed that the combination of dabrafenib and trametinib improves progression-free survival compared with dabrafenib and placebo in patients with BRAF Val600Lys/Glu mutation-positive metastatic melanoma.	dabrafenib	71-81	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	186-190
26037941-15	2015	INTERPRETATION: The improvement in overall survival establishes the combination of dabrafenib and trametinib as the standard targeted treatment for BRAF Val600 mutation-positive melanoma.	dabrafenib	83-93	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	148-152
30190849-3	2015	Dabrafenib, a potent kinase inhibitor of mutated BRAF, has been showed to have high response rates with a rapid onset of response, as well as improved overall and progression-free survival when compared with chemotherapy.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	49-53
30190849-4	2015	Dabrafenib in combination with trametinib, a MEK inhibitor, has demonstrated higher responses and improved clinical efficacy compared with monotherapy.	dabrafenib	0-10	mitogen-activated protein kinase kinase 7	Homo sapiens	45-48
25906420-0	2015	Dabrafenib for Treating Unresectable, Advanced or Metastatic BRAF V600 Mutation-Positive Melanoma: An Evidence Review Group Perspective.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	61-65
26347206-9	2015	The US Food and Drug Administration has approved the combination of dabrafenib (150 mg orally twice daily) and trametinib (2 mg orally once daily) for the treatment of patients with BRAF V600E/K-mutant metastatic melanoma, and their use seems to be currently the best approach.	dabrafenib	68-78	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	182-186
25906420-1	2015	The National Institute for Health and Care Excellence (NICE) invited GlaxoSmithKline, the manufacturer of dabrafenib, to submit evidence for the clinical and cost effectiveness of dabrafenib for the treatment of unresectable, advanced or metastatic BRAF V600 mutation-positive melanoma in accordance with the Institute"s Single Technology Appraisal (STA) process.	dabrafenib	180-190	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	249-253
25906420-14	2015	Applying the latest OS data from BREAK-3 to a less complex model structure increased the estimated ICER for dabrafenib compared with dacarbazine from $60,980 to $112,727 per QALY gained.	dabrafenib	108-118	cAMP responsive element modulator	Homo sapiens	99-103
26266008-8	2015	Given that the tumor was noted to be BRAF V600R mutated, the patient was started on single agent dabrafenib.	dabrafenib	97-107	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	37-41
25906420-17	2015	Since the overall costs of these two drugs were similar, the AC recommended the use of dabrafenib in patients with unresectable, advanced or metastatic BRAF V600 mutation-positive melanoma.	dabrafenib	87-97	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	152-156
26141621-4	2015	Positive results were also seen with combined dabrafenib and trametinib in patients with BRAF V600E/K metastatic melanoma and encorafenib plus binimetinib in BRAFV600-mutant cutaneous melanoma.	dabrafenib	46-56	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	89-93
26040620-1	2015	BACKGROUND: Patients with previously untreated BRAF V600E mutation-positive melanoma in BREAK-3 showed a median overall survival (OS) of 18.2 months for dabrafenib versus 15.6 months for dacarbazine (hazard ratio [HR], 0.76; 95% confidence interval, 0.48-1.21).	dabrafenib	153-163	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	47-51
26078801-1	2015	BACKGROUND: We report a case of severe bilateral panuveitis during melanoma therapy with a combination of Dabrafenib, a B-raf (BRAF) inhibitor, and Trametinib, a mitogen/extracellular signal-regulated kinase (MEK) inhibitor.	dabrafenib	106-116	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	120-125
26078801-1	2015	BACKGROUND: We report a case of severe bilateral panuveitis during melanoma therapy with a combination of Dabrafenib, a B-raf (BRAF) inhibitor, and Trametinib, a mitogen/extracellular signal-regulated kinase (MEK) inhibitor.	dabrafenib	106-116	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	127-131
26078801-1	2015	BACKGROUND: We report a case of severe bilateral panuveitis during melanoma therapy with a combination of Dabrafenib, a B-raf (BRAF) inhibitor, and Trametinib, a mitogen/extracellular signal-regulated kinase (MEK) inhibitor.	dabrafenib	106-116	mitogen-activated protein kinase kinase 7	Homo sapiens	209-212
25962795-3	2015	CASE PRESENTATION: We present a case of prolonged survival of a patient with BRAF V600E-mutant leptomeningeal disease who was treated with vemurafenib followed by whole brain radiation and a combination of dabrafenib and trametinib.	dabrafenib	206-216	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	77-81
26175403-4	2015	Dabrafenib, another BRAF inhibitor, has shown similar results and was approved in 2013.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	20-24
25965364-4	2015	However, since 2010 the anti-CTLA-4 antibody ipilimumab and the BRAF inhibitors, dabrafenib and vemurafenib, have demonstrated initial signs of efficacy in active brain metastases.	dabrafenib	81-91	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	64-68
25965804-2	2015	The kinase inhibitors vemurafenib and dabrafenib, which target oncogenic BRAF V600E, have shown significant clinical efficacy in melanoma patients harboring this mutation.	dabrafenib	38-48	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	73-77
26018524-5	2015	We show that the MEK inhibitor trametinib is more synergistic in combination with the BRAF inhibitor dabrafenib than with vemurafenib, another BRAF inhibitor.	dabrafenib	101-111	mitogen-activated protein kinase kinase 7	Homo sapiens	17-20
26018524-5	2015	We show that the MEK inhibitor trametinib is more synergistic in combination with the BRAF inhibitor dabrafenib than with vemurafenib, another BRAF inhibitor.	dabrafenib	101-111	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	86-90
25651238-0	2015	Multiple BRAF Wild-Type Melanomas During Dabrafenib Treatment for Metastatic BRAF-Mutant Melanoma.	dabrafenib	41-51	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
25159853-2	2015	We report a case of a 35-year-old man with BRAF(V600E) metastatic melanoma treated with dabrafenib (as well as ipilimumab and whole brain radiotherapy), who is alive, 25 months after the onset of his DMC.	dabrafenib	88-98	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	43-47
25619164-4	2015	In recent years, the United States Food and Drug Administration (FDA) - approved several novel agents targeting the RAS/RAF/MEK/ERK pathway (vemurafenib, dabrafenib, and trametinib) - critical in cell division and proliferation of melanoma, and an immune checkpoint inhibitor (ipilimumab) directed against the cytotoxic T lymphocyte Antigen - (CTLA-4).	dabrafenib	154-164	zinc fingers and homeoboxes 2	Homo sapiens	120-123
25619164-4	2015	In recent years, the United States Food and Drug Administration (FDA) - approved several novel agents targeting the RAS/RAF/MEK/ERK pathway (vemurafenib, dabrafenib, and trametinib) - critical in cell division and proliferation of melanoma, and an immune checkpoint inhibitor (ipilimumab) directed against the cytotoxic T lymphocyte Antigen - (CTLA-4).	dabrafenib	154-164	mitogen-activated protein kinase kinase 7	Homo sapiens	124-127
25619164-4	2015	In recent years, the United States Food and Drug Administration (FDA) - approved several novel agents targeting the RAS/RAF/MEK/ERK pathway (vemurafenib, dabrafenib, and trametinib) - critical in cell division and proliferation of melanoma, and an immune checkpoint inhibitor (ipilimumab) directed against the cytotoxic T lymphocyte Antigen - (CTLA-4).	dabrafenib	154-164	mitogen-activated protein kinase 1	Homo sapiens	128-131
25619164-4	2015	In recent years, the United States Food and Drug Administration (FDA) - approved several novel agents targeting the RAS/RAF/MEK/ERK pathway (vemurafenib, dabrafenib, and trametinib) - critical in cell division and proliferation of melanoma, and an immune checkpoint inhibitor (ipilimumab) directed against the cytotoxic T lymphocyte Antigen - (CTLA-4).	dabrafenib	154-164	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	344-350
25794603-0	2015	Health-related quality of life impact in a randomised phase III study of the combination of dabrafenib and trametinib versus dabrafenib monotherapy in patients with BRAF V600 metastatic melanoma.	dabrafenib	92-102	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	165-169
25651238-0	2015	Multiple BRAF Wild-Type Melanomas During Dabrafenib Treatment for Metastatic BRAF-Mutant Melanoma.	dabrafenib	41-51	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	77-81
30190840-2	2015	A 63-year-old female with widely metastatic BRAF V600E-mutant melanoma was treated with dabrafenib/trametinib.	dabrafenib	88-98	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	44-48
25597784-3	2015	Agents that target the RAS/RAF/MEK/ERK (MAPK) signaling pathway - the BRAF inhibitors vemurafenib and dabrafenib, and the MEK1/2 inhibitor trametinib - have increased survival in patients with metastatic melanoma.	dabrafenib	102-112	zinc fingers and homeoboxes 2	Homo sapiens	27-30
25597784-3	2015	Agents that target the RAS/RAF/MEK/ERK (MAPK) signaling pathway - the BRAF inhibitors vemurafenib and dabrafenib, and the MEK1/2 inhibitor trametinib - have increased survival in patients with metastatic melanoma.	dabrafenib	102-112	mitogen-activated protein kinase kinase 7	Homo sapiens	31-34
25597784-3	2015	Agents that target the RAS/RAF/MEK/ERK (MAPK) signaling pathway - the BRAF inhibitors vemurafenib and dabrafenib, and the MEK1/2 inhibitor trametinib - have increased survival in patients with metastatic melanoma.	dabrafenib	102-112	mitogen-activated protein kinase 1	Homo sapiens	35-38
25597784-3	2015	Agents that target the RAS/RAF/MEK/ERK (MAPK) signaling pathway - the BRAF inhibitors vemurafenib and dabrafenib, and the MEK1/2 inhibitor trametinib - have increased survival in patients with metastatic melanoma.	dabrafenib	102-112	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	70-74
25648338-3	2015	AREAS COVERED: This review covers the current data on the efficacy and safety of the selective BRAF (vemurafenib and dabrafenib) and MEK (trametinib) inhibitors as well as the available data on BRAF inhibitor + MEK inhibitor combination therapy (dabrafenib + trametinib and vemurafenib + cobimetinib).	dabrafenib	117-127	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	95-99
25673642-6	2015	Treatment with the BRAF inhibitor dabrafenib decreased tumor growth and induced senescence that was more pronounced in tumors with Atg7 deficiency.	dabrafenib	34-44	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	19-23
25797743-7	2015	After 14 days of dabrafenib therapy, there was a marked reduction in viable melanoma cells and a CD8 T-cell--rich infiltrate.	dabrafenib	17-27	CD8a molecule	Homo sapiens	97-100
25449654-0	2015	Assessment of the drug interaction potential and single- and repeat-dose pharmacokinetics of the BRAF inhibitor dabrafenib.	dabrafenib	112-122	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	97-101
25449654-1	2015	The induction of CYP2C9 by dabrafenib using S-warfarin as a probe and the effects of a CYP3A inhibitor (ketoconazole) and a CYP2C8 inhibitor (gemfibrozil) on dabrafenib pharmacokinetics were evaluated in patients with BRAF V600 mutation-positive tumors.	dabrafenib	27-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
25449654-11	2015	Substitution of strong inhibitors or strong inducers of CYP3A or CYP2C8 is recommended during treatment with dabrafenib.	dabrafenib	109-119	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	56-61
25449654-11	2015	Substitution of strong inhibitors or strong inducers of CYP3A or CYP2C8 is recommended during treatment with dabrafenib.	dabrafenib	109-119	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	65-71
25643238-3	2015	Here, we show that systemic treatment with BRAF inhibitor vemurafenib substituted by dual BRAF/MEK inhibition (dabrafenib and trametinib) before surgery can offer the potential to cure the initially difficult or inoperable melanoma.	dabrafenib	111-121	mitogen-activated protein kinase kinase 7	Homo sapiens	95-98
25480661-5	2015	Here, we investigated the biological and therapeutic importance of the activated BRAF-mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK) pathway in HCL by exposing in vitro primary leukemic cells purified from 26 patients to clinically available BRAF (vemurafenib; dabrafenib) or MEK (trametinib) inhibitors.	dabrafenib	304-314	mitogen-activated protein kinase kinase 7	Homo sapiens	127-130
25480661-5	2015	Here, we investigated the biological and therapeutic importance of the activated BRAF-mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK) pathway in HCL by exposing in vitro primary leukemic cells purified from 26 patients to clinically available BRAF (vemurafenib; dabrafenib) or MEK (trametinib) inhibitors.	dabrafenib	304-314	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	81-85
25467940-1	2015	The US Food and Drug Administration-approved BRAF inhibitors, vemurafenib and dabrafenib, have demonstrated superior efficacy in patients with BRAF-mutant melanomas but have limited efficacy in BRAF-mutant colorectal cancer.	dabrafenib	78-88	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	45-49
25116269-4	2015	After treatment with BRAF inhibitor (dabrafenib), the child"s clinical condition improved progressively.	dabrafenib	37-47	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	21-25
25488880-0	2015	Cost effectiveness of dabrafenib as a first-line treatment in patients with BRAF V600 mutation-positive unresectable or metastatic melanoma in Canada.	dabrafenib	22-32	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	76-80
25488880-1	2015	OBJECTIVE: To evaluate the cost effectiveness of dabrafenib versus dacarbazine and vemurafenib as first-line treatments in patients with BRAF V600 mutation-positive unresectable or metastatic melanoma from a Canadian healthcare system perspective.	dabrafenib	49-59	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	137-141
25488880-13	2015	Assuming a class effect for efficacy of BRAF inhibitors, dabrafenib was dominant versus vemurafenib (less costly, equally effective), reflecting its assumed lower daily cost.	dabrafenib	57-67	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	40-44
25787767-9	2015	Given the up-regulation of PD-L1 seen with dabrafenib and/or trametinib combined with antigen-specific ACT, we tested the combination of dabrafenib, trametinib, and anti-PD1 therapy in SM1 tumors, and observed superior antitumor effect.	dabrafenib	43-53	CD274 molecule	Homo sapiens	27-32
25810704-1	2015	BACKGROUND: Small molecules that inhibit V600 mutated BRAF protein, such as vemurafenib and dabrafenib, are effective in treatment of metastatic melanoma.	dabrafenib	92-102	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	54-58
25810704-2	2015	CASE REPORT: We here describe the clinical course of a V600E BRAF mutated metastatic melanoma patient with systemic disease, who developed tumor progression on superficial soft-tissue metastases during treatment with dabrafenib.	dabrafenib	217-227	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	61-65
25549723-0	2015	Redifferentiation of iodine-refractory BRAF V600E-mutant metastatic papillary thyroid cancer with dabrafenib.	dabrafenib	98-108	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	39-43
25549723-1	2015	PURPOSE: To determine whether the selective BRAF inhibitor, dabrafenib, can stimulate radioiodine uptake in BRAF V600E-mutated unresectable or metastatic iodine-refractory papillary thyroid cancer (PTC).	dabrafenib	60-70	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	44-48
25549723-1	2015	PURPOSE: To determine whether the selective BRAF inhibitor, dabrafenib, can stimulate radioiodine uptake in BRAF V600E-mutated unresectable or metastatic iodine-refractory papillary thyroid cancer (PTC).	dabrafenib	60-70	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	108-112
25549723-13	2015	CONCLUSIONS: Dabrafenib can stimulate radioiodine uptake in patients with metastatic BRAF V600E-mutant iodine-refractory PTC, representing a potential new therapeutic approach for these patients.	dabrafenib	13-23	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	85-89
25690538-1	2015	BACKGROUND: Selective BRAF inhibition (BRAFi) by vemurafenib or dabrafenib has become approved standard treatment in BRAF V600 mutated advanced stage melanoma.	dabrafenib	64-74	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	22-26
25690538-1	2015	BACKGROUND: Selective BRAF inhibition (BRAFi) by vemurafenib or dabrafenib has become approved standard treatment in BRAF V600 mutated advanced stage melanoma.	dabrafenib	64-74	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	39-43
