PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33887553-9	2021	In combination, sunitinib was able to overcome potential crizotinib-induced resistance through downregulation of ERK 1/2 activity and PDGFRss receptor expression; consequently, tumor growth was significantly decreased both in vitro and in vivo.	Sunitinib	16-25	mitogen-activated protein kinase 3	Homo sapiens	113-120
34036385-0	2021	QPCT regulation by CTCF leads to sunitinib resistance in renal cell carcinoma by promoting angiogenesis.	Sunitinib	33-42	glutaminyl-peptide cyclotransferase	Homo sapiens	0-4
34036385-0	2021	QPCT regulation by CTCF leads to sunitinib resistance in renal cell carcinoma by promoting angiogenesis.	Sunitinib	33-42	CCCTC-binding factor	Homo sapiens	19-23
34036385-3	2021	It has previously been suggested that the protein glutaminyl-peptide cyclotransferase (QPCT) is closely related to sunitinib resistance in RCC.	Sunitinib	115-124	glutaminyl-peptide cyclotransferase	Homo sapiens	50-85
34036385-3	2021	It has previously been suggested that the protein glutaminyl-peptide cyclotransferase (QPCT) is closely related to sunitinib resistance in RCC.	Sunitinib	115-124	glutaminyl-peptide cyclotransferase	Homo sapiens	87-91
34036385-6	2021	On the whole, the data from the present study suggest that QPCT, CCCTC-binding factor (CTCF) and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) may be used as targets for predicting, reversing and treating sunitinib-resistant RCC.	Sunitinib	239-248	glutaminyl-peptide cyclotransferase	Homo sapiens	59-63
34036385-6	2021	On the whole, the data from the present study suggest that QPCT, CCCTC-binding factor (CTCF) and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) may be used as targets for predicting, reversing and treating sunitinib-resistant RCC.	Sunitinib	239-248	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	97-167
34036385-6	2021	On the whole, the data from the present study suggest that QPCT, CCCTC-binding factor (CTCF) and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) may be used as targets for predicting, reversing and treating sunitinib-resistant RCC.	Sunitinib	239-248	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	169-175
34057619-3	2021	Variants of the HT-29 line with complete or partial knockout of the PROM1 gene were equally sensitive to protein kinase inhibitors sorafenib and sunitinib.	Sunitinib	145-154	prominin 1	Homo sapiens	68-73
33995090-0	2021	Sodium-Glucose CoTransporter-2 Inhibitor Empagliflozin Ameliorates Sunitinib-Induced Cardiac Dysfunction via Regulation of AMPK-mTOR Signaling Pathway-Mediated Autophagy.	Sunitinib	67-76	solute carrier family 5 member 2	Homo sapiens	0-30
33893075-3	2021	MATERIALS AND METHODS: Parental and sunitinib-resistant 786-O cells were treated with GPER1 agonist G-1, and quantitative phosphoproteomics was performed.	Sunitinib	36-45	G protein-coupled estrogen receptor 1	Homo sapiens	86-91
33893075-6	2021	Phosphoproteomic signatures, including phosphoinositide 3-kinase and protein kinase B (PI3K-AKT) as well as other pathways, were up-regulated in sunitinib-resistant cells but application of G-1 reversed this effect.	Sunitinib	145-154	protein tyrosine kinase 2 beta	Homo sapiens	69-85
33893075-6	2021	Phosphoproteomic signatures, including phosphoinositide 3-kinase and protein kinase B (PI3K-AKT) as well as other pathways, were up-regulated in sunitinib-resistant cells but application of G-1 reversed this effect.	Sunitinib	145-154	AKT serine/threonine kinase 1	Homo sapiens	92-95
33893075-7	2021	Among phosphoprotein candidates, activating transcription factor 2 (ATF2) Thr69/71 phosphorylation was antagonistically regulated by sunitinib resistance and G-1.	Sunitinib	133-142	activating transcription factor 2	Homo sapiens	33-66
33893075-7	2021	Among phosphoprotein candidates, activating transcription factor 2 (ATF2) Thr69/71 phosphorylation was antagonistically regulated by sunitinib resistance and G-1.	Sunitinib	133-142	activating transcription factor 2	Homo sapiens	68-72
33893075-8	2021	CONCLUSION: Our results open up the possibility for managing RCC and sunitinib resistance by GPER1 agonist G-1 and its regulated pathways.	Sunitinib	69-78	G protein-coupled estrogen receptor 1	Homo sapiens	93-98
33995090-0	2021	Sodium-Glucose CoTransporter-2 Inhibitor Empagliflozin Ameliorates Sunitinib-Induced Cardiac Dysfunction via Regulation of AMPK-mTOR Signaling Pathway-Mediated Autophagy.	Sunitinib	67-76	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	123-127
33995090-0	2021	Sodium-Glucose CoTransporter-2 Inhibitor Empagliflozin Ameliorates Sunitinib-Induced Cardiac Dysfunction via Regulation of AMPK-mTOR Signaling Pathway-Mediated Autophagy.	Sunitinib	67-76	mechanistic target of rapamycin kinase	Homo sapiens	128-132
33995090-12	2021	Conclusion: EMPA could ameliorate SNT-induced cardiac dysfunction via regulating cardiomyocyte autophagy, which was mediated by the AMPK-mTOR signaling pathway.	Sunitinib	34-37	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	132-136
33995090-12	2021	Conclusion: EMPA could ameliorate SNT-induced cardiac dysfunction via regulating cardiomyocyte autophagy, which was mediated by the AMPK-mTOR signaling pathway.	Sunitinib	34-37	mechanistic target of rapamycin kinase	Homo sapiens	137-141
33900546-4	2022	Here, we describe a hypotonic, thermosensitive gel-forming eye drop for effective delivery of sunitinib, a protein kinase inhibitor with activity against the neuroprotective targets dual leucine zipper kinase (DLK) and leucine zipper kinase (LZK), to enhance survival of RGCs after optic nerve injury.	Sunitinib	94-103	mitogen-activated protein kinase kinase kinase 12	Homo sapiens	182-208
33906367-7	2021	Cobimetinib at nontoxic doses prevented tumor formation, inhibited tumor growth and enhanced efficacy of 5-fluorouracil, sorafenib and sunitinib via suppressing Raf/MEK/ERK, leading to MAPK pathway inhibition.	Sunitinib	135-144	mitogen-activated protein kinase kinase 7	Homo sapiens	165-168
33906367-7	2021	Cobimetinib at nontoxic doses prevented tumor formation, inhibited tumor growth and enhanced efficacy of 5-fluorouracil, sorafenib and sunitinib via suppressing Raf/MEK/ERK, leading to MAPK pathway inhibition.	Sunitinib	135-144	mitogen-activated protein kinase 1	Homo sapiens	169-172
33900546-4	2022	Here, we describe a hypotonic, thermosensitive gel-forming eye drop for effective delivery of sunitinib, a protein kinase inhibitor with activity against the neuroprotective targets dual leucine zipper kinase (DLK) and leucine zipper kinase (LZK), to enhance survival of RGCs after optic nerve injury.	Sunitinib	94-103	mitogen-activated protein kinase kinase kinase 13	Homo sapiens	242-245
33900546-4	2022	Here, we describe a hypotonic, thermosensitive gel-forming eye drop for effective delivery of sunitinib, a protein kinase inhibitor with activity against the neuroprotective targets dual leucine zipper kinase (DLK) and leucine zipper kinase (LZK), to enhance survival of RGCs after optic nerve injury.	Sunitinib	94-103	mitogen-activated protein kinase kinase kinase 12	Homo sapiens	210-213
33900546-4	2022	Here, we describe a hypotonic, thermosensitive gel-forming eye drop for effective delivery of sunitinib, a protein kinase inhibitor with activity against the neuroprotective targets dual leucine zipper kinase (DLK) and leucine zipper kinase (LZK), to enhance survival of RGCs after optic nerve injury.	Sunitinib	94-103	mitogen-activated protein kinase kinase kinase 13	Homo sapiens	187-208
33854032-0	2021	Correction: ZHX2 drives cell growth and migration via activating MEK/ERK signal and induces Sunitinib resistance by regulating the autophagy in clear cell Renal Cell Carcinoma.	Sunitinib	92-101	zinc fingers and homeoboxes 2	Homo sapiens	12-16
33863648-1	2021	BACKGROUND: Limited data exist on the clinical effectiveness of second-line (2L) vascular endothelial growth factor (receptor) targeted inhibitor (VEGF(R)i) sunitinib after first-line (1L) immuno-oncology (IO) therapy for patients with metastatic renal cell carcinoma (mRCC) in real-world settings.	Sunitinib	157-166	vascular endothelial growth factor A	Homo sapiens	81-145
33936816-0	2021	Sunitinib Combined with Th1 Cytokines Potentiates Apoptosis in Human Breast Cancer Cells and Suppresses Tumor Growth in a Murine Model of HER-2pos Breast Cancer.	Sunitinib	0-9	erb-b2 receptor tyrosine kinase 2	Mus musculus	138-143
33936816-6	2021	Interestingly, sunitinib was found to have a profoundly suppressive effect of T cell"s capacity to secrete IFN-gamma, indicating that in vivo use of this drug may hinder robust Th1 responses.	Sunitinib	15-24	interferon gamma	Homo sapiens	107-116
33647840-4	2021	Compounds 1 and 4 inhibited VEGFR-2 kinase with activity better than or equal to that of sunitinib.	Sunitinib	89-98	kinase insert domain receptor	Homo sapiens	28-35
33732370-9	2021	Therefore, it is proposed that PDGFR inhibitors, including sunitinib and ponatinib, should be applied effectively to treat ER-alpha+ breast cancer.	Sunitinib	59-68	platelet derived growth factor receptor beta	Homo sapiens	31-36
33732370-9	2021	Therefore, it is proposed that PDGFR inhibitors, including sunitinib and ponatinib, should be applied effectively to treat ER-alpha+ breast cancer.	Sunitinib	59-68	estrogen receptor 1	Homo sapiens	123-131
33842334-7	2021	Application of AhR inhibitor DMF could efficiently suppress distant metastasis of renal cancer cells, and improve anticancer effects of sorafenib (Sor)/sunitinib (Sun), which described a promising therapeutic strategy for clinical renal cancer.	Sunitinib	152-161	aryl hydrocarbon receptor	Homo sapiens	15-18
33842334-7	2021	Application of AhR inhibitor DMF could efficiently suppress distant metastasis of renal cancer cells, and improve anticancer effects of sorafenib (Sor)/sunitinib (Sun), which described a promising therapeutic strategy for clinical renal cancer.	Sunitinib	163-166	aryl hydrocarbon receptor	Homo sapiens	15-18
33841146-9	2021	Furthermore, western blot analysis revealed that the expressions levels of phosphorylated IRS-1, Pellino-1, AKT and eNOS were significantly attenuated by sunitinib in rat mesenteric artery tissues and in the sunitinib-treated primary cultured mesenteric artery endothelial cells.	Sunitinib	154-163	insulin receptor substrate 1	Rattus norvegicus	90-95
33841146-9	2021	Furthermore, western blot analysis revealed that the expressions levels of phosphorylated IRS-1, Pellino-1, AKT and eNOS were significantly attenuated by sunitinib in rat mesenteric artery tissues and in the sunitinib-treated primary cultured mesenteric artery endothelial cells.	Sunitinib	154-163	pellino E3 ubiquitin protein ligase 1	Rattus norvegicus	97-106
33841146-9	2021	Furthermore, western blot analysis revealed that the expressions levels of phosphorylated IRS-1, Pellino-1, AKT and eNOS were significantly attenuated by sunitinib in rat mesenteric artery tissues and in the sunitinib-treated primary cultured mesenteric artery endothelial cells.	Sunitinib	154-163	AKT serine/threonine kinase 1	Rattus norvegicus	108-111
33841146-9	2021	Furthermore, western blot analysis revealed that the expressions levels of phosphorylated IRS-1, Pellino-1, AKT and eNOS were significantly attenuated by sunitinib in rat mesenteric artery tissues and in the sunitinib-treated primary cultured mesenteric artery endothelial cells.	Sunitinib	154-163	nitric oxide synthase 3	Rattus norvegicus	116-120
33841146-9	2021	Furthermore, western blot analysis revealed that the expressions levels of phosphorylated IRS-1, Pellino-1, AKT and eNOS were significantly attenuated by sunitinib in rat mesenteric artery tissues and in the sunitinib-treated primary cultured mesenteric artery endothelial cells.	Sunitinib	208-217	insulin receptor substrate 1	Rattus norvegicus	90-95
33841146-9	2021	Furthermore, western blot analysis revealed that the expressions levels of phosphorylated IRS-1, Pellino-1, AKT and eNOS were significantly attenuated by sunitinib in rat mesenteric artery tissues and in the sunitinib-treated primary cultured mesenteric artery endothelial cells.	Sunitinib	208-217	nitric oxide synthase 3	Rattus norvegicus	116-120
33841146-11	2021	Moreover, sunitinib-induced decrease in the expression levels of phosphorylated AKT and eNOS was further reduced by knocking down of Pellino-1 in MAECs.	Sunitinib	10-19	AKT serine/threonine kinase 1	Rattus norvegicus	80-83
33841146-11	2021	Moreover, sunitinib-induced decrease in the expression levels of phosphorylated AKT and eNOS was further reduced by knocking down of Pellino-1 in MAECs.	Sunitinib	10-19	nitric oxide synthase 3	Rattus norvegicus	88-92
33841146-11	2021	Moreover, sunitinib-induced decrease in the expression levels of phosphorylated AKT and eNOS was further reduced by knocking down of Pellino-1 in MAECs.	Sunitinib	10-19	pellino E3 ubiquitin protein ligase 1	Rattus norvegicus	133-142
33841146-12	2021	Our results suggest that sunitinib causes vascular dysfunction and hypertension, which are associated with insulin resistance- and Pellino-1-mediated inhibition of AKT/eNOS/NO signaling.	Sunitinib	25-34	pellino E3 ubiquitin protein ligase 1	Rattus norvegicus	131-140
33841146-12	2021	Our results suggest that sunitinib causes vascular dysfunction and hypertension, which are associated with insulin resistance- and Pellino-1-mediated inhibition of AKT/eNOS/NO signaling.	Sunitinib	25-34	AKT serine/threonine kinase 1	Rattus norvegicus	164-167
33841146-12	2021	Our results suggest that sunitinib causes vascular dysfunction and hypertension, which are associated with insulin resistance- and Pellino-1-mediated inhibition of AKT/eNOS/NO signaling.	Sunitinib	25-34	nitric oxide synthase 3	Rattus norvegicus	168-172
33976736-11	2021	C2 and C3 were corresponding to a better survival outcome and presented a low drug sensitivity to sorafenib and sunitinib.	Sunitinib	112-121	complement C2	Homo sapiens	0-9
32530390-4	2021	The cells were treated with an inhibitor of either ACK1 (dasatinib or sunitinib) or AKT (MK-2206 or GDC-0068), and the optimal concentrations of the two yielding synergistic tumor-killing effects were determined by applying the Chou-Talalay equation for drug combinations.	Sunitinib	70-79	tyrosine kinase non receptor 2	Homo sapiens	51-55
31331862-10	2021	CONCLUSIONS: Treatment with further TKIs or mTOR inhibitors for mRCC patients primarily refractory to first-line sunitinib in the observed time period achieved very minimal benefit, suggesting avoiding TKI rechallenge and possibly preferring alternative strategies, such as immune checkpoint inhibitors, after PD to a treatment line including a TKI in this setting.	Sunitinib	113-122	mechanistic target of rapamycin kinase	Homo sapiens	44-48
33732370-4	2021	To block the PDGF-BB signaling pathway, PDGFR inhibitors (sunitinib or ponatinib) were employed.	Sunitinib	58-67	platelet derived growth factor receptor beta	Homo sapiens	40-45
33723657-0	2021	Is there association between clinically relevant toxicities of pazopanib and sunitinib with the use of weak CYP3A4 and P-gp inhibitors?	Sunitinib	77-86	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	108-114
33723657-0	2021	Is there association between clinically relevant toxicities of pazopanib and sunitinib with the use of weak CYP3A4 and P-gp inhibitors?	Sunitinib	77-86	phosphoglycolate phosphatase	Homo sapiens	119-123
33135264-9	2021	Thus, sunitinib reduces the expression of KRT6A and SERPINB1 by inhibiting the ERK1/2 and p38 MAPK signaling pathways in the skin model.	Sunitinib	6-15	keratin 6A	Homo sapiens	42-47
33722287-11	2021	Sunitinib (SNT)-induced upregulation of glial fibrillary acidic protein (GFAP) (astrocyte) and ionized calcium-binding adaptor molecule 1 (Iba-1) (microglia) in the ipsilateral L4-5 dorsal and ventral horn relative to the contralateral side.	Sunitinib	0-9	glial fibrillary acidic protein	Homo sapiens	40-71
33722287-11	2021	Sunitinib (SNT)-induced upregulation of glial fibrillary acidic protein (GFAP) (astrocyte) and ionized calcium-binding adaptor molecule 1 (Iba-1) (microglia) in the ipsilateral L4-5 dorsal and ventral horn relative to the contralateral side.	Sunitinib	0-9	glial fibrillary acidic protein	Homo sapiens	73-77
33722287-11	2021	Sunitinib (SNT)-induced upregulation of glial fibrillary acidic protein (GFAP) (astrocyte) and ionized calcium-binding adaptor molecule 1 (Iba-1) (microglia) in the ipsilateral L4-5 dorsal and ventral horn relative to the contralateral side.	Sunitinib	0-9	allograft inflammatory factor 1	Homo sapiens	139-144
33859753-10	2021	Moreover, PRMT1 inhibition by DCPT1061 not only inhibited tumor growth but also sensitized ccRCC to sunitinib treatment in vivo by attenuating sunitinib-induced upregulation of LCN2-AKT-RB signaling.	Sunitinib	100-109	protein arginine methyltransferase 1	Homo sapiens	10-15
33859753-10	2021	Moreover, PRMT1 inhibition by DCPT1061 not only inhibited tumor growth but also sensitized ccRCC to sunitinib treatment in vivo by attenuating sunitinib-induced upregulation of LCN2-AKT-RB signaling.	Sunitinib	143-152	protein arginine methyltransferase 1	Homo sapiens	10-15
33859753-10	2021	Moreover, PRMT1 inhibition by DCPT1061 not only inhibited tumor growth but also sensitized ccRCC to sunitinib treatment in vivo by attenuating sunitinib-induced upregulation of LCN2-AKT-RB signaling.	Sunitinib	143-152	lipocalin 2	Homo sapiens	177-181
33707524-9	2021	In parallel, in rats exposed to sunitinib, glomerular thrombomodulin was upregulated in a dose-dependent manner, and the upregulation of glomerular thrombomodulin preceded the onset of histopathological changes.	Sunitinib	32-41	thrombomodulin	Rattus norvegicus	54-68
33707524-9	2021	In parallel, in rats exposed to sunitinib, glomerular thrombomodulin was upregulated in a dose-dependent manner, and the upregulation of glomerular thrombomodulin preceded the onset of histopathological changes.	Sunitinib	32-41	thrombomodulin	Rattus norvegicus	148-162
33707524-10	2021	Selective ETAR blockade, but not dual ETA/BR blockade, normalised the sunitinib-induced increase in thrombomodulin expression and albuminuria.	Sunitinib	70-79	endothelin receptor type A	Homo sapiens	10-14
33707524-10	2021	Selective ETAR blockade, but not dual ETA/BR blockade, normalised the sunitinib-induced increase in thrombomodulin expression and albuminuria.	Sunitinib	70-79	thrombomodulin	Rattus norvegicus	100-114
33307872-6	2021	Sunitinib and regorafenib are inhibitors of multiple tyrosine kinases, including KIT, PDGFRalpha, PDGFRbeta, and VEGFRs, and are approved for the management of imatinib- and imatinib/sunitinib-refractory GIST patients, respectively.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-84
33307872-6	2021	Sunitinib and regorafenib are inhibitors of multiple tyrosine kinases, including KIT, PDGFRalpha, PDGFRbeta, and VEGFRs, and are approved for the management of imatinib- and imatinib/sunitinib-refractory GIST patients, respectively.	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	86-96
33307872-6	2021	Sunitinib and regorafenib are inhibitors of multiple tyrosine kinases, including KIT, PDGFRalpha, PDGFRbeta, and VEGFRs, and are approved for the management of imatinib- and imatinib/sunitinib-refractory GIST patients, respectively.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	98-107
33135264-0	2021	Sunitinib decreases the expression of KRT6A and SERPINB1 in 3D human epidermal models.	Sunitinib	0-9	keratin 6A	Homo sapiens	38-43
33135264-0	2021	Sunitinib decreases the expression of KRT6A and SERPINB1 in 3D human epidermal models.	Sunitinib	0-9	serpin family B member 1	Homo sapiens	48-56
33135264-5	2021	Sunitinib treatment significantly decreased the expression of SERPINB1 and KRT6A in the immunohistochemical staining of the 3D epidermal model.	Sunitinib	0-9	serpin family B member 1	Homo sapiens	62-70
33135264-5	2021	Sunitinib treatment significantly decreased the expression of SERPINB1 and KRT6A in the immunohistochemical staining of the 3D epidermal model.	Sunitinib	0-9	keratin 6A	Homo sapiens	75-80
33135264-6	2021	In PSVK1 cells, but not in normal human epidermal keratinocyte cells, both of which are human normal keratinocyte cell lines, sunitinib decreased the expression of KRT6A with a concomitant decrease in levels of phosphorylated extracellular signal-regulated kinases (ERK)1/2 and phosphorylated p38 mitogen-activated protein kinase (MAPK).	Sunitinib	126-135	keratin 6A	Homo sapiens	164-169
33135264-6	2021	In PSVK1 cells, but not in normal human epidermal keratinocyte cells, both of which are human normal keratinocyte cell lines, sunitinib decreased the expression of KRT6A with a concomitant decrease in levels of phosphorylated extracellular signal-regulated kinases (ERK)1/2 and phosphorylated p38 mitogen-activated protein kinase (MAPK).	Sunitinib	126-135	mitogen-activated protein kinase 3	Homo sapiens	266-273
33135264-6	2021	In PSVK1 cells, but not in normal human epidermal keratinocyte cells, both of which are human normal keratinocyte cell lines, sunitinib decreased the expression of KRT6A with a concomitant decrease in levels of phosphorylated extracellular signal-regulated kinases (ERK)1/2 and phosphorylated p38 mitogen-activated protein kinase (MAPK).	Sunitinib	126-135	mitogen-activated protein kinase 14	Homo sapiens	293-329
33135264-8	2021	Sunitinib-induced decrease in KRT6A expression was suppressed by the inhibition of glycogen synthase kinase-3beta by enhancing ERK1/2 and p38 MAPK phosphorylation.	Sunitinib	0-9	keratin 6A	Homo sapiens	30-35
33135264-9	2021	Thus, sunitinib reduces the expression of KRT6A and SERPINB1 by inhibiting the ERK1/2 and p38 MAPK signaling pathways in the skin model.	Sunitinib	6-15	serpin family B member 1	Homo sapiens	52-60
33135264-8	2021	Sunitinib-induced decrease in KRT6A expression was suppressed by the inhibition of glycogen synthase kinase-3beta by enhancing ERK1/2 and p38 MAPK phosphorylation.	Sunitinib	0-9	glycogen synthase kinase 3 beta	Homo sapiens	83-113
33135264-8	2021	Sunitinib-induced decrease in KRT6A expression was suppressed by the inhibition of glycogen synthase kinase-3beta by enhancing ERK1/2 and p38 MAPK phosphorylation.	Sunitinib	0-9	mitogen-activated protein kinase 3	Homo sapiens	127-133
33135264-9	2021	Thus, sunitinib reduces the expression of KRT6A and SERPINB1 by inhibiting the ERK1/2 and p38 MAPK signaling pathways in the skin model.	Sunitinib	6-15	mitogen-activated protein kinase 3	Homo sapiens	79-85
33593885-14	2021	CONCLUSIONS: In patients with metastatic non-clear cell RCC, we identified several poor prognosis angiokines and immunomodulatory chemokines during treatment with sunitinib or everolimus, particularly OPN.	Sunitinib	163-172	secreted phosphoprotein 1	Homo sapiens	201-204
33455080-0	2021	Dysregulation of the Sirt5/IDH2 axis contributes to sunitinib resistance in human renal cancer cells.	Sunitinib	52-61	sirtuin 5	Homo sapiens	21-26
33455080-0	2021	Dysregulation of the Sirt5/IDH2 axis contributes to sunitinib resistance in human renal cancer cells.	Sunitinib	52-61	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	27-31
33455080-1	2021	Sunitinib (Sun), a tyrosine kinase inhibitor of vascular endothelial growth factor receptor (VEGFR), is the standard first-line treatment against advanced clear cell renal cell carcinoma (ccRCC), but resistance to therapy is inevitable.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	48-91
33455080-1	2021	Sunitinib (Sun), a tyrosine kinase inhibitor of vascular endothelial growth factor receptor (VEGFR), is the standard first-line treatment against advanced clear cell renal cell carcinoma (ccRCC), but resistance to therapy is inevitable.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	93-98
33455080-1	2021	Sunitinib (Sun), a tyrosine kinase inhibitor of vascular endothelial growth factor receptor (VEGFR), is the standard first-line treatment against advanced clear cell renal cell carcinoma (ccRCC), but resistance to therapy is inevitable.	Sunitinib	0-3	kinase insert domain receptor	Homo sapiens	48-91
33455080-1	2021	Sunitinib (Sun), a tyrosine kinase inhibitor of vascular endothelial growth factor receptor (VEGFR), is the standard first-line treatment against advanced clear cell renal cell carcinoma (ccRCC), but resistance to therapy is inevitable.	Sunitinib	0-3	kinase insert domain receptor	Homo sapiens	93-98
33717062-10	2021	Results: Along with its anti-proliferative and direct pro-apoptotic effect on sarcoma cell lines, sunitinib prompted PD-L1 upregulation on sarcoma cells.	Sunitinib	98-107	CD274 molecule	Homo sapiens	117-122
33717062-11	2021	Interestingly, sunitinib-treated sarcoma cells drive DCs to full maturation and increase their capacity to induce sarcoma-reactive T cells to produce IFN-gamma.	Sunitinib	15-24	interferon gamma	Sus scrofa	150-159
33717062-15	2021	Indeed, PD-1 blockade by nivolumab synergized with sunitinib in inducing IFN-gamma-producing effector T cells.	Sunitinib	51-60	interferon gamma	Sus scrofa	73-82
33717062-16	2021	Conclusions: Taken together, our in vitro data indicate that the treatment of sarcoma cells with sunitinib can exert significant changes on immune cell subsets toward immune activation, leading to DC-based cross-priming of IFN-gamma-producing effector T cells and reduced Treg induction.	Sunitinib	97-106	interferon gamma	Sus scrofa	223-232
33592176-17	2021	INTERPRETATION: Cabozantinib treatment resulted in significantly longer PFS compared with sunitinib in patients with metastatic PRCC.	Sunitinib	90-99	proline rich mitotic checkpoint control factor	Homo sapiens	128-132
33078449-7	2021	The docking study of the most potent compound against VEGFR-2 with the best-scored conformations displayed a binding affinity (-9.5 kcal/mol) comparable with the drug sunitinib (-9.9 kcal/mol) and exhibited that tighter interactions at the active adenosine triphosphate site might be responsible for anticancer potency.	Sunitinib	167-176	kinase insert domain receptor	Homo sapiens	54-61
33547392-8	2021	High Plk1 expression conferred a resistant phenotype of ccRCC to targeted therapeutics such as sunitinib, in vitro, in vivo, and in metastatic ccRCC patients.	Sunitinib	95-104	polo like kinase 1	Homo sapiens	5-9
33597889-7	2021	In vivo studies further confirmed that crizotinib and sunitinib decreased mitochondrial membrane potential and activated apoptosis-associated proteins (cleaved-PARP, cleaved caspase3, cytochrome c, Bcl2 and Bax).	Sunitinib	54-63	collagen type XI alpha 2 chain	Homo sapiens	160-164
33634984-0	2021	Epigenome screening highlights that JMJD6 confers an epigenetic vulnerability and mediates sunitinib sensitivity in renal cell carcinoma.	Sunitinib	91-100	jumonji domain containing 6, arginine demethylase and lysine hydroxylase	Homo sapiens	36-41
33634984-8	2021	Given the probable overlapped crosstalk between JMJD6 signature and tyrosine kinase inhibitors downstream targets, targeting JMJD6 sensitized RCC to sunitinib and was synergistic when they were combined together.	Sunitinib	149-158	jumonji domain containing 6, arginine demethylase and lysine hydroxylase	Homo sapiens	125-130
33597889-0	2021	Crizotinib and Sunitinib Induce Hepatotoxicity and Mitochondrial Apoptosis in L02 Cells via ROS and Nrf2 Signaling Pathway.	Sunitinib	15-24	NFE2 like bZIP transcription factor 2	Homo sapiens	100-104
33598481-12	2020	Both sunitinib and imatinib pre-treatment increased Angiotensin II-induced intracellular Ca2+ mobilization, with only sunitinib resulting in a significant effect and also causing increased CaMKII activation via oxidation.	Sunitinib	5-14	angiotensinogen	Rattus norvegicus	52-66
33597889-7	2021	In vivo studies further confirmed that crizotinib and sunitinib decreased mitochondrial membrane potential and activated apoptosis-associated proteins (cleaved-PARP, cleaved caspase3, cytochrome c, Bcl2 and Bax).	Sunitinib	54-63	caspase 3	Homo sapiens	174-182
33598481-16	2020	Sunitinib caused a significant increase in Angiotensin II-induced intracellular Ca2+ mobilization and both TKIs caused increased mitochondrial superoxide production.	Sunitinib	0-9	angiotensinogen	Rattus norvegicus	43-57
33597889-7	2021	In vivo studies further confirmed that crizotinib and sunitinib decreased mitochondrial membrane potential and activated apoptosis-associated proteins (cleaved-PARP, cleaved caspase3, cytochrome c, Bcl2 and Bax).	Sunitinib	54-63	cytochrome c, somatic	Homo sapiens	184-196
33597889-7	2021	In vivo studies further confirmed that crizotinib and sunitinib decreased mitochondrial membrane potential and activated apoptosis-associated proteins (cleaved-PARP, cleaved caspase3, cytochrome c, Bcl2 and Bax).	Sunitinib	54-63	BCL2 apoptosis regulator	Homo sapiens	198-202
33597889-7	2021	In vivo studies further confirmed that crizotinib and sunitinib decreased mitochondrial membrane potential and activated apoptosis-associated proteins (cleaved-PARP, cleaved caspase3, cytochrome c, Bcl2 and Bax).	Sunitinib	54-63	BCL2 associated X, apoptosis regulator	Homo sapiens	207-210
33597889-8	2021	Furthermore, mechanistic investigations demonstrated that crizotinib and sunitinib accumulated ROS and inhibited Nrf2 signaling, and that ROS scavenger NAC and Nrf2 agonist tBHQ alleviated the extent of cell damage and the mitochondrial apoptosis during crizotinib- and sunitinib-induced hepatotoxicity in L02 cells.	Sunitinib	73-82	NFE2 like bZIP transcription factor 2	Homo sapiens	113-117
33597889-8	2021	Furthermore, mechanistic investigations demonstrated that crizotinib and sunitinib accumulated ROS and inhibited Nrf2 signaling, and that ROS scavenger NAC and Nrf2 agonist tBHQ alleviated the extent of cell damage and the mitochondrial apoptosis during crizotinib- and sunitinib-induced hepatotoxicity in L02 cells.	Sunitinib	270-279	X-linked Kx blood group	Homo sapiens	152-155
33597889-8	2021	Furthermore, mechanistic investigations demonstrated that crizotinib and sunitinib accumulated ROS and inhibited Nrf2 signaling, and that ROS scavenger NAC and Nrf2 agonist tBHQ alleviated the extent of cell damage and the mitochondrial apoptosis during crizotinib- and sunitinib-induced hepatotoxicity in L02 cells.	Sunitinib	270-279	NFE2 like bZIP transcription factor 2	Homo sapiens	160-164
33657773-0	2021	[Gas-Producing Splenic Abscess after Spleen Metastasis of Left Renal Cell Carcinoma Spleen Metastasis Successfully Treated with Sunitinib].	Sunitinib	128-137	galactosamine (N-acetyl)-6-sulfatase	Homo sapiens	1-4
33597889-9	2021	Collectively, these findings indicated that NAC and tBHQ play the crucial roles in crizotinib- and sunitinib-induced mitochondrial apoptosis via the regulation of oxidative stress.	Sunitinib	99-108	X-linked Kx blood group	Homo sapiens	44-47
33376527-10	2021	rs191188930 on platelet-derived growth factor receptor (PDGFR) alpha was associated with numerous TKI drugs, including sunitinib, pazopanib, sorafenib, dasatinib and nilotinib.	Sunitinib	119-128	platelet derived growth factor receptor alpha	Homo sapiens	56-68
33410111-0	2021	Guanabenz Sensitizes Glioblastoma Cells to Sunitinib by Inhibiting GADD34-Mediated Autophagic Signaling.	Sunitinib	43-52	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	67-73
33410111-10	2021	Guanabenz, an alpha2-selective adrenergic agonist and GADD34 functional inhibitor, was identified to enhance the efficacy of sunitinib by targeting GADD34-induced protective autophagy in glioblastoma cells, TMZ-resistant cells, hypoxic cultured cells, sphere-forming cells, and colony formation abilities.	Sunitinib	125-134	glycoprotein hormone subunit alpha 2	Homo sapiens	14-20
33410111-8	2021	Growth arrest and DNA damage-inducible protein (GADD) 34 was identified as a candidate involved in sunitinib-promoted autophagy through activating p38-mitogen-activated protein kinase (MAPK) signaling.	Sunitinib	99-108	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	0-56
33410111-10	2021	Guanabenz, an alpha2-selective adrenergic agonist and GADD34 functional inhibitor, was identified to enhance the efficacy of sunitinib by targeting GADD34-induced protective autophagy in glioblastoma cells, TMZ-resistant cells, hypoxic cultured cells, sphere-forming cells, and colony formation abilities.	Sunitinib	125-134	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	54-60
33410111-10	2021	Guanabenz, an alpha2-selective adrenergic agonist and GADD34 functional inhibitor, was identified to enhance the efficacy of sunitinib by targeting GADD34-induced protective autophagy in glioblastoma cells, TMZ-resistant cells, hypoxic cultured cells, sphere-forming cells, and colony formation abilities.	Sunitinib	125-134	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	148-154
33410111-12	2021	Taken together, the sunitinib therapy combined with guanabenz in the inhibition of GADD34-enhanced protective autophagy may provide a new therapeutic strategy for glioblastoma.	Sunitinib	20-29	protein phosphatase 1, regulatory subunit 15A	Mus musculus	83-89
33410111-8	2021	Growth arrest and DNA damage-inducible protein (GADD) 34 was identified as a candidate involved in sunitinib-promoted autophagy through activating p38-mitogen-activated protein kinase (MAPK) signaling.	Sunitinib	99-108	mitogen-activated protein kinase 14	Homo sapiens	147-183
33410111-8	2021	Growth arrest and DNA damage-inducible protein (GADD) 34 was identified as a candidate involved in sunitinib-promoted autophagy through activating p38-mitogen-activated protein kinase (MAPK) signaling.	Sunitinib	99-108	mitogen-activated protein kinase 14	Homo sapiens	185-189
33410111-9	2021	Higher GADD34 levels predicted poor survival of glioblastoma patients and induced autophagy formation in desensitizing sunitinib cytotoxicity.	Sunitinib	119-128	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	7-13
33309571-11	2021	Among individual VEGFR-TKIs, Sunitinib (OR = 3.31, 95% CI 2.34-4.69) and Regorafenib (OR = 2.92, 95% CI 1.50-5.71) were associated with higher risk of hemorrhagic events in comparison to placebo.	Sunitinib	29-38	kinase insert domain receptor	Homo sapiens	17-22
33170322-1	2021	The objective of present work is to evaluate possible interactions among four clinically-used vascular epidermal growth factor receptor (VEGFR)-tyrosine kinase inhibitors (TKIs), including apatinib, cabozantinib, sorafenib, and sunitinib, with epidermal growth factor receptor (EGFR)-TKI gefitinib.	Sunitinib	228-237	kinase insert domain receptor	Homo sapiens	94-135
33170322-1	2021	The objective of present work is to evaluate possible interactions among four clinically-used vascular epidermal growth factor receptor (VEGFR)-tyrosine kinase inhibitors (TKIs), including apatinib, cabozantinib, sorafenib, and sunitinib, with epidermal growth factor receptor (EGFR)-TKI gefitinib.	Sunitinib	228-237	kinase insert domain receptor	Homo sapiens	137-142
33170322-1	2021	The objective of present work is to evaluate possible interactions among four clinically-used vascular epidermal growth factor receptor (VEGFR)-tyrosine kinase inhibitors (TKIs), including apatinib, cabozantinib, sorafenib, and sunitinib, with epidermal growth factor receptor (EGFR)-TKI gefitinib.	Sunitinib	228-237	epidermal growth factor receptor	Homo sapiens	103-135
33191180-0	2021	Sunitinib malate inhibits intestinal tumor development in male ApcMin/+ mice by down-regulating inflammation-related factors with suppressing beta-cateinin/c-Myc pathway and re-balancing Bcl-6 and Caspase-3.	Sunitinib	0-16	B cell leukemia/lymphoma 6	Mus musculus	187-192
33191180-0	2021	Sunitinib malate inhibits intestinal tumor development in male ApcMin/+ mice by down-regulating inflammation-related factors with suppressing beta-cateinin/c-Myc pathway and re-balancing Bcl-6 and Caspase-3.	Sunitinib	0-16	caspase 3	Mus musculus	197-206
33191180-9	2021	These results suggest that sunitinib malate can significantly improve the survival status and inhibit intestinal tumor development in male ApcMin/+ mice, through inhibiting inflammation-related factors, while suppressing beta-cateinin/c-Myc pathway and re-balancing protein levels of Bcl-6 and Caspase-3.	Sunitinib	27-43	B cell leukemia/lymphoma 6	Mus musculus	284-289
33191180-9	2021	These results suggest that sunitinib malate can significantly improve the survival status and inhibit intestinal tumor development in male ApcMin/+ mice, through inhibiting inflammation-related factors, while suppressing beta-cateinin/c-Myc pathway and re-balancing protein levels of Bcl-6 and Caspase-3.	Sunitinib	27-43	caspase 3	Mus musculus	294-303
33179075-6	2021	The results of the present study demonstrated that sunitinib reduced PARP1 expression and proliferation of melanoma cells.	Sunitinib	51-60	poly(ADP-ribose) polymerase 1	Homo sapiens	69-74
33179075-7	2021	Notably, one of the PARPis, veliparib, reversed the inhibitory effect of sunitinib on PARP1 expression and proliferation, indicating that inhibition of PARP1 enzyme activity by PARPi may be different from the inhibition of PARP1 expression in melanoma cell biological function.	Sunitinib	73-82	poly(ADP-ribose) polymerase 1	Homo sapiens	86-91
33179075-7	2021	Notably, one of the PARPis, veliparib, reversed the inhibitory effect of sunitinib on PARP1 expression and proliferation, indicating that inhibition of PARP1 enzyme activity by PARPi may be different from the inhibition of PARP1 expression in melanoma cell biological function.	Sunitinib	73-82	poly(ADP-ribose) polymerase 1	Homo sapiens	152-157
33179075-7	2021	Notably, one of the PARPis, veliparib, reversed the inhibitory effect of sunitinib on PARP1 expression and proliferation, indicating that inhibition of PARP1 enzyme activity by PARPi may be different from the inhibition of PARP1 expression in melanoma cell biological function.	Sunitinib	73-82	poly(ADP-ribose) polymerase 1	Homo sapiens	152-157
33374949-6	2020	The established sunitinib-resistant RCC cell line demonstrated significantly desuppressed protein kinase B (Akt) and mesenchymal-to-epithelial transition (MET) phosphorylation compared with the control RCC cell line under sunitinib exposure.	Sunitinib	16-25	thymoma viral proto-oncogene 1	Mus musculus	108-111
33374949-8	2020	Particularly, glutamine transporter (SLC1A5) expression was significantly increased in sunitinib-resistant RCC cells compared with control cells.	Sunitinib	87-96	solute carrier family 1 (neutral amino acid transporter), member 5	Mus musculus	37-43
33145941-0	2020	TFE3-PD-L1 axis is pivotal for sunitinib resistance in clear cell renal cell carcinoma.	Sunitinib	31-40	transcription factor binding to IGHM enhancer 3	Homo sapiens	0-4
32947227-0	2020	Novel 2-indolinone thiazole hybrids as sunitinib analogues: Design, synthesis, and potent VEGFR-2 inhibition with potential anti-renal cancer activity.	Sunitinib	39-48	kinase insert domain receptor	Homo sapiens	90-97
32947227-1	2020	Novel 2-indolinone thiazole hybrids were designed and synthesized as VEGFR-2 inhibitors based on sunitinib, an FDA-approved anticancer drug.	Sunitinib	97-106	kinase insert domain receptor	Homo sapiens	69-76
32947227-4	2020	All tested compounds exhibited a potent submicromolar inhibition of VEGFR-2 kinase with IC50 values ranging from 0.067 to 0.422 muM, relative to sunitinib reference drug (IC50 = 0.075 +- 0.002 muM).	Sunitinib	145-154	kinase insert domain receptor	Homo sapiens	68-75
32947227-6	2020	Compound 13b stood out as the most potent against VEGFR-2 showing IC50 value of 0.067 +- 0.002 muM, lower than that of sunitinib.	Sunitinib	119-128	kinase insert domain receptor	Homo sapiens	50-57
33038552-6	2020	Moreover, compounds 5a, 8c, 9d, 12c were equipotent to sunitinib against VEGFR-2 kinase.	Sunitinib	55-64	kinase insert domain receptor	Homo sapiens	73-80
33022096-7	2020	RESULTS: Across all utility combinations tested, Q-TWiST was found to be longer with cabozantinib versus sunitinib (range of differences, +24 days to +137 days).	Sunitinib	105-114	twist family bHLH transcription factor 1	Homo sapiens	51-56
32885522-4	2020	Sunitinib is the first oral indolin-2-one derivative marketed as a VEGFR inhibitor in the treatment of renal cell carcinoma and gastrointestinal stromal tumors.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	67-72
33145941-2	2020	Here, we investigated whether the resistance to sunitinib (Sun), the standard treatment for metastatic ccRCC, is due to up-regulation of programmed death ligand 1 (PD-L1) by the transcription factor E3 (TFE3).	Sunitinib	59-62	transcription factor binding to IGHM enhancer 3	Homo sapiens	178-201
33145941-2	2020	Here, we investigated whether the resistance to sunitinib (Sun), the standard treatment for metastatic ccRCC, is due to up-regulation of programmed death ligand 1 (PD-L1) by the transcription factor E3 (TFE3).	Sunitinib	59-62	transcription factor binding to IGHM enhancer 3	Homo sapiens	203-207
33145941-0	2020	TFE3-PD-L1 axis is pivotal for sunitinib resistance in clear cell renal cell carcinoma.	Sunitinib	31-40	CD274 molecule	Homo sapiens	5-10
33145941-2	2020	Here, we investigated whether the resistance to sunitinib (Sun), the standard treatment for metastatic ccRCC, is due to up-regulation of programmed death ligand 1 (PD-L1) by the transcription factor E3 (TFE3).	Sunitinib	48-57	CD274 molecule	Homo sapiens	137-162
33145941-2	2020	Here, we investigated whether the resistance to sunitinib (Sun), the standard treatment for metastatic ccRCC, is due to up-regulation of programmed death ligand 1 (PD-L1) by the transcription factor E3 (TFE3).	Sunitinib	48-57	CD274 molecule	Homo sapiens	164-169
33145941-2	2020	Here, we investigated whether the resistance to sunitinib (Sun), the standard treatment for metastatic ccRCC, is due to up-regulation of programmed death ligand 1 (PD-L1) by the transcription factor E3 (TFE3).	Sunitinib	48-57	transcription factor binding to IGHM enhancer 3	Homo sapiens	178-201
33145941-2	2020	Here, we investigated whether the resistance to sunitinib (Sun), the standard treatment for metastatic ccRCC, is due to up-regulation of programmed death ligand 1 (PD-L1) by the transcription factor E3 (TFE3).	Sunitinib	48-57	transcription factor binding to IGHM enhancer 3	Homo sapiens	203-207
33145941-2	2020	Here, we investigated whether the resistance to sunitinib (Sun), the standard treatment for metastatic ccRCC, is due to up-regulation of programmed death ligand 1 (PD-L1) by the transcription factor E3 (TFE3).	Sunitinib	59-62	CD274 molecule	Homo sapiens	137-162
33145941-2	2020	Here, we investigated whether the resistance to sunitinib (Sun), the standard treatment for metastatic ccRCC, is due to up-regulation of programmed death ligand 1 (PD-L1) by the transcription factor E3 (TFE3).	Sunitinib	59-62	CD274 molecule	Homo sapiens	164-169
33261151-9	2020	In addition, we inoculated 786-O cells to generate xenografted mice to evaluate the anti-tumor activity of AJ-HP-beta-CD in vivo and found that AJ-HP-beta-CD had a better tumor inhibitory effect than that of docetaxel and sunitinib in terms of tumor growth and endpoint tumor weight.	Sunitinib	222-231	adrenocortical dysplasia	Mus musculus	150-157
33510997-0	2021	The Beneficial Role of Sunitinib in Tumor Immune Surveillance by Regulating Tumor PD-L1.	Sunitinib	23-32	CD274 molecule	Homo sapiens	82-87
33510997-4	2021	Mechanistically, it is discovered that Sunitinib regulates the stability of tumor PD-L1 via p62, that p62 can bind to PD-L1 and specifically promote its translocation into autophagic lysosome for degradation.	Sunitinib	39-48	CD274 molecule	Homo sapiens	82-87
33510997-4	2021	Mechanistically, it is discovered that Sunitinib regulates the stability of tumor PD-L1 via p62, that p62 can bind to PD-L1 and specifically promote its translocation into autophagic lysosome for degradation.	Sunitinib	39-48	nucleoporin 62	Homo sapiens	92-95
33510997-4	2021	Mechanistically, it is discovered that Sunitinib regulates the stability of tumor PD-L1 via p62, that p62 can bind to PD-L1 and specifically promote its translocation into autophagic lysosome for degradation.	Sunitinib	39-48	CD274 molecule	Homo sapiens	118-123
33510997-5	2021	Preclinically, Sunitinib shows a synergistic antitumor effect with cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) monoclonal antibody (mAb) in melanoma and nonsmall cell lung cancer (NSCLC) immune competent mice by promoting the tumor-infiltrating lymphocytes activity.	Sunitinib	15-24	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	112-118
33510997-7	2021	Taken together, by utilizing rigorous computational analysis, functional characterization in vitro and in vivo, and neoadjuvent clinical trial, a novel molecular mechanism is revealed regarding the regulation of PD-L1 via p62, thus providing a novel therapeutic strategy by the combination treatment of CTLA-4 with Sunitinib.	Sunitinib	315-324	CD274 molecule	Homo sapiens	212-217
33510997-7	2021	Taken together, by utilizing rigorous computational analysis, functional characterization in vitro and in vivo, and neoadjuvent clinical trial, a novel molecular mechanism is revealed regarding the regulation of PD-L1 via p62, thus providing a novel therapeutic strategy by the combination treatment of CTLA-4 with Sunitinib.	Sunitinib	315-324	nucleoporin 62	Homo sapiens	222-225
33510997-7	2021	Taken together, by utilizing rigorous computational analysis, functional characterization in vitro and in vivo, and neoadjuvent clinical trial, a novel molecular mechanism is revealed regarding the regulation of PD-L1 via p62, thus providing a novel therapeutic strategy by the combination treatment of CTLA-4 with Sunitinib.	Sunitinib	315-324	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	303-309
33068284-0	2020	Sunitinib in Patients with Metastatic Colorectal Cancer (mCRC) with FLT-3 Amplification: Results from the Targeted Agent and Profiling Utilization Registry (TAPUR) Study.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	68-73
33068284-2	2020	Sunitinib is an oral multikinase inhibitor of FMS-like tyrosine kinase-3 (FLT-3), among other targets.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	46-72
33068284-2	2020	Sunitinib is an oral multikinase inhibitor of FMS-like tyrosine kinase-3 (FLT-3), among other targets.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	74-79
33068284-3	2020	Results from a cohort of patients with metastatic colorectal cancer (mCRC) with FLT-3 amplification treated with sunitinib are reported.	Sunitinib	113-122	fms related receptor tyrosine kinase 3	Homo sapiens	80-85
33068284-4	2020	OBJECTIVE: This study aimed to investigate whether patients with mCRC with FLT-3 amplification would be responsive to sunitinib, an oral multikinase inhibitor.	Sunitinib	118-127	fms related receptor tyrosine kinase 3	Homo sapiens	75-80
33201837-0	2020	Low DAPK1 expression correlates with poor prognosis and sunitinib resistance in clear cell renal cell carcinoma.	Sunitinib	56-65	death associated protein kinase 1	Homo sapiens	4-9
33218150-0	2020	Sunitinib-Containing Carborane Pharmacophore with the Ability to Inhibit Tyrosine Kinases Receptors FLT3, KIT and PDGFR-beta, Exhibits Powerful In Vivo Anti-Glioblastoma Activity.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	100-104
33218150-0	2020	Sunitinib-Containing Carborane Pharmacophore with the Ability to Inhibit Tyrosine Kinases Receptors FLT3, KIT and PDGFR-beta, Exhibits Powerful In Vivo Anti-Glioblastoma Activity.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	106-109
33218150-0	2020	Sunitinib-Containing Carborane Pharmacophore with the Ability to Inhibit Tyrosine Kinases Receptors FLT3, KIT and PDGFR-beta, Exhibits Powerful In Vivo Anti-Glioblastoma Activity.	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	114-124
33212804-0	2020	Small-Dose Sunitinib Modulates p53, Bcl-2, STAT3, and ERK1/2 Pathways and Protects against Adenine-Induced Nephrotoxicity.	Sunitinib	11-20	transformation related protein 53, pseudogene	Mus musculus	31-34
33212804-0	2020	Small-Dose Sunitinib Modulates p53, Bcl-2, STAT3, and ERK1/2 Pathways and Protects against Adenine-Induced Nephrotoxicity.	Sunitinib	11-20	B cell leukemia/lymphoma 2	Mus musculus	36-41
33212804-0	2020	Small-Dose Sunitinib Modulates p53, Bcl-2, STAT3, and ERK1/2 Pathways and Protects against Adenine-Induced Nephrotoxicity.	Sunitinib	11-20	signal transducer and activator of transcription 3	Mus musculus	43-48
33299657-0	2020	Soluble forms of PD-L1 and PD-1 as prognostic and predictive markers of sunitinib efficacy in patients with metastatic clear cell renal cell carcinoma.	Sunitinib	72-81	CD274 molecule	Homo sapiens	17-22
33299657-0	2020	Soluble forms of PD-L1 and PD-1 as prognostic and predictive markers of sunitinib efficacy in patients with metastatic clear cell renal cell carcinoma.	Sunitinib	72-81	programmed cell death 1	Homo sapiens	27-31
33299657-8	2020	Patients with high T0 plasmatic levels of sPD-L1 had a shorter PFS (11.3 vs 22.5 months, p = .011) in the sunitinib group.	Sunitinib	106-115	spindle apparatus coiled-coil protein 1	Homo sapiens	42-48
33299657-10	2020	mccRCC patients with high plasmatic levels of sPD-L1 or sPD-1 are poor responders to sunitinib.	Sunitinib	85-94	spindle apparatus coiled-coil protein 1	Homo sapiens	46-52
33299657-10	2020	mccRCC patients with high plasmatic levels of sPD-L1 or sPD-1 are poor responders to sunitinib.	Sunitinib	85-94	homeobox D13	Homo sapiens	56-61
33203399-9	2020	Grade 3/4 haematological toxicities were lower with docetaxel-sunitinib (18.2% vs 34.3%, p = 0.132), attributed to greater discretionary use of prophylactic G-CSF (90.9% vs 63.0%, p = 0.024).	Sunitinib	62-71	colony stimulating factor 3	Homo sapiens	157-162
33212804-0	2020	Small-Dose Sunitinib Modulates p53, Bcl-2, STAT3, and ERK1/2 Pathways and Protects against Adenine-Induced Nephrotoxicity.	Sunitinib	11-20	mitogen-activated protein kinase 3	Mus musculus	54-60
33201837-7	2020	Sunitinib-resistant ccRCC cells show significantly lower DAPK1 mRNA and protein levels than sunitinib-sensitive ccRCC cells.	Sunitinib	0-9	death associated protein kinase 1	Homo sapiens	57-62
33212804-3	2020	To test our hypothesis, we investigated sunitinib as an inhibitor for tyrosine kinase signaling for both vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptors (PDGFR) against adenine-induced nephrotoxicity.	Sunitinib	40-49	platelet derived growth factor receptor, beta polypeptide	Mus musculus	161-201
33212804-3	2020	To test our hypothesis, we investigated sunitinib as an inhibitor for tyrosine kinase signaling for both vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptors (PDGFR) against adenine-induced nephrotoxicity.	Sunitinib	40-49	platelet derived growth factor receptor, beta polypeptide	Mus musculus	203-208
33201837-8	2020	DAPK1 overexpression enhances apoptosis in sunitinib-resistant ccRCC cells via the ATF6-dependent ER stress pathway.	Sunitinib	43-52	death associated protein kinase 1	Homo sapiens	0-5
33201837-8	2020	DAPK1 overexpression enhances apoptosis in sunitinib-resistant ccRCC cells via the ATF6-dependent ER stress pathway.	Sunitinib	43-52	activating transcription factor 6	Homo sapiens	83-87
33212804-10	2020	Furthermore, sunitinib decreased (p < 0.5) renal levels of TGF-beta1, p-ERK1/2, and phospho-STAT3 while elevating Bcl-2 expression score.	Sunitinib	13-22	transforming growth factor, beta 1	Mus musculus	59-68
33201837-10	2020	Our finding demonstrates that low DAPK1 expression is an independent prognostic indicator that correlates with ccRCC progression and sunitinib resistance.	Sunitinib	133-142	death associated protein kinase 1	Mus musculus	34-39
33212804-10	2020	Furthermore, sunitinib decreased (p < 0.5) renal levels of TGF-beta1, p-ERK1/2, and phospho-STAT3 while elevating Bcl-2 expression score.	Sunitinib	13-22	mitogen-activated protein kinase 3	Mus musculus	72-78
33212804-10	2020	Furthermore, sunitinib decreased (p < 0.5) renal levels of TGF-beta1, p-ERK1/2, and phospho-STAT3 while elevating Bcl-2 expression score.	Sunitinib	13-22	signal transducer and activator of transcription 3	Mus musculus	92-97
33212804-10	2020	Furthermore, sunitinib decreased (p < 0.5) renal levels of TGF-beta1, p-ERK1/2, and phospho-STAT3 while elevating Bcl-2 expression score.	Sunitinib	13-22	B cell leukemia/lymphoma 2	Mus musculus	114-119
33083006-0	2020	Sunitinib reduces the infection of SARS-CoV, MERS-CoV and SARS-CoV-2 partially by inhibiting AP2M1 phosphorylation.	Sunitinib	0-9	adaptor related protein complex 2 subunit mu 1	Homo sapiens	93-98
32901843-4	2020	In the present study, we examined which splice variants of LAMP-2 contributed to sunitinib resistance in RCC cells.	Sunitinib	81-90	lysosomal associated membrane protein 2	Homo sapiens	59-65
32761670-0	2020	Sunitinib induces primary ectopic endometrial cell apoptosis through up-regulation of STAT1 in vitro.	Sunitinib	0-9	signal transducer and activator of transcription 1	Homo sapiens	86-91
32761670-11	2020	Protein spectrum analysis was conducted on ectopic intimal cells after sunitinib treatment, and it was found that STAT1 is specifically expressed in ectopic endometrial cells.	Sunitinib	71-80	signal transducer and activator of transcription 1	Homo sapiens	114-119
32761670-12	2020	In vitro, and through fludarabine interference, it was revealed that sunitinib specifically inhibited the phosphorylation site Tyr751 of PDGFR, while the expression of STAT1, p-STAT1, and caspase-3 was significantly upregulated, and the expression of STAT1 and p-STAT1 was positively correlated with the expression of caspase-3.	Sunitinib	69-78	platelet derived growth factor receptor beta	Homo sapiens	137-142
32761670-12	2020	In vitro, and through fludarabine interference, it was revealed that sunitinib specifically inhibited the phosphorylation site Tyr751 of PDGFR, while the expression of STAT1, p-STAT1, and caspase-3 was significantly upregulated, and the expression of STAT1 and p-STAT1 was positively correlated with the expression of caspase-3.	Sunitinib	69-78	signal transducer and activator of transcription 1	Homo sapiens	168-173
32761670-12	2020	In vitro, and through fludarabine interference, it was revealed that sunitinib specifically inhibited the phosphorylation site Tyr751 of PDGFR, while the expression of STAT1, p-STAT1, and caspase-3 was significantly upregulated, and the expression of STAT1 and p-STAT1 was positively correlated with the expression of caspase-3.	Sunitinib	69-78	signal transducer and activator of transcription 1	Homo sapiens	177-182
32761670-12	2020	In vitro, and through fludarabine interference, it was revealed that sunitinib specifically inhibited the phosphorylation site Tyr751 of PDGFR, while the expression of STAT1, p-STAT1, and caspase-3 was significantly upregulated, and the expression of STAT1 and p-STAT1 was positively correlated with the expression of caspase-3.	Sunitinib	69-78	caspase 3	Homo sapiens	188-197
32761670-12	2020	In vitro, and through fludarabine interference, it was revealed that sunitinib specifically inhibited the phosphorylation site Tyr751 of PDGFR, while the expression of STAT1, p-STAT1, and caspase-3 was significantly upregulated, and the expression of STAT1 and p-STAT1 was positively correlated with the expression of caspase-3.	Sunitinib	69-78	signal transducer and activator of transcription 1	Homo sapiens	177-182
32761670-12	2020	In vitro, and through fludarabine interference, it was revealed that sunitinib specifically inhibited the phosphorylation site Tyr751 of PDGFR, while the expression of STAT1, p-STAT1, and caspase-3 was significantly upregulated, and the expression of STAT1 and p-STAT1 was positively correlated with the expression of caspase-3.	Sunitinib	69-78	signal transducer and activator of transcription 1	Homo sapiens	177-182
32761670-12	2020	In vitro, and through fludarabine interference, it was revealed that sunitinib specifically inhibited the phosphorylation site Tyr751 of PDGFR, while the expression of STAT1, p-STAT1, and caspase-3 was significantly upregulated, and the expression of STAT1 and p-STAT1 was positively correlated with the expression of caspase-3.	Sunitinib	69-78	caspase 3	Homo sapiens	318-327
32761670-14	2020	CONCLUSION: The in vitro experiments revealed that sunitinib could upregulate the expression of STAT1 by inhibiting the phosphorylation site Tyr751 of PDGFR, thereby specifically inducing the apoptosis of the primary heterotopic mesenchymal endometrium.	Sunitinib	51-60	signal transducer and activator of transcription 1	Homo sapiens	96-101
32761670-14	2020	CONCLUSION: The in vitro experiments revealed that sunitinib could upregulate the expression of STAT1 by inhibiting the phosphorylation site Tyr751 of PDGFR, thereby specifically inducing the apoptosis of the primary heterotopic mesenchymal endometrium.	Sunitinib	51-60	platelet derived growth factor receptor beta	Homo sapiens	151-156
32879446-1	2020	Angiogenesis inhibitors, such as the receptor tyrosine kinase (RTK) inhibitor sunitinib, target vascular endothelial growth factor (VEGF) signaling in cancers.	Sunitinib	78-87	TYRO3 protein tyrosine kinase 3	Mus musculus	37-61
33041663-9	2020	In vitro validation showed RBL1 overexpression induced resistance to Sunitinib and Cabozantinib; KLHL33 silencing induced resistance to Sunitinib; ARHGAP28 silencing induced sensitivity to Cabozantinib.	Sunitinib	69-78	RB transcriptional corepressor like 1	Homo sapiens	27-31
33041663-9	2020	In vitro validation showed RBL1 overexpression induced resistance to Sunitinib and Cabozantinib; KLHL33 silencing induced resistance to Sunitinib; ARHGAP28 silencing induced sensitivity to Cabozantinib.	Sunitinib	136-145	kelch like family member 33	Homo sapiens	97-103
32788078-6	2020	The observed sunitinib concentrations were a little higher than those reported in the 421C>A polymorphism of the ATP-binding cassette subfamily G member 2 gene carrier.	Sunitinib	13-22	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	113-154
33115942-8	2020	We found that RFA caused PD-1 upregulation in tumor-infiltrated T cells by boosting hepatocyte growth factor (HGF) expression, which was suppressed by sunitinib treatment.	Sunitinib	151-160	hepatocyte growth factor	Mus musculus	84-108
33115942-8	2020	We found that RFA caused PD-1 upregulation in tumor-infiltrated T cells by boosting hepatocyte growth factor (HGF) expression, which was suppressed by sunitinib treatment.	Sunitinib	151-160	hepatocyte growth factor	Mus musculus	110-113
33115942-9	2020	We have also demonstrated that sunitinib suppressed VEGF"s effect in enhancing PD-L1 expression in DCs and attenuated heat-sink effect.	Sunitinib	31-40	vascular endothelial growth factor A	Mus musculus	52-56
33115942-9	2020	We have also demonstrated that sunitinib suppressed VEGF"s effect in enhancing PD-L1 expression in DCs and attenuated heat-sink effect.	Sunitinib	31-40	CD274 antigen	Mus musculus	79-84
33115942-11	2020	CONCLUSIONS: Sunitinib enables RFA-released in situ TSA to ignite an effective anti-tumor immune response by suppressing HGF and VEGF signaling pathways.	Sunitinib	13-22	hepatocyte growth factor	Mus musculus	121-124
33115942-11	2020	CONCLUSIONS: Sunitinib enables RFA-released in situ TSA to ignite an effective anti-tumor immune response by suppressing HGF and VEGF signaling pathways.	Sunitinib	13-22	vascular endothelial growth factor A	Mus musculus	129-133
32229739-12	2020	RESULTS: Under sunitinib therapy, assessment of the expression of VEGFR2 by ultrasound molecular imaging with BR55 reveals a significant difference as early as 12 hours after first dosing (-25%), whereas tumor size significant change occurs only after 24 hours.	Sunitinib	15-24	kinase insert domain receptor	Rattus norvegicus	66-72
32879446-1	2020	Angiogenesis inhibitors, such as the receptor tyrosine kinase (RTK) inhibitor sunitinib, target vascular endothelial growth factor (VEGF) signaling in cancers.	Sunitinib	78-87	TYRO3 protein tyrosine kinase 3	Mus musculus	63-66
32879446-1	2020	Angiogenesis inhibitors, such as the receptor tyrosine kinase (RTK) inhibitor sunitinib, target vascular endothelial growth factor (VEGF) signaling in cancers.	Sunitinib	78-87	vascular endothelial growth factor A	Mus musculus	96-130
32879446-1	2020	Angiogenesis inhibitors, such as the receptor tyrosine kinase (RTK) inhibitor sunitinib, target vascular endothelial growth factor (VEGF) signaling in cancers.	Sunitinib	78-87	vascular endothelial growth factor A	Mus musculus	132-136
32879446-7	2020	EC-specific PI3Kbeta knockout (EpsilonC-betaKO) in mice potentiated the sunitinib-induced reduction in subcutaneous growth of LLC1 and B16F10, and lung metastasis of B16F10 tumors.	Sunitinib	72-81	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta	Mus musculus	12-20
32879446-10	2020	Taken together, EC PI3Kbeta inactivation with sunitinib inhibition reduces microvessel turnover and decreases heterogeneity of the tumor microenvironment, hence PI3Kbeta inhibition may be a useful adjuvant antiangiogenesis therapy with sunitinib.	Sunitinib	46-55	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta	Mus musculus	19-27
32879446-10	2020	Taken together, EC PI3Kbeta inactivation with sunitinib inhibition reduces microvessel turnover and decreases heterogeneity of the tumor microenvironment, hence PI3Kbeta inhibition may be a useful adjuvant antiangiogenesis therapy with sunitinib.	Sunitinib	236-245	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta	Mus musculus	19-27
32546645-1	2020	PURPOSE: In the S-TRAC trial, adjuvant sunitinib improved disease-free survival (DFS) compared with placebo in patients with loco-regional renal cell carcinoma (RCC) at high risk of recurrence.	Sunitinib	39-48	T cell receptor alpha constant	Homo sapiens	18-22
32248228-3	2020	The objective of this study was to examine whether SAL enhances the cytotoxic effect of sunitinib in Gb3-expressing HeLa cells.	Sunitinib	88-97	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	101-104
32248228-8	2020	Furthermore, we observed that SAL promoted the formation of lysosome-like structures, which are LAMP1 positive but not acidic in HeLa cells, that can trap sunitinib.	Sunitinib	155-164	lysosomal associated membrane protein 1	Homo sapiens	96-101
32248228-10	2020	Our findings suggest that SAL/Gb3 interaction promoted sunitinib uptake and suppressed sunitinib excretion, and that sunitinib efficiently exerted cytotoxicity against HeLa cells.	Sunitinib	55-64	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	30-33
32248228-10	2020	Our findings suggest that SAL/Gb3 interaction promoted sunitinib uptake and suppressed sunitinib excretion, and that sunitinib efficiently exerted cytotoxicity against HeLa cells.	Sunitinib	87-96	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	30-33
32248228-10	2020	Our findings suggest that SAL/Gb3 interaction promoted sunitinib uptake and suppressed sunitinib excretion, and that sunitinib efficiently exerted cytotoxicity against HeLa cells.	Sunitinib	87-96	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	30-33
33072561-0	2020	Long Non-coding RNA CCAT1 Acts as an Oncogene and Promotes Sunitinib Resistance in Renal Cell Carcinoma.	Sunitinib	59-68	colon cancer associated transcript 1	Homo sapiens	20-25
33072561-3	2020	We found long non-coding RNA (lncRNA) colon cancer-associated transcript-1 (CCAT1) overexpressed in sunitinib-resistant cells while declined in the parental cells.	Sunitinib	100-109	colon cancer associated transcript 1	Homo sapiens	76-81
33072561-4	2020	Moreover, lncRNA CCAT1 increased significantly in samples with resistance to sunitinib compared with those with responses to sunitinib.	Sunitinib	77-86	colon cancer associated transcript 1	Homo sapiens	17-22
33072561-8	2020	Apart from the in vitro experiments, we demonstrated that knockdown of CCAT1 boosted response to sunitinib by performing sunitinib-resistant ACHN mouse models.	Sunitinib	97-106	colon cancer associated transcript 1	Homo sapiens	71-76
33072561-8	2020	Apart from the in vitro experiments, we demonstrated that knockdown of CCAT1 boosted response to sunitinib by performing sunitinib-resistant ACHN mouse models.	Sunitinib	121-130	colon cancer associated transcript 1	Homo sapiens	71-76
33072561-9	2020	Briefly, lncRNA CCAT1 conferred renal cell carcinoma resistance to sunitinib in a c-Myc-dependent manner, providing a novel target for improvement of sunitinib therapy.	Sunitinib	67-76	colon cancer associated transcript 1	Homo sapiens	16-21
33072561-9	2020	Briefly, lncRNA CCAT1 conferred renal cell carcinoma resistance to sunitinib in a c-Myc-dependent manner, providing a novel target for improvement of sunitinib therapy.	Sunitinib	67-76	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	82-87
33072561-9	2020	Briefly, lncRNA CCAT1 conferred renal cell carcinoma resistance to sunitinib in a c-Myc-dependent manner, providing a novel target for improvement of sunitinib therapy.	Sunitinib	150-159	colon cancer associated transcript 1	Homo sapiens	16-21
33072561-9	2020	Briefly, lncRNA CCAT1 conferred renal cell carcinoma resistance to sunitinib in a c-Myc-dependent manner, providing a novel target for improvement of sunitinib therapy.	Sunitinib	150-159	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	82-87
32830849-0	2020	Sunitinib inhibits RNase L by destabilizing its active dimer conformation.	Sunitinib	0-9	ribonuclease L	Homo sapiens	19-26
32830849-2	2020	The ribonuclease activity of RNase L can be regulated by the kinase inhibitor sunitinib.	Sunitinib	78-87	ribonuclease L	Homo sapiens	29-36
32830849-4	2020	In this study, we aimed to uncover the mechanism of action through which sunitinib inhibits RNase L.	Sunitinib	73-82	ribonuclease L	Homo sapiens	92-99
32830849-5	2020	We solved the crystal structures of RNase L in complex with sunitinib and its analogs toceranib and SU11652.	Sunitinib	60-69	ribonuclease L	Homo sapiens	36-43
32830849-6	2020	Our results showed that sunitinib bound to the ATP-binding pocket of RNase L.	Sunitinib	24-33	ribonuclease L	Homo sapiens	69-76
32830849-8	2020	Molecular dynamics simulations and dynamic light scattering results support that the binding of sunitinib in the pseudokinase domain destabilized the dimer conformation of RNase L and allosterically inhibited its ribonuclease activity.	Sunitinib	96-105	ribonuclease L	Homo sapiens	172-179
32993785-1	2020	BACKGROUND: Sunitinib, a receptor tyrosine kinase (RTK) inhibitor that targets multiple receptors such as vascular endothelial growth factor receptors (VEGFRs), was approved for cancer treatment in 2006.	Sunitinib	12-21	TYRO3 protein tyrosine kinase 3	Mus musculus	25-49
32993785-1	2020	BACKGROUND: Sunitinib, a receptor tyrosine kinase (RTK) inhibitor that targets multiple receptors such as vascular endothelial growth factor receptors (VEGFRs), was approved for cancer treatment in 2006.	Sunitinib	12-21	TYRO3 protein tyrosine kinase 3	Mus musculus	51-54
32921632-0	2020	LINC00160 mediates sunitinib resistance in renal cell carcinoma via SAA1 that is implicated in STAT3 activation and compound transportation.	Sunitinib	19-28	long intergenic non-protein coding RNA 160	Homo sapiens	0-9
33052225-0	2020	Restoring the epigenetically silenced PCK2 suppresses renal cell carcinoma progression and increases sensitivity to sunitinib by promoting endoplasmic reticulum stress.	Sunitinib	116-125	phosphoenolpyruvate carboxykinase 2, mitochondrial	Homo sapiens	38-42
33052225-11	2020	Restoration of PCK2 expression in RCC cells repressed tumor progression and increased their sensitivity to sunitinib.	Sunitinib	107-116	phosphoenolpyruvate carboxykinase 2, mitochondrial	Homo sapiens	15-19
33052225-13	2020	Conclusions: Collectively, our results identify a specific mechanism by which PCK2 suppresses the progression of renal cell carcinoma (RCC) and increases sensitivity to sunitinib by promoting endoplasmic reticulum stress.	Sunitinib	169-178	phosphoenolpyruvate carboxykinase 2, mitochondrial	Homo sapiens	78-82
32921632-0	2020	LINC00160 mediates sunitinib resistance in renal cell carcinoma via SAA1 that is implicated in STAT3 activation and compound transportation.	Sunitinib	19-28	serum amyloid A1	Homo sapiens	68-72
32921632-3	2020	In this study, we identified that LINC00160 was associated with sunitinib resistance in renal cell carcinoma.	Sunitinib	64-73	long intergenic non-protein coding RNA 160	Homo sapiens	34-43
32921632-5	2020	On one hand, SAA1 linked to ABCB1 protein, which facilitated sunitinib cellular efflux and diminished drug accumulation.	Sunitinib	61-70	serum amyloid A1	Homo sapiens	13-17
32921632-5	2020	On one hand, SAA1 linked to ABCB1 protein, which facilitated sunitinib cellular efflux and diminished drug accumulation.	Sunitinib	61-70	ATP binding cassette subfamily B member 1	Homo sapiens	28-33
32921632-8	2020	LINC00160 mediates sunitinib resistance in renal cell carcinoma via SAA1 that is implicated in STAT3 activation and compound transportation, which offers an opportunity for targeted intervention and molecular therapies in the future.	Sunitinib	19-28	long intergenic non-protein coding RNA 160	Homo sapiens	0-9