25711514-1	2015	Dabrafenib is a potent inhibitor of mutant BRAF.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	43-47
25755684-2	2015	Since 2011, the specific BRAF targeted agents, vemurafenib and dabrafenib, and the MEK inhibitor, trametinib, have been licensed for the treatment of patients with unresectable or metastatic BRAF mutant melanoma.	dabrafenib	63-73	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	25-29
25609506-2	2015	The targeted therapy with the B-RAF inhibitors vemurafenib and dabrafenib achieves rapid tumor reduction but is often followed by the development of resistance in the further course of therapy.	dabrafenib	63-73	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	30-35
25653539-1	2015	BRAF inhibitors vemurafenib and dabrafenib achieved improved overall survival over chemotherapy and have been approved for the treatment of BRAF-mutated metastatic melanoma.	dabrafenib	32-42	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
25653539-1	2015	BRAF inhibitors vemurafenib and dabrafenib achieved improved overall survival over chemotherapy and have been approved for the treatment of BRAF-mutated metastatic melanoma.	dabrafenib	32-42	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	140-144
25653539-2	2015	More recently, the combination of BRAF inhibitor dabrafenib with MEK inhibitor trametinib has shown improved progression-free survival, compared to dabrafenib monotherapy, in a Phase II study and has received approval by the US Food and Drug Administration.	dabrafenib	49-59	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	34-38
25653539-2	2015	More recently, the combination of BRAF inhibitor dabrafenib with MEK inhibitor trametinib has shown improved progression-free survival, compared to dabrafenib monotherapy, in a Phase II study and has received approval by the US Food and Drug Administration.	dabrafenib	148-158	mitogen-activated protein kinase kinase 7	Homo sapiens	65-68
25550132-5	2015	Moreover, trametinib is also indicated for use in combination with dabrafenib (a BRAF inhibitor).	dabrafenib	67-77	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	81-85
25993155-5	2015	The most dramatic example is the development of single-agent inhibitors of BRAF (vemurafenib, dabrafenib, encorafenib) and MEK (trametinib, cobimetinib, binimetinib) for patients with metastatic BRAFV600-mutant melanoma, a subset that represents 40% to 50% of patients with metastatic melanoma.	dabrafenib	94-104	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	75-79
24413374-5	2015	For most BRAF-mutated melanoma patients and particularly those with a high tumor load, vemurafenib or other BRAF inhibitors such as dabrafenib are the treatment of choice.	dabrafenib	132-142	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
24413374-5	2015	For most BRAF-mutated melanoma patients and particularly those with a high tumor load, vemurafenib or other BRAF inhibitors such as dabrafenib are the treatment of choice.	dabrafenib	132-142	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	108-112
25370473-7	2015	Consistent with these data, two BRAF-mutant cell lines with endogenous MEK1(P124) mutations showed intermediate sensitivity to dabrafenib, but were highly sensitive to downstream inhibition of MEK or ERK.	dabrafenib	127-137	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	32-36
25381152-5	2015	Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib).	dabrafenib	85-95	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	52-57
25370473-6	2015	Furthermore, MEK1(P124Q/S) mutations were shown to have independent kinase activity and introduction of these mutations into a BRAF-mutant melanoma cell line diminished inhibition of ERK phosphorylation by dabrafenib and enhanced clonogenic survival in the presence of dabrafenib compared with cells ectopically expressing wild-type MEK1.	dabrafenib	206-216	mitogen-activated protein kinase kinase 1	Homo sapiens	13-17
25370473-6	2015	Furthermore, MEK1(P124Q/S) mutations were shown to have independent kinase activity and introduction of these mutations into a BRAF-mutant melanoma cell line diminished inhibition of ERK phosphorylation by dabrafenib and enhanced clonogenic survival in the presence of dabrafenib compared with cells ectopically expressing wild-type MEK1.	dabrafenib	206-216	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	127-131
25370473-6	2015	Furthermore, MEK1(P124Q/S) mutations were shown to have independent kinase activity and introduction of these mutations into a BRAF-mutant melanoma cell line diminished inhibition of ERK phosphorylation by dabrafenib and enhanced clonogenic survival in the presence of dabrafenib compared with cells ectopically expressing wild-type MEK1.	dabrafenib	269-279	mitogen-activated protein kinase kinase 1	Homo sapiens	13-17
25370473-6	2015	Furthermore, MEK1(P124Q/S) mutations were shown to have independent kinase activity and introduction of these mutations into a BRAF-mutant melanoma cell line diminished inhibition of ERK phosphorylation by dabrafenib and enhanced clonogenic survival in the presence of dabrafenib compared with cells ectopically expressing wild-type MEK1.	dabrafenib	269-279	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	127-131
25370473-7	2015	Consistent with these data, two BRAF-mutant cell lines with endogenous MEK1(P124) mutations showed intermediate sensitivity to dabrafenib, but were highly sensitive to downstream inhibition of MEK or ERK.	dabrafenib	127-137	mitogen-activated protein kinase kinase 1	Homo sapiens	71-75
25370473-7	2015	Consistent with these data, two BRAF-mutant cell lines with endogenous MEK1(P124) mutations showed intermediate sensitivity to dabrafenib, but were highly sensitive to downstream inhibition of MEK or ERK.	dabrafenib	127-137	mitogen-activated protein kinase kinase 7	Homo sapiens	71-74
25473943-2	2015	Targeting BRAF mutations with either small molecule inhibitors of BRAF or one of the downstream mediators of oncogenic BRAF - MEK - is associated with improved outcomes compared with chemotherapy and has led to the US FDA approval of two BRAF inhibitors - vemurafenib and dabrafenib - and the MEK inhibitor trametinib.	dabrafenib	272-282	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	10-14
25467940-1	2015	The US Food and Drug Administration-approved BRAF inhibitors, vemurafenib and dabrafenib, have demonstrated superior efficacy in patients with BRAF-mutant melanomas but have limited efficacy in BRAF-mutant colorectal cancer.	dabrafenib	78-88	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	143-147
25467940-1	2015	The US Food and Drug Administration-approved BRAF inhibitors, vemurafenib and dabrafenib, have demonstrated superior efficacy in patients with BRAF-mutant melanomas but have limited efficacy in BRAF-mutant colorectal cancer.	dabrafenib	78-88	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	143-147
25473943-2	2015	Targeting BRAF mutations with either small molecule inhibitors of BRAF or one of the downstream mediators of oncogenic BRAF - MEK - is associated with improved outcomes compared with chemotherapy and has led to the US FDA approval of two BRAF inhibitors - vemurafenib and dabrafenib - and the MEK inhibitor trametinib.	dabrafenib	272-282	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	66-70
25473943-2	2015	Targeting BRAF mutations with either small molecule inhibitors of BRAF or one of the downstream mediators of oncogenic BRAF - MEK - is associated with improved outcomes compared with chemotherapy and has led to the US FDA approval of two BRAF inhibitors - vemurafenib and dabrafenib - and the MEK inhibitor trametinib.	dabrafenib	272-282	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	66-70
25473943-2	2015	Targeting BRAF mutations with either small molecule inhibitors of BRAF or one of the downstream mediators of oncogenic BRAF - MEK - is associated with improved outcomes compared with chemotherapy and has led to the US FDA approval of two BRAF inhibitors - vemurafenib and dabrafenib - and the MEK inhibitor trametinib.	dabrafenib	272-282	mitogen-activated protein kinase kinase 7	Homo sapiens	126-129
25473943-2	2015	Targeting BRAF mutations with either small molecule inhibitors of BRAF or one of the downstream mediators of oncogenic BRAF - MEK - is associated with improved outcomes compared with chemotherapy and has led to the US FDA approval of two BRAF inhibitors - vemurafenib and dabrafenib - and the MEK inhibitor trametinib.	dabrafenib	272-282	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	66-70
25473943-3	2015	Further, the combination of dabrafenib and trametinib is well tolerated and associated with higher responses and improved survival compared with single-agent BRAF inhibitors.	dabrafenib	28-38	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	158-162
25686114-4	2015	Other compounds such as the BRAF inhibitor dabrafenib and the immunotherapeutic agent ipilimumab are also approved in the same group of patients.	dabrafenib	43-53	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	28-32
25583765-0	2015	Cotreatment of hairy cell leukemia and melanoma with the BRAF inhibitor dabrafenib.	dabrafenib	72-82	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	57-61
25583765-3	2015	This report presents a patient with HCL and malignant melanoma with the BRAF p.V600E mutation, and discusses the successful treatment of both cancers with the BRAF inhibitor dabrafenib.	dabrafenib	174-184	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	72-76
25583765-3	2015	This report presents a patient with HCL and malignant melanoma with the BRAF p.V600E mutation, and discusses the successful treatment of both cancers with the BRAF inhibitor dabrafenib.	dabrafenib	174-184	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	159-163
26171248-2	2015	Two BRAF(V600E) targeted therapies, dabrafenib and vemurafenib, have received US approval for treatment of metastatic melanoma in BRAF(V600E) patients, a mutation that affects ~50% of patients.	dabrafenib	36-46	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-9
26171248-2	2015	Two BRAF(V600E) targeted therapies, dabrafenib and vemurafenib, have received US approval for treatment of metastatic melanoma in BRAF(V600E) patients, a mutation that affects ~50% of patients.	dabrafenib	36-46	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-8
25466451-0	2015	Response to dabrafenib after progression on vemurafenib in a patient with advanced BRAF V600E-mutant bronchial adenocarcinoma.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	83-87
25466451-1	2015	We present the case of a patient with rapidly accelerated fibrosarcoma gene F (BRAF) mutated adenocarcinoma of the lung, responding to BRAF inhibitor dabrafenib after progressing on vemurafenib followed by docetaxel.	dabrafenib	150-160	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	79-83
25466451-1	2015	We present the case of a patient with rapidly accelerated fibrosarcoma gene F (BRAF) mutated adenocarcinoma of the lung, responding to BRAF inhibitor dabrafenib after progressing on vemurafenib followed by docetaxel.	dabrafenib	150-160	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	135-139
25399551-1	2015	BACKGROUND: The BRAF inhibitors vemurafenib and dabrafenib have shown efficacy as monotherapies in patients with previously untreated metastatic melanoma with BRAF V600E or V600K mutations.	dabrafenib	48-58	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	16-20
25399551-1	2015	BACKGROUND: The BRAF inhibitors vemurafenib and dabrafenib have shown efficacy as monotherapies in patients with previously untreated metastatic melanoma with BRAF V600E or V600K mutations.	dabrafenib	48-58	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	159-163
25399551-11	2015	CONCLUSIONS: Dabrafenib plus trametinib, as compared with vemurafenib monotherapy, significantly improved overall survival in previously untreated patients with metastatic melanoma with BRAF V600E or V600K mutations, without increased overall toxicity.	dabrafenib	13-23	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	186-190
24863690-0	2014	Rapid and complete hematological response of refractory hairy cell leukemia to the BRAF inhibitor dabrafenib.	dabrafenib	98-108	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	83-87
25285888-0	2015	BRAF inhibitor dabrafenib in patients with metastatic BRAF-mutant thyroid cancer.	dabrafenib	15-25	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
25285888-0	2015	BRAF inhibitor dabrafenib in patients with metastatic BRAF-mutant thyroid cancer.	dabrafenib	15-25	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	54-58
25285888-3	2015	Our objectives were to analyze safety and efficacy of the selective BRAF inhibitor dabrafenib in patients with metastatic BRAF-mutant thyroid carcinoma.	dabrafenib	83-93	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	68-72
25285888-3	2015	Our objectives were to analyze safety and efficacy of the selective BRAF inhibitor dabrafenib in patients with metastatic BRAF-mutant thyroid carcinoma.	dabrafenib	83-93	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	122-126
25285888-13	2015	CONCLUSIONS: Dabrafenib was well tolerated and resulted in durable responses in BRAF-mutant differentiated thyroid carcinoma patients.	dabrafenib	13-23	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	80-84
25073704-8	2014	Application of the BRAF(V600E)-specific inhibitor vemurafenib and the BRAF(V6ooE/V600K)-inhibitor dabrafenib revealed predominant regulation of ETV-1 mRNA and protein via MAPK-pathway.	dabrafenib	98-108	ETS variant transcription factor 1	Homo sapiens	144-149
25056119-3	2014	Here, we demonstrate that melanoma cell lines possessing the RAC1 hotspot variant are resistant to RAF inhibitors (vemurafenib and dabrafenib).	dabrafenib	131-141	Rac family small GTPase 1	Homo sapiens	61-65
25452114-0	2014	Increased MAPK reactivation in early resistance to dabrafenib/trametinib combination therapy of BRAF-mutant metastatic melanoma.	dabrafenib	51-61	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	96-100
25452114-3	2014	Here we analyse 20 BRAF(V600)-mutant melanoma metastases derived from 10 patients treated with the combination of dabrafenib and trametinib for resistance mechanisms and genetic correlates of response.	dabrafenib	114-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	19-28
25287827-2	2014	This study assessed the safety and efficacy of dabrafenib and trametinib in patients who had received prior BRAF inhibitor treatment.	dabrafenib	47-57	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	108-112
25287827-8	2014	CONCLUSION: Dabrafenib plus trametinib has modest clinical efficacy in patients with BRAF inhibitor-resistant melanoma.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	85-89
25344914-2	2014	BRAF inhibitors vemurafenib and dabrafenib achieved improved overall survival over chemotherapy and have been approved for the treatment of BRAF-mutated metastatic melanoma.	dabrafenib	32-42	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
25344914-2	2014	BRAF inhibitors vemurafenib and dabrafenib achieved improved overall survival over chemotherapy and have been approved for the treatment of BRAF-mutated metastatic melanoma.	dabrafenib	32-42	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	140-144
25265492-12	2014	CONCLUSIONS: A combination of dabrafenib and trametinib, as compared with dabrafenib alone, improved the rate of progression-free survival in previously untreated patients who had metastatic melanoma with BRAF V600E or V600K mutations.	dabrafenib	30-40	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	205-209
25435907-0	2014	Dramatic response to dabrafenib and trametinib combination in a BRAF V600E-mutated cholangiocarcinoma: implementation of a molecular tumour board and next-generation sequencing for personalized medicine.	dabrafenib	21-31	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	64-68
25442474-6	2014	CONCLUSION: The patients treated by BRAF inhibitors (vemurafenib and dabrafenib) can present acantholytic dyskeratosis.	dabrafenib	69-79	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	36-40
24828387-2	2014	Treatments such as the FDA-approved RAF inhibitor vemurafenib and the more recently approved dabrafenib and trametinib combination therapy are designed to target the ERK1/2 pathway.	dabrafenib	93-103	mitogen-activated protein kinase 3	Homo sapiens	166-172
25364391-1	2014	The selective BRAF inhibitors, vemurafenib and dabrafenib, yield high response rates and improved overall survival in patients with BRAF V600E-mutant metastatic melanoma.	dabrafenib	47-57	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
25364391-1	2014	The selective BRAF inhibitors, vemurafenib and dabrafenib, yield high response rates and improved overall survival in patients with BRAF V600E-mutant metastatic melanoma.	dabrafenib	47-57	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	132-136
24985732-1	2014	BACKGROUND: The v-raf murine sarcoma viral oncogene homolog B (BRAF) inhibitor (BRAFi) drugs dabrafenib and vemurafenib have high response rates in BRAF-mutant, metastatic melanoma; however, 50% of patients progress by 7 months.	dabrafenib	93-103	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	16-61
24985732-1	2014	BACKGROUND: The v-raf murine sarcoma viral oncogene homolog B (BRAF) inhibitor (BRAFi) drugs dabrafenib and vemurafenib have high response rates in BRAF-mutant, metastatic melanoma; however, 50% of patients progress by 7 months.	dabrafenib	93-103	Braf transforming gene	Mus musculus	63-67
24985732-1	2014	BACKGROUND: The v-raf murine sarcoma viral oncogene homolog B (BRAF) inhibitor (BRAFi) drugs dabrafenib and vemurafenib have high response rates in BRAF-mutant, metastatic melanoma; however, 50% of patients progress by 7 months.	dabrafenib	93-103	Braf transforming gene	Mus musculus	80-84
25148599-4	2014	The discovery of the BRAF mutation has created a therapeutic target exploited by oral inhibitors like vemurafenib and dabrafenib.	dabrafenib	118-128	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	21-25
25501056-2	2014	Selective BRAF inhibitors such as vemurafenib and dabrafenib are currently approved for the treatment of advanced melanoma patients with BRAF mutation.	dabrafenib	50-60	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	10-14
25501056-2	2014	Selective BRAF inhibitors such as vemurafenib and dabrafenib are currently approved for the treatment of advanced melanoma patients with BRAF mutation.	dabrafenib	50-60	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	137-141
25526431-4	2014	Interestingly, the immediate therapeutic switch to a different BRAF inhibitor "dabrafenib?	dabrafenib	79-89	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	63-67
25437182-1	2014	INTRODUCTION: Selective inhibitors of BRAF, vemurafenib and dabrafenib are the standard of care for metastatic melanoma patients with BRAF V600, while chemotherapy continued to be widely used in BRAF wild type patients.	dabrafenib	60-70	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	134-138
25437182-1	2014	INTRODUCTION: Selective inhibitors of BRAF, vemurafenib and dabrafenib are the standard of care for metastatic melanoma patients with BRAF V600, while chemotherapy continued to be widely used in BRAF wild type patients.	dabrafenib	60-70	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	134-138
24313958-1	2014	BACKGROUND: The MEK inhibitor trametinib is currently undergoing clinical trials as the treatment of metastatic melanoma both alone and in combination with the BRAF inhibitor dabrafenib.	dabrafenib	175-185	mitogen-activated protein kinase kinase 7	Homo sapiens	16-19
24313958-1	2014	BACKGROUND: The MEK inhibitor trametinib is currently undergoing clinical trials as the treatment of metastatic melanoma both alone and in combination with the BRAF inhibitor dabrafenib.	dabrafenib	175-185	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	160-164
25305754-1	2014	BACKGROUND: Combination therapy with BRAF V600E inhibitor dabrafenib and MEK inhibitor trametinib significantly improves progression-free survival of patients with BRAF V600-positive metastatic melanoma, but their use can be associated with life-threatening toxicities.	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	37-41
25305754-1	2014	BACKGROUND: Combination therapy with BRAF V600E inhibitor dabrafenib and MEK inhibitor trametinib significantly improves progression-free survival of patients with BRAF V600-positive metastatic melanoma, but their use can be associated with life-threatening toxicities.	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	164-168
25305754-3	2014	Combination therapy with dabrafenib and trametinib improves progression-free survival of patients with BRAF V600-positive metastatic melanoma.	dabrafenib	25-35	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	103-107
25056119-5	2014	Conversely, RNAi-mediated silencing of endogenous RAC1 P29S in a melanoma cell line with a co-occurring BRAF V600 mutation increased sensitivity to vemurafenib and dabrafenib.	dabrafenib	164-174	Rac family small GTPase 1	Homo sapiens	50-54
25056119-5	2014	Conversely, RNAi-mediated silencing of endogenous RAC1 P29S in a melanoma cell line with a co-occurring BRAF V600 mutation increased sensitivity to vemurafenib and dabrafenib.	dabrafenib	164-174	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	104-108
24958809-0	2014	Dose selection, pharmacokinetics, and pharmacodynamics of BRAF inhibitor dabrafenib (GSK2118436).	dabrafenib	73-83	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	58-62
24958809-0	2014	Dose selection, pharmacokinetics, and pharmacodynamics of BRAF inhibitor dabrafenib (GSK2118436).	dabrafenib	85-95	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	58-62
24958809-3	2014	EXPERIMENTAL DESIGN: Dabrafenib was administered orally once, twice (BID), or three times daily (TID).	dabrafenib	21-31	BH3 interacting domain death agonist	Homo sapiens	69-72
24958809-7	2014	Pharmacokinetic assessment of dabrafenib demonstrated a less-than-dose-proportional increase in exposure after repeat dosing above 150 mg BID.	dabrafenib	30-40	BH3 interacting domain death agonist	Homo sapiens	138-141
24958809-13	2014	CONCLUSION: The RP2D of dabrafenib was determined to be 150 mg BID after considering multiple factors, including pharmacokinetics, tissue pharmacodynamics, FDG-PET pharmacodynamics, and the dose-response relationship.	dabrafenib	24-34	BH3 interacting domain death agonist	Homo sapiens	63-66
25014231-2	2014	Dabrafenib is the second approved selective BRAF inhibitor (after vemurafenib) for the treatment of unresectable or metastatic BRAF V600-positive melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	44-48
25054915-1	2014	The combination of dabrafenib and trametinib (CombiDT) is an effective treatment for BRAF-mutant metastatic melanoma; however, over 70% of patients develop drug-related pyrexia, and little is known about this toxicity.	dabrafenib	19-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	85-89
24858661-2	2014	This case report describes the use of multiplatform molecular profiling in sequential surgical samples of a treatment-resistant tumour site subjected to ongoing treatment with dabrafenib in a patient with metastatic cutaneous BRAF mutant melanoma.	dabrafenib	176-186	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	226-230
25014231-2	2014	Dabrafenib is the second approved selective BRAF inhibitor (after vemurafenib) for the treatment of unresectable or metastatic BRAF V600-positive melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	127-131
25014231-3	2014	AREAS COVERED: This review covers the current data on the efficacy and safety of the selective BRAF inhibitor dabrafenib in patients with metastatic BRAF V600 positive melanoma.	dabrafenib	110-120	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	95-99
25014231-3	2014	AREAS COVERED: This review covers the current data on the efficacy and safety of the selective BRAF inhibitor dabrafenib in patients with metastatic BRAF V600 positive melanoma.	dabrafenib	110-120	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	149-153
24769640-0	2014	Patient perception of the benefit of a BRAF inhibitor in metastatic melanoma: quality-of-life analyses of the BREAK-3 study comparing dabrafenib with dacarbazine.	dabrafenib	134-144	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	39-43
25324906-9	2014	Vemurafenib and dabrafenib are targeted agents for patients with BRAF mutation-positive melanoma.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	65-69
25074438-2	2014	METHODS: A human melanoma cell line with the B-RAF (V600E) mutation (A375mel) was exposed to B-RAF inhibitor (GSK2118436), MEK inhibitor (GSK1120212) and AurkA inhibitor (MLN8054) as single agents or in various combinations (BRAF plus AurkA inhibitor, MEK plus AurkA inhibitor or triple combination BRAF plus MEK plus AurkA inhibitor).	dabrafenib	110-120	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	45-50
24769640-1	2014	BACKGROUND: In a randomized phase III study (BREAK-3), dabrafenib showed prolonged progression-free survival (PFS) (median 5.1 versus 2.7 months; hazard ratio = 0.30; 95% confidence interval 0.18-0.53; P &lt; 0.0001) compared with dacarbazine (DTIC) in patients with BRAF V600E metastatic melanoma.	dabrafenib	55-65	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	267-271
24769640-9	2014	CONCLUSIONS: This first reported QoL analysis for a BRAF inhibitor in metastatic melanoma demonstrates that the high tumor response rates and PFS superiority of dabrafenib over DTIC is not only a theoretical advantage, but also transforms in a rapid functional and symptomatic benefit for the patient.	dabrafenib	161-171	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	52-56
24748562-1	2014	Dabrafenib is a potent ATP-competitive inhibitor for the V600 mutant b-rapidly accelerated fibrosarcoma (b-raf) kinase currently approved in the United States for the treatment of metastatic melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	69-103
24748562-1	2014	Dabrafenib is a potent ATP-competitive inhibitor for the V600 mutant b-rapidly accelerated fibrosarcoma (b-raf) kinase currently approved in the United States for the treatment of metastatic melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	105-110
24748562-7	2014	At 30 muM dabrafenib showed increases in CYP2B6 and CYP3A4 mRNA expression indicative of induction.	dabrafenib	10-20	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	41-47
24748562-7	2014	At 30 muM dabrafenib showed increases in CYP2B6 and CYP3A4 mRNA expression indicative of induction.	dabrafenib	10-20	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	52-58
24748562-9	2014	This risk-assessment approach indicated that dabrafenib is unlikely to perpetrate any in vivo DDIs by inhibition mechanisms, but is a likely inducer of CYP3A4 and a victim of CYP3A4 and CYP2C8 inhibitors.	dabrafenib	45-55	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	152-158
24748562-9	2014	This risk-assessment approach indicated that dabrafenib is unlikely to perpetrate any in vivo DDIs by inhibition mechanisms, but is a likely inducer of CYP3A4 and a victim of CYP3A4 and CYP2C8 inhibitors.	dabrafenib	45-55	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	175-181
24748562-9	2014	This risk-assessment approach indicated that dabrafenib is unlikely to perpetrate any in vivo DDIs by inhibition mechanisms, but is a likely inducer of CYP3A4 and a victim of CYP3A4 and CYP2C8 inhibitors.	dabrafenib	45-55	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	186-192
24983357-3	2014	We analyzed BCL-2 family member expression levels of 34 samples from 17 patients collected before and 10 to 14 days after treatment initiation with either vemurafenib or dabrafenib/trametinib combination.	dabrafenib	170-180	BCL2 apoptosis regulator	Homo sapiens	12-17
24901049-5	2014	Among them, dabrafenib showed the most potent inhibition on RIP3, which was achieved by its ATP-competitive binding to the enzyme.	dabrafenib	12-22	receptor interacting serine/threonine kinase 3	Homo sapiens	60-64
25037456-2	2014	Vemurafenib (Zelboraf) and dabrafenib (Tafinlar) are specific BRAF V600 inhibitors recently approved by the US FDA as single agent treatments for unresectable or metastatic melanoma in patients with the BRAF V600 mutation.	dabrafenib	27-37	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	62-66
25037456-2	2014	Vemurafenib (Zelboraf) and dabrafenib (Tafinlar) are specific BRAF V600 inhibitors recently approved by the US FDA as single agent treatments for unresectable or metastatic melanoma in patients with the BRAF V600 mutation.	dabrafenib	27-37	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	203-207
24901049-0	2014	The B-Raf(V600E) inhibitor dabrafenib selectively inhibits RIP3 and alleviates acetaminophen-induced liver injury.	dabrafenib	27-37	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-9
25018652-3	2014	Combining selective BRAF and MEK inhibition, such as the BRAF inhibitor dabrafenib and the MEK inhibitor trametinib, has been shown to improve the response rate and progression-free survival in patients with advanced melanoma while significantly alleviating the paradoxical activation of mitogen-activated protein kinase.	dabrafenib	72-82	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	20-24
25018652-3	2014	Combining selective BRAF and MEK inhibition, such as the BRAF inhibitor dabrafenib and the MEK inhibitor trametinib, has been shown to improve the response rate and progression-free survival in patients with advanced melanoma while significantly alleviating the paradoxical activation of mitogen-activated protein kinase.	dabrafenib	72-82	mitogen-activated protein kinase kinase 7	Homo sapiens	29-32
25018652-3	2014	Combining selective BRAF and MEK inhibition, such as the BRAF inhibitor dabrafenib and the MEK inhibitor trametinib, has been shown to improve the response rate and progression-free survival in patients with advanced melanoma while significantly alleviating the paradoxical activation of mitogen-activated protein kinase.	dabrafenib	72-82	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	57-61
24901049-0	2014	The B-Raf(V600E) inhibitor dabrafenib selectively inhibits RIP3 and alleviates acetaminophen-induced liver injury.	dabrafenib	27-37	receptor interacting serine/threonine kinase 3	Homo sapiens	59-63
24901049-6	2014	Dabrafenib displayed highly selective inhibition on RIP3 over RIP1, RIP2 and RIP5.	dabrafenib	0-10	receptor interacting serine/threonine kinase 3	Homo sapiens	52-56
24901049-6	2014	Dabrafenib displayed highly selective inhibition on RIP3 over RIP1, RIP2 and RIP5.	dabrafenib	0-10	receptor interacting serine/threonine kinase 1	Homo sapiens	62-66
24901049-6	2014	Dabrafenib displayed highly selective inhibition on RIP3 over RIP1, RIP2 and RIP5.	dabrafenib	0-10	receptor interacting serine/threonine kinase 2	Homo sapiens	68-72
24901049-6	2014	Dabrafenib displayed highly selective inhibition on RIP3 over RIP1, RIP2 and RIP5.	dabrafenib	0-10	dual serine/threonine and tyrosine protein kinase	Homo sapiens	77-81
24901049-7	2014	Moreover, only dabrafenib rescued cells from RIP3-mediated necroptosis induced by the necroptosis-induced combinations, that is, tumor necrosis factor (TNF)alpha, TNF-related apoptosis-inducing ligand or Fas ligand plus Smac mimetic and the caspase inhibitor z-VAD.	dabrafenib	15-25	receptor interacting serine/threonine kinase 3	Homo sapiens	45-49
24901049-7	2014	Moreover, only dabrafenib rescued cells from RIP3-mediated necroptosis induced by the necroptosis-induced combinations, that is, tumor necrosis factor (TNF)alpha, TNF-related apoptosis-inducing ligand or Fas ligand plus Smac mimetic and the caspase inhibitor z-VAD.	dabrafenib	15-25	tumor necrosis factor	Homo sapiens	129-150
24901049-7	2014	Moreover, only dabrafenib rescued cells from RIP3-mediated necroptosis induced by the necroptosis-induced combinations, that is, tumor necrosis factor (TNF)alpha, TNF-related apoptosis-inducing ligand or Fas ligand plus Smac mimetic and the caspase inhibitor z-VAD.	dabrafenib	15-25	tumor necrosis factor	Homo sapiens	152-161
24901049-7	2014	Moreover, only dabrafenib rescued cells from RIP3-mediated necroptosis induced by the necroptosis-induced combinations, that is, tumor necrosis factor (TNF)alpha, TNF-related apoptosis-inducing ligand or Fas ligand plus Smac mimetic and the caspase inhibitor z-VAD.	dabrafenib	15-25	Fas ligand	Homo sapiens	204-214
24901049-8	2014	Dabrafenib decreased the RIP3-mediated Ser358 phosphorylation of mixed lineage kinase domain-like protein (MLKL) and disrupted the interaction between RIP3 and MLKL.	dabrafenib	0-10	receptor interacting serine/threonine kinase 3	Homo sapiens	25-29
24901049-8	2014	Dabrafenib decreased the RIP3-mediated Ser358 phosphorylation of mixed lineage kinase domain-like protein (MLKL) and disrupted the interaction between RIP3 and MLKL.	dabrafenib	0-10	mixed lineage kinase domain like pseudokinase	Homo sapiens	65-105
24901049-8	2014	Dabrafenib decreased the RIP3-mediated Ser358 phosphorylation of mixed lineage kinase domain-like protein (MLKL) and disrupted the interaction between RIP3 and MLKL.	dabrafenib	0-10	mixed lineage kinase domain like pseudokinase	Homo sapiens	107-111
24901049-8	2014	Dabrafenib decreased the RIP3-mediated Ser358 phosphorylation of mixed lineage kinase domain-like protein (MLKL) and disrupted the interaction between RIP3 and MLKL.	dabrafenib	0-10	receptor interacting serine/threonine kinase 3	Homo sapiens	151-155
24901049-8	2014	Dabrafenib decreased the RIP3-mediated Ser358 phosphorylation of mixed lineage kinase domain-like protein (MLKL) and disrupted the interaction between RIP3 and MLKL.	dabrafenib	0-10	mixed lineage kinase domain like pseudokinase	Homo sapiens	160-164
24901049-9	2014	Notably, RIP3 inhibition of dabrafenib appeared to be independent of its B-Raf inhibition.	dabrafenib	28-38	receptor interacting serine/threonine kinase 3	Homo sapiens	9-13