32921632-8	2020	LINC00160 mediates sunitinib resistance in renal cell carcinoma via SAA1 that is implicated in STAT3 activation and compound transportation, which offers an opportunity for targeted intervention and molecular therapies in the future.	Sunitinib	19-28	serum amyloid A1	Homo sapiens	68-72
32552305-0	2020	Third-line sunitinib treatment in a VHL-mutated metastatic intrahepatic cholangiocarcinoma: a case report and literature review.	Sunitinib	11-20	von Hippel-Lindau tumor suppressor	Homo sapiens	36-39
32552305-5	2020	According to next-generation sequencing result of somatic Von Hippel-Lindau (VHL) gene mutation, the patient was administered third-line sunitinib and obtained a relatively longer survival of 9 months after taking sunitinib.	Sunitinib	137-146	von Hippel-Lindau tumor suppressor	Homo sapiens	58-75
32552305-5	2020	According to next-generation sequencing result of somatic Von Hippel-Lindau (VHL) gene mutation, the patient was administered third-line sunitinib and obtained a relatively longer survival of 9 months after taking sunitinib.	Sunitinib	137-146	von Hippel-Lindau tumor suppressor	Homo sapiens	77-80
32552305-5	2020	According to next-generation sequencing result of somatic Von Hippel-Lindau (VHL) gene mutation, the patient was administered third-line sunitinib and obtained a relatively longer survival of 9 months after taking sunitinib.	Sunitinib	214-223	von Hippel-Lindau tumor suppressor	Homo sapiens	58-75
32947305-4	2020	Evidence supporting the use of these therapies in the adjuvant setting is mixed, although one clinical trial, S-TRAC, has shown improvements in disease-free survival with 1 year of adjuvant sunitinib among patients with clear cell histology and high-risk features, leading to the first US Food and Drug Administration approval of an adjuvant therapy for high-risk RCC patients.	Sunitinib	190-199	T cell receptor alpha constant	Homo sapiens	112-116
32552305-5	2020	According to next-generation sequencing result of somatic Von Hippel-Lindau (VHL) gene mutation, the patient was administered third-line sunitinib and obtained a relatively longer survival of 9 months after taking sunitinib.	Sunitinib	214-223	von Hippel-Lindau tumor suppressor	Homo sapiens	77-80
32814829-0	2020	Enhanced YB1/EphA2 axis signaling promotes acquired resistance to sunitinib and metastatic potential in renal cell carcinoma.	Sunitinib	66-75	Y-box binding protein 1	Homo sapiens	9-12
32291709-2	2020	Imatinib and sunitinib are approved KIT-inhibiting therapies.	Sunitinib	13-22	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	36-39
32291709-9	2020	Our data show that dasatinib is more potent than imatinib or sunitinib at inhibiting the activity of drug-resistant KIT mutants.	Sunitinib	61-70	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	116-119
32783497-0	2020	Feedback activation of GATA1/miR-885-5p/PLIN3 pathway decreases sunitinib sensitivity in clear cell renal cell carcinoma.	Sunitinib	64-73	GATA binding protein 1	Homo sapiens	23-28
32783497-0	2020	Feedback activation of GATA1/miR-885-5p/PLIN3 pathway decreases sunitinib sensitivity in clear cell renal cell carcinoma.	Sunitinib	64-73	microRNA 885	Homo sapiens	29-36
32783497-0	2020	Feedback activation of GATA1/miR-885-5p/PLIN3 pathway decreases sunitinib sensitivity in clear cell renal cell carcinoma.	Sunitinib	64-73	perilipin 3	Homo sapiens	40-45
32783497-3	2020	Here, we discovered miR-885-5p was notably decreased after sunitinib treatment and associated with poor disease progression in clear cell renal cell carcinoma (ccRCC).	Sunitinib	59-68	microRNA 885	Homo sapiens	20-27
32783497-5	2020	Mechanistically, sunitinib treatment reduced GATA1 expression, which in turn reduced its binding to MIR885 promoter and resulted in miR-885-5p downregulation in transcriptional level.	Sunitinib	17-26	GATA binding protein 1	Homo sapiens	45-50
32783497-5	2020	Mechanistically, sunitinib treatment reduced GATA1 expression, which in turn reduced its binding to MIR885 promoter and resulted in miR-885-5p downregulation in transcriptional level.	Sunitinib	17-26	microRNA 885	Homo sapiens	100-106
32783497-5	2020	Mechanistically, sunitinib treatment reduced GATA1 expression, which in turn reduced its binding to MIR885 promoter and resulted in miR-885-5p downregulation in transcriptional level.	Sunitinib	17-26	microRNA 885	Homo sapiens	132-139
32783497-6	2020	In addition, PLIN3 was confirmed to be directly targeted by miR-885-5p and its upregulation significantly increased lipid droplets formation to decrease sunitinib sensitivity.	Sunitinib	153-162	perilipin 3	Homo sapiens	13-18
32783497-6	2020	In addition, PLIN3 was confirmed to be directly targeted by miR-885-5p and its upregulation significantly increased lipid droplets formation to decrease sunitinib sensitivity.	Sunitinib	153-162	microRNA 885	Homo sapiens	60-67
32783497-7	2020	Therefore, GATA1/miR-885-5p/ PLIN3 pathway may serve as a potential therapeutic strategy and a biomarker for sunitinib treatment in ccRCC.	Sunitinib	109-118	GATA binding protein 1	Homo sapiens	11-16
32783497-7	2020	Therefore, GATA1/miR-885-5p/ PLIN3 pathway may serve as a potential therapeutic strategy and a biomarker for sunitinib treatment in ccRCC.	Sunitinib	109-118	microRNA 885	Homo sapiens	17-24
32783497-7	2020	Therefore, GATA1/miR-885-5p/ PLIN3 pathway may serve as a potential therapeutic strategy and a biomarker for sunitinib treatment in ccRCC.	Sunitinib	109-118	perilipin 3	Homo sapiens	29-34
32814829-5	2020	In addition, our findings confirm that YB1 promotes the invasion, metastasis and sunitinib resistance of ccRCC by regulating the EphA2 signaling pathway.	Sunitinib	81-90	Y-box binding protein 1	Homo sapiens	39-42
32814829-6	2020	Furthermore, pharmacological inhibition of EphA2 through the small molecule inhibitor ALW-II-41-27 reduced the proliferation of sunitinib-resistant tumor cells, suppressed tumor growth in vivo, and restored the sensitivity of sunitinib-resistant tumor cells to sunitinib in vitro and in vivo.	Sunitinib	128-137	EPH receptor A2	Homo sapiens	43-48
32814829-6	2020	Furthermore, pharmacological inhibition of EphA2 through the small molecule inhibitor ALW-II-41-27 reduced the proliferation of sunitinib-resistant tumor cells, suppressed tumor growth in vivo, and restored the sensitivity of sunitinib-resistant tumor cells to sunitinib in vitro and in vivo.	Sunitinib	226-235	EPH receptor A2	Homo sapiens	43-48
32814829-6	2020	Furthermore, pharmacological inhibition of EphA2 through the small molecule inhibitor ALW-II-41-27 reduced the proliferation of sunitinib-resistant tumor cells, suppressed tumor growth in vivo, and restored the sensitivity of sunitinib-resistant tumor cells to sunitinib in vitro and in vivo.	Sunitinib	226-235	EPH receptor A2	Homo sapiens	43-48
32814829-0	2020	Enhanced YB1/EphA2 axis signaling promotes acquired resistance to sunitinib and metastatic potential in renal cell carcinoma.	Sunitinib	66-75	EPH receptor A2	Homo sapiens	13-18
32814829-2	2020	Receptor tyrosine kinase (RTK) inhibitors such as sunitinib have been demonstrated to target tumorigenic signaling pathways, delay tumor progression, and improve patient prognosis in metastatic renal cell carcinoma (mRCC).	Sunitinib	50-59	ret proto-oncogene	Homo sapiens	0-24
32814829-2	2020	Receptor tyrosine kinase (RTK) inhibitors such as sunitinib have been demonstrated to target tumorigenic signaling pathways, delay tumor progression, and improve patient prognosis in metastatic renal cell carcinoma (mRCC).	Sunitinib	50-59	ret proto-oncogene	Homo sapiens	26-29
32814829-4	2020	In our study, we found that increased expression of Y-box binding protein 1 (YB1, a multidrug resistance associated protein) and EphA2 (a member of the erythropoietin-producing hepatocellular (Eph) receptor family, belonging to the RTK family) mediated sunitinib resistance and mRCC exhibited a large phenotypic dependence on YB1 and EphA2.	Sunitinib	253-262	Y-box binding protein 1	Homo sapiens	52-75
32814829-4	2020	In our study, we found that increased expression of Y-box binding protein 1 (YB1, a multidrug resistance associated protein) and EphA2 (a member of the erythropoietin-producing hepatocellular (Eph) receptor family, belonging to the RTK family) mediated sunitinib resistance and mRCC exhibited a large phenotypic dependence on YB1 and EphA2.	Sunitinib	253-262	Y-box binding protein 1	Homo sapiens	77-80
32814829-4	2020	In our study, we found that increased expression of Y-box binding protein 1 (YB1, a multidrug resistance associated protein) and EphA2 (a member of the erythropoietin-producing hepatocellular (Eph) receptor family, belonging to the RTK family) mediated sunitinib resistance and mRCC exhibited a large phenotypic dependence on YB1 and EphA2.	Sunitinib	253-262	ATP binding cassette subfamily C member 3	Homo sapiens	84-123
32814829-4	2020	In our study, we found that increased expression of Y-box binding protein 1 (YB1, a multidrug resistance associated protein) and EphA2 (a member of the erythropoietin-producing hepatocellular (Eph) receptor family, belonging to the RTK family) mediated sunitinib resistance and mRCC exhibited a large phenotypic dependence on YB1 and EphA2.	Sunitinib	253-262	EPH receptor A2	Homo sapiens	129-134
32767163-4	2020	As the tumor may still be anti-VEGFR drug-naive, a tyrosine kinase inhibitor approved for first line treatment (e.g., sunitinib or pazopanib) may be beneficial.	Sunitinib	118-127	kinase insert domain receptor	Homo sapiens	31-36
32872567-7	2020	Furthermore, inhibition of AAK1 kinase activity using sunitinib decreased RABV infection.	Sunitinib	54-63	AP2 associated kinase 1	Homo sapiens	27-31
32492594-5	2020	Six small molecules that inhibit VEGFR1/2/3, namely, sunitinib, sorafenib, axitinib, pazopanib, cabozantinib, and lenvatinib, have been approved by the Food and Drug Administration (FDA) for the treatment of RCC.	Sunitinib	53-62	fms related receptor tyrosine kinase 1	Homo sapiens	33-43
32810161-0	2020	Cyclic pentapeptide cRGDfK enhances the inhibitory effect of sunitinib on TGF-beta1-induced epithelial-to-mesenchymal transition in human non-small cell lung cancer cells.	Sunitinib	61-70	transforming growth factor beta 1	Homo sapiens	74-83
32810161-5	2020	Sunitinib strongly inhibited the TGF-beta1-activated EMT through suppression of Wnt signaling, Smad and non-Smad signaling pathways.	Sunitinib	0-9	transforming growth factor beta 1	Homo sapiens	33-42
32874210-8	2020	Nivolumab plus ipilimumab and pembrolizumab plus axitinib achieved more health benefits than the other ICI regimens and sunitinib in programmed death ligand 1 (PD-L1)-positive and negative tumors, respectively.	Sunitinib	120-129	CD274 molecule	Homo sapiens	133-158
32874210-8	2020	Nivolumab plus ipilimumab and pembrolizumab plus axitinib achieved more health benefits than the other ICI regimens and sunitinib in programmed death ligand 1 (PD-L1)-positive and negative tumors, respectively.	Sunitinib	120-129	CD274 molecule	Homo sapiens	160-165
32628820-7	2020	CCNE1 gain was associated with resistance to Axitinib and LRP10 loss was associated with resistance to Sunitinib.	Sunitinib	103-112	LDL receptor related protein 10	Homo sapiens	58-63
32923192-1	2020	Spontaneous pneumothorax secondary to sunitinib, a vascular endothelial growth factor receptor (VEGFR) inhibitor, is an extremely rare side effect of this class of medications.	Sunitinib	38-47	kinase insert domain receptor	Homo sapiens	51-94
32923192-1	2020	Spontaneous pneumothorax secondary to sunitinib, a vascular endothelial growth factor receptor (VEGFR) inhibitor, is an extremely rare side effect of this class of medications.	Sunitinib	38-47	kinase insert domain receptor	Homo sapiens	96-101
32578660-3	2020	Herein, the multi-targeted receptor tyrosine kinase (RTK) inhibitor sunitinib (Sun) and photodynamic therapy (PDT) drug chlorin e6 (Ce6) were locally delivered to the postoperative tumor site via a zwitterionic hydrogel.	Sunitinib	68-77	ret proto-oncogene	Homo sapiens	27-51
32578660-3	2020	Herein, the multi-targeted receptor tyrosine kinase (RTK) inhibitor sunitinib (Sun) and photodynamic therapy (PDT) drug chlorin e6 (Ce6) were locally delivered to the postoperative tumor site via a zwitterionic hydrogel.	Sunitinib	68-77	ret proto-oncogene	Homo sapiens	53-56
32663095-0	2020	Depletion of lncRNA MALAT1 inhibited sunitinib resistance through regulating miR-362-3p-mediated G3BP1 in renal cell carcinoma.	Sunitinib	37-46	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	20-26
32663095-0	2020	Depletion of lncRNA MALAT1 inhibited sunitinib resistance through regulating miR-362-3p-mediated G3BP1 in renal cell carcinoma.	Sunitinib	37-46	G3BP stress granule assembly factor 1	Homo sapiens	97-102
32663095-4	2020	Further, RNA pull-down and luciferase reporter assay were applied to investigate the underlying mechanism of MALAT1 in SU resistance.	Sunitinib	119-121	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	109-115
32663095-2	2020	In this study, MALAT1 expression in SU-resistance tumor tissues and cells was tested by qRT-PCR.	Sunitinib	36-38	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	15-21
32663095-5	2020	The results showed that MALAT1 expression was dramatically upregulated in SU-resistance RCC tissues and cell lines.	Sunitinib	74-76	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	24-30
32760216-0	2020	LncRNA HOTAIR induces sunitinib resistance in renal cancer by acting as a competing endogenous RNA to regulate autophagy of renal cells.	Sunitinib	22-31	HOX transcript antisense RNA (non-protein coding)	Mus musculus	7-13
32663095-9	2020	Rescue experiments suggested that downregulation of miR-362-3p and overexpression of G3BP1 can reverse the SU chemosensitivity of MALAT1 knockdown in RCC cells.	Sunitinib	107-109	G3BP stress granule assembly factor 1	Homo sapiens	85-90
32663095-9	2020	Rescue experiments suggested that downregulation of miR-362-3p and overexpression of G3BP1 can reverse the SU chemosensitivity of MALAT1 knockdown in RCC cells.	Sunitinib	107-109	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	130-136
32663095-10	2020	In conclusion, depletion of LncRNA MALAT1 inhibited SU chemoresistance through modulating G3BP1 via sponging miR-362-3p in RCC cells, suggesting that targeting MALAT1 may be a potential therapeutic strategy for SU-resistance RCC.	Sunitinib	52-54	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	35-41
32663095-10	2020	In conclusion, depletion of LncRNA MALAT1 inhibited SU chemoresistance through modulating G3BP1 via sponging miR-362-3p in RCC cells, suggesting that targeting MALAT1 may be a potential therapeutic strategy for SU-resistance RCC.	Sunitinib	52-54	G3BP stress granule assembly factor 1	Homo sapiens	90-95
32663095-10	2020	In conclusion, depletion of LncRNA MALAT1 inhibited SU chemoresistance through modulating G3BP1 via sponging miR-362-3p in RCC cells, suggesting that targeting MALAT1 may be a potential therapeutic strategy for SU-resistance RCC.	Sunitinib	211-213	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	35-41
32663095-10	2020	In conclusion, depletion of LncRNA MALAT1 inhibited SU chemoresistance through modulating G3BP1 via sponging miR-362-3p in RCC cells, suggesting that targeting MALAT1 may be a potential therapeutic strategy for SU-resistance RCC.	Sunitinib	211-213	G3BP stress granule assembly factor 1	Homo sapiens	90-95
32511016-0	2020	Sunitinib inhibits PD-L1 expression in osteosarcoma by targeting STAT3 and remodels the immune system in tumor-bearing mice.	Sunitinib	0-9	CD274 antigen	Mus musculus	19-24
32511016-0	2020	Sunitinib inhibits PD-L1 expression in osteosarcoma by targeting STAT3 and remodels the immune system in tumor-bearing mice.	Sunitinib	0-9	signal transducer and activator of transcription 3	Mus musculus	65-70
32511016-5	2020	Results: Sunitinib reduced the expression of PD-L1 by inhibiting the activation of STAT3 and suppressed the migration and invasion in osteosarcoma cells.	Sunitinib	9-18	CD274 antigen	Mus musculus	45-50
32511016-5	2020	Results: Sunitinib reduced the expression of PD-L1 by inhibiting the activation of STAT3 and suppressed the migration and invasion in osteosarcoma cells.	Sunitinib	9-18	signal transducer and activator of transcription 3	Mus musculus	83-88
32511016-7	2020	Conclusion: Sunitinib inhibits PD-L1 expression by targeting STAT3 and remodels the immune system in tumor-bearing mice.	Sunitinib	12-21	CD274 antigen	Mus musculus	31-36
32511016-7	2020	Conclusion: Sunitinib inhibits PD-L1 expression by targeting STAT3 and remodels the immune system in tumor-bearing mice.	Sunitinib	12-21	signal transducer and activator of transcription 3	Mus musculus	61-66
32358665-3	2020	Present hypothesis was aimed to examine the nephroprotective potential of RIVA in SUN-induced nephrotoxicity, mediated through the inhibition of oxidative stress-induced apoptosis and inflammation, via the TNF-alpha/NFk-B signaling pathways.	Sunitinib	82-85	tumor necrosis factor	Rattus norvegicus	206-215
32358665-3	2020	Present hypothesis was aimed to examine the nephroprotective potential of RIVA in SUN-induced nephrotoxicity, mediated through the inhibition of oxidative stress-induced apoptosis and inflammation, via the TNF-alpha/NFk-B signaling pathways.	Sunitinib	82-85	nuclear factor kappa B subunit 1	Rattus norvegicus	216-221
32760216-3	2020	This study was assigned to probe the effect and mechanism of HOTAIR on sunitinib resistance of RC.	Sunitinib	71-80	HOX transcript antisense RNA (non-protein coding)	Mus musculus	61-67
32760216-11	2020	The role of HOTAIR knockdown in sunitinib resistance was verified in nude mice.	Sunitinib	32-41	HOX transcript antisense RNA (non-protein coding)	Mus musculus	12-18
32760216-12	2020	Results: HOTAIR expression in sunitinib-resistant cells is higher than that in parental cells.	Sunitinib	30-39	HOX transcript antisense RNA (non-protein coding)	Mus musculus	9-15
32760216-13	2020	Knockdown of HOTAIR in sunitinib-resistant cells lead to refrained sunitinib resistance and cell autophagy both in vivo and in vitro.	Sunitinib	23-32	HOX transcript antisense RNA (non-protein coding)	Mus musculus	13-19
32760216-13	2020	Knockdown of HOTAIR in sunitinib-resistant cells lead to refrained sunitinib resistance and cell autophagy both in vivo and in vitro.	Sunitinib	67-76	HOX transcript antisense RNA (non-protein coding)	Mus musculus	13-19
32760216-17	2020	Conclusion: HOTAIR negatively targets miR-17-5p to activate Beclin1-mediated cell autophagy, thereby enhancing sunitinib resistance in RC cells.	Sunitinib	111-120	HOX transcript antisense RNA (non-protein coding)	Mus musculus	12-18
32760216-17	2020	Conclusion: HOTAIR negatively targets miR-17-5p to activate Beclin1-mediated cell autophagy, thereby enhancing sunitinib resistance in RC cells.	Sunitinib	111-120	beclin 1, autophagy related	Mus musculus	60-67
32312893-0	2020	Identification of a RAS-activating TMEM87A-RASGRF1 fusion in an exceptional responder to sunitinib with non-small cell lung cancer.	Sunitinib	89-98	transmembrane protein 87A	Homo sapiens	35-42
32312893-0	2020	Identification of a RAS-activating TMEM87A-RASGRF1 fusion in an exceptional responder to sunitinib with non-small cell lung cancer.	Sunitinib	89-98	Ras protein specific guanine nucleotide releasing factor 1	Homo sapiens	43-50
32469384-15	2020	Following availability of external data on PFS with sunitinib in patients with MET-driven disease, study enrollment was closed.	Sunitinib	52-61	SAFB like transcription modulator	Homo sapiens	79-82
32792963-7	2020	Moreover, we found that the levels of p-RB, CDK4, and Cyclin D1 were up-regulated in sunitinib resistant 786-O, OS-RC-2, and TK-10 cells, and inhibition of CDK4 by palbociclib or wogonin effectively reversed the sunitinib resistance, indicating that the hyperactivation of CDK4-RB pathway may at least partially contribute to the resistance of RCC to sunitinib.	Sunitinib	85-94	RB transcriptional corepressor 1	Homo sapiens	38-42
32792963-7	2020	Moreover, we found that the levels of p-RB, CDK4, and Cyclin D1 were up-regulated in sunitinib resistant 786-O, OS-RC-2, and TK-10 cells, and inhibition of CDK4 by palbociclib or wogonin effectively reversed the sunitinib resistance, indicating that the hyperactivation of CDK4-RB pathway may at least partially contribute to the resistance of RCC to sunitinib.	Sunitinib	85-94	cyclin dependent kinase 4	Homo sapiens	44-48
32792963-7	2020	Moreover, we found that the levels of p-RB, CDK4, and Cyclin D1 were up-regulated in sunitinib resistant 786-O, OS-RC-2, and TK-10 cells, and inhibition of CDK4 by palbociclib or wogonin effectively reversed the sunitinib resistance, indicating that the hyperactivation of CDK4-RB pathway may at least partially contribute to the resistance of RCC to sunitinib.	Sunitinib	85-94	cyclin D1	Homo sapiens	54-63
32792963-7	2020	Moreover, we found that the levels of p-RB, CDK4, and Cyclin D1 were up-regulated in sunitinib resistant 786-O, OS-RC-2, and TK-10 cells, and inhibition of CDK4 by palbociclib or wogonin effectively reversed the sunitinib resistance, indicating that the hyperactivation of CDK4-RB pathway may at least partially contribute to the resistance of RCC to sunitinib.	Sunitinib	212-221	RB transcriptional corepressor 1	Homo sapiens	38-42
32641718-4	2020	SNHG12 promoted RCC proliferation, migration, invasion and sunitinib resistance via CDCA3 in vitro.	Sunitinib	59-68	small nucleolar RNA host gene 12	Homo sapiens	0-6
32792963-7	2020	Moreover, we found that the levels of p-RB, CDK4, and Cyclin D1 were up-regulated in sunitinib resistant 786-O, OS-RC-2, and TK-10 cells, and inhibition of CDK4 by palbociclib or wogonin effectively reversed the sunitinib resistance, indicating that the hyperactivation of CDK4-RB pathway may at least partially contribute to the resistance of RCC to sunitinib.	Sunitinib	212-221	cyclin dependent kinase 4	Homo sapiens	44-48
32792963-7	2020	Moreover, we found that the levels of p-RB, CDK4, and Cyclin D1 were up-regulated in sunitinib resistant 786-O, OS-RC-2, and TK-10 cells, and inhibition of CDK4 by palbociclib or wogonin effectively reversed the sunitinib resistance, indicating that the hyperactivation of CDK4-RB pathway may at least partially contribute to the resistance of RCC to sunitinib.	Sunitinib	212-221	cyclin D1	Homo sapiens	54-63
32792963-7	2020	Moreover, we found that the levels of p-RB, CDK4, and Cyclin D1 were up-regulated in sunitinib resistant 786-O, OS-RC-2, and TK-10 cells, and inhibition of CDK4 by palbociclib or wogonin effectively reversed the sunitinib resistance, indicating that the hyperactivation of CDK4-RB pathway may at least partially contribute to the resistance of RCC to sunitinib.	Sunitinib	212-221	cyclin dependent kinase 4	Homo sapiens	156-160
32792963-7	2020	Moreover, we found that the levels of p-RB, CDK4, and Cyclin D1 were up-regulated in sunitinib resistant 786-O, OS-RC-2, and TK-10 cells, and inhibition of CDK4 by palbociclib or wogonin effectively reversed the sunitinib resistance, indicating that the hyperactivation of CDK4-RB pathway may at least partially contribute to the resistance of RCC to sunitinib.	Sunitinib	212-221	cyclin dependent kinase 4	Homo sapiens	156-160
32792963-7	2020	Moreover, we found that the levels of p-RB, CDK4, and Cyclin D1 were up-regulated in sunitinib resistant 786-O, OS-RC-2, and TK-10 cells, and inhibition of CDK4 by palbociclib or wogonin effectively reversed the sunitinib resistance, indicating that the hyperactivation of CDK4-RB pathway may at least partially contribute to the resistance of RCC to sunitinib.	Sunitinib	212-221	RB transcriptional corepressor 1	Homo sapiens	38-42
32792963-7	2020	Moreover, we found that the levels of p-RB, CDK4, and Cyclin D1 were up-regulated in sunitinib resistant 786-O, OS-RC-2, and TK-10 cells, and inhibition of CDK4 by palbociclib or wogonin effectively reversed the sunitinib resistance, indicating that the hyperactivation of CDK4-RB pathway may at least partially contribute to the resistance of RCC to sunitinib.	Sunitinib	212-221	cyclin dependent kinase 4	Homo sapiens	44-48
32792963-7	2020	Moreover, we found that the levels of p-RB, CDK4, and Cyclin D1 were up-regulated in sunitinib resistant 786-O, OS-RC-2, and TK-10 cells, and inhibition of CDK4 by palbociclib or wogonin effectively reversed the sunitinib resistance, indicating that the hyperactivation of CDK4-RB pathway may at least partially contribute to the resistance of RCC to sunitinib.	Sunitinib	212-221	cyclin D1	Homo sapiens	54-63
32792963-7	2020	Moreover, we found that the levels of p-RB, CDK4, and Cyclin D1 were up-regulated in sunitinib resistant 786-O, OS-RC-2, and TK-10 cells, and inhibition of CDK4 by palbociclib or wogonin effectively reversed the sunitinib resistance, indicating that the hyperactivation of CDK4-RB pathway may at least partially contribute to the resistance of RCC to sunitinib.	Sunitinib	212-221	cyclin dependent kinase 4	Homo sapiens	156-160
32792963-7	2020	Moreover, we found that the levels of p-RB, CDK4, and Cyclin D1 were up-regulated in sunitinib resistant 786-O, OS-RC-2, and TK-10 cells, and inhibition of CDK4 by palbociclib or wogonin effectively reversed the sunitinib resistance, indicating that the hyperactivation of CDK4-RB pathway may at least partially contribute to the resistance of RCC to sunitinib.	Sunitinib	212-221	cyclin dependent kinase 4	Homo sapiens	156-160
32698382-8	2020	Furthermore, a decrease in nitric oxide (NO) levels and endothelial nitric oxide synthase (eNOS) activation was observed in aortas from Su-treated animals.	Sunitinib	136-138	nitric oxide synthase 3	Rattus norvegicus	56-89
32698382-8	2020	Furthermore, a decrease in nitric oxide (NO) levels and endothelial nitric oxide synthase (eNOS) activation was observed in aortas from Su-treated animals.	Sunitinib	136-138	nitric oxide synthase 3	Rattus norvegicus	91-95
32234492-8	2020	Low expression of JAK2 were resistant to QL-VIII-58, TL-1-85, Ruxolitinib, TG101348 and Sunitinib.	Sunitinib	88-97	Janus kinase 2	Homo sapiens	18-22
32641718-0	2020	Long noncoding RNA SNHG12 promotes tumour progression and sunitinib resistance by upregulating CDCA3 in renal cell carcinoma.	Sunitinib	58-67	small nucleolar RNA host gene 12	Homo sapiens	19-25
32641718-2	2020	Long noncoding RNA SNHG12 (lncRNA SNHG12) has emerged as a key molecule in numerous human cancers, but its functions in renal cell carcinoma (RCC) sunitinib resistance remain unclear.	Sunitinib	147-156	small nucleolar RNA host gene 12	Homo sapiens	19-25
32641718-2	2020	Long noncoding RNA SNHG12 (lncRNA SNHG12) has emerged as a key molecule in numerous human cancers, but its functions in renal cell carcinoma (RCC) sunitinib resistance remain unclear.	Sunitinib	147-156	small nucleolar RNA host gene 12	Homo sapiens	34-40
32641718-3	2020	In this study, we found SNHG12 was highly expressed in RCC tissues and in sunitinib-resistant RCC cells and was associated with a poor clinical prognosis.	Sunitinib	74-83	small nucleolar RNA host gene 12	Homo sapiens	24-30
32667929-7	2020	In RCC cells from mice treated with disulfiram and/or sunitinib, several genes associated with serine biosynthesis and aldose reductase were downregulated in cells treated with disulfiram or sunitinib alone and further downregulated in cells treated with both disulfiram and sunitinib.	Sunitinib	54-63	aldo-keto reductase family 1, member B3 (aldose reductase)	Mus musculus	119-135
32667929-7	2020	In RCC cells from mice treated with disulfiram and/or sunitinib, several genes associated with serine biosynthesis and aldose reductase were downregulated in cells treated with disulfiram or sunitinib alone and further downregulated in cells treated with both disulfiram and sunitinib.	Sunitinib	191-200	aldo-keto reductase family 1, member B3 (aldose reductase)	Mus musculus	119-135
32667929-7	2020	In RCC cells from mice treated with disulfiram and/or sunitinib, several genes associated with serine biosynthesis and aldose reductase were downregulated in cells treated with disulfiram or sunitinib alone and further downregulated in cells treated with both disulfiram and sunitinib.	Sunitinib	191-200	aldo-keto reductase family 1, member B3 (aldose reductase)	Mus musculus	119-135
32802186-14	2020	Moreover, silencing of GYS1 increased the synthetic lethality of ccRCC cells to sunitinib treatment by concomitantly suppressing p65.	Sunitinib	80-89	glycogen synthase 1	Homo sapiens	23-27
32802186-16	2020	Re-sensitization of ccRCC cells to sunitinib suggests that GYS1 is a useful indicator of unfavorable prognosis as well as a therapeutic target for patients with ccRCC.	Sunitinib	35-44	glycogen synthase 1	Homo sapiens	59-63
32641718-7	2020	Furthermore, in vivo experiments showed that SNHG12 increased tumour growth and that knocking down SNHG12 could reverse RCC sunitinib resistance.	Sunitinib	124-133	small nucleolar RNA host gene 12	Homo sapiens	99-105
32641718-8	2020	Our study revealed that the lncRNA SNHG12/SP1/CDCA3 axis promoted RCC progression and sunitinib resistance, which could provide a new therapeutic target for sunitinib-resistant RCC.	Sunitinib	86-95	small nucleolar RNA host gene 12	Homo sapiens	35-41
32641718-8	2020	Our study revealed that the lncRNA SNHG12/SP1/CDCA3 axis promoted RCC progression and sunitinib resistance, which could provide a new therapeutic target for sunitinib-resistant RCC.	Sunitinib	86-95	cell division cycle associated 3	Homo sapiens	46-51
32641718-8	2020	Our study revealed that the lncRNA SNHG12/SP1/CDCA3 axis promoted RCC progression and sunitinib resistance, which could provide a new therapeutic target for sunitinib-resistant RCC.	Sunitinib	157-166	small nucleolar RNA host gene 12	Homo sapiens	35-41
32641718-8	2020	Our study revealed that the lncRNA SNHG12/SP1/CDCA3 axis promoted RCC progression and sunitinib resistance, which could provide a new therapeutic target for sunitinib-resistant RCC.	Sunitinib	157-166	cell division cycle associated 3	Homo sapiens	46-51
32233096-5	2020	Through screening, we identified two FDA-approved drugs, Oxytetracycline and Sunitinib, which were able to dissociate Abeta oligomers and plaques to monomers in 5XFAD transgenic mice.	Sunitinib	77-86	amyloid beta (A4) precursor protein	Mus musculus	118-123
32334266-4	2020	The multi-kinase inhibitor, sunitinib, has demonstrated potent nanomolar inhibition of AMPK activity and has scope for modification.	Sunitinib	28-37	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	87-91
32126313-6	2020	Sunitinib, a tyrosine receptor kinase inhibitor that also blocks VEGFR2 blocked sildenafil-/vardenafil-induced osteoblast differentiation.	Sunitinib	0-9	kinase insert domain protein receptor	Mus musculus	65-71
32334266-6	2020	We identified two potent, novel oxindole-based AMPK inhibitors that were designed to interact with the DFG motif in the ATP-binding site of AMPK, this key feature evades interaction with the common recptor tyrosine kinase targets of sunitinib.	Sunitinib	233-242	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	47-51
32334266-6	2020	We identified two potent, novel oxindole-based AMPK inhibitors that were designed to interact with the DFG motif in the ATP-binding site of AMPK, this key feature evades interaction with the common recptor tyrosine kinase targets of sunitinib.	Sunitinib	233-242	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	140-144
32661119-8	2020	The most commonly used IO and VEGF-TKIs were nivolumab (66%) and sunitinib (40%).	Sunitinib	65-74	vascular endothelial growth factor A	Homo sapiens	30-34
32382017-0	2020	ZHX2 drives cell growth and migration via activating MEK/ERK signal and induces Sunitinib resistance by regulating the autophagy in clear cell Renal Cell Carcinoma.	Sunitinib	80-89	zinc fingers and homeoboxes 2	Homo sapiens	0-4
32409702-0	2020	Targeting the ERbeta/Angiopoietin-2/Tie-2 signaling-mediated angiogenesis with the FDA-approved anti-estrogen Faslodex to increase the Sunitinib sensitivity in RCC.	Sunitinib	135-144	estrogen receptor 1 (alpha)	Mus musculus	14-20
32409702-0	2020	Targeting the ERbeta/Angiopoietin-2/Tie-2 signaling-mediated angiogenesis with the FDA-approved anti-estrogen Faslodex to increase the Sunitinib sensitivity in RCC.	Sunitinib	135-144	angiopoietin 2	Mus musculus	21-35
32409702-0	2020	Targeting the ERbeta/Angiopoietin-2/Tie-2 signaling-mediated angiogenesis with the FDA-approved anti-estrogen Faslodex to increase the Sunitinib sensitivity in RCC.	Sunitinib	135-144	TEK receptor tyrosine kinase	Mus musculus	36-41
32409702-6	2020	Our study is the first to explore (i) how estrogen receptor beta (ERbeta) can up-regulate ANGPT-2 in RCC cells, and (ii) how ERbeta-increased ANGPT-2 can promote the HUVEC tube formation and reduce sunitinib sensitivity.	Sunitinib	198-207	estrogen receptor 1 (alpha)	Mus musculus	66-72
32409702-6	2020	Our study is the first to explore (i) how estrogen receptor beta (ERbeta) can up-regulate ANGPT-2 in RCC cells, and (ii) how ERbeta-increased ANGPT-2 can promote the HUVEC tube formation and reduce sunitinib sensitivity.	Sunitinib	198-207	estrogen receptor 1 (alpha)	Mus musculus	125-131
32409702-6	2020	Our study is the first to explore (i) how estrogen receptor beta (ERbeta) can up-regulate ANGPT-2 in RCC cells, and (ii) how ERbeta-increased ANGPT-2 can promote the HUVEC tube formation and reduce sunitinib sensitivity.	Sunitinib	198-207	angiopoietin 2	Mus musculus	142-149
32409702-8	2020	We found the up-regulated ANGPT-2 of RCC cells could then increase the Tie-2 phosphorylation to promote the angiogenesis and increase sunitinib treatment resistance of endothelial cells.	Sunitinib	134-143	angiopoietin 2	Mus musculus	26-33
32409702-8	2020	We found the up-regulated ANGPT-2 of RCC cells could then increase the Tie-2 phosphorylation to promote the angiogenesis and increase sunitinib treatment resistance of endothelial cells.	Sunitinib	134-143	TEK receptor tyrosine kinase	Mus musculus	71-76
32409702-10	2020	Targeting this newly identified ERbeta/ANGPT-2/Tie-2 signaling pathway with the FDA-approved anti-estrogen, Faslodex, may help in the development of a novel combined therapy with sunitinib to better suppress the ccRCC progression.	Sunitinib	179-188	estrogen receptor 1 (alpha)	Mus musculus	32-38
32409702-10	2020	Targeting this newly identified ERbeta/ANGPT-2/Tie-2 signaling pathway with the FDA-approved anti-estrogen, Faslodex, may help in the development of a novel combined therapy with sunitinib to better suppress the ccRCC progression.	Sunitinib	179-188	angiopoietin 2	Mus musculus	39-46
32409702-10	2020	Targeting this newly identified ERbeta/ANGPT-2/Tie-2 signaling pathway with the FDA-approved anti-estrogen, Faslodex, may help in the development of a novel combined therapy with sunitinib to better suppress the ccRCC progression.	Sunitinib	179-188	TEK receptor tyrosine kinase	Mus musculus	47-52
32382017-9	2020	We also found ZHX2 overexpression induce Sunitinib resistance though activating autophagy and the combination treatment of Sunitinib and Chloroquine could significantly rescue the phenomenon.	Sunitinib	41-50	zinc fingers and homeoboxes 2	Homo sapiens	14-18
32382017-9	2020	We also found ZHX2 overexpression induce Sunitinib resistance though activating autophagy and the combination treatment of Sunitinib and Chloroquine could significantly rescue the phenomenon.	Sunitinib	123-132	zinc fingers and homeoboxes 2	Homo sapiens	14-18
32382017-10	2020	In summary, these results indicate that ZHX2 drivers cell growth, migration though increase VEGF expression, and transcriptional activate MEK/ERK1/2 signaling pathway, and could induce Sunitinib resistance by regulating self-protective autophagy, these may provide new insight in advanced ccRCC treatment.	Sunitinib	185-194	zinc fingers and homeoboxes 2	Homo sapiens	40-44
32379831-0	2020	Oncogenic effects of RAB27B through exosome independent function in renal cell carcinoma including sunitinib-resistant.	Sunitinib	99-108	RAB27B, member RAS oncogene family	Homo sapiens	21-27
32232883-0	2020	Potential new therapy of Rapalink-1, a new generation mTOR inhibitor, against sunitinib-resistant renal cell carcinoma.	Sunitinib	78-87	mechanistic target of rapamycin kinase	Homo sapiens	54-58
32379831-7	2020	The present study aimed to elucidate the role of RAB27B in RCC including sunitinib-resistant and its role in exosomes.	Sunitinib	73-82	RAB27B, member RAS oncogene family	Homo sapiens	49-55
32379831-10	2020	Furthermore, RAB27B protein expression was enhanced in all of the tested sunitinib-resistant RCC cell lines compared to parental cells.	Sunitinib	73-82	RAB27B, member RAS oncogene family	Homo sapiens	13-19
32379831-12	2020	Moreover, anti-tumor effects of RAB27B downregulation were also observed in sunitinib-resistant RCC cells.	Sunitinib	76-85	RAB27B, member RAS oncogene family	Homo sapiens	32-38
32379831-14	2020	These results showed that RAB27B is a prognostic marker and a novel therapeutic target in sunitinib-sensitive and -resistant RCCs.	Sunitinib	90-99	RAB27B, member RAS oncogene family	Homo sapiens	26-32
32232883-1	2020	Sunitinib, a muiti-targeted receptor tyrosine kinase inhibitor including vascular endothelial growth factor, has been widely used as a first-line treatment against metastatic renal cell carcinoma (mRCC).	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	73-107
32272660-0	2020	The Efficacy of Sunitinib Treatment of Renal Cancer Cells Is Associated with the Protein PHAX In Vitro.	Sunitinib	16-25	phosphorylated adaptor for RNA export	Homo sapiens	89-93
32355171-11	2020	There was a significantly lower expression of both VEGFR-1 and FSHR molecular ultrasound imaging signals in the sunitinib group at all times of treatment (Days 7, 14 and 28).	Sunitinib	112-121	fms related receptor tyrosine kinase 1	Homo sapiens	51-58
32355171-11	2020	There was a significantly lower expression of both VEGFR-1 and FSHR molecular ultrasound imaging signals in the sunitinib group at all times of treatment (Days 7, 14 and 28).	Sunitinib	112-121	follicle stimulating hormone receptor	Homo sapiens	63-67
32355171-14	2020	This study demonstrated for the first time the potential of VEGFR1 and FSHR, by ultrasound-based molecular imaging, to follow-up the longitudinal response to sunitinib in ccRCC.	Sunitinib	158-167	fms related receptor tyrosine kinase 1	Homo sapiens	60-66
32355171-14	2020	This study demonstrated for the first time the potential of VEGFR1 and FSHR, by ultrasound-based molecular imaging, to follow-up the longitudinal response to sunitinib in ccRCC.	Sunitinib	158-167	follicle stimulating hormone receptor	Homo sapiens	71-75
32321460-0	2020	Tumor endothelial ELTD1 as a predictive marker for treatment of renal cancer patients with sunitinib.	Sunitinib	91-100	adhesion G protein-coupled receptor L4	Homo sapiens	18-23
32321460-9	2020	RESULTS: Patients with high ELTD1 expression in the tumor vasculature experienced a significantly better progression free survival (PFS) with sunitinib treatment as compared to patients with low ELTD1 expression (8 versus 5.5 months, respectively).	Sunitinib	142-151	adhesion G protein-coupled receptor L4	Homo sapiens	28-33
32321460-12	2020	CONCLUSIONS: Our results identify tumor vessel ELTD1 expression as a positive predictive marker for sunitinib-treatment in patients suffering from mRCC.	Sunitinib	100-109	adhesion G protein-coupled receptor L4	Homo sapiens	47-52
32272660-2	2020	Here, we take steps towards validating a computational prediction based on differential transcriptome network analysis that phosphorylated adapter RNA export protein (PHAX) is associated with sunitinib drug treatment.	Sunitinib	192-201	phosphorylated adaptor for RNA export	Homo sapiens	124-165
32272660-2	2020	Here, we take steps towards validating a computational prediction based on differential transcriptome network analysis that phosphorylated adapter RNA export protein (PHAX) is associated with sunitinib drug treatment.	Sunitinib	192-201	phosphorylated adaptor for RNA export	Homo sapiens	167-171
32272660-4	2020	Immunofluorescence staining of patient tumours showed strong localisation of PHAX to the microvasculature consistent with the anti-angiogenic effect of sunitinib.	Sunitinib	152-161	phosphorylated adaptor for RNA export	Homo sapiens	77-81
32272660-6	2020	In organ culture, ccRCC cells had higher levels of PHAX protein expression than normal kidney cells, and sunitinib increased PHAX protein expression in a dose dependent manner (untreated vs. 100 microM; p < 0.05).	Sunitinib	105-114	phosphorylated adaptor for RNA export	Homo sapiens	125-129
32272660-7	2020	PHAX knockdown in a ccRCC organ culture model impacted the ability of sunitinib to cause cancer cell death (p < 0.0001 untreated vs. treated), suggesting a role for PHAX in mediating the efficacy of sunitinib.	Sunitinib	70-79	phosphorylated adaptor for RNA export	Homo sapiens	0-4
32272660-7	2020	PHAX knockdown in a ccRCC organ culture model impacted the ability of sunitinib to cause cancer cell death (p < 0.0001 untreated vs. treated), suggesting a role for PHAX in mediating the efficacy of sunitinib.	Sunitinib	199-208	phosphorylated adaptor for RNA export	Homo sapiens	0-4
32272660-7	2020	PHAX knockdown in a ccRCC organ culture model impacted the ability of sunitinib to cause cancer cell death (p < 0.0001 untreated vs. treated), suggesting a role for PHAX in mediating the efficacy of sunitinib.	Sunitinib	199-208	phosphorylated adaptor for RNA export	Homo sapiens	165-169
31369705-4	2020	Interestingly, our data indicated that one candidate aptamer, called V15, can specifically inhibit the in vitro kinase activity of mutant c-KITD816V with an IC50 value that is 9-fold more potent than the sunitinib drug tested under the same conditions.	Sunitinib	204-213	immunoglobulin lambda variable 2-18	Homo sapiens	69-72
31999483-9	2020	Besides, we found that sunitinib, a multi-targeted tyrosine kinase inhibitor, could significantly inhibit ufmylation, whereas overexpression of active Ufm1 partially inhibited the antitumor effects of sunitinib.	Sunitinib	201-210	ubiquitin fold modifier 1	Homo sapiens	151-155
31866228-3	2020	Another class of therapeutic agents that has been implicated in TMA is the vascular endothelial growth factor (VEGF) pathway inhibitors, including the anti-VEGF monoclonal antibody bevacizumab and the VEGF receptor tyrosine kinase inhibitor sunitinib.	Sunitinib	241-250	vascular endothelial growth factor A	Homo sapiens	75-109
31866228-3	2020	Another class of therapeutic agents that has been implicated in TMA is the vascular endothelial growth factor (VEGF) pathway inhibitors, including the anti-VEGF monoclonal antibody bevacizumab and the VEGF receptor tyrosine kinase inhibitor sunitinib.	Sunitinib	241-250	vascular endothelial growth factor A	Homo sapiens	111-115
32234883-0	2020	PTEN Is Involved in Sunitinib and Sorafenib Resistance in Renal Cell Carcinoma.	Sunitinib	20-29	phosphatase and tensin homolog	Homo sapiens	0-4
32234883-5	2020	RESULTS: PTEN knockout promoted spheroid formation and decreased sunitinib/sorafenib sensitivity in RCC cell lines.	Sunitinib	65-74	phosphatase and tensin homolog	Homo sapiens	9-13
32234883-6	2020	PTEN immunohistochemistry in 74 metastatic RCCs treated with sunitinib and sorafenib revealed negative PTEN expression in 23% of samples.	Sunitinib	61-70	phosphatase and tensin homolog	Homo sapiens	0-4
32234883-7	2020	Kaplan-Meier analysis showed a significant association of negative PTEN expression with poor progression-free survival in metastatic RCC treated with sunitinib and sorafenib (p=0.024) or sunitinib alone (p=0.009).	Sunitinib	150-159	phosphatase and tensin homolog	Homo sapiens	67-71
32234883-7	2020	Kaplan-Meier analysis showed a significant association of negative PTEN expression with poor progression-free survival in metastatic RCC treated with sunitinib and sorafenib (p=0.024) or sunitinib alone (p=0.009).	Sunitinib	187-196	phosphatase and tensin homolog	Homo sapiens	67-71
32078941-6	2020	Sunitinib malate increased infiltration of CD8+ T cells and decreased regulatory T cells (Tregs), accompanied by inhibited expression of TGF-beta1 and IL-10 and increased CCL-28, IFN-gamma and IL-12, but no significant inhibition of myeloid-derived suppressor cells (MDSCs) was observed.	Sunitinib	0-16	transforming growth factor beta 1	Homo sapiens	137-146
32078941-6	2020	Sunitinib malate increased infiltration of CD8+ T cells and decreased regulatory T cells (Tregs), accompanied by inhibited expression of TGF-beta1 and IL-10 and increased CCL-28, IFN-gamma and IL-12, but no significant inhibition of myeloid-derived suppressor cells (MDSCs) was observed.	Sunitinib	0-16	interleukin 10	Homo sapiens	151-156
32078941-6	2020	Sunitinib malate increased infiltration of CD8+ T cells and decreased regulatory T cells (Tregs), accompanied by inhibited expression of TGF-beta1 and IL-10 and increased CCL-28, IFN-gamma and IL-12, but no significant inhibition of myeloid-derived suppressor cells (MDSCs) was observed.	Sunitinib	0-16	C-C motif chemokine ligand 28	Homo sapiens	171-177
32078941-6	2020	Sunitinib malate increased infiltration of CD8+ T cells and decreased regulatory T cells (Tregs), accompanied by inhibited expression of TGF-beta1 and IL-10 and increased CCL-28, IFN-gamma and IL-12, but no significant inhibition of myeloid-derived suppressor cells (MDSCs) was observed.	Sunitinib	0-16	interferon gamma	Homo sapiens	179-188
32078941-7	2020	In addition, sunitinib malate increased the levels of PD-1 and PD-L1 in TME, combined with anti-PD-1 therapy showed a significant reduction in tumor burden compared with either monotherapy, suggesting that anti-PD-1 therapy is reasonable after sunitinib malate treatment.	Sunitinib	13-29	CD274 molecule	Homo sapiens	63-68
32078941-7	2020	In addition, sunitinib malate increased the levels of PD-1 and PD-L1 in TME, combined with anti-PD-1 therapy showed a significant reduction in tumor burden compared with either monotherapy, suggesting that anti-PD-1 therapy is reasonable after sunitinib malate treatment.	Sunitinib	244-260	CD274 molecule	Homo sapiens	63-68
31702819-3	2020	Previous reports have found success with sunitinib in imatinib-resistant GIST, but we report a certain wild-type KIT mutation GIST with cutaneous and subcutaneous metastasis that was unresponsive to multiple tyrosine kinase inhibitor (TKI) treatments.	Sunitinib	41-50	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	113-116
32041631-8	2020	RESULTS: We demonstrate that YB-1 and ABCB-1 are upregulated in sunitinib-resistant in vitro, ex vivo, in vivo and patient samples compared to the sensitive samples.	Sunitinib	64-73	Y-box binding protein 1	Homo sapiens	29-33
31023123-0	2020	Influence of ABCB1 (1236C &gt; T, 2677G &gt; T and 3435C &gt; T) polymorphisms on the transport ability of P-gp-mediated sunitinib in Caco-2 cell line.	Sunitinib	121-130	ATP binding cassette subfamily B member 1	Homo sapiens	13-18
31023123-0	2020	Influence of ABCB1 (1236C &gt; T, 2677G &gt; T and 3435C &gt; T) polymorphisms on the transport ability of P-gp-mediated sunitinib in Caco-2 cell line.	Sunitinib	121-130	ATP binding cassette subfamily B member 1	Homo sapiens	107-111
31023123-2	2020	The aim of the current research was to observe in vitro the impacts of ABCB1 (1236 C &gt; T, 2677G &gt; T, and 3435C &gt; T) polymorphisms on the efflux activity of P-gp-mediated sunitinib.	Sunitinib	179-188	ATP binding cassette subfamily B member 1	Homo sapiens	71-76
31023123-2	2020	The aim of the current research was to observe in vitro the impacts of ABCB1 (1236 C &gt; T, 2677G &gt; T, and 3435C &gt; T) polymorphisms on the efflux activity of P-gp-mediated sunitinib.	Sunitinib	179-188	ATP binding cassette subfamily B member 1	Homo sapiens	165-169
31023123-6	2020	The recombinant cell lines transfected with ABCB1 variant alleles (1236 T, 2677T, and 3435T) showed higher resistance to sunitinib compared to cells transfecting with ABCB1 wild-type allele (p &lt; .05).	Sunitinib	121-130	ATP binding cassette subfamily B member 1	Homo sapiens	44-49
31023123-7	2020	The intracellular accumulation of sunitinib was significantly decreased in the three types of recombinant cell lines overexpressing ABCB1 variant alleles in comparison of their wild-type cell lines (p &lt; .05).	Sunitinib	34-43	ATP binding cassette subfamily B member 1	Homo sapiens	132-137
31023123-9	2020	The P-gp activity in recombinant variant cells is stronger when mediated transport of sunitinib than wild-type counterpart.	Sunitinib	86-95	ATP binding cassette subfamily B member 1	Homo sapiens	4-8
31023123-10	2020	P-gp encoded by ABCB1 (1236 T, 2677T, and 3435T) variant alleles may be more efficient to transport sunitinib than wild-type allele.	Sunitinib	100-109	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
31023123-10	2020	P-gp encoded by ABCB1 (1236 T, 2677T, and 3435T) variant alleles may be more efficient to transport sunitinib than wild-type allele.	Sunitinib	100-109	ATP binding cassette subfamily B member 1	Homo sapiens	16-21
31023123-11	2020	Our observation suggests that ABCB1 (1236 C &gt; T, 2677G &gt; T, and 3435C &gt; T) polymorphisms affect the transport ability of P-gp-mediated sunitinib.	Sunitinib	144-153	ATP binding cassette subfamily B member 1	Homo sapiens	30-35
31023123-11	2020	Our observation suggests that ABCB1 (1236 C &gt; T, 2677G &gt; T, and 3435C &gt; T) polymorphisms affect the transport ability of P-gp-mediated sunitinib.	Sunitinib	144-153	ATP binding cassette subfamily B member 1	Homo sapiens	130-134
31023123-12	2020	Collectively, ABCB1 polymorphisms may alter the P-gp-mediated sunitinib sensitivity via regulating drug transport.	Sunitinib	62-71	ATP binding cassette subfamily B member 1	Homo sapiens	14-19
31023123-12	2020	Collectively, ABCB1 polymorphisms may alter the P-gp-mediated sunitinib sensitivity via regulating drug transport.	Sunitinib	62-71	ATP binding cassette subfamily B member 1	Homo sapiens	48-52
32041631-8	2020	RESULTS: We demonstrate that YB-1 and ABCB-1 are upregulated in sunitinib-resistant in vitro, ex vivo, in vivo and patient samples compared to the sensitive samples.	Sunitinib	64-73	ATP binding cassette subfamily B member 1	Homo sapiens	38-44
32041631-10	2020	Furthermore, our results establish that inhibiting ABCB-1 with elacridar, in addition to sunitinib, has a positive impact on reverting sunitinib-resistance development in in vitro, ex vivo and in vivo models.	Sunitinib	135-144	ATP binding cassette subfamily B member 1	Homo sapiens	51-57
31922424-3	2020	In November 2017, sunitinib was approved in the USA as the first adjuvant therapy for patients at high risk for recurrent RCC postnephrectomy based on results from the S-TRAC trial.	Sunitinib	18-27	T cell receptor alpha constant	Homo sapiens	170-174
32206105-2	2020	Using a new multimodal preclinical imaging instrument, we explored a sequence of events leading to sunitinib-induced resistance in a murine model of paraganglioma (PGL) invalidated for the expression of succinate dehydrogenase subunit B (Sdhb -/-).	Sunitinib	99-108	succinate dehydrogenase complex, subunit B, iron sulfur (Ip)	Mus musculus	238-242
32206105-10	2020	Conclusion: These results demonstrate an adaptive resistance of Sdhb -/- tumors to six weeks of sunitinib treatment.	Sunitinib	96-105	succinate dehydrogenase complex, subunit B, iron sulfur (Ip)	Mus musculus	64-68
31789391-7	2020	The results of western blotting demonstrated that sunitinib induced upregulation of LAMP-1 and LC3-II, and downregulation of sequestosome 1/p62, indicating the activation of autophagy.	Sunitinib	50-59	lysosomal associated membrane protein 1	Homo sapiens	84-90
32005261-2	2020	The events that drive GIST oncogenesis are primarily KIT or PDGFRA mutations, which lead to the susceptibility of these tumors to small-molecule tyrosine kinase inhibitors such as imatinib and sunitinib.	Sunitinib	193-202	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-56
32005261-2	2020	The events that drive GIST oncogenesis are primarily KIT or PDGFRA mutations, which lead to the susceptibility of these tumors to small-molecule tyrosine kinase inhibitors such as imatinib and sunitinib.	Sunitinib	193-202	platelet derived growth factor receptor alpha	Homo sapiens	60-66
31975150-4	2020	First, the PBPK model for sunitinib was established, then the cytochrome P450 3A4-mediated metabolism of sunitinib was used as the input for SU012662.	Sunitinib	105-114	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	62-81
30825427-8	2020	Sunitinib malate, a multi tyrosine kinase inhibitor, market authorised for cancer, reversed the ocular behavioural and morphological phenotypes observed in vhl-/- zebrafish.	Sunitinib	0-16	von Hippel-Lindau tumor suppressor	Danio rerio	156-159
30825427-9	2020	We conclude that the zebrafish vhl gene contributes to an endogenous molecular barrier that prevents development of intraretinal vasculature, and that pharmacological intervention with sunitinib can improve visual function and hyaloid vessel patterning while reducing abnormally formed ectopic intraretinal vessels in vhl-/- zebrafish.	Sunitinib	185-194	von Hippel-Lindau tumor suppressor	Danio rerio	31-34
30825427-9	2020	We conclude that the zebrafish vhl gene contributes to an endogenous molecular barrier that prevents development of intraretinal vasculature, and that pharmacological intervention with sunitinib can improve visual function and hyaloid vessel patterning while reducing abnormally formed ectopic intraretinal vessels in vhl-/- zebrafish.	Sunitinib	185-194	von Hippel-Lindau tumor suppressor	Danio rerio	318-321
31744648-1	2020	INTRODUCTION: Sunitinib (SUN) and pazopanib (PAZ) are 2 oral tyrosine kinase inhibitors against vascular endothelial growth factor.	Sunitinib	14-23	vascular endothelial growth factor A	Homo sapiens	96-130
31535851-7	2020	Docking experiments in the CYP3A4 active site were performed and showed that pazopanib and sunitinib fitting in the catalytic site are in accordance with their regioselective oxidation to aldehydes.	Sunitinib	91-100	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	27-33
31789391-7	2020	The results of western blotting demonstrated that sunitinib induced upregulation of LAMP-1 and LC3-II, and downregulation of sequestosome 1/p62, indicating the activation of autophagy.	Sunitinib	50-59	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	95-98
31789391-7	2020	The results of western blotting demonstrated that sunitinib induced upregulation of LAMP-1 and LC3-II, and downregulation of sequestosome 1/p62, indicating the activation of autophagy.	Sunitinib	50-59	sequestosome 1	Homo sapiens	125-139
31789391-7	2020	The results of western blotting demonstrated that sunitinib induced upregulation of LAMP-1 and LC3-II, and downregulation of sequestosome 1/p62, indicating the activation of autophagy.	Sunitinib	50-59	sequestosome 1	Homo sapiens	140-143
31371341-0	2019	PD-L1 Expression and Clinical Outcomes to Cabozantinib, Everolimus, and Sunitinib in Patients with Metastatic Renal Cell Carcinoma: Analysis of the Randomized Clinical Trials METEOR and CABOSUN.	Sunitinib	72-81	CD274 molecule	Homo sapiens	0-5
31905947-6	2019	Inhibition of AAK1 kinase activity by sunitinib blocked AP2M1 phosphorylation, significantly inhibiting RABV infection and preventing RABV from entering early endosomes.	Sunitinib	38-47	AP2 associated kinase 1	Homo sapiens	14-18
31905947-6	2019	Inhibition of AAK1 kinase activity by sunitinib blocked AP2M1 phosphorylation, significantly inhibiting RABV infection and preventing RABV from entering early endosomes.	Sunitinib	38-47	adaptor related protein complex 2 subunit mu 1	Homo sapiens	56-61
31471313-2	2019	Approved KIT inhibitors sunitinib and regorafenib have complementary activity against KIT resistance mutations.	Sunitinib	24-33	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	9-12
31471313-2	2019	Approved KIT inhibitors sunitinib and regorafenib have complementary activity against KIT resistance mutations.	Sunitinib	24-33	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	86-89
31463627-6	2019	Sunitinib also significantly decreased the number of tumor-infiltrating CD8 + T and B cells, MDSCs, and macrophages.	Sunitinib	0-9	CD8a molecule	Homo sapiens	72-75
31485624-10	2019	GNF-5837 also enhanced the cytotoxic effects of sunitinib via inhibition of ERK kinase.	Sunitinib	48-57	mitogen-activated protein kinase 1	Homo sapiens	76-79
31501521-0	2020	Targeting the TR4 nuclear receptor-mediated lncTASR/AXL signaling with tretinoin increases the sunitinib sensitivity to better suppress the RCC progression.	Sunitinib	95-104	nuclear receptor subfamily 2 group C member 2	Homo sapiens	14-17
31501521-0	2020	Targeting the TR4 nuclear receptor-mediated lncTASR/AXL signaling with tretinoin increases the sunitinib sensitivity to better suppress the RCC progression.	Sunitinib	95-104	AXL receptor tyrosine kinase	Homo sapiens	52-55
31501521-4	2020	Here we found TR4 nuclear receptor might alter the sunitinib resistance to RCC via altering the TR4/lncTASR/AXL signaling.	Sunitinib	51-60	nuclear receptor subfamily 2 group C member 2	Homo sapiens	14-17
31501521-4	2020	Here we found TR4 nuclear receptor might alter the sunitinib resistance to RCC via altering the TR4/lncTASR/AXL signaling.	Sunitinib	51-60	nuclear receptor subfamily 2 group C member 2	Homo sapiens	96-99
31501521-4	2020	Here we found TR4 nuclear receptor might alter the sunitinib resistance to RCC via altering the TR4/lncTASR/AXL signaling.	Sunitinib	51-60	AXL receptor tyrosine kinase	Homo sapiens	108-111
31501521-5	2020	Mechanism dissection revealed that TR4 could modulate lncTASR (ENST00000600671.1) expression via transcriptional regulation, which might then increase AXL protein expression via enhancing the stability of AXL mRNA to increase the sunitinib resistance in RCC.	Sunitinib	230-239	nuclear receptor subfamily 2 group C member 2	Homo sapiens	35-38
31501521-6	2020	Human clinical surveys also linked the expression of TR4, lncTASR, and AXL to the RCC survival, and results from multiple RCC cell lines revealed that targeting this newly identified TR4-mediated signaling with small molecules, including tretinoin, metformin, or TR4-shRNAs, all led to increase the sunitinib sensitivity to better suppress the RCC progression, and our preclinical study using the in vivo mouse model further proved tretinoin had a better synergistic effect to increase sunitinib sensitivity to suppress RCC progression.	Sunitinib	299-308	nuclear receptor subfamily 2 group C member 2	Homo sapiens	183-186
31501521-6	2020	Human clinical surveys also linked the expression of TR4, lncTASR, and AXL to the RCC survival, and results from multiple RCC cell lines revealed that targeting this newly identified TR4-mediated signaling with small molecules, including tretinoin, metformin, or TR4-shRNAs, all led to increase the sunitinib sensitivity to better suppress the RCC progression, and our preclinical study using the in vivo mouse model further proved tretinoin had a better synergistic effect to increase sunitinib sensitivity to suppress RCC progression.	Sunitinib	299-308	nuclear receptor subfamily 2 group C member 2	Homo sapiens	183-186
31501521-6	2020	Human clinical surveys also linked the expression of TR4, lncTASR, and AXL to the RCC survival, and results from multiple RCC cell lines revealed that targeting this newly identified TR4-mediated signaling with small molecules, including tretinoin, metformin, or TR4-shRNAs, all led to increase the sunitinib sensitivity to better suppress the RCC progression, and our preclinical study using the in vivo mouse model further proved tretinoin had a better synergistic effect to increase sunitinib sensitivity to suppress RCC progression.	Sunitinib	486-495	nuclear receptor subfamily 2 group C member 2	Homo sapiens	183-186
31501521-6	2020	Human clinical surveys also linked the expression of TR4, lncTASR, and AXL to the RCC survival, and results from multiple RCC cell lines revealed that targeting this newly identified TR4-mediated signaling with small molecules, including tretinoin, metformin, or TR4-shRNAs, all led to increase the sunitinib sensitivity to better suppress the RCC progression, and our preclinical study using the in vivo mouse model further proved tretinoin had a better synergistic effect to increase sunitinib sensitivity to suppress RCC progression.	Sunitinib	486-495	nuclear receptor subfamily 2 group C member 2	Homo sapiens	183-186
31231785-1	2019	Purpose Sunitinib is a vascular endothelial growth factor receptor (VEGFR) inhibitor with antitumor activity against bladder cancer.	Sunitinib	8-17	kinase insert domain receptor	Homo sapiens	23-66
31231785-1	2019	Purpose Sunitinib is a vascular endothelial growth factor receptor (VEGFR) inhibitor with antitumor activity against bladder cancer.	Sunitinib	8-17	kinase insert domain receptor	Homo sapiens	68-73
31775817-9	2019	Finally, we show that the FDA-approved protein kinase inhibitor, sunitinib, which has activity against DLK and LZK, is able to produce similar increases in RGC survival.	Sunitinib	65-74	mitogen-activated protein kinase kinase kinase 12	Mus musculus	103-106
31775817-9	2019	Finally, we show that the FDA-approved protein kinase inhibitor, sunitinib, which has activity against DLK and LZK, is able to produce similar increases in RGC survival.	Sunitinib	65-74	mitogen-activated protein kinase kinase kinase 13	Mus musculus	111-114
31427001-0	2019	HP-1 inhibits the progression of ccRCC and enhances sunitinib therapeutic effects by suppressing EMT.	Sunitinib	52-61	haptoglobin	Mus musculus	0-4
31427001-7	2019	In addition, the HP-1/sunitinib combination inhibited the PI3K/Akt/VEGFR pathway, reducing the expression of pathway-related proteins.	Sunitinib	22-31	haptoglobin	Mus musculus	17-21
31427001-7	2019	In addition, the HP-1/sunitinib combination inhibited the PI3K/Akt/VEGFR pathway, reducing the expression of pathway-related proteins.	Sunitinib	22-31	thymoma viral proto-oncogene 1	Mus musculus	63-66
31427001-8	2019	The HP-1-induced enhancement of sunitinib effects on tumor growth were also observed in vivo in a xenograft mouse model.	Sunitinib	32-41	haptoglobin	Mus musculus	4-8
31427001-9	2019	Overall, these results indicated that HP-1 exerted antitumor effects against clear cell renal cell carcinoma (ccRCC) and enhanced the therapeutic efficacy of sunitinib.	Sunitinib	158-167	haptoglobin	Mus musculus	38-42
31348025-7	2019	Based on the S-TRAC data, sunitinib is approved for use in the adjuvant setting, and can be considered under select circumstances.	Sunitinib	26-35	T cell receptor alpha constant	Homo sapiens	15-19
31545458-1	2019	The present study aimed to investigate the potential mechanisms of human miR-942 in the sunitinib-resistance of renal cell carcinoma (RCC).	Sunitinib	88-97	microRNA 942	Homo sapiens	73-80
31545458-11	2019	The expression level of miR-942 was significantly increased in sunitinib-resistant cells.	Sunitinib	63-72	microRNA 942	Homo sapiens	24-31
31471309-6	2019	RESULTS: VEGF and PlGF increased after 4 weeks on sunitinib or sorafenib (P < 0.0001 for both) and returned to baseline at 6 weeks on sunitinib (corresponding to the break in the sunitinib schedule) but not sorafenib (which was administered continuously).	Sunitinib	50-59	vascular endothelial growth factor A	Homo sapiens	9-13
31471309-10	2019	CXCL10 was elevated at 4 and 6 weeks on sunitinib and sorafenib but not on placebo.	Sunitinib	40-49	C-X-C motif chemokine ligand 10	Homo sapiens	0-6
31371341-4	2019	Our primary aim was to correlate progression-free survival (PFS) by independent central review with PD-L1 status in patients treated with cabozantinib, everolimus (METEOR), or sunitinib (CABOSUN).	Sunitinib	176-185	CD274 molecule	Homo sapiens	100-105
31385548-7	2019	PDGF-BB promoted the proliferation, migration and invasion of hPFs, which can be significantly suppressed by sunitinib via inhibition of the PDGFR-beta/extracellular signal-regulated kinase (ERK) pathway.	Sunitinib	109-118	platelet derived growth factor receptor alpha	Homo sapiens	141-151
31400051-13	2019	Hypermethylated PON1 promoted migration, invasion and proliferation of sunitinib-resistance renal cancer cells and arrested more cells in G0/G1 phase.	Sunitinib	71-80	paraoxonase 1	Homo sapiens	16-20
31445075-8	2019	Accordingly, sunitinib caused caspase 3 activation and DNA fragmentation in H9c2 cells.	Sunitinib	13-22	caspase 3	Rattus norvegicus	30-39
31445075-9	2019	Co-exposure with mito-TEMPO (mitochondrial-specific ROS scavenger) for 24 h prevented ATP and GSH depletion, as well as the increases in H2O2 and caspase 3/7 activity observed with sunitinib.	Sunitinib	181-190	caspase 3	Rattus norvegicus	146-155
31519573-0	2019	Inhibition of Tumor Growth and Sensitization to Sunitinib by RNA Interference Targeting Programmed Death-ligand 1 in Mouse Renal Cell Carcinoma RenCa Model.	Sunitinib	48-57	CD274 antigen	Mus musculus	88-113
31519573-2	2019	The purpose of this study was to address the inhibitory effects of programmed death-ligand 1 (PD-L1) expression on growth and sensitivity to sunitinib in the mouse RCC RenCa model.	Sunitinib	141-150	CD274 antigen	Mus musculus	67-92
31519573-2	2019	The purpose of this study was to address the inhibitory effects of programmed death-ligand 1 (PD-L1) expression on growth and sensitivity to sunitinib in the mouse RCC RenCa model.	Sunitinib	141-150	CD274 antigen	Mus musculus	94-99
31519573-7	2019	Treatment of mice bearing each tumor with sunitinib resulted in a significant reduction of the RenCa/sh-PD-L1 tumor compared to the RenCa/Co tumor.	Sunitinib	42-51	CD274 antigen	Mus musculus	104-109
31519573-9	2019	CONCLUSION: Suppressed expression of PD-L1 could increase tumor-infiltrating CD8+ T cells and result in growth inhibition as well as enhanced sensitivity to sunitinib in the RenCa model.	Sunitinib	157-166	CD274 antigen	Mus musculus	37-42
31467229-0	2019	MiR-376b-3p Is Associated With Long-term Response to Sunitinib in Metastatic Renal Cell Carcinoma Patients.	Sunitinib	53-62	microRNA 376b	Homo sapiens	0-8
31385548-7	2019	PDGF-BB promoted the proliferation, migration and invasion of hPFs, which can be significantly suppressed by sunitinib via inhibition of the PDGFR-beta/extracellular signal-regulated kinase (ERK) pathway.	Sunitinib	109-118	mitogen-activated protein kinase 1	Homo sapiens	191-194
31385548-8	2019	In the ex vivo model, the knockout of PDGFRB and sunitinib treatment blocked the proliferation and motility of fibroblasts in the pterygial stroma via the suppression of PDGFR-beta/ERK pathway.	Sunitinib	49-58	platelet derived growth factor receptor alpha	Homo sapiens	170-180
31385548-8	2019	In the ex vivo model, the knockout of PDGFRB and sunitinib treatment blocked the proliferation and motility of fibroblasts in the pterygial stroma via the suppression of PDGFR-beta/ERK pathway.	Sunitinib	49-58	mitogen-activated protein kinase 1	Homo sapiens	181-184
31385548-9	2019	Conclusion: This study demonstrates that PDGFR-beta may be a potential therapeutic target for pterygium, and inhibition of PDGFR-beta by sunitinib is a promising and effective approach for pterygium treatment.	Sunitinib	137-146	platelet derived growth factor receptor alpha	Homo sapiens	123-133
31464635-10	2019	The sunitinib-axitinib sequence was safe and effective, the mOS was 41.15 months.	Sunitinib	4-13	Moloney sarcoma oncogene	Mus musculus	60-63
31401413-9	2019	In vitro, we found that adiponectin inhibited migration, invasion and sensitized RCC cells to sunitinib though interacting with AdipoR1, but not AdipoR2.	Sunitinib	94-103	adiponectin, C1Q and collagen domain containing	Homo sapiens	24-35
31401413-10	2019	Furthermore, we demonstrated that adiponentin-AdipoR1 axis inhibits tumor cells migration and invasion by blocking the GSK3beta/beta-Catenin pathway and enhances sunitinib sensitivity via abrogating PI3K/AKT/NF-kappaB signaling.	Sunitinib	162-171	adiponectin receptor 1	Homo sapiens	46-53
31443471-5	2019	Currently vascular endothelial growth factor (VEGF) targeted therapy based on tyrosine kinase inhibitors (TKI), sunitinib and pazopanib is the alternative regimen for patients who cannot tolerate immune checkpoint inhibitors (ICI).	Sunitinib	112-121	vascular endothelial growth factor A	Homo sapiens	10-44
31507414-0	2019	Downregulation of miR-146a Contributes to Cardiac Dysfunction Induced by the Tyrosine Kinase Inhibitor Sunitinib.	Sunitinib	103-112	microRNA 146	Mus musculus	18-26
31507414-4	2019	A significant downregulation of miR-146a was observed in the myocardium of sunitinib-treated mice, along with a 20% decrease in left ventricle ejection fraction (LVEF).	Sunitinib	75-84	microRNA 146	Mus musculus	32-40
31507414-8	2019	Significant upregulation of PLN and ANK2 at the mRNA and protein levels was observed in the myocardium of sunitinib-treated mice.	Sunitinib	106-115	phospholamban	Mus musculus	28-31
31507414-8	2019	Significant upregulation of PLN and ANK2 at the mRNA and protein levels was observed in the myocardium of sunitinib-treated mice.	Sunitinib	106-115	ankyrin 2, brain	Mus musculus	36-40
31507414-10	2019	SiRNA knockdown of PLN or ANK2 prevented sunitinib-induced suppression of contractility in hiPSC-CMs.	Sunitinib	41-50	phospholamban	Mus musculus	19-22
31507414-10	2019	SiRNA knockdown of PLN or ANK2 prevented sunitinib-induced suppression of contractility in hiPSC-CMs.	Sunitinib	41-50	ankyrin 2, brain	Mus musculus	26-30
31507414-11	2019	Therefore, our in vivo and in vitro results showed that sunitinib downregulated miR-146a, which contributes to cardiac contractile dysfunction by regulating the downstream targets PLN and ANK2, and that upregulation of miR-146a alleviated the inhibitory effect of SNT on cardiac contractility.	Sunitinib	56-65	microRNA 146	Mus musculus	80-88
31507414-11	2019	Therefore, our in vivo and in vitro results showed that sunitinib downregulated miR-146a, which contributes to cardiac contractile dysfunction by regulating the downstream targets PLN and ANK2, and that upregulation of miR-146a alleviated the inhibitory effect of SNT on cardiac contractility.	Sunitinib	56-65	phospholamban	Mus musculus	180-183
31507414-11	2019	Therefore, our in vivo and in vitro results showed that sunitinib downregulated miR-146a, which contributes to cardiac contractile dysfunction by regulating the downstream targets PLN and ANK2, and that upregulation of miR-146a alleviated the inhibitory effect of SNT on cardiac contractility.	Sunitinib	56-65	ankyrin 2, brain	Mus musculus	188-192
31507414-11	2019	Therefore, our in vivo and in vitro results showed that sunitinib downregulated miR-146a, which contributes to cardiac contractile dysfunction by regulating the downstream targets PLN and ANK2, and that upregulation of miR-146a alleviated the inhibitory effect of SNT on cardiac contractility.	Sunitinib	56-65	microRNA 146	Mus musculus	219-227
31462260-11	2019	Mechanistic studies confirmed that HM-3 and Sunitinib regulated distribution of integrin alphavbeta3, alpha5beta1, VEGFR2 and alphavbeta3-VEGFR2 complexes, both inside and outside of the lipid raft regions to regulate endothelial cell migration and intracellular RhoGTPase activities.	Sunitinib	44-53	kinase insert domain protein receptor	Mus musculus	115-121
31462260-11	2019	Mechanistic studies confirmed that HM-3 and Sunitinib regulated distribution of integrin alphavbeta3, alpha5beta1, VEGFR2 and alphavbeta3-VEGFR2 complexes, both inside and outside of the lipid raft regions to regulate endothelial cell migration and intracellular RhoGTPase activities.	Sunitinib	44-53	kinase insert domain protein receptor	Mus musculus	138-144
31507414-11	2019	Therefore, our in vivo and in vitro results showed that sunitinib downregulated miR-146a, which contributes to cardiac contractile dysfunction by regulating the downstream targets PLN and ANK2, and that upregulation of miR-146a alleviated the inhibitory effect of SNT on cardiac contractility.	Sunitinib	56-65	fibroblast growth factor receptor substrate 2	Homo sapiens	264-267
31507414-12	2019	Thus, miR-146a could be a useful protective agent against sunitinib-induced cardiac dysfunction.	Sunitinib	58-67	microRNA 146	Mus musculus	6-14
31443471-5	2019	Currently vascular endothelial growth factor (VEGF) targeted therapy based on tyrosine kinase inhibitors (TKI), sunitinib and pazopanib is the alternative regimen for patients who cannot tolerate immune checkpoint inhibitors (ICI).	Sunitinib	112-121	vascular endothelial growth factor A	Homo sapiens	46-50
31411627-3	2019	The pH-sensitive micelle core encapsulates PTX, while beta-cyclodextrin molecules being conjugated to the micelle shell via matrix metalloproteinase 2 (MMP-2) sensitive peptides include sunitinib.	Sunitinib	186-195	matrix metallopeptidase 2	Homo sapiens	152-157
31411627-4	2019	Following the pH and MMP-2 dual sensitive structure design, the micelle may sequentially release sunitinib inside the tumor extracellular matrix and PTX into cancer cells through responding to enriched MMP-2 levels and decreased pH, respectively.	Sunitinib	97-106	matrix metallopeptidase 2	Homo sapiens	21-26
31411627-4	2019	Following the pH and MMP-2 dual sensitive structure design, the micelle may sequentially release sunitinib inside the tumor extracellular matrix and PTX into cancer cells through responding to enriched MMP-2 levels and decreased pH, respectively.	Sunitinib	97-106	matrix metallopeptidase 2	Homo sapiens	202-207
31294623-9	2019	Sunitinib therapy substantially mitigated both AAA formation and further progression of established AAAs, attenuated aneurysmal aortic MMP2 (matrix metalloproteinase) and MMP9 protein expression, inhibited inflammatory monocyte and neutrophil chemotaxis to VEGF-A, and reduced MMP2, MMP9, and VEGF-A mRNA expression in macrophages and smooth muscle cells in vitro.	Sunitinib	0-9	matrix metallopeptidase 2	Mus musculus	135-139
31534544-0	2019	DNA methylation-regulated QPCT promotes sunitinib resistance by increasing HRAS stability in renal cell carcinoma.	Sunitinib	40-49	glutaminyl-peptide cyclotransferase	Homo sapiens	26-30
31534544-0	2019	DNA methylation-regulated QPCT promotes sunitinib resistance by increasing HRAS stability in renal cell carcinoma.	Sunitinib	40-49	HRas proto-oncogene, GTPase	Homo sapiens	75-79
31534544-4	2019	We verified glutaminyl peptide cyclotransferase (QPCT) expression in sunitinib-nonresponsive and -responsive RCC tissues via qRT-PCR, western blot and immunohistochemical assays.	Sunitinib	69-78	glutaminyl-peptide cyclotransferase	Homo sapiens	12-47
31534544-4	2019	We verified glutaminyl peptide cyclotransferase (QPCT) expression in sunitinib-nonresponsive and -responsive RCC tissues via qRT-PCR, western blot and immunohistochemical assays.	Sunitinib	69-78	glutaminyl-peptide cyclotransferase	Homo sapiens	49-53
31534544-5	2019	Then, cell counting kit 8 (CCK-8), plate colony formation and flow cytometric assays were used to verify the function of QPCT in RCC sunitinib resistance after QPCT intervention or overexpression.	Sunitinib	133-142	glutaminyl-peptide cyclotransferase	Homo sapiens	121-125
31534544-8	2019	Results: We found that the degree of methylation in the QPCT promoter region was significantly different between sunitinib-nonresponsive and -responsive RCC tissues.	Sunitinib	113-122	glutaminyl-peptide cyclotransferase	Homo sapiens	56-60
31534544-9	2019	In the sunitinib-nonresponsive tissues, the degree of methylation in the QPCT promoter region was significantly reduced, and the expression of QPCT was upregulated, which correlated with a clinically poor response to sunitinib.	Sunitinib	7-16	glutaminyl-peptide cyclotransferase	Homo sapiens	73-77
31534544-9	2019	In the sunitinib-nonresponsive tissues, the degree of methylation in the QPCT promoter region was significantly reduced, and the expression of QPCT was upregulated, which correlated with a clinically poor response to sunitinib.	Sunitinib	7-16	glutaminyl-peptide cyclotransferase	Homo sapiens	143-147
31534544-9	2019	In the sunitinib-nonresponsive tissues, the degree of methylation in the QPCT promoter region was significantly reduced, and the expression of QPCT was upregulated, which correlated with a clinically poor response to sunitinib.	Sunitinib	217-226	glutaminyl-peptide cyclotransferase	Homo sapiens	143-147
31534544-10	2019	A knockdown of QPCT conferred sunitinib sensitivity traits to RCC cells, whereas an overexpression of QPCT restored sunitinib resistance in RCC cells.	Sunitinib	116-125	glutaminyl-peptide cyclotransferase	Homo sapiens	102-106
31534544-13	2019	Conclusion: QPCT may be a novel predictor of the response to sunitinib therapy in RCC patients and a potential therapeutic target.	Sunitinib	61-70	glutaminyl-peptide cyclotransferase	Homo sapiens	12-16
31294623-9	2019	Sunitinib therapy substantially mitigated both AAA formation and further progression of established AAAs, attenuated aneurysmal aortic MMP2 (matrix metalloproteinase) and MMP9 protein expression, inhibited inflammatory monocyte and neutrophil chemotaxis to VEGF-A, and reduced MMP2, MMP9, and VEGF-A mRNA expression in macrophages and smooth muscle cells in vitro.	Sunitinib	0-9	matrix metallopeptidase 9	Mus musculus	171-175
31294623-9	2019	Sunitinib therapy substantially mitigated both AAA formation and further progression of established AAAs, attenuated aneurysmal aortic MMP2 (matrix metalloproteinase) and MMP9 protein expression, inhibited inflammatory monocyte and neutrophil chemotaxis to VEGF-A, and reduced MMP2, MMP9, and VEGF-A mRNA expression in macrophages and smooth muscle cells in vitro.	Sunitinib	0-9	vascular endothelial growth factor A	Mus musculus	257-263
31294623-9	2019	Sunitinib therapy substantially mitigated both AAA formation and further progression of established AAAs, attenuated aneurysmal aortic MMP2 (matrix metalloproteinase) and MMP9 protein expression, inhibited inflammatory monocyte and neutrophil chemotaxis to VEGF-A, and reduced MMP2, MMP9, and VEGF-A mRNA expression in macrophages and smooth muscle cells in vitro.	Sunitinib	0-9	matrix metallopeptidase 2	Mus musculus	277-281
31294623-9	2019	Sunitinib therapy substantially mitigated both AAA formation and further progression of established AAAs, attenuated aneurysmal aortic MMP2 (matrix metalloproteinase) and MMP9 protein expression, inhibited inflammatory monocyte and neutrophil chemotaxis to VEGF-A, and reduced MMP2, MMP9, and VEGF-A mRNA expression in macrophages and smooth muscle cells in vitro.	Sunitinib	0-9	matrix metallopeptidase 9	Mus musculus	283-287
31294623-9	2019	Sunitinib therapy substantially mitigated both AAA formation and further progression of established AAAs, attenuated aneurysmal aortic MMP2 (matrix metalloproteinase) and MMP9 protein expression, inhibited inflammatory monocyte and neutrophil chemotaxis to VEGF-A, and reduced MMP2, MMP9, and VEGF-A mRNA expression in macrophages and smooth muscle cells in vitro.	Sunitinib	0-9	vascular endothelial growth factor A	Mus musculus	293-299
30644033-0	2019	Carnitine Supplementation Attenuates Sunitinib-Induced Inhibition of AMP-Activated Protein Kinase Downstream Signals in Cardiac Tissues.	Sunitinib	37-46	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	69-97
31423209-0	2019	Significance of cyclooxygenase-2, prostaglandin E2 and CD133 levels in sunitinib-resistant renal cell carcinoma.	Sunitinib	71-80	prostaglandin-endoperoxide synthase 2	Homo sapiens	16-32
31268155-2	2019	The Von Hippel-Lindau tumor suppressor (VHL)-hypoxia-inducible factor 1 subunit alpha (HIF1A)/hypoxia-inducible factor 2alpha (HIF2A)-vascular endothelial growth factor A (VEGFA) protein axis is involved in the development and progression of ccRCC, whereas sunitinib, a tyrosine kinase inhibitor, blocks the binding of VEGFA to its receptor.	Sunitinib	257-266	von Hippel-Lindau tumor suppressor	Homo sapiens	40-43
31268155-2	2019	The Von Hippel-Lindau tumor suppressor (VHL)-hypoxia-inducible factor 1 subunit alpha (HIF1A)/hypoxia-inducible factor 2alpha (HIF2A)-vascular endothelial growth factor A (VEGFA) protein axis is involved in the development and progression of ccRCC, whereas sunitinib, a tyrosine kinase inhibitor, blocks the binding of VEGFA to its receptor.	Sunitinib	257-266	vascular endothelial growth factor A	Homo sapiens	134-170
31268155-3	2019	The aim of the present study was to examine the possible association of the gene expression of VHL, HIF1A, HIF2A, VEGFA and tumor protein P53 (P53) in cancer tissue with the outcome of ccRCC patients who were treated with sunitinib as first-line therapy following nephrectomy.	Sunitinib	222-231	von Hippel-Lindau tumor suppressor	Homo sapiens	95-98
31268155-3	2019	The aim of the present study was to examine the possible association of the gene expression of VHL, HIF1A, HIF2A, VEGFA and tumor protein P53 (P53) in cancer tissue with the outcome of ccRCC patients who were treated with sunitinib as first-line therapy following nephrectomy.	Sunitinib	222-231	tumor protein p53	Homo sapiens	138-141
31268155-3	2019	The aim of the present study was to examine the possible association of the gene expression of VHL, HIF1A, HIF2A, VEGFA and tumor protein P53 (P53) in cancer tissue with the outcome of ccRCC patients who were treated with sunitinib as first-line therapy following nephrectomy.	Sunitinib	222-231	tumor protein p53	Homo sapiens	143-146
31268155-8	2019	Sunitinib resistance was associated with high HIF2A and VEGFA protein levels (b=0.57 and b=0.69 for OS and PFS, respectively; P&lt;0.001).	Sunitinib	0-9	endothelial PAS domain protein 1	Homo sapiens	46-51
31268155-8	2019	Sunitinib resistance was associated with high HIF2A and VEGFA protein levels (b=0.57 and b=0.69 for OS and PFS, respectively; P&lt;0.001).	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	56-61
31339065-3	2019	This Review focuses on the existing evidence on patient-reported outcomes and health-related quality of life with several tyrosine kinase inhibitors (pazopanib, sunitinib, cabozantinib and tivozanib) used as first-line treatment for metastatic renal cell carcinoma.	Sunitinib	161-170	TXK tyrosine kinase	Homo sapiens	122-137
31392045-15	2019	Nine patients received sunitinib, of them 3 had germline mutation (2 in MEN1 and 1 in VHL genes).	Sunitinib	23-32	menin 1	Homo sapiens	72-82
31423209-0	2019	Significance of cyclooxygenase-2, prostaglandin E2 and CD133 levels in sunitinib-resistant renal cell carcinoma.	Sunitinib	71-80	prominin 1	Homo sapiens	55-60
31423209-13	2019	In summary, the results indicate that activation of the COX-2-PGE2 pathway in RCC leads to the development of sunitinib resistance and may serve an important role in the maintenance of the characteristics of stem cells that are closely associated with drug resistance.	Sunitinib	110-119	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	56-66
31366950-0	2019	SQSTM1/p62 loss reverses the inhibitory effect of sunitinib on autophagy independent of AMPK signaling.	Sunitinib	50-59	sequestosome 1	Homo sapiens	0-6
31366950-0	2019	SQSTM1/p62 loss reverses the inhibitory effect of sunitinib on autophagy independent of AMPK signaling.	Sunitinib	50-59	sequestosome 1	Homo sapiens	7-10
30875096-8	2019	Activation of PPARalpha and inhibition of xenobiotic metabolism may be of value in attenuating sunitinib hepatotoxicity.	Sunitinib	95-104	peroxisome proliferator activated receptor alpha	Mus musculus	14-23
31054432-7	2019	IC50 of the promising compounds were in the range of 247-793 nM for VEGFR-2 in reference to sunitinib (IC50 320 nM), and 369-725 nM for EGFR in reference to erlotinib (IC50 568 nM).	Sunitinib	92-101	kinase insert domain receptor	Homo sapiens	68-75
31054432-7	2019	IC50 of the promising compounds were in the range of 247-793 nM for VEGFR-2 in reference to sunitinib (IC50 320 nM), and 369-725 nM for EGFR in reference to erlotinib (IC50 568 nM).	Sunitinib	92-101	epidermal growth factor receptor	Homo sapiens	69-73
31319613-5	2019	The administration of a small molecule inhibitor of CAIX, SLC-0111, significantly reduced overall metastatic burden, whereas exposure to sunitinib increased hypoxia and CAIX expression in primary tumors, and failed to inhibit metastasis.	Sunitinib	137-146	carbonic anhydrase 9	Homo sapiens	169-173
31319613-7	2019	Furthermore, combining sunitinib and SLC-0111 significantly reduced both primary tumor growth and sunitinib-induced metastasis to the lung.	Sunitinib	98-107	C-C motif chemokine ligand 21	Homo sapiens	37-40
31039345-2	2019	A tyrosine kinase inhibitor (TKIs), sunitinib, was screened in our group previously and showed antagonistic activity for cytokine release in a TLR7 stimulation model.	Sunitinib	36-45	toll-like receptor 7	Mus musculus	143-147
31039345-4	2019	In vitro, nearly all of the eleven TKIs decreased the TNF-alpha levels induced by the TLR7 agonist, especially sunitinib.	Sunitinib	111-120	tumor necrosis factor	Mus musculus	54-63
31039345-4	2019	In vitro, nearly all of the eleven TKIs decreased the TNF-alpha levels induced by the TLR7 agonist, especially sunitinib.	Sunitinib	111-120	toll-like receptor 7	Mus musculus	86-90
31039345-5	2019	Furthermore, sunitinib displayed potent inhibition of the cytokine levels triggered by several types of TLR ligands, including TLR3, TLR4, TLR7/8 and TLR9, in mouse spleen lymphocytes, mouse BMDCs and human PBMCs.	Sunitinib	13-22	toll-like receptor 3	Mus musculus	127-131
31039345-5	2019	Furthermore, sunitinib displayed potent inhibition of the cytokine levels triggered by several types of TLR ligands, including TLR3, TLR4, TLR7/8 and TLR9, in mouse spleen lymphocytes, mouse BMDCs and human PBMCs.	Sunitinib	13-22	toll-like receptor 4	Mus musculus	133-137
31039345-5	2019	Furthermore, sunitinib displayed potent inhibition of the cytokine levels triggered by several types of TLR ligands, including TLR3, TLR4, TLR7/8 and TLR9, in mouse spleen lymphocytes, mouse BMDCs and human PBMCs.	Sunitinib	13-22	toll-like receptor 7	Mus musculus	139-145
31039345-5	2019	Furthermore, sunitinib displayed potent inhibition of the cytokine levels triggered by several types of TLR ligands, including TLR3, TLR4, TLR7/8 and TLR9, in mouse spleen lymphocytes, mouse BMDCs and human PBMCs.	Sunitinib	13-22	toll-like receptor 9	Mus musculus	150-154
31039345-6	2019	The in vivo results showed that sunitinib efficiently depressed the LPS-induced cytokine storm, i.e., rapid and intense production of TNF-alpha and IL-6.	Sunitinib	32-41	tumor necrosis factor	Mus musculus	134-143
31039345-6	2019	The in vivo results showed that sunitinib efficiently depressed the LPS-induced cytokine storm, i.e., rapid and intense production of TNF-alpha and IL-6.	Sunitinib	32-41	interleukin 6	Mus musculus	148-152
31039345-8	2019	As for the immunosuppressive mechanisms of sunitinib, at least the PDGFR-activated ERK and p38 pathways were critical, although we could not rule out the possibility of other pathways being involved.	Sunitinib	43-52	platelet derived growth factor receptor, beta polypeptide	Mus musculus	67-72
31039345-8	2019	As for the immunosuppressive mechanisms of sunitinib, at least the PDGFR-activated ERK and p38 pathways were critical, although we could not rule out the possibility of other pathways being involved.	Sunitinib	43-52	Eph receptor B2	Mus musculus	83-86
31039345-8	2019	As for the immunosuppressive mechanisms of sunitinib, at least the PDGFR-activated ERK and p38 pathways were critical, although we could not rule out the possibility of other pathways being involved.	Sunitinib	43-52	mitogen-activated protein kinase 14	Mus musculus	91-94
31297023-6	2019	Moreover, a molecular docking simulation was performed for compound 16 and sunitinib to predict the protein-ligand interactions with the active site of VEGFR2.	Sunitinib	75-84	kinase insert domain receptor	Homo sapiens	152-158
30914797-5	2019	Only two trials of an autologous renal tumour cell vaccine and of the vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor sunitinib have shown positive results, but these have been criticized for methodological reasons and conflicting data, respectively.	Sunitinib	148-157	kinase insert domain receptor	Homo sapiens	70-113
30914797-5	2019	Only two trials of an autologous renal tumour cell vaccine and of the vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor sunitinib have shown positive results, but these have been criticized for methodological reasons and conflicting data, respectively.	Sunitinib	148-157	kinase insert domain receptor	Homo sapiens	115-120
30806670-6	2019	Sunitinib exerts its regenerative effects via transient inhibition of SHP-2 and subsequent activation of the STAT3 pathway.	Sunitinib	0-9	protein tyrosine phosphatase, non-receptor type 11	Mus musculus	70-75
30806670-6	2019	Sunitinib exerts its regenerative effects via transient inhibition of SHP-2 and subsequent activation of the STAT3 pathway.	Sunitinib	0-9	signal transducer and activator of transcription 3	Mus musculus	109-114
31018963-0	2019	Multiple conformational states of the HPK1 kinase domain in complex with sunitinib reveal the structural changes accompanying HPK1 trans-regulation.	Sunitinib	73-82	mitogen-activated protein kinase kinase kinase kinase 1	Homo sapiens	38-42
31293642-0	2019	Overexpression of miR-15b Promotes Resistance to Sunitinib in Renal Cell Carcinoma.	Sunitinib	49-58	microRNA 15b	Mus musculus	18-25
31293642-5	2019	Results: Reproduction of GEO datasets revealed miR-15b significantly upregulated in sunitinib- resistant ccRCC.	Sunitinib	84-93	microRNA 15b	Mus musculus	47-54
31293642-6	2019	Five out of seven ccRCC cell lines demonstrated significantly overexpressed miR-15b after sunitinib treatment.	Sunitinib	90-99	microRNA 15b	Mus musculus	76-83
31293642-7	2019	Vector-mediated overexpression of miR-15b significantly induced resistance to sunitinib in ccRCC cells.	Sunitinib	78-87	microRNA 15b	Mus musculus	34-41
31293642-8	2019	Overexpression of miR-15b significantly induced less population in G1 phase of cell cycle and less apoptosis in cells treated sunitinib.	Sunitinib	126-135	microRNA 15b	Mus musculus	18-25
31293642-12	2019	Silencing of CCNC mimicked overexpression of miR-25 inducing cell cycle progression passing G1 phase and less apoptosis in ccRCC cells treated by sunitinib.	Sunitinib	146-155	cyclin C	Mus musculus	13-17
31293642-12	2019	Silencing of CCNC mimicked overexpression of miR-25 inducing cell cycle progression passing G1 phase and less apoptosis in ccRCC cells treated by sunitinib.	Sunitinib	146-155	microRNA 25	Mus musculus	45-51
31248045-0	2019	Heightened JNK Activation and Reduced XIAP Levels Promote TRAIL and Sunitinib-Mediated Apoptosis in Colon Cancer Models.	Sunitinib	68-77	X-linked inhibitor of apoptosis	Homo sapiens	38-42
31248045-3	2019	We hypothesized that a disruption of pro-survival signaling cascades with the multi-tyrosine kinase inhibitor sunitinib and would be an effective strategy to enhance TRAIL-mediated apoptosis.	Sunitinib	110-119	TNF superfamily member 10	Homo sapiens	166-171
31248045-4	2019	Here we demonstrate that sunitinib significantly augments the anticancer activity of TRAIL in models of colon cancer.	Sunitinib	25-34	TNF superfamily member 10	Homo sapiens	85-90
31248045-5	2019	The therapeutic benefit of the TRAIL/sunitinib combination was associated with increased apoptosis marked by enhanced caspase-3 cleavage and DNA fragmentation.	Sunitinib	37-46	caspase 3	Homo sapiens	118-127
31248045-6	2019	Overexpression of the anti-apoptotic factor B-cell lymphoma 2 (BCL-2) in HCT116 cells reduced TRAIL/sunitinib-mediated apoptosis, further supporting that sunitinib enhances the anticancer activity of TRAIL via augmented apoptosis.	Sunitinib	100-109	BCL2 apoptosis regulator	Homo sapiens	44-61
31248045-6	2019	Overexpression of the anti-apoptotic factor B-cell lymphoma 2 (BCL-2) in HCT116 cells reduced TRAIL/sunitinib-mediated apoptosis, further supporting that sunitinib enhances the anticancer activity of TRAIL via augmented apoptosis.	Sunitinib	100-109	BCL2 apoptosis regulator	Homo sapiens	63-68
31248045-6	2019	Overexpression of the anti-apoptotic factor B-cell lymphoma 2 (BCL-2) in HCT116 cells reduced TRAIL/sunitinib-mediated apoptosis, further supporting that sunitinib enhances the anticancer activity of TRAIL via augmented apoptosis.	Sunitinib	154-163	BCL2 apoptosis regulator	Homo sapiens	44-61
31248045-6	2019	Overexpression of the anti-apoptotic factor B-cell lymphoma 2 (BCL-2) in HCT116 cells reduced TRAIL/sunitinib-mediated apoptosis, further supporting that sunitinib enhances the anticancer activity of TRAIL via augmented apoptosis.	Sunitinib	154-163	BCL2 apoptosis regulator	Homo sapiens	63-68
31248045-6	2019	Overexpression of the anti-apoptotic factor B-cell lymphoma 2 (BCL-2) in HCT116 cells reduced TRAIL/sunitinib-mediated apoptosis, further supporting that sunitinib enhances the anticancer activity of TRAIL via augmented apoptosis.	Sunitinib	154-163	TNF superfamily member 10	Homo sapiens	94-99
31248045-6	2019	Overexpression of the anti-apoptotic factor B-cell lymphoma 2 (BCL-2) in HCT116 cells reduced TRAIL/sunitinib-mediated apoptosis, further supporting that sunitinib enhances the anticancer activity of TRAIL via augmented apoptosis.	Sunitinib	154-163	TNF superfamily member 10	Homo sapiens	200-205
31248045-7	2019	Analysis of pro-survival factors identified that the combination of TRAIL and sunitinib significantly downregulated the anti-apoptotic protein X-linked inhibitor of apoptosis protein (XIAP) through a c-Jun N-terminal kinase (JNK)-mediated mechanism.	Sunitinib	78-87	X-linked inhibitor of apoptosis	Homo sapiens	143-182
31248045-7	2019	Analysis of pro-survival factors identified that the combination of TRAIL and sunitinib significantly downregulated the anti-apoptotic protein X-linked inhibitor of apoptosis protein (XIAP) through a c-Jun N-terminal kinase (JNK)-mediated mechanism.	Sunitinib	78-87	X-linked inhibitor of apoptosis	Homo sapiens	184-188
31248045-7	2019	Analysis of pro-survival factors identified that the combination of TRAIL and sunitinib significantly downregulated the anti-apoptotic protein X-linked inhibitor of apoptosis protein (XIAP) through a c-Jun N-terminal kinase (JNK)-mediated mechanism.	Sunitinib	78-87	mitogen-activated protein kinase 8	Homo sapiens	200-223
31248045-7	2019	Analysis of pro-survival factors identified that the combination of TRAIL and sunitinib significantly downregulated the anti-apoptotic protein X-linked inhibitor of apoptosis protein (XIAP) through a c-Jun N-terminal kinase (JNK)-mediated mechanism.	Sunitinib	78-87	mitogen-activated protein kinase 8	Homo sapiens	225-228
31248045-8	2019	Short hairpin RNA (shRNA)-mediated knockdown of JNK confirmed its key role in the regulation of sensitivity to this combination as cells with suppressed JNK expression exhibited significantly reduced TRAIL/sunitinib-mediated apoptosis.	Sunitinib	206-215	mitogen-activated protein kinase 8	Homo sapiens	48-51
31248045-8	2019	Short hairpin RNA (shRNA)-mediated knockdown of JNK confirmed its key role in the regulation of sensitivity to this combination as cells with suppressed JNK expression exhibited significantly reduced TRAIL/sunitinib-mediated apoptosis.	Sunitinib	206-215	mitogen-activated protein kinase 8	Homo sapiens	153-156
31248045-10	2019	Collectively, our data demonstrate that sunitinib enhances TRAIL-mediated apoptosis by heightened JNK activation, diminished XIAP levels, and augmented apoptosis.	Sunitinib	40-49	TNF superfamily member 10	Homo sapiens	59-64
31248045-10	2019	Collectively, our data demonstrate that sunitinib enhances TRAIL-mediated apoptosis by heightened JNK activation, diminished XIAP levels, and augmented apoptosis.	Sunitinib	40-49	mitogen-activated protein kinase 8	Homo sapiens	98-101
31248045-10	2019	Collectively, our data demonstrate that sunitinib enhances TRAIL-mediated apoptosis by heightened JNK activation, diminished XIAP levels, and augmented apoptosis.	Sunitinib	40-49	X-linked inhibitor of apoptosis	Homo sapiens	125-129
31293642-13	2019	Overexpression of miR-15b also counteracted suppression of migration and colony formation by sunitinib in ccRCC cell lines.	Sunitinib	93-102	microRNA 15b	Mus musculus	18-25
31293642-14	2019	In vivo mouse xenograft models showed recovered tumor growth with miR-15b expression in mice treated with sunitinib.	Sunitinib	106-115	microRNA 15b	Mus musculus	66-73
31293642-15	2019	Conclusion: We here show miR-15b as a possible culprit for sunitinib resistance in ccRCC.	Sunitinib	59-68	microRNA 15b	Mus musculus	25-32
31018963-0	2019	Multiple conformational states of the HPK1 kinase domain in complex with sunitinib reveal the structural changes accompanying HPK1 trans-regulation.	Sunitinib	73-82	mitogen-activated protein kinase kinase kinase kinase 1	Homo sapiens	126-130
31289593-0	2019	Tumoral Pyruvate Kinase L/R as a Predictive Marker for the Treatment of Renal Cancer Patients with Sunitinib and Sorafenib.	Sunitinib	99-108	pyruvate kinase L/R	Homo sapiens	8-27
31289593-4	2019	We have previously shown that the tumoral expression of cubilin (CUBN) is associated with progression free survival (PFS) in mRCC patients treated with sunitinib and sorafenib.	Sunitinib	152-161	cubilin	Homo sapiens	56-63
31289593-4	2019	We have previously shown that the tumoral expression of cubilin (CUBN) is associated with progression free survival (PFS) in mRCC patients treated with sunitinib and sorafenib.	Sunitinib	152-161	cubilin	Homo sapiens	65-69
29792121-0	2019	ABCG2 Polymorphism rs2231142 and hypothyroidism in metastatic renal cell carcinoma patients treated with sunitinib.	Sunitinib	105-114	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
31289593-14	2019	Conclusions: In this real world study we show that tumoral PKLR membrane expression is a positive predictive biomarker for sunitinib and sorafenib treatment in patients suffering from mRCC.	Sunitinib	123-132	pyruvate kinase L/R	Homo sapiens	59-63
29792121-10	2019	CONCLUSION: Polymorphism rs2231142 in the efflux pump ABCG2 is associated with hypothyroidism in mRCC patients treated with sunitinib.	Sunitinib	124-133	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	54-59
31025080-1	2019	Sunitinib (SNT) is a multi-targeted receptor tyrosine kinase inhibitor that has been approved by the FDA for cancer therapy.	Sunitinib	0-9	ret proto-oncogene	Homo sapiens	36-60
30707374-6	2019	KIT inhibitors that have been investigated in relevant clinical trials in advanced melanoma include imatinib, sunitinib, dasatinib, and nilotinib.	Sunitinib	110-119	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
31025080-1	2019	Sunitinib (SNT) is a multi-targeted receptor tyrosine kinase inhibitor that has been approved by the FDA for cancer therapy.	Sunitinib	11-14	ret proto-oncogene	Homo sapiens	36-60
31025080-7	2019	Oral SNT administration (40 mg/kg/day) in mice progressively decreased the PI3K activity and cardiac function in 2 weeks with a significant decrease in the expression and activity of Cav1.2 and SERCA.	Sunitinib	5-8	calcium channel, voltage-dependent, L type, alpha 1C subunit	Mus musculus	183-189
30837208-0	2019	Metastatic Clear-cell Renal Cell Carcinoma With a Long-term Response to Sunitinib: A Distinct Phenotype Independently Associated With Low PD-L1 Expression.	Sunitinib	72-81	CD274 molecule	Homo sapiens	138-143
30953637-8	2019	Moreover, the combination of SN-38 and sunitinib caused synergism on colon cancer cells, with significant inhibition of the ABCG2 gene expression and an increase of SN-38 intracellular concentrations.	Sunitinib	39-48	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	124-129
31035254-0	2019	EGF and IGF1 affect sunitinib activity in BP-NEN: new putative targets beyond VEGFR?	Sunitinib	20-29	epidermal growth factor	Homo sapiens	0-3
31035254-0	2019	EGF and IGF1 affect sunitinib activity in BP-NEN: new putative targets beyond VEGFR?	Sunitinib	20-29	insulin like growth factor 1	Homo sapiens	8-12
31035254-7	2019	Our results showed that after treatment with sunitinib and/or IGF1, EGF and VEGF, the antiproliferative effect of sunitinib was counteracted by EGF and IGF1 but not by VEGF.	Sunitinib	45-54	insulin like growth factor 1	Homo sapiens	152-156
31035254-7	2019	Our results showed that after treatment with sunitinib and/or IGF1, EGF and VEGF, the antiproliferative effect of sunitinib was counteracted by EGF and IGF1 but not by VEGF.	Sunitinib	114-123	insulin like growth factor 1	Homo sapiens	62-66
31035254-7	2019	Our results showed that after treatment with sunitinib and/or IGF1, EGF and VEGF, the antiproliferative effect of sunitinib was counteracted by EGF and IGF1 but not by VEGF.	Sunitinib	114-123	epidermal growth factor	Homo sapiens	68-80
31035254-7	2019	Our results showed that after treatment with sunitinib and/or IGF1, EGF and VEGF, the antiproliferative effect of sunitinib was counteracted by EGF and IGF1 but not by VEGF.	Sunitinib	114-123	epidermal growth factor	Homo sapiens	68-71
31035254-7	2019	Our results showed that after treatment with sunitinib and/or IGF1, EGF and VEGF, the antiproliferative effect of sunitinib was counteracted by EGF and IGF1 but not by VEGF.	Sunitinib	114-123	insulin like growth factor 1	Homo sapiens	152-156
31035254-7	2019	Our results showed that after treatment with sunitinib and/or IGF1, EGF and VEGF, the antiproliferative effect of sunitinib was counteracted by EGF and IGF1 but not by VEGF.	Sunitinib	114-123	vascular endothelial growth factor A	Homo sapiens	76-80
31035254-8	2019	Therefore, we evaluated with AlphaScreen technology the phosphorylated EGFR and IGF1R levels in primary cultures treated with sunitinib and/or EGF and IGF1.	Sunitinib	126-135	epidermal growth factor receptor	Homo sapiens	71-75
31035254-8	2019	Therefore, we evaluated with AlphaScreen technology the phosphorylated EGFR and IGF1R levels in primary cultures treated with sunitinib and/or EGF and IGF1.	Sunitinib	126-135	insulin like growth factor 1 receptor	Homo sapiens	80-85
31035254-8	2019	Therefore, we evaluated with AlphaScreen technology the phosphorylated EGFR and IGF1R levels in primary cultures treated with sunitinib and/or EGF and IGF1.	Sunitinib	126-135	epidermal growth factor	Homo sapiens	71-74
31035254-8	2019	Therefore, we evaluated with AlphaScreen technology the phosphorylated EGFR and IGF1R levels in primary cultures treated with sunitinib and/or EGF and IGF1.	Sunitinib	126-135	insulin like growth factor 1	Homo sapiens	80-84
31035254-9	2019	Results showed a decrease of p-IGF1R after treatment with sunitinib and an increase after co-treatment with IGF1.	Sunitinib	58-67	insulin like growth factor 1 receptor	Homo sapiens	31-36
31035254-9	2019	Results showed a decrease of p-IGF1R after treatment with sunitinib and an increase after co-treatment with IGF1.	Sunitinib	58-67	insulin like growth factor 1	Homo sapiens	31-35
31186733-0	2019	Effect of the Nrf2-ARE signaling pathway on biological characteristics and sensitivity to sunitinib in renal cell carcinoma.	Sunitinib	90-99	NFE2 like bZIP transcription factor 2	Homo sapiens	14-18
31186733-7	2019	Following shRNA-Nrf2 transfection, the 786-0 cells demonstrated a significant decrease in viability, cell invasion and scratch healing rate, and the mRNA and protein expression levels of Nrf2, NQO1, HO-1 and glutathione transferase were significantly decreased, which enhanced the sensitivity to sunitinib, arrested cells in the G0/G1 phase and increased apoptosis.	Sunitinib	296-305	NFE2 like bZIP transcription factor 2	Homo sapiens	16-20
31217744-5	2019	After exposure to sunitinib (a kind of tyrosine kinase inhibitor, TKI), cell proliferation inhibition was tested by MTT, cell cycle and apoptosis were measured by FCM, autophagy was assessed by fluorescence microscopy and immunoblotting.	Sunitinib	18-27	TXK tyrosine kinase	Homo sapiens	39-54
31217744-8	2019	After sunitinib inhibited the c-KIT activity, the colony formation efficiency was reduced, and the half-maximal inhibitory concentration (IC50) of sunitinib was low (0.44+-0.17muM) at 48 hours.	Sunitinib	6-15	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-35
31217744-8	2019	After sunitinib inhibited the c-KIT activity, the colony formation efficiency was reduced, and the half-maximal inhibitory concentration (IC50) of sunitinib was low (0.44+-0.17muM) at 48 hours.	Sunitinib	147-156	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-35
31054006-3	2019	The S-TRAC study demonstrated a statistically significant improvement in disease-free survival (DFS) of greater than 1 year with adjuvant sunitinib compared to placebo in patients with high-risk localized RCC and earned it FDA approval.	Sunitinib	138-147	T cell receptor alpha constant	Homo sapiens	6-10
30689282-0	2019	Exploring binding mechanisms of VEGFR2 with three drugs lenvatinib, sorafenib, and sunitinib by molecular dynamics simulation and free energy calculation.	Sunitinib	83-92	kinase insert domain receptor	Homo sapiens	32-38
30689282-1	2019	Lenvatinib (LEN), sorafenib (SOR), and sunitinib (SUN) are drugs targeting vascular endothelial growth factor receptor 2 (VEGFR2).	Sunitinib	39-48	kinase insert domain receptor	Homo sapiens	75-120
30705246-7	2019	However, a greater-fold increase in sorafenib/sunitinib resistance was observed during hypoxia, particularly in pVHL-deficient cells.	Sunitinib	46-55	von Hippel-Lindau tumor suppressor	Homo sapiens	112-116
30689282-1	2019	Lenvatinib (LEN), sorafenib (SOR), and sunitinib (SUN) are drugs targeting vascular endothelial growth factor receptor 2 (VEGFR2).	Sunitinib	39-48	kinase insert domain receptor	Homo sapiens	122-128
30523507-4	2019	Second-line sunitinib potently inhibits KIT exon 13/14 mutants but is ineffective against exon 17 mutations.	Sunitinib	12-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	40-43
30816432-0	2019	Potential tumor-suppressive role of microRNA-99a-3p in sunitinib-resistant renal cell carcinoma cells through the regulation of RRM2.	Sunitinib	55-64	ribonucleotide reductase regulatory subunit M2	Homo sapiens	128-132
31083182-0	2019	Relationship between efficacy of sunitinib and KIT mutation of patients with advanced gastrointestinal stromal tumors after failure of imatinib: A systematic review.	Sunitinib	33-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-50
31083182-3	2019	We initiated a systematic review to compare the efficacy of SU after failure of Imatinib (IM) in different KIT mutations.	Sunitinib	60-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	107-110
31083182-9	2019	CONCLUSION: The results show that efficacy of SU is closely associated with KIT genotypes in GISTs.	Sunitinib	46-48	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	76-79
30722031-2	2019	The first VEGF inhibitors approved for mRCC were sorafenib and sunitinib.	Sunitinib	63-72	vascular endothelial growth factor A	Homo sapiens	10-14
31013908-4	2019	Here, the antitumor effects of three conjugates possessing a selective binder of the extracellular portion of integrin alphaVbeta3 covalently linked to the tyrosine kinase inhibitor sunitinib were investigated in cisplatin-sensitive and -resistant ovarian carcinoma cells expressing both tyrosine kinase VEGFR2 and alphaVbeta3 at different levels.	Sunitinib	182-191	integrin subunit alpha V	Homo sapiens	110-130
30527746-0	2019	Fibroblast Growth Factor Receptor-2 Polymorphism rs2981582 is Correlated With Progression-free Survival and Overall Survival in Patients With Metastatic Clear-cell Renal Cell Carcinoma Treated With Sunitinib.	Sunitinib	198-207	fibroblast growth factor receptor 2	Homo sapiens	0-35
30684595-2	2019	Sunitinib and regorafenib have been approved as the second and third line therapies to overcome some of these drug-resistance mutations; however, their limited clinical response, toxicity and resistance of the activation loop mutants still makes new therapies bearing different cKIT mutants activity spectrum profile highly demanded.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	278-282
30984366-10	2019	Our data also support the hypothesis that the use of KIT/PDGFRA inhibitors, including non-approved agents, has improved OS for patients with imatinib- and sunitinib-resistant GIST.	Sunitinib	155-164	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-56
30984366-10	2019	Our data also support the hypothesis that the use of KIT/PDGFRA inhibitors, including non-approved agents, has improved OS for patients with imatinib- and sunitinib-resistant GIST.	Sunitinib	155-164	platelet derived growth factor receptor alpha	Homo sapiens	57-63
30640790-6	2019	Sunitinib is an oral tyrosine kinase inhibitor that interacts with several angiogenesis receptors including platelet-derived growth factor receptors and VEGF receptors, and is approved for the first-line treatment in metastatic RCC.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	153-157
30527746-2	2019	Recently, single nucleotide polymorphism (SNP) rs2981582 in Fibroblast Growth Factor Receptor 2 (FGFR2) was found to be associated with clinical outcome in patients with mccRCC treated with pazopanib and sunitinib.	Sunitinib	204-213	fibroblast growth factor receptor 2	Homo sapiens	60-95
30527746-2	2019	Recently, single nucleotide polymorphism (SNP) rs2981582 in Fibroblast Growth Factor Receptor 2 (FGFR2) was found to be associated with clinical outcome in patients with mccRCC treated with pazopanib and sunitinib.	Sunitinib	204-213	fibroblast growth factor receptor 2	Homo sapiens	97-102
30527746-12	2019	CONCLUSION: Polymorphism rs2981582 in FGFR2 is correlated to PFS and OS in patients with mccRCC treated with sunitinib.	Sunitinib	109-118	fibroblast growth factor receptor 2	Homo sapiens	38-43
30527746-12	2019	CONCLUSION: Polymorphism rs2981582 in FGFR2 is correlated to PFS and OS in patients with mccRCC treated with sunitinib.	Sunitinib	109-118	Moloney sarcoma oncogene	Mus musculus	69-71
30792533-2	2019	Once resistance emerges, targeting KIT with tyrosine kinase inhibitors (TKIs) sunitinib and regorafenib provides clinical benefit, albeit of limited duration.	Sunitinib	78-87	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	35-38
30689992-8	2019	Combination of sunitinib and TSA increased cell death with PARP cleavage, an early marker of mitochondrial apoptosis, whereas receptor tyrosine kinase signaling, which is the target of sunitinib, was not altered by TSA.	Sunitinib	15-24	poly(ADP-ribose) polymerase 1	Homo sapiens	59-63
30620878-0	2019	Combination of Sunitinib and PD-L1 Blockade Enhances Anticancer Efficacy of TLR7/8 Agonist-Based Nanovaccine.	Sunitinib	15-24	toll-like receptor 7	Mus musculus	76-82
30552230-5	2019	Here, we report that the ER-associated protein degradation (ERAD) inhibitor eeyarestatin sensitized MTC cells to the TKIs, sunitinib and vandetanib, thereby leading to synergistic upregulation of ATF4 expression, accumulation of reactive oxygen species, and subsequent cell death.	Sunitinib	123-132	activating transcription factor 4	Homo sapiens	196-200
30821250-8	2019	Analysis of post-receptor pathways controlling proliferation and migration of HUVECs showed suppression of phosphorylated PI3K/Akt and ERK1/2 after exposure to sunitinib but not to 3PO in 10 microM concentration.	Sunitinib	160-169	AKT serine/threonine kinase 1	Homo sapiens	127-130
30821250-8	2019	Analysis of post-receptor pathways controlling proliferation and migration of HUVECs showed suppression of phosphorylated PI3K/Akt and ERK1/2 after exposure to sunitinib but not to 3PO in 10 microM concentration.	Sunitinib	160-169	mitogen-activated protein kinase 3	Homo sapiens	135-141
30693663-7	2019	Subsequent sunitinib (P = 0.066) and regorafenib (P = 0.003) were more commonly administered in period 2.	Sunitinib	11-20	period circadian regulator 2	Homo sapiens	96-104
30779084-0	2019	Effect of miR-34a on resistance to sunitinib in breast cancer by regulating the Wnt/beta-catenin signaling pathway.	Sunitinib	35-44	catenin beta 1	Homo sapiens	84-96
31031856-2	2019	Mammalian target of rapamycin (mTOR) inhibitor everolimus is currently used as a second-line therapy for sorafenib or sunitinib-refractory metastatic RCC patients.	Sunitinib	118-127	mechanistic target of rapamycin kinase	Homo sapiens	31-35
31031856-2	2019	Mammalian target of rapamycin (mTOR) inhibitor everolimus is currently used as a second-line therapy for sorafenib or sunitinib-refractory metastatic RCC patients.	Sunitinib	118-127	mechanistic target of rapamycin kinase	Homo sapiens	0-29
30401688-1	2019	PURPOSE: In the S-TRAC trial, adjuvant sunitinib prolonged disease-free survival (DFS) versus placebo in patients with loco-regional renal cell carcinoma at high risk of recurrence after nephrectomy.	Sunitinib	39-48	T cell receptor alpha constant	Homo sapiens	18-22
30401688-8	2019	Shorter DFS was observed for VEGFR1 rs9582036 C/A versus C/C with sunitinib, placebo, and combined therapies (P &lt;= 0.05), and A/A versus C/C with sunitinib (P = 0.022).	Sunitinib	66-75	fms related receptor tyrosine kinase 1	Homo sapiens	29-35
30401688-8	2019	Shorter DFS was observed for VEGFR1 rs9582036 C/A versus C/C with sunitinib, placebo, and combined therapies (P &lt;= 0.05), and A/A versus C/C with sunitinib (P = 0.022).	Sunitinib	149-158	fms related receptor tyrosine kinase 1	Homo sapiens	29-35
30401688-10	2019	CONCLUSIONS: Correlations between VEGFR1 and VEGFR2 SNPs and longer DFS with sunitinib suggest germline SNPs are predictive of improved outcomes with adjuvant sunitinib in patients with renal cell carcinoma.	Sunitinib	77-86	fms related receptor tyrosine kinase 1	Homo sapiens	34-40
30401688-10	2019	CONCLUSIONS: Correlations between VEGFR1 and VEGFR2 SNPs and longer DFS with sunitinib suggest germline SNPs are predictive of improved outcomes with adjuvant sunitinib in patients with renal cell carcinoma.	Sunitinib	77-86	kinase insert domain receptor	Homo sapiens	45-51
30401688-10	2019	CONCLUSIONS: Correlations between VEGFR1 and VEGFR2 SNPs and longer DFS with sunitinib suggest germline SNPs are predictive of improved outcomes with adjuvant sunitinib in patients with renal cell carcinoma.	Sunitinib	159-168	fms related receptor tyrosine kinase 1	Homo sapiens	34-40
30401688-10	2019	CONCLUSIONS: Correlations between VEGFR1 and VEGFR2 SNPs and longer DFS with sunitinib suggest germline SNPs are predictive of improved outcomes with adjuvant sunitinib in patients with renal cell carcinoma.	Sunitinib	159-168	kinase insert domain receptor	Homo sapiens	45-51
30648632-11	2019	CONCLUSIONS: Individualised sunitinib therapy is feasible, safe and an effective method to manage toxicity with one of the best efficacy seen for oral vascular endothelial growth factor inhibitors in metastatic renal cell carcinoma.	Sunitinib	28-37	vascular endothelial growth factor A	Homo sapiens	151-185
30779084-0	2019	Effect of miR-34a on resistance to sunitinib in breast cancer by regulating the Wnt/beta-catenin signaling pathway.	Sunitinib	35-44	microRNA 34a	Homo sapiens	10-17
30779084-0	2019	Effect of miR-34a on resistance to sunitinib in breast cancer by regulating the Wnt/beta-catenin signaling pathway.	Sunitinib	35-44	Wnt family member 1	Homo sapiens	80-83
30779084-8	2019	RESULTS: The overexpression of miR-34a significantly reduced the invasive ability of MCF-7 cells after treatment with sunitinib.	Sunitinib	118-127	microRNA 34a	Homo sapiens	31-38
30779084-9	2019	After miR-34a expression was downregulated, the sensitivity of MCF-7 cells to sunitinib was significantly lowered.	Sunitinib	78-87	microRNA 34a	Homo sapiens	6-13
30779084-12	2019	CONCLUSIONS: MiR-34a affects the sensitivity to sunitinib in breast cancer by regulating the Wnt/beta-catenin signaling pathway.	Sunitinib	48-57	microRNA 34a	Homo sapiens	13-20
30779084-12	2019	CONCLUSIONS: MiR-34a affects the sensitivity to sunitinib in breast cancer by regulating the Wnt/beta-catenin signaling pathway.	Sunitinib	48-57	Wnt family member 1	Homo sapiens	93-96
30779084-12	2019	CONCLUSIONS: MiR-34a affects the sensitivity to sunitinib in breast cancer by regulating the Wnt/beta-catenin signaling pathway.	Sunitinib	48-57	catenin beta 1	Homo sapiens	97-109
30788170-6	2019	Sunitinib is required for KIT exon 9, 13, and 14 mutations, while ponatinib is used for exon 17 mutations and regorafenib for highly refractory tumors.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	26-29
28990511-1	2019	BACKGROUND: Sunitinib (SU11248) is an oral multi-target tyrosine kinase inhibitor (TKI) with low molecular weight, that inhibits platelet-derived growth factor receptors (PDGF-Rs) and vascular endothelial growth factor receptors (VEGFRs), c-KIT, fms-related tyrosine kinase 3 (FLT3) and RET.	Sunitinib	12-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	239-244
30867824-12	2019	One of the most up-regulated genes in sunitinib-resistant cells was the CXCL5 cytokine.	Sunitinib	38-47	C-X-C motif chemokine ligand 5	Homo sapiens	72-77
30867824-15	2019	The levels of CXCL5 present in the plasma of patients treated with sunitinib were predictive of the efficacy of sunitinib but not of the VEGF-directed antibody bevacizumab.	Sunitinib	67-76	C-X-C motif chemokine ligand 5	Homo sapiens	14-19
30867824-15	2019	The levels of CXCL5 present in the plasma of patients treated with sunitinib were predictive of the efficacy of sunitinib but not of the VEGF-directed antibody bevacizumab.	Sunitinib	112-121	C-X-C motif chemokine ligand 5	Homo sapiens	14-19
30498230-1	2019	BACKGROUND: There are phase 3 clinical trials underway evaluating anti-PD-L1 antibodies as adjuvant (postoperative) monotherapies for resectable renal cell carcinoma (RCC) and triple-negative breast cancer (TNBC); in combination with antiangiogenic VEGF/VEGFR2 inhibitors (e.g., bevacizumab and sunitinib) for metastatic RCC; and in combination with chemotherapeutics as neoadjuvant (preoperative) therapies for resectable TNBC.	Sunitinib	295-304	CD274 antigen	Mus musculus	71-76
30913495-0	2019	Elevated plasma interleukin 6 predicts poor response in patients treated with sunitinib for metastatic clear cell renal cell carcinoma.	Sunitinib	78-87	interleukin 6	Homo sapiens	16-29
30566287-0	2019	Synthesis, Characterization and in vitro Studies of a Cathepsin B-Cleavable Prodrug of the VEGFR Inhibitor Sunitinib.	Sunitinib	107-116	cathepsin B	Homo sapiens	54-65
30566287-0	2019	Synthesis, Characterization and in vitro Studies of a Cathepsin B-Cleavable Prodrug of the VEGFR Inhibitor Sunitinib.	Sunitinib	107-116	kinase insert domain receptor	Homo sapiens	91-96
30566287-3	2019	Here, we present the synthesis and biological investigation of a cathepsin B-cleavable prodrug of the VEGFR inhibitor sunitinib.	Sunitinib	118-127	cathepsin B	Homo sapiens	65-76
30566287-3	2019	Here, we present the synthesis and biological investigation of a cathepsin B-cleavable prodrug of the VEGFR inhibitor sunitinib.	Sunitinib	118-127	kinase insert domain receptor	Homo sapiens	102-107
30854133-0	2019	Overexpression of FZD1 is Associated with a Good Prognosis and Resistance of Sunitinib in Clear Cell Renal Cell Carcinoma.	Sunitinib	77-86	frizzled class receptor 1	Homo sapiens	18-22
30854133-5	2019	We then detected FZD1 mRNA expression in sunitinib-resistant cells and the corresponding parental cells by qRT-PCR.	Sunitinib	41-50	frizzled class receptor 1	Homo sapiens	17-21
30854133-6	2019	FZD1 level was significantly upregulated in renal cancer tissues, renal cancer cell lines and their corresponding sunitinib-resistant cells.	Sunitinib	114-123	frizzled class receptor 1	Homo sapiens	0-4
30854133-13	2019	In conclusion, our results suggested that expression status of FZD1 had a diagnostic value and prognostic value in ccRCC patients, it also may serve as a potential drug target to relieve sunitinib resistance in renal cancer patients.	Sunitinib	187-196	frizzled class receptor 1	Homo sapiens	63-67
30719230-0	2019	ATF4 contributes to autophagy and survival in sunitinib treated brain tumor initiating cells (BTICs).	Sunitinib	46-55	activating transcription factor 4	Homo sapiens	0-4
30719230-5	2019	We found that the ATF4/p-eIF2alpha pathway is activated in response to Sunitinib in primary tumor initiating progenitor cell cultures (BTICs).	Sunitinib	71-80	activating transcription factor 4	Homo sapiens	18-22
30719230-5	2019	We found that the ATF4/p-eIF2alpha pathway is activated in response to Sunitinib in primary tumor initiating progenitor cell cultures (BTICs).	Sunitinib	71-80	eukaryotic translation initiation factor 2A	Homo sapiens	25-34
30719230-7	2019	In case of Sunitinib treated cells, autophagy is additionally increased by ATF4 mediated upregulation of autophagy genes.	Sunitinib	11-20	activating transcription factor 4	Homo sapiens	75-79
30719230-8	2019	Inhibition of ATF4 by small interfering RNA (siRNA) reduced autophagy and cell proliferation after Sunitinib treatment in a subset of BTIC cultures.	Sunitinib	99-108	activating transcription factor 4	Homo sapiens	14-18
30559346-5	2019	We additionally show, using preclinical mouse as well as patient data, that treatment with the inhibitor sunitinib significantly reduces the expression of INSR-A.	Sunitinib	105-114	insulin receptor	Homo sapiens	155-159
30073769-16	2019	CONCLUSIONS: Blocking of PlGF or injection of sunitinib results in a similar inhibition of neovascularization as by anti-VEGF treatment in the mouse model of ROP.	Sunitinib	46-55	vascular endothelial growth factor A	Mus musculus	121-125
30073769-17	2019	However, physiological angiogenesis that occurs after anti-VEGF treatment is blocked by anti-PlGF or sunitinib treatment, indicating that pathological neovascularization may follow different pathways than physiological angiogenesis.	Sunitinib	101-110	vascular endothelial growth factor A	Mus musculus	59-63
28990511-1	2019	BACKGROUND: Sunitinib (SU11248) is an oral multi-target tyrosine kinase inhibitor (TKI) with low molecular weight, that inhibits platelet-derived growth factor receptors (PDGF-Rs) and vascular endothelial growth factor receptors (VEGFRs), c-KIT, fms-related tyrosine kinase 3 (FLT3) and RET.	Sunitinib	12-21	fms related receptor tyrosine kinase 3	Homo sapiens	246-275
28990511-1	2019	BACKGROUND: Sunitinib (SU11248) is an oral multi-target tyrosine kinase inhibitor (TKI) with low molecular weight, that inhibits platelet-derived growth factor receptors (PDGF-Rs) and vascular endothelial growth factor receptors (VEGFRs), c-KIT, fms-related tyrosine kinase 3 (FLT3) and RET.	Sunitinib	12-21	fms related receptor tyrosine kinase 3	Homo sapiens	277-281
28990511-1	2019	BACKGROUND: Sunitinib (SU11248) is an oral multi-target tyrosine kinase inhibitor (TKI) with low molecular weight, that inhibits platelet-derived growth factor receptors (PDGF-Rs) and vascular endothelial growth factor receptors (VEGFRs), c-KIT, fms-related tyrosine kinase 3 (FLT3) and RET.	Sunitinib	12-21	ret proto-oncogene	Homo sapiens	287-290
28990511-1	2019	BACKGROUND: Sunitinib (SU11248) is an oral multi-target tyrosine kinase inhibitor (TKI) with low molecular weight, that inhibits platelet-derived growth factor receptors (PDGF-Rs) and vascular endothelial growth factor receptors (VEGFRs), c-KIT, fms-related tyrosine kinase 3 (FLT3) and RET.	Sunitinib	23-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	239-244
28990511-1	2019	BACKGROUND: Sunitinib (SU11248) is an oral multi-target tyrosine kinase inhibitor (TKI) with low molecular weight, that inhibits platelet-derived growth factor receptors (PDGF-Rs) and vascular endothelial growth factor receptors (VEGFRs), c-KIT, fms-related tyrosine kinase 3 (FLT3) and RET.	Sunitinib	23-30	fms related receptor tyrosine kinase 3	Homo sapiens	246-275
28990511-1	2019	BACKGROUND: Sunitinib (SU11248) is an oral multi-target tyrosine kinase inhibitor (TKI) with low molecular weight, that inhibits platelet-derived growth factor receptors (PDGF-Rs) and vascular endothelial growth factor receptors (VEGFRs), c-KIT, fms-related tyrosine kinase 3 (FLT3) and RET.	Sunitinib	23-30	fms related receptor tyrosine kinase 3	Homo sapiens	277-281
28990511-1	2019	BACKGROUND: Sunitinib (SU11248) is an oral multi-target tyrosine kinase inhibitor (TKI) with low molecular weight, that inhibits platelet-derived growth factor receptors (PDGF-Rs) and vascular endothelial growth factor receptors (VEGFRs), c-KIT, fms-related tyrosine kinase 3 (FLT3) and RET.	Sunitinib	23-30	ret proto-oncogene	Homo sapiens	287-290
28990511-5	2019	RESULTS: In vitro studies showed that sunitinib targeted the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell inhibiting cell proliferation and causing stimulation of sodium/iodide symporter (NIS) gene expression in RET/PTC1 cells.	Sunitinib	38-47	mitogen-activated protein kinase kinase 7	Homo sapiens	71-74
28990511-5	2019	RESULTS: In vitro studies showed that sunitinib targeted the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell inhibiting cell proliferation and causing stimulation of sodium/iodide symporter (NIS) gene expression in RET/PTC1 cells.	Sunitinib	38-47	ret proto-oncogene	Homo sapiens	108-111
28990511-5	2019	RESULTS: In vitro studies showed that sunitinib targeted the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell inhibiting cell proliferation and causing stimulation of sodium/iodide symporter (NIS) gene expression in RET/PTC1 cells.	Sunitinib	38-47	patched 1	Homo sapiens	112-116
28990511-5	2019	RESULTS: In vitro studies showed that sunitinib targeted the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell inhibiting cell proliferation and causing stimulation of sodium/iodide symporter (NIS) gene expression in RET/PTC1 cells.	Sunitinib	38-47	ret proto-oncogene	Homo sapiens	228-231
28990511-5	2019	RESULTS: In vitro studies showed that sunitinib targeted the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell inhibiting cell proliferation and causing stimulation of sodium/iodide symporter (NIS) gene expression in RET/PTC1 cells.	Sunitinib	38-47	patched 1	Homo sapiens	232-236
30281919-0	2019	NT5E inhibition suppresses the growth of sunitinib-resistant cells and EMT course and AKT/GSK-3beta signaling pathway in renal cell cancer.	Sunitinib	41-50	5'-nucleotidase ecto	Homo sapiens	0-4
30148679-8	2019	Functional studies confirm that E-cadherin is a key contributor to the survival of RCC cells under sunitinib treatment.	Sunitinib	99-108	cadherin 1	Homo sapiens	32-42
30558998-7	2019	A positive correlation between gankyrin and sunitinib-resistance was also observed in RCC cell lines and in an orthotopic RCC model.	Sunitinib	44-53	proteasome 26S subunit, non-ATPase 10	Homo sapiens	31-39
30281919-2	2019	Microarray analysis, quantitative real time PCR (qRT-PCR), Western blot, and immunohistochemistry were used to detect Ecto-5"-nucleotidase (NT5E) expressions in sunitinib-resistant tissues in RCC.	Sunitinib	161-170	5'-nucleotidase ecto	Homo sapiens	118-138
30281919-2	2019	Microarray analysis, quantitative real time PCR (qRT-PCR), Western blot, and immunohistochemistry were used to detect Ecto-5"-nucleotidase (NT5E) expressions in sunitinib-resistant tissues in RCC.	Sunitinib	161-170	5'-nucleotidase ecto	Homo sapiens	140-144
30281919-5	2019	In vivo experiment was performed using NCr-nu/nu mice to explore the effects of NT5E on cell growth and EMT signal in sunitinib environment.	Sunitinib	118-127	5'-nucleotidase ecto	Homo sapiens	80-84
30281919-6	2019	NT5E expression was upregulated in sunitinib-resistant RCC tissues and cells.	Sunitinib	35-44	5'-nucleotidase ecto	Homo sapiens	0-4
30281919-8	2019	EMT course and AKT/GSK-3beta signal pathway both in vitro and in vivo in sunitinib environment was suppressed to varying degrees via NT5E inhibition.	Sunitinib	73-82	AKT serine/threonine kinase 1	Homo sapiens	15-18
30281919-8	2019	EMT course and AKT/GSK-3beta signal pathway both in vitro and in vivo in sunitinib environment was suppressed to varying degrees via NT5E inhibition.	Sunitinib	73-82	glycogen synthase kinase 3 beta	Homo sapiens	19-28
30281919-8	2019	EMT course and AKT/GSK-3beta signal pathway both in vitro and in vivo in sunitinib environment was suppressed to varying degrees via NT5E inhibition.	Sunitinib	73-82	5'-nucleotidase ecto	Homo sapiens	133-137
30281919-9	2019	NT5E inhibition could suppress the growth of sunitinib-resistant RCC cells and restrain EMT course and AKT/GSK-3beta signal pathway in sunitinib environment in RCC.	Sunitinib	45-54	5'-nucleotidase ecto	Homo sapiens	0-4
30281919-9	2019	NT5E inhibition could suppress the growth of sunitinib-resistant RCC cells and restrain EMT course and AKT/GSK-3beta signal pathway in sunitinib environment in RCC.	Sunitinib	135-144	5'-nucleotidase ecto	Homo sapiens	0-4
30281919-9	2019	NT5E inhibition could suppress the growth of sunitinib-resistant RCC cells and restrain EMT course and AKT/GSK-3beta signal pathway in sunitinib environment in RCC.	Sunitinib	135-144	glycogen synthase kinase 3 beta	Homo sapiens	107-116
31195398-7	2019	We evaluated the relationship between miR-130b and PTEN and also analyzed the effect of miR-130b on sunitinib resistance.	Sunitinib	100-109	microRNA 130b	Homo sapiens	88-96
29570259-11	2019	CONCLUSION: Our study suggests that dynamic changes in CRP can better predict survival in patients with mRCC who are treated with sunitinib.	Sunitinib	130-139	C-reactive protein	Homo sapiens	55-58
30653116-3	2019	We report the 1st case of metastatic jejunum GIST with a KIT exon 11 deletion that showed complete response (CR) to sunitinib for more than 3 years.	Sunitinib	116-125	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-60
30653116-10	2019	LESSONS: In cases of metastatic jejunum GIST with a KIT exon 11 deletion, sunitinib as second-line therapy can be used to achieve CR for more than 3 years.	Sunitinib	74-83	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-55
31195398-0	2019	miR-130b Promotes Sunitinib Resistance through Regulation of PTEN in Renal Cell Carcinoma.	Sunitinib	18-27	microRNA 130b	Homo sapiens	0-8
31195398-0	2019	miR-130b Promotes Sunitinib Resistance through Regulation of PTEN in Renal Cell Carcinoma.	Sunitinib	18-27	phosphatase and tensin homolog	Homo sapiens	61-65
31195398-4	2019	This study aimed to examine the expression and functional role of miR-130b and to analyze the association between miR-130b and sunitinib resistance in RCC.	Sunitinib	127-136	microRNA 130b	Homo sapiens	114-122
31195398-12	2019	Additionally, miR-130b was associated with sunitinib resistance through regulation of PTEN.	Sunitinib	43-52	microRNA 130b	Homo sapiens	14-22
31195398-12	2019	Additionally, miR-130b was associated with sunitinib resistance through regulation of PTEN.	Sunitinib	43-52	phosphatase and tensin homolog	Homo sapiens	86-90
31195398-13	2019	We established the sunitinib-resistant Caki-1 (Caki-1-SR) cells and observed that the expression of miR-130b was elevated in Caki-1-SR cells compared with parental Caki-1 cells.	Sunitinib	19-28	microRNA 130b	Homo sapiens	100-108
31195398-14	2019	Knockdown of miR-130b improved sunitinib resistance in Caki-1-SR cells.	Sunitinib	31-40	microRNA 130b	Homo sapiens	13-21
31195398-16	2019	miR-130b promoted cell growth and was associated with sunitinib resistance through regulating PTEN expression.	Sunitinib	54-63	microRNA 130b	Homo sapiens	0-8
31195398-16	2019	miR-130b promoted cell growth and was associated with sunitinib resistance through regulating PTEN expression.	Sunitinib	54-63	phosphatase and tensin homolog	Homo sapiens	94-98
30070687-5	2018	The impact of BCRP/ABCG2 on response to sunitinib treatment was investigated in two independent sunitinib-treated ccRCC-cohorts based on mRNA levels.	Sunitinib	40-49	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	14-18
30393206-0	2019	Ageing alters the severity of Sunitinib-induced cardiotoxicity: Investigating the mitogen activated kinase kinase 7 pathway association.	Sunitinib	30-39	mitogen activated protein kinase kinase 7	Rattus norvegicus	82-115
30393206-1	2019	Anti-cancer drug Sunitinib is linked to adverse cardiovascular events, which have shown to involve mitogen activated kinase kinase 7 (MKK7) pathway.	Sunitinib	17-26	mitogen activated protein kinase kinase 7	Rattus norvegicus	99-132
30393206-1	2019	Anti-cancer drug Sunitinib is linked to adverse cardiovascular events, which have shown to involve mitogen activated kinase kinase 7 (MKK7) pathway.	Sunitinib	17-26	mitogen activated protein kinase kinase 7	Rattus norvegicus	134-138
30393206-8	2019	Sunitinib treatment decreased the expression of miR-27a in all age groups, while miR-133a and miR-133b levels were increased in 3 months and decreased in 24 months groups.	Sunitinib	0-9	microRNA 27a	Rattus norvegicus	48-55
30393206-9	2019	MKK7 mRNA and p-MKK7 levels were decreased in the 3 months group after Sunitinib treatment.	Sunitinib	71-80	mitogen activated protein kinase kinase 7	Rattus norvegicus	0-4
30393206-9	2019	MKK7 mRNA and p-MKK7 levels were decreased in the 3 months group after Sunitinib treatment.	Sunitinib	71-80	mitogen activated protein kinase kinase 7	Rattus norvegicus	16-20
30393206-10	2019	MKK7 mRNA level was increased in 24 months group and p-MKK7 levels were increased in 12 months group following Sunitinib treatment.	Sunitinib	111-120	mitogen activated protein kinase kinase 7	Rattus norvegicus	0-4
30393206-10	2019	MKK7 mRNA level was increased in 24 months group and p-MKK7 levels were increased in 12 months group following Sunitinib treatment.	Sunitinib	111-120	mitogen activated protein kinase kinase 7	Rattus norvegicus	55-59
30393183-2	2018	In this study, our objective was to determine whether co-delivery of sunitinib, a member of tyrosine kinase inhibitor (TKI) family, and siRNA against Alox15 (siAlox15) could reverse the new-onset of T1D in non-obese diabetic (NOD)/ShiLtJ female mice which spontaneously develop diabetes.	Sunitinib	69-78	arachidonate 15-lipoxygenase	Mus musculus	150-156
30393183-4	2018	These micellar formulations exhibited sustained release of sunitinib for around 50% at 24 h and protected siAlox15 from serum degradation for at least 10 h. Further, both sunitinib and siAlox15 inhibited human peripheral blood mononuclear cell (PBMC) proliferation and activation by downregulating the phosphorylation of Akt, platelet-derived growth factor receptor (PDGFR) at protein levels and Alox15 in mRNA levels, respectively.	Sunitinib	171-180	arachidonate 15-lipoxygenase	Homo sapiens	108-114
30446580-9	2018	The patient received first-line sunitinib to target PDGFRA and PDGFRB and had stable disease for &gt;6 mo, followed by nivolumab upon progression.	Sunitinib	32-41	platelet derived growth factor receptor alpha	Homo sapiens	52-58
30446580-9	2018	The patient received first-line sunitinib to target PDGFRA and PDGFRB and had stable disease for &gt;6 mo, followed by nivolumab upon progression.	Sunitinib	32-41	platelet derived growth factor receptor beta	Homo sapiens	63-69
30070687-9	2018	BCRP/ABCG2 and MDR1/ABCB1 mRNA expression were linked to decreased progression-free survival after sunitinib treatment.	Sunitinib	99-108	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-4
30070687-9	2018	BCRP/ABCG2 and MDR1/ABCB1 mRNA expression were linked to decreased progression-free survival after sunitinib treatment.	Sunitinib	99-108	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	5-10
30070687-9	2018	BCRP/ABCG2 and MDR1/ABCB1 mRNA expression were linked to decreased progression-free survival after sunitinib treatment.	Sunitinib	99-108	ATP binding cassette subfamily B member 1	Homo sapiens	15-19
30070687-9	2018	BCRP/ABCG2 and MDR1/ABCB1 mRNA expression were linked to decreased progression-free survival after sunitinib treatment.	Sunitinib	99-108	ATP binding cassette subfamily B member 1	Homo sapiens	20-25
30070687-12	2018	In summary, BCRP/ABCG2 expression in ccRCC underlies considerable interindividual variability with impact on patient survival and response to sunitinib treatment.	Sunitinib	142-151	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	12-16
30070687-12	2018	In summary, BCRP/ABCG2 expression in ccRCC underlies considerable interindividual variability with impact on patient survival and response to sunitinib treatment.	Sunitinib	142-151	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	17-22
30369518-15	2018	And we found that 786-O RCC cells secrete high IL-6 levels after low dose stimulation with the TKIs sorafenib, sunitinib and pazopanib, inducing activation of AKT-mTOR pathway, NFkappaB, HIF-2alpha and VEGF expression.	Sunitinib	111-120	AKT serine/threonine kinase 1	Homo sapiens	159-162
30651932-8	2018	Our findings suggest that axitinib works better than mTOR inhibitors after the first-line treatment with sunitinib.	Sunitinib	105-114	mechanistic target of rapamycin kinase	Homo sapiens	53-57
30651923-8	2018	Dynamic upward variations were also observed with respect to IL-8 levels in sunitinib-refractory individuals: 28.5 pg/mL at baseline vs. 38.3 pg/mL at 3 months, p-value=0.024.	Sunitinib	76-85	C-X-C motif chemokine ligand 8	Homo sapiens	61-65
30651923-9	2018	In conclusion, two VEGFR-3 SNPs as well as various serum biomarkers were associated with diverse clinical outcomes in patients with well-differentiated pancreatic neuroendocrine tumors treated with sunitinib.	Sunitinib	198-207	fms related receptor tyrosine kinase 4	Homo sapiens	19-26
30369518-15	2018	And we found that 786-O RCC cells secrete high IL-6 levels after low dose stimulation with the TKIs sorafenib, sunitinib and pazopanib, inducing activation of AKT-mTOR pathway, NFkappaB, HIF-2alpha and VEGF expression.	Sunitinib	111-120	mechanistic target of rapamycin kinase	Homo sapiens	163-167
30369518-15	2018	And we found that 786-O RCC cells secrete high IL-6 levels after low dose stimulation with the TKIs sorafenib, sunitinib and pazopanib, inducing activation of AKT-mTOR pathway, NFkappaB, HIF-2alpha and VEGF expression.	Sunitinib	111-120	interleukin 6	Homo sapiens	47-51
30369518-15	2018	And we found that 786-O RCC cells secrete high IL-6 levels after low dose stimulation with the TKIs sorafenib, sunitinib and pazopanib, inducing activation of AKT-mTOR pathway, NFkappaB, HIF-2alpha and VEGF expression.	Sunitinib	111-120	nuclear factor kappa B subunit 1	Homo sapiens	177-185