24901049-10	2014	Dabrafenib was further revealed to prevent acetaminophen-induced necrosis in normal human hepatocytes, which is considered to be mediated by RIP3.	dabrafenib	0-10	receptor interacting serine/threonine kinase 3	Homo sapiens	141-145
24901049-12	2014	The results indicate that the anticancer B-Raf(V600E) inhibitor dabrafenib is a RIP3 inhibitor, which could serve as a sharp tool for probing the RIP3 biology and as a potential preventive or therapeutic agent for RIP3-involved necroptosis-related diseases such as acetaminophen-induced liver damage.	dabrafenib	64-74	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	41-46
24901049-12	2014	The results indicate that the anticancer B-Raf(V600E) inhibitor dabrafenib is a RIP3 inhibitor, which could serve as a sharp tool for probing the RIP3 biology and as a potential preventive or therapeutic agent for RIP3-involved necroptosis-related diseases such as acetaminophen-induced liver damage.	dabrafenib	64-74	receptor interacting serine/threonine kinase 3	Homo sapiens	80-84
24901049-12	2014	The results indicate that the anticancer B-Raf(V600E) inhibitor dabrafenib is a RIP3 inhibitor, which could serve as a sharp tool for probing the RIP3 biology and as a potential preventive or therapeutic agent for RIP3-involved necroptosis-related diseases such as acetaminophen-induced liver damage.	dabrafenib	64-74	receptor interacting serine/threonine kinase 3	Homo sapiens	146-150
24901049-12	2014	The results indicate that the anticancer B-Raf(V600E) inhibitor dabrafenib is a RIP3 inhibitor, which could serve as a sharp tool for probing the RIP3 biology and as a potential preventive or therapeutic agent for RIP3-involved necroptosis-related diseases such as acetaminophen-induced liver damage.	dabrafenib	64-74	receptor interacting serine/threonine kinase 3	Homo sapiens	146-150
24867225-1	2014	Patients treated with ipilimumab or targeted inhibitors of the RAF-MEK-ERK pathway (vemurafenib, dabrafenib, and trametinib) for advanced cutaneous melanoma often experience drug-related skin toxicities denoted as dermatologic adverse events (DAEs).	dabrafenib	97-107	zinc fingers and homeoboxes 2	Homo sapiens	63-66
24867225-1	2014	Patients treated with ipilimumab or targeted inhibitors of the RAF-MEK-ERK pathway (vemurafenib, dabrafenib, and trametinib) for advanced cutaneous melanoma often experience drug-related skin toxicities denoted as dermatologic adverse events (DAEs).	dabrafenib	97-107	mitogen-activated protein kinase kinase 7	Homo sapiens	67-70
24867225-1	2014	Patients treated with ipilimumab or targeted inhibitors of the RAF-MEK-ERK pathway (vemurafenib, dabrafenib, and trametinib) for advanced cutaneous melanoma often experience drug-related skin toxicities denoted as dermatologic adverse events (DAEs).	dabrafenib	97-107	mitogen-activated protein kinase 1	Homo sapiens	71-74
24880943-3	2014	In cutaneous melanomas with BRAF V600 mutations the selective RAF inhibitors, vemurafenib and dabrafenib, and the MEK inhibitor, trametinib, have demonstrated survival benefits.	dabrafenib	94-104	zinc fingers and homeoboxes 2	Homo sapiens	29-32
24766074-3	2014	Two of these compounds, vemurafenib and dabrafenib, have been licensed for the treatment of BRAF-mutant advanced melanoma.	dabrafenib	40-50	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	92-96
24664307-4	2014	There are currently two inhibitors, vemurafenib and dabrafenib, approved for treatment of malignant melanoma having activating BRaf mutations.	dabrafenib	52-62	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	127-131
24408395-0	2014	Population pharmacokinetics of dabrafenib, a BRAF inhibitor: effect of dose, time, covariates, and relationship with its metabolites.	dabrafenib	31-41	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	45-49
24408395-1	2014	Dabrafenib is a BRAF kinase inhibitor indicated for the treatment of BRAF V600E mutation-positive melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	16-20
24408395-1	2014	Dabrafenib is a BRAF kinase inhibitor indicated for the treatment of BRAF V600E mutation-positive melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	69-73
24403169-6	2014	Recently, novel drugs such as vemurafenib, dabrafenib and trametinib were approved for treatment of advanced disease harbouring BRAF V600E and V600K mutations.	dabrafenib	43-53	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	128-132
24885690-7	2014	Among tested agents, the B-Raf inhibitor dabrafenib was found to induce a strong V600E-dependent shift in cell viability.	dabrafenib	41-51	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	25-30
24885690-9	2014	Treatment with dabrafenib efficiently inhibited phosphorylation of the B-Raf downstream targets Mek 1/2 and Erk 1/2.	dabrafenib	15-25	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	71-76
24885690-9	2014	Treatment with dabrafenib efficiently inhibited phosphorylation of the B-Raf downstream targets Mek 1/2 and Erk 1/2.	dabrafenib	15-25	mitogen-activated protein kinase kinase 1	Homo sapiens	96-103
24885690-9	2014	Treatment with dabrafenib efficiently inhibited phosphorylation of the B-Raf downstream targets Mek 1/2 and Erk 1/2.	dabrafenib	15-25	mitogen-activated protein kinase 3	Homo sapiens	108-115
24520098-1	2014	UNLABELLED: Resistance to RAF inhibitors such as vemurafenib and dabrafenib is a major clinical problem in the treatment of melanoma.	dabrafenib	65-75	zinc fingers and homeoboxes 2	Homo sapiens	26-29
24720932-4	2014	The BRAF inhibitor dabrafenib recently was approved for use in patients with BRAF V600-mutated metastatic melanoma.	dabrafenib	19-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	4-8
24720932-4	2014	The BRAF inhibitor dabrafenib recently was approved for use in patients with BRAF V600-mutated metastatic melanoma.	dabrafenib	19-29	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	77-81
24720932-5	2014	AREAS COVERED: This article discusses the mechanisms of action and pharmacokinetic and pharmacodynamic changes as well as clinical efficacy and safety of dabrafenib for treatment of patients with advanced melanoma including unresectable stage IIIc and stage IV patients who harbor a BRAF V600 mutation.	dabrafenib	154-164	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	283-287
24720932-7	2014	EXPERT OPINION: Despite rapid and significant tumor reduction in a majority of patients with BRAF-mutant metastatic melanoma who are treated with dabrafenib, this drug"s use as a single agent is limited because of its relatively short duration of response.	dabrafenib	146-156	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	93-97
25089220-0	2014	Dabrafenib: A New Therapy for Use in BRAF-Mutated Metastatic Melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	37-41
24812130-4	2014	Recently developed treatment options for patients with BRAF-mutant melanoma include BRAF inhibitors (vemurafenib, dabrafenib), MEK inhibitors (trametinib), and immune-based therapeutics (interleukin-2 or ipilimumab), but the most effective strategy for first-line therapy is heavily debated.	dabrafenib	114-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	55-59
24325952-8	2014	Combination of the BRAF inhibitor dabrafenib with the MEK inhibitor trametinib has significantly prolonged progression free survival compared to dabrafenib alone in metastatic melanoma.	dabrafenib	34-44	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	19-23
24504448-2	2014	http://www.sanger.ac.uk/genetics/CGP/cosmic/) and pharmacological BRAF inhibitors such as vemurafenib and dabrafenib achieve dramatic responses in patients whose tumours harbour BRAF(V600) mutations.	dabrafenib	106-116	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	66-70
24504448-2	2014	http://www.sanger.ac.uk/genetics/CGP/cosmic/) and pharmacological BRAF inhibitors such as vemurafenib and dabrafenib achieve dramatic responses in patients whose tumours harbour BRAF(V600) mutations.	dabrafenib	106-116	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	178-187
24325952-8	2014	Combination of the BRAF inhibitor dabrafenib with the MEK inhibitor trametinib has significantly prolonged progression free survival compared to dabrafenib alone in metastatic melanoma.	dabrafenib	145-155	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	19-23
24259661-8	2014	Dabrafenib has been approved to treat patients with BRAF(V600E)-positive unresectable or metastatic melanoma based on its clinical benefit demonstrated in a randomized phase III study.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	52-56
24735930-3	2014	METHODS: Anti-tumor effects of the combination of the BRAF inhibitor (BRAFi) dabrafenib and GSK2141795B (AKTi) in a panel of 23 BRAF mutated melanoma cell lines were evaluated on growth inhibition by an ATP-based luminescent assay, on cell cycle and apoptosis by flow cytometry and on cell signaling by western blot.	dabrafenib	77-87	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	54-58
24735930-3	2014	METHODS: Anti-tumor effects of the combination of the BRAF inhibitor (BRAFi) dabrafenib and GSK2141795B (AKTi) in a panel of 23 BRAF mutated melanoma cell lines were evaluated on growth inhibition by an ATP-based luminescent assay, on cell cycle and apoptosis by flow cytometry and on cell signaling by western blot.	dabrafenib	77-87	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	70-74
24735930-8	2014	In long term cultures of a PTEN-/- cell line, combinatorial treatment with the MAPK inhibitors, dabrafenib and trametinib, and AKTi markedly delayed the emergence of drug resistance.	dabrafenib	96-106	phosphatase and tensin homolog	Homo sapiens	27-31
24583796-0	2014	Dabrafenib and trametinib, alone and in combination for BRAF-mutant metastatic melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	56-60
24583796-1	2014	Dabrafenib and trametinib were approved for use as monotherapies in BRAF-mutant metastatic melanoma by the U.S. Food and Drug Administration (FDA) in 2013, and most recently, their use in combination has received accelerated FDA approval.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	68-72
24583796-2	2014	Both drugs target the mitogen-activated protein kinase (MAPK) pathway: dabrafenib selectively inhibits mutant BRAF that constitutively activates the pathway, and trametinib selectively inhibits MEK1 and MEK2 proteins activated by RAF kinases.	dabrafenib	71-81	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	110-114
24583796-3	2014	The phase III study of dabrafenib in BRAF(V600E) metastatic melanoma reported rapid tumor regression in most patients and a 59% objective RECIST response rate.	dabrafenib	23-33	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	37-41
24422853-1	2014	Vemurafenib and dabrafenib block MEK-ERK1/2 signaling and cause tumor regression in the majority of advanced-stage BRAF(V600E) melanoma patients; however, acquired resistance and paradoxical signaling have driven efforts for more potent and selective RAF inhibitors.	dabrafenib	16-26	mitogen-activated protein kinase kinase 7	Homo sapiens	33-36
24422853-1	2014	Vemurafenib and dabrafenib block MEK-ERK1/2 signaling and cause tumor regression in the majority of advanced-stage BRAF(V600E) melanoma patients; however, acquired resistance and paradoxical signaling have driven efforts for more potent and selective RAF inhibitors.	dabrafenib	16-26	mitogen-activated protein kinase 3	Homo sapiens	37-43
24422853-1	2014	Vemurafenib and dabrafenib block MEK-ERK1/2 signaling and cause tumor regression in the majority of advanced-stage BRAF(V600E) melanoma patients; however, acquired resistance and paradoxical signaling have driven efforts for more potent and selective RAF inhibitors.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	115-119
24422853-1	2014	Vemurafenib and dabrafenib block MEK-ERK1/2 signaling and cause tumor regression in the majority of advanced-stage BRAF(V600E) melanoma patients; however, acquired resistance and paradoxical signaling have driven efforts for more potent and selective RAF inhibitors.	dabrafenib	16-26	zinc fingers and homeoboxes 2	Homo sapiens	116-119
24422853-4	2014	Acquired resistance to vemurafenib and dabrafenib is also frequently driven by expression of mutation BRAF splice variants; thus, we tested the effects of PLX7904 and its clinical analog, PLX8394 (PB03), in BRAF(V600E) splice variant-mediated vemurafenib-resistant cells.	dabrafenib	39-49	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	102-106
24422853-6	2014	These data support the further investigation of paradox-breaker RAF inhibitors as a second-line treatment option for patients failing on vemurafenib or dabrafenib.	dabrafenib	152-162	zinc fingers and homeoboxes 2	Homo sapiens	64-67
24259661-13	2014	CONCLUSIONS: Dabrafenib joins vemurafenib to confirm the superior clinical outcome of the BRAF inhibitors when compared with dacarbazine in patients with BRAF(V600E)-positive advanced melanoma.	dabrafenib	13-23	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	90-94
24456413-2	2014	Objective response rates of approximately 50% have been observed in the Phase III studies of the BRAF inhibitors vemurafenib and dabrafenib.	dabrafenib	129-139	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	97-101
24259661-7	2014	This discovery led to the development of BRAF kinase inhibitors like vemurafenib and dabrafenib.	dabrafenib	85-95	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	41-45
24596183-1	2014	The U.S. Food and Drug Administration approved the use of trametinib and dabrafenib in combination for patients with metastatic or unresectable melanoma with BRAF V600K or V600E mutations-the first combination therapy approved for the disease.	dabrafenib	73-83	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	158-162
24352115-1	2014	IMPORTANCE: Targeted BRAF inhibitor therapy (vemurafenib, dabrafenib) is an effective, novel treatment for patients with metastatic melanoma with the V600E BRAF mutation.	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	21-25
24352115-1	2014	IMPORTANCE: Targeted BRAF inhibitor therapy (vemurafenib, dabrafenib) is an effective, novel treatment for patients with metastatic melanoma with the V600E BRAF mutation.	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	156-160
24352115-5	2014	In case 1, after 2 months of treatment with dabrafenib and trametinib (MEK inhibitor), a papular eruption concerning for progression of disease prompted cessation of treatment.	dabrafenib	44-54	mitogen-activated protein kinase kinase 7	Homo sapiens	71-74
24756796-1	2014	Dabrafenib was developed as a highly specific reversible inhibitor of V600-mutant BRAF kinase, an oncogenic mutation driving proliferation in many different types of aggressive tumors.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	82-86
24600206-2	2014	Although activation of the PI3K/Akt pathway resulting from genetic mutations and epigenetic deregulation of its major regulators is known to cause resistance of melanoma to therapeutic agents, including the conventional chemotherapeutic drug dacarbazine and the Food and Drug Administration-approved mutant BRAF inhibitors vemurafenib and dabrafenib, the role of extracellular stimuli of the pathway, such as insulin, in drug resistance of melanoma remains less understood.	dabrafenib	339-349	AKT serine/threonine kinase 1	Homo sapiens	32-35
24496868-0	2014	Patterns of response and progression in patients with BRAF-mutant melanoma metastatic to the brain who were treated with dabrafenib.	dabrafenib	121-131	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	54-58
24291778-4	2014	Recently, two different mutant-selective small molecule inhibitors of BRAF, vemurafenib and dabrafenib, have gained regulatory approval based on positive results in randomized phase III trials.	dabrafenib	92-102	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	70-74
24114495-13	2014	GSK2118436 (dabrafenib), the second BRAF inhibitor, in phase I and II trial obtained similar results to vemurafenib.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	36-40
24971404-0	2014	Dabrafenib in advanced melanoma with BRAF V600E mutation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	37-41
24971404-1	2014	Dabrafenib was recently approved by the US Food and Drug Administration for treatment of unresectable or metastatic melanoma with BRAF V600E mutations as detected by an FDA-approved test.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	130-134
24971404-5	2014	Dabrafenib is a reversible, ATP-competitive inhibitor that selectively inhibits BRAF V600E kinase; preclinical data indicate that dabrafenib inhibits the MAPK pathway in BRAF V600E-mutated melanoma cells, leading to decreased proliferation and regression in xenograft models.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	80-84