30369518-15	2018	And we found that 786-O RCC cells secrete high IL-6 levels after low dose stimulation with the TKIs sorafenib, sunitinib and pazopanib, inducing activation of AKT-mTOR pathway, NFkappaB, HIF-2alpha and VEGF expression.	Sunitinib	111-120	endothelial PAS domain protein 1	Homo sapiens	187-197
30369518-15	2018	And we found that 786-O RCC cells secrete high IL-6 levels after low dose stimulation with the TKIs sorafenib, sunitinib and pazopanib, inducing activation of AKT-mTOR pathway, NFkappaB, HIF-2alpha and VEGF expression.	Sunitinib	111-120	vascular endothelial growth factor A	Homo sapiens	202-206
30267660-0	2018	RCAN1.4 acts as a suppressor of cancer progression and sunitinib resistance in clear cell renal cell carcinoma.	Sunitinib	55-64	regulator of calcineurin 1	Homo sapiens	0-5
28782406-0	2018	Severe sunitinib-induced myelosuppression in a patient with a CYP 3A4 polymorphism.	Sunitinib	7-16	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	62-69
30514344-4	2018	In this review, we summarized the preclinical and clinical studies on new FLT3 inhibitors, including sorafenib, lestaurtinib, sunitinib, tandutinib, quizartinib, midostaurin, gilteritinib, crenolanib, cabozantinib, Sel24-B489, G-749, AMG 925, TTT-3002, and FF-10101.	Sunitinib	126-135	fms related receptor tyrosine kinase 3	Homo sapiens	74-78
30267660-8	2018	In addition, RCAN1.4 expression was downregulated in sunitinib-resistant renal cancer cell lines, and inhibition of RCAN1.4 promoted sunitinib resistance.	Sunitinib	53-62	regulator of calcineurin 1	Homo sapiens	13-18
30267660-8	2018	In addition, RCAN1.4 expression was downregulated in sunitinib-resistant renal cancer cell lines, and inhibition of RCAN1.4 promoted sunitinib resistance.	Sunitinib	133-142	regulator of calcineurin 1	Homo sapiens	116-121
30267660-9	2018	We also found that RCAN1.4 could regulate epithelial-mesenchymal transition (EMT) and the expression of HIF2alpha in sunitinib-resistant cell lines.	Sunitinib	117-126	regulator of calcineurin 1	Homo sapiens	19-24
30267660-9	2018	We also found that RCAN1.4 could regulate epithelial-mesenchymal transition (EMT) and the expression of HIF2alpha in sunitinib-resistant cell lines.	Sunitinib	117-126	endothelial PAS domain protein 1	Homo sapiens	104-113
30267660-10	2018	Taken together, these findings indicate that downregulation of RCAN1.4 may be crucial for the metastasis of ccRCC and may induce sunitinib resistance.	Sunitinib	129-138	regulator of calcineurin 1	Homo sapiens	63-68
30428867-11	2018	CONCLUSIONS: Sunitinib is a multi-targeted inhibitor of vascular endothelial growth factor (VEGF) receptors.	Sunitinib	13-22	vascular endothelial growth factor A	Homo sapiens	56-90
30428867-11	2018	CONCLUSIONS: Sunitinib is a multi-targeted inhibitor of vascular endothelial growth factor (VEGF) receptors.	Sunitinib	13-22	vascular endothelial growth factor A	Homo sapiens	92-96
30348622-0	2018	Screening of FDA-approved drugs identifies sutent as a modulator of UCP1 expression in brown adipose tissue.	Sunitinib	43-49	uncoupling protein 1 (mitochondrial, proton carrier)	Mus musculus	68-72
30713805-7	2019	Sunitinib improved pericyte coverage on endothelial cells and the expression levels of regulator of G-protein signaling 5, suggesting blood vessel normalization.	Sunitinib	0-9	regulator of G protein signaling 5	Homo sapiens	87-121
30419914-0	2018	Sunitinib-suppressed miR-452-5p facilitates renal cancer cell invasion and metastasis through modulating SMAD4/SMAD7 signals.	Sunitinib	0-9	microRNA 452	Homo sapiens	21-28
30419914-0	2018	Sunitinib-suppressed miR-452-5p facilitates renal cancer cell invasion and metastasis through modulating SMAD4/SMAD7 signals.	Sunitinib	0-9	SMAD family member 4	Homo sapiens	105-110
30419914-0	2018	Sunitinib-suppressed miR-452-5p facilitates renal cancer cell invasion and metastasis through modulating SMAD4/SMAD7 signals.	Sunitinib	0-9	SMAD family member 7	Homo sapiens	111-116
30419914-3	2018	EXPERIMENTAL DESIGN: We focused on 2 published microarray data to select out our anchored miRNA and then explored the roles of miR-452-5p both in vitro and in vivo, which was downregulated after Sunitinib treatment while upregulated in metastasis renal cell carcinoma (RCC) tissues.	Sunitinib	195-204	microRNA 452	Homo sapiens	127-134
30419914-4	2018	RESULTS: Here, we discovered that treating with Sunitinib, the targeted receptor tyrosine kinase inhibitor (TKI), inhibited renal cancer cell migration and invasion via attenuating the expression of miR-452-5p.	Sunitinib	48-57	microRNA 4525	Homo sapiens	199-209
30055290-0	2018	Targeting autophagy by small molecule inhibitors of vacuolar protein sorting 34 (Vps34) improves the sensitivity of breast cancer cells to Sunitinib.	Sunitinib	139-148	phosphatidylinositol 3-kinase catalytic subunit type 3	Homo sapiens	81-86
30372397-7	2018	Because 3p loss and VHL inactivation are nearly universal truncal events in ccRCC, the resulting HIF1/2 signaling overdrive and accompanied tumor hypervascularization probably underlie the therapeutic benefits observed with vascular endothelial growth factor receptor inhibitors, including sorafenib, sunitinib, pazopanib, axitinib, bevacizumab, cabozantinib, and lenvatinib.	Sunitinib	301-310	SET domain containing 2, histone lysine methyltransferase	Homo sapiens	97-101
30031043-5	2018	Sunitinib did not affect body weight, but increased plasma ALT activity 6-fold.	Sunitinib	0-9	glutamic pyruvic transaminase, soluble	Mus musculus	59-62
30031043-10	2018	Protein expression of PGC-1alpha, citrate synthase activity and mtDNA copy number were all decreased in livers of sunitinib-treated mice, indicating impaired mitochondrial proliferation.	Sunitinib	114-123	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	22-32
30031043-10	2018	Protein expression of PGC-1alpha, citrate synthase activity and mtDNA copy number were all decreased in livers of sunitinib-treated mice, indicating impaired mitochondrial proliferation.	Sunitinib	114-123	citrate synthase	Mus musculus	34-50
30031043-11	2018	Caspase 3 activation and TUNEL-positive hepatocytes were increased in livers of sunitinib-treated mice, indicating hepatocyte apoptosis.	Sunitinib	80-89	caspase 3	Mus musculus	0-9
30055290-0	2018	Targeting autophagy by small molecule inhibitors of vacuolar protein sorting 34 (Vps34) improves the sensitivity of breast cancer cells to Sunitinib.	Sunitinib	139-148	phosphatidylinositol 3-kinase catalytic subunit type 3	Homo sapiens	52-79
30055290-7	2018	Vps34 inhibitor significantly potentiated cytotoxicity of Sunitinib and Erlotinib in MCF-7 and MDA-MB-231 in vitro in monolayer cultures and when grown as multicellular spheroids.	Sunitinib	58-67	phosphatidylinositol 3-kinase catalytic subunit type 3	Homo sapiens	0-5
30071205-7	2018	Treatment of mice with sunitinib, a VEGF receptor tyrosine kinase inhibitor, once (day 2) or twice (days 1 and 2) post-infection reduced mortality by 50-80% compared with untreated mice.	Sunitinib	23-32	vascular endothelial growth factor A	Mus musculus	36-40
30071205-8	2018	Notably, sunitinib treatment decreased serum TNF levels, white blood cell counts, and hematocrit levels relative to untreated mice, but had only marginal effects on tissue viral burden.	Sunitinib	9-18	tumor necrosis factor	Mus musculus	45-48
30412222-2	2018	We report safety, therapy management, and patient-reported outcomes for patients receiving sunitinib and placebo in the S-TRAC trial.	Sunitinib	91-100	T cell receptor alpha constant	Homo sapiens	122-126
29896907-9	2018	Sunitinib +ABCC2 blocker group showed a significant response to therapy compared to the other treatment groups both in vitro (P &lt;= 0.0001) and in vivo (P = 0.0132).	Sunitinib	0-9	ATP binding cassette subfamily C member 2	Homo sapiens	11-16
29896907-10	2018	ABCC2 blockage resulted in higher sunitinib uptake, both in vitro (P = 0.0016) and in vivo (P = 0.0031).	Sunitinib	34-43	ATP binding cassette subfamily C member 2	Homo sapiens	0-5
30524898-0	2018	Sphingosine kinase 1 overexpression contributes to sunitinib resistance in clear cell renal cell carcinoma.	Sunitinib	51-60	sphingosine kinase 1	Homo sapiens	0-20
30524898-8	2018	Our results unraveled that increased SphK1 kinase activation defines an important mechanism for sunitinib resistance, therefore contributes to tumour development and represents therapeutic targets for ccRCC.	Sunitinib	96-105	sphingosine kinase 1	Homo sapiens	37-42
30200486-0	2018	Effects of Sunitinib and Other Kinase Inhibitors on Cells Harboring a PDGFRB Mutation Associated with Infantile Myofibromatosis.	Sunitinib	11-20	platelet derived growth factor receptor beta	Homo sapiens	70-76
30371202-0	2018	Renal Soluble Guanylate Cyclase Is Downregulated in Sunitinib-Induced Hypertension.	Sunitinib	52-61	guanylate cyclase 1 soluble subunit alpha 1	Rattus norvegicus	6-31
29983397-9	2018	Sunitinib inhibited Complex I with an IC50 value of 38 microM and caused ATP depletion, caspase 3/7 activation, an increase in reactive oxygen species (ROS), and decreased nucleoside and glucose uptake.	Sunitinib	0-9	caspase 3	Mus musculus	88-97
30194077-7	2018	In renal clear cell carcinoma, the target FLT1 of pazopanib, sunitinib, sorafenib, and axitinib was recurrently deleted, whereas FLT4 bound by the same drugs, was recurrently amplified.	Sunitinib	61-70	fms related receptor tyrosine kinase 1	Homo sapiens	42-46
29764854-2	2018	Treatment with the small-molecule inhibitors imatinib, sunitinib, and regorafenib resulted in resistance (c-KIT mutant tumors) or limited activity (c-KIT wild-type tumors).	Sunitinib	55-64	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	106-111
29764854-2	2018	Treatment with the small-molecule inhibitors imatinib, sunitinib, and regorafenib resulted in resistance (c-KIT mutant tumors) or limited activity (c-KIT wild-type tumors).	Sunitinib	55-64	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	148-153
30371202-9	2018	Renal cortical sGC mRNA and sGC alpha1-subunit protein abundance were less in sunitinib-treated rats than in controls, and cinaciguat effectively lowered arterial pressure by 15-20 mm Hg in sunitinib-treated rats.	Sunitinib	78-87	guanylate cyclase 1 soluble subunit alpha 1	Rattus norvegicus	15-18
30371202-10	2018	Conclusions Renal cortical sGC is downregulated in the presence of intact endothelium-dependent renal vascular resistance regulation in developing sunitinib-induced hypertension.	Sunitinib	147-156	guanylate cyclase 1 soluble subunit alpha 1	Rattus norvegicus	27-30
30371202-11	2018	This suggests that sGC downregulation occurs outside the renal vasculature, increases renal sodium retention, and contributes to nitrate resistance of sunitinib-induced hypertension.	Sunitinib	151-160	guanylate cyclase 1 soluble subunit alpha 1	Rattus norvegicus	19-22
30200486-7	2018	We also observed that PDGFR-beta phosphorylation in tumor cells is reduced by the receptor tyrosine kinase inhibitor sunitinib.	Sunitinib	117-126	platelet derived growth factor receptor beta	Homo sapiens	22-32
30200486-8	2018	In contrast, MAPK/ERK kinases (MEK) 1/2 and ERK1/2 kinases remained constitutively phosphorylated after treatment with sunitinib and other relevant protein kinase inhibitors.	Sunitinib	119-128	mitogen-activated protein kinase kinase 1	Homo sapiens	18-39
30200486-8	2018	In contrast, MAPK/ERK kinases (MEK) 1/2 and ERK1/2 kinases remained constitutively phosphorylated after treatment with sunitinib and other relevant protein kinase inhibitors.	Sunitinib	119-128	mitogen-activated protein kinase 3	Homo sapiens	44-50
30200486-9	2018	Our study showed that sunitinib is a very promising agent that affects the proliferation of tumor cells with a p.R561C mutation in PDGFR-beta.	Sunitinib	22-31	platelet derived growth factor receptor beta	Homo sapiens	131-141
30008308-4	2018	Therefore, a novel linkable sunitinib derivative, designated SB1, was rationally designed and synthesized.	Sunitinib	28-37	Sh3kbp1 binding protein 1	Mus musculus	61-64
30224936-1	2018	Objectives: Sunitinib (a second-line chemotherapeutic agent that inhibits multiple kinases, including KIT and PDGFR) is widely used in imatinib-resistant patients with gastrointestinal stromal tumors (GISTs).	Sunitinib	12-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	102-105
30224936-1	2018	Objectives: Sunitinib (a second-line chemotherapeutic agent that inhibits multiple kinases, including KIT and PDGFR) is widely used in imatinib-resistant patients with gastrointestinal stromal tumors (GISTs).	Sunitinib	12-21	platelet derived growth factor receptor beta	Homo sapiens	110-115
30224936-8	2018	Patients with KIT mutations showed an improved CBR to sunitinib compared to those with PDGFRA mutations.	Sunitinib	54-63	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
30008308-7	2018	Cytotoxicity evaluation in three glioma cells showed that SB1 preserved the antiproliferative effect of sunitinib.	Sunitinib	104-113	Sh3kbp1 binding protein 1	Mus musculus	58-61
29803017-0	2018	Hypoxia-Targeting Drug Evofosfamide (TH-302) Enhances Sunitinib Activity in Neuroblastoma Xenograft Models.	Sunitinib	54-63	Rho guanine nucleotide exchange factor (GEF) 16	Mus musculus	76-89
30109169-9	2018	IL-8 was increased in sunitinib-resistant Caki-2 and SN12K1 cells and decreased in 786-0 without any significant changes in Caki-1.	Sunitinib	22-31	C-X-C motif chemokine ligand 8	Homo sapiens	0-4
30109169-12	2018	The increased IL-6 may contribute to sunitinib resistance either via VEGF-mediated angiogenesis or through shifting of the Bcl2/Bax balance in favour of anti-apoptosis.	Sunitinib	37-46	interleukin 6	Homo sapiens	14-18
30109169-12	2018	The increased IL-6 may contribute to sunitinib resistance either via VEGF-mediated angiogenesis or through shifting of the Bcl2/Bax balance in favour of anti-apoptosis.	Sunitinib	37-46	vascular endothelial growth factor A	Homo sapiens	69-73
30109169-12	2018	The increased IL-6 may contribute to sunitinib resistance either via VEGF-mediated angiogenesis or through shifting of the Bcl2/Bax balance in favour of anti-apoptosis.	Sunitinib	37-46	BCL2 apoptosis regulator	Homo sapiens	123-127
30109169-12	2018	The increased IL-6 may contribute to sunitinib resistance either via VEGF-mediated angiogenesis or through shifting of the Bcl2/Bax balance in favour of anti-apoptosis.	Sunitinib	37-46	BCL2 associated X, apoptosis regulator	Homo sapiens	128-131
29935772-2	2018	Sunitinib, a multikinase inhibitor, was the first Fms-like tyrosine kinase 3 (FLT3) inhibitor clinically used against AML.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	50-76
29935772-2	2018	Sunitinib, a multikinase inhibitor, was the first Fms-like tyrosine kinase 3 (FLT3) inhibitor clinically used against AML.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	78-82
29986726-15	2018	Sunitinib, gemcitabine and chloroquine treated mice showed a significant reduction of GRP78 expression, reduced cell proliferation and increased apoptosis in pancreas, compatible with a tumor response.	Sunitinib	0-9	heat shock protein 5	Mus musculus	86-91
29963235-2	2018	We aimed to establish molecular imaging during treatment with sunitinib using the fibronectin extradomain A specific small immunoprotein(SIP)-F8 in glioma.	Sunitinib	62-71	fibronectin 1	Mus musculus	82-93
29729400-5	2018	Motherwort total alkaloids significantly increased angiogenesis in transgenic Tg (flk1: EGFP) zebrafish embryos treated with sunitinib, as did stachydrine, the most abundant alkaloid produced by motherwort.	Sunitinib	125-134	kinase insert domain receptor (a type III receptor tyrosine kinase)	Danio rerio	82-86
29704617-10	2018	Based upon the X-ray crystallographic structures, imatinib, sunitinib, and ponatinib are Type II Kit inhibitors.	Sunitinib	60-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	97-100
29915248-8	2018	Gefitinib, imatinib, pazopanib, sorafenib, and sunitinib also inhibited MATE1-mediated creatinine uptake.	Sunitinib	47-56	solute carrier family 47 member 1	Rattus norvegicus	72-77
29396852-5	2018	Then the in vitro data also demonstrated the efficacy of Sunitinib, a currently used drug to treat ccRCC, could be increased after targeting this newly identified miR-32-5p/TR4/HGF/Met signaling.	Sunitinib	57-66	microRNA 32	Homo sapiens	163-169
29396852-5	2018	Then the in vitro data also demonstrated the efficacy of Sunitinib, a currently used drug to treat ccRCC, could be increased after targeting this newly identified miR-32-5p/TR4/HGF/Met signaling.	Sunitinib	57-66	nuclear receptor subfamily 2 group C member 2	Homo sapiens	173-176
29396852-5	2018	Then the in vitro data also demonstrated the efficacy of Sunitinib, a currently used drug to treat ccRCC, could be increased after targeting this newly identified miR-32-5p/TR4/HGF/Met signaling.	Sunitinib	57-66	hepatocyte growth factor	Homo sapiens	177-180
29678462-2	2018	Clinically used kinase inhibitors imatinib and sunitinib are potent inhibitors of wild-type PDGFR family members, but show reduced binding to mutant forms.	Sunitinib	47-56	platelet derived growth factor receptor beta	Homo sapiens	92-97
29572225-6	2018	Additionally, AR overexpression resulted in acquired sunitinib resistance and the AR antagonist enzalutamide-induced AR degradation and attenuated AR downstream activity in sunitinib-resistant cells, also indicated by decreased secretion of human kallikrein 2.	Sunitinib	173-182	androgen receptor	Homo sapiens	14-16
29877179-6	2018	In contrast, the S-TRAC trial showed improved DFS after one year of adjuvant sunitinib using central review process, but not using investigator review process.	Sunitinib	77-86	T cell receptor alpha constant	Homo sapiens	19-23
29572225-0	2018	Therapeutic Targeting of Sunitinib-Induced AR Phosphorylation in Renal Cell Carcinoma.	Sunitinib	25-34	androgen receptor	Homo sapiens	43-45
29572225-3	2018	Through integrative analysis of a reverse phase protein array, we discovered increased expression of AR in an RCC patient-derived xenograft model of acquired resistance to the receptor tyrosine kinase inhibitor (RTKi) sunitinib.	Sunitinib	218-227	androgen receptor	Homo sapiens	101-103
29572225-6	2018	Additionally, AR overexpression resulted in acquired sunitinib resistance and the AR antagonist enzalutamide-induced AR degradation and attenuated AR downstream activity in sunitinib-resistant cells, also indicated by decreased secretion of human kallikrein 2.	Sunitinib	173-182	androgen receptor	Homo sapiens	82-84
29572225-4	2018	AR expression was increased in RCC cell lines with either acquired or intrinsic sunitinib resistance in vitro An AR signaling gene array profiler indicated elevated levels of AR target genes in sunitinib-resistant cells.	Sunitinib	80-89	androgen receptor	Homo sapiens	0-2
29572225-4	2018	AR expression was increased in RCC cell lines with either acquired or intrinsic sunitinib resistance in vitro An AR signaling gene array profiler indicated elevated levels of AR target genes in sunitinib-resistant cells.	Sunitinib	194-203	androgen receptor	Homo sapiens	0-2
29572225-6	2018	Additionally, AR overexpression resulted in acquired sunitinib resistance and the AR antagonist enzalutamide-induced AR degradation and attenuated AR downstream activity in sunitinib-resistant cells, also indicated by decreased secretion of human kallikrein 2.	Sunitinib	173-182	androgen receptor	Homo sapiens	82-84
29572225-4	2018	AR expression was increased in RCC cell lines with either acquired or intrinsic sunitinib resistance in vitro An AR signaling gene array profiler indicated elevated levels of AR target genes in sunitinib-resistant cells.	Sunitinib	194-203	androgen receptor	Homo sapiens	113-115
29572225-4	2018	AR expression was increased in RCC cell lines with either acquired or intrinsic sunitinib resistance in vitro An AR signaling gene array profiler indicated elevated levels of AR target genes in sunitinib-resistant cells.	Sunitinib	194-203	androgen receptor	Homo sapiens	113-115
29572225-6	2018	Additionally, AR overexpression resulted in acquired sunitinib resistance and the AR antagonist enzalutamide-induced AR degradation and attenuated AR downstream activity in sunitinib-resistant cells, also indicated by decreased secretion of human kallikrein 2.	Sunitinib	173-182	androgen receptor	Homo sapiens	82-84
29572225-5	2018	Sunitinib-induced AR transcriptional activity was associated with increased phosphorylation of serine 81 (pS81) on AR.	Sunitinib	0-9	androgen receptor	Homo sapiens	18-20
29572225-6	2018	Additionally, AR overexpression resulted in acquired sunitinib resistance and the AR antagonist enzalutamide-induced AR degradation and attenuated AR downstream activity in sunitinib-resistant cells, also indicated by decreased secretion of human kallikrein 2.	Sunitinib	173-182	kallikrein related peptidase 2	Homo sapiens	247-259
29572225-5	2018	Sunitinib-induced AR transcriptional activity was associated with increased phosphorylation of serine 81 (pS81) on AR.	Sunitinib	0-9	androgen receptor	Homo sapiens	115-117
29572225-6	2018	Additionally, AR overexpression resulted in acquired sunitinib resistance and the AR antagonist enzalutamide-induced AR degradation and attenuated AR downstream activity in sunitinib-resistant cells, also indicated by decreased secretion of human kallikrein 2.	Sunitinib	53-62	androgen receptor	Homo sapiens	14-16
29490989-0	2018	A Genetic Polymorphism in CTLA-4 Is Associated with Overall Survival in Sunitinib-Treated Patients with Clear Cell Metastatic Renal Cell Carcinoma.	Sunitinib	72-81	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	26-32
28874077-0	2018	Effects of sunitinib and bevacizumab on VEGF and miRNA levels on corneal neovascularization.	Sunitinib	11-20	vascular endothelial growth factor A	Rattus norvegicus	40-44
28874077-9	2018	Also, in comparison with the control group; VEGF-A expression was downregulated by nearly 0.75 times in sunitinib group and nearly 0.52 times in bevacizumab group.	Sunitinib	104-113	vascular endothelial growth factor A	Rattus norvegicus	44-50
28874077-10	2018	VEGFR-2 expression was downregulated by 0.89 times in sunitinib group and 0.68 times in bevacizumab group, compared to the control group.	Sunitinib	54-63	kinase insert domain receptor	Rattus norvegicus	0-7
28874077-11	2018	miR-15 b, miR-16 and miR-126 levels were statistically lower in sunitinib and bevacizumab groups, but miR-188 and miR-410 levels were two-fold higher compared to the control group.	Sunitinib	64-73	microRNA 15b	Rattus norvegicus	0-8
28874077-12	2018	The miR-210 level was found higher only in sunitinib group compared to the control group.	Sunitinib	43-52	microRNA 210	Rattus norvegicus	4-11
28874077-14	2018	CONCLUSION: Topical application of bevacizumab (5 mg/ml) and sunitinib (0.5 mg/ml) decreases the levels of VEGFR-2 and VEGF-A in CNV.	Sunitinib	61-70	kinase insert domain receptor	Rattus norvegicus	107-114
28874077-14	2018	CONCLUSION: Topical application of bevacizumab (5 mg/ml) and sunitinib (0.5 mg/ml) decreases the levels of VEGFR-2 and VEGF-A in CNV.	Sunitinib	61-70	vascular endothelial growth factor A	Rattus norvegicus	119-125
29633072-0	2018	Association of Expression Levels or Activation Status of STAT3 with Treatment Outcomes of Sunitinib in Patients with Renal Cell Carcinoma.	Sunitinib	90-99	signal transducer and activator of transcription 3	Homo sapiens	57-62
29633072-2	2018	OBJECTIVE: This retrospective study aimed to elucidate the association of STAT3 expression in tumor cells with the therapeutic outcomes of sunitinib in patients with renal cell carcinoma (RCC).	Sunitinib	139-148	signal transducer and activator of transcription 3	Homo sapiens	74-79
29633072-10	2018	CONCLUSIONS: Activated STAT3 in tumor tissues shows a significant association with poor prognosis in patients with RCC who received sunitinib as a first-line therapy, and positive p-STAT3 expression could be a potential biomarker for refractoriness to sunitinib therapy.	Sunitinib	132-141	signal transducer and activator of transcription 3	Homo sapiens	23-28
29633072-10	2018	CONCLUSIONS: Activated STAT3 in tumor tissues shows a significant association with poor prognosis in patients with RCC who received sunitinib as a first-line therapy, and positive p-STAT3 expression could be a potential biomarker for refractoriness to sunitinib therapy.	Sunitinib	252-261	signal transducer and activator of transcription 3	Homo sapiens	23-28
29490989-8	2018	No significant associations with PFS were found.Conclusions: The G-allele of rs231775 in the CTLA-4 gene is associated with an improved OS in sunitinib-treated cc-mRCC patients and could potentially be used as a prognostic biomarker.	Sunitinib	142-151	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	93-99
30202791-3	2018	The second wave of tyrosine kinase inhibitors (TKIs), which target the intracellular site of VEGF receptor kinases, began with the approval of sorafenib in 2005 and sunitinib in 2006.	Sunitinib	165-174	vascular endothelial growth factor A	Homo sapiens	93-97
29382533-2	2018	Sunitinib, a multi-targeted tyrosine kinase inhibitor, is known to selectively inhibit several growth factor receptors, including vascular endothelial growth factor receptor, platelet-derived growth factor receptor and stem cell factor.	Sunitinib	0-9	KIT ligand	Homo sapiens	219-235
29532289-7	2018	RESULTS: In vitro, sunitinib and sorafenib significantly inhibited platelet aggregation (20 muM sunitinib: 71.3%, p &lt; 0.001; 25 muM sorafenib: 55.8%, p = 0.042).	Sunitinib	19-28	latexin	Homo sapiens	92-95
29532289-7	2018	RESULTS: In vitro, sunitinib and sorafenib significantly inhibited platelet aggregation (20 muM sunitinib: 71.3%, p &lt; 0.001; 25 muM sorafenib: 55.8%, p = 0.042).	Sunitinib	19-28	latexin	Homo sapiens	131-134
29532289-8	2018	Sorafenib and sunitinib significantly inhibited P-selectin expression on platelets.	Sunitinib	14-23	selectin P	Homo sapiens	48-58
29760553-4	2018	The immunohistochemistry in this patient revealed abundant expression of platelet-derived growth factor receptor-beta on tumor cells, which is one of the drug targets of sunitinib.	Sunitinib	170-179	platelet derived growth factor receptor beta	Homo sapiens	73-117
29796168-4	2018	Here, we aimed to elucidate the anti-cancer effects of JQ1 and the mechanisms underlying BRD4 inhibition in sunitinib-sensitive and -resistant ccRCCs.	Sunitinib	108-117	bromodomain containing 4	Homo sapiens	89-93
29796168-8	2018	Chromatin immunoprecipitation assays revealed that these oncogenes may be promising BRD4 targets, particularly in sunitinib-resistant ccRCC cells.	Sunitinib	114-123	bromodomain containing 4	Homo sapiens	84-88
29796168-9	2018	These results identified SCG5, SPOCD1, RGS19, and ARHGAP22 as potential prognostic markers and showed that BRD4 inhibition may have applications as a potential therapeutic approach in sunitinib-sensitive and -resistant ccRCC.	Sunitinib	184-193	bromodomain containing 4	Homo sapiens	107-111
29854307-8	2018	Moreover, TRC105 enhanced the inhibitory effect of Sunitinib on VEGF signaling and reduced VEGFR2-Akt-Creb activation, suggesting a molecular cooperation between the two drugs.	Sunitinib	51-60	vascular endothelial growth factor A	Homo sapiens	64-68
29563634-0	2018	The tyrosine-kinase inhibitor sunitinib targets vascular endothelial (VE)-cadherin: a marker of response to antitumoural treatment in metastatic renal cell carcinoma.	Sunitinib	30-39	cadherin 5	Homo sapiens	48-82
29563634-7	2018	RESULTS: Human VE-cadherin is a direct target for sunitinib which inhibits its VEGF-induced phosphorylation and cleavage on endothelial monolayer and endothelial cell migration in the 3D model.	Sunitinib	50-59	cadherin 5	Homo sapiens	15-26
29563634-7	2018	RESULTS: Human VE-cadherin is a direct target for sunitinib which inhibits its VEGF-induced phosphorylation and cleavage on endothelial monolayer and endothelial cell migration in the 3D model.	Sunitinib	50-59	vascular endothelial growth factor A	Homo sapiens	79-83
29854303-0	2018	The role of netrin-1 in metastatic renal cell carcinoma treated with sunitinib.	Sunitinib	69-78	netrin 1	Homo sapiens	12-20
29854303-7	2018	NTN1 was assessed in our in vivo sunitinib-conditioned mouse model using immunostaining.	Sunitinib	33-42	netrin 1	Mus musculus	0-4
29854303-9	2018	Results: Human renal cell carcinoma sunitinib-conditioned cell lines showed upregulation of netrin-1 in microarray and q-PCR.	Sunitinib	36-45	netrin 1	Homo sapiens	92-100
29854303-11	2018	Silencing of netrin-1 in sunitinib-conditioned Caki-1 cells did not demonstrate a significant reduction in cell migration.	Sunitinib	25-34	netrin 1	Homo sapiens	13-21
29854303-12	2018	Conclusion: Netrin-1 is highly upregulated in renal cell carcinoma treated with sunitinib, but has no influence on cell viability or cell migration in metastatic RCC.	Sunitinib	80-89	netrin 1	Homo sapiens	12-20
29854307-7	2018	At a molecular level, we showed that the combination of TRC105 and Sunitinib induced the phosphorylation of Smad 2/3 to promote endothelial cell death.	Sunitinib	67-76	SMAD family member 2	Homo sapiens	108-116
29382533-5	2018	We found that Sunitinib could inhibit the proliferation of Hacat/E cell in a time and concentration dependent manner by influencing the expression level of cell cycle protein D1, cycle protein E1, in addition, Sunitinib could induce the apoptosis of Hacat/E cell and up-regulate the expression of poly ADP-ribose polymerase (PARP).	Sunitinib	14-23	poly(ADP-ribose) polymerase 1	Homo sapiens	297-323
29382533-5	2018	We found that Sunitinib could inhibit the proliferation of Hacat/E cell in a time and concentration dependent manner by influencing the expression level of cell cycle protein D1, cycle protein E1, in addition, Sunitinib could induce the apoptosis of Hacat/E cell and up-regulate the expression of poly ADP-ribose polymerase (PARP).	Sunitinib	14-23	poly(ADP-ribose) polymerase 1	Homo sapiens	325-329
29382533-5	2018	We found that Sunitinib could inhibit the proliferation of Hacat/E cell in a time and concentration dependent manner by influencing the expression level of cell cycle protein D1, cycle protein E1, in addition, Sunitinib could induce the apoptosis of Hacat/E cell and up-regulate the expression of poly ADP-ribose polymerase (PARP).	Sunitinib	210-219	poly(ADP-ribose) polymerase 1	Homo sapiens	297-323
29382533-5	2018	We found that Sunitinib could inhibit the proliferation of Hacat/E cell in a time and concentration dependent manner by influencing the expression level of cell cycle protein D1, cycle protein E1, in addition, Sunitinib could induce the apoptosis of Hacat/E cell and up-regulate the expression of poly ADP-ribose polymerase (PARP).	Sunitinib	210-219	poly(ADP-ribose) polymerase 1	Homo sapiens	325-329
29374054-1	2018	Purpose: Adjuvant sunitinib therapy compared with placebo prolonged disease-free survival (DFS) in patients with locoregional high-risk renal cell carcinoma (RCC) in the S-TRAC trial (ClinicalTrials.gov number NCT00375674).	Sunitinib	18-27	T cell receptor alpha constant	Homo sapiens	172-176
29095068-1	2018	OBJECTIVES: Clear-cell renal cell carcinomas (ccRCC) are characterized by hyper-vascularization and can respond to vascular endothelial growth factor receptor (VEGFR) inhibitors such as sunitinib.	Sunitinib	186-195	kinase insert domain receptor	Homo sapiens	115-158
29095068-1	2018	OBJECTIVES: Clear-cell renal cell carcinomas (ccRCC) are characterized by hyper-vascularization and can respond to vascular endothelial growth factor receptor (VEGFR) inhibitors such as sunitinib.	Sunitinib	186-195	kinase insert domain receptor	Homo sapiens	160-165
29095068-9	2018	HIF2A, VEGFA, VEGFR1, VEGFR2 and VEGFR3 were highly expressed in the transcriptomic ccrcc2-subtype of tumors, known to be highly sensitive to sunitinib.	Sunitinib	142-151	endothelial PAS domain protein 1	Homo sapiens	0-5
29095068-9	2018	HIF2A, VEGFA, VEGFR1, VEGFR2 and VEGFR3 were highly expressed in the transcriptomic ccrcc2-subtype of tumors, known to be highly sensitive to sunitinib.	Sunitinib	142-151	vascular endothelial growth factor A	Homo sapiens	7-12
29095068-9	2018	HIF2A, VEGFA, VEGFR1, VEGFR2 and VEGFR3 were highly expressed in the transcriptomic ccrcc2-subtype of tumors, known to be highly sensitive to sunitinib.	Sunitinib	142-151	fms related receptor tyrosine kinase 1	Homo sapiens	14-20
29095068-9	2018	HIF2A, VEGFA, VEGFR1, VEGFR2 and VEGFR3 were highly expressed in the transcriptomic ccrcc2-subtype of tumors, known to be highly sensitive to sunitinib.	Sunitinib	142-151	kinase insert domain receptor	Homo sapiens	22-28
29095068-9	2018	HIF2A, VEGFA, VEGFR1, VEGFR2 and VEGFR3 were highly expressed in the transcriptomic ccrcc2-subtype of tumors, known to be highly sensitive to sunitinib.	Sunitinib	142-151	fms related receptor tyrosine kinase 4	Homo sapiens	33-39
29095068-12	2018	CONCLUSIONS: Intratumoral expression of genes involved in the HIF-VEGF-VEGFR-pro-angiogenic pathway, especially VEGFR2, is associated with favorable outcome on sunitinib in m-ccRCCs.	Sunitinib	160-169	vascular endothelial growth factor A	Homo sapiens	66-70
29095068-12	2018	CONCLUSIONS: Intratumoral expression of genes involved in the HIF-VEGF-VEGFR-pro-angiogenic pathway, especially VEGFR2, is associated with favorable outcome on sunitinib in m-ccRCCs.	Sunitinib	160-169	kinase insert domain receptor	Homo sapiens	71-76
29095068-12	2018	CONCLUSIONS: Intratumoral expression of genes involved in the HIF-VEGF-VEGFR-pro-angiogenic pathway, especially VEGFR2, is associated with favorable outcome on sunitinib in m-ccRCCs.	Sunitinib	160-169	kinase insert domain receptor	Homo sapiens	112-118
29374054-5	2018	Among patients with IHC, longer DFS was observed in patients with tumor CD8+ T-cell density &gt;= versus &lt; median [median (95% CI), not reached (6.83-not reached) versus 3.47 years (1.73-not reached); hazard ratio (HR) 0.40 (95% CI, 0.20-0.81); P = 0.009] treated with sunitinib (n = 101), but not with placebo (n = 90).	Sunitinib	272-281	CD8a molecule	Homo sapiens	72-75
29374054-8	2018	Among all patients with PD-L1+ tumors, DFS was numerically longer with sunitinib versus placebo (HR 0.58; P = 0.175).Conclusions: Greater CD8+ T-cell density in tumor tissue was associated with longer DFS with sunitinib but not placebo, suggesting predictive treatment effect utility.	Sunitinib	71-80	CD8a molecule	Homo sapiens	138-141
29374054-8	2018	Among all patients with PD-L1+ tumors, DFS was numerically longer with sunitinib versus placebo (HR 0.58; P = 0.175).Conclusions: Greater CD8+ T-cell density in tumor tissue was associated with longer DFS with sunitinib but not placebo, suggesting predictive treatment effect utility.	Sunitinib	210-219	CD8a molecule	Homo sapiens	138-141
29532881-12	2018	By contrast, the sunitinib-adapted cells exhibited increased neuropilin-1 (NRP1) expression levels compared with the control cells.	Sunitinib	17-26	neuropilin 1	Homo sapiens	61-73
29532881-12	2018	By contrast, the sunitinib-adapted cells exhibited increased neuropilin-1 (NRP1) expression levels compared with the control cells.	Sunitinib	17-26	neuropilin 1	Homo sapiens	75-79
29532881-13	2018	In the sunitinib-adapted cells, NRP1 interacted with phosphorylated cMet, and the cMet activation was dependent on NRP1.	Sunitinib	7-16	neuropilin 1	Homo sapiens	32-36
29532881-13	2018	In the sunitinib-adapted cells, NRP1 interacted with phosphorylated cMet, and the cMet activation was dependent on NRP1.	Sunitinib	7-16	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-72
29532881-13	2018	In the sunitinib-adapted cells, NRP1 interacted with phosphorylated cMet, and the cMet activation was dependent on NRP1.	Sunitinib	7-16	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-86
29532881-13	2018	In the sunitinib-adapted cells, NRP1 interacted with phosphorylated cMet, and the cMet activation was dependent on NRP1.	Sunitinib	7-16	neuropilin 1	Homo sapiens	115-119
29532881-14	2018	Thus, NRP1 or cMet blockade suppressed the evasive activation of the sunitinib-adapted cells.	Sunitinib	69-78	neuropilin 1	Homo sapiens	6-10
29532881-14	2018	Thus, NRP1 or cMet blockade suppressed the evasive activation of the sunitinib-adapted cells.	Sunitinib	69-78	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-18
29532881-15	2018	These results suggest that the sunitinib-adapted cells switched from a VEGF-R-dependent pathway to an alternative NRP1/cMet-dependent one.	Sunitinib	31-40	vascular endothelial growth factor A	Homo sapiens	71-75
29532881-15	2018	These results suggest that the sunitinib-adapted cells switched from a VEGF-R-dependent pathway to an alternative NRP1/cMet-dependent one.	Sunitinib	31-40	neuropilin 1	Homo sapiens	114-118
29532881-15	2018	These results suggest that the sunitinib-adapted cells switched from a VEGF-R-dependent pathway to an alternative NRP1/cMet-dependent one.	Sunitinib	31-40	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	119-123
29554654-9	2018	This article reviews the literature behind the preclinical and clinical data of the combination of RT with VEGFR-TKIs currently approved for RCC (sunitinib, sorafenib, pazopanib, and axitinib), with a focus on dose schedules as well as efficacy and toxicity.	Sunitinib	146-155	kinase insert domain receptor	Homo sapiens	107-112
29283974-9	2018	After 14 days of treatment, renal medullary beta-ENaC protein abundance was higher in rats that received sunitinib than in controls, whereas alpha-ENaC, gamma-ENaC, and NCC abundances were similar in both groups.	Sunitinib	105-114	sodium channel epithelial 1 subunit beta	Rattus norvegicus	44-53
29665322-9	2018	Low tumour cell expression of IL6Ralpha was significantly associated with improved response to sunitinib (Fisher"s exact test, p = 0.03), but not with PFS or OS.	Sunitinib	95-104	interleukin 6 receptor	Homo sapiens	30-39
29665322-13	2018	Loss of tumour cell expression of IL6Ralpha in mccRCC patients treated with sunitinib predicts improved treatment response, and might represent a candidate predictive marker.	Sunitinib	76-85	interleukin 6 receptor	Homo sapiens	34-43
29721091-0	2018	Soluble CD146 is a predictive marker of pejorative evolution and of sunitinib efficacy in clear cell renal cell carcinoma.	Sunitinib	68-77	melanoma cell adhesion molecule	Homo sapiens	8-13
29721091-7	2018	In vitro, resistant cells to sunitinib expressed high levels of CD146 mRNA and protein in comparison to sensitive cells.	Sunitinib	29-38	melanoma cell adhesion molecule	Homo sapiens	64-69
29721091-8	2018	Moreover, recombinant CD146 protected cells from the sunitinib-dependent decrease of cell viability.	Sunitinib	53-62	melanoma cell adhesion molecule	Homo sapiens	22-27
29721091-9	2018	Conclusion: CD146/sCD146 produced by tumor cells is a relevant biological marker of ccRCC aggressiveness and relapse on sunitinib treatment.	Sunitinib	120-129	melanoma cell adhesion molecule	Homo sapiens	12-17
29615901-2	2018	It was hypothesized that sunitinib-induced fatigue may be related to off target inhibition of the AMPK enzyme, which results in impairment of energy-producing processes at a systemic level.	Sunitinib	25-34	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	98-102
29356495-3	2018	To address tractability of multiple RTKs for chemical degradation by the E3 ligase CUL4-RBX1-DDB1-CRBN (CRL4CRBN), we synthesized a series of phthalimide degraders based on the promiscuous kinase inhibitors sunitinib and PHA665752.	Sunitinib	207-216	damage specific DNA binding protein 1	Homo sapiens	93-97
29356495-3	2018	To address tractability of multiple RTKs for chemical degradation by the E3 ligase CUL4-RBX1-DDB1-CRBN (CRL4CRBN), we synthesized a series of phthalimide degraders based on the promiscuous kinase inhibitors sunitinib and PHA665752.	Sunitinib	207-216	cereblon	Homo sapiens	98-102
29376753-9	2018	Left ventricular systolic dysfunction was increased after tyrosine kinase inhibitor therapy (relative risk = 2.53; 95% confidence interval:1.79 - 3.57; p &lt; 0.001), with the highest risks reported for sunitinib and hepatocellular cancer.	Sunitinib	203-212	TXK tyrosine kinase	Homo sapiens	58-73
29515108-0	2018	The convergent roles of NF-kappaB and ER stress in sunitinib-mediated expression of pro-tumorigenic cytokines and refractory phenotype in renal cell carcinoma.	Sunitinib	51-60	nuclear factor kappa B subunit 1	Homo sapiens	24-33
29515108-4	2018	Our studies reveal that sunitinib triggers two resistance-promoting signaling pathways in RCC cells, which emanate from the endoplasmic reticulum (ER) stress response: a PERK-driven ER stress response that induces expression of the pro-tumorigenic cytokines IL-6, IL-8, and TNF-alpha, and a TRAF2-mediated NF-kappaB survival program that protects tumor cells against cell death.	Sunitinib	24-33	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	170-174
29515108-4	2018	Our studies reveal that sunitinib triggers two resistance-promoting signaling pathways in RCC cells, which emanate from the endoplasmic reticulum (ER) stress response: a PERK-driven ER stress response that induces expression of the pro-tumorigenic cytokines IL-6, IL-8, and TNF-alpha, and a TRAF2-mediated NF-kappaB survival program that protects tumor cells against cell death.	Sunitinib	24-33	interleukin 6	Homo sapiens	258-262
29515108-4	2018	Our studies reveal that sunitinib triggers two resistance-promoting signaling pathways in RCC cells, which emanate from the endoplasmic reticulum (ER) stress response: a PERK-driven ER stress response that induces expression of the pro-tumorigenic cytokines IL-6, IL-8, and TNF-alpha, and a TRAF2-mediated NF-kappaB survival program that protects tumor cells against cell death.	Sunitinib	24-33	C-X-C motif chemokine ligand 8	Homo sapiens	264-268
29515108-4	2018	Our studies reveal that sunitinib triggers two resistance-promoting signaling pathways in RCC cells, which emanate from the endoplasmic reticulum (ER) stress response: a PERK-driven ER stress response that induces expression of the pro-tumorigenic cytokines IL-6, IL-8, and TNF-alpha, and a TRAF2-mediated NF-kappaB survival program that protects tumor cells against cell death.	Sunitinib	24-33	tumor necrosis factor	Homo sapiens	274-283
29515108-4	2018	Our studies reveal that sunitinib triggers two resistance-promoting signaling pathways in RCC cells, which emanate from the endoplasmic reticulum (ER) stress response: a PERK-driven ER stress response that induces expression of the pro-tumorigenic cytokines IL-6, IL-8, and TNF-alpha, and a TRAF2-mediated NF-kappaB survival program that protects tumor cells against cell death.	Sunitinib	24-33	TNF receptor associated factor 2	Homo sapiens	291-296
29515108-4	2018	Our studies reveal that sunitinib triggers two resistance-promoting signaling pathways in RCC cells, which emanate from the endoplasmic reticulum (ER) stress response: a PERK-driven ER stress response that induces expression of the pro-tumorigenic cytokines IL-6, IL-8, and TNF-alpha, and a TRAF2-mediated NF-kappaB survival program that protects tumor cells against cell death.	Sunitinib	24-33	nuclear factor kappa B subunit 1	Homo sapiens	306-315
29515108-5	2018	PERK blockade completely prevents sunitinib-induced expression of IL-6, IL-8 and TNF-alpha, whereas NF-kappaB inhibition reinstates sensitivity of RCC cells to sunitinib both in vitro and in vivo.	Sunitinib	34-43	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	0-4
29515108-5	2018	PERK blockade completely prevents sunitinib-induced expression of IL-6, IL-8 and TNF-alpha, whereas NF-kappaB inhibition reinstates sensitivity of RCC cells to sunitinib both in vitro and in vivo.	Sunitinib	34-43	interleukin 6	Homo sapiens	66-70
29515108-5	2018	PERK blockade completely prevents sunitinib-induced expression of IL-6, IL-8 and TNF-alpha, whereas NF-kappaB inhibition reinstates sensitivity of RCC cells to sunitinib both in vitro and in vivo.	Sunitinib	34-43	C-X-C motif chemokine ligand 8	Homo sapiens	72-76
29515108-5	2018	PERK blockade completely prevents sunitinib-induced expression of IL-6, IL-8 and TNF-alpha, whereas NF-kappaB inhibition reinstates sensitivity of RCC cells to sunitinib both in vitro and in vivo.	Sunitinib	34-43	tumor necrosis factor	Homo sapiens	81-90
29248607-0	2018	Involvement of mitogen activated kinase kinase 7 intracellular signalling pathway in Sunitinib-induced cardiotoxicity.	Sunitinib	85-94	mitogen-activated protein kinase kinase 7	Homo sapiens	15-48
29435010-5	2018	The inhibition of autophagy by CQ enhanced sunitinib-induced apoptosis, which was characterized by the activation of caspase-3, caspase-9, Bcl-2 and p53.	Sunitinib	43-52	caspase 3	Homo sapiens	117-126
29435010-5	2018	The inhibition of autophagy by CQ enhanced sunitinib-induced apoptosis, which was characterized by the activation of caspase-3, caspase-9, Bcl-2 and p53.	Sunitinib	43-52	caspase 9	Homo sapiens	128-137
29435010-5	2018	The inhibition of autophagy by CQ enhanced sunitinib-induced apoptosis, which was characterized by the activation of caspase-3, caspase-9, Bcl-2 and p53.	Sunitinib	43-52	BCL2 apoptosis regulator	Homo sapiens	139-144
29435010-5	2018	The inhibition of autophagy by CQ enhanced sunitinib-induced apoptosis, which was characterized by the activation of caspase-3, caspase-9, Bcl-2 and p53.	Sunitinib	43-52	tumor protein p53	Homo sapiens	149-152
29435010-6	2018	Additionally, the exposure of OS-RC-2 cells to CQ and sunitinib resulted in the inhibition of AKT, tuberous sclerosis complex 2, mechanistic target of rapamycin and p70 ribosomal S6 kinase, which are associated with cell proliferation.	Sunitinib	54-63	AKT serine/threonine kinase 1	Homo sapiens	94-97
29345296-9	2018	Among the test agents, sunitinib and cisplatin decreased the secretion of vascular endothelial growth factor (VEGF)-A from the A549 lung cancer cells.	Sunitinib	23-32	vascular endothelial growth factor A	Homo sapiens	74-108
29345296-9	2018	Among the test agents, sunitinib and cisplatin decreased the secretion of vascular endothelial growth factor (VEGF)-A from the A549 lung cancer cells.	Sunitinib	23-32	vascular endothelial growth factor A	Homo sapiens	110-114
29248607-7	2018	Administration of Sunitinib (1 muM) during Langendorff perfusion resulted in increased infarct size, increased miR-133a expression, and decreased phosphorylation of the ASK1/MKK7/JNK pathway compared to control.	Sunitinib	18-27	mitogen-activated protein kinase 8	Homo sapiens	179-182
29248607-8	2018	Co-administration of NQDI-1 (2.5 muM) attenuated the increased Sunitinib-induced infarct size, reversed miR-133a expression and restored phosphorylated levels of ASK1/MKK7/JNK.	Sunitinib	63-72	mitogen-activated protein kinase kinase 7	Homo sapiens	167-171
29248607-8	2018	Co-administration of NQDI-1 (2.5 muM) attenuated the increased Sunitinib-induced infarct size, reversed miR-133a expression and restored phosphorylated levels of ASK1/MKK7/JNK.	Sunitinib	63-72	mitogen-activated protein kinase 8	Homo sapiens	172-175
29248607-4	2018	This study investigates the role of ASK1, MKK7 and JNK during Sunitinib-induced cardiotoxicity.	Sunitinib	62-71	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	36-40
29248607-9	2018	These findings suggest that the ASK1/MKK7/JNK intracellular signalling pathway is important in Sunitinib-induced cardiotoxicity.	Sunitinib	95-104	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	32-36
29248607-9	2018	These findings suggest that the ASK1/MKK7/JNK intracellular signalling pathway is important in Sunitinib-induced cardiotoxicity.	Sunitinib	95-104	mitogen-activated protein kinase kinase 7	Homo sapiens	37-41
29248607-9	2018	These findings suggest that the ASK1/MKK7/JNK intracellular signalling pathway is important in Sunitinib-induced cardiotoxicity.	Sunitinib	95-104	mitogen-activated protein kinase 8	Homo sapiens	42-45
29248607-13	2018	Investigations into the ASK1/MKK7/JNK transduction pathway could lead to development of cardioprotective adjunct therapy, which could prevent Sunitinib-induced cardiac injury.	Sunitinib	142-151	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	24-28
29248607-13	2018	Investigations into the ASK1/MKK7/JNK transduction pathway could lead to development of cardioprotective adjunct therapy, which could prevent Sunitinib-induced cardiac injury.	Sunitinib	142-151	mitogen-activated protein kinase kinase 7	Homo sapiens	29-33
29248607-13	2018	Investigations into the ASK1/MKK7/JNK transduction pathway could lead to development of cardioprotective adjunct therapy, which could prevent Sunitinib-induced cardiac injury.	Sunitinib	142-151	mitogen-activated protein kinase 8	Homo sapiens	34-37
29248607-4	2018	This study investigates the role of ASK1, MKK7 and JNK during Sunitinib-induced cardiotoxicity.	Sunitinib	62-71	mitogen-activated protein kinase 8	Homo sapiens	51-54
29248607-7	2018	Administration of Sunitinib (1 muM) during Langendorff perfusion resulted in increased infarct size, increased miR-133a expression, and decreased phosphorylation of the ASK1/MKK7/JNK pathway compared to control.	Sunitinib	18-27	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	169-173
29248607-7	2018	Administration of Sunitinib (1 muM) during Langendorff perfusion resulted in increased infarct size, increased miR-133a expression, and decreased phosphorylation of the ASK1/MKK7/JNK pathway compared to control.	Sunitinib	18-27	mitogen-activated protein kinase kinase 7	Homo sapiens	174-178
29551130-6	2018	The first TK to be targeted, Bcr-Abl, led to the generation of several drugs including imatinib, dasatinib, and sunitinib that provided a rich understanding of this phenomenon.	Sunitinib	112-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
28676023-1	2018	BACKGROUND: Sunitinib, a tyrosine kinase inhibitor of vascular endothelial growth factor (VEGF), is approved for first and second line treatment of advanced renal cell carcinoma (RCC).	Sunitinib	12-21	vascular endothelial growth factor A	Homo sapiens	54-88
28676023-1	2018	BACKGROUND: Sunitinib, a tyrosine kinase inhibitor of vascular endothelial growth factor (VEGF), is approved for first and second line treatment of advanced renal cell carcinoma (RCC).	Sunitinib	12-21	vascular endothelial growth factor A	Homo sapiens	90-94
29662541-2	2018	Chronic treatment with vascular endothelial growth factor receptor (VEGFR)-targeting sunitinib upregulates MET and AXL in RCC, indicating that cabozantinib may be particularly effective in patients with advanced RCC whose disease progressed on prior VEGFR-targeted treatment.	Sunitinib	85-94	kinase insert domain receptor	Homo sapiens	23-66
29662541-2	2018	Chronic treatment with vascular endothelial growth factor receptor (VEGFR)-targeting sunitinib upregulates MET and AXL in RCC, indicating that cabozantinib may be particularly effective in patients with advanced RCC whose disease progressed on prior VEGFR-targeted treatment.	Sunitinib	85-94	kinase insert domain receptor	Homo sapiens	68-73
29662541-2	2018	Chronic treatment with vascular endothelial growth factor receptor (VEGFR)-targeting sunitinib upregulates MET and AXL in RCC, indicating that cabozantinib may be particularly effective in patients with advanced RCC whose disease progressed on prior VEGFR-targeted treatment.	Sunitinib	85-94	AXL receptor tyrosine kinase	Homo sapiens	115-118
29662541-2	2018	Chronic treatment with vascular endothelial growth factor receptor (VEGFR)-targeting sunitinib upregulates MET and AXL in RCC, indicating that cabozantinib may be particularly effective in patients with advanced RCC whose disease progressed on prior VEGFR-targeted treatment.	Sunitinib	85-94	kinase insert domain receptor	Homo sapiens	250-255
29298329-12	2018	In addition, 48 h sutent treatment significantly down-regulated the protein expression of PDGFRbeta, MYCN, SOX2 and Survivin in the AI tumorspheres and inhibited tumorsphere self-renewal.	Sunitinib	18-24	platelet derived growth factor receptor beta	Homo sapiens	90-99
29298329-12	2018	In addition, 48 h sutent treatment significantly down-regulated the protein expression of PDGFRbeta, MYCN, SOX2 and Survivin in the AI tumorspheres and inhibited tumorsphere self-renewal.	Sunitinib	18-24	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	101-105
29298329-12	2018	In addition, 48 h sutent treatment significantly down-regulated the protein expression of PDGFRbeta, MYCN, SOX2 and Survivin in the AI tumorspheres and inhibited tumorsphere self-renewal.	Sunitinib	18-24	SRY-box transcription factor 2	Homo sapiens	107-111
29581831-6	2018	Results: Necessary dose reductions of sunitinib were significantly correlated with SNP rs1933437 in FLT3.	Sunitinib	38-47	fms related receptor tyrosine kinase 3	Homo sapiens	100-104
29581831-9	2018	Our study provides a population PK model of sunitinib with the ABCB1 genotype as a predictive covariate for apparent oral clearance.	Sunitinib	44-53	ATP binding cassette subfamily B member 1	Homo sapiens	63-68
30205729-0	2018	HMGB1 represses the anti-cancer activity of sunitinib by governing TP53 autophagic degradation via its nucleus-to-cytoplasm transport.	Sunitinib	44-53	high mobility group box 1	Homo sapiens	0-5
30205729-0	2018	HMGB1 represses the anti-cancer activity of sunitinib by governing TP53 autophagic degradation via its nucleus-to-cytoplasm transport.	Sunitinib	44-53	tumor protein p53	Homo sapiens	67-71
30205729-3	2018	Here we report that resistance to sunitinib therapy was driven by autophagic degradation of TP53/p53.	Sunitinib	34-43	tumor protein p53	Homo sapiens	92-96
30205729-3	2018	Here we report that resistance to sunitinib therapy was driven by autophagic degradation of TP53/p53.	Sunitinib	34-43	tumor protein p53	Homo sapiens	97-100
30205729-5	2018	Mechanistically, the transport of TP53 from the nucleus to the cytoplasm was essential for the sunitinib-induced autophagic degradation of TP53 and did not require TP53 nuclear export signals (NESs).	Sunitinib	95-104	tumor protein p53	Homo sapiens	34-38
30205729-5	2018	Mechanistically, the transport of TP53 from the nucleus to the cytoplasm was essential for the sunitinib-induced autophagic degradation of TP53 and did not require TP53 nuclear export signals (NESs).	Sunitinib	95-104	tumor protein p53	Homo sapiens	139-143
30205729-5	2018	Mechanistically, the transport of TP53 from the nucleus to the cytoplasm was essential for the sunitinib-induced autophagic degradation of TP53 and did not require TP53 nuclear export signals (NESs).	Sunitinib	95-104	tumor protein p53	Homo sapiens	139-143
30205729-7	2018	The inhibition of HMGB1 sensitized cancer cells to sunitinib.	Sunitinib	51-60	high mobility group box 1	Homo sapiens	18-23
30205729-8	2018	Importantly, sunitinib induced the degradation of all TP53 proteins, except for TP53 proteins with mutations in the interaction domain of TP53 with HMGB1 (amino acids 313 to 352).	Sunitinib	13-22	tumor protein p53	Homo sapiens	54-58
30205729-9	2018	In conclusion, our data identify an alternative HMGB1-mediated TP53 protein turnover mechanism that participates in the resistance of sunitinib and suggest HMGB1 as a potential therapeutic target for improving clinical outcomes of sunitinib.	Sunitinib	134-143	high mobility group box 1	Homo sapiens	48-53
30205729-9	2018	In conclusion, our data identify an alternative HMGB1-mediated TP53 protein turnover mechanism that participates in the resistance of sunitinib and suggest HMGB1 as a potential therapeutic target for improving clinical outcomes of sunitinib.	Sunitinib	134-143	tumor protein p53	Homo sapiens	63-67
30205729-9	2018	In conclusion, our data identify an alternative HMGB1-mediated TP53 protein turnover mechanism that participates in the resistance of sunitinib and suggest HMGB1 as a potential therapeutic target for improving clinical outcomes of sunitinib.	Sunitinib	231-240	high mobility group box 1	Homo sapiens	48-53
30205729-9	2018	In conclusion, our data identify an alternative HMGB1-mediated TP53 protein turnover mechanism that participates in the resistance of sunitinib and suggest HMGB1 as a potential therapeutic target for improving clinical outcomes of sunitinib.	Sunitinib	231-240	tumor protein p53	Homo sapiens	63-67
30205729-9	2018	In conclusion, our data identify an alternative HMGB1-mediated TP53 protein turnover mechanism that participates in the resistance of sunitinib and suggest HMGB1 as a potential therapeutic target for improving clinical outcomes of sunitinib.	Sunitinib	231-240	high mobility group box 1	Homo sapiens	156-161
29161241-10	2018	A 10% reduction in marker lesions was associated with improved PFS in the whole sunitinib population (HR 0.55 (95 CI 0.3-0.9); P=0.04); mostly in patients on sunitinib CDD (HR 0.33 (95% CI 0.2-0.7); P=0.005).	Sunitinib	80-89	natriuretic peptide A	Homo sapiens	168-171
29652183-0	2018	Effects of sunitinib on immunoreactivity of vimentin, E-cadherin and S100 in kidneys of streptozotocin induced diabetic mice.	Sunitinib	11-20	vimentin	Mus musculus	44-52
29652183-14	2018	We found that the number of vimentin and E-cadherin positive glomeruli and tubules were increased after sunitinib treatment compared to saline treated diabetic mice.	Sunitinib	104-113	vimentin	Mus musculus	28-36
29652183-14	2018	We found that the number of vimentin and E-cadherin positive glomeruli and tubules were increased after sunitinib treatment compared to saline treated diabetic mice.	Sunitinib	104-113	cadherin 1	Mus musculus	41-51
29652183-15	2018	The number of vimentin labeled tubules was decreased in the sunitinib treated group compared to diabetic + saline groups.	Sunitinib	60-69	vimentin	Mus musculus	14-22
29652183-17	2018	The effect of sunitinib on experimental diabetic mice appears to be related to levels of vimentin, E-cadherin and S100 in the glomeruli and tubules of the kidney, and sunitinib may protect against renal damage from DM.	Sunitinib	14-23	vimentin	Mus musculus	89-97
29652183-17	2018	The effect of sunitinib on experimental diabetic mice appears to be related to levels of vimentin, E-cadherin and S100 in the glomeruli and tubules of the kidney, and sunitinib may protect against renal damage from DM.	Sunitinib	14-23	cadherin 1	Mus musculus	99-109
29652183-17	2018	The effect of sunitinib on experimental diabetic mice appears to be related to levels of vimentin, E-cadherin and S100 in the glomeruli and tubules of the kidney, and sunitinib may protect against renal damage from DM.	Sunitinib	14-23	S100 calcium binding protein A1	Mus musculus	114-118
30636586-4	2018	We have presented that VEGF blockage in neoadjuvant setting via bevacizumab, aflibercept and sunitinib not only has revealed some promising benefits but also has shown a large negative outcome in the adjuvant trials.	Sunitinib	93-102	vascular endothelial growth factor A	Homo sapiens	23-27
30168120-2	2018	In 2005, with the advent of vascular endothelial growth factor (VEGF) tyrosine kinase inhibitor (TKI) therapy, the standard of care shifted to agents such as sunitinib and pazopanib.	Sunitinib	158-167	vascular endothelial growth factor A	Homo sapiens	28-62
30168120-2	2018	In 2005, with the advent of vascular endothelial growth factor (VEGF) tyrosine kinase inhibitor (TKI) therapy, the standard of care shifted to agents such as sunitinib and pazopanib.	Sunitinib	158-167	vascular endothelial growth factor A	Homo sapiens	64-68
30539696-8	2018	RESULTS: HepG2 cells with high CBS expression were less sensitive to DOX and sunitinib and knockdown of CBS significantly elevated the sensitivity to DOX and sunitinib in HepG2 cells.	Sunitinib	77-86	cystathionine beta-synthase	Homo sapiens	31-34
30539696-8	2018	RESULTS: HepG2 cells with high CBS expression were less sensitive to DOX and sunitinib and knockdown of CBS significantly elevated the sensitivity to DOX and sunitinib in HepG2 cells.	Sunitinib	158-167	cystathionine beta-synthase	Homo sapiens	104-107
30539696-9	2018	In contrast, CBS overexpression increased the resistance of DOX and sunitinib in BEL-7404 cells.	Sunitinib	68-77	cystathionine beta-synthase	Homo sapiens	13-16
29174910-0	2018	Corrigendum to "Enhanced expression of caveolin-1 possesses diagnostic and prognostic value and promotes cell migration, invasion and sunitinib resistance in the clear cell renal cell carcinoma" [Exp.	Sunitinib	134-143	caveolin 1	Homo sapiens	39-49
28885866-5	2018	Of particular interest is the novel use of tyrosine kinase inhibitors (sunitinib and its derivatives) for the prevention and treatment of age-related ocular diseases via inhibition of the caspase-3, dual-leucine zipper kinase (DLK) and leucine zipper-bearing kinase (LZK) pathways.	Sunitinib	71-80	caspase 3	Homo sapiens	188-197
28885866-5	2018	Of particular interest is the novel use of tyrosine kinase inhibitors (sunitinib and its derivatives) for the prevention and treatment of age-related ocular diseases via inhibition of the caspase-3, dual-leucine zipper kinase (DLK) and leucine zipper-bearing kinase (LZK) pathways.	Sunitinib	71-80	mitogen-activated protein kinase kinase kinase 12	Homo sapiens	199-225
28885866-5	2018	Of particular interest is the novel use of tyrosine kinase inhibitors (sunitinib and its derivatives) for the prevention and treatment of age-related ocular diseases via inhibition of the caspase-3, dual-leucine zipper kinase (DLK) and leucine zipper-bearing kinase (LZK) pathways.	Sunitinib	71-80	mitogen-activated protein kinase kinase kinase 12	Homo sapiens	227-230
28885866-5	2018	Of particular interest is the novel use of tyrosine kinase inhibitors (sunitinib and its derivatives) for the prevention and treatment of age-related ocular diseases via inhibition of the caspase-3, dual-leucine zipper kinase (DLK) and leucine zipper-bearing kinase (LZK) pathways.	Sunitinib	71-80	mitogen-activated protein kinase kinase kinase 13	Homo sapiens	236-265
28885866-5	2018	Of particular interest is the novel use of tyrosine kinase inhibitors (sunitinib and its derivatives) for the prevention and treatment of age-related ocular diseases via inhibition of the caspase-3, dual-leucine zipper kinase (DLK) and leucine zipper-bearing kinase (LZK) pathways.	Sunitinib	71-80	mitogen-activated protein kinase kinase kinase 13	Homo sapiens	267-270
29289530-9	2018	This model enables the study of anti-angiogenic drugs which target a specific factor/receptor pathway, as demonstrated by the use of the clinically approved sorafenib and sunitinib for targeting the VEGF-A/VEGFR-2 pathway.	Sunitinib	171-180	vascular endothelial growth factor A	Homo sapiens	199-205
29289530-9	2018	This model enables the study of anti-angiogenic drugs which target a specific factor/receptor pathway, as demonstrated by the use of the clinically approved sorafenib and sunitinib for targeting the VEGF-A/VEGFR-2 pathway.	Sunitinib	171-180	kinase insert domain receptor	Homo sapiens	206-213
30123861-6	2018	Flow cytometry showed that treatment with sunitinib, not sorafenib, significantly reduced the frequency of regulatory T cells (Tregs) and myeloid-derived suppressive cells (MDSCs) in tumor-bearing mice; and allowed splenic lymphocytes to produce equivalent levels of IFN-gamma and TNF-alpha in response to vaccination as that in wild type mice.	Sunitinib	42-51	interferon gamma	Mus musculus	267-276
30123861-6	2018	Flow cytometry showed that treatment with sunitinib, not sorafenib, significantly reduced the frequency of regulatory T cells (Tregs) and myeloid-derived suppressive cells (MDSCs) in tumor-bearing mice; and allowed splenic lymphocytes to produce equivalent levels of IFN-gamma and TNF-alpha in response to vaccination as that in wild type mice.	Sunitinib	42-51	tumor necrosis factor	Mus musculus	281-290
28966072-6	2018	PFS1 and 2 were defined as the time between the start of sunitinib and first progression and the time between dose-escalation and second progression respectively.	Sunitinib	57-66	GINS complex subunit 2	Homo sapiens	0-10
30286478-10	2018	In 3 patients KIT mutations (e.g. pM541L, pV654A) known to be tissue-based biomarkers with level 1 evidence for the treatment with imatinib and sunitinib were found.	Sunitinib	144-153	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
29290798-10	2018	SU inhibits signaling of vascular endothelial growth factor (VEGF), which is responsible for the sprouting of new vasculature, and GSI inhibits the Notch pathway, which is a key factor in the correct maturation of newly formed vasculature.	Sunitinib	0-2	vascular endothelial growth factor A	Mus musculus	25-59
29290798-10	2018	SU inhibits signaling of vascular endothelial growth factor (VEGF), which is responsible for the sprouting of new vasculature, and GSI inhibits the Notch pathway, which is a key factor in the correct maturation of newly formed vasculature.	Sunitinib	0-2	vascular endothelial growth factor A	Mus musculus	61-65
29290798-13	2018	Results The results show that MI can detect changes in VEGFR-2 expression in the group treated with SU within a week of the start of treatment, while differences in volume only become apparent after the mice have been treated for three weeks.	Sunitinib	100-102	kinase insert domain protein receptor	Mus musculus	55-62
28479237-16	2018	S-TRAC provides evidence that 1 year of adjuvant sunitinib in patients with higher risk locoregional disease increases the median time to recurrence.	Sunitinib	49-58	T cell receptor alpha constant	Homo sapiens	2-6
29399154-0	2018	Lysosome-associated membrane protein 2 (LAMP-2) expression induced by miR-194-5p downregulation contributes to sunitinib resistance in human renal cell carcinoma cells.	Sunitinib	111-120	lysosomal associated membrane protein 2	Homo sapiens	40-46
29399154-0	2018	Lysosome-associated membrane protein 2 (LAMP-2) expression induced by miR-194-5p downregulation contributes to sunitinib resistance in human renal cell carcinoma cells.	Sunitinib	111-120	membrane associated ring-CH-type finger 8	Homo sapiens	70-73
29399154-5	2018	Transfection of miR-194-5p, though not with negative control miR, in SR-ACHN cells could significantly inhibit cell proliferation following sunitinib treatment (2.5-40 microM; P&lt;0.05).	Sunitinib	140-149	membrane associated ring-CH-type finger 8	Homo sapiens	16-19
29399154-6	2018	Western blotting demonstrated that the expression of lysosome-associated membrane protein-2 (LAMP-2), which attenuates the anti-proliferative effect of sunitinib, was significantly higher in SR-ACHN than in ACHN cells (P&lt;0.01).	Sunitinib	152-161	lysosomal associated membrane protein 2	Homo sapiens	53-91
29399154-6	2018	Western blotting demonstrated that the expression of lysosome-associated membrane protein-2 (LAMP-2), which attenuates the anti-proliferative effect of sunitinib, was significantly higher in SR-ACHN than in ACHN cells (P&lt;0.01).	Sunitinib	152-161	lysosomal associated membrane protein 2	Homo sapiens	93-99
29399154-8	2018	These data suggested that miR-194-5p downregulation may be associated with sunitinib resistance via the induction of LAMP-2 expression in human RCC.	Sunitinib	75-84	membrane associated ring-CH-type finger 8	Homo sapiens	26-29
29399154-8	2018	These data suggested that miR-194-5p downregulation may be associated with sunitinib resistance via the induction of LAMP-2 expression in human RCC.	Sunitinib	75-84	lysosomal associated membrane protein 2	Homo sapiens	117-123
28986088-0	2018	Expression of tyrosine kinase receptor AXL is associated with worse outcome of metastatic renal cell carcinomas treated with sunitinib.	Sunitinib	125-134	AXL receptor tyrosine kinase	Homo sapiens	39-42
28986088-4	2018	Recently, others and our group suggested that the receptor tyrosine kinase AXL may modify the response to sunitinib.	Sunitinib	106-115	AXL receptor tyrosine kinase	Homo sapiens	75-78
28986088-5	2018	OBJECTIVE: To study the expression of AXL in a series patients with of mRCC treated with sunitinib and to correlate it with patient"s clinic-pathological features and therapeutic response.	Sunitinib	89-98	AXL receptor tyrosine kinase	Homo sapiens	38-41
28986088-10	2018	Moreover, AXL expression was associated with shorter progression to sunitinib.	Sunitinib	68-77	AXL receptor tyrosine kinase	Homo sapiens	10-13
28986088-12	2018	CONCLUSION: AXL expression was associated with worse clinical outcome and may be an important prognostic biomarker in sunitinib-treated patients with metastatic renal cell carcinoma.	Sunitinib	118-127	AXL receptor tyrosine kinase	Homo sapiens	12-15
29416656-4	2018	Western blot showed that propranolol and sunitinib combination significantly down-regulated phospho-Rb, phospho-ERK, Cyclin D1, and Cyclin E, but had no effect on Bax, Bcl-2, or cleaved PARP expression.	Sunitinib	41-50	cyclin D1	Mus musculus	117-126
28978636-0	2017	EZH2 Modifies Sunitinib Resistance in Renal Cell Carcinoma by Kinome Reprogramming.	Sunitinib	14-23	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	0-4
28978636-6	2017	Modulating EZH2 expression or activity suppressed phosphorylation of certain RTKs, restoring the antitumor effects of sunitinib in models of acquired or intrinsically resistant ccRCC.	Sunitinib	118-127	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	11-15