24971404-5	2014	Dabrafenib is a reversible, ATP-competitive inhibitor that selectively inhibits BRAF V600E kinase; preclinical data indicate that dabrafenib inhibits the MAPK pathway in BRAF V600E-mutated melanoma cells, leading to decreased proliferation and regression in xenograft models.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	170-174
24971404-5	2014	Dabrafenib is a reversible, ATP-competitive inhibitor that selectively inhibits BRAF V600E kinase; preclinical data indicate that dabrafenib inhibits the MAPK pathway in BRAF V600E-mutated melanoma cells, leading to decreased proliferation and regression in xenograft models.	dabrafenib	130-140	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	170-174
24971404-6	2014	Dabrafenib also inhibits other mutated forms of BRAF kinases, including BRAF V600K and BRAF V600D enzymes and, at higher concentrations, wild-type BRAF and CRAF kinases and other kinases (eg, SIK1, NEK11, and LIMK1).	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	48-52
24971404-6	2014	Dabrafenib also inhibits other mutated forms of BRAF kinases, including BRAF V600K and BRAF V600D enzymes and, at higher concentrations, wild-type BRAF and CRAF kinases and other kinases (eg, SIK1, NEK11, and LIMK1).	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	72-76
24971404-6	2014	Dabrafenib also inhibits other mutated forms of BRAF kinases, including BRAF V600K and BRAF V600D enzymes and, at higher concentrations, wild-type BRAF and CRAF kinases and other kinases (eg, SIK1, NEK11, and LIMK1).	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	72-76
24971404-6	2014	Dabrafenib also inhibits other mutated forms of BRAF kinases, including BRAF V600K and BRAF V600D enzymes and, at higher concentrations, wild-type BRAF and CRAF kinases and other kinases (eg, SIK1, NEK11, and LIMK1).	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	72-76
24971404-6	2014	Dabrafenib also inhibits other mutated forms of BRAF kinases, including BRAF V600K and BRAF V600D enzymes and, at higher concentrations, wild-type BRAF and CRAF kinases and other kinases (eg, SIK1, NEK11, and LIMK1).	dabrafenib	0-10	salt inducible kinase 1	Homo sapiens	192-196
24971404-6	2014	Dabrafenib also inhibits other mutated forms of BRAF kinases, including BRAF V600K and BRAF V600D enzymes and, at higher concentrations, wild-type BRAF and CRAF kinases and other kinases (eg, SIK1, NEK11, and LIMK1).	dabrafenib	0-10	NIMA related kinase 11	Homo sapiens	198-203
24971404-6	2014	Dabrafenib also inhibits other mutated forms of BRAF kinases, including BRAF V600K and BRAF V600D enzymes and, at higher concentrations, wild-type BRAF and CRAF kinases and other kinases (eg, SIK1, NEK11, and LIMK1).	dabrafenib	0-10	LIM domain kinase 1	Homo sapiens	209-214
24265154-1	2014	Treatment of BRAF-mutant melanoma with combined dabrafenib and trametinib, which target RAF and the downstream MAP-ERK kinase (MEK)1 and MEK2 kinases, respectively, improves progression-free survival and response rates compared with dabrafenib monotherapy.	dabrafenib	48-58	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	13-17
24265154-1	2014	Treatment of BRAF-mutant melanoma with combined dabrafenib and trametinib, which target RAF and the downstream MAP-ERK kinase (MEK)1 and MEK2 kinases, respectively, improves progression-free survival and response rates compared with dabrafenib monotherapy.	dabrafenib	48-58	zinc fingers and homeoboxes 2	Homo sapiens	14-17
24265154-1	2014	Treatment of BRAF-mutant melanoma with combined dabrafenib and trametinib, which target RAF and the downstream MAP-ERK kinase (MEK)1 and MEK2 kinases, respectively, improves progression-free survival and response rates compared with dabrafenib monotherapy.	dabrafenib	48-58	mitogen-activated protein kinase kinase 1	Homo sapiens	111-132
24265154-1	2014	Treatment of BRAF-mutant melanoma with combined dabrafenib and trametinib, which target RAF and the downstream MAP-ERK kinase (MEK)1 and MEK2 kinases, respectively, improves progression-free survival and response rates compared with dabrafenib monotherapy.	dabrafenib	48-58	mitogen-activated protein kinase kinase 2	Homo sapiens	137-141
24265154-1	2014	Treatment of BRAF-mutant melanoma with combined dabrafenib and trametinib, which target RAF and the downstream MAP-ERK kinase (MEK)1 and MEK2 kinases, respectively, improves progression-free survival and response rates compared with dabrafenib monotherapy.	dabrafenib	233-243	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	13-17
24265154-1	2014	Treatment of BRAF-mutant melanoma with combined dabrafenib and trametinib, which target RAF and the downstream MAP-ERK kinase (MEK)1 and MEK2 kinases, respectively, improves progression-free survival and response rates compared with dabrafenib monotherapy.	dabrafenib	233-243	zinc fingers and homeoboxes 2	Homo sapiens	14-17
24353011-8	2014	Finally, in melanoma, the B-raf inhibitors vemurafenib and dabrafenib, and the immunomodulator, ipilumimab, have reported CNS activity.	dabrafenib	59-69	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	26-31
24756796-2	2014	Metastatic melanoma has a high prevalence of V600-mutant BRAF, and clinical trials showed that dabrafenib improved response rates and median progression-free survival in patients with V600E BRAF mutations, including those with brain metastasis.	dabrafenib	95-105	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	57-61
24756796-2	2014	Metastatic melanoma has a high prevalence of V600-mutant BRAF, and clinical trials showed that dabrafenib improved response rates and median progression-free survival in patients with V600E BRAF mutations, including those with brain metastasis.	dabrafenib	95-105	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	190-194
24516336-0	2014	Dabrafenib for treatment of BRAF-mutant melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	28-32
24516336-4	2014	Dabrafenib, a reversible inhibitor of mutant BRAF kinase, improved response rates and median progression-free survival in patients with V600E BRAF-mutant metastatic melanoma, including those with brain metastases.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	45-49
24516336-4	2014	Dabrafenib, a reversible inhibitor of mutant BRAF kinase, improved response rates and median progression-free survival in patients with V600E BRAF-mutant metastatic melanoma, including those with brain metastases.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	142-146
28609051-0	2013	Dabrafenib -- Benefit Assessment According to  35a Social Code Book V The aim of this report was to assess the added benefit of dabrafenib in adult patients with BRAF V600 mutation-positive unresectable or metastatic melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	162-166
28609051-0	2013	Dabrafenib -- Benefit Assessment According to  35a Social Code Book V The aim of this report was to assess the added benefit of dabrafenib in adult patients with BRAF V600 mutation-positive unresectable or metastatic melanoma.	dabrafenib	128-138	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	162-166
24121489-3	2013	Recently, the BRAF inhibitors vemurafenib and dabrafenib have emerged as promising agents for the treatment of melanoma patients with BRAF-activating mutations.	dabrafenib	46-56	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
24121489-3	2013	Recently, the BRAF inhibitors vemurafenib and dabrafenib have emerged as promising agents for the treatment of melanoma patients with BRAF-activating mutations.	dabrafenib	46-56	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	134-138
24121492-1	2013	Activation of the ERK1/2 mitogen-activated protein kinases (MAPK) confers resistance to the RAF inhibitors vemurafenib and dabrafenib in mutant BRAF-driven melanomas.	dabrafenib	123-133	mitogen-activated protein kinase 3	Homo sapiens	18-24
24121492-1	2013	Activation of the ERK1/2 mitogen-activated protein kinases (MAPK) confers resistance to the RAF inhibitors vemurafenib and dabrafenib in mutant BRAF-driven melanomas.	dabrafenib	123-133	mitogen-activated protein kinase 3	Homo sapiens	60-64
24121492-1	2013	Activation of the ERK1/2 mitogen-activated protein kinases (MAPK) confers resistance to the RAF inhibitors vemurafenib and dabrafenib in mutant BRAF-driven melanomas.	dabrafenib	123-133	zinc fingers and homeoboxes 2	Homo sapiens	92-95
24121492-1	2013	Activation of the ERK1/2 mitogen-activated protein kinases (MAPK) confers resistance to the RAF inhibitors vemurafenib and dabrafenib in mutant BRAF-driven melanomas.	dabrafenib	123-133	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	144-148
23918947-0	2013	Phase II trial (BREAK-2) of the BRAF inhibitor dabrafenib (GSK2118436) in patients with metastatic melanoma.	dabrafenib	47-57	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	32-36
24114495-13	2014	GSK2118436 (dabrafenib), the second BRAF inhibitor, in phase I and II trial obtained similar results to vemurafenib.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	36-40
24114495-15	2014	Taken together, the early clinical development of vemurafenib and dabrafenib clearly confirms that BRAF inhibitors can halt or reverse disease in patients with melanomas carrying this mutation, improving survival times compared with historically standard treatments (chemotherapy and interleukin-2).	dabrafenib	66-76	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	99-103
24196789-1	2013	BACKGROUND: The detection of V600E BRAF mutations has fundamental clinical consequences as the treatment option with BRAF inhibitors such as vemurafenib or dabrafenib yields response rates of ~48%.	dabrafenib	156-166	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	35-39
24196789-1	2013	BACKGROUND: The detection of V600E BRAF mutations has fundamental clinical consequences as the treatment option with BRAF inhibitors such as vemurafenib or dabrafenib yields response rates of ~48%.	dabrafenib	156-166	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	117-121
24201813-2	2013	Recent clinical studies have demonstrated that vemurafenib (PLX4032) and dabrafenib, potent and selective inhibitors of mutant v-raf murine sarcoma viral oncogene homolog B1 (BRAF), exhibit remarkable activities in patients with V600 BRAF mutant melanomas.	dabrafenib	73-83	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	127-173
24201813-2	2013	Recent clinical studies have demonstrated that vemurafenib (PLX4032) and dabrafenib, potent and selective inhibitors of mutant v-raf murine sarcoma viral oncogene homolog B1 (BRAF), exhibit remarkable activities in patients with V600 BRAF mutant melanomas.	dabrafenib	73-83	Braf transforming gene	Mus musculus	175-179
24201813-2	2013	Recent clinical studies have demonstrated that vemurafenib (PLX4032) and dabrafenib, potent and selective inhibitors of mutant v-raf murine sarcoma viral oncogene homolog B1 (BRAF), exhibit remarkable activities in patients with V600 BRAF mutant melanomas.	dabrafenib	73-83	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	234-238
24192036-1	2013	Vemurafenib and dabrafenib selectively inhibit the v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) kinase, resulting in high response rates and increased survival in melanoma.	dabrafenib	16-26	Braf transforming gene	Mus musculus	99-103
24055054-3	2013	We also identified the same MEK2-Q60P mutation along with BRAF amplification in a xenograft tumor derived from a second melanoma patient resistant to the combination of dabrafenib and trametinib.	dabrafenib	169-179	mitogen-activated protein kinase kinase 2	Homo sapiens	28-32
24055054-3	2013	We also identified the same MEK2-Q60P mutation along with BRAF amplification in a xenograft tumor derived from a second melanoma patient resistant to the combination of dabrafenib and trametinib.	dabrafenib	169-179	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	58-62
23918947-0	2013	Phase II trial (BREAK-2) of the BRAF inhibitor dabrafenib (GSK2118436) in patients with metastatic melanoma.	dabrafenib	59-69	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	32-36
23918947-1	2013	PURPOSE: Dabrafenib (GSK2118436) is a potent inhibitor of mutated BRAF kinase.	dabrafenib	9-19	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	66-70
23918947-1	2013	PURPOSE: Dabrafenib (GSK2118436) is a potent inhibitor of mutated BRAF kinase.	dabrafenib	21-31	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	66-70
23918947-2	2013	Our multicenter, single-arm, phase II study assessed the safety and clinical activity of dabrafenib in BRAF(V600E/K) mutation-positive metastatic melanoma (mut(+) MM).	dabrafenib	89-99	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	103-107
23918947-14	2013	CONCLUSION: Dabrafenib was well tolerated and clinically active in patients with BRAF(V600E/K) mut(+) MM.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	93-104
24341237-5	2013	Clinical trials involving specific BRAF inhibitors--vemurafenib and dabrafenib--demonstrated high efficacy of these agents towards BRAF-mutated melanoma.	dabrafenib	68-78	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	35-39
24341237-5	2013	Clinical trials involving specific BRAF inhibitors--vemurafenib and dabrafenib--demonstrated high efficacy of these agents towards BRAF-mutated melanoma.	dabrafenib	68-78	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	131-135
23833299-0	2013	Tumor genetic analyses of patients with metastatic melanoma treated with the BRAF inhibitor dabrafenib (GSK2118436).	dabrafenib	92-102	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	77-81
23833299-0	2013	Tumor genetic analyses of patients with metastatic melanoma treated with the BRAF inhibitor dabrafenib (GSK2118436).	dabrafenib	104-114	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	77-81
23833299-1	2013	PURPOSE: Dabrafenib is a selective inhibitor of V600-mutant BRAF kinase, which recently showed improved progression-free survival (PFS) as compared with dacarbazine, in metastatic melanoma patients.	dabrafenib	9-19	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	60-64
23833299-9	2013	CONCLUSIONS: Copy number changes in CDKN2A, CCND1, and mutation/copy number changes in PTEN correlated with the duration of PFS in patients treated with dabrafenib.	dabrafenib	153-163	cyclin dependent kinase inhibitor 2A	Homo sapiens	36-42
23833299-9	2013	CONCLUSIONS: Copy number changes in CDKN2A, CCND1, and mutation/copy number changes in PTEN correlated with the duration of PFS in patients treated with dabrafenib.	dabrafenib	153-163	cyclin D1	Homo sapiens	44-49
23833299-9	2013	CONCLUSIONS: Copy number changes in CDKN2A, CCND1, and mutation/copy number changes in PTEN correlated with the duration of PFS in patients treated with dabrafenib.	dabrafenib	153-163	phosphatase and tensin homolog	Homo sapiens	87-91
23846776-0	2013	Concomitant oral and intravenous pharmacokinetics of dabrafenib, a BRAF inhibitor, in patients with BRAF V600 mutation-positive solid tumors.	dabrafenib	53-63	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	67-71
23846776-0	2013	Concomitant oral and intravenous pharmacokinetics of dabrafenib, a BRAF inhibitor, in patients with BRAF V600 mutation-positive solid tumors.	dabrafenib	53-63	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	100-104
23846776-1	2013	Dabrafenib is an orally bioavailable, potent, and selective inhibitor of human wild-type BRAF and CRAF kinases as well as mutant forms of BRAF kinase.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	89-93
23846776-1	2013	Dabrafenib is an orally bioavailable, potent, and selective inhibitor of human wild-type BRAF and CRAF kinases as well as mutant forms of BRAF kinase.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	138-142
23846776-2	2013	The aim of this phase 1, single-center, open-label study in four patients with BRAF mutation-positive solid tumors was to determine the absolute bioavailability of a 150 mg oral dose of dabrafenib.	dabrafenib	186-196	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	79-83
23608920-0	2013	Effects of particle size, food, and capsule shell composition on the oral bioavailability of dabrafenib, a BRAF inhibitor, in patients with BRAF mutation-positive tumors.	dabrafenib	93-103	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	107-111
23608920-0	2013	Effects of particle size, food, and capsule shell composition on the oral bioavailability of dabrafenib, a BRAF inhibitor, in patients with BRAF mutation-positive tumors.	dabrafenib	93-103	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	140-144
23608920-1	2013	Dabrafenib is a small-molecule inhibitor of BRAF kinase activity that is currently being developed for the treatment of BRAF V600 mutation-positive melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	44-48
23608920-1	2013	Dabrafenib is a small-molecule inhibitor of BRAF kinase activity that is currently being developed for the treatment of BRAF V600 mutation-positive melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	120-124
23844038-3	2013	In this report we characterize the novel, potent, and selective BRAF inhibitor, dabrafenib (GSK2118436).	dabrafenib	80-90	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	64-68
24034635-1	2013	Recent developments and therapeutic use of selective BRAF inhibitors (e.g. dabrafenib and vemurafenib) have significantly improved overall survival and disease-free survival of patients with BRAF V600 mutation-positive metastatic melanoma.	dabrafenib	75-85	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	53-57
24034635-1	2013	Recent developments and therapeutic use of selective BRAF inhibitors (e.g. dabrafenib and vemurafenib) have significantly improved overall survival and disease-free survival of patients with BRAF V600 mutation-positive metastatic melanoma.	dabrafenib	75-85	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	191-195
23881668-1	2013	Dabrafenib (Tafinlar ), a mutant-BRAF kinase inhibitor, emerged from GlaxoSmithKline"s research programme for the discovery of selective inhibitors of mutant BRAF kinase activity, for the treatment of solid tumours; mutations in the BRAF gene are associated with increased growth and proliferation of cancer cells.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	33-37
23881668-1	2013	Dabrafenib (Tafinlar ), a mutant-BRAF kinase inhibitor, emerged from GlaxoSmithKline"s research programme for the discovery of selective inhibitors of mutant BRAF kinase activity, for the treatment of solid tumours; mutations in the BRAF gene are associated with increased growth and proliferation of cancer cells.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	158-162
23881668-1	2013	Dabrafenib (Tafinlar ), a mutant-BRAF kinase inhibitor, emerged from GlaxoSmithKline"s research programme for the discovery of selective inhibitors of mutant BRAF kinase activity, for the treatment of solid tumours; mutations in the BRAF gene are associated with increased growth and proliferation of cancer cells.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	158-162
23881668-1	2013	Dabrafenib (Tafinlar ), a mutant-BRAF kinase inhibitor, emerged from GlaxoSmithKline"s research programme for the discovery of selective inhibitors of mutant BRAF kinase activity, for the treatment of solid tumours; mutations in the BRAF gene are associated with increased growth and proliferation of cancer cells.	dabrafenib	12-20	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	33-37
23881668-1	2013	Dabrafenib (Tafinlar ), a mutant-BRAF kinase inhibitor, emerged from GlaxoSmithKline"s research programme for the discovery of selective inhibitors of mutant BRAF kinase activity, for the treatment of solid tumours; mutations in the BRAF gene are associated with increased growth and proliferation of cancer cells.	dabrafenib	12-20	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	158-162
23881668-1	2013	Dabrafenib (Tafinlar ), a mutant-BRAF kinase inhibitor, emerged from GlaxoSmithKline"s research programme for the discovery of selective inhibitors of mutant BRAF kinase activity, for the treatment of solid tumours; mutations in the BRAF gene are associated with increased growth and proliferation of cancer cells.	dabrafenib	12-20	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	158-162
23881668-2	2013	GlaxoSmithKline has focused the development of dabrafenib on the treatment of malignant melanoma, as BRAF mutations are present in 50 % of these cancers.	dabrafenib	47-57	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	101-105
23881668-3	2013	Dabrafenib is approved in the US as a single agent treatment for unresectable or metastatic melanoma in patients with the BRAF V600E mutation, and has received a positive opinion in the EU in this indication.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	122-126
23881668-4	2013	Submissions have also been made in the US and the EU for the use of dabrafenib in combination with trametinib for the treatment of metastatic melanoma with a BRAF V600E/K mutation.	dabrafenib	68-78	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	158-162
23881668-7	2013	Dabrafenib is intended to treat the patient population with a BRAF V600E/K mutation.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	62-66
23881668-11	2013	This article summarises the milestones in the development of dabrafenib leading to this first approval as a single agent treatment for unresectable or metastatic melanoma in patients with the BRAF V600E mutation.	dabrafenib	61-71	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	192-196
23844038-3	2013	In this report we characterize the novel, potent, and selective BRAF inhibitor, dabrafenib (GSK2118436).	dabrafenib	92-102	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	64-68
23844038-4	2013	Cellular inhibition of BRAF(V600E) kinase activity by dabrafenib resulted in decreased MEK and ERK phosphorylation and inhibition of cell proliferation through an initial G1 cell cycle arrest, followed by cell death.	dabrafenib	54-64	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	23-28
23844038-4	2013	Cellular inhibition of BRAF(V600E) kinase activity by dabrafenib resulted in decreased MEK and ERK phosphorylation and inhibition of cell proliferation through an initial G1 cell cycle arrest, followed by cell death.	dabrafenib	54-64	mitogen-activated protein kinase kinase 7	Homo sapiens	87-90
23844038-4	2013	Cellular inhibition of BRAF(V600E) kinase activity by dabrafenib resulted in decreased MEK and ERK phosphorylation and inhibition of cell proliferation through an initial G1 cell cycle arrest, followed by cell death.	dabrafenib	54-64	mitogen-activated protein kinase 1	Homo sapiens	95-98
23844038-5	2013	In a BRAF(V600E)-containing xenograft model of human melanoma, orally administered dabrafenib inhibited ERK activation, downregulated Ki67, and upregulated p27, leading to tumor growth inhibition.	dabrafenib	83-93	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	5-10
23844038-5	2013	In a BRAF(V600E)-containing xenograft model of human melanoma, orally administered dabrafenib inhibited ERK activation, downregulated Ki67, and upregulated p27, leading to tumor growth inhibition.	dabrafenib	83-93	mitogen-activated protein kinase 1	Homo sapiens	104-107
23844038-5	2013	In a BRAF(V600E)-containing xenograft model of human melanoma, orally administered dabrafenib inhibited ERK activation, downregulated Ki67, and upregulated p27, leading to tumor growth inhibition.	dabrafenib	83-93	interferon alpha inducible protein 27	Homo sapiens	156-159
23844038-6	2013	However, as reported for other BRAF inhibitors, dabrafenib also induced MAPK pathway activation in wild-type BRAF cells through CRAF (RAF1) signalling, potentially explaining the squamous cell carcinomas and keratoacanthomas arising in patients treated with BRAF inhibitors.	dabrafenib	48-58	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	31-35
23844038-6	2013	However, as reported for other BRAF inhibitors, dabrafenib also induced MAPK pathway activation in wild-type BRAF cells through CRAF (RAF1) signalling, potentially explaining the squamous cell carcinomas and keratoacanthomas arising in patients treated with BRAF inhibitors.	dabrafenib	48-58	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	109-113
23844038-6	2013	However, as reported for other BRAF inhibitors, dabrafenib also induced MAPK pathway activation in wild-type BRAF cells through CRAF (RAF1) signalling, potentially explaining the squamous cell carcinomas and keratoacanthomas arising in patients treated with BRAF inhibitors.	dabrafenib	48-58	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	128-132
23844038-6	2013	However, as reported for other BRAF inhibitors, dabrafenib also induced MAPK pathway activation in wild-type BRAF cells through CRAF (RAF1) signalling, potentially explaining the squamous cell carcinomas and keratoacanthomas arising in patients treated with BRAF inhibitors.	dabrafenib	48-58	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	134-138
23844038-6	2013	However, as reported for other BRAF inhibitors, dabrafenib also induced MAPK pathway activation in wild-type BRAF cells through CRAF (RAF1) signalling, potentially explaining the squamous cell carcinomas and keratoacanthomas arising in patients treated with BRAF inhibitors.	dabrafenib	48-58	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	109-113
23844038-8	2013	Taken together, our findings offer preclinical proof of concept for dabrafenib as a specific and highly efficacious BRAF inhibitor and provide evidence for its potential clinical benefits when used in combination with a MEK inhibitor.	dabrafenib	68-78	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	116-120
23844038-8	2013	Taken together, our findings offer preclinical proof of concept for dabrafenib as a specific and highly efficacious BRAF inhibitor and provide evidence for its potential clinical benefits when used in combination with a MEK inhibitor.	dabrafenib	68-78	mitogen-activated protein kinase kinase 7	Homo sapiens	220-223
23807941-3	2013	Similar to the first-in-class selective serine/threonine-protein kinase B-raf inhibitor vemurafenib, dabrafenib is highly efficacious in melanoma patients with BRAF V600E mutations, with response rates of approximately 50% and progression-free survival of 6 months.	dabrafenib	101-111	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	160-164
23621583-0	2013	Clinical development of dabrafenib in BRAF mutant melanoma and other malignancies.	dabrafenib	24-34	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	38-42
23621583-2	2013	While vemurafenib was the first approved BRAF inhibitor for this indication, another selective BRAF inhibitor, dabrafenib, has demonstrated efficacy in patients with BRAF mutant melanoma, including those with active brain metastases and other malignancies.	dabrafenib	111-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	95-99
23621583-2	2013	While vemurafenib was the first approved BRAF inhibitor for this indication, another selective BRAF inhibitor, dabrafenib, has demonstrated efficacy in patients with BRAF mutant melanoma, including those with active brain metastases and other malignancies.	dabrafenib	111-121	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	95-99
23621583-3	2013	AREAS COVERED: This review covers the current role of BRAF inhibitors in patients with metastatic melanoma and the clinical development of dabrafenib.	dabrafenib	139-149	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	54-58
23420410-6	2013	Dabrafenib, another BRAF inhibitor, and trametinib, a MEK inhibitor, also have been shown to be effective in phase III trials for BRAF mutant melanoma and may be additional treatment options as monotherapy or in combination pending regulatory approval.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	20-24
23420410-6	2013	Dabrafenib, another BRAF inhibitor, and trametinib, a MEK inhibitor, also have been shown to be effective in phase III trials for BRAF mutant melanoma and may be additional treatment options as monotherapy or in combination pending regulatory approval.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	130-134
23807941-4	2013	There is data to suggest that dabrafenib not only shows activity in V600E-mutated melanoma, but also in non-V600E BRAF-mutated disease such as V600K.	dabrafenib	30-40	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	114-118
23709751-0	2013	Ipilimumab, vemurafenib, dabrafenib, and trametinib: synergistic competitors in the clinical management of BRAF mutant malignant melanoma.	dabrafenib	25-35	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	107-111
25806238-6	2013	The use of vemurafenib and dabrafenib, agents that block MAPK signaling in patients with melanoma and the BRAF V600E mutation, has been associated with prolonged survival and progression-free survival.	dabrafenib	27-37	mitogen-activated protein kinase 1	Homo sapiens	57-61
25806238-6	2013	The use of vemurafenib and dabrafenib, agents that block MAPK signaling in patients with melanoma and the BRAF V600E mutation, has been associated with prolonged survival and progression-free survival.	dabrafenib	27-37	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	106-110
25806238-8	2013	Treatment of V600E BRAF-mutant lung adenocarcinomas with dabrafenib is under evaluation in a phase 2 trial, and could represent another milestone in individualized therapy for lung cancer patients.	dabrafenib	57-67	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	19-23
25806238-9	2013	The next step will be a combination therapy of BRAF inhibitor dabrafenib and MEK inhibitor trametinib.	dabrafenib	62-72	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	47-51
23807941-8	2013	The U.S. Food and Drug Administration has recently approved dabrafenib as a single agent for the treatment of unresectable or metastatic melanoma in adult patients with BRAF V600E mutation.	dabrafenib	60-70	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	169-173
23535073-1	2013	BACKGROUND: Although remarkable clinical response rates in melanoma have been observed using vemurafenib or dabrafenib in patients with tumors carrying oncogenic mutations in BRAF, a substantial unmet medical need remains for the subset of patients with wild-type BRAF tumors.	dabrafenib	108-118	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	175-179
23524406-0	2013	Molecular characterization of acquired resistance to the BRAF inhibitor dabrafenib in a patient with BRAF-mutant non-small-cell lung cancer.	dabrafenib	72-82	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	57-61
23524406-0	2013	Molecular characterization of acquired resistance to the BRAF inhibitor dabrafenib in a patient with BRAF-mutant non-small-cell lung cancer.	dabrafenib	72-82	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	101-105
23432625-9	2013	Current clinical investigations have shown great promise with the combination of trametinib and dabrafenib in patients with BRAF-mutant melanoma; a number of clinical trials of trametinib in combination with other targeted drugs are underway.	dabrafenib	96-106	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	124-128
23537694-0	2013	Liquid chromatography-tandem mass spectrometric assay for the mutated BRAF inhibitor dabrafenib in mouse plasma.	dabrafenib	85-95	Braf transforming gene	Mus musculus	70-74
23537694-1	2013	A quantitative bioanalytical liquid chromatography-tandem mass spectrometric (LC-MS/MS) assay for the mutated BRAF inhibitor dabrafenib was developed and validated.	dabrafenib	125-135	Braf transforming gene	Mus musculus	110-114
23290787-2	2013	Treatment of these patients with either of two BRAF inhibitors (vemurafenib, dabrafenib) or the MEK inhibitor trametinib is associated with improved clinical benefit (response rate, progression free survival, and overall survival) compared with treatment with chemotherapy in three phase III trials.	dabrafenib	77-87	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	47-51
23515890-4	2013	In particular we discuss the mutant BRAF inhibitors Vemurafenib and Dabrafenib, which markedly inhibit tumor growth and advance patients" overall survival.	dabrafenib	68-78	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	36-40
23403819-2	2013	METHODS: Fifty-eight BRAF(V600E) metastatic melanoma patients treated with dabrafenib or vemurafenib on clinical trials had pre-treatment tumour BRAF(V600E) protein expression immunohistochemically (IHC) assessed using the BRAF V600E mutant-specific antibody VE1.	dabrafenib	75-85	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	21-25
23288408-1	2013	RAF inhibitors such as vemurafenib and dabrafenib block BRAF-mediated cell proliferation and achieve meaningful clinical benefit in the vast majority of patients with BRAF(V600E)-mutant melanoma.	dabrafenib	39-49	zinc fingers and homeoboxes 2	Homo sapiens	0-3
23249624-0	2013	Mechanisms limiting distribution of the threonine-protein kinase B-RaF(V600E) inhibitor dabrafenib to the brain: implications for the treatment of melanoma brain metastases.	dabrafenib	88-98	zinc fingers and homeoboxes 2	Mus musculus	67-70
23249624-2	2013	Dabrafenib is a BRAF (gene encoding serine/threonine-protein kinase B-Raf) inhibitor that has been developed to selectively target the valine 600 to glutamic acid substitution (BRAF(V600E)), which is commonly found in metastatic melanoma.	dabrafenib	0-10	Braf transforming gene	Mus musculus	16-20
23249624-2	2013	Dabrafenib is a BRAF (gene encoding serine/threonine-protein kinase B-Raf) inhibitor that has been developed to selectively target the valine 600 to glutamic acid substitution (BRAF(V600E)), which is commonly found in metastatic melanoma.	dabrafenib	0-10	Braf transforming gene	Mus musculus	36-73
23249624-2	2013	Dabrafenib is a BRAF (gene encoding serine/threonine-protein kinase B-Raf) inhibitor that has been developed to selectively target the valine 600 to glutamic acid substitution (BRAF(V600E)), which is commonly found in metastatic melanoma.	dabrafenib	0-10	Braf transforming gene	Mus musculus	177-181