28978636-7	2017	Overall, our results highlight EZH2 as a rational target for therapeutic intervention in sunitinib-resistant ccRCC as well as a predictive marker for RTKi response in this disease.	Sunitinib	89-98	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	31-35
30381648-11	2018	As a result, the ICER associated with replacing IFN-alpha with sunitinib was 22,695,839 yen/QALYs.	Sunitinib	63-72	interferon alpha 1	Homo sapiens	48-57
28745317-8	2017	Moreover, we demonstrated that RCN2 knockout sensitized HCC cells to tyrosine kinase inhibitors, including erlotinib, lapatinib and sunitinib.	Sunitinib	132-141	reticulocalbin 2	Homo sapiens	31-35
29416656-4	2018	Western blot showed that propranolol and sunitinib combination significantly down-regulated phospho-Rb, phospho-ERK, Cyclin D1, and Cyclin E, but had no effect on Bax, Bcl-2, or cleaved PARP expression.	Sunitinib	41-50	B cell leukemia/lymphoma 2	Mus musculus	168-173
29416656-4	2018	Western blot showed that propranolol and sunitinib combination significantly down-regulated phospho-Rb, phospho-ERK, Cyclin D1, and Cyclin E, but had no effect on Bax, Bcl-2, or cleaved PARP expression.	Sunitinib	41-50	mitogen-activated protein kinase 1	Mus musculus	112-115
29416656-4	2018	Western blot showed that propranolol and sunitinib combination significantly down-regulated phospho-Rb, phospho-ERK, Cyclin D1, and Cyclin E, but had no effect on Bax, Bcl-2, or cleaved PARP expression.	Sunitinib	41-50	poly (ADP-ribose) polymerase family, member 1	Mus musculus	186-190
29416656-7	2018	This synergistic effect between propranolol and sunitinib to inhibit MM proliferation was through suppressing ERK/Cyclin D1/Rb/Cyclin E pathways and inducing G0/G1/S phase arrest, rather than by inducing tumor cell apoptosis.	Sunitinib	48-57	mitogen-activated protein kinase 1	Mus musculus	110-113
29416656-7	2018	This synergistic effect between propranolol and sunitinib to inhibit MM proliferation was through suppressing ERK/Cyclin D1/Rb/Cyclin E pathways and inducing G0/G1/S phase arrest, rather than by inducing tumor cell apoptosis.	Sunitinib	48-57	cyclin D1	Mus musculus	114-123
28898759-8	2017	In addition, CONPs downregulate the expression of AXL, MET, AKT, and ERK to recover sunitinib responsiveness in RCC cells with sunitinib resistance (SR) and may therefore facilitate the development of promising new pathways to treat patients with acquired SRRCC.	Sunitinib	84-93	AXL receptor tyrosine kinase	Homo sapiens	50-53
29290991-7	2017	In addition, we identified adrenomedullin (ADM), previously shown to be implicated in sunitinib resistance, as the earliest response gene upon ALK inhibition.	Sunitinib	86-95	ALK receptor tyrosine kinase	Homo sapiens	143-146
28811127-2	2017	Using rat Langendorff heart model and human acute myeloid leukaemia 60 (HL60) cell line we detected the involvement of protein kinase C (PKC) alpha during Sunitinib-induced cardiotoxicity and the effect of Sunitinib on cancer progression.	Sunitinib	155-164	protein kinase C alpha	Homo sapiens	119-147
28811127-12	2017	This study reveals that A3 adenosine receptor activation by IB-MECA attenuates Sunitinib-induced cardiotoxicity through the involvement of PKCalpha.	Sunitinib	79-88	protein kinase C alpha	Homo sapiens	139-147
28898759-8	2017	In addition, CONPs downregulate the expression of AXL, MET, AKT, and ERK to recover sunitinib responsiveness in RCC cells with sunitinib resistance (SR) and may therefore facilitate the development of promising new pathways to treat patients with acquired SRRCC.	Sunitinib	84-93	AKT serine/threonine kinase 1	Homo sapiens	60-63
28729403-10	2017	Sunitinib also induced lysosomal membrane permeabilization, which further increased in the presence of chloroquine or knockdown of lysosome-associated membrane protein (LAMP2).	Sunitinib	0-9	lysosomal associated membrane protein 2	Homo sapiens	169-174
28898759-8	2017	In addition, CONPs downregulate the expression of AXL, MET, AKT, and ERK to recover sunitinib responsiveness in RCC cells with sunitinib resistance (SR) and may therefore facilitate the development of promising new pathways to treat patients with acquired SRRCC.	Sunitinib	84-93	mitogen-activated protein kinase 1	Homo sapiens	69-72
28898759-8	2017	In addition, CONPs downregulate the expression of AXL, MET, AKT, and ERK to recover sunitinib responsiveness in RCC cells with sunitinib resistance (SR) and may therefore facilitate the development of promising new pathways to treat patients with acquired SRRCC.	Sunitinib	127-136	AXL receptor tyrosine kinase	Homo sapiens	50-53
28898759-8	2017	In addition, CONPs downregulate the expression of AXL, MET, AKT, and ERK to recover sunitinib responsiveness in RCC cells with sunitinib resistance (SR) and may therefore facilitate the development of promising new pathways to treat patients with acquired SRRCC.	Sunitinib	127-136	mitogen-activated protein kinase 1	Homo sapiens	69-72
29262588-2	2017	Agents targeting angiogenesis and mTOR, such as sunitinib and everolimus (RAD001), have been shown to result in progression-free survival of approximately 11 months in patients with advanced pNETs.	Sunitinib	48-57	mechanistic target of rapamycin kinase	Homo sapiens	34-38
29187872-0	2017	Tumoral ANXA1 Is a Predictive Marker for Sunitinib Treatment of Renal Cancer Patients.	Sunitinib	41-50	annexin A1	Homo sapiens	8-13
29187872-4	2017	Our aim with the current study was to assess annexin A1 (ANXA1), which stimulates angiogenesis, as a predictive marker for sunitinib therapy in mRCC patients.	Sunitinib	123-132	annexin A1	Homo sapiens	45-55
29187872-4	2017	Our aim with the current study was to assess annexin A1 (ANXA1), which stimulates angiogenesis, as a predictive marker for sunitinib therapy in mRCC patients.	Sunitinib	123-132	annexin A1	Homo sapiens	57-62
29187872-13	2017	Conclusions: Our results indicate that cytoplasmic expression of ANXA1 is a negative predictive marker for sunitinib therapy in mRCC patients.	Sunitinib	107-116	annexin A1	Homo sapiens	65-70
29212269-0	2017	Low neighbor of Brca1 gene expression predicts poor clinical outcome and resistance of sunitinib in clear cell renal cell carcinoma.	Sunitinib	87-96	BRCA1 DNA repair associated	Homo sapiens	16-21
29212269-8	2017	Low level of NBR1 mRNA showed a significance poor prognostic of overall survival (OS), disease-free survival (DFS) with univariate and multivariate analyses in ccRCC patients and sunitinib resistance.	Sunitinib	179-188	NBR1 autophagy cargo receptor	Homo sapiens	13-17
29212269-9	2017	Conclusions: Taken together, our results suggest that low level of NBR1 can predict poor clinical outcome and resistance of sunitinib in patients with ccRCC.	Sunitinib	124-133	NBR1 autophagy cargo receptor	Homo sapiens	67-71
28805145-7	2017	An increase in extracellular TGase activity on the HPT cell membrane was observed in a dose-dependent manner after treatment with Sunitinib malate.	Sunitinib	130-146	transglutaminase 1	Homo sapiens	29-34
28850564-0	2017	CXCL7 is a predictive marker of sunitinib efficacy in clear cell renal cell carcinomas.	Sunitinib	32-41	pro-platelet basic protein	Homo sapiens	0-5
28330808-1	2017	BACKGROUND: Sunitinib, the vascular endothelial growth factor pathway inhibitor, is an established standard-of-care for advanced renal cell carcinoma (RCC).	Sunitinib	12-21	vascular endothelial growth factor A	Homo sapiens	27-61
28850564-9	2017	CONCLUSIONS: CXCL7 may be considered as a predictive marker of sunitinib efficacy for ccRCC patients.	Sunitinib	63-72	pro-platelet basic protein	Homo sapiens	13-18
29296523-8	2017	Mechanistically, sunitinib treatment primes the antitumor immune response by significantly decreasing Treg frequency, reducing TGF-beta and IL-10 production by Tregs, and also protecting TAS CD8+ T cells from tumor-induced deletion in the setting of HCC.	Sunitinib	17-26	transforming growth factor, beta 1	Mus musculus	127-135
28756150-7	2017	The cytotoxicity of 4-CF was reversed by co-treatment with the VEGF and Akt inhibitors sunitinib and perifosine, respectively or by the addition of neutralizing VEGF antibodies.	Sunitinib	87-96	vascular endothelial growth factor A	Mus musculus	63-67
28756150-7	2017	The cytotoxicity of 4-CF was reversed by co-treatment with the VEGF and Akt inhibitors sunitinib and perifosine, respectively or by the addition of neutralizing VEGF antibodies.	Sunitinib	87-96	thymoma viral proto-oncogene 1	Mus musculus	72-75
28993730-8	2017	However, targeting the altered biological pathways (mTOR, PDGFRB, FGF2, HDAC) guided identification of possibly beneficial treatment with a combination of sirolimus, thalidomide, sunitinib, and vorinostat.	Sunitinib	179-188	mechanistic target of rapamycin kinase	Homo sapiens	52-56
28993730-8	2017	However, targeting the altered biological pathways (mTOR, PDGFRB, FGF2, HDAC) guided identification of possibly beneficial treatment with a combination of sirolimus, thalidomide, sunitinib, and vorinostat.	Sunitinib	179-188	histone deacetylase 9	Homo sapiens	72-76
29296523-8	2017	Mechanistically, sunitinib treatment primes the antitumor immune response by significantly decreasing Treg frequency, reducing TGF-beta and IL-10 production by Tregs, and also protecting TAS CD8+ T cells from tumor-induced deletion in the setting of HCC.	Sunitinib	17-26	interleukin 10	Mus musculus	140-145
29033582-0	2017	HIF pathway and c-Myc as biomarkers for response to sunitinib in metastatic clear-cell renal cell carcinoma.	Sunitinib	52-61	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	16-21
28870911-5	2017	Apoptotic death induced by sunitinib in MCF7 cells was mediated by activation of caspase-3 and p53 mRNA and protein expression and an increase in the percentage of apoptotic cells (40%) as determined by flow cytometry.	Sunitinib	27-36	caspase 3	Homo sapiens	81-90
28684115-0	2017	Enhanced expression of caveolin-1 possesses diagnostic and prognostic value and promotes cell migration, invasion and sunitinib resistance in the clear cell renal cell carcinoma.	Sunitinib	118-127	caveolin 1	Homo sapiens	23-33
28684115-6	2017	Moreover, CAV1 expression was up-regulated in sunitinib-resistant renal cancer cell lines, and its overexpression promoted sunitinib resistance.	Sunitinib	46-55	caveolin 1	Homo sapiens	10-14
28684115-6	2017	Moreover, CAV1 expression was up-regulated in sunitinib-resistant renal cancer cell lines, and its overexpression promoted sunitinib resistance.	Sunitinib	123-132	caveolin 1	Homo sapiens	10-14
28684115-7	2017	In general, our results confirm that CAV1 plays an important role in the metastasis of kidney cancer and induces sunitinib resistance, so CAV1 function suppression may become a promising clinical treatment strategy during renal cell carcinoma metastasis and sunitinib resistance.	Sunitinib	113-122	caveolin 1	Homo sapiens	37-41
28684115-7	2017	In general, our results confirm that CAV1 plays an important role in the metastasis of kidney cancer and induces sunitinib resistance, so CAV1 function suppression may become a promising clinical treatment strategy during renal cell carcinoma metastasis and sunitinib resistance.	Sunitinib	258-267	caveolin 1	Homo sapiens	37-41
28684115-7	2017	In general, our results confirm that CAV1 plays an important role in the metastasis of kidney cancer and induces sunitinib resistance, so CAV1 function suppression may become a promising clinical treatment strategy during renal cell carcinoma metastasis and sunitinib resistance.	Sunitinib	258-267	caveolin 1	Homo sapiens	138-142
29262547-10	2017	In addition, crotonoside alone or the combination of sunitinib/RFP966/HPOB exhibited a significant post-inhibition effect in AML cells by the inhibition of FLT3 and HDAC3/6.	Sunitinib	53-62	fms related receptor tyrosine kinase 3	Homo sapiens	156-160
29262547-10	2017	In addition, crotonoside alone or the combination of sunitinib/RFP966/HPOB exhibited a significant post-inhibition effect in AML cells by the inhibition of FLT3 and HDAC3/6.	Sunitinib	53-62	histone deacetylase 3	Homo sapiens	165-170
28870911-5	2017	Apoptotic death induced by sunitinib in MCF7 cells was mediated by activation of caspase-3 and p53 mRNA and protein expression and an increase in the percentage of apoptotic cells (40%) as determined by flow cytometry.	Sunitinib	27-36	tumor protein p53	Homo sapiens	95-98
28870911-7	2017	Mechanistically, blocking of de novo RNA synthesis by actinomycin D significantly inhibited sunitinib-induced expression of p53 mRNA, but not that of caspase-3, indicating involvement of a transcriptional mechanism.	Sunitinib	92-101	tumor protein p53	Homo sapiens	124-127
28870911-9	2017	In addition, sunitinib exhibited concentration-dependent induction of oxidative stress genes (heme oxygenase 1 and glutathione transferase A1) through the nuclear factor erythroid 2-related factor 2 pathway.	Sunitinib	13-22	heme oxygenase 1	Homo sapiens	94-110
28870911-9	2017	In addition, sunitinib exhibited concentration-dependent induction of oxidative stress genes (heme oxygenase 1 and glutathione transferase A1) through the nuclear factor erythroid 2-related factor 2 pathway.	Sunitinib	13-22	NFE2 like bZIP transcription factor 2	Homo sapiens	155-198
28796254-0	2017	Sunitinib induces genomic instability of renal carcinoma cells through affecting the interaction of LC3-II and PARP-1.	Sunitinib	0-9	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	100-103
28778562-5	2017	Compound 2 exhibited angiogenesis effect against sunitinib-induced damage on intersegmental blood vessels in Tg (flk1: EGFP) and Tg (fli1: nEGFP) transgenic zebrafish at concentrations of 3.13, 6.25, 12.50, and 25.00muM.	Sunitinib	49-58	kinase insert domain receptor (a type III receptor tyrosine kinase)	Danio rerio	113-117
28778562-5	2017	Compound 2 exhibited angiogenesis effect against sunitinib-induced damage on intersegmental blood vessels in Tg (flk1: EGFP) and Tg (fli1: nEGFP) transgenic zebrafish at concentrations of 3.13, 6.25, 12.50, and 25.00muM.	Sunitinib	49-58	Fli-1 proto-oncogene, ETS transcription factor	Danio rerio	133-137
28859644-0	2017	Predictive value of C-reactive protein in patients treated with sunitinib for metastatic clear cell renal cell carcinoma.	Sunitinib	64-73	C-reactive protein	Homo sapiens	20-38
28859644-13	2017	CONCLUSION: Baseline CRP was a significant predictive factor of sunitinib response and a prognostic factor of survival.	Sunitinib	64-73	C-reactive protein	Homo sapiens	21-24
28624441-0	2017	Hsp90 inhibitor geldanamycin attenuates the cytotoxicity of sunitinib in cardiomyocytes via inhibition of the autophagy pathway.	Sunitinib	60-69	heat shock protein 90 alpha family class A member 1	Homo sapiens	0-5
28624441-3	2017	Here, we examined the effect of geldanamycin, an inhibitor of heat shock protein (Hsp) 90, on sunitinib-induced cytotoxicity in cardiomyocytes.	Sunitinib	94-103	heat shock protein 90 alpha family class A member 1	Homo sapiens	62-89
28624441-4	2017	First, we found that treatment with geldanamycin or other Hsp90 inhibitors (tanespimycin, ganetespib, or BIIB021) significantly attenuated sunitinib-induced cytotoxicity in rat H9c2 cardiomyocytes, suggesting a drug-class effect of Hsp90 inhibitors.	Sunitinib	139-148	heat shock protein 90 alpha family class A member 1	Rattus norvegicus	58-63
28624441-4	2017	First, we found that treatment with geldanamycin or other Hsp90 inhibitors (tanespimycin, ganetespib, or BIIB021) significantly attenuated sunitinib-induced cytotoxicity in rat H9c2 cardiomyocytes, suggesting a drug-class effect of Hsp90 inhibitors.	Sunitinib	139-148	heat shock protein 90 alpha family class A member 1	Rattus norvegicus	232-237
28624441-5	2017	We then examined the mechanisms underlying sunitinib-induced cytotoxicity and found that sunitinib induced autophagy in H9c2 cells and that pretreatment with geldanamycin inhibited the induction of autophagy by promoting degradation of the autophagy-related proteins Atg7, Beclin-1, and ULK1.	Sunitinib	43-52	autophagy related 7	Rattus norvegicus	267-271
28624441-5	2017	We then examined the mechanisms underlying sunitinib-induced cytotoxicity and found that sunitinib induced autophagy in H9c2 cells and that pretreatment with geldanamycin inhibited the induction of autophagy by promoting degradation of the autophagy-related proteins Atg7, Beclin-1, and ULK1.	Sunitinib	43-52	beclin 1	Rattus norvegicus	273-281
28624441-5	2017	We then examined the mechanisms underlying sunitinib-induced cytotoxicity and found that sunitinib induced autophagy in H9c2 cells and that pretreatment with geldanamycin inhibited the induction of autophagy by promoting degradation of the autophagy-related proteins Atg7, Beclin-1, and ULK1.	Sunitinib	43-52	unc-51 like autophagy activating kinase 1	Rattus norvegicus	287-291
28624441-10	2017	Thus, the further investigation of combination or sequential treatment with an Hsp90 inhibitor and sunitinib is warranted as a potential strategy of attenuating the cardiotoxicity associated with sunitinib administration in the clinical setting.	Sunitinib	196-205	heat shock protein 90 alpha family class A member 1	Homo sapiens	79-84
28796254-0	2017	Sunitinib induces genomic instability of renal carcinoma cells through affecting the interaction of LC3-II and PARP-1.	Sunitinib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	111-117
28978162-0	2017	Effects of VEGF and VEGFR polymorphisms on the outcome of patients with metastatic renal cell carcinoma treated with sunitinib: a systematic review and meta-analysis.	Sunitinib	117-126	kinase insert domain receptor	Homo sapiens	20-25
28978162-4	2017	VEGFR1 rs9582036 AA/AC carriers and rs9554320 CC/AC carriers had more favorable overall survival (OS) in patients with mRCC treated with sunitinib (n = 3), but not in progression-free survival (PFS).	Sunitinib	137-146	fms related receptor tyrosine kinase 1	Homo sapiens	0-6
28978162-7	2017	VEGFR2 rs1870377 was verified to be associated with sunitinib OS (n = 1).	Sunitinib	52-61	kinase insert domain receptor	Homo sapiens	0-6
28978162-8	2017	Furthermore, patients with VEGFR3 rs307826 and rs307821 had shorter PFS and OS during sunitinib therapy (n = 2, respectively).	Sunitinib	86-95	fms related receptor tyrosine kinase 4	Homo sapiens	27-33
28978162-9	2017	Our results suggested that VEGF and VEGFR polymorphisms were associated with outcomes in sunitinib treated mRCC patients, especially VEGFR1 polymorphisms.	Sunitinib	89-98	vascular endothelial growth factor A	Homo sapiens	27-31
28978162-9	2017	Our results suggested that VEGF and VEGFR polymorphisms were associated with outcomes in sunitinib treated mRCC patients, especially VEGFR1 polymorphisms.	Sunitinib	89-98	kinase insert domain receptor	Homo sapiens	36-41
28978162-9	2017	Our results suggested that VEGF and VEGFR polymorphisms were associated with outcomes in sunitinib treated mRCC patients, especially VEGFR1 polymorphisms.	Sunitinib	89-98	fms related receptor tyrosine kinase 1	Homo sapiens	133-139
28544544-4	2017	Screening of a library of compounds containing approximately 90 molecular-targeting drugs revealed that this process was suppressed by the insulin-like growth factor-1 (IGF-1) receptor (IGF-1R)-specific kinase inhibitor OSI-906, as well as the multikinase inhibitors axitinib and sunitinib.	Sunitinib	280-289	insulin like growth factor 1 receptor	Homo sapiens	186-192
28449948-3	2017	This study aims to analyse whether sunitinib has specific and direct effects on insulin secreting beta-cells.	Sunitinib	35-44	insulin	Homo sapiens	80-87
28449948-8	2017	Sunitinib further augmented insulin secretion in the presence of elevated cAMP levels and the FFAR1 agonists.	Sunitinib	0-9	free fatty acid receptor 1	Homo sapiens	94-99
28819401-10	2017	Analyses of two open source, RNA expression data sets on sunitinib response revealed that SLC10A2 was downregulated in tyrosine kinase inhibitor-resistant samples.	Sunitinib	57-66	solute carrier family 10 member 2	Homo sapiens	90-97
28237182-0	2017	Correlation of c-Met Expression and Outcome in Patients With Renal Cell Carcinoma Treated With Sunitinib.	Sunitinib	95-104	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	15-20
28237182-3	2017	The main objective was to evaluate c-Met expression in sunitinib-treated patients with mRCC, including patients with bone metastases.	Sunitinib	55-64	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	35-40
28237182-8	2017	CONCLUSIONS: High c-Met expression was associated with poor survival in patients with mRCC treated with sunitinib.	Sunitinib	104-113	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-23
28672196-2	2017	Therapeutic alternatives such as other tyrosine kinase inhibitors, VEGF inhibitors, or mTOR inhibitors emphasize the clinical need to predict the patient"s response to sunitinib therapy before treatment initiation.	Sunitinib	168-177	vascular endothelial growth factor A	Homo sapiens	67-71
28672196-2	2017	Therapeutic alternatives such as other tyrosine kinase inhibitors, VEGF inhibitors, or mTOR inhibitors emphasize the clinical need to predict the patient"s response to sunitinib therapy before treatment initiation.	Sunitinib	168-177	mechanistic target of rapamycin kinase	Homo sapiens	87-91
28903416-7	2017	786-O RCC cells secrete high IL-6 levels after low dose stimulation with the TKIs sorafenib, sunitinib and pazopanib, inducing activation of AKT-mTOR pathway, NFkappaB, HIF-2alpha and VEGF expression.	Sunitinib	93-102	interleukin 6	Homo sapiens	29-33
28903416-7	2017	786-O RCC cells secrete high IL-6 levels after low dose stimulation with the TKIs sorafenib, sunitinib and pazopanib, inducing activation of AKT-mTOR pathway, NFkappaB, HIF-2alpha and VEGF expression.	Sunitinib	93-102	AKT serine/threonine kinase 1	Homo sapiens	141-144
28903416-7	2017	786-O RCC cells secrete high IL-6 levels after low dose stimulation with the TKIs sorafenib, sunitinib and pazopanib, inducing activation of AKT-mTOR pathway, NFkappaB, HIF-2alpha and VEGF expression.	Sunitinib	93-102	mechanistic target of rapamycin kinase	Homo sapiens	145-149
28903416-7	2017	786-O RCC cells secrete high IL-6 levels after low dose stimulation with the TKIs sorafenib, sunitinib and pazopanib, inducing activation of AKT-mTOR pathway, NFkappaB, HIF-2alpha and VEGF expression.	Sunitinib	93-102	endothelial PAS domain protein 1	Homo sapiens	169-179
28903416-7	2017	786-O RCC cells secrete high IL-6 levels after low dose stimulation with the TKIs sorafenib, sunitinib and pazopanib, inducing activation of AKT-mTOR pathway, NFkappaB, HIF-2alpha and VEGF expression.	Sunitinib	93-102	vascular endothelial growth factor A	Homo sapiens	184-188
28196874-10	2017	These elevations similarly tended to occur early and resolved over time.Conclusions: On average, patients with mRCC receiving sunitinib exhibit modest declines in LVEF and nonsignificant changes in hsTnI and BNP.	Sunitinib	126-135	natriuretic peptide B	Homo sapiens	208-211
29086859-2	2017	Compared to sunitinib, the C(5)-Br derivative of 2-pyrrolidone-fused (2-oxoindolin-3-ylidene)methylpyrrole has significantly greater in vitro activities against VEGFR-2, PDGFRbeta, and tube formation.	Sunitinib	12-21	kinase insert domain receptor	Homo sapiens	161-168
29086859-8	2017	Graphical abstract IC50 comparison of sunitinib, 14, and 15 against VEGFR-2 and PDGFRbeta.	Sunitinib	38-47	platelet derived growth factor receptor beta	Homo sapiens	80-89
28796048-10	2017	Four patients (33.3%) developed disease progression during imatinib treatment after initial resection, but all of these patients regained disease control when the treatment was altered to sunitinib targeted therapy.SDH-deficient GISTs arise exclusively in the stomach and account for approximately 7.4% (12/162) of gastric GISTs.	Sunitinib	188-197	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	215-218
28550387-0	2017	Correlation of c-MET Expression with PD-L1 Expression in Metastatic Clear Cell Renal Cell Carcinoma Treated by Sunitinib First-Line Therapy.	Sunitinib	111-120	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	15-20
28550387-0	2017	Correlation of c-MET Expression with PD-L1 Expression in Metastatic Clear Cell Renal Cell Carcinoma Treated by Sunitinib First-Line Therapy.	Sunitinib	111-120	CD274 molecule	Homo sapiens	37-42
28572533-7	2017	We found that the anti-angiogenic TKI sunitinib disrupted the balance between HIF-1alpha and HIF-2alpha in RCCs and led to a protective effect on HUVECs against sunitinib treatment when cultured with conditioned medium.	Sunitinib	38-47	hypoxia inducible factor 1 subunit alpha	Homo sapiens	78-88
28572533-7	2017	We found that the anti-angiogenic TKI sunitinib disrupted the balance between HIF-1alpha and HIF-2alpha in RCCs and led to a protective effect on HUVECs against sunitinib treatment when cultured with conditioned medium.	Sunitinib	38-47	endothelial PAS domain protein 1	Homo sapiens	93-103
28572533-8	2017	Mechanistically, RCCs treated with sunitinib resulted in down-regulation of HIF-1alpha, but not HIF-2alpha, through reduction of both mRNA and protein levels.	Sunitinib	35-44	hypoxia inducible factor 1 subunit alpha	Homo sapiens	76-86
28572533-8	2017	Mechanistically, RCCs treated with sunitinib resulted in down-regulation of HIF-1alpha, but not HIF-2alpha, through reduction of both mRNA and protein levels.	Sunitinib	35-44	endothelial PAS domain protein 1	Homo sapiens	96-106
28572533-9	2017	The down-regulation of HIF-1alpha by sunitinib occurred via hypoxia associated factor (HAF), which also enhanced HIF-2alpha transactivation activity to increase the production of pro-angiogenic factors and cytokines and promote HUVEC proliferation.	Sunitinib	37-46	hypoxia inducible factor 1 subunit alpha	Homo sapiens	23-33
28572533-9	2017	The down-regulation of HIF-1alpha by sunitinib occurred via hypoxia associated factor (HAF), which also enhanced HIF-2alpha transactivation activity to increase the production of pro-angiogenic factors and cytokines and promote HUVEC proliferation.	Sunitinib	37-46	coagulation factor XII	Homo sapiens	60-85
28572533-9	2017	The down-regulation of HIF-1alpha by sunitinib occurred via hypoxia associated factor (HAF), which also enhanced HIF-2alpha transactivation activity to increase the production of pro-angiogenic factors and cytokines and promote HUVEC proliferation.	Sunitinib	37-46	coagulation factor XII	Homo sapiens	87-90
28572533-9	2017	The down-regulation of HIF-1alpha by sunitinib occurred via hypoxia associated factor (HAF), which also enhanced HIF-2alpha transactivation activity to increase the production of pro-angiogenic factors and cytokines and promote HUVEC proliferation.	Sunitinib	37-46	endothelial PAS domain protein 1	Homo sapiens	113-123
28978115-1	2017	OBJECTIVE: This study aims to investigate biological behavior changes in a murine lung cancer cell characterized by acquired resistance to sunitinib, a potent inhibitor of multiple-targeted receptor tyrosine kinase.	Sunitinib	139-148	TYRO3 protein tyrosine kinase 3	Mus musculus	190-214
28781191-11	2017	The increased anti-factor Xa levels during combination treatment suggest that sunitinib might increase the anticoagulation activity of dalteparin.	Sunitinib	78-87	coagulation factor X	Homo sapiens	19-28
28640223-3	2017	The TKI erlotinib targets the epidermal growth factor receptor (EGFR), whereas sunitinib targets primarily vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR).TKIs that impact the function of non-malignant cells and have on- and off-target toxicities, including cardiotoxicities.	Sunitinib	79-88	platelet derived growth factor receptor, beta polypeptide	Mus musculus	163-202
29662544-6	2017	Sunitinib has also been tested in the adjuvant setting, within the ASSURE and S-TRAC trials, with opposite results; indeed, equivocal risk-stratification criteria, as well as immature overall survival (OS) data prevent any definitive conclusion on this important issue.	Sunitinib	0-9	T cell receptor alpha constant	Homo sapiens	80-84
28287633-10	2017	On the other hand, the VASH1 density was significantly higher in the metastatic ccRCCs treated with sunitinib compared with non-treated ones (P=0.010), indicating that VASH1 may be associated with the resistance of ECs to sunitinib treatment.	Sunitinib	100-109	vasohibin 1	Homo sapiens	23-28
28287633-10	2017	On the other hand, the VASH1 density was significantly higher in the metastatic ccRCCs treated with sunitinib compared with non-treated ones (P=0.010), indicating that VASH1 may be associated with the resistance of ECs to sunitinib treatment.	Sunitinib	100-109	vasohibin 1	Homo sapiens	168-173
28287633-10	2017	On the other hand, the VASH1 density was significantly higher in the metastatic ccRCCs treated with sunitinib compared with non-treated ones (P=0.010), indicating that VASH1 may be associated with the resistance of ECs to sunitinib treatment.	Sunitinib	222-231	vasohibin 1	Homo sapiens	168-173
28693255-1	2017	Sunitinib (SU) is a small molecule that inhibits the receptor tyrosine kinase (RTK) signaling pathway, and has been clinically used to treat advanced renal cell carcinoma (RCC).	Sunitinib	0-9	ret proto-oncogene	Homo sapiens	53-77
28693255-1	2017	Sunitinib (SU) is a small molecule that inhibits the receptor tyrosine kinase (RTK) signaling pathway, and has been clinically used to treat advanced renal cell carcinoma (RCC).	Sunitinib	0-9	ret proto-oncogene	Homo sapiens	79-82
28693255-1	2017	Sunitinib (SU) is a small molecule that inhibits the receptor tyrosine kinase (RTK) signaling pathway, and has been clinically used to treat advanced renal cell carcinoma (RCC).	Sunitinib	11-13	ret proto-oncogene	Homo sapiens	53-77
28693255-1	2017	Sunitinib (SU) is a small molecule that inhibits the receptor tyrosine kinase (RTK) signaling pathway, and has been clinically used to treat advanced renal cell carcinoma (RCC).	Sunitinib	11-13	ret proto-oncogene	Homo sapiens	79-82
28640223-3	2017	The TKI erlotinib targets the epidermal growth factor receptor (EGFR), whereas sunitinib targets primarily vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR).TKIs that impact the function of non-malignant cells and have on- and off-target toxicities, including cardiotoxicities.	Sunitinib	79-88	platelet derived growth factor receptor, beta polypeptide	Mus musculus	204-209
28376387-0	2017	Comprehensive insight into the binding of sunitinib, a multi-targeted anticancer drug to human serum albumin.	Sunitinib	42-51	albumin	Homo sapiens	95-108
28376387-1	2017	Binding studies between a multi-targeted anticancer drug, sunitinib (SU) and human serum albumin (HSA) were made using fluorescence, UV-vis absorption, circular dichroism (CD) and molecular docking analysis.	Sunitinib	58-67	albumin	Homo sapiens	83-96
28376387-1	2017	Binding studies between a multi-targeted anticancer drug, sunitinib (SU) and human serum albumin (HSA) were made using fluorescence, UV-vis absorption, circular dichroism (CD) and molecular docking analysis.	Sunitinib	69-71	albumin	Homo sapiens	83-96
28327411-0	2017	Gas6-Axl signaling in presence of Sunitinib is enhanced, diversified and sustained in renal tumor cells, resulting in tumor-progressive advantages.	Sunitinib	34-43	AXL receptor tyrosine kinase	Homo sapiens	5-8
28422745-2	2017	We rationally designed and evaluated preclinically a novel sunitinib analogue, SAP, with favourable pharmacological properties and the ability to be readily conjugated to a targeting peptide or antibody for active tumour targeting.SAP was evaluated in silico and in vitro in order to verify target engagement (e.g., VEGFR2).	Sunitinib	59-68	SH2 domain containing 1A	Mus musculus	79-82
28422745-2	2017	We rationally designed and evaluated preclinically a novel sunitinib analogue, SAP, with favourable pharmacological properties and the ability to be readily conjugated to a targeting peptide or antibody for active tumour targeting.SAP was evaluated in silico and in vitro in order to verify target engagement (e.g., VEGFR2).	Sunitinib	59-68	SH2 domain containing 1A	Mus musculus	231-234
28422745-2	2017	We rationally designed and evaluated preclinically a novel sunitinib analogue, SAP, with favourable pharmacological properties and the ability to be readily conjugated to a targeting peptide or antibody for active tumour targeting.SAP was evaluated in silico and in vitro in order to verify target engagement (e.g., VEGFR2).	Sunitinib	59-68	kinase insert domain protein receptor	Mus musculus	316-322
28327411-0	2017	Gas6-Axl signaling in presence of Sunitinib is enhanced, diversified and sustained in renal tumor cells, resulting in tumor-progressive advantages.	Sunitinib	34-43	growth arrest specific 6	Homo sapiens	0-4
28327411-2	2017	Investigation of Gas6-mediated Axl signaling in CCRCC and endothelial cells reveals a Sunitinib resistant Gas6-Axl signaling that is sustained and enhanced and specifically triggers downstream AKT and PRAS40 activation in an intensified manner.	Sunitinib	86-95	growth arrest specific 6	Homo sapiens	17-21
28327411-2	2017	Investigation of Gas6-mediated Axl signaling in CCRCC and endothelial cells reveals a Sunitinib resistant Gas6-Axl signaling that is sustained and enhanced and specifically triggers downstream AKT and PRAS40 activation in an intensified manner.	Sunitinib	86-95	AXL receptor tyrosine kinase	Homo sapiens	31-34
28327411-2	2017	Investigation of Gas6-mediated Axl signaling in CCRCC and endothelial cells reveals a Sunitinib resistant Gas6-Axl signaling that is sustained and enhanced and specifically triggers downstream AKT and PRAS40 activation in an intensified manner.	Sunitinib	86-95	growth arrest specific 6	Homo sapiens	106-110
28327411-2	2017	Investigation of Gas6-mediated Axl signaling in CCRCC and endothelial cells reveals a Sunitinib resistant Gas6-Axl signaling that is sustained and enhanced and specifically triggers downstream AKT and PRAS40 activation in an intensified manner.	Sunitinib	86-95	AXL receptor tyrosine kinase	Homo sapiens	111-114
28327411-2	2017	Investigation of Gas6-mediated Axl signaling in CCRCC and endothelial cells reveals a Sunitinib resistant Gas6-Axl signaling that is sustained and enhanced and specifically triggers downstream AKT and PRAS40 activation in an intensified manner.	Sunitinib	86-95	AKT serine/threonine kinase 1	Homo sapiens	193-196
28327411-2	2017	Investigation of Gas6-mediated Axl signaling in CCRCC and endothelial cells reveals a Sunitinib resistant Gas6-Axl signaling that is sustained and enhanced and specifically triggers downstream AKT and PRAS40 activation in an intensified manner.	Sunitinib	86-95	AKT1 substrate 1	Homo sapiens	201-207
28327411-3	2017	Gas6-induced Axl signaling in presence of Sunitinib is also diversified displaying onset of Axl-dependent EGFR and METR activation and activation of classical MAPK pathways.	Sunitinib	42-51	growth arrest specific 6	Homo sapiens	0-4
28327411-3	2017	Gas6-induced Axl signaling in presence of Sunitinib is also diversified displaying onset of Axl-dependent EGFR and METR activation and activation of classical MAPK pathways.	Sunitinib	42-51	AXL receptor tyrosine kinase	Homo sapiens	13-16
28327411-3	2017	Gas6-induced Axl signaling in presence of Sunitinib is also diversified displaying onset of Axl-dependent EGFR and METR activation and activation of classical MAPK pathways.	Sunitinib	42-51	epidermal growth factor receptor	Homo sapiens	106-110
28327411-4	2017	Gas6+Sunitinib-adapted CCRCC cells present increased viability and decreased apoptosis and enhanced production of the multi-tumorigenic Osteopontin (OPN) and of one of its activator matrix metalloproteinase-7.	Sunitinib	5-14	growth arrest specific 6	Homo sapiens	0-4
28327411-4	2017	Gas6+Sunitinib-adapted CCRCC cells present increased viability and decreased apoptosis and enhanced production of the multi-tumorigenic Osteopontin (OPN) and of one of its activator matrix metalloproteinase-7.	Sunitinib	5-14	secreted phosphoprotein 1	Homo sapiens	136-147
28327411-4	2017	Gas6+Sunitinib-adapted CCRCC cells present increased viability and decreased apoptosis and enhanced production of the multi-tumorigenic Osteopontin (OPN) and of one of its activator matrix metalloproteinase-7.	Sunitinib	5-14	secreted phosphoprotein 1	Homo sapiens	149-152
28327411-4	2017	Gas6+Sunitinib-adapted CCRCC cells present increased viability and decreased apoptosis and enhanced production of the multi-tumorigenic Osteopontin (OPN) and of one of its activator matrix metalloproteinase-7.	Sunitinib	5-14	matrix metallopeptidase 7	Homo sapiens	182-208
28327411-6	2017	In addition, Gas6+Sunitinib-adapted CCRCC cells displayed enhanced migration and sphere formation, both mechanisms being Axl and OPN dependent.	Sunitinib	18-27	growth arrest specific 6	Homo sapiens	13-17
28327411-6	2017	In addition, Gas6+Sunitinib-adapted CCRCC cells displayed enhanced migration and sphere formation, both mechanisms being Axl and OPN dependent.	Sunitinib	18-27	AXL receptor tyrosine kinase	Homo sapiens	121-124
28327411-6	2017	In addition, Gas6+Sunitinib-adapted CCRCC cells displayed enhanced migration and sphere formation, both mechanisms being Axl and OPN dependent.	Sunitinib	18-27	secreted phosphoprotein 1	Homo sapiens	129-132
28327411-7	2017	Altogether, this suggests that Sunitinib while targeting endothelial cells and tumor angiogenesis, simultaneously provides protumorigenic effects due to a constitutively, intensified and divergent Gas6-Axl system.	Sunitinib	31-40	growth arrest specific 6	Homo sapiens	197-201
28327411-7	2017	Altogether, this suggests that Sunitinib while targeting endothelial cells and tumor angiogenesis, simultaneously provides protumorigenic effects due to a constitutively, intensified and divergent Gas6-Axl system.	Sunitinib	31-40	AXL receptor tyrosine kinase	Homo sapiens	202-205
28327411-8	2017	IMPLICATIONS: Gas6-mediated Axl signaling, which is enhanced and diversified in the presence of Sunitinib possibly contributes to acquired chemoresistance, recurrence of aggressive disease and metastasis of CCRCC tumors.	Sunitinib	96-105	growth arrest specific 6	Homo sapiens	14-18
28327411-8	2017	IMPLICATIONS: Gas6-mediated Axl signaling, which is enhanced and diversified in the presence of Sunitinib possibly contributes to acquired chemoresistance, recurrence of aggressive disease and metastasis of CCRCC tumors.	Sunitinib	96-105	AXL receptor tyrosine kinase	Homo sapiens	28-31
28327411-9	2017	Therefore, combinatorial Axl-targeted therapy might be beneficial for CCRCC patients intended for Sunitinib treatment.	Sunitinib	98-107	AXL receptor tyrosine kinase	Homo sapiens	25-28
28736633-3	2017	Through a number of clinical trials, the mTOR inhibitor everolimus and the receptor tyrosine kinase (RTK) inhibitor sunitinib were recently approved for NETs.	Sunitinib	116-125	ret proto-oncogene	Homo sapiens	75-99
28260162-0	2017	Tumoral cubilin is a predictive marker for treatment of renal cancer patients with sunitinib and sorafenib.	Sunitinib	83-92	cubilin	Homo sapiens	8-15
28260162-12	2017	CONCLUSIONS: We show for the first time that tumoral expression of cubilin is a positive predictive marker for treatment of metastatic renal cell cancer patients with sunitinib and sorafenib.	Sunitinib	167-176	cubilin	Homo sapiens	67-74
28736633-3	2017	Through a number of clinical trials, the mTOR inhibitor everolimus and the receptor tyrosine kinase (RTK) inhibitor sunitinib were recently approved for NETs.	Sunitinib	116-125	ret proto-oncogene	Homo sapiens	101-104
28599497-7	2017	In A549-xenografted nude mice treated with sunitinib or cetuximab, a decrease in the plasma AMF concentration was accompanied by a reduction in tumor weight, suggesting an association between the plasma AMF concentration and anticancer activity.	Sunitinib	43-52	glucose-6-phosphate isomerase	Homo sapiens	92-95
28452850-0	2017	Sunitinib Induces NK-kappaB-dependent NKG2D Ligand Expression in Nasopharyngeal Carcinoma and Hepatoma Cells.	Sunitinib	0-9	killer cell lectin like receptor C1	Homo sapiens	38-42
28452850-4	2017	In this study, we confirmed sunitinib induced downregulation of its targets, such as vascular endothelial growth factor, platelet-derived growth factor, and c-kit in multiple-drug-resistant nasopharyngeal carcinoma cell line CNE2/DDP and hepatoma cell line HepG2.	Sunitinib	28-37	vascular endothelial growth factor A	Homo sapiens	85-119
28452850-4	2017	In this study, we confirmed sunitinib induced downregulation of its targets, such as vascular endothelial growth factor, platelet-derived growth factor, and c-kit in multiple-drug-resistant nasopharyngeal carcinoma cell line CNE2/DDP and hepatoma cell line HepG2.	Sunitinib	28-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	157-162
28452850-8	2017	Silencing of NF-kappabeta1, NF-kappabeta2, or RelB (NF-kappabeta pathway) inhibited sunitinib-induced upregulation of NKG2DLs.	Sunitinib	84-93	RELB proto-oncogene, NF-kB subunit	Homo sapiens	46-50
28452850-8	2017	Silencing of NF-kappabeta1, NF-kappabeta2, or RelB (NF-kappabeta pathway) inhibited sunitinib-induced upregulation of NKG2DLs.	Sunitinib	84-93	nuclear factor kappa B subunit 1	Homo sapiens	13-25
28452850-9	2017	Taken together, we concluded that sunitinib upregulated NKG2DLs through NF-kappabeta signaling noncanonical pathway which might mediate higher cytotoxic sensitivity of CNE2/DDP and HepG2 cells to NK cells.	Sunitinib	34-43	nuclear factor kappa B subunit 1	Homo sapiens	72-84
28602541-0	2017	Connexin 43 enhances Bax activation via JNK activation in sunitinib-induced apoptosis in mesothelioma cells.	Sunitinib	58-67	gap junction protein alpha 1	Homo sapiens	0-11
28602541-0	2017	Connexin 43 enhances Bax activation via JNK activation in sunitinib-induced apoptosis in mesothelioma cells.	Sunitinib	58-67	BCL2 associated X, apoptosis regulator	Homo sapiens	21-24
28602541-0	2017	Connexin 43 enhances Bax activation via JNK activation in sunitinib-induced apoptosis in mesothelioma cells.	Sunitinib	58-67	mitogen-activated protein kinase 8	Homo sapiens	40-43
28602541-3	2017	In our previous work, Cx43 was found to interact directly with Bax and in the presence of sunitinib, lead to the Bax-mediated apoptosis in mesothelioma cells.	Sunitinib	90-99	gap junction protein alpha 1	Homo sapiens	22-26
28602541-3	2017	In our previous work, Cx43 was found to interact directly with Bax and in the presence of sunitinib, lead to the Bax-mediated apoptosis in mesothelioma cells.	Sunitinib	90-99	BCL2 associated X, apoptosis regulator	Homo sapiens	113-116
28602541-5	2017	Treatment with sunitinib increased the expression of the active conformation of the Bax protein, which was predominantly localized at the mitochondria, only in Cx43-transfected cells.	Sunitinib	15-24	BCL2 associated X, apoptosis regulator	Homo sapiens	84-87
28602541-5	2017	Treatment with sunitinib increased the expression of the active conformation of the Bax protein, which was predominantly localized at the mitochondria, only in Cx43-transfected cells.	Sunitinib	15-24	gap junction protein alpha 1	Homo sapiens	160-164
28602541-8	2017	Treatment with sunitinib increased the expression of phosphorylated (active) form of JNK only in the Cx43-transfected cells.	Sunitinib	15-24	mitogen-activated protein kinase 8	Homo sapiens	85-88
28602541-8	2017	Treatment with sunitinib increased the expression of phosphorylated (active) form of JNK only in the Cx43-transfected cells.	Sunitinib	15-24	gap junction protein alpha 1	Homo sapiens	101-105
28599497-7	2017	In A549-xenografted nude mice treated with sunitinib or cetuximab, a decrease in the plasma AMF concentration was accompanied by a reduction in tumor weight, suggesting an association between the plasma AMF concentration and anticancer activity.	Sunitinib	43-52	glucose-6-phosphate isomerase	Homo sapiens	203-206
28330784-8	2017	Small molecule VEGFR1/2/3 inhibitors including axitinib, cabozantinib, lenvatinib, sorafenib, sunitinib, and pazopanib are approved by the FDA for the treatment of renal cell carcinomas.	Sunitinib	94-103	fms related receptor tyrosine kinase 1	Homo sapiens	15-25
28561780-4	2017	Of these, 11 and 12 had the highest potency and, compared to sunitinib, showed: (1) significant increase in anti-proliferation of various cancer cells with a favorable selective index (SI); (2) higher inhibitory potency against both VEGFR-2 and PDGFRbeta.	Sunitinib	61-70	kinase insert domain receptor	Homo sapiens	233-240
28430711-0	2017	Evaluation of KDR rs34231037 as a predictor of sunitinib efficacy in patients with metastatic renal cell carcinoma.	Sunitinib	47-56	kinase insert domain receptor	Homo sapiens	14-17
28430711-5	2017	KDR-rs34231037 association with sunitinib response, clinical benefit, and progression-free survival was analyzed using logistic and Cox regression analyses.	Sunitinib	32-41	kinase insert domain receptor	Homo sapiens	0-3
28478525-3	2017	Three tyrosine kinase inhibitors (TKIs) with KIT inhibitory activity - imatinib, sunitinib, and regorafenib - are approved to treat advanced GIST and have successfully exploited this addiction to KIT oncogenic signaling, demonstrating remarkable activity in a disease that historically had no successful systemic therapy options.	Sunitinib	81-90	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	196-199
28561780-5	2017	The molecular modeling results showed that, in terms of VEGFR-2 binding, the synthesized products had a similar binding mode to sunitinib but with tighter interaction.	Sunitinib	128-137	kinase insert domain receptor	Homo sapiens	56-63
28529744-0	2017	Prognostic effect of serum C-reactive protein kinetics on advanced renal cell carcinoma treated with sunitinib.	Sunitinib	101-110	C-reactive protein	Homo sapiens	27-45
28205224-5	2017	Silencing of MUC13 expression inhibited migration and invasion, and sensitized renal cancer cells to killing by the multi-kinase inhibitors used clinically, sorafenib and sunitinib, and reversed acquired resistance to these drugs.	Sunitinib	171-180	mucin 13, cell surface associated	Homo sapiens	13-18
28423742-15	2017	HEYL, hsa-miR-27b, hsa-miR-23b and hsa-miR-628-5p could be potentially used as biomarkers of sunitinib response.	Sunitinib	93-102	hes related family bHLH transcription factor with YRPW motif like	Homo sapiens	0-4
28423742-15	2017	HEYL, hsa-miR-27b, hsa-miR-23b and hsa-miR-628-5p could be potentially used as biomarkers of sunitinib response.	Sunitinib	93-102	microRNA 27b	Homo sapiens	10-17
28423742-15	2017	HEYL, hsa-miR-27b, hsa-miR-23b and hsa-miR-628-5p could be potentially used as biomarkers of sunitinib response.	Sunitinib	93-102	microRNA 628	Homo sapiens	35-46
28529744-2	2017	The aim of the present study was to investigate the prognostic effect of pretreatment serum CRP level and CRP kinetics on patients with advanced RCC treated with sunitinib.	Sunitinib	162-171	C-reactive protein	Homo sapiens	106-109
28529744-9	2017	Therefore, CRP kinetics and normal pretreatment CRP level are prognostic indicators in patients with advanced RCC treated with sunitinib.	Sunitinib	127-136	C-reactive protein	Homo sapiens	11-14
28529744-2	2017	The aim of the present study was to investigate the prognostic effect of pretreatment serum CRP level and CRP kinetics on patients with advanced RCC treated with sunitinib.	Sunitinib	162-171	C-reactive protein	Homo sapiens	92-95
28529744-9	2017	Therefore, CRP kinetics and normal pretreatment CRP level are prognostic indicators in patients with advanced RCC treated with sunitinib.	Sunitinib	127-136	C-reactive protein	Homo sapiens	48-51
28418873-6	2017	Besides, combined treatment with sunitinib, PF-04691502 and GANT61 significantly prolonged the survival of mice transplanted with FLT3-mutated MV4-11 cells compared to the single agent treatments.	Sunitinib	33-42	FMS-like tyrosine kinase 3	Mus musculus	130-134
28670632-1	2017	PURPOSE: To describe the clinical course of advanced juxtapapillary retinal capillary hemangioblastomas (RCH) associated with von Hippel-Lindau (VHL) disease treated with systemic sunitinib malate, an agent that inhibits both anti-vascular endothelial growth factor and anti-platelet-derived growth factor signaling.	Sunitinib	180-196	vascular endothelial growth factor A	Homo sapiens	231-265
28105557-3	2017	Although no treatments are currently available to manage HAND, we have previously shown that sunitinib, an anticancer drug that blocks receptor tyrosine-kinase and cyclin kinase pathways, might be of interest.	Sunitinib	93-102	ret proto-oncogene	Homo sapiens	135-159
28240606-6	2017	In cultured cells, treatment with sunitinib and erlotinib, approved anticancer drugs that inhibit AAK1 or GAK activity, or with more selective compounds inhibited intracellular trafficking of HCV and multiple unrelated RNA viruses with a high barrier to resistance.	Sunitinib	34-43	AP2 associated kinase 1	Homo sapiens	98-102
28240606-6	2017	In cultured cells, treatment with sunitinib and erlotinib, approved anticancer drugs that inhibit AAK1 or GAK activity, or with more selective compounds inhibited intracellular trafficking of HCV and multiple unrelated RNA viruses with a high barrier to resistance.	Sunitinib	34-43	cyclin G associated kinase	Homo sapiens	106-109
28240606-8	2017	We validated sunitinib- and erlotinib-mediated inhibition of AAK1 and GAK activity as an important mechanism of antiviral action.	Sunitinib	13-22	AP2 associated kinase 1	Homo sapiens	61-65
28240606-8	2017	We validated sunitinib- and erlotinib-mediated inhibition of AAK1 and GAK activity as an important mechanism of antiviral action.	Sunitinib	13-22	cyclin G associated kinase	Homo sapiens	70-73
28413468-6	2017	In addition, sunitinib activated ERK1/2 and inhibited mTOR/p70S6K signaling.	Sunitinib	13-22	mitogen-activated protein kinase 3	Homo sapiens	33-39
28413468-6	2017	In addition, sunitinib activated ERK1/2 and inhibited mTOR/p70S6K signaling.	Sunitinib	13-22	mechanistic target of rapamycin kinase	Homo sapiens	54-58
28413468-6	2017	In addition, sunitinib activated ERK1/2 and inhibited mTOR/p70S6K signaling.	Sunitinib	13-22	ribosomal protein S6 kinase B1	Homo sapiens	59-65
28413468-7	2017	Sunitinib-induced autophagy was notably reversed by ERK1/2 kinase inhibitor, U0126.	Sunitinib	0-9	mitogen-activated protein kinase 3	Homo sapiens	52-58
28105557-8	2017	Moreover, in these animals, sunitinib reduced the hyperactivation of CDK5, tau hyperphosphorylation, and p35 cleavage to p25.	Sunitinib	28-37	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	121-124
28105557-10	2017	Alterations in autophagy in the Tat tg mice were associated with reduced levels of a CDK5 substrate, EndoB1, and levels of total EndoB1 were normalized by sunitinib treatment.	Sunitinib	155-164	cyclin-dependent kinase 5	Mus musculus	85-89
28105557-10	2017	Alterations in autophagy in the Tat tg mice were associated with reduced levels of a CDK5 substrate, EndoB1, and levels of total EndoB1 were normalized by sunitinib treatment.	Sunitinib	155-164	SH3-domain GRB2-like B1 (endophilin)	Mus musculus	101-107
28105557-10	2017	Alterations in autophagy in the Tat tg mice were associated with reduced levels of a CDK5 substrate, EndoB1, and levels of total EndoB1 were normalized by sunitinib treatment.	Sunitinib	155-164	SH3-domain GRB2-like B1 (endophilin)	Mus musculus	129-135
28384190-12	2017	HPLC analysis of the cell culture supernatant demonstrated saturation of the cell medium within approximately 4 hours for each amount added, with sunitinib achieving a final concentration of 17.61 muM (SE +-1.01).	Sunitinib	146-155	latexin	Homo sapiens	197-200
28278077-12	2017	Moreover, the VM-associated proteins VE-cadherin and Twist1 upregulated in the sunitinib-treated MDA-MB-231 and Hs578T tumors.	Sunitinib	79-88	cadherin 5	Homo sapiens	37-48
28278077-12	2017	Moreover, the VM-associated proteins VE-cadherin and Twist1 upregulated in the sunitinib-treated MDA-MB-231 and Hs578T tumors.	Sunitinib	79-88	twist family bHLH transcription factor 1	Homo sapiens	53-59
28105557-6	2017	In neuronal cultures challenged with low levels of Tat, sunitinib increased markers of autophagy such as LC3-II and reduced p62 accumulation in a dose-dependent manner.	Sunitinib	56-65	nucleoporin 62	Homo sapiens	124-127
28105557-7	2017	In vivo, sunitinib treatment restored LC3-II, p62, and endophilin B1 (EndoB1) levels in doxycycline-induced Tat transgenic mice.	Sunitinib	9-18	nucleoporin 62	Mus musculus	46-49
28105557-7	2017	In vivo, sunitinib treatment restored LC3-II, p62, and endophilin B1 (EndoB1) levels in doxycycline-induced Tat transgenic mice.	Sunitinib	9-18	SH3-domain GRB2-like B1 (endophilin)	Mus musculus	55-68
28105557-7	2017	In vivo, sunitinib treatment restored LC3-II, p62, and endophilin B1 (EndoB1) levels in doxycycline-induced Tat transgenic mice.	Sunitinib	9-18	SH3-domain GRB2-like B1 (endophilin)	Mus musculus	70-76
28105557-8	2017	Moreover, in these animals, sunitinib reduced the hyperactivation of CDK5, tau hyperphosphorylation, and p35 cleavage to p25.	Sunitinib	28-37	cyclin dependent kinase 5	Homo sapiens	69-73
28105557-8	2017	Moreover, in these animals, sunitinib reduced the hyperactivation of CDK5, tau hyperphosphorylation, and p35 cleavage to p25.	Sunitinib	28-37	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	105-108
28274318-0	2017	[Knockdown of ATG5 enhances the sensitivity of human renal carcinoma cells to sunitinib].	Sunitinib	78-87	autophagy related 5	Homo sapiens	14-18
28423517-6	2017	The expression levels of sunitinib targeted-kinases were measured by transcriptome sequencing for KDR, PDGFRA/B, KIT, RET, FLT1, and FLT4.	Sunitinib	25-34	kinase insert domain receptor	Homo sapiens	98-101
28184014-8	2017	These results were confirmed by siRNA targeting the autophagy-related gene Atg5 In CCOC tumor xenografts, Lys05 potentiated the antitumor activity of sunitinib compared with either treatment alone.	Sunitinib	150-159	autophagy related 5	Homo sapiens	75-79
28231773-2	2017	METHODS: Eighteen patients with pathologically proven advanced GEP-NENs treated with sunitinib were enrolled in the study.	Sunitinib	85-94	granulin precursor	Homo sapiens	63-66
28231773-13	2017	CONCLUSION: The Choi criteria appear to be more sensitive and more precise than RECIST 1.1 in assessing the early response of advanced GEP-NENs treated with sunitinib.	Sunitinib	157-166	granulin precursor	Homo sapiens	135-138
28401187-3	2017	Inhibition of MCL-1 or mTORC1 sensitized cancer cells to sunitinib.	Sunitinib	57-66	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	14-19
28167241-7	2017	Sunitinib treatment reduced vessel densities and induced hypoxia in all melanoma lines, and the magnitude of the effect was associated with the gene expression and protein secretion rate of VEGF-A.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	190-196
28276433-5	2017	However, over the past decade, marked advances in the treatment of metastatic RCC have been made, with targeted agents including sorafenib, sunitinib, bevacizumab, pazopanib and axitinib, which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGFR), and everolimus and temsirolimus, which inhibit mechanistic target of rapamycin complex 1 (mTORC1), being approved.	Sunitinib	140-149	vascular endothelial growth factor A	Homo sapiens	202-236
28276433-5	2017	However, over the past decade, marked advances in the treatment of metastatic RCC have been made, with targeted agents including sorafenib, sunitinib, bevacizumab, pazopanib and axitinib, which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGFR), and everolimus and temsirolimus, which inhibit mechanistic target of rapamycin complex 1 (mTORC1), being approved.	Sunitinib	140-149	vascular endothelial growth factor A	Homo sapiens	238-242
28276433-5	2017	However, over the past decade, marked advances in the treatment of metastatic RCC have been made, with targeted agents including sorafenib, sunitinib, bevacizumab, pazopanib and axitinib, which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGFR), and everolimus and temsirolimus, which inhibit mechanistic target of rapamycin complex 1 (mTORC1), being approved.	Sunitinib	140-149	kinase insert domain receptor	Homo sapiens	262-267
28276433-5	2017	However, over the past decade, marked advances in the treatment of metastatic RCC have been made, with targeted agents including sorafenib, sunitinib, bevacizumab, pazopanib and axitinib, which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGFR), and everolimus and temsirolimus, which inhibit mechanistic target of rapamycin complex 1 (mTORC1), being approved.	Sunitinib	140-149	CREB regulated transcription coactivator 1	Mus musculus	360-366
28087600-0	2017	Sunitinib Stimulates Expression of VEGFC by Tumor Cells and Promotes Lymphangiogenesis in Clear Cell Renal Cell Carcinomas.	Sunitinib	0-9	vascular endothelial growth factor C	Homo sapiens	35-40
28087600-4	2017	In this study, we found that sunitinib can stimulate vegfc gene transcription and increase VEGFC mRNA half-life.	Sunitinib	29-38	vascular endothelial growth factor C	Homo sapiens	53-58
28087600-4	2017	In this study, we found that sunitinib can stimulate vegfc gene transcription and increase VEGFC mRNA half-life.	Sunitinib	29-38	vascular endothelial growth factor C	Homo sapiens	91-96
28087600-5	2017	In addition, sunitinib activated p38 MAPK, which resulted in the upregulation/activity of HuR and inactivation of tristetraprolin, two AU-rich element-binding proteins.	Sunitinib	13-22	ELAV like RNA binding protein 1	Homo sapiens	90-93
28087600-5	2017	In addition, sunitinib activated p38 MAPK, which resulted in the upregulation/activity of HuR and inactivation of tristetraprolin, two AU-rich element-binding proteins.	Sunitinib	13-22	ZFP36 ring finger protein	Homo sapiens	114-129
28087600-6	2017	Sunitinib stimulated a VEGFC-dependent development of lymphatic vessels in experimental tumors.	Sunitinib	0-9	vascular endothelial growth factor C	Homo sapiens	23-28
27751729-8	2017	With first-line sunitinib, KDM5C mutations were associated with longer PFS1L (median [95% CI] of 20.6 [12.4, 27.3] vs 8.3 [7.8, 11.0] mo).	Sunitinib	16-25	lysine demethylase 5C	Homo sapiens	27-32
27395374-1	2017	PURPOSE: To identify prognostic molecular profiles in patients with mRCC treated with sunitinib, we performed immunohistochemical analysis for VEGF and PI3K/Akt/mTOR pathway components.	Sunitinib	86-95	vascular endothelial growth factor A	Homo sapiens	143-147
27395374-7	2017	CONCLUSION: Immunohistochemistry for VEGF and p-mTOR proteins may discriminate patients refractory to first-line sunitinib with poor prognosis.	Sunitinib	113-122	vascular endothelial growth factor A	Homo sapiens	37-41
27395374-7	2017	CONCLUSION: Immunohistochemistry for VEGF and p-mTOR proteins may discriminate patients refractory to first-line sunitinib with poor prognosis.	Sunitinib	113-122	mechanistic target of rapamycin kinase	Homo sapiens	48-52
27477693-7	2017	Taken together, our study suggests a model in which overexpression of wild-type PDGFRA associated with NF1 deficiency leads to aberrant activation of downstream RAS signaling and thus contributes importantly to MPNST development-a prediction supported by the ability of the kinase inhibitor sunitinib alone and in combination with the MEK inhibitor trametinib to retard MPNST progression in transgenic fish overexpressing the wild-type receptor.	Sunitinib	291-300	platelet-derived growth factor receptor, alpha polypeptide	Danio rerio	80-86
28401187-3	2017	Inhibition of MCL-1 or mTORC1 sensitized cancer cells to sunitinib.	Sunitinib	57-66	CREB regulated transcription coactivator 1	Mus musculus	23-29
28401187-4	2017	Analysis of tissues from patients correlated MCL-1/mTORC1 induction with resistance to sunitinib.	Sunitinib	87-96	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	45-50
28401187-4	2017	Analysis of tissues from patients correlated MCL-1/mTORC1 induction with resistance to sunitinib.	Sunitinib	87-96	CREB regulated transcription coactivator 1	Mus musculus	51-57
28274318-1	2017	Objective To investigate the expression levels of autophagy-related gene 5 (ATG5) and microtubule-associated protein 1 light chain 3 (LC3) and their effects on sunitinib resistance in human renal carcinoma cells.	Sunitinib	160-169	autophagy related 5	Homo sapiens	50-74
28274318-1	2017	Objective To investigate the expression levels of autophagy-related gene 5 (ATG5) and microtubule-associated protein 1 light chain 3 (LC3) and their effects on sunitinib resistance in human renal carcinoma cells.	Sunitinib	160-169	autophagy related 5	Homo sapiens	76-80
28274318-1	2017	Objective To investigate the expression levels of autophagy-related gene 5 (ATG5) and microtubule-associated protein 1 light chain 3 (LC3) and their effects on sunitinib resistance in human renal carcinoma cells.	Sunitinib	160-169	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	134-137
28274318-11	2017	Compared with control group, the survival rate in ATG5 low expression group were significantly reduced in a dose-dependent manner after sunitinib treatment.	Sunitinib	136-145	autophagy related 5	Homo sapiens	50-54
28274318-12	2017	Conclusion Autophagy is active in renal clear cell carcinoma, and the drug sensitivity to sunitinib in renal cancer cells can be enhanced by the downregulation of ATG5.	Sunitinib	90-99	autophagy related 5	Homo sapiens	163-167
27896475-9	2017	We also highlighted the association with sunitinib-related toxicity; in particular, VEGFA polymorphism rs3025039 (CT+TT vs. CC, OR 15.3, 95% CI 2.2-102.1; P = 0.005) is associated with severe toxicity, with the presence of the variant T allele associated with a grade &gt;=3 AE.	Sunitinib	41-50	vascular endothelial growth factor A	Homo sapiens	84-89
28143610-10	2017	In this case, the patient was homozygous for the ABCG2 421C allele, but was capable of potentially harboring polymorphisms in other genes, such as ABCB1, an efflux pump of sunitinib.	Sunitinib	172-181	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	49-54
27030134-1	2017	AIM: Although targeting angiogenesis with vascular endothelial growth factor receptor (VEGFR) inhibitors has demonstrated efficacy in the treatment of renal cell carcinoma, primary, intrinsic resistance to the VEGFR inhibitor sunitinib is not fully understood in a subset of metastatic RCC (mRCC) patients.	Sunitinib	226-235	kinase insert domain receptor	Homo sapiens	42-85
27030134-1	2017	AIM: Although targeting angiogenesis with vascular endothelial growth factor receptor (VEGFR) inhibitors has demonstrated efficacy in the treatment of renal cell carcinoma, primary, intrinsic resistance to the VEGFR inhibitor sunitinib is not fully understood in a subset of metastatic RCC (mRCC) patients.	Sunitinib	226-235	kinase insert domain receptor	Homo sapiens	87-92
27030134-1	2017	AIM: Although targeting angiogenesis with vascular endothelial growth factor receptor (VEGFR) inhibitors has demonstrated efficacy in the treatment of renal cell carcinoma, primary, intrinsic resistance to the VEGFR inhibitor sunitinib is not fully understood in a subset of metastatic RCC (mRCC) patients.	Sunitinib	226-235	kinase insert domain receptor	Homo sapiens	210-215
28143610-10	2017	In this case, the patient was homozygous for the ABCG2 421C allele, but was capable of potentially harboring polymorphisms in other genes, such as ABCB1, an efflux pump of sunitinib.	Sunitinib	172-181	ATP binding cassette subfamily B member 1	Homo sapiens	147-152
28117391-0	2017	Functional PTGS2 polymorphism-based models as novel predictive markers in metastatic renal cell carcinoma patients receiving first-line sunitinib.	Sunitinib	136-145	prostaglandin-endoperoxide synthase 2	Homo sapiens	11-16
28217462-5	2017	In conjunction with the restricted expression of HIF-2alpha in normal adult physiology, these studies suggest that such therapeutic approach might be favorable for patients with lower toxicity than current anti-angiogenic drugs like sunitinib.	Sunitinib	233-242	endothelial PAS domain protein 1	Homo sapiens	49-59
28114889-3	2017	METHODS: In this study, in a clinical aspect, we retrospectively investigated the prognostic and predictive impact of tumoral CCR7 expression in 110 mRCC patients treated with sunitinib and sorafenib, and its correlation with pre- or post-administration lymphatic involvement.	Sunitinib	176-185	C-C motif chemokine receptor 7	Homo sapiens	126-130
28178124-1	2017	RATIONALE: The case reported the rapid remission of disease recurrence achieved adding foscarnet, a DNA polymerase inhibitor that interacts with fibroblast growth factor 2, to low molecular weight heparin and sunitinib for the first time in a patient with an anaplastic thyroid cancer (ATC).	Sunitinib	209-218	fibroblast growth factor 2	Homo sapiens	145-171
27958294-0	2017	Targeted therapy: Sunitinib modulates MCL-1 and mTOR signalling.	Sunitinib	18-27	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	38-43
27958294-0	2017	Targeted therapy: Sunitinib modulates MCL-1 and mTOR signalling.	Sunitinib	18-27	mechanistic target of rapamycin kinase	Homo sapiens	48-52
27893461-0	2017	Dual modulation of MCL-1 and mTOR determines the response to sunitinib.	Sunitinib	61-70	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	19-24
28117425-2	2017	The endothelial cell-specific mitogen vascular endothelial growth factor (VEGF), as well as its receptors, VEGFR1, VEGFR2, are thought to be the major mediators of pathological angiogenesis, and sunitinib exhibits anti-angiogenesis property through VEGF blockage and has been widely used to treat various cancers.	Sunitinib	195-204	vascular endothelial growth factor A	Rattus norvegicus	38-72
28117425-2	2017	The endothelial cell-specific mitogen vascular endothelial growth factor (VEGF), as well as its receptors, VEGFR1, VEGFR2, are thought to be the major mediators of pathological angiogenesis, and sunitinib exhibits anti-angiogenesis property through VEGF blockage and has been widely used to treat various cancers.	Sunitinib	195-204	vascular endothelial growth factor A	Rattus norvegicus	74-78
28117425-2	2017	The endothelial cell-specific mitogen vascular endothelial growth factor (VEGF), as well as its receptors, VEGFR1, VEGFR2, are thought to be the major mediators of pathological angiogenesis, and sunitinib exhibits anti-angiogenesis property through VEGF blockage and has been widely used to treat various cancers.	Sunitinib	195-204	Fms related receptor tyrosine kinase 1	Rattus norvegicus	107-113
28117425-2	2017	The endothelial cell-specific mitogen vascular endothelial growth factor (VEGF), as well as its receptors, VEGFR1, VEGFR2, are thought to be the major mediators of pathological angiogenesis, and sunitinib exhibits anti-angiogenesis property through VEGF blockage and has been widely used to treat various cancers.	Sunitinib	195-204	kinase insert domain receptor	Rattus norvegicus	115-121
28117425-2	2017	The endothelial cell-specific mitogen vascular endothelial growth factor (VEGF), as well as its receptors, VEGFR1, VEGFR2, are thought to be the major mediators of pathological angiogenesis, and sunitinib exhibits anti-angiogenesis property through VEGF blockage and has been widely used to treat various cancers.	Sunitinib	195-204	vascular endothelial growth factor A	Rattus norvegicus	107-111
28117425-5	2017	Sunitinib treatment was associated with less angiogenesis in small-airway remodelling with a slightly disordered lung architecture, and lower expression level of VEGF, VEGFR1, VEGFR2.	Sunitinib	0-9	vascular endothelial growth factor A	Rattus norvegicus	162-166
28117425-5	2017	Sunitinib treatment was associated with less angiogenesis in small-airway remodelling with a slightly disordered lung architecture, and lower expression level of VEGF, VEGFR1, VEGFR2.	Sunitinib	0-9	Fms related receptor tyrosine kinase 1	Rattus norvegicus	168-174
28117425-5	2017	Sunitinib treatment was associated with less angiogenesis in small-airway remodelling with a slightly disordered lung architecture, and lower expression level of VEGF, VEGFR1, VEGFR2.	Sunitinib	0-9	kinase insert domain receptor	Rattus norvegicus	176-182
28117425-6	2017	Overall, our results indicate that VEGF is a vital important factor that contributes to the small-airway remodelling in a rat model of COPD through promoting angiogenesis, which mainly depend on the specific binding between VEGF and VEGFR1 and can be effectively attenuated by sunitinib.	Sunitinib	277-286	vascular endothelial growth factor A	Rattus norvegicus	35-39
28117425-6	2017	Overall, our results indicate that VEGF is a vital important factor that contributes to the small-airway remodelling in a rat model of COPD through promoting angiogenesis, which mainly depend on the specific binding between VEGF and VEGFR1 and can be effectively attenuated by sunitinib.	Sunitinib	277-286	vascular endothelial growth factor A	Rattus norvegicus	224-228
28117425-6	2017	Overall, our results indicate that VEGF is a vital important factor that contributes to the small-airway remodelling in a rat model of COPD through promoting angiogenesis, which mainly depend on the specific binding between VEGF and VEGFR1 and can be effectively attenuated by sunitinib.	Sunitinib	277-286	Fms related receptor tyrosine kinase 1	Rattus norvegicus	233-239