23249624-4	2013	Thus, the objective of the current study was to evaluate the brain distribution of dabrafenib in mice, and to see whether active efflux by P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) restricts its delivery across the blood-brain barrier (BBB).	dabrafenib	83-93	phosphoglycolate phosphatase	Mus musculus	155-159
23249624-5	2013	In vitro accumulation studies conducted in Madin-Darby canine kidney II cells indicate that dabrafenib is an avid substrate for both P-gp and BCRP.	dabrafenib	92-102	PGP	Canis lupus familiaris	133-137
23249624-5	2013	In vitro accumulation studies conducted in Madin-Darby canine kidney II cells indicate that dabrafenib is an avid substrate for both P-gp and BCRP.	dabrafenib	92-102	ATP binding cassette subfamily G member 2	Canis lupus familiaris	142-146
23249624-9	2013	Dabrafenib plasma exposure was ~2-fold greater in Mdr1 a/b(-/-)Bcrp1(-/-) mice as compared with wild-type with an oral dose (25 mg/kg); however, the brain distribution was increased by ~10-fold with a resulting K(p) of 0.25.	dabrafenib	0-10	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	50-56
23249624-9	2013	Dabrafenib plasma exposure was ~2-fold greater in Mdr1 a/b(-/-)Bcrp1(-/-) mice as compared with wild-type with an oral dose (25 mg/kg); however, the brain distribution was increased by ~10-fold with a resulting K(p) of 0.25.	dabrafenib	0-10	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	63-68
23249624-10	2013	Further, compared with vemurafenib, another BRAF(V600E) inhibitor, dabrafenib showed greater brain penetration with a similar dose.	dabrafenib	67-77	Braf transforming gene	Mus musculus	44-48
22878367-2	2013	In this case report, we describe alterations of tumor morphology and patterns of cyclin-dependent kinase inhibitor (CDKI) expression in a patient who received GSK2118436, a second-generation RAF inhibitor, for stage IV (M1c) metastatic melanoma.	dabrafenib	159-169	cyclin dependent kinase inhibitor 3	Homo sapiens	81-114
22878367-2	2013	In this case report, we describe alterations of tumor morphology and patterns of cyclin-dependent kinase inhibitor (CDKI) expression in a patient who received GSK2118436, a second-generation RAF inhibitor, for stage IV (M1c) metastatic melanoma.	dabrafenib	159-169	cyclin dependent kinase inhibitor 3	Homo sapiens	116-120
22878367-2	2013	In this case report, we describe alterations of tumor morphology and patterns of cyclin-dependent kinase inhibitor (CDKI) expression in a patient who received GSK2118436, a second-generation RAF inhibitor, for stage IV (M1c) metastatic melanoma.	dabrafenib	159-169	zinc fingers and homeoboxes 2	Homo sapiens	191-194
23294221-2	2013	Some of the drugs thus developed, such as vemurafenib and dabrafenib, show impressive responses in melanoma patients harbouring a BRAF mutation.	dabrafenib	58-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	130-134
23237741-5	2013	We have treated 45 patients with V600 mutated melanoma including patients with V600R mutation between July 2011 and October 2012 with the selective BRAF inhibitor dabrafenib (n=43) or vemurafenib (n=2) via a compassionate access programme.	dabrafenib	163-173	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	148-152
23552670-0	2013	Merkel cell polyomavirus and HPV-17 associated with cutaneous squamous cell carcinoma arising in a patient with melanoma treated with the BRAF inhibitor dabrafenib.	dabrafenib	153-163	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	138-142
23552670-2	2013	We report what we believe to be the first case in which Merkel cell polyomavirus (MCPyV) and human papillomavirus subtype 17 (HPV-17) were associated with cutaneous SCC that developed during treatment with the BRAF inhibitor dabrafenib.	dabrafenib	225-235	serpin family B member 3	Homo sapiens	165-168
23552670-2	2013	We report what we believe to be the first case in which Merkel cell polyomavirus (MCPyV) and human papillomavirus subtype 17 (HPV-17) were associated with cutaneous SCC that developed during treatment with the BRAF inhibitor dabrafenib.	dabrafenib	225-235	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	210-214
23552670-3	2013	OBSERVATIONS: A 62-year-old woman with V600E BRAF -mutant metastatic melanoma enrolled in a phase 1 trial of dabrafenib, a selective inhibitor of V600-mutant BRAF kinase.	dabrafenib	109-119	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	45-49
23552670-3	2013	OBSERVATIONS: A 62-year-old woman with V600E BRAF -mutant metastatic melanoma enrolled in a phase 1 trial of dabrafenib, a selective inhibitor of V600-mutant BRAF kinase.	dabrafenib	109-119	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	158-162
24900673-0	2013	Discovery of Dabrafenib: A Selective Inhibitor of Raf Kinases with Antitumor Activity against B-Raf-Driven Tumors.	dabrafenib	13-23	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	94-99
24900673-2	2013	Herein we report the discovery and biological evaluation of GSK2118436, a selective inhibitor of Raf kinases with potent in vitro activity in oncogenic B-Raf-driven melanoma and colorectal carcinoma cells and robust in vivo antitumor and pharmacodynamic activity in mouse models of B-Raf(V600E) human melanoma.	dabrafenib	60-70	Braf transforming gene	Mus musculus	152-157
24900673-2	2013	Herein we report the discovery and biological evaluation of GSK2118436, a selective inhibitor of Raf kinases with potent in vitro activity in oncogenic B-Raf-driven melanoma and colorectal carcinoma cells and robust in vivo antitumor and pharmacodynamic activity in mouse models of B-Raf(V600E) human melanoma.	dabrafenib	60-70	Braf transforming gene	Mus musculus	282-287
24900673-3	2013	GSK2118436 was identified as a development candidate, and early clinical results have shown significant activity in patients with B-Raf mutant melanoma.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	130-135
23215674-6	2013	EXPERT OPINION: Elucidation of the crucial role of MAPK pathway and BRAF kinase mutations in particular has led to development of specific small molecule kinase inhibitors (vemurafenib, dabrafenib, trametinib), and new insight into molecular mechanisms responsible for immune response and tolerance resulted in development of immunomodulatory agents (ipilimumab, anti-PD1, anti-PD-L1).	dabrafenib	186-196	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	68-72
23215674-6	2013	EXPERT OPINION: Elucidation of the crucial role of MAPK pathway and BRAF kinase mutations in particular has led to development of specific small molecule kinase inhibitors (vemurafenib, dabrafenib, trametinib), and new insight into molecular mechanisms responsible for immune response and tolerance resulted in development of immunomodulatory agents (ipilimumab, anti-PD1, anti-PD-L1).	dabrafenib	186-196	programmed cell death 1	Homo sapiens	368-371
23215674-6	2013	EXPERT OPINION: Elucidation of the crucial role of MAPK pathway and BRAF kinase mutations in particular has led to development of specific small molecule kinase inhibitors (vemurafenib, dabrafenib, trametinib), and new insight into molecular mechanisms responsible for immune response and tolerance resulted in development of immunomodulatory agents (ipilimumab, anti-PD1, anti-PD-L1).	dabrafenib	186-196	CD274 molecule	Homo sapiens	378-383
23369684-3	2013	The selective inhibitors of mutant BRAF Val600, vemurafenib and dabrafenib, showed major tumour responses, resulting in improved progression-free and overall survival in patients with metastatic disease, compared with chemotherapy.	dabrafenib	64-74	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	35-39
23288408-1	2013	RAF inhibitors such as vemurafenib and dabrafenib block BRAF-mediated cell proliferation and achieve meaningful clinical benefit in the vast majority of patients with BRAF(V600E)-mutant melanoma.	dabrafenib	39-49	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	56-60
23288408-1	2013	RAF inhibitors such as vemurafenib and dabrafenib block BRAF-mediated cell proliferation and achieve meaningful clinical benefit in the vast majority of patients with BRAF(V600E)-mutant melanoma.	dabrafenib	39-49	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	167-171
23317446-0	2013	Effect of dabrafenib on melanoma cell lines harbouring the BRAF(V600D/R) mutations.	dabrafenib	10-20	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	59-63
23317446-7	2013	To evaluate the inhibition of MAPK pathway and the consequent inhibition of cellular proliferation, the phosphorylation of ERK was examined by Western Blot analysis performed on total protein extracts from cell lines after treatment with dabrafenib.	dabrafenib	238-248	mitogen-activated protein kinase 1	Homo sapiens	30-34
23317446-7	2013	To evaluate the inhibition of MAPK pathway and the consequent inhibition of cellular proliferation, the phosphorylation of ERK was examined by Western Blot analysis performed on total protein extracts from cell lines after treatment with dabrafenib.	dabrafenib	238-248	mitogen-activated protein kinase 1	Homo sapiens	123-126
23714462-1	2013	Treatment of V600E/K BRAF-mutated melanomas with RAF inhibitors (either vemurafenib or dabrafenib) results in rapid and dramatic responses in most patients-results that are associated with improved progression-free survival (PFS) and in the case of vemurafenib, overall survival (OS).	dabrafenib	87-97	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	21-25
23714462-1	2013	Treatment of V600E/K BRAF-mutated melanomas with RAF inhibitors (either vemurafenib or dabrafenib) results in rapid and dramatic responses in most patients-results that are associated with improved progression-free survival (PFS) and in the case of vemurafenib, overall survival (OS).	dabrafenib	87-97	zinc fingers and homeoboxes 2	Homo sapiens	22-25
23714558-4	2013	Since 2010, three drugs have demonstrated activity in progressing or "active" brain metastases including the anti-CTLA4 antibody ipilimumab (phase II study of 72 patients), and the BRAF inhibitors dabrafenib (phase II study of 172 patients, both previously treated and untreated brain metastases) and vemurafenib (a pilot study of 24 patients with heavily pretreated brain metastases).	dabrafenib	197-207	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	181-185
22981500-0	2013	(18)F-labelled fluorodeoxyglucose-positron emission tomography (FDG-PET) heterogeneity of response is prognostic in dabrafenib treated BRAF mutant metastatic melanoma.	dabrafenib	116-126	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	135-139
22584957-3	2012	Selective BRAF-V600 inhibitors (vemurafenib, dabrafenib) have high antitumor activity against BRAF-V600-mutant melanoma with objective tumor response rates.	dabrafenib	45-55	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	10-14
23306915-5	2013	Another BRAF inhibitor, dabrafenib, and a MEK inhibitor, trametinib, have shown excellent efficacy in clinical studies.	dabrafenib	24-34	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	8-12
23276366-1	2013	The RAF inhibitors vemurafenib and dabrafenib are emerging as the standard of care for Val600 BRAF-mutant metastatic melanoma.	dabrafenib	35-45	zinc fingers and homeoboxes 2	Homo sapiens	4-7
23470635-0	2013	BRAF mutant gastrointestinal stromal tumor: first report of regression with BRAF inhibitor dabrafenib (GSK2118436) and whole exomic sequencing for analysis of acquired resistance.	dabrafenib	91-101	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
22584957-3	2012	Selective BRAF-V600 inhibitors (vemurafenib, dabrafenib) have high antitumor activity against BRAF-V600-mutant melanoma with objective tumor response rates.	dabrafenib	45-55	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	94-98
22584957-6	2012	Two patients with BRAF-V600E mutant melanoma who had documented progression during treatment with dabrafenib/GSK1120212 and dabrafenib, respectively, were rechallenged with dabrafenib and vemurafenib after a treatment-free interval of 8 and 4 months during which further progression was documented.	dabrafenib	98-108	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	18-22
23020132-2	2012	To address this problem, we conducted a phase 1 and 2 trial of combined treatment with dabrafenib, a selective BRAF inhibitor, and trametinib, a selective MAPK kinase (MEK) inhibitor.	dabrafenib	87-97	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	111-115
23470635-0	2013	BRAF mutant gastrointestinal stromal tumor: first report of regression with BRAF inhibitor dabrafenib (GSK2118436) and whole exomic sequencing for analysis of acquired resistance.	dabrafenib	91-101	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	76-80
23470635-0	2013	BRAF mutant gastrointestinal stromal tumor: first report of regression with BRAF inhibitor dabrafenib (GSK2118436) and whole exomic sequencing for analysis of acquired resistance.	dabrafenib	103-113	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
23470635-2	2013	Dabrafenib is a potent ATP-competitive inhibitor of BRAF kinase and is highly selective for mutant BRAF in kinase panel screening, cell lines, and xenografts.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	52-56
23470635-2	2013	Dabrafenib is a potent ATP-competitive inhibitor of BRAF kinase and is highly selective for mutant BRAF in kinase panel screening, cell lines, and xenografts.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	99-103
22804352-0	2012	Cutaneous manifestations of dabrafenib (GSK2118436): a selective inhibitor of mutant BRAF in patients with metastatic melanoma.	dabrafenib	28-38	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	85-89
22804352-0	2012	Cutaneous manifestations of dabrafenib (GSK2118436): a selective inhibitor of mutant BRAF in patients with metastatic melanoma.	dabrafenib	40-50	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	85-89
22804352-3	2012	We conducted a systematic prospective dermatological review of all patients enrolled at a single institution in the phase I/II clinical trial of the mutant BRAF inhibitor dabrafenib (GSK2118436).	dabrafenib	171-181	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	156-160
22804352-4	2012	OBJECTIVES: To identify the cutaneous manifestations of the BRAF inhibitor dabrafenib; to form diagnostic criteria to standardize the diagnosis of verrucal keratotic squamoproliferative lesions; and to bring awareness to the medical community of the importance of dermatological assessment of patients taking dabrafenib.	dabrafenib	75-85	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	60-64
22804352-4	2012	OBJECTIVES: To identify the cutaneous manifestations of the BRAF inhibitor dabrafenib; to form diagnostic criteria to standardize the diagnosis of verrucal keratotic squamoproliferative lesions; and to bring awareness to the medical community of the importance of dermatological assessment of patients taking dabrafenib.	dabrafenib	309-319	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	60-64
22804352-14	2012	CONCLUSIONS: Administration of the mutant BRAF inhibitor dabrafenib is associated with induction of keratinocytic proliferation, which in some cases develops features of low-grade malignancy.	dabrafenib	57-67	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	42-46
23431672-1	2012	Vemurafenib is a chemotherapeutic BRAF inhibitor, or dabrafenib, that has been FDA-approved for treatment in metastatic melanoma positive for the V600E mutation.	dabrafenib	53-63	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	34-38
23031422-0	2012	Overwhelming response to Dabrafenib in a patient with double BRAF mutation (V600E; V600M) metastatic malignant melanoma.	dabrafenib	25-35	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	61-65
22437314-3	2012	To investigate the efficacy of combination BRAF and MEK inhibition, we generated melanoma cell clones resistant to the BRAF inhibitor GSK2118436.	dabrafenib	134-144	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	119-123
23051966-0	2012	Dabrafenib in patients with Val600Glu or Val600Lys BRAF-mutant melanoma metastatic to the brain (BREAK-MB): a multicentre, open-label, phase 2 trial.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	51-55
23051966-2	2012	We assessed dabrafenib in patients with Val600Glu or Val600Lys BRAF-mutant melanoma metastatic to the brain.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	63-67
23051966-20	2012	INTERPRETATION: Dabrafenib has activity and an acceptable safety profile in patients with Val600Glu BRAF-mutant melanoma and brain metastases irrespective of whether they are untreated or have been previously treated but have progressed.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	100-104
22744255-3	2012	He was started on targeted biological therapy with BRAF inhibitor GSK2118436, and is having a good clinical and radiological response without significant lasting toxicity.	dabrafenib	66-76	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	51-55
22609219-3	2012	OBJECTIVE: We sought to detail additional cutaneous adverse effects of vemurafenib and a similar BRAF inhibitor, dabrafenib.	dabrafenib	113-123	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	97-101