27997164-0	2017	Synthesis of Novel c(AmpRGD)-Sunitinib Dual Conjugates as Molecular Tools Targeting the alphavbeta3 Integrin/VEGFR2 Couple and Impairing Tumor-Associated Angiogenesis.	Sunitinib	29-38	kinase insert domain protein receptor	Mus musculus	109-115
28057017-6	2017	RESULTS: The in vivo experiments demonstrated that bevacizumab and sunitinib increase the in vivo expression of CXCR4, SDF-1alpha, and TGFbeta1.	Sunitinib	67-76	C-X-C motif chemokine receptor 4	Homo sapiens	112-117
28057017-6	2017	RESULTS: The in vivo experiments demonstrated that bevacizumab and sunitinib increase the in vivo expression of CXCR4, SDF-1alpha, and TGFbeta1.	Sunitinib	67-76	transforming growth factor beta 1	Homo sapiens	135-143
28057017-7	2017	In addition, we demonstrate that the co-administration of the novel brain-penetrating CXCR4 antagonist, PRX177561, with bevacizumab or sunitinib inhibited tumor growth and reduced the inflammation.	Sunitinib	135-144	C-X-C motif chemokine receptor 4	Homo sapiens	86-91
28057017-0	2017	The brain-penetrating CXCR4 antagonist, PRX177561, increases the antitumor effects of bevacizumab and sunitinib in preclinical models of human glioblastoma.	Sunitinib	102-111	C-X-C motif chemokine receptor 4	Homo sapiens	22-27
27893461-0	2017	Dual modulation of MCL-1 and mTOR determines the response to sunitinib.	Sunitinib	61-70	mechanistic target of rapamycin kinase	Homo sapiens	29-33
27901483-0	2017	Meta-analysis on the association of VEGFR1 genetic variants with sunitinib outcome in metastatic renal cell carcinoma patients.	Sunitinib	65-74	fms related receptor tyrosine kinase 1	Homo sapiens	36-42
27893461-3	2017	Here, we have shown that cancer cells respond to clinically relevant doses of sunitinib by enhancing the stability of the antiapoptotic protein MCL-1 and inducing mTORC1 signaling, thus evoking little cytotoxicity.	Sunitinib	78-87	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	144-149
27901483-1	2017	VEGFR1 rs9582036 and rs9554320 were previously reported the association with sunitinib progression-free survival (PFS) and overall survival (OS) in patients with metastatic renal cell carcinoma (mRCC).	Sunitinib	77-86	fms related receptor tyrosine kinase 1	Homo sapiens	0-6
27901483-8	2017	Our findings suggest that, although VEGFR1 rs9582036 and rs9554320 are involved in sunitinib therapy outcome, its clinical use as biomarkers for prediction of sunitinib outcome in mRCC patients is limited, due to inconsistent findings when analyzing all existing studies together.	Sunitinib	83-92	fms related receptor tyrosine kinase 1	Homo sapiens	36-42
27893461-3	2017	Here, we have shown that cancer cells respond to clinically relevant doses of sunitinib by enhancing the stability of the antiapoptotic protein MCL-1 and inducing mTORC1 signaling, thus evoking little cytotoxicity.	Sunitinib	78-87	CREB regulated transcription coactivator 1	Mus musculus	163-169
27926489-9	2017	The expression of GM-CSF was substantially inhibited by celecoxib and sunitinib.	Sunitinib	70-79	colony stimulating factor 2	Homo sapiens	18-24
27893461-4	2017	Inhibition of MCL-1 or mTORC1 signaling sensitized cells to clinically relevant doses of sunitinib in vitro and was synergistic with sunitinib in impairing tumor growth in vivo, indicating that these responses are triggered as prosurvival mechanisms that enable cells to tolerate the cytotoxic effects of sunitinib.	Sunitinib	89-98	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	14-19
27893461-4	2017	Inhibition of MCL-1 or mTORC1 signaling sensitized cells to clinically relevant doses of sunitinib in vitro and was synergistic with sunitinib in impairing tumor growth in vivo, indicating that these responses are triggered as prosurvival mechanisms that enable cells to tolerate the cytotoxic effects of sunitinib.	Sunitinib	89-98	CREB regulated transcription coactivator 1	Mus musculus	23-29
27893461-4	2017	Inhibition of MCL-1 or mTORC1 signaling sensitized cells to clinically relevant doses of sunitinib in vitro and was synergistic with sunitinib in impairing tumor growth in vivo, indicating that these responses are triggered as prosurvival mechanisms that enable cells to tolerate the cytotoxic effects of sunitinib.	Sunitinib	133-142	CREB regulated transcription coactivator 1	Mus musculus	23-29
27893461-4	2017	Inhibition of MCL-1 or mTORC1 signaling sensitized cells to clinically relevant doses of sunitinib in vitro and was synergistic with sunitinib in impairing tumor growth in vivo, indicating that these responses are triggered as prosurvival mechanisms that enable cells to tolerate the cytotoxic effects of sunitinib.	Sunitinib	133-142	CREB regulated transcription coactivator 1	Mus musculus	23-29
27893461-5	2017	Furthermore, higher doses of sunitinib were cytotoxic, triggered a decline in MCL-1 levels, and inhibited mTORC1 signaling.	Sunitinib	29-38	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	78-83
27893461-5	2017	Furthermore, higher doses of sunitinib were cytotoxic, triggered a decline in MCL-1 levels, and inhibited mTORC1 signaling.	Sunitinib	29-38	CREB regulated transcription coactivator 1	Mus musculus	106-112
27893461-6	2017	Mechanistically, we determined that sunitinib modulates MCL-1 stability by affecting its proteasomal degradation.	Sunitinib	36-45	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	56-61
27893461-7	2017	Dual modulation of MCL-1 stability at different dose ranges of sunitinib was due to differential effects on ERK and GSK3beta activity, and the latter also accounted for dual modulation of mTORC1 activity.	Sunitinib	63-72	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	19-24
27893461-7	2017	Dual modulation of MCL-1 stability at different dose ranges of sunitinib was due to differential effects on ERK and GSK3beta activity, and the latter also accounted for dual modulation of mTORC1 activity.	Sunitinib	63-72	EPH receptor B2	Homo sapiens	108-111
27893461-7	2017	Dual modulation of MCL-1 stability at different dose ranges of sunitinib was due to differential effects on ERK and GSK3beta activity, and the latter also accounted for dual modulation of mTORC1 activity.	Sunitinib	63-72	glycogen synthase kinase 3 beta	Homo sapiens	116-124
27893461-8	2017	Finally, comparison of patient samples prior to and following sunitinib treatment suggested that increases in MCL-1 levels and mTORC1 activity correlate with resistance to sunitinib in patients.	Sunitinib	62-71	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	110-115
27893461-8	2017	Finally, comparison of patient samples prior to and following sunitinib treatment suggested that increases in MCL-1 levels and mTORC1 activity correlate with resistance to sunitinib in patients.	Sunitinib	62-71	CREB regulated transcription coactivator 1	Mus musculus	127-133
27893461-8	2017	Finally, comparison of patient samples prior to and following sunitinib treatment suggested that increases in MCL-1 levels and mTORC1 activity correlate with resistance to sunitinib in patients.	Sunitinib	172-181	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	110-115
27893461-8	2017	Finally, comparison of patient samples prior to and following sunitinib treatment suggested that increases in MCL-1 levels and mTORC1 activity correlate with resistance to sunitinib in patients.	Sunitinib	172-181	CREB regulated transcription coactivator 1	Mus musculus	127-133
27564227-7	2017	In conclusion, our data showed that the ABCB1 rs2032582 GG genotype was associated with individual adverse events" susceptibility among Japanese patients treated with sunitinib in routine clinical settings.	Sunitinib	167-176	ATP binding cassette subfamily B member 1	Homo sapiens	40-45
28381801-9	2017	In conclusion, STAT3 polymorphism may be a novel risk factor for sunitinib-induced stomatitis in patients with mRCC.	Sunitinib	65-74	signal transducer and activator of transcription 3	Homo sapiens	15-20
27737332-0	2017	Sunitinib in the therapy of malignant paragangliomas: report on the efficacy in a SDHB mutation carrier and review of the literature.	Sunitinib	0-9	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	82-86
27737332-4	2017	Their therapy is palliative and represented by different options among which antiangiogenic drugs, like sunitinib, have been hypothesized to be effective especially in malignant SDHB mutated tumors.	Sunitinib	104-113	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	178-182
27737332-5	2017	We report the effects of sunitinib therapy in a SDHB mutation carrier affected by a malignant sPGL.	Sunitinib	25-34	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	48-52
28381801-0	2017	Association of Single Nucleotide Polymorphisms in STAT3, ABCB1, and ABCG2 with Stomatitis in Patients with Metastatic Renal Cell Carcinoma Treated with Sunitinib: A Retrospective Analysis in Japanese Patients.	Sunitinib	152-161	signal transducer and activator of transcription 3	Homo sapiens	50-55
28381801-2	2017	Sunitinib is a substrate of P-glycoprotein (multidrug resistance (MDR)-1/ABCB1) and breast-cancer resistance protein (BCRP/ABCG2).	Sunitinib	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	44-72
27942928-1	2017	PURPOSE: Efficacy of targeted agents, such as everolimus and sunitinib, has been demonstrated in prospective trials on patients with gastroenteropancreatic neuroendocrine tumors (GEP-NETs).	Sunitinib	61-70	granulin precursor	Homo sapiens	179-182
28381801-2	2017	Sunitinib is a substrate of P-glycoprotein (multidrug resistance (MDR)-1/ABCB1) and breast-cancer resistance protein (BCRP/ABCG2).	Sunitinib	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	73-78
28381801-2	2017	Sunitinib is a substrate of P-glycoprotein (multidrug resistance (MDR)-1/ABCB1) and breast-cancer resistance protein (BCRP/ABCG2).	Sunitinib	0-9	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	84-116
28381801-2	2017	Sunitinib is a substrate of P-glycoprotein (multidrug resistance (MDR)-1/ABCB1) and breast-cancer resistance protein (BCRP/ABCG2).	Sunitinib	0-9	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	118-122
28381801-2	2017	Sunitinib is a substrate of P-glycoprotein (multidrug resistance (MDR)-1/ABCB1) and breast-cancer resistance protein (BCRP/ABCG2).	Sunitinib	0-9	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	123-128
28381801-3	2017	In this retrospective study, we evaluated the association between sunitinib-induced stomatitis and STAT3, ABCB1, and ABCG2 polymorphisms in patients with metastatic renal cell carcinoma (mRCC).	Sunitinib	66-75	signal transducer and activator of transcription 3	Homo sapiens	99-104
28381801-3	2017	In this retrospective study, we evaluated the association between sunitinib-induced stomatitis and STAT3, ABCB1, and ABCG2 polymorphisms in patients with metastatic renal cell carcinoma (mRCC).	Sunitinib	66-75	ATP binding cassette subfamily B member 1	Homo sapiens	106-111
28381801-3	2017	In this retrospective study, we evaluated the association between sunitinib-induced stomatitis and STAT3, ABCB1, and ABCG2 polymorphisms in patients with metastatic renal cell carcinoma (mRCC).	Sunitinib	66-75	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	117-122
27942928-10	2017	CONCLUSIONS: Both everolimus and sunitinib were effective in GEP-NET patients.	Sunitinib	33-42	granulin precursor	Homo sapiens	61-64
27942928-3	2017	METHODS: Clinical records of 44 patients with GEP-NET who were treated with everolimus or sunitinib between March 2007 and October 2014 were retrospectively reviewed.	Sunitinib	90-99	granulin precursor	Homo sapiens	46-49
29073615-0	2017	Mir-144-3p Promotes Cell Proliferation, Metastasis, Sunitinib Resistance in Clear Cell Renal Cell Carcinoma by Downregulating ARID1A.	Sunitinib	52-61	microRNA 144	Mus musculus	0-7
29359059-5	2017	Four other cases of AIN reported along with inhibition of the vascular endothelial growth factor (VEGF) by either TKI (sunitinib and sorafenib) or antibodies (bevacizumab) suggest a possible class effect.	Sunitinib	119-128	vascular endothelial growth factor A	Homo sapiens	62-96
29359059-5	2017	Four other cases of AIN reported along with inhibition of the vascular endothelial growth factor (VEGF) by either TKI (sunitinib and sorafenib) or antibodies (bevacizumab) suggest a possible class effect.	Sunitinib	119-128	vascular endothelial growth factor A	Homo sapiens	98-102
28478450-4	2017	RESULTS: The results revealed that both the PDGF receptor-tyrosine kinase inhibitor imatinib and the multi-targeted VEGF and PDGF receptor inhibit or sunitinib malate reversed hypoxia-induced increases in right ventricular systolic pressure (RVSP), right ventricular function and thickening of the medial walls.	Sunitinib	150-166	vascular endothelial growth factor A	Rattus norvegicus	116-120
29073615-3	2017	This study aims to explore the roles of miR-144-3p in the invasion, migration and Sunitinib-resistance in ccRCC and to elucidate the underlying mechanisms.	Sunitinib	82-91	microRNA 144	Mus musculus	40-47
29073615-12	2017	CONCLUSION: Higher miR-144-3p may enhance malignancy and resistance to Sunitinib in ccRCC by targeting ARID1A, the observations may uncover novel strategies of ccRCC treatment.	Sunitinib	71-80	microRNA 144	Mus musculus	19-26
29073615-12	2017	CONCLUSION: Higher miR-144-3p may enhance malignancy and resistance to Sunitinib in ccRCC by targeting ARID1A, the observations may uncover novel strategies of ccRCC treatment.	Sunitinib	71-80	AT rich interactive domain 1A (SWI-like)	Mus musculus	103-109
28994095-12	2017	The immunoreactivities of Notch1, Jagged1, DLL-1 and VEGF in hepatocytes were significantly lower in the DM group when compared with the C, DM + S and C + S group treated with sunitinib.	Sunitinib	176-185	notch 1	Mus musculus	26-32
27784207-11	2017	Specifically, in tumors resistant to single-agent sunitinib we detected a transcriptional response to hypoxia characterized by over-expression of several HIF1alpha target genes.	Sunitinib	50-59	hypoxia inducible factor 1 subunit alpha	Homo sapiens	154-163
28994095-12	2017	The immunoreactivities of Notch1, Jagged1, DLL-1 and VEGF in hepatocytes were significantly lower in the DM group when compared with the C, DM + S and C + S group treated with sunitinib.	Sunitinib	176-185	jagged 1	Mus musculus	34-41
28994095-12	2017	The immunoreactivities of Notch1, Jagged1, DLL-1 and VEGF in hepatocytes were significantly lower in the DM group when compared with the C, DM + S and C + S group treated with sunitinib.	Sunitinib	176-185	delta like canonical Notch ligand 1	Mus musculus	43-48
28994095-12	2017	The immunoreactivities of Notch1, Jagged1, DLL-1 and VEGF in hepatocytes were significantly lower in the DM group when compared with the C, DM + S and C + S group treated with sunitinib.	Sunitinib	176-185	vascular endothelial growth factor A	Mus musculus	53-57
28994095-13	2017	CONCLUSIONS: These results suggest that sunitinib effectively protects the liver from diabetes-induced damage through the inhibition of the Notch pathway.	Sunitinib	40-49	notch 1	Mus musculus	140-145
28954991-0	2017	Antiangiogenic agent sunitinib induces epithelial to mesenchymal transition and accelerates motility of colorectal cancer cells.	Sunitinib	21-30	collagen type XVIII alpha 1 chain	Homo sapiens	0-20
28954991-4	2017	To elucidate a direct effect of VEGF-R-targeting drug (sunitinib), we established a human colorectal cancer cell model adapted to sunitinib.	Sunitinib	55-64	kinase insert domain receptor	Homo sapiens	32-38
28954991-6	2017	Consistent with the phenotype, the sunitinib-conditioned cells decreased the expression levels of E-cadherin (an epithelial marker), while significantly increased the levels of Slug and Zeb1 (mesenchymal markers).	Sunitinib	35-44	cadherin 1	Homo sapiens	98-108
28954991-6	2017	Consistent with the phenotype, the sunitinib-conditioned cells decreased the expression levels of E-cadherin (an epithelial marker), while significantly increased the levels of Slug and Zeb1 (mesenchymal markers).	Sunitinib	35-44	snail family transcriptional repressor 2	Homo sapiens	177-181
28954991-6	2017	Consistent with the phenotype, the sunitinib-conditioned cells decreased the expression levels of E-cadherin (an epithelial marker), while significantly increased the levels of Slug and Zeb1 (mesenchymal markers).	Sunitinib	35-44	zinc finger E-box binding homeobox 1	Homo sapiens	186-190
28954991-7	2017	Expression profiles of VEGF-R in the sunitinib-conditioned cells showed that only neuropilin-1 (NRP1) expression was significantly increased among all VEGF-R tested.	Sunitinib	37-46	kinase insert domain receptor	Homo sapiens	23-29
28954991-7	2017	Expression profiles of VEGF-R in the sunitinib-conditioned cells showed that only neuropilin-1 (NRP1) expression was significantly increased among all VEGF-R tested.	Sunitinib	37-46	neuropilin 1	Homo sapiens	82-94
28954991-7	2017	Expression profiles of VEGF-R in the sunitinib-conditioned cells showed that only neuropilin-1 (NRP1) expression was significantly increased among all VEGF-R tested.	Sunitinib	37-46	neuropilin 1	Homo sapiens	96-100
28954991-7	2017	Expression profiles of VEGF-R in the sunitinib-conditioned cells showed that only neuropilin-1 (NRP1) expression was significantly increased among all VEGF-R tested.	Sunitinib	37-46	kinase insert domain receptor	Homo sapiens	151-157
28954991-8	2017	Blockade of NRP1 using its antagonist clearly repressed the migration activation in sunitinib-conditioned cells, but not in the control cells.	Sunitinib	84-93	neuropilin 1	Homo sapiens	12-16
28478454-8	2017	RESULTS: VEGF (50 and 100 ng/ml) significantly augmented endothelial arginine transport in a time dependent manner, an effect which was prevented by Sunitinib (2 microM), a multi targeted receptor tyrosine kinase inhibitor.	Sunitinib	149-158	vascular endothelial growth factor A	Homo sapiens	9-13
28123542-0	2017	Influence of VEGFR single nucleotide polymorphisms on the efficacy of sunitinib therapy against renal cell carcinoma.	Sunitinib	70-79	kinase insert domain receptor	Homo sapiens	13-18
26810136-0	2017	Sunitinib-induced hypertension in CYP3A4 rs4646437 A-allele carriers with metastatic renal cell carcinoma.	Sunitinib	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	34-40
26810136-1	2017	The single nucleotide polymorphism (SNP) rs4646437G&gt;A in CYP3A4 was suggested to be related to sunitinib toxicity.	Sunitinib	98-107	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	60-66
27840968-8	2017	Knockdown of ERK reduced sensitivity to sorafenib in both cell lines, knockdown of ERK and 4EBP1 reduced sensitivity to sunitinib in 769-P cells, and knockdown of 4EBP1 and p70 reduced sensitivity to everolimus in 786-O cells.	Sunitinib	120-129	mitogen-activated protein kinase 1	Homo sapiens	83-96
27840968-8	2017	Knockdown of ERK reduced sensitivity to sorafenib in both cell lines, knockdown of ERK and 4EBP1 reduced sensitivity to sunitinib in 769-P cells, and knockdown of 4EBP1 and p70 reduced sensitivity to everolimus in 786-O cells.	Sunitinib	120-129	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	91-96
27840968-9	2017	High expression of phospho-ERK, -4EBP1 and -p70 correlated with better progression-free survival in patients treated with sorafenib, sunitinib and everolimus, respectively.	Sunitinib	133-142	mitogen-activated protein kinase 1	Homo sapiens	27-30
27840968-9	2017	High expression of phospho-ERK, -4EBP1 and -p70 correlated with better progression-free survival in patients treated with sorafenib, sunitinib and everolimus, respectively.	Sunitinib	133-142	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	32-38
27840968-9	2017	High expression of phospho-ERK, -4EBP1 and -p70 correlated with better progression-free survival in patients treated with sorafenib, sunitinib and everolimus, respectively.	Sunitinib	133-142	annexin A6	Homo sapiens	44-47
26810136-7	2017	In conclusion, hypertension is more likely to occur in A-allele carriers of the CYP3A4 rs4646437 variant in our cohort of mRCC patients treated with sunitinib.	Sunitinib	149-158	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	80-86
28123542-1	2017	Single nucleotide polymorphisms (SNPs) of vascular endothelial growth factor receptor (VEGFR) may have effects on the MAPK/ERK/STAT3 signaling pathway, and the resulting phenotypes may influence the response to sunitinib-targeted therapy for renal cell carcinoma.	Sunitinib	211-220	kinase insert domain receptor	Homo sapiens	42-85
28123542-1	2017	Single nucleotide polymorphisms (SNPs) of vascular endothelial growth factor receptor (VEGFR) may have effects on the MAPK/ERK/STAT3 signaling pathway, and the resulting phenotypes may influence the response to sunitinib-targeted therapy for renal cell carcinoma.	Sunitinib	211-220	kinase insert domain receptor	Homo sapiens	87-92
28123542-1	2017	Single nucleotide polymorphisms (SNPs) of vascular endothelial growth factor receptor (VEGFR) may have effects on the MAPK/ERK/STAT3 signaling pathway, and the resulting phenotypes may influence the response to sunitinib-targeted therapy for renal cell carcinoma.	Sunitinib	211-220	mitogen-activated protein kinase 1	Homo sapiens	123-126
28123542-1	2017	Single nucleotide polymorphisms (SNPs) of vascular endothelial growth factor receptor (VEGFR) may have effects on the MAPK/ERK/STAT3 signaling pathway, and the resulting phenotypes may influence the response to sunitinib-targeted therapy for renal cell carcinoma.	Sunitinib	211-220	signal transducer and activator of transcription 3	Homo sapiens	127-132
28123542-14	2017	VEGFR SNPs are able to mediate the MAPK/ERK/STAT3 signaling pathway and therefore influence the effectiveness of sunitinib-targeted therapy, which makes them possible new therapeutic targets.	Sunitinib	113-122	kinase insert domain receptor	Homo sapiens	0-5
28123542-14	2017	VEGFR SNPs are able to mediate the MAPK/ERK/STAT3 signaling pathway and therefore influence the effectiveness of sunitinib-targeted therapy, which makes them possible new therapeutic targets.	Sunitinib	113-122	mitogen-activated protein kinase 1	Homo sapiens	40-43
28123542-14	2017	VEGFR SNPs are able to mediate the MAPK/ERK/STAT3 signaling pathway and therefore influence the effectiveness of sunitinib-targeted therapy, which makes them possible new therapeutic targets.	Sunitinib	113-122	signal transducer and activator of transcription 3	Homo sapiens	44-49
27974690-4	2016	The specific VHL CNL has not previously been associated with PNET, but has been reported in other tumors and has been associated with response to Sunitinib.	Sunitinib	146-155	von Hippel-Lindau tumor suppressor	Homo sapiens	13-16
28042343-3	2017	In the first mouse model, only sunitinib exhibited broad-spectrum antivascular and antitumor activities by simultaneously suppressing vascular endothelial growth factor receptor-2 (VEGFR2) and desmin expression, and by increasing intratumoral hypoxia and inhibiting both tumor growth and vascularisation significantly.	Sunitinib	31-40	kinase insert domain protein receptor	Mus musculus	134-179
28042343-3	2017	In the first mouse model, only sunitinib exhibited broad-spectrum antivascular and antitumor activities by simultaneously suppressing vascular endothelial growth factor receptor-2 (VEGFR2) and desmin expression, and by increasing intratumoral hypoxia and inhibiting both tumor growth and vascularisation significantly.	Sunitinib	31-40	kinase insert domain protein receptor	Mus musculus	181-187
27873490-7	2017	EGF activated epidermal growth factor receptor (EGFR) and triggered resistance to sunitinib, E7080, vandetanib, and sorafenib by transducing bypass survival signaling through ERK and AKT.	Sunitinib	82-91	epidermal growth factor	Homo sapiens	0-3
27974690-6	2016	To our knowledge, this is the first report of pulmonary PNET with CNL of VHL gene that benefits from Sunitinib treatment.	Sunitinib	101-110	von Hippel-Lindau tumor suppressor	Homo sapiens	73-76
28723497-9	2016	In the sunitinib cohort, the CYP3A4 rs464637 AG variant was associated with a lower risk of high-grade AEs (odds ratio 0.27, 95% confidence interval 0.08-0.88; p=0.03), but no SNPs were associated with hypertension.	Sunitinib	7-16	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	29-35
28723497-11	2016	CONCLUSIONS: We observed an association between CYP3A4 polymorphisms and toxicity outcomes in mRCC patients treated with sunitinib, but not with everolimus or temsirolimus.	Sunitinib	121-130	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	48-54
28723497-13	2016	PATIENT SUMMARY: We found that variants of CYP3A4, a gene involved in drug metabolism, are associated with sunitinib toxicity.	Sunitinib	107-116	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	43-49
27921007-0	2016	Long-term Response to Nivolumab and Acute Renal Failure in a Patient with Metastatic Papillary Renal Cell Carcinoma and a PD-L1 Tumor Expression Increased with Sunitinib Therapy: A Case Report.	Sunitinib	160-169	CD274 molecule	Homo sapiens	122-127
27718781-1	2016	BACKGROUND: Sunitinib, a vascular endothelial growth factor pathway inhibitor, is an effective treatment for metastatic renal-cell carcinoma.	Sunitinib	12-21	vascular endothelial growth factor A	Homo sapiens	25-59
27417418-0	2016	Validation of VEGFR1 rs9582036 as predictive biomarker in metastatic clear-cell renal cell carcinoma patients treated with sunitinib.	Sunitinib	123-132	fms related receptor tyrosine kinase 1	Homo sapiens	14-20
27417418-1	2016	OBJECTIVES: To validate vascular endothelial growth factor receptor-1 (VEGFR1) single nucleotide polymorphism (SNP) rs9582036 as a potential predictive biomarker in metastatic clear-cell renal cell carcinoma (m-ccRCC) patients treated with sunitinib.	Sunitinib	240-249	fms related receptor tyrosine kinase 1	Homo sapiens	24-69
27417418-1	2016	OBJECTIVES: To validate vascular endothelial growth factor receptor-1 (VEGFR1) single nucleotide polymorphism (SNP) rs9582036 as a potential predictive biomarker in metastatic clear-cell renal cell carcinoma (m-ccRCC) patients treated with sunitinib.	Sunitinib	240-249	fms related receptor tyrosine kinase 1	Homo sapiens	71-77
27417418-13	2016	CONCLUSION: VEGFR1 rs9582036 is a candidate predictive biomarker in m-ccRCC-patients treated with sunitinib.	Sunitinib	98-107	fms related receptor tyrosine kinase 1	Homo sapiens	12-18
28008275-5	2016	GISTs with KIT mutations at exon 9 and the so-called wild-type GISTs seem to better respond to sunitinib.	Sunitinib	95-104	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	11-14
28008275-6	2016	Nonetheless, further investigation is required to confirm these findings as well as to understand the mechanisms of sunitinib resistance such as the development of new KIT mutations or conformational changes in KIT receptor.	Sunitinib	116-125	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	168-171
28008275-6	2016	Nonetheless, further investigation is required to confirm these findings as well as to understand the mechanisms of sunitinib resistance such as the development of new KIT mutations or conformational changes in KIT receptor.	Sunitinib	116-125	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	211-214
28105174-11	2016	Thus, sunitinib confers radiosensitivity to esophageal cancer cells, which is associated with the downregulation of HIF-1alpha and VEGF expression.	Sunitinib	6-15	hypoxia inducible factor 1 subunit alpha	Homo sapiens	116-126
28105174-11	2016	Thus, sunitinib confers radiosensitivity to esophageal cancer cells, which is associated with the downregulation of HIF-1alpha and VEGF expression.	Sunitinib	6-15	vascular endothelial growth factor A	Homo sapiens	131-135
27459381-1	2016	Sunitinib and sorafenib are broad-spectrum tyrosine kinase inhibitors (TKI) targeting, for example, VEGF1-3, PDGFRb, RET, FLT3, CD117 (c-KIT) and CSF-1R cell membrane receptors thus suppressing tumor angiogenesis and cancer cell growth.	Sunitinib	0-9	platelet derived growth factor receptor, beta polypeptide	Mus musculus	109-115
27459381-1	2016	Sunitinib and sorafenib are broad-spectrum tyrosine kinase inhibitors (TKI) targeting, for example, VEGF1-3, PDGFRb, RET, FLT3, CD117 (c-KIT) and CSF-1R cell membrane receptors thus suppressing tumor angiogenesis and cancer cell growth.	Sunitinib	0-9	ret proto-oncogene	Mus musculus	117-120
27459381-1	2016	Sunitinib and sorafenib are broad-spectrum tyrosine kinase inhibitors (TKI) targeting, for example, VEGF1-3, PDGFRb, RET, FLT3, CD117 (c-KIT) and CSF-1R cell membrane receptors thus suppressing tumor angiogenesis and cancer cell growth.	Sunitinib	0-9	FMS-like tyrosine kinase 3	Mus musculus	122-126
27459381-1	2016	Sunitinib and sorafenib are broad-spectrum tyrosine kinase inhibitors (TKI) targeting, for example, VEGF1-3, PDGFRb, RET, FLT3, CD117 (c-KIT) and CSF-1R cell membrane receptors thus suppressing tumor angiogenesis and cancer cell growth.	Sunitinib	0-9	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	128-133
27459381-1	2016	Sunitinib and sorafenib are broad-spectrum tyrosine kinase inhibitors (TKI) targeting, for example, VEGF1-3, PDGFRb, RET, FLT3, CD117 (c-KIT) and CSF-1R cell membrane receptors thus suppressing tumor angiogenesis and cancer cell growth.	Sunitinib	0-9	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	135-140
27633584-8	2016	Immunohistochemistry analyses found that both sunitinib (60 mg/kg) and HM-3 (3 and 48 mg/kg) decreased microvascular density and increased percent of HIF-1alpha and VEGF expressing cells.	Sunitinib	46-55	hypoxia inducible factor 1 subunit alpha	Homo sapiens	150-160
27841748-5	2016	Suppressing RET activity using Sunitinib, a clinically-approved tyrosine kinase inhibitor, rescued differentiation in both DUX4-expressing murine myoblasts and in FSHD patient-derived myoblasts.	Sunitinib	31-40	ret proto-oncogene	Mus musculus	12-15
27841748-5	2016	Suppressing RET activity using Sunitinib, a clinically-approved tyrosine kinase inhibitor, rescued differentiation in both DUX4-expressing murine myoblasts and in FSHD patient-derived myoblasts.	Sunitinib	31-40	double homeobox	Mus musculus	123-127
27841748-8	2016	Rescue of DUX4-induced pathology by Sunitinib highlights the therapeutic potential of tyrosine kinase inhibitors for treatment of FSHD.	Sunitinib	36-45	double homeobox	Mus musculus	10-14
27706901-5	2016	These data, together with molecular docking simulations, revealed distinct differences in the impact of structural modifications on drug binding to the enzymes: whereas the catalytic pocket of the epidermal growth factor receptor (EGFR) accepted all new erlotinib derivatives, the vascular endothelial growth factor receptor (VEGFR)-inhibitory potential in the case of the sunitinib prodrugs was dramatically diminished by derivatization.	Sunitinib	373-382	epidermal growth factor receptor	Homo sapiens	197-229
27706901-5	2016	These data, together with molecular docking simulations, revealed distinct differences in the impact of structural modifications on drug binding to the enzymes: whereas the catalytic pocket of the epidermal growth factor receptor (EGFR) accepted all new erlotinib derivatives, the vascular endothelial growth factor receptor (VEGFR)-inhibitory potential in the case of the sunitinib prodrugs was dramatically diminished by derivatization.	Sunitinib	373-382	epidermal growth factor receptor	Homo sapiens	231-235
27793938-0	2016	FoxO3a is Essential for the Antiproliferative and Apoptogenic Effects of Sunitinib in MDA-MB231 Cell Line.	Sunitinib	73-82	forkhead box O3	Homo sapiens	0-6
27930642-4	2016	In a phase 3 adjuvant therapy trial (S-TRAC), sunitinib increased median disease-free survival in patients with clear cell RCC who were at very high risk.	Sunitinib	46-55	T cell receptor alpha constant	Homo sapiens	39-43
27822356-5	2016	However, several molecularly targeted drugs have been proposed as potentially beneficial, including tyrosine kinase inhibitors (TKIs) directed at vascular endothelial growth factor receptor (VEGFR), like pazopanib and sunitinib.	Sunitinib	218-227	kinase insert domain receptor	Homo sapiens	191-196
28133332-6	2016	Mutational analysis revealed a PDGFRA mutation in exon 18, which causes resistance to both imatinib and sunitinib.	Sunitinib	104-113	platelet derived growth factor receptor alpha	Homo sapiens	31-37
27633584-8	2016	Immunohistochemistry analyses found that both sunitinib (60 mg/kg) and HM-3 (3 and 48 mg/kg) decreased microvascular density and increased percent of HIF-1alpha and VEGF expressing cells.	Sunitinib	46-55	vascular endothelial growth factor A	Homo sapiens	165-169
27495788-1	2016	PURPOSE: Pharmacokinetic interaction of sunitinib with diclofenac, paracetamol, mefenamic acid and ibuprofen was evaluated due to their P450 mediated metabolism and OATP1B1, OATP1B3, ABCB1, ABCG2 transporters overlapping features.	Sunitinib	40-49	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	183-188
27560553-0	2016	MEK inhibition abrogates sunitinib resistance in a renal cell carcinoma patient-derived xenograft model.	Sunitinib	25-34	mitogen-activated protein kinase kinase 7	Homo sapiens	0-3
26416414-7	2016	No difference was found in patients treated with sunitinib (P = 0.370).A second line with sunitinib was associated with an improved TTP in KIT exon 11 mutated patients progressing on imatinib 400 mg/die.	Sunitinib	90-99	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	139-142
27920695-5	2016	We report two individuals with metastatic ASPS who obtained disease stabilization from sunitinib lasting over a year.	Sunitinib	87-96	ASPSCR1 tether for SLC2A4, UBX domain containing	Homo sapiens	42-46
27495788-1	2016	PURPOSE: Pharmacokinetic interaction of sunitinib with diclofenac, paracetamol, mefenamic acid and ibuprofen was evaluated due to their P450 mediated metabolism and OATP1B1, OATP1B3, ABCB1, ABCG2 transporters overlapping features.	Sunitinib	40-49	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	190-195
27525572-9	2016	Also, sunitinib dose dependently reduced collagen- and ADP-induced aggregation, collagen-dependent thrombus formation and collagen-induced secretion of platelet-derived growth factor and beta-thromboglobulin.	Sunitinib	6-15	pro-platelet basic protein	Homo sapiens	187-207
27450971-2	2016	The first-generation FLT3 inhibitors were developed several years ago and include midostaurin, lestaurtinib, sunitinib, and sorafenib.	Sunitinib	109-118	fms related receptor tyrosine kinase 3	Homo sapiens	21-25
27525572-13	2016	CONCLUSIONS: Sunitinib uptake by platelets inhibits collagen receptor-induced aggregation and thrombus formation via reduction of protein tyrosine phosphorylation and alpha-granule secretion.	Sunitinib	13-22	integrin subunit alpha 2	Homo sapiens	52-69
27432152-8	2016	Tumorsphere formation is one of the indicators of aggressiveness in malignant cancers, which was significantly inhibited in IMR-32 cells after L1-CAM KD or Sutent treatment, however, no synergistic effect was observed with dual treatments, rather L1-CAM KD alone showed a greater inhibition on tumorsphere formation compared to Sutent treatment alone.	Sunitinib	328-334	L1 cell adhesion molecule	Homo sapiens	143-149
26755746-8	2016	Of interest, VEGF inhibition with drugs like sunitinib, applied in cancer patients, results in a PE-like syndrome, characterized by hypertension, proteinuria and renal toxicity.	Sunitinib	45-54	vascular endothelial growth factor A	Homo sapiens	13-17
26755746-9	2016	Both in cancer patients treated with sunitinib and in pregnant women with PE, significant rises in endothelin-1 occur.	Sunitinib	37-46	endothelin 1	Homo sapiens	99-111
27733829-12	2016	The sequence Sunitinib-Axitinib was well-tolerated without worsening in side effects, with a median OS of 34.7 months (95% CI 18.4-51.0 months).	Sunitinib	13-22	Moloney sarcoma oncogene	Mus musculus	100-102
27686636-3	2016	Results: The levels of CD3+ , CD8+ T lymphocyte, NK cell, B lymphocyte were significantly increased after the therapy of Sunitinib for 1 cycle(I-J was 212+-22, 163+-18, 59+-12, 13.8+-1.4, respectively, all P&lt;0.05).	Sunitinib	121-130	CD8a molecule	Homo sapiens	30-33
27686636-4	2016	The levels of CD3+ , CD8+ T lymphocyte, NK cell, B lymphocyte were significantly increased after the therapy of Sunitinib for 2 cycles(I-J was 362+-43, 299+-28, 91+-19, 28.1+-3.9, respectively, all P&lt;0.05), while the level of CD4+ lymphocyte was decreased, but no significant difference(F=0.873, P&gt;0.05).	Sunitinib	112-121	CD8a molecule	Homo sapiens	21-24
27686636-4	2016	The levels of CD3+ , CD8+ T lymphocyte, NK cell, B lymphocyte were significantly increased after the therapy of Sunitinib for 2 cycles(I-J was 362+-43, 299+-28, 91+-19, 28.1+-3.9, respectively, all P&lt;0.05), while the level of CD4+ lymphocyte was decreased, but no significant difference(F=0.873, P&gt;0.05).	Sunitinib	112-121	CD4 molecule	Homo sapiens	229-232
27686636-5	2016	CD4+ /CD8+ was significantly decreased after the therapy of Sunitinib for 1 cycle, and it went on decreasing after the therapy of Sunitinib for 2 cycles(I-J was -0.31+-0.03, -0.44+-0.04, respectively, all P&lt;0.05).	Sunitinib	60-69	CD4 molecule	Homo sapiens	0-3
27686636-5	2016	CD4+ /CD8+ was significantly decreased after the therapy of Sunitinib for 1 cycle, and it went on decreasing after the therapy of Sunitinib for 2 cycles(I-J was -0.31+-0.03, -0.44+-0.04, respectively, all P&lt;0.05).	Sunitinib	60-69	CD8a molecule	Homo sapiens	6-9
27686636-5	2016	CD4+ /CD8+ was significantly decreased after the therapy of Sunitinib for 1 cycle, and it went on decreasing after the therapy of Sunitinib for 2 cycles(I-J was -0.31+-0.03, -0.44+-0.04, respectively, all P&lt;0.05).	Sunitinib	130-139	CD4 molecule	Homo sapiens	0-3
27506945-8	2016	Compared with HR-negative tumor, HR-positive tumor had significantly better response to sunitinib (p = 0.035).	Sunitinib	88-97	nuclear receptor subfamily 4 group A member 1	Homo sapiens	33-35
27556517-0	2016	Adrenomedullin blockade suppresses sunitinib-resistant renal cell carcinoma growth by targeting the ERK/MAPK pathway.	Sunitinib	35-44	mitogen-activated protein kinase 1	Mus musculus	100-103
27556517-0	2016	Adrenomedullin blockade suppresses sunitinib-resistant renal cell carcinoma growth by targeting the ERK/MAPK pathway.	Sunitinib	35-44	mitogen-activated protein kinase 1	Mus musculus	104-108
27556517-3	2016	And adrenomedullin expression was increased in sunitinib-resistant tumor xenografts, accompanied by upregulation of phospho-ERK levels.	Sunitinib	47-56	mitogen-activated protein kinase 1	Mus musculus	124-127
27164264-9	2016	Sensitive markers for sunitinib therapy include KDR positivity and early-developed treatment-induced hypertension.	Sunitinib	22-31	kinase insert domain receptor	Homo sapiens	48-51
27164264-10	2016	Resistance factors for sunitinib include VEGF positivity, CAIX positivity and squamous cell carcinoma pathology type.	Sunitinib	23-32	carbonic anhydrase 9	Homo sapiens	58-62
27487138-8	2016	Ubiquitin-like with PHD and ring finger domains 1 (UHRF1) was directly suppressed by miR-101 in RCC cells, and overexpression of UHRF1 was confirmed in sunitinib-treated RCC tissues.	Sunitinib	152-161	ubiquitin like with PHD and ring finger domains 1	Homo sapiens	0-49
27487138-8	2016	Ubiquitin-like with PHD and ring finger domains 1 (UHRF1) was directly suppressed by miR-101 in RCC cells, and overexpression of UHRF1 was confirmed in sunitinib-treated RCC tissues.	Sunitinib	152-161	ubiquitin like with PHD and ring finger domains 1	Homo sapiens	51-56
27487138-8	2016	Ubiquitin-like with PHD and ring finger domains 1 (UHRF1) was directly suppressed by miR-101 in RCC cells, and overexpression of UHRF1 was confirmed in sunitinib-treated RCC tissues.	Sunitinib	152-161	ubiquitin like with PHD and ring finger domains 1	Homo sapiens	129-134
27487138-10	2016	Our findings showed that antitumor miR-101- mediated UHRF1 pathways may be suppressed by sunitinib treatment.	Sunitinib	89-98	ubiquitin like with PHD and ring finger domains 1	Homo sapiens	53-58
27288242-0	2016	The tyrosine kinase inhibitor, sunitinib malate, induces cognitive impairment in vivo via dysregulating VEGFR signaling, apoptotic and autophagic machineries.	Sunitinib	31-47	kinase insert domain receptor	Homo sapiens	104-109
26597115-1	2016	PURPOSE: This study aimed to clarify the molecular mechanism mediating the cytotoxicity of axitinib, a selective inhibitor of the vascular endothelial growth factor receptor (VEGFR), in sunitinib-resistant renal cell carcinoma (RCC).	Sunitinib	186-195	kinase insert domain receptor	Homo sapiens	130-173
26597115-1	2016	PURPOSE: This study aimed to clarify the molecular mechanism mediating the cytotoxicity of axitinib, a selective inhibitor of the vascular endothelial growth factor receptor (VEGFR), in sunitinib-resistant renal cell carcinoma (RCC).	Sunitinib	186-195	kinase insert domain receptor	Homo sapiens	175-180
27485537-0	2016	BSA and ABCB1 polymorphism affect the pharmacokinetics of sunitinib and its active metabolite in Asian mRCC patients receiving an attenuated sunitinib dosing regimen.	Sunitinib	58-67	ATP binding cassette subfamily B member 1	Homo sapiens	8-13
27485537-7	2016	RESULTS: Sunitinib population means for CL/F and V d /F central were 13.8 L/h and 1720 L, respectively.	Sunitinib	9-18	CLQTL1	Homo sapiens	40-52
27485537-9	2016	Body surface area (BSA) and ABCB1 polymorphism significantly influenced the CL/F variability of sunitinib: CL/F parent = 13.8 x exp((BSA - 1.75) x 2.08 + (ABCB1 genotype - 0.67) x 0.61), ABCB1-0: wild genotype, 1: mutant genotype.	Sunitinib	96-105	ATP binding cassette subfamily B member 1	Homo sapiens	28-33
27485537-9	2016	Body surface area (BSA) and ABCB1 polymorphism significantly influenced the CL/F variability of sunitinib: CL/F parent = 13.8 x exp((BSA - 1.75) x 2.08 + (ABCB1 genotype - 0.67) x 0.61), ABCB1-0: wild genotype, 1: mutant genotype.	Sunitinib	96-105	ATP binding cassette subfamily B member 1	Homo sapiens	155-160
27485537-9	2016	Body surface area (BSA) and ABCB1 polymorphism significantly influenced the CL/F variability of sunitinib: CL/F parent = 13.8 x exp((BSA - 1.75) x 2.08 + (ABCB1 genotype - 0.67) x 0.61), ABCB1-0: wild genotype, 1: mutant genotype.	Sunitinib	96-105	ATP binding cassette subfamily B member 1	Homo sapiens	155-160
27485537-10	2016	The effect size of ABCB1 mutant genotype and BSA greater than 1.75 m(2) in relation to sunitinib clearance was 31.14 % (p = 0.006) and 22.11 % (p = 0.011), respectively, relative to the reference group.	Sunitinib	87-96	ATP binding cassette subfamily B member 1	Homo sapiens	19-24
27485537-11	2016	CONCLUSIONS: Adjusting doses of sunitinib according to BSA and ABCB1 polymorphism in Asian mRCC patients may be recommended for sufficient attainment of a target TTL of sunitinib and its metabolite.	Sunitinib	32-41	ATP binding cassette subfamily B member 1	Homo sapiens	63-68
27288242-11	2016	Besides, sunitinib boosted cortical and hippocampal p53 and executioner caspase-3 and decreased nuclear factor kappa B and Bcl-2 levels promoting apoptotic cell death.	Sunitinib	9-18	tumor protein p53	Homo sapiens	52-55
27288242-11	2016	Besides, sunitinib boosted cortical and hippocampal p53 and executioner caspase-3 and decreased nuclear factor kappa B and Bcl-2 levels promoting apoptotic cell death.	Sunitinib	9-18	caspase 3	Homo sapiens	72-81
27288242-11	2016	Besides, sunitinib boosted cortical and hippocampal p53 and executioner caspase-3 and decreased nuclear factor kappa B and Bcl-2 levels promoting apoptotic cell death.	Sunitinib	9-18	BCL2 apoptosis regulator	Homo sapiens	123-128
27288242-13	2016	To our knowledge, this is the first study to provide molecular insights into sunitinib-induced chemofog where impeded VEGFR2 signaling and autophagic and hyperactivated apoptotic machineries act in neurodegenerative concert.	Sunitinib	77-86	kinase insert domain receptor	Homo sapiens	118-124
27485825-1	2016	The von Hippel-Lindau tumor suppressor (VHL; E3 ubiquitin ligase gene) is frequently mutated or undetectable in clear cell renal cell carcinoma (CCRCC), and therefore these tumors are highly resistant to chemotherapeutic agents, including adriamycin (ADM) and sunitinib.	Sunitinib	260-269	von Hippel-Lindau tumor suppressor	Homo sapiens	40-43
27602218-0	2016	GLI2 expression levels in radical nephrectomy specimens as a predictor of disease progression in patients with metastatic clear cell renal cell carcinoma following treatment with sunitinib.	Sunitinib	179-188	GLI family zinc finger 2	Homo sapiens	0-4
27485825-1	2016	The von Hippel-Lindau tumor suppressor (VHL; E3 ubiquitin ligase gene) is frequently mutated or undetectable in clear cell renal cell carcinoma (CCRCC), and therefore these tumors are highly resistant to chemotherapeutic agents, including adriamycin (ADM) and sunitinib.	Sunitinib	260-269	Cbl proto-oncogene like 2	Homo sapiens	45-64
27485825-5	2016	The expression of VHL in the MZ1257 cell line sensitized these cells to ADM and sunitinib, and a knockdown of VHL in the ACHN cells increased their chemoresistance.	Sunitinib	80-89	von Hippel-Lindau tumor suppressor	Homo sapiens	18-21
27602218-6	2016	Furthermore, treatment with sunitinib resulted in a marked inhibition of GLI2 expression in the parental human RCC ACHN cell line, but not in ACHN cells with acquired resistance to sunitinib.	Sunitinib	28-37	GLI family zinc finger 2	Homo sapiens	73-77
27602218-7	2016	These findings suggested that GLI2 may be involved in the acquisition of resistance to sunitinib in RCC; thus, it may be useful to consider the expression levels of GLI2 in addition to conventional prognostic parameters when selecting m-ccRCC patients likely to benefit from treatment with sunitinib.	Sunitinib	87-96	GLI family zinc finger 2	Homo sapiens	30-34
27485825-9	2016	Further analysis indicated that co-expression of VHL and P53 inhibited cell proliferation by completely inhibiting the cell cycle at the G0/G1 phase, and promoted apoptosis following treatment with ADM or sunitinib.	Sunitinib	205-214	von Hippel-Lindau tumor suppressor	Homo sapiens	49-52
27485825-9	2016	Further analysis indicated that co-expression of VHL and P53 inhibited cell proliferation by completely inhibiting the cell cycle at the G0/G1 phase, and promoted apoptosis following treatment with ADM or sunitinib.	Sunitinib	205-214	tumor protein p53	Homo sapiens	57-60
29263493-0	2016	[Sunitinib induces autophagy via suppressing Akt/mTOR pathway in renal cell carcinoma].	Sunitinib	1-10	AKT serine/threonine kinase 1	Homo sapiens	45-48
27235791-6	2016	Regarding the studied antifibrotics, gene levels of HSP47 and PCOL1A1 could be down-regulated with sunitinib and valproic acid, while PCOL1A1 expression was reduced following treatment with rosmarinic acid, tetrandrine and pirfenidone.	Sunitinib	99-108	serpin family H member 1	Homo sapiens	52-57
27297795-6	2016	Examination of the underlying mechanisms indicated that venetoclax resistance may be induced by microenvironmental signals that upregulate antiapoptotic Bcl-xl, Mcl-1, and A1, which can be counteracted more efficiently by sunitinib than by ibrutinib or idelalisib.	Sunitinib	222-231	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	161-166
27580750-4	2016	Discontinuation of an anti-VEGF antibody-based drug and sunitinib markedly promotes liver metastasis.	Sunitinib	56-65	vascular endothelial growth factor A	Homo sapiens	27-31
29263493-0	2016	[Sunitinib induces autophagy via suppressing Akt/mTOR pathway in renal cell carcinoma].	Sunitinib	1-10	mechanistic target of rapamycin kinase	Homo sapiens	49-53
29263493-14	2016	The rapamycin (mTOR inhibitor) or knocking down Akt subunits could change the sunitinib-induced LC3 -II accumulation, whereas overexpression of Akt subunits decreased the autophagic flux, indicating that Akt/mTOR was the target of sunitinib in autophagy.	Sunitinib	78-87	mechanistic target of rapamycin kinase	Homo sapiens	208-212
29263493-10	2016	And the nuclear-to-cytosol translocation as well as aggregation of LC3-II was presented after sunitinib treatment by the fluorescence microscope, which was the proof of the enhanced autophagy.	Sunitinib	94-103	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	67-70
29263493-14	2016	The rapamycin (mTOR inhibitor) or knocking down Akt subunits could change the sunitinib-induced LC3 -II accumulation, whereas overexpression of Akt subunits decreased the autophagic flux, indicating that Akt/mTOR was the target of sunitinib in autophagy.	Sunitinib	231-240	mechanistic target of rapamycin kinase	Homo sapiens	208-212
29263493-15	2016	CONCLUSION: Sunitinib induced autophagy via suppressing Akt/mTOR pathway, and the autophagy was involved in apopotosis.	Sunitinib	12-21	AKT serine/threonine kinase 1	Homo sapiens	56-59
29263493-11	2016	According to the immunoblotting, sunitinib was able to increase the accumulation of LC3-II .	Sunitinib	33-42	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	84-87
29263493-15	2016	CONCLUSION: Sunitinib induced autophagy via suppressing Akt/mTOR pathway, and the autophagy was involved in apopotosis.	Sunitinib	12-21	mechanistic target of rapamycin kinase	Homo sapiens	60-64
29263493-12	2016	At the same time, the result of sunitinib combined with chloroquine, a drug which blocked the fusion of autophagosomes and lysosomes, demonstrated that the increasing amount of LC3-II was due to the enhanced autophagy flux by sunitinib treatment in ACHN cells.	Sunitinib	32-41	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	177-180
29263494-11	2016	CONCLUSION: MEK/ERK signaling pathways may play an important role in the metastasis and the resistance of sunitinib in RCC patients with bone metastasis.	Sunitinib	106-115	mitogen-activated protein kinase kinase 7	Homo sapiens	12-15
29263493-12	2016	At the same time, the result of sunitinib combined with chloroquine, a drug which blocked the fusion of autophagosomes and lysosomes, demonstrated that the increasing amount of LC3-II was due to the enhanced autophagy flux by sunitinib treatment in ACHN cells.	Sunitinib	226-235	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	177-180
29263494-11	2016	CONCLUSION: MEK/ERK signaling pathways may play an important role in the metastasis and the resistance of sunitinib in RCC patients with bone metastasis.	Sunitinib	106-115	mitogen-activated protein kinase 1	Homo sapiens	16-19
29263493-14	2016	The rapamycin (mTOR inhibitor) or knocking down Akt subunits could change the sunitinib-induced LC3 -II accumulation, whereas overexpression of Akt subunits decreased the autophagic flux, indicating that Akt/mTOR was the target of sunitinib in autophagy.	Sunitinib	78-87	mechanistic target of rapamycin kinase	Homo sapiens	15-19
29263493-14	2016	The rapamycin (mTOR inhibitor) or knocking down Akt subunits could change the sunitinib-induced LC3 -II accumulation, whereas overexpression of Akt subunits decreased the autophagic flux, indicating that Akt/mTOR was the target of sunitinib in autophagy.	Sunitinib	78-87	AKT serine/threonine kinase 1	Homo sapiens	48-51
29263493-14	2016	The rapamycin (mTOR inhibitor) or knocking down Akt subunits could change the sunitinib-induced LC3 -II accumulation, whereas overexpression of Akt subunits decreased the autophagic flux, indicating that Akt/mTOR was the target of sunitinib in autophagy.	Sunitinib	78-87	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	96-99
27016208-0	2016	Schedule-dependent cytotoxicity of sunitinib and TRAIL in human non-small cell lung cancer cells with or without EGFR and KRAS mutations.	Sunitinib	35-44	epidermal growth factor receptor	Homo sapiens	113-117
27046396-0	2016	Sunitinib, a Clinically Used Anticancer Drug, Is a Potent AChE Inhibitor and Attenuates Cognitive Impairments in Mice.	Sunitinib	0-9	acetylcholinesterase	Mus musculus	58-62
27046396-2	2016	In this study, we found for the first time that sunitinib inhibits acetylcholinesterase (AChE) at submicromolar concentrations in vitro.	Sunitinib	48-57	acetylcholinesterase	Mus musculus	67-87
27046396-2	2016	In this study, we found for the first time that sunitinib inhibits acetylcholinesterase (AChE) at submicromolar concentrations in vitro.	Sunitinib	48-57	acetylcholinesterase	Mus musculus	89-93
27046396-3	2016	In addition, sunitinib dramatically decreased the hippocampal and cortical activity of AChE in a time-dependent manner in mice.	Sunitinib	13-22	acetylcholinesterase	Mus musculus	87-91
27046396-4	2016	Molecular docking analysis further demonstrates that sunitinib might interact with both the catalytic anion and peripheral anionic sites within AChE, which is in accordance with enzymatic activity results showing that sunitinib inhibits AChE in a mixed pattern.	Sunitinib	53-62	acetylcholinesterase	Mus musculus	144-148
27046396-4	2016	Molecular docking analysis further demonstrates that sunitinib might interact with both the catalytic anion and peripheral anionic sites within AChE, which is in accordance with enzymatic activity results showing that sunitinib inhibits AChE in a mixed pattern.	Sunitinib	53-62	acetylcholinesterase	Mus musculus	237-241
27046396-4	2016	Molecular docking analysis further demonstrates that sunitinib might interact with both the catalytic anion and peripheral anionic sites within AChE, which is in accordance with enzymatic activity results showing that sunitinib inhibits AChE in a mixed pattern.	Sunitinib	218-227	acetylcholinesterase	Mus musculus	144-148
27046396-4	2016	Molecular docking analysis further demonstrates that sunitinib might interact with both the catalytic anion and peripheral anionic sites within AChE, which is in accordance with enzymatic activity results showing that sunitinib inhibits AChE in a mixed pattern.	Sunitinib	218-227	acetylcholinesterase	Mus musculus	237-241
27046396-6	2016	Surprisingly, sunitinib could attenuate cognitive impairments to a similar extent as donepezil, a marketed AChE inhibitor used for the treatment of Alzheimer"s disease.	Sunitinib	14-23	acetylcholinesterase	Mus musculus	107-111
27046396-7	2016	In summary, our results have shown that sunitinib could potently inhibit AChE and attenuate cognitive impairments in mice.	Sunitinib	40-49	acetylcholinesterase	Mus musculus	73-77
27488093-6	2016	Namely high HIF-2alpha, CD31, and CAIX expression levels along with low VEGFR1 and PDGFRB expression levels improved the benefit of sunitinib treatment compared with sorafenib treatment.	Sunitinib	132-141	carbonic anhydrase 9	Homo sapiens	34-38
27488093-6	2016	Namely high HIF-2alpha, CD31, and CAIX expression levels along with low VEGFR1 and PDGFRB expression levels improved the benefit of sunitinib treatment compared with sorafenib treatment.	Sunitinib	132-141	fms related receptor tyrosine kinase 1	Homo sapiens	72-78
27488093-6	2016	Namely high HIF-2alpha, CD31, and CAIX expression levels along with low VEGFR1 and PDGFRB expression levels improved the benefit of sunitinib treatment compared with sorafenib treatment.	Sunitinib	132-141	platelet derived growth factor receptor beta	Homo sapiens	83-89
27488093-5	2016	We found that patients with high HIF-2alpha, CD31 expression showed greater relative PFS and OS benefit and patients with high CAIX expression presented greater relative OS benefit from sunitinib than from sorafenib, patients with high VEGFR1 or PDGFRB expression levels exhibited worse relative PFS benefit from sunitinib than from sorafenib.	Sunitinib	186-195	carbonic anhydrase 9	Homo sapiens	127-131
27488093-6	2016	Namely high HIF-2alpha, CD31, and CAIX expression levels along with low VEGFR1 and PDGFRB expression levels improved the benefit of sunitinib treatment compared with sorafenib treatment.	Sunitinib	132-141	endothelial PAS domain protein 1	Homo sapiens	12-22
27488093-6	2016	Namely high HIF-2alpha, CD31, and CAIX expression levels along with low VEGFR1 and PDGFRB expression levels improved the benefit of sunitinib treatment compared with sorafenib treatment.	Sunitinib	132-141	platelet and endothelial cell adhesion molecule 1	Homo sapiens	24-28
27016208-7	2016	We found that sunitinib enhances TRAIL-induced G0/G1-phase cell cycle arrest and blocks TRAIL-triggered activation of AKT as the underlying mechanism.	Sunitinib	14-23	TNF superfamily member 10	Homo sapiens	33-38
27016208-7	2016	We found that sunitinib enhances TRAIL-induced G0/G1-phase cell cycle arrest and blocks TRAIL-triggered activation of AKT as the underlying mechanism.	Sunitinib	14-23	TNF superfamily member 10	Homo sapiens	88-93
27016208-7	2016	We found that sunitinib enhances TRAIL-induced G0/G1-phase cell cycle arrest and blocks TRAIL-triggered activation of AKT as the underlying mechanism.	Sunitinib	14-23	AKT serine/threonine kinase 1	Homo sapiens	118-121
27016208-8	2016	In contrast, we observed antagonistic effects when sunitinib was administered after TRAIL to the cell lines tested.	Sunitinib	51-60	TNF superfamily member 10	Homo sapiens	84-89
27016208-10	2016	CONCLUSION: From our data we conclude that administration of sunitinib followed by TRAIL, as well as a simultaneous administration of both agents, serve as favorable treatment regimens for NSCLC-derived cells, irrespective of their EGFR and/or KRAS mutation status.	Sunitinib	61-70	KRAS proto-oncogene, GTPase	Homo sapiens	244-248
27374084-4	2016	We showed that Ela-myc pancreatic tumors express PDGFR and VEGFR in blood vessels and epithelial cells, rendering these tumors sensitive to sunitinib by more than only its anti-angiogenic activity.	Sunitinib	140-149	platelet derived growth factor receptor, beta polypeptide	Mus musculus	49-54
27123883-7	2016	Potential activity of VEGF (vascular endothelial growth factor) inhibitors such as sunitinib, valatinib, and bevacizumab is suggested in small non-controlled studies and requires validation in randomized trials.	Sunitinib	83-92	vascular endothelial growth factor A	Homo sapiens	22-26
27123883-7	2016	Potential activity of VEGF (vascular endothelial growth factor) inhibitors such as sunitinib, valatinib, and bevacizumab is suggested in small non-controlled studies and requires validation in randomized trials.	Sunitinib	83-92	vascular endothelial growth factor A	Homo sapiens	28-62
27439438-12	2016	Moreover, sunitinib reduced the degree of phosphorylation of serine residues on Smad2/3 that was induced by TGF-beta in HBEs.	Sunitinib	10-19	SMAD family member 2	Mus musculus	80-87
27374084-5	2016	However, sunitinib treatment of Ela-myc mice with either early or advanced tumor progression had no impact on either survival or tumor burden.	Sunitinib	9-18	apelin receptor early endogenous ligand	Mus musculus	32-35
27374084-7	2016	In stark contrast, in vitro sunitinib treatment of Ela-myc- derived cell lines showed high sensitivity to the drug, with increased apoptosis and reduced proliferation.	Sunitinib	28-37	apelin receptor early endogenous ligand	Mus musculus	51-54
27304187-8	2016	Finally, we also found that PDGFRB is one of the components of a complex that includes Beclin 1 and VPS34.The results of these tissue-based analyses provide new insights into sunitinib"s mechanism of action in SFT patients.	Sunitinib	175-184	platelet derived growth factor receptor beta	Homo sapiens	28-34
27304187-8	2016	Finally, we also found that PDGFRB is one of the components of a complex that includes Beclin 1 and VPS34.The results of these tissue-based analyses provide new insights into sunitinib"s mechanism of action in SFT patients.	Sunitinib	175-184	beclin 1	Homo sapiens	87-95
27304187-8	2016	Finally, we also found that PDGFRB is one of the components of a complex that includes Beclin 1 and VPS34.The results of these tissue-based analyses provide new insights into sunitinib"s mechanism of action in SFT patients.	Sunitinib	175-184	phosphatidylinositol 3-kinase catalytic subunit type 3	Homo sapiens	100-105
27181063-7	2016	Although the patient had refractory disease after salvage therapy for the second relapse, treatment with the FLT3 inhibitor sunitinib rapidly induced a near complete molecular response, permitting the patient to proceed to a matched-unrelated donor stem cell transplantation.	Sunitinib	124-133	fms related receptor tyrosine kinase 3	Homo sapiens	109-113
27109549-1	2016	Sunitinib malate is a small multi-targeted tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) and stem cell factor receptor (KIT), which are highly expressed by some high-grade brain tumors.	Sunitinib	0-16	kinase insert domain receptor	Homo sapiens	83-126
27109549-1	2016	Sunitinib malate is a small multi-targeted tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) and stem cell factor receptor (KIT), which are highly expressed by some high-grade brain tumors.	Sunitinib	0-16	kinase insert domain receptor	Homo sapiens	128-133
27109549-1	2016	Sunitinib malate is a small multi-targeted tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) and stem cell factor receptor (KIT), which are highly expressed by some high-grade brain tumors.	Sunitinib	0-16	platelet derived growth factor receptor beta	Homo sapiens	136-175
27109549-1	2016	Sunitinib malate is a small multi-targeted tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) and stem cell factor receptor (KIT), which are highly expressed by some high-grade brain tumors.	Sunitinib	0-16	platelet derived growth factor receptor beta	Homo sapiens	177-182
27109549-1	2016	Sunitinib malate is a small multi-targeted tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) and stem cell factor receptor (KIT), which are highly expressed by some high-grade brain tumors.	Sunitinib	0-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	215-218
27109549-9	2016	While there was a statistically significant modulation of plasma VEGFR2 with sunitinib exposure, there were no sustained tumor responses.	Sunitinib	77-86	kinase insert domain receptor	Homo sapiens	65-71
27156227-10	2016	Nine patients (35%) had a best response of stable disease, including two patients who had KIT mutations known to be associated with resistance to imatinib and sunitinib.	Sunitinib	159-168	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-93
27479949-10	2016	Treatment of EHE with VEGF inhibition, potentially in combination with other antiangiogenic and tumor-inhibiting therapies such as lenalidomide, thalidomide, sorafenib, and sunitinib, may also hold promise.	Sunitinib	173-182	vascular endothelial growth factor A	Homo sapiens	22-26
30058926-9	2016	Targeted agents, such as everolimus and sunitinib, have improved PFS in GEP-NET.	Sunitinib	40-49	granulin precursor	Homo sapiens	72-75
27564279-0	2016	Sunitinib treatment in patients with advanced renal cell cancer: the Brazilian National Cancer Institute (INCA) experience.	Sunitinib	0-9	caspase recruitment domain family member 17	Homo sapiens	106-110
27237035-1	2016	BACKGROUND: Sunitinib is a potent oral tyrosine kinase inhibitor of VEGFRs, KIT, and PDGFRs.	Sunitinib	12-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	76-79
27385210-0	2016	Sunitinib enhances the antitumor responses of agonistic CD40-antibody by reducing MDSCs and synergistically improving endothelial activation and T-cell recruitment.	Sunitinib	0-9	CD40 molecule	Homo sapiens	56-60
27385210-4	2016	Treatment of tumor-bearing mice with anti-CD40 mAb led to increased activation of CD11c+ dendritic cells in the tumor draining lymph node, while sunitinib treatment reduced vessel density and decreased accumulation of CD11b+Gr1+ myeloid derived suppressor cells.	Sunitinib	145-154	integrin subunit alpha M	Homo sapiens	218-223
27385210-5	2016	The expression of ICAM-1 and VCAM-1 adhesion molecules was up-regulated on tumor endothelial cells only when anti-CD40 mAb treatment was combined with sunitinib.	Sunitinib	151-160	intercellular adhesion molecule 1	Homo sapiens	18-24
27385210-5	2016	The expression of ICAM-1 and VCAM-1 adhesion molecules was up-regulated on tumor endothelial cells only when anti-CD40 mAb treatment was combined with sunitinib.	Sunitinib	151-160	vascular cell adhesion molecule 1	Homo sapiens	29-35
27385210-7	2016	Our results show that combining CD40-stimulating immunotherapy with sunitinib treatment exerts potent complementary antitumor effects mediated by dendritic cell activation, a reduction in myeloid derived suppressor cells and increased endothelial activation, resulting in enhanced recruitment of cytotoxic T-cells.	Sunitinib	68-77	CD40 molecule	Homo sapiens	32-36
27175586-2	2016	We previously reported how VEGF and VEGFR polymorphisms might have a predictive role in patients treated with first-line sunitinib.	Sunitinib	121-130	vascular endothelial growth factor A	Homo sapiens	27-31
26733173-6	2016	EGCG enhanced the antiproliferation and VEGF secretion-reducing effects of sunitinib in the three tested cell lines.	Sunitinib	75-84	vascular endothelial growth factor A	Homo sapiens	40-44
26733173-8	2016	We further demonstrated that sunitinib exposure induces insulin receptor substrate-1 (IRS-1) upregulation and activation of MAPK signaling.	Sunitinib	29-38	insulin receptor substrate 1	Homo sapiens	56-84
26733173-8	2016	We further demonstrated that sunitinib exposure induces insulin receptor substrate-1 (IRS-1) upregulation and activation of MAPK signaling.	Sunitinib	29-38	insulin receptor substrate 1	Homo sapiens	86-91
27175586-2	2016	We previously reported how VEGF and VEGFR polymorphisms might have a predictive role in patients treated with first-line sunitinib.	Sunitinib	121-130	kinase insert domain receptor	Homo sapiens	36-41
27175586-7	2016	CONCLUSIONS: in our analysis patients with opposite polymorphisms of rs833061, rs2010963, rs699947 of VEGF A seems to have a better PFS if treated with either sunitinib or pazopanib.	Sunitinib	159-168	vascular endothelial growth factor A	Homo sapiens	102-108
27770111-0	2016	Correction: Sunitinib prevents cachexia and prolongs survival of mice bearing renal cancer by restraining STAT3 and MuRF-1 activation in muscle.	Sunitinib	12-21	signal transducer and activator of transcription 3	Mus musculus	106-111
27141054-7	2016	Sunitinib sensitivity correlated with vascular endothelial growth factor (VEGF) production.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	38-72
27770111-0	2016	Correction: Sunitinib prevents cachexia and prolongs survival of mice bearing renal cancer by restraining STAT3 and MuRF-1 activation in muscle.	Sunitinib	12-21	tripartite motif-containing 63	Mus musculus	116-122
26815723-0	2016	Sunitinib activates Axl signaling in renal cell cancer.	Sunitinib	0-9	AXL receptor tyrosine kinase	Homo sapiens	20-23
26815723-7	2016	Compared to control, incubation with sunitinib at its IC50 of 2 microM resulted in downregulation of 86 phosphopeptides including CDK5, DYRK3, DYRK4, G6PD, PKM and LDH-A, while 94 phosphopeptides including Axl, FAK, EPHA2 and p38alpha were upregulated.	Sunitinib	37-46	cyclin dependent kinase 5	Homo sapiens	130-134
26815723-7	2016	Compared to control, incubation with sunitinib at its IC50 of 2 microM resulted in downregulation of 86 phosphopeptides including CDK5, DYRK3, DYRK4, G6PD, PKM and LDH-A, while 94 phosphopeptides including Axl, FAK, EPHA2 and p38alpha were upregulated.	Sunitinib	37-46	dual specificity tyrosine phosphorylation regulated kinase 3	Homo sapiens	136-141
26815723-7	2016	Compared to control, incubation with sunitinib at its IC50 of 2 microM resulted in downregulation of 86 phosphopeptides including CDK5, DYRK3, DYRK4, G6PD, PKM and LDH-A, while 94 phosphopeptides including Axl, FAK, EPHA2 and p38alpha were upregulated.	Sunitinib	37-46	dual specificity tyrosine phosphorylation regulated kinase 4	Homo sapiens	143-148
26815723-7	2016	Compared to control, incubation with sunitinib at its IC50 of 2 microM resulted in downregulation of 86 phosphopeptides including CDK5, DYRK3, DYRK4, G6PD, PKM and LDH-A, while 94 phosphopeptides including Axl, FAK, EPHA2 and p38alpha were upregulated.	Sunitinib	37-46	glucose-6-phosphate dehydrogenase	Homo sapiens	150-154
26815723-7	2016	Compared to control, incubation with sunitinib at its IC50 of 2 microM resulted in downregulation of 86 phosphopeptides including CDK5, DYRK3, DYRK4, G6PD, PKM and LDH-A, while 94 phosphopeptides including Axl, FAK, EPHA2 and p38alpha were upregulated.	Sunitinib	37-46	pyruvate kinase M1/2	Homo sapiens	156-159
26815723-7	2016	Compared to control, incubation with sunitinib at its IC50 of 2 microM resulted in downregulation of 86 phosphopeptides including CDK5, DYRK3, DYRK4, G6PD, PKM and LDH-A, while 94 phosphopeptides including Axl, FAK, EPHA2 and p38alpha were upregulated.	Sunitinib	37-46	lactate dehydrogenase A	Homo sapiens	164-169
26815723-7	2016	Compared to control, incubation with sunitinib at its IC50 of 2 microM resulted in downregulation of 86 phosphopeptides including CDK5, DYRK3, DYRK4, G6PD, PKM and LDH-A, while 94 phosphopeptides including Axl, FAK, EPHA2 and p38alpha were upregulated.	Sunitinib	37-46	AXL receptor tyrosine kinase	Homo sapiens	206-209
26815723-7	2016	Compared to control, incubation with sunitinib at its IC50 of 2 microM resulted in downregulation of 86 phosphopeptides including CDK5, DYRK3, DYRK4, G6PD, PKM and LDH-A, while 94 phosphopeptides including Axl, FAK, EPHA2 and p38alpha were upregulated.	Sunitinib	37-46	protein tyrosine kinase 2	Homo sapiens	211-214
26815723-7	2016	Compared to control, incubation with sunitinib at its IC50 of 2 microM resulted in downregulation of 86 phosphopeptides including CDK5, DYRK3, DYRK4, G6PD, PKM and LDH-A, while 94 phosphopeptides including Axl, FAK, EPHA2 and p38alpha were upregulated.	Sunitinib	37-46	EPH receptor A2	Homo sapiens	216-221
26815723-7	2016	Compared to control, incubation with sunitinib at its IC50 of 2 microM resulted in downregulation of 86 phosphopeptides including CDK5, DYRK3, DYRK4, G6PD, PKM and LDH-A, while 94 phosphopeptides including Axl, FAK, EPHA2 and p38alpha were upregulated.	Sunitinib	37-46	mitogen-activated protein kinase 14	Homo sapiens	226-234
26815723-9	2016	Subsequent proliferation assays revealed that inhibition of Axl with a small molecule inhibitor (R428) sensitized 786-O RCC cells and immortalized endothelial cells to sunitinib up to 3 fold.	Sunitinib	168-177	AXL receptor tyrosine kinase	Homo sapiens	60-63
27141054-7	2016	Sunitinib sensitivity correlated with vascular endothelial growth factor (VEGF) production.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	74-78
26815723-10	2016	In conclusion, incubation with sunitinib of RCC cells causes significant upregulation of multiple phosphopeptides including Axl.	Sunitinib	31-40	AXL receptor tyrosine kinase	Homo sapiens	124-127
26815723-11	2016	Simultaneous inhibition of Axl improves the antitumor activity of sunitinib.	Sunitinib	66-75	AXL receptor tyrosine kinase	Homo sapiens	27-30
27141054-8	2016	RCC induced paracrine extracellular signal-regulated kinase (ERK) activation in EC which was inhibited by sunitinib in sensitive but not in resistant tumors.	Sunitinib	106-115	mitogen-activated protein kinase 1	Homo sapiens	22-59
27141054-8	2016	RCC induced paracrine extracellular signal-regulated kinase (ERK) activation in EC which was inhibited by sunitinib in sensitive but not in resistant tumors.	Sunitinib	106-115	mitogen-activated protein kinase 1	Homo sapiens	61-64
27141054-11	2016	Our data show that RCC activates EC through VEGF-dependent and -independent pathways, that sunitinib sensitivity correlates with VEGF-mediated ERK activation, and that combined inhibition of VEGF/PDGF/FGF receptors is sufficient to inhibit mitogenic signaling in EC but not in fibroblasts.	Sunitinib	91-100	vascular endothelial growth factor A	Homo sapiens	129-133
27141054-11	2016	Our data show that RCC activates EC through VEGF-dependent and -independent pathways, that sunitinib sensitivity correlates with VEGF-mediated ERK activation, and that combined inhibition of VEGF/PDGF/FGF receptors is sufficient to inhibit mitogenic signaling in EC but not in fibroblasts.	Sunitinib	91-100	mitogen-activated protein kinase 1	Homo sapiens	143-146
27141054-11	2016	Our data show that RCC activates EC through VEGF-dependent and -independent pathways, that sunitinib sensitivity correlates with VEGF-mediated ERK activation, and that combined inhibition of VEGF/PDGF/FGF receptors is sufficient to inhibit mitogenic signaling in EC but not in fibroblasts.	Sunitinib	91-100	vascular endothelial growth factor A	Homo sapiens	129-133
27103123-1	2016	PURPOSE: Sirolimus, an oral mTOR inhibitor, may complement the anti-angiogenic and anti-tumor activity of sunitinib, an oral small molecule inhibitor of multiple receptor tyrosine kinases, by vertical disruption of vascular epithelial growth factor receptor (VEGFR) signaling, by reducing the compensatory production of VEGF in sunitinib-treated patients and also by directly inhibiting tumor cell proliferation.	Sunitinib	106-115	mechanistic target of rapamycin kinase	Homo sapiens	28-32
27103123-1	2016	PURPOSE: Sirolimus, an oral mTOR inhibitor, may complement the anti-angiogenic and anti-tumor activity of sunitinib, an oral small molecule inhibitor of multiple receptor tyrosine kinases, by vertical disruption of vascular epithelial growth factor receptor (VEGFR) signaling, by reducing the compensatory production of VEGF in sunitinib-treated patients and also by directly inhibiting tumor cell proliferation.	Sunitinib	106-115	kinase insert domain receptor	Homo sapiens	215-257
27103123-1	2016	PURPOSE: Sirolimus, an oral mTOR inhibitor, may complement the anti-angiogenic and anti-tumor activity of sunitinib, an oral small molecule inhibitor of multiple receptor tyrosine kinases, by vertical disruption of vascular epithelial growth factor receptor (VEGFR) signaling, by reducing the compensatory production of VEGF in sunitinib-treated patients and also by directly inhibiting tumor cell proliferation.	Sunitinib	106-115	kinase insert domain receptor	Homo sapiens	259-264
27103123-1	2016	PURPOSE: Sirolimus, an oral mTOR inhibitor, may complement the anti-angiogenic and anti-tumor activity of sunitinib, an oral small molecule inhibitor of multiple receptor tyrosine kinases, by vertical disruption of vascular epithelial growth factor receptor (VEGFR) signaling, by reducing the compensatory production of VEGF in sunitinib-treated patients and also by directly inhibiting tumor cell proliferation.	Sunitinib	106-115	vascular endothelial growth factor A	Homo sapiens	259-263
27149458-6	2016	Gene mutations in the genes encoding EGFR, FGFR2, KDR, and RET were discovered in the patient"s tumor tissue by whole exome sequencing and the patient was treated with a combination of the targeted drugs cetuximab and sunitinib.	Sunitinib	218-227	epidermal growth factor receptor	Homo sapiens	37-41
27300260-5	2016	The results suggest that 1) active drug concentration (i.e., sunitinib and its metabolite) inhibits the release of sVEGFR2 and that such inhibition is associated with TGI, and 2) daily sVEGFR2 exposure is likely a reliable predictor for the TTP in HCC patients.	Sunitinib	61-70	ZFP36 ring finger protein	Homo sapiens	241-244
26626617-7	2016	At final analysis, mOS was 16.2 and 14.9 mo with sunitinib and everolimus, respectively (p=0.18).	Sunitinib	49-58	Moloney sarcoma oncogene	Mus musculus	19-22
26626617-9	2016	In patients without sarcomatoid features in their tumors (n=49), mOS was 31.6 mo with sunitinib and 10.5 mo with everolimus (p=0.075).	Sunitinib	86-95	Moloney sarcoma oncogene	Mus musculus	65-68
26681729-0	2016	Effect of high salt diet on blood pressure and renal damage during vascular endothelial growth factor inhibition with sunitinib.	Sunitinib	118-127	vascular endothelial growth factor A	Rattus norvegicus	67-101
26681729-1	2016	BACKGROUND: Antiangiogenic treatment with the multitargeted vascular endothelial growth factor (VEGF) receptor inhibitor sunitinib associates with a blood pressure (BP) rise and glomerular renal injury.	Sunitinib	121-130	vascular endothelial growth factor A	Rattus norvegicus	60-94
26681729-1	2016	BACKGROUND: Antiangiogenic treatment with the multitargeted vascular endothelial growth factor (VEGF) receptor inhibitor sunitinib associates with a blood pressure (BP) rise and glomerular renal injury.	Sunitinib	121-130	vascular endothelial growth factor A	Rattus norvegicus	96-100
27117758-4	2016	lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells.	Sunitinib	17-26	microRNA 34a	Homo sapiens	64-70
27117758-4	2016	lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells.	Sunitinib	17-26	AXL receptor tyrosine kinase	Homo sapiens	93-96
27117758-4	2016	lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells.	Sunitinib	17-26	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-106
27117758-6	2016	Treatment of sunitinib-resistant RCC with locked nucleic acids targeting lncARSR or an AXL/c-MET inhibitor restored sunitinib response.	Sunitinib	13-22	AXL receptor tyrosine kinase	Homo sapiens	87-90
27117758-6	2016	Treatment of sunitinib-resistant RCC with locked nucleic acids targeting lncARSR or an AXL/c-MET inhibitor restored sunitinib response.	Sunitinib	116-125	AXL receptor tyrosine kinase	Homo sapiens	87-90
27117758-6	2016	Treatment of sunitinib-resistant RCC with locked nucleic acids targeting lncARSR or an AXL/c-MET inhibitor restored sunitinib response.	Sunitinib	116-125	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	91-96
27149458-6	2016	Gene mutations in the genes encoding EGFR, FGFR2, KDR, and RET were discovered in the patient"s tumor tissue by whole exome sequencing and the patient was treated with a combination of the targeted drugs cetuximab and sunitinib.	Sunitinib	218-227	fibroblast growth factor receptor 2	Homo sapiens	43-48
27149458-6	2016	Gene mutations in the genes encoding EGFR, FGFR2, KDR, and RET were discovered in the patient"s tumor tissue by whole exome sequencing and the patient was treated with a combination of the targeted drugs cetuximab and sunitinib.	Sunitinib	218-227	kinase insert domain receptor	Homo sapiens	50-53
27149458-6	2016	Gene mutations in the genes encoding EGFR, FGFR2, KDR, and RET were discovered in the patient"s tumor tissue by whole exome sequencing and the patient was treated with a combination of the targeted drugs cetuximab and sunitinib.	Sunitinib	218-227	ret proto-oncogene	Homo sapiens	59-62
26959741-7	2016	PKM2 was also found to determine the sensitivity of targeted drugs, such as sorafenib, brivanib, and sunitinib, by SHP-1 activation.	Sunitinib	101-110	pyruvate kinase M1/2	Homo sapiens	0-4
26434595-4	2016	describe the mechanisms linking Axl and Met activation to acquired resistance to sunitinib in renal cell carcinoma (RCC), providing a pre-clinical rationale for the development of Axl and Met inhibitors including cabozantinib in anti-angiogenic resistant RCC.	Sunitinib	81-90	AXL receptor tyrosine kinase	Homo sapiens	180-183
27077705-2	2016	Clinically used c-KIT kinase inhibitors, i.e., Imatinib and Sunitinib, bear other important targets such as ABL or FLT3 kinases.	Sunitinib	60-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	16-21
27100185-0	2016	Association of Angiopoietin-2 and Ki-67 Expression with Vascular Density and Sunitinib Response in Metastatic Renal Cell Carcinoma.	Sunitinib	77-86	angiopoietin 2	Homo sapiens	15-29
27100185-5	2016	Ang2 protein expression was restrained to RCC tumour vessels, and correlated with tumour vascularization and response to sunitinib.	Sunitinib	121-130	angiopoietin 2	Homo sapiens	0-4
27100185-8	2016	In summary, in this study to investigate endothelial Ang2 in mRCC patients treated with first-line sunitinib, high cancer Ang2 expression was associated with the CBR, but not PFS or OS, whereas low Ki-67 expression was significantly associated with long PFS and OS.	Sunitinib	99-108	angiopoietin 2	Homo sapiens	53-57
26364599-0	2016	Targeting MET and AXL overcomes resistance to sunitinib therapy in renal cell carcinoma.	Sunitinib	46-55	AXL receptor tyrosine kinase	Homo sapiens	18-21
26364599-3	2016	We hypothesized that sunitinib-induced upregulation of the prometastatic MET and AXL receptors is associated with resistance to sunitinib and with more aggressive tumor behavior.	Sunitinib	21-30	AXL receptor tyrosine kinase	Homo sapiens	81-84
26364599-3	2016	We hypothesized that sunitinib-induced upregulation of the prometastatic MET and AXL receptors is associated with resistance to sunitinib and with more aggressive tumor behavior.	Sunitinib	128-137	AXL receptor tyrosine kinase	Homo sapiens	81-84
26364599-10	2016	Chronic sunitinib treatment of RCC cell lines activated both AXL and MET, induced EMT-associated gene expression changes, including upregulation of Snail and beta-catenin, and increased cell migration and invasion.	Sunitinib	8-17	AXL receptor tyrosine kinase	Homo sapiens	61-64
26364599-10	2016	Chronic sunitinib treatment of RCC cell lines activated both AXL and MET, induced EMT-associated gene expression changes, including upregulation of Snail and beta-catenin, and increased cell migration and invasion.	Sunitinib	8-17	catenin beta 1	Homo sapiens	158-170
26364599-12	2016	The suppression of AXL or MET expression and the inhibition of AXL and MET activation using cabozantinib both impaired chronic sunitinib treatment-induced prometastatic behavior in cell culture and rescued acquired resistance to sunitinib in xenograft models.	Sunitinib	127-136	AXL receptor tyrosine kinase	Homo sapiens	63-66
26364599-12	2016	The suppression of AXL or MET expression and the inhibition of AXL and MET activation using cabozantinib both impaired chronic sunitinib treatment-induced prometastatic behavior in cell culture and rescued acquired resistance to sunitinib in xenograft models.	Sunitinib	229-238	AXL receptor tyrosine kinase	Homo sapiens	63-66
26364599-13	2016	In summary, chronic sunitinib treatment induces the activation of AXL and MET signaling and promotes prometastatic behavior and angiogenesis.	Sunitinib	20-29	AXL receptor tyrosine kinase	Homo sapiens	66-69
26364599-14	2016	The inhibition of AXL and MET activity may overcome resistance induced by prolonged sunitinib therapy in metastatic RCC.	Sunitinib	84-93	AXL receptor tyrosine kinase	Homo sapiens	18-21
26959741-7	2016	PKM2 was also found to determine the sensitivity of targeted drugs, such as sorafenib, brivanib, and sunitinib, by SHP-1 activation.	Sunitinib	101-110	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	115-120
26934000-5	2016	The combination of the ERBB1/2/4 inhibitor afatinib with the SRC family inhibitor dasatinib killed afatinib resistant H1975 cells in a greater than additive fashion; other drugs used in combination with dasatinib such as sunitinib, crizotinib and amufatinib were less effective.	Sunitinib	221-230	epidermal growth factor receptor	Homo sapiens	23-32
26447463-0	2016	The early effect of sunitinib on insulin clearance in patients with metastatic renal cell carcinoma.	Sunitinib	20-29	insulin	Homo sapiens	33-40
26896780-3	2016	In this study, protein-ligand interactions between FLT3 and kinase inhibitors (CEP701, PKC412, sunitinib, imatinib and dasatinib) were obtained through homology modelling and molecular docking.	Sunitinib	95-104	FMS-like tyrosine kinase 3	Mus musculus	51-55
26896780-6	2016	CEP701, PKC412 and sunitinib interacted with the ATP-binding pocket of FLT3, forming H-bonds with Cys694 and Glu692.	Sunitinib	19-28	FMS-like tyrosine kinase 3	Mus musculus	71-75
26896780-9	2016	The potency of sunitinib and to a lesser extent CEP701 in inhibition of FLT3 autophosphorylation was lower than the cell proliferation inhibition, indicating that inhibition of FLT3 downstream proteins may contribute to the cellular effects.	Sunitinib	15-24	FMS-like tyrosine kinase 3	Mus musculus	72-76
26896780-9	2016	The potency of sunitinib and to a lesser extent CEP701 in inhibition of FLT3 autophosphorylation was lower than the cell proliferation inhibition, indicating that inhibition of FLT3 downstream proteins may contribute to the cellular effects.	Sunitinib	15-24	FMS-like tyrosine kinase 3	Mus musculus	177-181
26912111-1	2016	Sunitinib (Sutent ) is a receptor tyrosine kinase (RTK) and angiogenesis inhibitor approved for the treatment of renal cell carcinomas, gastrointestinal stromal tumours and pancreatic neuroendocrine tumours.	Sunitinib	0-9	erb-b2 receptor tyrosine kinase 4	Rattus norvegicus	25-49
26912111-1	2016	Sunitinib (Sutent ) is a receptor tyrosine kinase (RTK) and angiogenesis inhibitor approved for the treatment of renal cell carcinomas, gastrointestinal stromal tumours and pancreatic neuroendocrine tumours.	Sunitinib	0-9	erb-b2 receptor tyrosine kinase 4	Rattus norvegicus	51-54
26912111-1	2016	Sunitinib (Sutent ) is a receptor tyrosine kinase (RTK) and angiogenesis inhibitor approved for the treatment of renal cell carcinomas, gastrointestinal stromal tumours and pancreatic neuroendocrine tumours.	Sunitinib	11-17	erb-b2 receptor tyrosine kinase 4	Rattus norvegicus	25-49
26912111-1	2016	Sunitinib (Sutent ) is a receptor tyrosine kinase (RTK) and angiogenesis inhibitor approved for the treatment of renal cell carcinomas, gastrointestinal stromal tumours and pancreatic neuroendocrine tumours.	Sunitinib	11-17	erb-b2 receptor tyrosine kinase 4	Rattus norvegicus	51-54
26447463-2	2016	To explore the mechanism of this adverse effect we performed a prospective study to investigate the effect of sunitinib on insulin concentration, insulin clearance and insulin sensitivity.	Sunitinib	110-119	insulin	Homo sapiens	123-130
26447463-6	2016	Steady-state insulin concentrations during the clamp increased after 1 week of sunitinib (from 128.9 +- 9.0 mU l-1 to 170.8 +- 12.8 mU l-1, P &lt; 0.05; 95% CI on difference - 64.3, -19.6).	Sunitinib	79-88	insulin	Homo sapiens	13-20
26447463-9	2016	CONCLUSION: Sunitinib affects insulin clearance which could possibly lead to overexposure to insulin in patients using insulin or insulin-secretion stimulating agents.	Sunitinib	12-21	insulin	Homo sapiens	30-37
26447463-9	2016	CONCLUSION: Sunitinib affects insulin clearance which could possibly lead to overexposure to insulin in patients using insulin or insulin-secretion stimulating agents.	Sunitinib	12-21	insulin	Homo sapiens	93-100
26447463-9	2016	CONCLUSION: Sunitinib affects insulin clearance which could possibly lead to overexposure to insulin in patients using insulin or insulin-secretion stimulating agents.	Sunitinib	12-21	insulin	Homo sapiens	93-100
26447463-9	2016	CONCLUSION: Sunitinib affects insulin clearance which could possibly lead to overexposure to insulin in patients using insulin or insulin-secretion stimulating agents.	Sunitinib	12-21	insulin	Homo sapiens	93-100
27031198-1	2016	In metastatic ccRCC , the treatment options in 1st line treatment are still the tyrosinkinase inhibitors (TKI) pazopanib and sunitinib, for patients with low or intermediate risk additionally IFNalpha/bevacizumab and for high risk patients the mTOR inhibitor temsirolimus.	Sunitinib	125-134	mechanistic target of rapamycin kinase	Homo sapiens	244-248
27453754-4	2016	Sunitinib represents an inhibitor of VEGFR 1-3, c-kit, FLT-3 and PDGFR.	Sunitinib	0-9	fms related receptor tyrosine kinase 1	Homo sapiens	37-46
27453754-4	2016	Sunitinib represents an inhibitor of VEGFR 1-3, c-kit, FLT-3 and PDGFR.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-53
27453754-4	2016	Sunitinib represents an inhibitor of VEGFR 1-3, c-kit, FLT-3 and PDGFR.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	55-60
27453754-4	2016	Sunitinib represents an inhibitor of VEGFR 1-3, c-kit, FLT-3 and PDGFR.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	65-70
27073655-4	2016	A patient with a c-kit mutation-positive thymic carcinoma received imatinib followed by sunitinib consecutively, which are both c-Kit inhibitors.	Sunitinib	88-97	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-22
27073655-4	2016	A patient with a c-kit mutation-positive thymic carcinoma received imatinib followed by sunitinib consecutively, which are both c-Kit inhibitors.	Sunitinib	88-97	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	128-133
27034725-2	2016	Improvements in response rates and survival, with more manageable side effects compared with interleukin 2/interferon immunotherapy, have been reported with the use of targeted therapy agents, including vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitors (sunitinib, sorafenib, pazopanib, axitinib), mammalian target of rapamycin (mTOR) inhibitors (everolimus and temsirolimus) and VEGF receptor antibodies (bevacizumab).	Sunitinib	282-291	vascular endothelial growth factor A	Homo sapiens	203-237
27035144-4	2016	Sunitinib exposure significantly reduced (i) corpora lutea number per ovary (1.1 +- 0.38 in sunitinib group versus 4 +- 0.79 in control group, p&lt;0.01) and (ii) serum Anti Mullerian hormone (AMH) levels in sunitinib treated mice (12.01 +- 1.16) compared to control mice (14.33 +- 0.87 ng/ml, p&lt; 0.05).	Sunitinib	0-9	anti-Mullerian hormone	Mus musculus	193-196
27053605-8	2016	CONCLUSION: Sunitinib inhibits the expressions of CD80, PD-L1 and B7-H4 on DCs induced by LPS.	Sunitinib	12-21	CD80 molecule	Homo sapiens	50-54
27053605-8	2016	CONCLUSION: Sunitinib inhibits the expressions of CD80, PD-L1 and B7-H4 on DCs induced by LPS.	Sunitinib	12-21	CD274 molecule	Homo sapiens	56-61
27053605-7	2016	Compared with the LPS-treated group, the expressions of CD80, PD-L1 and B7-H4 on DCs significantly decreased in the sunitinib-LPS group; the expressions of PD-L1, PD-L2, CD80, CD86, B7-H4 and HVEM were lower in the DMSO group.	Sunitinib	116-125	CD80 molecule	Homo sapiens	56-60
27053605-7	2016	Compared with the LPS-treated group, the expressions of CD80, PD-L1 and B7-H4 on DCs significantly decreased in the sunitinib-LPS group; the expressions of PD-L1, PD-L2, CD80, CD86, B7-H4 and HVEM were lower in the DMSO group.	Sunitinib	116-125	CD274 molecule	Homo sapiens	62-67
27053605-7	2016	Compared with the LPS-treated group, the expressions of CD80, PD-L1 and B7-H4 on DCs significantly decreased in the sunitinib-LPS group; the expressions of PD-L1, PD-L2, CD80, CD86, B7-H4 and HVEM were lower in the DMSO group.	Sunitinib	116-125	CD274 molecule	Homo sapiens	156-161
27053605-7	2016	Compared with the LPS-treated group, the expressions of CD80, PD-L1 and B7-H4 on DCs significantly decreased in the sunitinib-LPS group; the expressions of PD-L1, PD-L2, CD80, CD86, B7-H4 and HVEM were lower in the DMSO group.	Sunitinib	116-125	programmed cell death 1 ligand 2	Homo sapiens	163-168
27053605-7	2016	Compared with the LPS-treated group, the expressions of CD80, PD-L1 and B7-H4 on DCs significantly decreased in the sunitinib-LPS group; the expressions of PD-L1, PD-L2, CD80, CD86, B7-H4 and HVEM were lower in the DMSO group.	Sunitinib	116-125	CD80 molecule	Homo sapiens	170-174
27053605-7	2016	Compared with the LPS-treated group, the expressions of CD80, PD-L1 and B7-H4 on DCs significantly decreased in the sunitinib-LPS group; the expressions of PD-L1, PD-L2, CD80, CD86, B7-H4 and HVEM were lower in the DMSO group.	Sunitinib	116-125	CD86 molecule	Homo sapiens	176-180
27053605-7	2016	Compared with the LPS-treated group, the expressions of CD80, PD-L1 and B7-H4 on DCs significantly decreased in the sunitinib-LPS group; the expressions of PD-L1, PD-L2, CD80, CD86, B7-H4 and HVEM were lower in the DMSO group.	Sunitinib	116-125	TNF receptor superfamily member 14	Homo sapiens	192-196
27034725-2	2016	Improvements in response rates and survival, with more manageable side effects compared with interleukin 2/interferon immunotherapy, have been reported with the use of targeted therapy agents, including vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitors (sunitinib, sorafenib, pazopanib, axitinib), mammalian target of rapamycin (mTOR) inhibitors (everolimus and temsirolimus) and VEGF receptor antibodies (bevacizumab).	Sunitinib	282-291	vascular endothelial growth factor A	Homo sapiens	239-243
26786874-5	2016	We show that frequencies of monocytic CD14(+)HLA-DR(-/low) MDSCs derived from mature monocytes were significantly and dose-dependently reduced in the presence of dasatinib, nilotinib and sorafenib, whereas sunitinib had no effect.	Sunitinib	206-215	CD14 molecule	Homo sapiens	38-42
26923603-1	2016	Autocrine VEGF signaling is critical for sustaining prostate and other cancer stem cells (CSCs), and it is a potential therapeutic target, but we observed that CSCs isolated from prostate tumors are resistant to anti-VEGF (bevacizumab) and anti-VEGFR (sunitinib) therapy.	Sunitinib	252-261	vascular endothelial growth factor A	Homo sapiens	10-14
26832420-2	2016	Oral tyrosine kinase inhibitors (TKI) targeting the VEGF receptor, including sunitinib, sorafenib, axitinib, regorafenib, pazopanib, and vandetanib reduce tumor growth and metastasis.	Sunitinib	77-86	vascular endothelial growth factor A	Homo sapiens	52-56
26914831-0	2016	Association Study of a Functional Variant on ABCG2 Gene with Sunitinib-Induced Severe Adverse Drug Reaction.	Sunitinib	61-70	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	45-50
26359568-0	2016	Combined Treatment With 131I-MIBG and Sunitinib Induces Remission in a Patient With Metastatic Paraganglioma Due to Hereditary Paraganglioma-Pheochromocytoma Syndrome From an SDHB Mutation.	Sunitinib	38-47	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	175-179
26914831-3	2016	This study is to investigate the association of a functional germline variant on ABCG2 that affects the pharmacokinetics of sunitinib with sunitinib-induced toxicity of RCC patients in the Japanese population.	Sunitinib	124-133	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	81-86
26914831-3	2016	This study is to investigate the association of a functional germline variant on ABCG2 that affects the pharmacokinetics of sunitinib with sunitinib-induced toxicity of RCC patients in the Japanese population.	Sunitinib	139-148	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	81-86
26914831-8	2016	In the univariate analysis, both age (P = 7.77x10(-3), odds ratio (OR) = 1.04, 95%CI = 1.01-1.07) and ABCG2 421C&gt;A (P = 1.87x10(-2), OR = 1.71, 95%CI = 1.09-2.68) showed association with sunitinib-induced severe thrombocytopenia.	Sunitinib	190-199	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	102-107
26914831-12	2016	ABCG2 421C&gt;A could explain part of the inter-individual variability of sunitinib-induced severe thrombocytopenia.	Sunitinib	74-83	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
27538132-0	2016	[Sunitinib induces autophagy via suppressing Akt/mTOR pathway in renal cell carcinoma].	Sunitinib	1-10	AKT serine/threonine kinase 1	Homo sapiens	45-48
27538132-0	2016	[Sunitinib induces autophagy via suppressing Akt/mTOR pathway in renal cell carcinoma].	Sunitinib	1-10	mechanistic target of rapamycin kinase	Homo sapiens	49-53
27538132-10	2016	And the nuclear-to-cytosol translocation as well as aggregation of LC3-II was presented after sunitinib treatment by the fluorescence microscope, which was the proof of the enhanced autophagy.	Sunitinib	94-103	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	67-70
27538132-11	2016	According to the immunoblotting, sunitinib was able to increase the accumulation of LC3-II .	Sunitinib	33-42	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	84-87
27538132-12	2016	At the same time, the result of sunitinib combined with chloroquine, a drug which blocked the fusion of autophagosomes and lysosomes, demonstrated that the increasing amount of LC3-II was due to the enhanced autophagy flux by sunitinib treatment in ACHN cells.	Sunitinib	32-41	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	177-180
27538132-12	2016	At the same time, the result of sunitinib combined with chloroquine, a drug which blocked the fusion of autophagosomes and lysosomes, demonstrated that the increasing amount of LC3-II was due to the enhanced autophagy flux by sunitinib treatment in ACHN cells.	Sunitinib	226-235	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	177-180
27538132-14	2016	The rapamycin (mTOR inhibitor) or knocking down Akt subunits could change the sunitinib-induced LC3 -II accumulation, whereas overexpression of Akt subunits decreased the autophagic flux, indicating that Akt/mTOR was the target of sunitinib in autophagy.	Sunitinib	78-87	mechanistic target of rapamycin kinase	Homo sapiens	15-19
27538132-14	2016	The rapamycin (mTOR inhibitor) or knocking down Akt subunits could change the sunitinib-induced LC3 -II accumulation, whereas overexpression of Akt subunits decreased the autophagic flux, indicating that Akt/mTOR was the target of sunitinib in autophagy.	Sunitinib	78-87	AKT serine/threonine kinase 1	Homo sapiens	48-51
27538132-14	2016	The rapamycin (mTOR inhibitor) or knocking down Akt subunits could change the sunitinib-induced LC3 -II accumulation, whereas overexpression of Akt subunits decreased the autophagic flux, indicating that Akt/mTOR was the target of sunitinib in autophagy.	Sunitinib	78-87	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	96-99
27538132-14	2016	The rapamycin (mTOR inhibitor) or knocking down Akt subunits could change the sunitinib-induced LC3 -II accumulation, whereas overexpression of Akt subunits decreased the autophagic flux, indicating that Akt/mTOR was the target of sunitinib in autophagy.	Sunitinib	78-87	mechanistic target of rapamycin kinase	Homo sapiens	208-212
27538132-14	2016	The rapamycin (mTOR inhibitor) or knocking down Akt subunits could change the sunitinib-induced LC3 -II accumulation, whereas overexpression of Akt subunits decreased the autophagic flux, indicating that Akt/mTOR was the target of sunitinib in autophagy.	Sunitinib	231-240	mechanistic target of rapamycin kinase	Homo sapiens	208-212
27538132-15	2016	CONCLUSION: Sunitinib induced autophagy via suppressing Akt/mTOR pathway, and the autophagy was involved in apopotosis.	Sunitinib	12-21	AKT serine/threonine kinase 1	Homo sapiens	56-59
27538132-15	2016	CONCLUSION: Sunitinib induced autophagy via suppressing Akt/mTOR pathway, and the autophagy was involved in apopotosis.	Sunitinib	12-21	mechanistic target of rapamycin kinase	Homo sapiens	60-64
27538133-11	2016	CONCLUSION: MEK/ERK signaling pathways may play an important role in the metastasis and the resistance of sunitinib in RCC patients with bone metastasis.	Sunitinib	106-115	mitogen-activated protein kinase kinase 7	Homo sapiens	12-15
27538133-11	2016	CONCLUSION: MEK/ERK signaling pathways may play an important role in the metastasis and the resistance of sunitinib in RCC patients with bone metastasis.	Sunitinib	106-115	mitogen-activated protein kinase 1	Homo sapiens	16-19
26831065-3	2016	Aberrant platelet-derived growth factor receptor beta (PDGFRbeta) signaling in cancer has motivated the development of several antagonists currently in clinical use, including imatinib, sunitinib, and sorafenib.	Sunitinib	186-195	platelet derived growth factor receptor beta	Homo sapiens	9-53
26831065-3	2016	Aberrant platelet-derived growth factor receptor beta (PDGFRbeta) signaling in cancer has motivated the development of several antagonists currently in clinical use, including imatinib, sunitinib, and sorafenib.	Sunitinib	186-195	platelet derived growth factor receptor beta	Homo sapiens	55-64
26893877-5	2016	Sunitinib is suggested to have preventive effects on the pathogenesis of liver fibrosis and cirrhosis in vitro, via an anti-vascular endothelial growth factor and anti-platelet-derived growth factor mechanism.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	124-158
26540173-6	2016	Sunitinib was the most common VEGF-targeted therapy (77%), and it was followed by sorafenib (18.4%).	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	30-34
26375012-8	2016	RESULTS: Sunitinib suppressed multiple in vitro gain-in-functions of Nf1(+/-) mast cells and fibroblasts and attenuated Erk1/2 phosphorylation.	Sunitinib	9-18	neurofibromin 1	Mus musculus	69-72
26375012-8	2016	RESULTS: Sunitinib suppressed multiple in vitro gain-in-functions of Nf1(+/-) mast cells and fibroblasts and attenuated Erk1/2 phosphorylation.	Sunitinib	9-18	mitogen-activated protein kinase 3	Mus musculus	120-126
26375012-9	2016	Sunitinib treated Krox20;Nf1(flox/-) mice exhibited significant reductions in pNF size, tumor number, and FDG uptake compared to control mice.	Sunitinib	0-9	early growth response 2	Mus musculus	18-24
25778465-0	2016	Effect of the CYP3A5 and ABCB1 genotype on exposure, clinical response and manifestation of toxicities from sunitinib in Asian patients.	Sunitinib	108-117	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	14-20
26375012-3	2016	Sunitinib malate is a potent, highly selective RTK inhibitor with activity against c-Kit, PDGFR, and VEGFR, which have also been implicated in the pathogenesis of these lesions.	Sunitinib	0-16	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	83-88
26375012-3	2016	Sunitinib malate is a potent, highly selective RTK inhibitor with activity against c-Kit, PDGFR, and VEGFR, which have also been implicated in the pathogenesis of these lesions.	Sunitinib	0-16	platelet derived growth factor receptor, beta polypeptide	Mus musculus	90-95
26375012-9	2016	Sunitinib treated Krox20;Nf1(flox/-) mice exhibited significant reductions in pNF size, tumor number, and FDG uptake compared to control mice.	Sunitinib	0-9	neurofibromin 1	Mus musculus	25-28
26375012-5	2016	EXPERIMENTAL DESIGN: Proliferation, beta-hexosaminidase release (degranulation), and Erk1/2 phosphorylation were assessed in sunitinib treated Nf1(+/-) mast cells and fibroblasts, respectively.	Sunitinib	125-134	neurofibromin 1	Mus musculus	143-146
25778465-0	2016	Effect of the CYP3A5 and ABCB1 genotype on exposure, clinical response and manifestation of toxicities from sunitinib in Asian patients.	Sunitinib	108-117	ATP binding cassette subfamily B member 1	Homo sapiens	25-30
25778465-1	2016	The objective of this study was to determine the effect of the CYP3A5 and ATP binding cassette subfamily B member 1 (ABCB1) single-nucleotide polymorphisms on the disposition of sunitinib and SU12662, on clinical response, and on the manifestation of toxicities in Asian metastatic renal cell carcinoma patients.	Sunitinib	178-187	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	63-69
25778465-1	2016	The objective of this study was to determine the effect of the CYP3A5 and ATP binding cassette subfamily B member 1 (ABCB1) single-nucleotide polymorphisms on the disposition of sunitinib and SU12662, on clinical response, and on the manifestation of toxicities in Asian metastatic renal cell carcinoma patients.	Sunitinib	178-187	ATP binding cassette subfamily B member 1	Homo sapiens	74-115
26375012-11	2016	CONCLUSIONS: Collectively, these results demonstrate the efficacy of sunitinib in reducing tumor burden in Krox20;Nf1(flox/-) mice.	Sunitinib	69-78	early growth response 2	Mus musculus	107-113
25778465-1	2016	The objective of this study was to determine the effect of the CYP3A5 and ATP binding cassette subfamily B member 1 (ABCB1) single-nucleotide polymorphisms on the disposition of sunitinib and SU12662, on clinical response, and on the manifestation of toxicities in Asian metastatic renal cell carcinoma patients.	Sunitinib	178-187	ATP binding cassette subfamily B member 1	Homo sapiens	117-122
25778465-5	2016	The CC genotype for ABCB1 was associated with a higher sunitinib exposure (76.81 vs 56.55 ng ml(-1), P=0.03), higher risk of all-grade rash (RR 3.00, 95% CI 1.17-7.67) and mucositis (RR 1.60, 95% CI 1.10-2.34) and disease progression than compared with the CT/TT genotype.	Sunitinib	55-64	ATP binding cassette subfamily B member 1	Homo sapiens	20-25
26375012-11	2016	CONCLUSIONS: Collectively, these results demonstrate the efficacy of sunitinib in reducing tumor burden in Krox20;Nf1(flox/-) mice.	Sunitinib	69-78	neurofibromin 1	Mus musculus	114-117
26312563-9	2016	S100P knockdown also promoted CCA cell apoptosis by up-regulating expression of apoptosis related factors, DR5, TRADD, caspase 3 and BAX, and increased the sensitivity of CCA cells to the chemotherapeutic agents sunitinib and apigenin.	Sunitinib	212-221	S100 calcium binding protein P	Homo sapiens	0-5
26772734-0	2016	Correlation of KIT and PDGFRA mutational status with clinical benefit in patients with gastrointestinal stromal tumor treated with sunitinib in a worldwide treatment-use trial.	Sunitinib	131-140	platelet derived growth factor receptor alpha	Homo sapiens	23-29
26772734-1	2016	BACKGROUND: Several small studies indicated that the genotype of KIT or platelet-derived growth factor receptor-alpha (PDGFRA) contributes in part to the level of clinical effectiveness of sunitinib in gastrointestinal stromal tumor (GIST) patients.	Sunitinib	189-198	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	65-68
26772734-1	2016	BACKGROUND: Several small studies indicated that the genotype of KIT or platelet-derived growth factor receptor-alpha (PDGFRA) contributes in part to the level of clinical effectiveness of sunitinib in gastrointestinal stromal tumor (GIST) patients.	Sunitinib	189-198	platelet derived growth factor receptor alpha	Homo sapiens	72-117
26772734-1	2016	BACKGROUND: Several small studies indicated that the genotype of KIT or platelet-derived growth factor receptor-alpha (PDGFRA) contributes in part to the level of clinical effectiveness of sunitinib in gastrointestinal stromal tumor (GIST) patients.	Sunitinib	189-198	platelet derived growth factor receptor alpha	Homo sapiens	119-125
26772734-10	2016	The data available were limited to investigate the effects of additional KIT or PDGFRA mutations on the efficacy of sunitinib treatment.	Sunitinib	116-125	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
26772734-10	2016	The data available were limited to investigate the effects of additional KIT or PDGFRA mutations on the efficacy of sunitinib treatment.	Sunitinib	116-125	platelet derived growth factor receptor alpha	Homo sapiens	80-86
26239999-3	2016	Here, we report that a remarkably synergistic antitumor responses elicited by the combined treatment of Sunitinib and an agonistic antibody against glucocorticoid-induced TNFR related protein (GITR) in a model of metastatic renal cell carcinoma.	Sunitinib	104-113	tumor necrosis factor receptor superfamily, member 18	Mus musculus	148-191
25864572-7	2016	RESULTS: VEGFR-2 mRNA expression levels (DeltaCt, median, min-max) were reduced in the everolimus 1.0 (0.25-1.81) and sunitinib 1.06 (0.24-2.68) treated groups compared with the control 4.74 (1.02-14.74) and DMSO groups 7.41 (0.72-13.10).	Sunitinib	118-127	kinase insert domain receptor	Rattus norvegicus	9-16
26239999-3	2016	Here, we report that a remarkably synergistic antitumor responses elicited by the combined treatment of Sunitinib and an agonistic antibody against glucocorticoid-induced TNFR related protein (GITR) in a model of metastatic renal cell carcinoma.	Sunitinib	104-113	tumor necrosis factor receptor superfamily, member 18	Mus musculus	193-197
26239999-4	2016	Sunitinib significantly increased the infiltration, activation, and proliferation and/or cytotoxicity of CD8(+) T cells and NK cells in liver metastatic foci when combined with the anti (alpha)-GITR agonist, which was associated with treatment-induced prominent upregulation of Th1-biased immune genes in the livers from mice receiving combined therapy versus single treatment.	Sunitinib	0-9	tumor necrosis factor receptor superfamily, member 18	Mus musculus	194-198
26239999-5	2016	Sunitinib/alpha-GITR treatment also markedly promoted the maturation, activation and cytokine production of liver-resident macrophages and DCs compared with that achieved by alpha-GITR or Sunitinib treatment alone in mice.	Sunitinib	0-9	tumor necrosis factor receptor superfamily, member 18	Mus musculus	180-184
26569132-10	2016	Moreover, treatment with bFGF enhanced cell growth and the PDGF-BB-induced migratory activity of cultured pericytes, which were significantly suppressed by SU5402 or Sunitinib, an inhibitor of PDGFR.	Sunitinib	166-175	fibroblast growth factor 2	Homo sapiens	25-29
26569132-10	2016	Moreover, treatment with bFGF enhanced cell growth and the PDGF-BB-induced migratory activity of cultured pericytes, which were significantly suppressed by SU5402 or Sunitinib, an inhibitor of PDGFR.	Sunitinib	166-175	platelet derived growth factor receptor beta	Homo sapiens	193-198
26439451-1	2016	BACKGROUND: Sorafenib and sunitinib are oral vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) approved in 2005 and 2006, respectively, for the treatment of patients with renal cell carcinoma (RCC).	Sunitinib	26-35	kinase insert domain receptor	Homo sapiens	45-88
26439451-1	2016	BACKGROUND: Sorafenib and sunitinib are oral vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) approved in 2005 and 2006, respectively, for the treatment of patients with renal cell carcinoma (RCC).	Sunitinib	26-35	kinase insert domain receptor	Homo sapiens	90-95
25701259-0	2016	FGF2 Prevents Sunitinib-Induced Cardiotoxicity in Zebrafish and Cardiomyoblast H9c2 Cells.	Sunitinib	14-23	fibroblast growth factor 2	Danio rerio	0-4
25701259-4	2016	Here, we reported that the injection of fibroblast growth factor 2 (FGF2) mRNA into one- to two-cell stage embryos protected against sunitinib-induced cardiotoxicity in zebrafish.	Sunitinib	133-142	fibroblast growth factor 2	Danio rerio	40-66
25701259-4	2016	Here, we reported that the injection of fibroblast growth factor 2 (FGF2) mRNA into one- to two-cell stage embryos protected against sunitinib-induced cardiotoxicity in zebrafish.	Sunitinib	133-142	fibroblast growth factor 2	Danio rerio	68-72
25701259-5	2016	In addition, FGF2 significantly prevented sunitinib-induced cardiotoxicity in cardiomyoblast H9c2 cells, possibly via activating the PLC-gamma/c-Raf/CREB pathway.	Sunitinib	42-51	fibroblast growth factor 2	Rattus norvegicus	13-17
25701259-5	2016	In addition, FGF2 significantly prevented sunitinib-induced cardiotoxicity in cardiomyoblast H9c2 cells, possibly via activating the PLC-gamma/c-Raf/CREB pathway.	Sunitinib	42-51	Raf-1 proto-oncogene, serine/threonine kinase	Rattus norvegicus	143-148
25701259-5	2016	In addition, FGF2 significantly prevented sunitinib-induced cardiotoxicity in cardiomyoblast H9c2 cells, possibly via activating the PLC-gamma/c-Raf/CREB pathway.	Sunitinib	42-51	cAMP responsive element binding protein 1	Rattus norvegicus	149-153
25701259-7	2016	Molecular docking simulations further revealed an interaction between the tyrosine kinase domain of FGF receptor 1 (FGFR1) and sunitinib.	Sunitinib	127-136	Fibroblast growth factor receptor 1	Rattus norvegicus	100-114
25701259-7	2016	Molecular docking simulations further revealed an interaction between the tyrosine kinase domain of FGF receptor 1 (FGFR1) and sunitinib.	Sunitinib	127-136	Fibroblast growth factor receptor 1	Rattus norvegicus	116-121
25701259-8	2016	Taken together, our results clearly demonstrated that FGF2 inhibition plays an important role in sunitinib-induced cardiotoxicity both in vitro and in vivo.	Sunitinib	97-106	fibroblast growth factor 2	Rattus norvegicus	54-58
25864572-10	2016	CONCLUSION: Topical administration of both everolimus and sunitinib reduced VEGFR-2 levels and inhibited CNV.	Sunitinib	58-67	kinase insert domain receptor	Rattus norvegicus	76-83
26779618-3	2016	The antitumor effect of second-line agents is correlated with the type of secondary mutation: indeed, sunitinib is effective against tumors with C-KIT exon 13 or 14 mutations.	Sunitinib	102-111	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	145-150
27990160-13	2016	Sunitinib inhibited phospho-ERK1/2 and phospho-mTOR.	Sunitinib	0-9	mitogen-activated protein kinase 3	Homo sapiens	28-34
27990160-13	2016	Sunitinib inhibited phospho-ERK1/2 and phospho-mTOR.	Sunitinib	0-9	mechanistic target of rapamycin kinase	Homo sapiens	47-51
27072203-4	2016	We here review the normal physiology of vascular endothelial growth factor in the kidney, and discuss the pathogenesis, clinical and laboratory manifestations, pathological changes in the kidney, and the management of this uncommon complication of sunitinib.	Sunitinib	248-257	vascular endothelial growth factor A	Homo sapiens	40-74
26617188-1	2016	Over the last few years, the most recent advances of the molecular mechanisms involved in renal cell carcinoma have led to the use of new drugs targeting VEGF, such as bevacizumab plus interferon, sorafenib, sunitinib, pazopanib, and axitinib, or the mTOR, such as temsirolimus and everolimus.	Sunitinib	208-217	vascular endothelial growth factor A	Homo sapiens	154-158
26262503-0	2016	Oral Platelet-Derived Growth Factor and Vascular Endothelial Growth Factor Inhibitor Sunitinib Prevents Chronic Allograft Injury in Experimental Kidney Transplantation Model.	Sunitinib	85-94	vascular endothelial growth factor A	Rattus norvegicus	40-74
26262503-2	2016	Sunitinib is a tyrosine kinase inhibitor which inhibits both VEGF and PDGF receptors.	Sunitinib	0-9	vascular endothelial growth factor A	Rattus norvegicus	61-65
26262503-12	2016	Sunitinib also inhibited chronic PDGF-A and -B and VEGF-A and -B expressions.	Sunitinib	0-9	platelet derived growth factor subunit A	Rattus norvegicus	33-46
26385865-5	2016	Furthermore, knockdown of the human ortholog POLG of S. pombe POG1 in human cells significantly increased the cytotoxicity of sunitinib.	Sunitinib	126-135	DNA polymerase gamma, catalytic subunit	Homo sapiens	45-49
26385865-6	2016	Notably, sunitinib dramatically decreased the levels of POLG mRNAs and proteins, of which downregulation was already known to induce mitochondrial damage of cardiomyocytes, causing cardiotoxicity.	Sunitinib	9-18	DNA polymerase gamma, catalytic subunit	Homo sapiens	56-60
26385865-7	2016	These results indicate that POLG might play a crucial role in mitochondrial damage as a gene of which expressional pathway is targeted by sunitinib for cardiotoxicity, and that genome-wide drug target screening with GPScreen can be applied to drug toxicity target discovery to understand the molecular insights regarding drug toxicity.	Sunitinib	138-147	DNA polymerase gamma, catalytic subunit	Homo sapiens	28-32
26262503-12	2016	Sunitinib also inhibited chronic PDGF-A and -B and VEGF-A and -B expressions.	Sunitinib	0-9	vascular endothelial growth factor A	Rattus norvegicus	51-64
26262503-13	2016	CONCLUSIONS: These results demonstrate that combined inhibition of PGDF and VEGF with sunitinib prevents chronic rejection changes in experimental kidney transplantation which indicates that sunitinib could be a potential intervention also in clinical kidney transplantation.	Sunitinib	191-200	vascular endothelial growth factor A	Rattus norvegicus	76-80
30695560-1	2016	Sunitinib is one of first targeted agents and tyrosine kinase inhibitors of vascular endothelial growth factor receptor (VEGFR) that approved for therapy of metastatic renal cell carcinoma.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	76-119
30695560-1	2016	Sunitinib is one of first targeted agents and tyrosine kinase inhibitors of vascular endothelial growth factor receptor (VEGFR) that approved for therapy of metastatic renal cell carcinoma.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	121-126
26387812-0	2015	Association of single nucleotide polymorphisms in IL8 and IL13 with sunitinib-induced toxicity in patients with metastatic renal cell carcinoma.	Sunitinib	68-77	C-X-C motif chemokine ligand 8	Homo sapiens	50-53
25971960-0	2015	Receptor Tyrosine Kinase Expression Predicts Response to Sunitinib in Breast Cancer.	Sunitinib	57-66	ret proto-oncogene	Homo sapiens	0-24
25971960-11	2015	Both ERalpha-positive and low-EGFR-expressing tumors had an increased in vitro sunitinib response, as determined by alteration of Erk activation.	Sunitinib	79-88	estrogen receptor 1	Homo sapiens	5-12
25971960-11	2015	Both ERalpha-positive and low-EGFR-expressing tumors had an increased in vitro sunitinib response, as determined by alteration of Erk activation.	Sunitinib	79-88	epidermal growth factor receptor	Homo sapiens	30-34
25971960-11	2015	Both ERalpha-positive and low-EGFR-expressing tumors had an increased in vitro sunitinib response, as determined by alteration of Erk activation.	Sunitinib	79-88	EPH receptor B2	Homo sapiens	130-133
26575424-9	2015	Moreover, formononetin enhanced the effect of VEGFR2 inhibitor sunitinib on tumor growth inhibition.	Sunitinib	63-72	kinase insert domain receptor	Rattus norvegicus	46-52
26484875-2	2015	Clinical trials enrolling ACC patients with high tissue vascular endothelial growth factor receptor (VEGFR) expression levels showed controversial results after treatment with Sunitinib, possibly due to variability in the expression of drug targets, which include epidermal growth factor receptor (EGFR).	Sunitinib	176-185	kinase insert domain receptor	Homo sapiens	56-99
26484875-2	2015	Clinical trials enrolling ACC patients with high tissue vascular endothelial growth factor receptor (VEGFR) expression levels showed controversial results after treatment with Sunitinib, possibly due to variability in the expression of drug targets, which include epidermal growth factor receptor (EGFR).	Sunitinib	176-185	kinase insert domain receptor	Homo sapiens	101-106
26484875-2	2015	Clinical trials enrolling ACC patients with high tissue vascular endothelial growth factor receptor (VEGFR) expression levels showed controversial results after treatment with Sunitinib, possibly due to variability in the expression of drug targets, which include epidermal growth factor receptor (EGFR).	Sunitinib	176-185	epidermal growth factor receptor	Homo sapiens	264-296
26484875-2	2015	Clinical trials enrolling ACC patients with high tissue vascular endothelial growth factor receptor (VEGFR) expression levels showed controversial results after treatment with Sunitinib, possibly due to variability in the expression of drug targets, which include epidermal growth factor receptor (EGFR).	Sunitinib	176-185	epidermal growth factor receptor	Homo sapiens	102-106
26484875-5	2015	In addition, by cell viability, proliferation and caspase activation assays we found that Sunitinib inhibits adrenocortical cell viability acting, at least in part, through EGFR, that, in turn, is crucial for EGF proliferative effect on adrenocortical cells.	Sunitinib	90-99	epidermal growth factor receptor	Homo sapiens	173-177
26387812-0	2015	Association of single nucleotide polymorphisms in IL8 and IL13 with sunitinib-induced toxicity in patients with metastatic renal cell carcinoma.	Sunitinib	68-77	interleukin 13	Homo sapiens	58-62
26387812-4	2015	METHODS: In this exploratory study, we selected SNPs in genes CYP3A4, NR1I2, POR, IL8, IL13, IL4-R, HIF1A and MET that might possibly be associated with sunitinib treatment outcome.	Sunitinib	153-162	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	62-68
26387812-4	2015	METHODS: In this exploratory study, we selected SNPs in genes CYP3A4, NR1I2, POR, IL8, IL13, IL4-R, HIF1A and MET that might possibly be associated with sunitinib treatment outcome.	Sunitinib	153-162	nuclear receptor subfamily 1 group I member 2	Homo sapiens	70-75
26387812-4	2015	METHODS: In this exploratory study, we selected SNPs in genes CYP3A4, NR1I2, POR, IL8, IL13, IL4-R, HIF1A and MET that might possibly be associated with sunitinib treatment outcome.	Sunitinib	153-162	cytochrome p450 oxidoreductase	Homo sapiens	77-80
26387812-4	2015	METHODS: In this exploratory study, we selected SNPs in genes CYP3A4, NR1I2, POR, IL8, IL13, IL4-R, HIF1A and MET that might possibly be associated with sunitinib treatment outcome.	Sunitinib	153-162	C-X-C motif chemokine ligand 8	Homo sapiens	82-85
26387812-4	2015	METHODS: In this exploratory study, we selected SNPs in genes CYP3A4, NR1I2, POR, IL8, IL13, IL4-R, HIF1A and MET that might possibly be associated with sunitinib treatment outcome.	Sunitinib	153-162	interleukin 13	Homo sapiens	87-91
26387812-4	2015	METHODS: In this exploratory study, we selected SNPs in genes CYP3A4, NR1I2, POR, IL8, IL13, IL4-R, HIF1A and MET that might possibly be associated with sunitinib treatment outcome.	Sunitinib	153-162	interleukin 4 receptor	Homo sapiens	93-98
26387812-4	2015	METHODS: In this exploratory study, we selected SNPs in genes CYP3A4, NR1I2, POR, IL8, IL13, IL4-R, HIF1A and MET that might possibly be associated with sunitinib treatment outcome.	Sunitinib	153-162	hypoxia inducible factor 1 subunit alpha	Homo sapiens	100-105
26387812-10	2015	CONCLUSIONS: We show that polymorphisms in IL8 rs1126647 and IL13 rs1800925 are associated with sunitinib-induced toxicities.	Sunitinib	96-105	C-X-C motif chemokine ligand 8	Homo sapiens	43-46
26387812-10	2015	CONCLUSIONS: We show that polymorphisms in IL8 rs1126647 and IL13 rs1800925 are associated with sunitinib-induced toxicities.	Sunitinib	96-105	interleukin 13	Homo sapiens	61-65
26555641-0	2015	Spectroscopic and molecular docking studies of binding interaction of gefitinib, lapatinib and sunitinib with bovine serum albumin (BSA).	Sunitinib	95-104	albumin	Homo sapiens	117-130
26555641-1	2015	The binding interactions of three kinds of tyrosine kinase inhibitors (TKIs), such as gefitinib, lapatinib and sunitinib, with bovine serum albumin (BSA) were studied using ultraviolet spectrophotometry, fluorescence spectroscopy, circular dichroism (CD), Fourier transform infrared spectroscopy (FT-IR) and molecular docking methods.	Sunitinib	111-120	albumin	Homo sapiens	134-147
26201448-0	2015	miR-221/222 Are Involved in Response to Sunitinib Treatment in Metastatic Renal Cell Carcinoma.	Sunitinib	40-49	microRNA 221	Homo sapiens	0-7
26474454-8	2015	In contrast, seven other mutations, including phospholipase C-gamma1 (PLCG1) R707Q mutation, were found only in the metastatic tumor, indicating selection of cells with the resistant genotype under sunitinib pressure.	Sunitinib	198-207	phospholipase C gamma 1	Homo sapiens	46-68
26474454-8	2015	In contrast, seven other mutations, including phospholipase C-gamma1 (PLCG1) R707Q mutation, were found only in the metastatic tumor, indicating selection of cells with the resistant genotype under sunitinib pressure.	Sunitinib	198-207	phospholipase C gamma 1	Homo sapiens	70-75
26386874-3	2015	VEGF-inhibiting strategies include the use of tyrosine kinase inhibitors (sunitinib, axitinib, pazopanib, and sorafenib) and neutralizing antibodies such as bevacizumab.	Sunitinib	74-83	vascular endothelial growth factor A	Homo sapiens	0-4
26199386-11	2015	Additional analyses suggested (i) prior bevacizumab therapy to be associated with unusually low baseline [sVEGFR2] and (ii) sunitinib causes measurable changes in CTx.	Sunitinib	124-133	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	163-166
26199386-13	2015	Sunitinib caused measurable declines in serum CTx.	Sunitinib	0-9	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	46-49
28031890-4	2015	STAT3 is also involved in the response to tyrosine kinase inhibitors sunitinib and axitinib, in patients with metastatic renal cell carcinoma, and to second-generation androgen receptor inhibitor enzalutamide in patients with advanced prostate cancer.	Sunitinib	69-78	signal transducer and activator of transcription 3	Homo sapiens	0-5
26306766-0	2015	Induction of epithelial-mesenchymal transition via activation of epidermal growth factor receptor contributes to sunitinib resistance in human renal cell carcinoma cell lines.	Sunitinib	113-122	epidermal growth factor receptor	Homo sapiens	65-97
26306766-3	2015	We aimed to study the association between sunitinib sensitivity and epithelial-mesenchymal transition (EMT) regulation via epidermal growth factor receptor (EGFR) signaling, which is a mechanism of resistance to anticancer drugs.	Sunitinib	42-51	epidermal growth factor receptor	Homo sapiens	123-155
26306766-3	2015	We aimed to study the association between sunitinib sensitivity and epithelial-mesenchymal transition (EMT) regulation via epidermal growth factor receptor (EGFR) signaling, which is a mechanism of resistance to anticancer drugs.	Sunitinib	42-51	epidermal growth factor receptor	Homo sapiens	157-161
26306766-6	2015	After treatment with sunitinib, EGFR phosphorylation increased in 786-O cells, resulting in an increase in the phosphorylation of extracellular signal-regulated kinase, nuclear translocation of beta-catenin, and expression of mesenchymal markers.	Sunitinib	21-30	epidermal growth factor receptor	Homo sapiens	32-36
26306766-6	2015	After treatment with sunitinib, EGFR phosphorylation increased in 786-O cells, resulting in an increase in the phosphorylation of extracellular signal-regulated kinase, nuclear translocation of beta-catenin, and expression of mesenchymal markers.	Sunitinib	21-30	catenin beta 1	Homo sapiens	194-206
26306766-7	2015	These results suggest that sunitinib induced EMT via activation of EGFR in 786-O cells, but not in ACHN and Caki-1 cells.	Sunitinib	27-36	epidermal growth factor receptor	Homo sapiens	67-71
26108242-1	2015	AIMS AND BACKGROUND: The introduction of agents targeting vascular endothelial growth factor has radically changed the approach to metastatic renal cell carcinoma (mRCC): sunitinib and pazopanib are now the standard first-line therapy in mRCC.	Sunitinib	171-180	vascular endothelial growth factor A	Homo sapiens	58-92
26306766-8	2015	Caki-1/SN cells, a resistant cell line generated by continuous exposure to sunitinib, displayed increased phosphorylation of EGFR.	Sunitinib	75-84	epidermal growth factor receptor	Homo sapiens	125-129
26306766-9	2015	Cell viability in the presence of sunitinib was decreased by erlotinib, as the selective inhibitor of EGFR, treatment in 786-O and Caki-1/SN cells.	Sunitinib	34-43	epidermal growth factor receptor	Homo sapiens	102-106
26306766-10	2015	Similarly, erlotinib suppressed sunitinib-induced EGFR activation and upregulated mesenchymal markers.	Sunitinib	32-41	epidermal growth factor receptor	Homo sapiens	50-54
26306766-11	2015	Thus, we postulate that resistance to sunitinib in RCC may be associated with EMT caused by activation of EGFR.	Sunitinib	38-47	epidermal growth factor receptor	Homo sapiens	106-110
25963915-8	2015	The VEGF score was significantly decreased similarly by pazopanib, sunitinib, and sorafenib compared to normal saline (P &lt; .05).	Sunitinib	67-76	vascular endothelial growth factor A	Rattus norvegicus	4-8
26408725-2	2015	Thirteen patients with temozolomide-refractory recurrent anaplastic or low-grade glioma were treated with sunitinib malate, a small-molecule tyrosine kinase inhibitor of the VEGFR, PDGFR, and KIT receptors, in combination with lomustine.	Sunitinib	106-122	kinase insert domain receptor	Homo sapiens	174-179
26472187-9	2015	Finally, GRP78 knockdown showed potent suppression of tumor growth and enhanced the antitumor effect of sunitinib in RCC xenografts.	Sunitinib	104-113	heat shock protein family A (Hsp70) member 5	Homo sapiens	9-14
26513662-0	2015	Prodrug AST-003 Improves the Therapeutic Index of the Multi-Targeted Tyrosine Kinase Inhibitor Sunitinib.	Sunitinib	95-104	solute carrier family 17 member 5	Homo sapiens	8-11
26513662-4	2015	The inactive prodrug AST-003 can be converted to Sunitinib in vitro and in vivo.	Sunitinib	49-58	solute carrier family 17 member 5	Homo sapiens	21-24
26408740-12	2015	CONCLUSION: A significantly higher expression of VEGF in CRCC in comparison to healthy parenchyma can predict a better response to sunitinib.	Sunitinib	131-140	vascular endothelial growth factor A	Homo sapiens	49-53
26451083-3	2015	A better understanding of angiogenesis has led to the investigation of drugs that inhibit the vascular endothelial growth factor (VEGF) pathway including anti-VEGF antibody therapy (eg, bevacizumab), inhibitors of angiogenic receptor tyrosine kinases (eg, sunitinib, sorafenib, apatinib, regorafenib), and inhibitors of vascular endothelial growth factor receptors (VEGFRs) (eg, ramucirumab).	Sunitinib	256-265	vascular endothelial growth factor A	Homo sapiens	94-128
26126494-1	2015	Vascular endothelial growth factor [VEGF] pathway, which plays a key role in angiogenesis, may be blocked by either extracellular interference with VEGF itself (bevacizumab [BEV] or aflibercept), or intracytoplasmic inhibition of VEGF receptor (pazopanib, nintedanib, cediranid, sunitinib and sorafenib).	Sunitinib	279-288	vascular endothelial growth factor A	Homo sapiens	0-34
26126494-1	2015	Vascular endothelial growth factor [VEGF] pathway, which plays a key role in angiogenesis, may be blocked by either extracellular interference with VEGF itself (bevacizumab [BEV] or aflibercept), or intracytoplasmic inhibition of VEGF receptor (pazopanib, nintedanib, cediranid, sunitinib and sorafenib).	Sunitinib	279-288	vascular endothelial growth factor A	Homo sapiens	36-40
26126494-1	2015	Vascular endothelial growth factor [VEGF] pathway, which plays a key role in angiogenesis, may be blocked by either extracellular interference with VEGF itself (bevacizumab [BEV] or aflibercept), or intracytoplasmic inhibition of VEGF receptor (pazopanib, nintedanib, cediranid, sunitinib and sorafenib).	Sunitinib	279-288	vascular endothelial growth factor A	Homo sapiens	148-152
26126494-1	2015	Vascular endothelial growth factor [VEGF] pathway, which plays a key role in angiogenesis, may be blocked by either extracellular interference with VEGF itself (bevacizumab [BEV] or aflibercept), or intracytoplasmic inhibition of VEGF receptor (pazopanib, nintedanib, cediranid, sunitinib and sorafenib).	Sunitinib	279-288	vascular endothelial growth factor A	Homo sapiens	148-152
25930089-0	2015	CYP3A5 and ABCB1 polymorphisms as predictors for sunitinib outcome in metastatic renal cell carcinoma.	Sunitinib	49-58	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	0-6
25930089-0	2015	CYP3A5 and ABCB1 polymorphisms as predictors for sunitinib outcome in metastatic renal cell carcinoma.	Sunitinib	49-58	ATP binding cassette subfamily B member 1	Homo sapiens	11-16
25930089-11	2015	CONCLUSIONS: The confirmation of previously reported associations between polymorphisms in CYP3A5 and ABCB1 with sunitinib toxicity and efficacy, respectively, indicates that genotyping of these genetic variants will be useful for guiding sunitinib treatment.	Sunitinib	113-122	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	91-97
25930089-11	2015	CONCLUSIONS: The confirmation of previously reported associations between polymorphisms in CYP3A5 and ABCB1 with sunitinib toxicity and efficacy, respectively, indicates that genotyping of these genetic variants will be useful for guiding sunitinib treatment.	Sunitinib	113-122	ATP binding cassette subfamily B member 1	Homo sapiens	102-107
25930089-11	2015	CONCLUSIONS: The confirmation of previously reported associations between polymorphisms in CYP3A5 and ABCB1 with sunitinib toxicity and efficacy, respectively, indicates that genotyping of these genetic variants will be useful for guiding sunitinib treatment.	Sunitinib	239-248	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	91-97
25930089-11	2015	CONCLUSIONS: The confirmation of previously reported associations between polymorphisms in CYP3A5 and ABCB1 with sunitinib toxicity and efficacy, respectively, indicates that genotyping of these genetic variants will be useful for guiding sunitinib treatment.	Sunitinib	239-248	ATP binding cassette subfamily B member 1	Homo sapiens	102-107
26451083-3	2015	A better understanding of angiogenesis has led to the investigation of drugs that inhibit the vascular endothelial growth factor (VEGF) pathway including anti-VEGF antibody therapy (eg, bevacizumab), inhibitors of angiogenic receptor tyrosine kinases (eg, sunitinib, sorafenib, apatinib, regorafenib), and inhibitors of vascular endothelial growth factor receptors (VEGFRs) (eg, ramucirumab).	Sunitinib	256-265	vascular endothelial growth factor A	Homo sapiens	130-134
26015515-1	2015	PURPOSE: The aim of this study was to investigate the effect of VEGF-targeted therapy (sunitinib) on molecular intratumoral heterogeneity (ITH) in metastatic clear cell renal cancer (mccRCC).	Sunitinib	87-96	vascular endothelial growth factor A	Homo sapiens	64-68
26396737-0	2015	Response to sunitinib of a gastrointestinal stromal tumor with a rare exon 12 PDGFRA mutation.	Sunitinib	12-21	platelet derived growth factor receptor alpha	Homo sapiens	78-84
26396737-7	2015	CONCLUSIONS: This is the first report detailing a response to treatment with sunitinib of a gastrointestinal stromal tumor with an uncommon exon 12 PDGFRA mutation.	Sunitinib	77-86	platelet derived growth factor receptor alpha	Homo sapiens	148-154
25922428-5	2015	Sunitinib treatment resulted in a significant reduction in monocytic MDSC, phosphorylated STAT3, and arginase levels in monocytic MDSC (CD33(+)CD14(+)CD16(+)), and an increase in T-cell proliferative activity in cancer patients.	Sunitinib	0-9	signal transducer and activator of transcription 3	Homo sapiens	90-95
25922428-5	2015	Sunitinib treatment resulted in a significant reduction in monocytic MDSC, phosphorylated STAT3, and arginase levels in monocytic MDSC (CD33(+)CD14(+)CD16(+)), and an increase in T-cell proliferative activity in cancer patients.	Sunitinib	0-9	CD33 molecule	Homo sapiens	136-140
26380584-7	2015	In contrast, in RCCs with FLT1 hypermethylation, proliferation inhibition was counteracted by treatment with an anti-FLT1 peptide and both VEGF-TKIs (sunitinib and axitinib).	Sunitinib	150-159	fms related receptor tyrosine kinase 1	Homo sapiens	26-30
26380584-7	2015	In contrast, in RCCs with FLT1 hypermethylation, proliferation inhibition was counteracted by treatment with an anti-FLT1 peptide and both VEGF-TKIs (sunitinib and axitinib).	Sunitinib	150-159	vascular endothelial growth factor A	Homo sapiens	139-143
26380584-8	2015	Demethylation with sunitinib or axitinib synergistically increased proliferation inhibition in the RCCs exhibiting FLT1 hypermethylation.	Sunitinib	19-28	fms related receptor tyrosine kinase 1	Homo sapiens	115-119
26380584-9	2015	Using in vitro FLT1 or KDR knockdown models, decreased proliferation inhibition following anti-FLT1 peptide, sunitinib, and axitinib treatment was observed only in FLT1-knockdown cells.	Sunitinib	109-118	fms related receptor tyrosine kinase 1	Homo sapiens	15-19
25922428-5	2015	Sunitinib treatment resulted in a significant reduction in monocytic MDSC, phosphorylated STAT3, and arginase levels in monocytic MDSC (CD33(+)CD14(+)CD16(+)), and an increase in T-cell proliferative activity in cancer patients.	Sunitinib	0-9	CD14 molecule	Homo sapiens	143-147
26380584-9	2015	Using in vitro FLT1 or KDR knockdown models, decreased proliferation inhibition following anti-FLT1 peptide, sunitinib, and axitinib treatment was observed only in FLT1-knockdown cells.	Sunitinib	109-118	kinase insert domain receptor	Homo sapiens	23-26
26015515-8	2015	Despite this variability, significant chromosomal and transcript changes to key targets of sunitinib, such as VHL, PBRM1, and CAIX, occurred in the treated samples.	Sunitinib	91-100	polybromo 1	Homo sapiens	115-120
26380584-10	2015	In patients with renal cancer who received sunitinib, FLT1 promoter methylation was higher in renal cancer tissues from eight nonresponders (stable or progressive disease assessed by the Response Evaluation Criteria in Solid Tumors) than in cancer tissues from five responders (complete response or partial response).	Sunitinib	43-52	fms related receptor tyrosine kinase 1	Homo sapiens	54-58
25922428-5	2015	Sunitinib treatment resulted in a significant reduction in monocytic MDSC, phosphorylated STAT3, and arginase levels in monocytic MDSC (CD33(+)CD14(+)CD16(+)), and an increase in T-cell proliferative activity in cancer patients.	Sunitinib	0-9	Fc gamma receptor IIIa	Homo sapiens	150-154
25922428-7	2015	SBRT synergized the therapeutic effects of sunitinib, especially as related to decreased numbers of monocytic MDSC, Treg, and B cells, and augmented Tbet expression in primary CD4 and CD8 T cells.	Sunitinib	43-52	T-box transcription factor 21	Homo sapiens	149-153
25922428-7	2015	SBRT synergized the therapeutic effects of sunitinib, especially as related to decreased numbers of monocytic MDSC, Treg, and B cells, and augmented Tbet expression in primary CD4 and CD8 T cells.	Sunitinib	43-52	CD4 molecule	Homo sapiens	176-179
26015515-8	2015	Despite this variability, significant chromosomal and transcript changes to key targets of sunitinib, such as VHL, PBRM1, and CAIX, occurred in the treated samples.	Sunitinib	91-100	carbonic anhydrase 9	Homo sapiens	126-130
25922428-7	2015	SBRT synergized the therapeutic effects of sunitinib, especially as related to decreased numbers of monocytic MDSC, Treg, and B cells, and augmented Tbet expression in primary CD4 and CD8 T cells.	Sunitinib	43-52	CD8a molecule	Homo sapiens	184-187
25922428-9	2015	Most interestingly, the responders, defined by sunitinib-mediated reduction in CD33(+)CD11b(+) myeloid cell populations, tend to exhibit improved progression-free survival and cause-specific survival.	Sunitinib	47-56	CD33 molecule	Homo sapiens	79-83
25922428-9	2015	Most interestingly, the responders, defined by sunitinib-mediated reduction in CD33(+)CD11b(+) myeloid cell populations, tend to exhibit improved progression-free survival and cause-specific survival.	Sunitinib	47-56	integrin subunit alpha M	Homo sapiens	86-91
25701807-1	2015	Sunitinib is a multi-targeted receptor tyrosine kinase (RTK) inhibitor that blocks several angiogenesis related pathways.	Sunitinib	0-9	EPH receptor A3	Gallus gallus	30-54
26366997-8	2015	CONCLUSIONS: The WX-ETK-model-derived vC was an effective prognostic biomarker for advanced HCC treated with sunitinib.	Sunitinib	109-118	BMX non-receptor tyrosine kinase	Homo sapiens	20-23
25783986-6	2015	Furthermore, TIM-3 rendered RCC cells with the ability to induce resistance to sunitinib and mTOR inhibitors, the standard regimen for patients with ccRCC, as well as stem cell activities.	Sunitinib	79-88	hepatitis A virus cellular receptor 2	Homo sapiens	13-18
26014097-8	2015	Treatment of RCC cell lines and RCC xenografts in immunodeficient mice with sunitinib also increased tumor PD-L1 expression.	Sunitinib	76-85	CD274 antigen	Mus musculus	107-112
25701807-1	2015	Sunitinib is a multi-targeted receptor tyrosine kinase (RTK) inhibitor that blocks several angiogenesis related pathways.	Sunitinib	0-9	EPH receptor A3	Gallus gallus	56-59