22934253-2	2012	While treatment with selective BRAF(V600E) inhibitors (like vemurafenib or dabrafenib) leads to high response rates but short response duration, CTLA-4 blocking therapies induce sustained responses, but only in a limited number of patients.	dabrafenib	75-85	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	31-35
22735384-0	2012	Dabrafenib in BRAF-mutated metastatic melanoma: a multicentre, open-label, phase 3 randomised controlled trial.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
22735384-1	2012	BACKGROUND: Dabrafenib, an inhibitor of mutated BRAF, has clinical activity with a manageable safety profile in studies of phase 1 and 2 in patients with BRAF(V600)-mutated metastatic melanoma.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	48-52
22735384-1	2012	BACKGROUND: Dabrafenib, an inhibitor of mutated BRAF, has clinical activity with a manageable safety profile in studies of phase 1 and 2 in patients with BRAF(V600)-mutated metastatic melanoma.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	154-163
22735384-2	2012	We studied the efficacy of dabrafenib in patients with BRAF(V600E)-mutated metastatic melanoma.	dabrafenib	27-37	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	55-60
22554099-14	2012	Preliminary data seem to indicate that an additional inhibitor of mutated BRAF, GSK2118436, might be also active on a wider range of BRAF mutations (V600E-K-D-R); actually, treatment with such a compound is under evaluation in a phase III study among stage III-IV melanoma patients positive for BRAF mutations.	dabrafenib	80-90	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	74-78
22554099-14	2012	Preliminary data seem to indicate that an additional inhibitor of mutated BRAF, GSK2118436, might be also active on a wider range of BRAF mutations (V600E-K-D-R); actually, treatment with such a compound is under evaluation in a phase III study among stage III-IV melanoma patients positive for BRAF mutations.	dabrafenib	80-90	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	133-137
22554099-14	2012	Preliminary data seem to indicate that an additional inhibitor of mutated BRAF, GSK2118436, might be also active on a wider range of BRAF mutations (V600E-K-D-R); actually, treatment with such a compound is under evaluation in a phase III study among stage III-IV melanoma patients positive for BRAF mutations.	dabrafenib	80-90	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	133-137
22355009-0	2012	BRAF(V600) inhibitor GSK2118436 targeted inhibition of mutant BRAF in cancer patients does not impair overall immune competency.	dabrafenib	21-31	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-9
22594466-8	2012	For this reason, she was enrolled into another clinical trial with the GSK2118436 BRAF inhibitor, dabrafenib, as a second line of therapy.	dabrafenib	71-81	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	82-86
22594466-8	2012	For this reason, she was enrolled into another clinical trial with the GSK2118436 BRAF inhibitor, dabrafenib, as a second line of therapy.	dabrafenib	98-108	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	82-86
25562798-4	2012	Similarly in melanoma, 50% of cases have BRAF mutations in exon 15 mostly V600E and these cases are sensitive to the BRAF inhibitors vemurafenib or dabrafenib.	dabrafenib	148-158	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	41-45
25562798-4	2012	Similarly in melanoma, 50% of cases have BRAF mutations in exon 15 mostly V600E and these cases are sensitive to the BRAF inhibitors vemurafenib or dabrafenib.	dabrafenib	148-158	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	117-121
22355009-0	2012	BRAF(V600) inhibitor GSK2118436 targeted inhibition of mutant BRAF in cancer patients does not impair overall immune competency.	dabrafenib	21-31	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
22389471-0	2012	Combinations of BRAF, MEK, and PI3K/mTOR inhibitors overcome acquired resistance to the BRAF inhibitor GSK2118436 dabrafenib, mediated by NRAS or MEK mutations.	dabrafenib	103-113	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	16-20
22389471-0	2012	Combinations of BRAF, MEK, and PI3K/mTOR inhibitors overcome acquired resistance to the BRAF inhibitor GSK2118436 dabrafenib, mediated by NRAS or MEK mutations.	dabrafenib	103-113	mitogen-activated protein kinase kinase 7	Homo sapiens	22-25
22389471-0	2012	Combinations of BRAF, MEK, and PI3K/mTOR inhibitors overcome acquired resistance to the BRAF inhibitor GSK2118436 dabrafenib, mediated by NRAS or MEK mutations.	dabrafenib	103-113	mechanistic target of rapamycin kinase	Homo sapiens	36-40
22389471-0	2012	Combinations of BRAF, MEK, and PI3K/mTOR inhibitors overcome acquired resistance to the BRAF inhibitor GSK2118436 dabrafenib, mediated by NRAS or MEK mutations.	dabrafenib	103-113	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	88-92
22389471-0	2012	Combinations of BRAF, MEK, and PI3K/mTOR inhibitors overcome acquired resistance to the BRAF inhibitor GSK2118436 dabrafenib, mediated by NRAS or MEK mutations.	dabrafenib	103-113	NRAS proto-oncogene, GTPase	Homo sapiens	138-142
22389471-0	2012	Combinations of BRAF, MEK, and PI3K/mTOR inhibitors overcome acquired resistance to the BRAF inhibitor GSK2118436 dabrafenib, mediated by NRAS or MEK mutations.	dabrafenib	103-113	mitogen-activated protein kinase kinase 7	Homo sapiens	146-149
22389471-0	2012	Combinations of BRAF, MEK, and PI3K/mTOR inhibitors overcome acquired resistance to the BRAF inhibitor GSK2118436 dabrafenib, mediated by NRAS or MEK mutations.	dabrafenib	114-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	16-20
22389471-0	2012	Combinations of BRAF, MEK, and PI3K/mTOR inhibitors overcome acquired resistance to the BRAF inhibitor GSK2118436 dabrafenib, mediated by NRAS or MEK mutations.	dabrafenib	114-124	mitogen-activated protein kinase kinase 7	Homo sapiens	22-25
22389471-0	2012	Combinations of BRAF, MEK, and PI3K/mTOR inhibitors overcome acquired resistance to the BRAF inhibitor GSK2118436 dabrafenib, mediated by NRAS or MEK mutations.	dabrafenib	114-124	mechanistic target of rapamycin kinase	Homo sapiens	36-40
22389471-0	2012	Combinations of BRAF, MEK, and PI3K/mTOR inhibitors overcome acquired resistance to the BRAF inhibitor GSK2118436 dabrafenib, mediated by NRAS or MEK mutations.	dabrafenib	114-124	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	88-92
22389471-0	2012	Combinations of BRAF, MEK, and PI3K/mTOR inhibitors overcome acquired resistance to the BRAF inhibitor GSK2118436 dabrafenib, mediated by NRAS or MEK mutations.	dabrafenib	114-124	NRAS proto-oncogene, GTPase	Homo sapiens	138-142
22389471-0	2012	Combinations of BRAF, MEK, and PI3K/mTOR inhibitors overcome acquired resistance to the BRAF inhibitor GSK2118436 dabrafenib, mediated by NRAS or MEK mutations.	dabrafenib	114-124	mitogen-activated protein kinase kinase 7	Homo sapiens	146-149
22389471-1	2012	Recent results from clinical trials with the BRAF inhibitors GSK2118436 (dabrafenib) and PLX4032 (vemurafenib) have shown encouraging response rates; however, the duration of response has been limited.	dabrafenib	61-71	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	45-49
22389471-1	2012	Recent results from clinical trials with the BRAF inhibitors GSK2118436 (dabrafenib) and PLX4032 (vemurafenib) have shown encouraging response rates; however, the duration of response has been limited.	dabrafenib	73-83	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	45-49
22389471-2	2012	To identify determinants of acquired resistance to GSK2118436 and strategies to overcome the resistance, we isolated GSK2118436 drug-resistant clones from the A375 BRAF(V600E) and the YUSIT1 BRAF(V600K) melanoma cell lines.	dabrafenib	117-127	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	164-169
22389471-2	2012	To identify determinants of acquired resistance to GSK2118436 and strategies to overcome the resistance, we isolated GSK2118436 drug-resistant clones from the A375 BRAF(V600E) and the YUSIT1 BRAF(V600K) melanoma cell lines.	dabrafenib	117-127	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	164-168
22389471-5	2012	Stable knockdown of NRAS with short hairpin RNA partially restored GSK2118436 sensitivity in mutant NRAS clones, whereas expression of NRAS(Q61K) or NRAS(A146T) in the A375 parental cells decreased sensitivity to GSK2118436.	dabrafenib	67-77	NRAS proto-oncogene, GTPase	Homo sapiens	20-24
22389471-5	2012	Stable knockdown of NRAS with short hairpin RNA partially restored GSK2118436 sensitivity in mutant NRAS clones, whereas expression of NRAS(Q61K) or NRAS(A146T) in the A375 parental cells decreased sensitivity to GSK2118436.	dabrafenib	67-77	NRAS proto-oncogene, GTPase	Homo sapiens	100-104
22389471-5	2012	Stable knockdown of NRAS with short hairpin RNA partially restored GSK2118436 sensitivity in mutant NRAS clones, whereas expression of NRAS(Q61K) or NRAS(A146T) in the A375 parental cells decreased sensitivity to GSK2118436.	dabrafenib	67-77	NRAS proto-oncogene, GTPase	Homo sapiens	100-104
22389471-5	2012	Stable knockdown of NRAS with short hairpin RNA partially restored GSK2118436 sensitivity in mutant NRAS clones, whereas expression of NRAS(Q61K) or NRAS(A146T) in the A375 parental cells decreased sensitivity to GSK2118436.	dabrafenib	67-77	NRAS proto-oncogene, GTPase	Homo sapiens	100-104
22389471-5	2012	Stable knockdown of NRAS with short hairpin RNA partially restored GSK2118436 sensitivity in mutant NRAS clones, whereas expression of NRAS(Q61K) or NRAS(A146T) in the A375 parental cells decreased sensitivity to GSK2118436.	dabrafenib	213-223	NRAS proto-oncogene, GTPase	Homo sapiens	20-24
22389471-6	2012	Similarly, expression of MEK1(K59del), but not MEK1(P387S), decreased sensitivity of A375 cells to GSK2118436.	dabrafenib	99-109	mitogen-activated protein kinase kinase 1	Homo sapiens	25-29
22389471-7	2012	The combination of GSK2118436 and GSK1120212 effectively inhibited cell growth, decreased ERK phosphorylation, decreased cyclin D1 protein, and increased p27(kip1) protein in the resistant clones.	dabrafenib	19-29	cyclin D1	Homo sapiens	121-130
22389471-7	2012	The combination of GSK2118436 and GSK1120212 effectively inhibited cell growth, decreased ERK phosphorylation, decreased cyclin D1 protein, and increased p27(kip1) protein in the resistant clones.	dabrafenib	19-29	dynactin subunit 6	Homo sapiens	154-157
22389471-7	2012	The combination of GSK2118436 and GSK1120212 effectively inhibited cell growth, decreased ERK phosphorylation, decreased cyclin D1 protein, and increased p27(kip1) protein in the resistant clones.	dabrafenib	19-29	cyclin dependent kinase inhibitor 1B	Homo sapiens	158-162
22389471-8	2012	Moreover, the combination of GSK2118436 or GSK1120212 with the phosphoinositide 3-kinase/mTOR inhibitor GSK2126458 enhanced cell growth inhibition and decreased S6 ribosomal protein phosphorylation in these clones.	dabrafenib	29-39	mechanistic target of rapamycin kinase	Homo sapiens	89-93
22253555-4	2012	The second group of agents to show a survival benefit were the selective BRAF inhibitors, vemurafenib and GSK2118436, in patients who are BRAF V600 mutation positive.	dabrafenib	106-116	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	138-142
22156613-1	2012	PURPOSE: To evaluate the effects of treatment with the potent mutant BRAF inhibitors GSK2118436 or vemurafenib (PLX4720) on immune responses to metastatic melanoma in tissues taken before and after treatment.	dabrafenib	85-95	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	69-73
22608338-1	2012	BACKGROUND: Dabrafenib is an inhibitor of BRAF kinase that is selective for mutant BRAF.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	42-46
22608338-1	2012	BACKGROUND: Dabrafenib is an inhibitor of BRAF kinase that is selective for mutant BRAF.	dabrafenib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	83-87
22608338-23	2012	INTERPRETATION: Dabrafenib is safe in patients with solid tumours, and an active inhibitor of Val600-mutant BRAF with responses noted in patients with melanoma, brain metastases, and other solid tumours.	dabrafenib	16-26	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	108-112
23788912-7	2012	Ipilimumab or BRAF inhibitors (vemurafenib, dabrafenib) seem to be active in patients with brain metastases.	dabrafenib	44-54	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
21818706-7	2012	Early clinical results with the BRAF-selective inhibitors PLX4032 and GSK2118436 suggest that this strategy will prove successful in a select group of patients whose tumors are driven by oncogenic BRAF.	dabrafenib	70-80	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	32-36
21818706-7	2012	Early clinical results with the BRAF-selective inhibitors PLX4032 and GSK2118436 suggest that this strategy will prove successful in a select group of patients whose tumors are driven by oncogenic BRAF.	dabrafenib	70-80	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	197-201
23251089-3	2012	Dabrafenib inhibits the mutant BRAF (BRAF(mut)) protein in melanomas with BRAF(V600E) and BRAF(V600K) genotypes.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	31-35
23251089-3	2012	Dabrafenib inhibits the mutant BRAF (BRAF(mut)) protein in melanomas with BRAF(V600E) and BRAF(V600K) genotypes.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	37-46
23251089-3	2012	Dabrafenib inhibits the mutant BRAF (BRAF(mut)) protein in melanomas with BRAF(V600E) and BRAF(V600K) genotypes.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	37-41
23251089-3	2012	Dabrafenib inhibits the mutant BRAF (BRAF(mut)) protein in melanomas with BRAF(V600E) and BRAF(V600K) genotypes.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	37-41
23251089-4	2012	BRAF(V600E) metastatic melanoma patients who receive dabrafenib treatment exhibit high clinical response rates and compared with dacarbazine chemotherapy, progression-free survival.	dabrafenib	53-63	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
23251089-9	2012	It is expected that new combinations of targeted drugs, such as the combination of dabrafenib and trametinib (GSK1120212, a MEK inhibitor), will provide higher response rates and more durable clinical benefit than dabrafenib monotherapy.	dabrafenib	83-93	mitogen-activated protein kinase kinase 7	Homo sapiens	124-127
23102194-0	2012	[Dabrafenib: the new inhibitor of hyperactive B-RAF kinase].	dabrafenib	1-11	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	46-51
23102194-4	2012	In this study, we focus on the reversible ATP-competitive inhibitor dabrafenib (GSK-2118436), which is now in phase III clinical trial for use in subjects with various cancers expressing hyperactive B-RAF.	dabrafenib	68-78	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	199-204
23102194-4	2012	In this study, we focus on the reversible ATP-competitive inhibitor dabrafenib (GSK-2118436), which is now in phase III clinical trial for use in subjects with various cancers expressing hyperactive B-RAF.	dabrafenib	80-91	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	199-204
23102194-5	2012	Dabrafenib is selective for B-RAFV600E and B-RAFV600K (less for B-RAFV600D) over wild-type B-RAF.	dabrafenib	0-10	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	28-33
23102194-8	2012	Most of the cancers expressing hyperactive B-RAF respond to dabrafenib treatment, but the complete response is only rarely achieved.	dabrafenib	60-70	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	43-48
23102194-13	2012	Since B-RAF mutations alone cause only the formation of benign naevi, since the tumors frequently and quickly acquire resistance to B-RAF inhibitors, and because the B-RAF-inhibitor-mediated treatment outcomes are severely affected by changes in the activity and expression of a number of signaling molecules (among them PI3K/mTOR, PTEN, AKT, MEK, PDGFRbeta), it can be anticipated that dabrafenib treatment should be suggested only as a part of combined therapy targeting simultaneously the other pathways responsible for cancer onset and progression.	dabrafenib	387-397	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	6-11
21656352-3	2011	This article provides a review of GSK2118436 and PLX4032 as potential therapeutics for the treatment of melanomas by inhibiting oncogenic BRAF.	dabrafenib	34-44	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	138-142
21426297-4	2011	This review article will address: (a) preclinical data on the antitumor activity of BRAF inhibitors in cell lines/ in vivo models and their opposing functions as inhibitors or activators of the MAPK pathway, depending on the cellular context; (b) drug development from non-selective RAF inhibitors to selective BRAF inhibitors, such as PLX4032 and GSK2118436, with emphasis in the clinical efficacy and toxicity of these agents; and (c) possible mechanisms of resistance to BRAF inhibitors and strategies to overcome its development in BRAF mutant tumors.	dabrafenib	348-358	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	84-88