26713520-0	2015	[Sunitinib suppresses migration of ovarian cancer cells through negative modulation of TGF-beta-mediated epithelial-mesenchymal transition].	Sunitinib	1-10	transforming growth factor beta 1	Homo sapiens	87-95
26067856-5	2015	RESULTS: Sunitinib, which targets the imatinib-inhibited tyrosine kinases of VEGFR, KIT, PDGFR, and FLT-3, was without effect in COV434 and KGN cell lines.	Sunitinib	9-18	kinase insert domain receptor	Homo sapiens	77-82
26291023-0	2015	Rapid Response to Sunitinib in a Patient with Lung Adenocarcinoma Harboring KIF5B-RET Fusion Gene.	Sunitinib	18-27	kinesin family member 5B	Homo sapiens	76-81
26291023-0	2015	Rapid Response to Sunitinib in a Patient with Lung Adenocarcinoma Harboring KIF5B-RET Fusion Gene.	Sunitinib	18-27	ret proto-oncogene	Homo sapiens	82-85
26713520-1	2015	OBJECTIVE: To investigate the effect of sunitinib on the migration of ovarian cells and its mechanism of the negative regulation TGF-beta mediated of epithelial-mesenchymal transition(EMT) by sunitinib to inhibit ovarian cancer metastasis.	Sunitinib	40-49	transforming growth factor beta 1	Homo sapiens	129-137
26713520-1	2015	OBJECTIVE: To investigate the effect of sunitinib on the migration of ovarian cells and its mechanism of the negative regulation TGF-beta mediated of epithelial-mesenchymal transition(EMT) by sunitinib to inhibit ovarian cancer metastasis.	Sunitinib	192-201	transforming growth factor beta 1	Homo sapiens	129-137
26713520-3	2015	The effects of sunitinib on TGF-beta-induced E-cadherin expression was assessed by Western-blotting, real time RT-PCR and immunofluorescence assay.	Sunitinib	15-24	transforming growth factor beta 1	Homo sapiens	28-36
26713520-3	2015	The effects of sunitinib on TGF-beta-induced E-cadherin expression was assessed by Western-blotting, real time RT-PCR and immunofluorescence assay.	Sunitinib	15-24	cadherin 1	Homo sapiens	45-55
26713520-4	2015	The protein levels of Snail and the transcriptional activity of Smad in sunitinib-treated cells were examined by Western-blotting and SBE-luciferase assay.	Sunitinib	72-81	snail family transcriptional repressor 1	Homo sapiens	22-27
26713520-6	2015	TGF-beta stimulation reduced E-cadherin protein level, which was attenuated by sunitinib.	Sunitinib	79-88	transforming growth factor beta 1	Homo sapiens	0-8
26713520-6	2015	TGF-beta stimulation reduced E-cadherin protein level, which was attenuated by sunitinib.	Sunitinib	79-88	cadherin 1	Homo sapiens	29-39
26713520-7	2015	Sunitinib inhibited the up-regulation of Snail protein level induced by TGF-beta treatment.	Sunitinib	0-9	snail family transcriptional repressor 1	Homo sapiens	41-46
26713520-7	2015	Sunitinib inhibited the up-regulation of Snail protein level induced by TGF-beta treatment.	Sunitinib	0-9	transforming growth factor beta 1	Homo sapiens	72-80
26713520-9	2015	A remarkable increment of transcriptional activity of Smads complexes was observed in SKOV3 cells exposed to TGF-beta, which was significantly prohibited by sunitinib.	Sunitinib	157-166	transforming growth factor beta 1	Homo sapiens	109-117
26713520-10	2015	CONCLUSION: Sunitinib can inhibit the migration of SKOV3 cells and attenuate the down-regulation of E-cadherin protein level induced by TGF-beta.	Sunitinib	12-21	cadherin 1	Homo sapiens	100-110
26713520-10	2015	CONCLUSION: Sunitinib can inhibit the migration of SKOV3 cells and attenuate the down-regulation of E-cadherin protein level induced by TGF-beta.	Sunitinib	12-21	transforming growth factor beta 1	Homo sapiens	136-144
26713520-11	2015	Sunitinib can abolish TGF-beta-induced up-regulation of Snail protein and decrease the transcriptional activity of Smad complexes.	Sunitinib	0-9	transforming growth factor beta 1	Homo sapiens	22-30
26713520-11	2015	Sunitinib can abolish TGF-beta-induced up-regulation of Snail protein and decrease the transcriptional activity of Smad complexes.	Sunitinib	0-9	snail family transcriptional repressor 1	Homo sapiens	56-61
26713520-12	2015	The results indicate that sunitinib suppresses migration of ovarian cancer cells through negative modulation of TGF-beta-mediated epithelial-mesenchymal transition.	Sunitinib	26-35	transforming growth factor beta 1	Homo sapiens	112-120
25893276-8	2015	RESULTS: Sunitinib strongly reduced proliferation of PC-3 and DU-145 cells in a dose dependent manner, and decreased levels of p-Akt, p-Erk1/2, and Id-1, compared to untreated cells.	Sunitinib	9-18	mitogen-activated protein kinase 3	Homo sapiens	136-142
25963382-6	2015	Tyrosine kinase inhibitors and mammalian target of rapamycin inhibitors are now established classes of drugs used in the treatment of renal cancer, with a total of six having received regulatory approval to date (sorafenib, sunitinib, pazopanib, axitinib, temsirolimus, and everolimus).	Sunitinib	224-233	mechanistic target of rapamycin kinase	Homo sapiens	31-60
26480622-9	2015	The biologic therapies for metastatic renal cell carcinoma belong to two main groups: angiogenesis inhibitors (VEGF-R inhibitors like sunitinib, sorafenib, pazopanib and axitinib), and inhibitors of the mTOR protein (everolimus and temsirolimus).	Sunitinib	134-143	vascular endothelial growth factor A	Homo sapiens	111-115
24727344-1	2015	BACKGROUND: Vascular endothelial growth factor inhibitors such as bevacizumab, sorafenib, and sunitinib are utilized in the treatment of multiple cancers.	Sunitinib	94-103	vascular endothelial growth factor A	Homo sapiens	12-46
26309414-0	2015	Heme oxygenase-1 is a predictive biomarker for therapeutic targeting of advanced clear cell renal cell carcinoma treated with sorafenib or sunitinib.	Sunitinib	139-148	heme oxygenase 1	Homo sapiens	0-16
26309414-1	2015	BACKGROUND: We analyzed the expression of heme oxygenase-1 (HO-1) in patients undergoing radical nephrectomy for advanced clear cell renal cell carcinoma (CC-RCC) and evaluated the effects of the targeted therapies treated with sorafenib and sunitinib.	Sunitinib	242-251	heme oxygenase 1	Homo sapiens	42-58
26309414-1	2015	BACKGROUND: We analyzed the expression of heme oxygenase-1 (HO-1) in patients undergoing radical nephrectomy for advanced clear cell renal cell carcinoma (CC-RCC) and evaluated the effects of the targeted therapies treated with sorafenib and sunitinib.	Sunitinib	242-251	heme oxygenase 1	Homo sapiens	60-64
26309414-6	2015	In the low HO-1 level group, a higher tumor response rate and a longer survival time was achieved in patients who received sorafenib or sunitinib.	Sunitinib	136-145	heme oxygenase 1	Homo sapiens	11-15
26309414-9	2015	Overall, HO-1 expression might be a useful biomarker for predicting the response to sunitinib and sorafenib for patients with metastatic CC-RCC.	Sunitinib	84-93	heme oxygenase 1	Homo sapiens	9-13
26244574-0	2015	Association of ABCB1 and FLT3 Polymorphisms with Toxicities and Survival in Asian Patients Receiving Sunitinib for Renal Cell Carcinoma.	Sunitinib	101-110	ATP binding cassette subfamily B member 1	Homo sapiens	15-20
26244574-0	2015	Association of ABCB1 and FLT3 Polymorphisms with Toxicities and Survival in Asian Patients Receiving Sunitinib for Renal Cell Carcinoma.	Sunitinib	101-110	fms related receptor tyrosine kinase 3	Homo sapiens	25-29
26244574-9	2015	In conclusion, ABCB1 and FLT3 polymorphisms may be helpful in predicting sunitinib toxicities, response and survival benefit in Asian mRCC patients.	Sunitinib	73-82	ATP binding cassette subfamily B member 1	Homo sapiens	15-20
26244574-9	2015	In conclusion, ABCB1 and FLT3 polymorphisms may be helpful in predicting sunitinib toxicities, response and survival benefit in Asian mRCC patients.	Sunitinib	73-82	fms related receptor tyrosine kinase 3	Homo sapiens	25-29
26244574-10	2015	We have also validated the association between FLT3 738T and sunitinib-induced leucopenia previously reported in Caucasian populations, but have not validated other reported genetic associations.	Sunitinib	61-70	fms related receptor tyrosine kinase 3	Homo sapiens	47-51
26011058-1	2015	Tyrosine kinase inhibitor sunitinib (used in GIST, advanced RCC, and pancreatic neuroendocrine tumors) undergoes CYP3A4 metabolism and is an ABCB1B and ABCG2 efflux transporters substrate.	Sunitinib	26-35	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	141-147
26011058-1	2015	Tyrosine kinase inhibitor sunitinib (used in GIST, advanced RCC, and pancreatic neuroendocrine tumors) undergoes CYP3A4 metabolism and is an ABCB1B and ABCG2 efflux transporters substrate.	Sunitinib	26-35	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	152-157
25893276-8	2015	RESULTS: Sunitinib strongly reduced proliferation of PC-3 and DU-145 cells in a dose dependent manner, and decreased levels of p-Akt, p-Erk1/2, and Id-1, compared to untreated cells.	Sunitinib	9-18	inhibitor of DNA binding 1, HLH protein	Homo sapiens	148-152
28162293-3	2015	VEGF-inhibiting strategies include the use of tyrosine kinase inhibitors (sunitinib, axitinib, pazopanib, and sorafenib) and neutralizing antibodies such as bevacizumab.	Sunitinib	74-83	vascular endothelial growth factor A	Homo sapiens	0-4
25893276-10	2015	Depletion of Hif-1alpha levels in vitro and a decrease in FMISO uptake in vivo showed that Sunitinib inhibits tumor hypoxia.	Sunitinib	91-100	hypoxia inducible factor 1 subunit alpha	Homo sapiens	13-23
26151457-2	2015	We investigated the efficacy of sunitinib, a multikinase VEGF inhibitor, in patients with relapsed/refractory GE/oesophageal cancer.	Sunitinib	32-41	vascular endothelial growth factor A	Homo sapiens	57-61
26198000-1	2015	BACKGROUND: Clinical studies implying the sunitinib multi-kinase inhibitor have led to disappointing results for breast cancer care but mostly focused on HER2-negative subtypes.	Sunitinib	42-51	erb-b2 receptor tyrosine kinase 2	Mus musculus	154-158
26198000-13	2015	CONCLUSIONS: [(18)F]FDG and [(18)F]FMISO PET were relevant approaches to study the response to sunitinib in this luminal B (HER2-positive) model.	Sunitinib	95-104	erb-b2 receptor tyrosine kinase 2	Mus musculus	124-128
25980323-1	2015	The aim of this study was to evaluate the capacity of BR55, an ultrasound contrast agent specifically targeting vascular endothelial growth factor receptor 2 (VEGFR2), to distinguish the specific anti-VEGFR2 therapy effect of sunitinib from other anti-angiogenic effects of a therapy (imatinib) that does not directly inhibit VEGFR2.	Sunitinib	226-235	kinase insert domain protein receptor	Mus musculus	112-157
25980323-1	2015	The aim of this study was to evaluate the capacity of BR55, an ultrasound contrast agent specifically targeting vascular endothelial growth factor receptor 2 (VEGFR2), to distinguish the specific anti-VEGFR2 therapy effect of sunitinib from other anti-angiogenic effects of a therapy (imatinib) that does not directly inhibit VEGFR2.	Sunitinib	226-235	kinase insert domain protein receptor	Mus musculus	159-165
25980323-1	2015	The aim of this study was to evaluate the capacity of BR55, an ultrasound contrast agent specifically targeting vascular endothelial growth factor receptor 2 (VEGFR2), to distinguish the specific anti-VEGFR2 therapy effect of sunitinib from other anti-angiogenic effects of a therapy (imatinib) that does not directly inhibit VEGFR2.	Sunitinib	226-235	kinase insert domain protein receptor	Mus musculus	201-207
25980323-1	2015	The aim of this study was to evaluate the capacity of BR55, an ultrasound contrast agent specifically targeting vascular endothelial growth factor receptor 2 (VEGFR2), to distinguish the specific anti-VEGFR2 therapy effect of sunitinib from other anti-angiogenic effects of a therapy (imatinib) that does not directly inhibit VEGFR2.	Sunitinib	226-235	kinase insert domain protein receptor	Mus musculus	201-207
25980323-9	2015	Targeted contrast-enhanced imaging revealed lower differential targeted enhancement, that is, lower levels of VEGFR2 expression, in sunitinib-treated mice relative to placebo-treated mice from 24 h (p &lt; 0.05) and relative to both placebo- and imatinib-treated mice from 48 h (p &lt; 0.05).	Sunitinib	132-141	kinase insert domain protein receptor	Mus musculus	110-116
26009164-3	2015	Results reveal that some compounds have potent antitumor activity, and the most active 13c7 (IC50s: 4.49-15.39 muM) was found to be more active than Sunitinib (IC50s: 4.70-&gt;30 muM) against all of the tested cancer cell lines.	Sunitinib	149-158	latexin	Homo sapiens	179-182
26151457-18	2015	On this study, patients with clinical benefit from sunitinib had higher tumour CFB expression, and thus has identified CFB as a potential predictor for efficacy of anti-angiogenic therapy.	Sunitinib	51-60	complement factor B	Homo sapiens	79-82
26114873-0	2015	Role of IL13RA2 in Sunitinib Resistance in Clear Cell Renal Cell Carcinoma.	Sunitinib	19-28	interleukin 13 receptor subunit alpha 2	Homo sapiens	8-15
26114873-2	2015	Sunitinib is an agent that targets VEGF receptors and is considered to be a standard treatment for metastatic or unresectable clear cell RCC (ccRCC).	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	35-39
26114873-7	2015	Comparing gene expression profiles between the two xenograft models with different sensitivity to sunitinib, we identified interleukin 13 receptor alpha 2 (IL13RA2) as a candidate molecule associated with the acquired sunitinib-resistance in ccRCC.	Sunitinib	98-107	interleukin 13 receptor subunit alpha 2	Homo sapiens	123-154
26114873-7	2015	Comparing gene expression profiles between the two xenograft models with different sensitivity to sunitinib, we identified interleukin 13 receptor alpha 2 (IL13RA2) as a candidate molecule associated with the acquired sunitinib-resistance in ccRCC.	Sunitinib	98-107	interleukin 13 receptor subunit alpha 2	Homo sapiens	156-163
26114873-7	2015	Comparing gene expression profiles between the two xenograft models with different sensitivity to sunitinib, we identified interleukin 13 receptor alpha 2 (IL13RA2) as a candidate molecule associated with the acquired sunitinib-resistance in ccRCC.	Sunitinib	218-227	interleukin 13 receptor subunit alpha 2	Homo sapiens	123-154
26114873-7	2015	Comparing gene expression profiles between the two xenograft models with different sensitivity to sunitinib, we identified interleukin 13 receptor alpha 2 (IL13RA2) as a candidate molecule associated with the acquired sunitinib-resistance in ccRCC.	Sunitinib	218-227	interleukin 13 receptor subunit alpha 2	Homo sapiens	156-163
26114873-8	2015	And patients with high IL13RA2 expression in immunohistochemistry in primary ccRCC tumor tends to have sunitinib-resistant metastatic site.	Sunitinib	103-112	interleukin 13 receptor subunit alpha 2	Homo sapiens	23-30
26114873-9	2015	Next, we showed that sunitinib-sensitive 786-O cells acquired resistance in vivo when IL13RA2 was overexpressed.	Sunitinib	21-30	interleukin 13 receptor subunit alpha 2	Homo sapiens	86-93
26114873-10	2015	Conversely, shRNA-mediated knockdown of IL13RA2 successfully overcame the sunitinib-resistance in Caki-1 cells.	Sunitinib	74-83	interleukin 13 receptor subunit alpha 2	Homo sapiens	40-47
26114873-11	2015	Histopathological analyses revealed that IL13RA2 repressed sunitinib-induced apoptosis without increasing tumor vasculature in vivo.	Sunitinib	59-68	interleukin 13 receptor subunit alpha 2	Homo sapiens	41-48
26114873-12	2015	To our knowledge, this is a novel mechanism of developing resistance to sunitinib in a certain population of ccRCC, and these results indicate that IL13RA2 could be one of potential target to overcome sunitinib resistance.	Sunitinib	72-81	interleukin 13 receptor subunit alpha 2	Homo sapiens	148-155
26114873-12	2015	To our knowledge, this is a novel mechanism of developing resistance to sunitinib in a certain population of ccRCC, and these results indicate that IL13RA2 could be one of potential target to overcome sunitinib resistance.	Sunitinib	201-210	interleukin 13 receptor subunit alpha 2	Homo sapiens	148-155
26070816-9	2015	In the melanoma xenograft model, serum phospho-CSE1L level declined 5 days after vemurafenib/sunitinib treatment and 3 days after sorafenib/lapatinib treatment in the HT-29 colon cancer xenograft model.	Sunitinib	93-102	chromosome segregation 1-like (S. cerevisiae)	Mus musculus	47-52
25564360-0	2015	Synthetic miR-145 Mimic Enhances the Cytotoxic Effect of the Antiangiogenic Drug Sunitinib in Glioblastoma.	Sunitinib	81-90	microRNA 145	Homo sapiens	10-17
25861727-0	2015	MiRNA-21 silencing mediated by tumor-targeted nanoparticles combined with sunitinib: A new multimodal gene therapy approach for glioblastoma.	Sunitinib	74-83	microRNA 21	Homo sapiens	0-8
25861727-5	2015	Decreased tumor cell proliferation and tumor size, as well as enhanced apoptosis activation and, to a lesser extent, improvement of animal survival, were also observed in GBM-bearing mice upon systemic delivery of targeted nanoparticle-formulated anti-miR-21 oligonucleotides and exposure to the tyrosine kinase inhibitor sunitinib.	Sunitinib	322-331	microRNA 21a	Mus musculus	252-258
25818407-0	2015	A phase I/II study of sunitinib and intensive chemotherapy in patients over 60 years of age with acute myeloid leukaemia and activating FLT3 mutations.	Sunitinib	22-31	fms related receptor tyrosine kinase 3	Homo sapiens	136-140
26070816-0	2015	Early decline in serum phospho-CSE1L levels in vemurafenib/sunitinib-treated melanoma and sorafenib/lapatinib-treated colorectal tumor xenografts.	Sunitinib	59-68	chromosome segregation 1-like (S. cerevisiae)	Mus musculus	31-36
26042424-1	2015	Inhibitors of VEGF receptor (VEGFR) signaling such as sorafenib and sunitinib that are currently used in the treatment of malignant diseases have been shown to affect immunological responses by inhibition of the function of antigen presenting cells and T lymphocytes.	Sunitinib	68-77	kinase insert domain receptor	Homo sapiens	14-27
26042424-1	2015	Inhibitors of VEGF receptor (VEGFR) signaling such as sorafenib and sunitinib that are currently used in the treatment of malignant diseases have been shown to affect immunological responses by inhibition of the function of antigen presenting cells and T lymphocytes.	Sunitinib	68-77	kinase insert domain receptor	Homo sapiens	29-34
25564360-4	2015	In addition, we suggested that the enhanced cytotoxicity of Sunitinib by miR-145 mimic was mediated by inhibition of both P-gp and Bcrp.	Sunitinib	60-69	microRNA 145	Homo sapiens	73-80
25564360-4	2015	In addition, we suggested that the enhanced cytotoxicity of Sunitinib by miR-145 mimic was mediated by inhibition of both P-gp and Bcrp.	Sunitinib	60-69	phosphoglycolate phosphatase	Homo sapiens	122-126
25564360-4	2015	In addition, we suggested that the enhanced cytotoxicity of Sunitinib by miR-145 mimic was mediated by inhibition of both P-gp and Bcrp.	Sunitinib	60-69	BCR pseudogene 1	Homo sapiens	131-135
25488966-2	2015	Recent placebo-controlled phase III trials of the mammalian target of rapamycin (mTOR) inhibitor everolimus and the vascular endothelial growth factor (VEGF)/platelet-derived growth factor receptor inhibitor sunitinib have noted improved progression-free survival (PFS).	Sunitinib	208-217	vascular endothelial growth factor A	Homo sapiens	116-150
25917740-5	2015	However, compared with PC3/C, PC3/sh-Akt1 showed a significantly higher sensitivity to sunitinib, accompanying impaired phosphorylation of p44/42 mitogen-activated protein kinase, downregulation of Bcl-2, and upregulation of Bax.	Sunitinib	87-96	proprotein convertase subtilisin/kexin type 1	Homo sapiens	30-33
25948774-5	2015	At variance, only VEGF-receptor inhibition using the non-specific tyrosine kinase inhibitor Sunitinib or the anti-VEGF-receptor 2 neutralizing antibody, but not VEGF blockade using Bevacizumab, impaired the process of endothelial differentiation in vitro, suggesting a VEGF-independent mechanism.	Sunitinib	92-101	vascular endothelial growth factor A	Mus musculus	18-22
25907705-4	2015	Its potent and selective inhibition of VEGFR was the rationale for its development in the second-line setting after failure of prior cytokines or sunitinib.	Sunitinib	146-155	kinase insert domain receptor	Homo sapiens	39-44
26003083-0	2015	Effect of enhanced expression of connexin 43 on sunitinib-induced cytotoxicity in mesothelioma cells.	Sunitinib	48-57	gap junction protein alpha 1	Homo sapiens	33-44
26003083-4	2015	This work aims to evaluate the effect of the restoration of connexin 43 (Cx43) (the most ubiquitous Cx subtype) expression on sunitinib (SU)-induced cytotoxicity in malignant mesothelioma (MM) cells.	Sunitinib	126-135	gap junction protein alpha 1	Homo sapiens	60-71
26003083-4	2015	This work aims to evaluate the effect of the restoration of connexin 43 (Cx43) (the most ubiquitous Cx subtype) expression on sunitinib (SU)-induced cytotoxicity in malignant mesothelioma (MM) cells.	Sunitinib	126-135	gap junction protein alpha 1	Homo sapiens	73-77
26003083-4	2015	This work aims to evaluate the effect of the restoration of connexin 43 (Cx43) (the most ubiquitous Cx subtype) expression on sunitinib (SU)-induced cytotoxicity in malignant mesothelioma (MM) cells.	Sunitinib	126-135	LOC100128922	Homo sapiens	73-75
26003083-4	2015	This work aims to evaluate the effect of the restoration of connexin 43 (Cx43) (the most ubiquitous Cx subtype) expression on sunitinib (SU)-induced cytotoxicity in malignant mesothelioma (MM) cells.	Sunitinib	137-139	gap junction protein alpha 1	Homo sapiens	60-71
26003083-4	2015	This work aims to evaluate the effect of the restoration of connexin 43 (Cx43) (the most ubiquitous Cx subtype) expression on sunitinib (SU)-induced cytotoxicity in malignant mesothelioma (MM) cells.	Sunitinib	137-139	gap junction protein alpha 1	Homo sapiens	73-77
26003083-4	2015	This work aims to evaluate the effect of the restoration of connexin 43 (Cx43) (the most ubiquitous Cx subtype) expression on sunitinib (SU)-induced cytotoxicity in malignant mesothelioma (MM) cells.	Sunitinib	137-139	LOC100128922	Homo sapiens	73-75
26003083-5	2015	Increased Cx43 expression in an MM cell line (H28) improved the ability of SU to inhibit receptor tyrosine kinase (RTK) signaling.	Sunitinib	75-77	gap junction protein alpha 1	Homo sapiens	10-14
26003083-5	2015	Increased Cx43 expression in an MM cell line (H28) improved the ability of SU to inhibit receptor tyrosine kinase (RTK) signaling.	Sunitinib	75-77	ret proto-oncogene	Homo sapiens	89-113
26003083-5	2015	Increased Cx43 expression in an MM cell line (H28) improved the ability of SU to inhibit receptor tyrosine kinase (RTK) signaling.	Sunitinib	75-77	ret proto-oncogene	Homo sapiens	115-118
26003083-6	2015	Moreover, higher Cx43 expression promoted SU-induced apoptosis.	Sunitinib	42-44	gap junction protein alpha 1	Homo sapiens	17-21
26003083-7	2015	The cell viability test revealed that Cx43 enhanced the cytotoxic effect of SU in a GJ-independent manner.	Sunitinib	76-78	gap junction protein alpha 1	Homo sapiens	38-42
26003083-10	2015	Furthermore, higher Cx43 expression increased the production of a cleaved (active) form of Bax during SU-induced apoptosis with no alteration in total Bax expression.	Sunitinib	102-104	gap junction protein alpha 1	Homo sapiens	20-24
26003083-10	2015	Furthermore, higher Cx43 expression increased the production of a cleaved (active) form of Bax during SU-induced apoptosis with no alteration in total Bax expression.	Sunitinib	102-104	BCL2 associated X, apoptosis regulator	Homo sapiens	91-94
26003083-11	2015	These findings indicate that Cx43 most likely increases sensitivity to SU in H28 through direct interaction with Bax.	Sunitinib	71-73	gap junction protein alpha 1	Homo sapiens	29-33
26003083-11	2015	These findings indicate that Cx43 most likely increases sensitivity to SU in H28 through direct interaction with Bax.	Sunitinib	71-73	BCL2 associated X, apoptosis regulator	Homo sapiens	113-116
25917740-0	2015	Enhanced Sensitivity to Sunitinib by Inhibition of Akt1 Expression in Human Castration-resistant Prostate Cancer PC3 Cells Both In Vitro and In Vivo.	Sunitinib	24-33	AKT serine/threonine kinase 1	Homo sapiens	51-55
25917740-0	2015	Enhanced Sensitivity to Sunitinib by Inhibition of Akt1 Expression in Human Castration-resistant Prostate Cancer PC3 Cells Both In Vitro and In Vivo.	Sunitinib	24-33	proprotein convertase subtilisin/kexin type 1	Homo sapiens	113-116
25917740-1	2015	OBJECTIVE: To investigate whether antitumor activity of sunitinib is enhanced by silencing Akt1 in a human castration-resistant prostate cancer PC3 model.	Sunitinib	56-65	AKT serine/threonine kinase 1	Homo sapiens	91-95
25917740-3	2015	Changes in various phenotypes of PC3/sh-Akt1 after treatment with sunitinib were compared with those of PC3 transfected with control vector alone (PC3/C) both in vitro and in vivo.	Sunitinib	66-75	proprotein convertase subtilisin/kexin type 1	Homo sapiens	33-36
25917740-3	2015	Changes in various phenotypes of PC3/sh-Akt1 after treatment with sunitinib were compared with those of PC3 transfected with control vector alone (PC3/C) both in vitro and in vivo.	Sunitinib	66-75	AKT serine/threonine kinase 1	Homo sapiens	40-44
25752672-8	2015	Vascular endothelial growth factor-A blocker 1 effectively restored VEGF levels, decreased cerebral oedema, and reduced vascular leakage under hypobaric hypoxia when compared to sunitinib-treated rats.	Sunitinib	178-187	vascular endothelial growth factor A	Rattus norvegicus	0-36
25917740-5	2015	However, compared with PC3/C, PC3/sh-Akt1 showed a significantly higher sensitivity to sunitinib, accompanying impaired phosphorylation of p44/42 mitogen-activated protein kinase, downregulation of Bcl-2, and upregulation of Bax.	Sunitinib	87-96	AKT serine/threonine kinase 1	Homo sapiens	37-41
25917740-6	2015	In addition, treatment with sunitinib significantly suppressed the migration ability of PC3/sh-Akt1 compared with that of PC3/C.	Sunitinib	28-37	proprotein convertase subtilisin/kexin type 1	Homo sapiens	88-91
25917740-6	2015	In addition, treatment with sunitinib significantly suppressed the migration ability of PC3/sh-Akt1 compared with that of PC3/C.	Sunitinib	28-37	AKT serine/threonine kinase 1	Homo sapiens	95-99
25917740-6	2015	In addition, treatment with sunitinib significantly suppressed the migration ability of PC3/sh-Akt1 compared with that of PC3/C.	Sunitinib	28-37	proprotein convertase subtilisin/kexin type 1	Homo sapiens	122-125
25917740-7	2015	In vivo, administration of sunitinib induced the significantly marked growth inhibition of PC3/sh-Akt1 compared with that of PC3/C, and apoptotic index in PC3/sh-Akt1 tumor in mice treated with sunitinib was significantly greater than that in PC3/C tumor.	Sunitinib	27-36	proprotein convertase subtilisin/kexin type 1	Mus musculus	91-94
25917740-7	2015	In vivo, administration of sunitinib induced the significantly marked growth inhibition of PC3/sh-Akt1 compared with that of PC3/C, and apoptotic index in PC3/sh-Akt1 tumor in mice treated with sunitinib was significantly greater than that in PC3/C tumor.	Sunitinib	27-36	thymoma viral proto-oncogene 1	Mus musculus	98-102
25917740-7	2015	In vivo, administration of sunitinib induced the significantly marked growth inhibition of PC3/sh-Akt1 compared with that of PC3/C, and apoptotic index in PC3/sh-Akt1 tumor in mice treated with sunitinib was significantly greater than that in PC3/C tumor.	Sunitinib	27-36	proprotein convertase subtilisin/kexin type 1	Mus musculus	125-128
25917740-7	2015	In vivo, administration of sunitinib induced the significantly marked growth inhibition of PC3/sh-Akt1 compared with that of PC3/C, and apoptotic index in PC3/sh-Akt1 tumor in mice treated with sunitinib was significantly greater than that in PC3/C tumor.	Sunitinib	27-36	proprotein convertase subtilisin/kexin type 1	Mus musculus	125-128
25917740-7	2015	In vivo, administration of sunitinib induced the significantly marked growth inhibition of PC3/sh-Akt1 compared with that of PC3/C, and apoptotic index in PC3/sh-Akt1 tumor in mice treated with sunitinib was significantly greater than that in PC3/C tumor.	Sunitinib	27-36	thymoma viral proto-oncogene 1	Mus musculus	162-166
25917740-7	2015	In vivo, administration of sunitinib induced the significantly marked growth inhibition of PC3/sh-Akt1 compared with that of PC3/C, and apoptotic index in PC3/sh-Akt1 tumor in mice treated with sunitinib was significantly greater than that in PC3/C tumor.	Sunitinib	27-36	proprotein convertase subtilisin/kexin type 1	Mus musculus	125-128
25917740-7	2015	In vivo, administration of sunitinib induced the significantly marked growth inhibition of PC3/sh-Akt1 compared with that of PC3/C, and apoptotic index in PC3/sh-Akt1 tumor in mice treated with sunitinib was significantly greater than that in PC3/C tumor.	Sunitinib	194-203	thymoma viral proto-oncogene 1	Mus musculus	98-102
25917740-7	2015	In vivo, administration of sunitinib induced the significantly marked growth inhibition of PC3/sh-Akt1 compared with that of PC3/C, and apoptotic index in PC3/sh-Akt1 tumor in mice treated with sunitinib was significantly greater than that in PC3/C tumor.	Sunitinib	194-203	thymoma viral proto-oncogene 1	Mus musculus	162-166
25862847-15	2015	Everolimus, sorafenib and sunitinib significantly reduced mTOR expression.	Sunitinib	26-35	mechanistic target of rapamycin kinase	Homo sapiens	58-62
25862847-17	2015	Sunitinib and sorafenib increased AREG expression in HNSCC 11A and 14C but not in CERV196.	Sunitinib	0-9	amphiregulin	Homo sapiens	34-38
25862847-19	2015	Interestingly, sorafenib and sunitinib increased AREG in HNSCC 11A and 14C, which could be a possible evasive mechanism following incubation with these drugs.	Sunitinib	29-38	amphiregulin	Homo sapiens	49-53
25862847-20	2015	On the contrary, p16-positive CERV196 showed increased susceptibility to sorafenib and sunitinib concerning suppression of AREG expression.	Sunitinib	87-96	cyclin dependent kinase inhibitor 2A	Homo sapiens	17-20
25862847-20	2015	On the contrary, p16-positive CERV196 showed increased susceptibility to sorafenib and sunitinib concerning suppression of AREG expression.	Sunitinib	87-96	amphiregulin	Homo sapiens	123-127
25123505-0	2015	Expression of TNF-alpha and CD44 is implicated in poor prognosis, cancer cell invasion, metastasis and resistance to the sunitinib treatment in clear cell renal cell carcinomas.	Sunitinib	121-130	tumor necrosis factor	Homo sapiens	14-23
25123505-0	2015	Expression of TNF-alpha and CD44 is implicated in poor prognosis, cancer cell invasion, metastasis and resistance to the sunitinib treatment in clear cell renal cell carcinomas.	Sunitinib	121-130	CD44 molecule (Indian blood group)	Homo sapiens	28-32
25123505-9	2015	Among the 25 ccRCC patients treated with sunitinib for metastatic disease, high CD44 expression was associated with poor treatment outcome.	Sunitinib	41-50	CD44 molecule (Indian blood group)	Homo sapiens	80-84
25123505-10	2015	Importantly, residual carcinoma cells in the sunitinib-treated metastatic ccRCCs were strongly positive for CD44, and the CD44 expression was significantly higher in the tumors from the sunitinib-treated patients than in those from untreated ones.	Sunitinib	45-54	CD44 molecule (Indian blood group)	Homo sapiens	108-112
25123505-10	2015	Importantly, residual carcinoma cells in the sunitinib-treated metastatic ccRCCs were strongly positive for CD44, and the CD44 expression was significantly higher in the tumors from the sunitinib-treated patients than in those from untreated ones.	Sunitinib	45-54	CD44 molecule (Indian blood group)	Homo sapiens	122-126
25123505-10	2015	Importantly, residual carcinoma cells in the sunitinib-treated metastatic ccRCCs were strongly positive for CD44, and the CD44 expression was significantly higher in the tumors from the sunitinib-treated patients than in those from untreated ones.	Sunitinib	186-195	CD44 molecule (Indian blood group)	Homo sapiens	122-126
26097571-5	2015	Dual luciferase analysis confirmed that Raf/MEK/ERK pathway could directly be regulated by SOX9, and sequential experiments demonstrated that, renal carcinoma cells could sensitize to Sorafenib/Sunitinib through Raf/MEK/ERK signaling pathway inhibition regulated by SOX9 down-regulation.	Sunitinib	194-203	zinc fingers and homeoboxes 2	Homo sapiens	212-215
26097571-5	2015	Dual luciferase analysis confirmed that Raf/MEK/ERK pathway could directly be regulated by SOX9, and sequential experiments demonstrated that, renal carcinoma cells could sensitize to Sorafenib/Sunitinib through Raf/MEK/ERK signaling pathway inhibition regulated by SOX9 down-regulation.	Sunitinib	194-203	zinc fingers and homeoboxes 2	Homo sapiens	40-43
26097571-5	2015	Dual luciferase analysis confirmed that Raf/MEK/ERK pathway could directly be regulated by SOX9, and sequential experiments demonstrated that, renal carcinoma cells could sensitize to Sorafenib/Sunitinib through Raf/MEK/ERK signaling pathway inhibition regulated by SOX9 down-regulation.	Sunitinib	194-203	mitogen-activated protein kinase kinase 7	Homo sapiens	44-47
26097571-5	2015	Dual luciferase analysis confirmed that Raf/MEK/ERK pathway could directly be regulated by SOX9, and sequential experiments demonstrated that, renal carcinoma cells could sensitize to Sorafenib/Sunitinib through Raf/MEK/ERK signaling pathway inhibition regulated by SOX9 down-regulation.	Sunitinib	194-203	mitogen-activated protein kinase 1	Homo sapiens	48-51
26097571-5	2015	Dual luciferase analysis confirmed that Raf/MEK/ERK pathway could directly be regulated by SOX9, and sequential experiments demonstrated that, renal carcinoma cells could sensitize to Sorafenib/Sunitinib through Raf/MEK/ERK signaling pathway inhibition regulated by SOX9 down-regulation.	Sunitinib	194-203	SRY-box transcription factor 9	Homo sapiens	91-95
26097571-5	2015	Dual luciferase analysis confirmed that Raf/MEK/ERK pathway could directly be regulated by SOX9, and sequential experiments demonstrated that, renal carcinoma cells could sensitize to Sorafenib/Sunitinib through Raf/MEK/ERK signaling pathway inhibition regulated by SOX9 down-regulation.	Sunitinib	194-203	mitogen-activated protein kinase kinase 7	Homo sapiens	216-219
26097571-5	2015	Dual luciferase analysis confirmed that Raf/MEK/ERK pathway could directly be regulated by SOX9, and sequential experiments demonstrated that, renal carcinoma cells could sensitize to Sorafenib/Sunitinib through Raf/MEK/ERK signaling pathway inhibition regulated by SOX9 down-regulation.	Sunitinib	194-203	mitogen-activated protein kinase 1	Homo sapiens	220-223
26097571-5	2015	Dual luciferase analysis confirmed that Raf/MEK/ERK pathway could directly be regulated by SOX9, and sequential experiments demonstrated that, renal carcinoma cells could sensitize to Sorafenib/Sunitinib through Raf/MEK/ERK signaling pathway inhibition regulated by SOX9 down-regulation.	Sunitinib	194-203	SRY-box transcription factor 9	Homo sapiens	266-270
25123505-11	2015	Our data show that TNF-alpha plays an important role in progression of ccRCCs by inducing EMT and CD44 expression, and suggest that CD44 induced by TNF-alpha may be involved in the resistance to the sunitinib treatment.	Sunitinib	199-208	tumor necrosis factor	Homo sapiens	19-28
26097571-6	2015	In a small cases with mRCC treated with Sorafenib/Sunitinib (n=38), comparative analysis showed that patients with SOX9 (-) had much better therapeutic response to TKIs than those with SOX9 (+) (PD: 9.1% vs. 56.2%, P=0.002, DCR: 90.9% vs. 43.8%, P=0.002).	Sunitinib	50-59	SRY-box transcription factor 9	Homo sapiens	115-119
25123505-11	2015	Our data show that TNF-alpha plays an important role in progression of ccRCCs by inducing EMT and CD44 expression, and suggest that CD44 induced by TNF-alpha may be involved in the resistance to the sunitinib treatment.	Sunitinib	199-208	CD44 molecule (Indian blood group)	Homo sapiens	98-102
25123505-11	2015	Our data show that TNF-alpha plays an important role in progression of ccRCCs by inducing EMT and CD44 expression, and suggest that CD44 induced by TNF-alpha may be involved in the resistance to the sunitinib treatment.	Sunitinib	199-208	CD44 molecule (Indian blood group)	Homo sapiens	132-136
25123505-11	2015	Our data show that TNF-alpha plays an important role in progression of ccRCCs by inducing EMT and CD44 expression, and suggest that CD44 induced by TNF-alpha may be involved in the resistance to the sunitinib treatment.	Sunitinib	199-208	tumor necrosis factor	Homo sapiens	148-157
25695485-0	2015	IL8 polymorphisms and overall survival in pazopanib- or sunitinib-treated patients with renal cell carcinoma.	Sunitinib	56-65	C-X-C motif chemokine ligand 8	Homo sapiens	0-3
25653444-4	2015	We also discovered that AAK1 and GAK inhibitors, including the approved anticancer drugs sunitinib and erlotinib, could block HCV assembly.	Sunitinib	89-98	AP2 associated kinase 1	Homo sapiens	24-28
25653444-4	2015	We also discovered that AAK1 and GAK inhibitors, including the approved anticancer drugs sunitinib and erlotinib, could block HCV assembly.	Sunitinib	89-98	cyclin G associated kinase	Homo sapiens	33-36
25653444-9	2015	Last, in addition to affecting assembly, sunitinib and erlotinib inhibited HCV entry at a postbinding step, their combination was synergistic, and their antiviral effect was reversed by either AAK1 or GAK overexpression.	Sunitinib	41-50	AP2 associated kinase 1	Homo sapiens	193-197
25653444-9	2015	Last, in addition to affecting assembly, sunitinib and erlotinib inhibited HCV entry at a postbinding step, their combination was synergistic, and their antiviral effect was reversed by either AAK1 or GAK overexpression.	Sunitinib	41-50	cyclin G associated kinase	Homo sapiens	201-204
25653444-10	2015	Together, these results validate AAK1 and GAK as critical regulators of HCV entry that function in part by activating EGFR, AP2M1, and NUMB and as the molecular targets underlying the antiviral effect of sunitinib and erlotinib (in addition to EGFR), respectively.	Sunitinib	204-213	AP2 associated kinase 1	Homo sapiens	33-37
25653444-10	2015	Together, these results validate AAK1 and GAK as critical regulators of HCV entry that function in part by activating EGFR, AP2M1, and NUMB and as the molecular targets underlying the antiviral effect of sunitinib and erlotinib (in addition to EGFR), respectively.	Sunitinib	204-213	cyclin G associated kinase	Homo sapiens	42-45
25756398-10	2015	CONCLUSIONS: Interleukin-8, sVEGFR-3, and SDF-1alpha were identified as predictors of sunitinib clinical outcome.	Sunitinib	86-95	C-X-C motif chemokine ligand 8	Homo sapiens	13-26
25695485-7	2015	CONCLUSIONS: Variant alleles of IL8 polymorphisms are associated with poorer survival outcomes in pazopanib- or sunitinib-treated patients with aRCC.	Sunitinib	112-121	C-X-C motif chemokine ligand 8	Homo sapiens	32-35
25756398-11	2015	Putative pro-tumorigenic CXCR4+ and VEGFR-1+ monocytes represent novel candidate markers and biologically relevant targets explaining the activity of sunitinib.	Sunitinib	150-159	C-X-C motif chemokine receptor 4	Homo sapiens	25-30
25776476-0	2015	Cytotoxic activity of sunitinib and everolimus in Caki-1 renal cancer cells is accompanied by modulations in the expression of apoptosis-related microRNA clusters and BCL2 family genes.	Sunitinib	22-31	BCL2 apoptosis regulator	Homo sapiens	167-171
25756398-11	2015	Putative pro-tumorigenic CXCR4+ and VEGFR-1+ monocytes represent novel candidate markers and biologically relevant targets explaining the activity of sunitinib.	Sunitinib	150-159	fms related receptor tyrosine kinase 1	Homo sapiens	36-43
25849942-4	2015	Upon Cox-2 inhibition PGE2 levels were normalized and efficacy of anti-vascular endothelial growth factor receptor 2 (anti-VEGFR-2) antibodies and sunitinib was enhanced.	Sunitinib	147-156	prostaglandin-endoperoxide synthase 2	Homo sapiens	5-10
25750290-7	2015	Sunitinib, sorafenib and everolimus significantly reduced the expression of VEGFR1 and -2, especially in p16-positive CERV196 cells.	Sunitinib	0-9	fms related receptor tyrosine kinase 1	Homo sapiens	76-89
25750290-8	2015	Sunitinib appeared to be more effective in reducing VEGFR1 and -2 expression than sorafenib and everolimus.	Sunitinib	0-9	fms related receptor tyrosine kinase 1	Homo sapiens	52-65
25750290-10	2015	PTEN expression increased significantly under sunitinib and sorafenib in HNSCC 11A and CERV196 cells.	Sunitinib	46-55	phosphatase and tensin homolog	Homo sapiens	0-4
25750290-13	2015	Sunitinib and sorafenib were able to increase PTEN expression, which might induce apoptosis of cancer cells.	Sunitinib	0-9	phosphatase and tensin homolog	Homo sapiens	46-50
25776476-3	2015	Herein, we sought to evaluate the cytotoxic activity of sunitinib and everolimus against renal cancer cells Caki-1 and moreover to assess their impact on the expression levels of three BCL2 family members and three apoptosis-related microRNA clusters upon incubation with the drugs or following recovery from treatment.	Sunitinib	56-65	BCL2 apoptosis regulator	Homo sapiens	185-189
25776476-7	2015	In parallel, significant modulations were observed in the expression levels of miR-145, miR-15a, and miR-16 in case of sunitinib, whereas BCL2, BAX, miR-145 and miR-15a expression was strongly affected by everolimus.	Sunitinib	119-128	microRNA 145	Homo sapiens	79-86
25776476-7	2015	In parallel, significant modulations were observed in the expression levels of miR-145, miR-15a, and miR-16 in case of sunitinib, whereas BCL2, BAX, miR-145 and miR-15a expression was strongly affected by everolimus.	Sunitinib	119-128	microRNA 15a	Homo sapiens	88-95
25260394-6	2015	The antitumor activity of hispidulin and its enhancement of the antitumor activity of sunitinib correlated with the suppression of pStat3 signaling and the consequent downregulation of Bcl-2 and survivin.	Sunitinib	86-95	BCL2 apoptosis regulator	Homo sapiens	185-190
25776476-7	2015	In parallel, significant modulations were observed in the expression levels of miR-145, miR-15a, and miR-16 in case of sunitinib, whereas BCL2, BAX, miR-145 and miR-15a expression was strongly affected by everolimus.	Sunitinib	119-128	glycerophosphodiester phosphodiesterase 1	Homo sapiens	101-107
25776476-7	2015	In parallel, significant modulations were observed in the expression levels of miR-145, miR-15a, and miR-16 in case of sunitinib, whereas BCL2, BAX, miR-145 and miR-15a expression was strongly affected by everolimus.	Sunitinib	119-128	microRNA 15a	Homo sapiens	161-168
25776476-8	2015	Overall, our data support the notion that sunitinib and everolimus are able to directly induce cell death in renal cancer cells and simultaneously affect the expression levels of their apoptosis-related microRNAs and BCL2 family members upon this process.	Sunitinib	42-51	BCL2 apoptosis regulator	Homo sapiens	217-221
25663899-6	2015	Functionally, the role of ABCG2 in the resistance to sunitinib was confirmed by the use of the ABCG2 inhibitors fumitremorgin C and diethylstilbestrol, which blocked cell resistance.	Sunitinib	53-62	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	26-31
25637219-0	2015	AXL as a modulator of sunitinib response in glioblastoma cell lines.	Sunitinib	22-31	AXL receptor tyrosine kinase	Homo sapiens	0-3
25637219-3	2015	We recently identified the RTK AXL as a putative target for the pan-RTK inhibitors cediranib and sunitinib, which are under clinical trials for glioblastoma patients.	Sunitinib	97-106	ret proto-oncogene	Homo sapiens	27-30
25637219-3	2015	We recently identified the RTK AXL as a putative target for the pan-RTK inhibitors cediranib and sunitinib, which are under clinical trials for glioblastoma patients.	Sunitinib	97-106	AXL receptor tyrosine kinase	Homo sapiens	31-34
25637219-3	2015	We recently identified the RTK AXL as a putative target for the pan-RTK inhibitors cediranib and sunitinib, which are under clinical trials for glioblastoma patients.	Sunitinib	97-106	ret proto-oncogene	Homo sapiens	68-71
25637219-4	2015	Here, we provide evidence that AXL activity can modulate sunitinib response in glioblastoma cell lines.	Sunitinib	57-66	AXL receptor tyrosine kinase	Homo sapiens	31-34
25637219-5	2015	We found that AXL knockdown conferred lower sensitivity to sunitinib by rescuing migratory defects and inhibiting apoptosis in cells expressing high AXL basal levels.	Sunitinib	59-68	AXL receptor tyrosine kinase	Homo sapiens	14-17
25637219-5	2015	We found that AXL knockdown conferred lower sensitivity to sunitinib by rescuing migratory defects and inhibiting apoptosis in cells expressing high AXL basal levels.	Sunitinib	59-68	AXL receptor tyrosine kinase	Homo sapiens	149-152
25637219-6	2015	Accordingly, overactivation of AXL by its ligand GAS6 rendered AXL positive glioblastoma cells more sensitive to sunitinib.	Sunitinib	113-122	AXL receptor tyrosine kinase	Homo sapiens	31-34
25637219-6	2015	Accordingly, overactivation of AXL by its ligand GAS6 rendered AXL positive glioblastoma cells more sensitive to sunitinib.	Sunitinib	113-122	growth arrest specific 6	Homo sapiens	49-53
25637219-6	2015	Accordingly, overactivation of AXL by its ligand GAS6 rendered AXL positive glioblastoma cells more sensitive to sunitinib.	Sunitinib	113-122	AXL receptor tyrosine kinase	Homo sapiens	63-66
25637219-8	2015	The combination of sunitinib with a specific AKT inhibitor reverted the resistance of AXL-silenced cells to sunitinib.	Sunitinib	19-28	AKT serine/threonine kinase 1	Homo sapiens	45-48
25637219-8	2015	The combination of sunitinib with a specific AKT inhibitor reverted the resistance of AXL-silenced cells to sunitinib.	Sunitinib	19-28	AXL receptor tyrosine kinase	Homo sapiens	86-89
25637219-8	2015	The combination of sunitinib with a specific AKT inhibitor reverted the resistance of AXL-silenced cells to sunitinib.	Sunitinib	108-117	AKT serine/threonine kinase 1	Homo sapiens	45-48
25637219-8	2015	The combination of sunitinib with a specific AKT inhibitor reverted the resistance of AXL-silenced cells to sunitinib.	Sunitinib	108-117	AXL receptor tyrosine kinase	Homo sapiens	86-89
25637219-9	2015	Together, our results suggest that sunitinib inhibits AXL and AXL activation status modulates therapy response of glioblastoma cells to sunitinib.	Sunitinib	35-44	AXL receptor tyrosine kinase	Homo sapiens	54-57
25637219-9	2015	Together, our results suggest that sunitinib inhibits AXL and AXL activation status modulates therapy response of glioblastoma cells to sunitinib.	Sunitinib	35-44	AXL receptor tyrosine kinase	Homo sapiens	62-65
25637219-9	2015	Together, our results suggest that sunitinib inhibits AXL and AXL activation status modulates therapy response of glioblastoma cells to sunitinib.	Sunitinib	136-145	AXL receptor tyrosine kinase	Homo sapiens	62-65
25637219-10	2015	Moreover, it indicates that combining sunitinib therapy with AKT pathway inhibitors could overcome sunitinib resistance.	Sunitinib	99-108	AKT serine/threonine kinase 1	Homo sapiens	61-64
25837361-9	2015	The expressions of Fas ligand and PARP in T24 cells treated with sunitinib malate exhibited a concentration-dependent increase.	Sunitinib	65-81	Fas ligand	Homo sapiens	19-29
25837361-9	2015	The expressions of Fas ligand and PARP in T24 cells treated with sunitinib malate exhibited a concentration-dependent increase.	Sunitinib	65-81	poly(ADP-ribose) polymerase 1	Homo sapiens	34-38
25663899-6	2015	Functionally, the role of ABCG2 in the resistance to sunitinib was confirmed by the use of the ABCG2 inhibitors fumitremorgin C and diethylstilbestrol, which blocked cell resistance.	Sunitinib	53-62	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	95-100
25675297-0	2015	p21-activated kinase 1 determines stem-like phenotype and sunitinib resistance via NF-kappaB/IL-6 activation in renal cell carcinoma.	Sunitinib	58-67	nuclear factor kappa B subunit 1	Homo sapiens	83-92
25460504-0	2015	Sunitinib prevents cachexia and prolongs survival of mice bearing renal cancer by restraining STAT3 and MuRF-1 activation in muscle.	Sunitinib	0-9	signal transducer and activator of transcription 3	Mus musculus	94-99
25460504-0	2015	Sunitinib prevents cachexia and prolongs survival of mice bearing renal cancer by restraining STAT3 and MuRF-1 activation in muscle.	Sunitinib	0-9	tripartite motif-containing 63	Mus musculus	104-110
25460504-9	2015	Among the mechanisms, we herein show that sunitinib is able to restrain the overactivation of STAT3 and MuRF-1 pathways, involved in enhanced muscle protein catabolism during cancer cachexia.	Sunitinib	42-51	signal transducer and activator of transcription 3	Mus musculus	94-99
25460504-9	2015	Among the mechanisms, we herein show that sunitinib is able to restrain the overactivation of STAT3 and MuRF-1 pathways, involved in enhanced muscle protein catabolism during cancer cachexia.	Sunitinib	42-51	tripartite motif-containing 63	Mus musculus	104-110
25880253-0	2015	Melan-A/MART-1 immunity in a EWS-ATF1 translocated clear cell sarcoma patient treated with sunitinib: a case report.	Sunitinib	91-100	melan-A	Homo sapiens	0-7
25880253-0	2015	Melan-A/MART-1 immunity in a EWS-ATF1 translocated clear cell sarcoma patient treated with sunitinib: a case report.	Sunitinib	91-100	melan-A	Homo sapiens	8-14
25880253-0	2015	Melan-A/MART-1 immunity in a EWS-ATF1 translocated clear cell sarcoma patient treated with sunitinib: a case report.	Sunitinib	91-100	activating transcription factor 1	Homo sapiens	29-37
25880253-4	2015	In the case we report here, treatment with sunitinib induced a long-lasting clinical response that was associated with an immune activation directed against Melan-A/MART-1 antigen.	Sunitinib	43-52	melan-A	Homo sapiens	157-164
25880253-4	2015	In the case we report here, treatment with sunitinib induced a long-lasting clinical response that was associated with an immune activation directed against Melan-A/MART-1 antigen.	Sunitinib	43-52	melan-A	Homo sapiens	165-171
25675297-7	2015	Furthermore, nuclear factor-kappaB (NF-kappaB)/interleukin-6 (IL-6) activation was found to be responsible for PAK1-mediated stem-like phenotype following sunitinib treatment.	Sunitinib	155-164	interleukin 6	Homo sapiens	62-66
25675297-7	2015	Furthermore, nuclear factor-kappaB (NF-kappaB)/interleukin-6 (IL-6) activation was found to be responsible for PAK1-mediated stem-like phenotype following sunitinib treatment.	Sunitinib	155-164	p21 (RAC1) activated kinase 1	Homo sapiens	111-115
25675297-8	2015	Both IL-6 neutralizing antibody and IPA3 administration enhanced tumor growth inhibition effect of sunitinib treatment on RCC cells in vitro and in vivo.	Sunitinib	99-108	interleukin 6	Homo sapiens	5-9
25675297-9	2015	Our results unraveled that oncogenic activation of PAK1 defines an important mechanism for maintaining stem-like phenotype and sunitinib resistance through NF-kappaB/IL-6 activation in RCC, lending PAK1-mediated NF-kappaB/IL-6 activation considerable appeal as novel pharmacological therapeutic targets against sunitinib resistance.	Sunitinib	127-136	p21 (RAC1) activated kinase 1	Homo sapiens	51-55
25675297-9	2015	Our results unraveled that oncogenic activation of PAK1 defines an important mechanism for maintaining stem-like phenotype and sunitinib resistance through NF-kappaB/IL-6 activation in RCC, lending PAK1-mediated NF-kappaB/IL-6 activation considerable appeal as novel pharmacological therapeutic targets against sunitinib resistance.	Sunitinib	127-136	nuclear factor kappa B subunit 1	Homo sapiens	156-165
25675297-9	2015	Our results unraveled that oncogenic activation of PAK1 defines an important mechanism for maintaining stem-like phenotype and sunitinib resistance through NF-kappaB/IL-6 activation in RCC, lending PAK1-mediated NF-kappaB/IL-6 activation considerable appeal as novel pharmacological therapeutic targets against sunitinib resistance.	Sunitinib	127-136	interleukin 6	Homo sapiens	166-170
25675297-9	2015	Our results unraveled that oncogenic activation of PAK1 defines an important mechanism for maintaining stem-like phenotype and sunitinib resistance through NF-kappaB/IL-6 activation in RCC, lending PAK1-mediated NF-kappaB/IL-6 activation considerable appeal as novel pharmacological therapeutic targets against sunitinib resistance.	Sunitinib	127-136	nuclear factor kappa B subunit 1	Homo sapiens	212-221
25675297-0	2015	p21-activated kinase 1 determines stem-like phenotype and sunitinib resistance via NF-kappaB/IL-6 activation in renal cell carcinoma.	Sunitinib	58-67	interleukin 6	Homo sapiens	93-97
25675297-9	2015	Our results unraveled that oncogenic activation of PAK1 defines an important mechanism for maintaining stem-like phenotype and sunitinib resistance through NF-kappaB/IL-6 activation in RCC, lending PAK1-mediated NF-kappaB/IL-6 activation considerable appeal as novel pharmacological therapeutic targets against sunitinib resistance.	Sunitinib	127-136	interleukin 6	Homo sapiens	222-226
25675297-9	2015	Our results unraveled that oncogenic activation of PAK1 defines an important mechanism for maintaining stem-like phenotype and sunitinib resistance through NF-kappaB/IL-6 activation in RCC, lending PAK1-mediated NF-kappaB/IL-6 activation considerable appeal as novel pharmacological therapeutic targets against sunitinib resistance.	Sunitinib	311-320	p21 (RAC1) activated kinase 1	Homo sapiens	51-55
25675297-6	2015	Stem-like phenotype due to sunitinib administration via increased PAK1 kinase activation could be ameliorated by PAK1 shRNA, PAK1 mutant K299R and IPA3.	Sunitinib	27-36	p21 (RAC1) activated kinase 1	Homo sapiens	66-70
25675297-9	2015	Our results unraveled that oncogenic activation of PAK1 defines an important mechanism for maintaining stem-like phenotype and sunitinib resistance through NF-kappaB/IL-6 activation in RCC, lending PAK1-mediated NF-kappaB/IL-6 activation considerable appeal as novel pharmacological therapeutic targets against sunitinib resistance.	Sunitinib	311-320	nuclear factor kappa B subunit 1	Homo sapiens	156-165
25675297-9	2015	Our results unraveled that oncogenic activation of PAK1 defines an important mechanism for maintaining stem-like phenotype and sunitinib resistance through NF-kappaB/IL-6 activation in RCC, lending PAK1-mediated NF-kappaB/IL-6 activation considerable appeal as novel pharmacological therapeutic targets against sunitinib resistance.	Sunitinib	311-320	interleukin 6	Homo sapiens	166-170
25675297-9	2015	Our results unraveled that oncogenic activation of PAK1 defines an important mechanism for maintaining stem-like phenotype and sunitinib resistance through NF-kappaB/IL-6 activation in RCC, lending PAK1-mediated NF-kappaB/IL-6 activation considerable appeal as novel pharmacological therapeutic targets against sunitinib resistance.	Sunitinib	311-320	p21 (RAC1) activated kinase 1	Homo sapiens	198-202
25675297-6	2015	Stem-like phenotype due to sunitinib administration via increased PAK1 kinase activation could be ameliorated by PAK1 shRNA, PAK1 mutant K299R and IPA3.	Sunitinib	27-36	p21 (RAC1) activated kinase 1	Homo sapiens	113-117
25675297-9	2015	Our results unraveled that oncogenic activation of PAK1 defines an important mechanism for maintaining stem-like phenotype and sunitinib resistance through NF-kappaB/IL-6 activation in RCC, lending PAK1-mediated NF-kappaB/IL-6 activation considerable appeal as novel pharmacological therapeutic targets against sunitinib resistance.	Sunitinib	311-320	nuclear factor kappa B subunit 1	Homo sapiens	212-221
25675297-9	2015	Our results unraveled that oncogenic activation of PAK1 defines an important mechanism for maintaining stem-like phenotype and sunitinib resistance through NF-kappaB/IL-6 activation in RCC, lending PAK1-mediated NF-kappaB/IL-6 activation considerable appeal as novel pharmacological therapeutic targets against sunitinib resistance.	Sunitinib	311-320	interleukin 6	Homo sapiens	222-226
25675297-6	2015	Stem-like phenotype due to sunitinib administration via increased PAK1 kinase activation could be ameliorated by PAK1 shRNA, PAK1 mutant K299R and IPA3.	Sunitinib	27-36	p21 (RAC1) activated kinase 1	Homo sapiens	113-117
25675301-1	2015	The angiogenesis inhibitor sunitinib is a tyrosine kinase inhibitor that acts mainly on the VEGF and PDGF pathways.	Sunitinib	27-36	vascular endothelial growth factor A	Mus musculus	92-96
25675297-7	2015	Furthermore, nuclear factor-kappaB (NF-kappaB)/interleukin-6 (IL-6) activation was found to be responsible for PAK1-mediated stem-like phenotype following sunitinib treatment.	Sunitinib	155-164	nuclear factor kappa B subunit 1	Homo sapiens	13-34
25675297-7	2015	Furthermore, nuclear factor-kappaB (NF-kappaB)/interleukin-6 (IL-6) activation was found to be responsible for PAK1-mediated stem-like phenotype following sunitinib treatment.	Sunitinib	155-164	nuclear factor kappa B subunit 1	Homo sapiens	36-46
25675297-7	2015	Furthermore, nuclear factor-kappaB (NF-kappaB)/interleukin-6 (IL-6) activation was found to be responsible for PAK1-mediated stem-like phenotype following sunitinib treatment.	Sunitinib	155-164	interleukin 6	Homo sapiens	47-60
25363319-7	2015	Tumour growth and intratumour VEGF receptor-2 expressions were significantly reduced in sunitinib-treated mice, while the expression of the other targeted receptors, PDGF receptor -alpha or -beta and fibroblast growth factor receptor-1, remained unaffected.	Sunitinib	88-97	kinase insert domain protein receptor	Mus musculus	30-45
25363319-9	2015	There were intratumour areas where the signal intensity of sunitinib correlated with expression of VEGF receptor-2.	Sunitinib	59-68	kinase insert domain protein receptor	Mus musculus	99-114
25344452-9	2015	The LBM (p &lt; 0.0001) and a polymorphism in the ABCG2 transporter (421C&gt;A) (p = 0.014) were two independent parameters accounting for the variability of composite (sunitinib + SU12662) exposure.	Sunitinib	169-178	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	50-55
25458015-10	2015	We determined the underlying pathways by which sunitinib operates as a toxin on gliomas and found vascular endothelial growth factor receptor 2 (VEGFR2, KDR/Flk1) as the main target to execute gliomatoxicity.	Sunitinib	47-56	kinase insert domain receptor	Homo sapiens	98-143
25458015-10	2015	We determined the underlying pathways by which sunitinib operates as a toxin on gliomas and found vascular endothelial growth factor receptor 2 (VEGFR2, KDR/Flk1) as the main target to execute gliomatoxicity.	Sunitinib	47-56	kinase insert domain receptor	Homo sapiens	153-156
25458015-10	2015	We determined the underlying pathways by which sunitinib operates as a toxin on gliomas and found vascular endothelial growth factor receptor 2 (VEGFR2, KDR/Flk1) as the main target to execute gliomatoxicity.	Sunitinib	47-56	kinase insert domain receptor	Homo sapiens	157-161
25458015-11	2015	The apoptosis-inducing effect of sunitinib can be mimicked by inhibition of VEGFR2.	Sunitinib	33-42	kinase insert domain receptor	Homo sapiens	76-82
24403097-5	2015	RESULTS: Sunitinib interacts with CYP3A4 inducers or inhibitors and with P-glycoprotein and ABCG2 substrates.	Sunitinib	9-18	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	92-97
25444514-10	2015	It is concluded that an mTOR-inhibitor for second-line therapy could be the strategy of choice after first-line sunitinib failure.	Sunitinib	112-121	mechanistic target of rapamycin kinase	Homo sapiens	24-28
25422908-1	2015	BACKGROUND: Sunitinib (VEGFR/PDGFR inhibitor) and everolimus (mTOR inhibitor) are both approved for advanced renal cell carcinoma (RCC) as first-line and second-line therapy, respectively.	Sunitinib	12-21	kinase insert domain receptor	Homo sapiens	23-28
25519701-12	2015	Furthermore, specific EZH2 inhibition resulted in increased in vitro antitumor effect of sunitinib.	Sunitinib	89-98	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	22-26
25437118-5	2015	We found that chronic restraint stress markedly weakened the efficacy of sunitinib, primarily through promoting the expression of vascular endothelial growth factor (VEGF) and interleukin-8 (IL-8) to stimulate tumor angiogenesis in vivo.	Sunitinib	73-82	vascular endothelial growth factor A	Mus musculus	130-164
25437118-5	2015	We found that chronic restraint stress markedly weakened the efficacy of sunitinib, primarily through promoting the expression of vascular endothelial growth factor (VEGF) and interleukin-8 (IL-8) to stimulate tumor angiogenesis in vivo.	Sunitinib	73-82	vascular endothelial growth factor A	Mus musculus	166-170
25437118-5	2015	We found that chronic restraint stress markedly weakened the efficacy of sunitinib, primarily through promoting the expression of vascular endothelial growth factor (VEGF) and interleukin-8 (IL-8) to stimulate tumor angiogenesis in vivo.	Sunitinib	73-82	chemokine (C-X-C motif) ligand 15	Mus musculus	176-189
25437118-5	2015	We found that chronic restraint stress markedly weakened the efficacy of sunitinib, primarily through promoting the expression of vascular endothelial growth factor (VEGF) and interleukin-8 (IL-8) to stimulate tumor angiogenesis in vivo.	Sunitinib	73-82	chemokine (C-X-C motif) ligand 15	Mus musculus	191-195
25437118-7	2015	In vitro, norepinephrine up-regulated expression of VEGF and IL-8 in sunitinib-treated cancer cells mainly through the beta-adrenoceptor-cAMP-PKA signaling pathway.	Sunitinib	69-78	vascular endothelial growth factor A	Mus musculus	52-56
25437118-7	2015	In vitro, norepinephrine up-regulated expression of VEGF and IL-8 in sunitinib-treated cancer cells mainly through the beta-adrenoceptor-cAMP-PKA signaling pathway.	Sunitinib	69-78	chemokine (C-X-C motif) ligand 15	Mus musculus	61-65
25422908-1	2015	BACKGROUND: Sunitinib (VEGFR/PDGFR inhibitor) and everolimus (mTOR inhibitor) are both approved for advanced renal cell carcinoma (RCC) as first-line and second-line therapy, respectively.	Sunitinib	12-21	platelet derived growth factor receptor beta	Homo sapiens	29-34
25455500-6	2015	We hypothesized that inhibition of multidrug resistant transporters by elacridar (dual inhibitor of P-glycoprotein and ABCG 2) might overcome sunitinib resistance in experimental renal cell carcinoma.	Sunitinib	142-151	ATP binding cassette subfamily B member 1	Homo sapiens	100-114
25455500-6	2015	We hypothesized that inhibition of multidrug resistant transporters by elacridar (dual inhibitor of P-glycoprotein and ABCG 2) might overcome sunitinib resistance in experimental renal cell carcinoma.	Sunitinib	142-151	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	119-125
25455500-11	2015	ABCG2 function was inhibited by sunitinib alone or combination with elacridar but not elacridar alone.	Sunitinib	32-41	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
25455500-12	2015	These findings suggest that sunitinib resistance involves multidrug resistance transporters, and in combination with elacridar, can be reversed in renal carcinoma cells by P-glycoprotein inhibition.	Sunitinib	28-37	ATP binding cassette subfamily B member 1	Homo sapiens	172-186
26064968-0	2015	miR-155 and miR-484 Are Associated with Time to Progression in Metastatic Renal Cell Carcinoma Treated with Sunitinib.	Sunitinib	108-117	microRNA 155	Homo sapiens	0-7
26312386-6	2015	At these concentrations, sunitinib accumulated in lysosomes, which downregulated the activity of the lysosomal protease CTSB (cathepsin B) and led to incomplete autophagic flux.	Sunitinib	25-34	cathepsin B	Homo sapiens	120-124
26312386-6	2015	At these concentrations, sunitinib accumulated in lysosomes, which downregulated the activity of the lysosomal protease CTSB (cathepsin B) and led to incomplete autophagic flux.	Sunitinib	25-34	cathepsin B	Homo sapiens	126-137
26312386-8	2015	Sunitinib stimulated the expression of ABCB1 (ATP-binding cassette, sub-family B [MDR/TAP], member 1), which participates in the accumulation of the drug in autolysosomes and favor its cellular efflux.	Sunitinib	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	39-44
26312386-8	2015	Sunitinib stimulated the expression of ABCB1 (ATP-binding cassette, sub-family B [MDR/TAP], member 1), which participates in the accumulation of the drug in autolysosomes and favor its cellular efflux.	Sunitinib	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	46-100
25446042-2	2015	Sunitinib, a tyrosine kinase inhibitor of the VEGF receptor, has become the mainstay of treatment for these patients.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	46-50
25993161-7	2015	For recurrent and aggressive tumors, inhibitors of the vascular endothelial growth factor (VEGF) pathway, such as vatalinib, bevacizumab, and sunitinib, showed signs of activity in small, uncontrolled studies, and prospective clinical studies will test the efficacy of the tetrahydroisoquinoline trabectedin and of SMO and AKT1 inhibitors.	Sunitinib	142-151	vascular endothelial growth factor A	Homo sapiens	55-89
25993161-7	2015	For recurrent and aggressive tumors, inhibitors of the vascular endothelial growth factor (VEGF) pathway, such as vatalinib, bevacizumab, and sunitinib, showed signs of activity in small, uncontrolled studies, and prospective clinical studies will test the efficacy of the tetrahydroisoquinoline trabectedin and of SMO and AKT1 inhibitors.	Sunitinib	142-151	vascular endothelial growth factor A	Homo sapiens	91-95
25993161-7	2015	For recurrent and aggressive tumors, inhibitors of the vascular endothelial growth factor (VEGF) pathway, such as vatalinib, bevacizumab, and sunitinib, showed signs of activity in small, uncontrolled studies, and prospective clinical studies will test the efficacy of the tetrahydroisoquinoline trabectedin and of SMO and AKT1 inhibitors.	Sunitinib	142-151	smoothened, frizzled class receptor	Homo sapiens	315-318
25993161-7	2015	For recurrent and aggressive tumors, inhibitors of the vascular endothelial growth factor (VEGF) pathway, such as vatalinib, bevacizumab, and sunitinib, showed signs of activity in small, uncontrolled studies, and prospective clinical studies will test the efficacy of the tetrahydroisoquinoline trabectedin and of SMO and AKT1 inhibitors.	Sunitinib	142-151	AKT serine/threonine kinase 1	Homo sapiens	323-327
26320436-8	2015	Six month disease control rate (complete response, partial response and stable disease) in response to sunitinib was significantly higher in patients with normal (&lt;=0.5 mg/dl) than elevated baseline CRP (p&lt;0.001).	Sunitinib	103-112	C-reactive protein	Homo sapiens	202-205
26320436-9	2015	CONCLUSIONS: CRP is a significant independent predictor of PFS for Japanese patients with mCCRCC treated with first-line sunitinib.	Sunitinib	121-130	C-reactive protein	Homo sapiens	13-16
26320436-10	2015	Pretreatment CRP concentration may be a useful biomarker predicting response to sunitinib treatment.	Sunitinib	80-89	C-reactive protein	Homo sapiens	13-16
26064968-0	2015	miR-155 and miR-484 Are Associated with Time to Progression in Metastatic Renal Cell Carcinoma Treated with Sunitinib.	Sunitinib	108-117	microRNA 484	Homo sapiens	12-19
26064968-12	2015	miR-155 and miR-484 are potentially connected with sunitinib resistance and failure of the therapy.	Sunitinib	51-60	microRNA 155	Homo sapiens	0-7
26064968-12	2015	miR-155 and miR-484 are potentially connected with sunitinib resistance and failure of the therapy.	Sunitinib	51-60	microRNA 484	Homo sapiens	12-19
26788996-5	2015	Sunitinib inhibited PDGF-stimulated proliferation, migration, phosphorylation of MAPK and PI3K/Akt proteins and changes in the expression of cell-cycle regulatory proteins in vascular smooth-muscle cells as well as VEGF-stimulated endothelial cell proliferation in vitro.	Sunitinib	0-9	AKT serine/threonine kinase 1	Homo sapiens	95-98
25376776-7	2015	In the presence of VEGF stimulation, the ROCK inhibitor suppressed stretch-induced sprout alignment but did not affect stretch-induced sprout density; in contrast, the receptor tyrosine kinase (RTK) inhibitor sunitinib had no effect on stretch-induced alignment but trended toward suppressed stretch-induced sprout density.	Sunitinib	209-218	ret proto-oncogene	Homo sapiens	194-197
24865476-13	2015	Sunitinib also blocked LRP1 phosphorylation in response to PDGF-BB and induced phosphorylation of ERK, but this latter event was not affected by LRP1 knockdown.	Sunitinib	0-9	LDL receptor related protein 1	Rattus norvegicus	23-27
24865476-13	2015	Sunitinib also blocked LRP1 phosphorylation in response to PDGF-BB and induced phosphorylation of ERK, but this latter event was not affected by LRP1 knockdown.	Sunitinib	0-9	Eph receptor B1	Rattus norvegicus	98-101
25361735-6	2015	Inhibition of VEGF signaling in B16 melanoma tumor-bearing mice by sunitinib treatment resulted in up-regulation of CXCL10 and CXCL11 in tumor vessels, accompanied by up to 18-fold increased infiltration of CD3(+) T-lymphocytes in B16 tumors.	Sunitinib	67-76	vascular endothelial growth factor A	Mus musculus	14-18
25361735-6	2015	Inhibition of VEGF signaling in B16 melanoma tumor-bearing mice by sunitinib treatment resulted in up-regulation of CXCL10 and CXCL11 in tumor vessels, accompanied by up to 18-fold increased infiltration of CD3(+) T-lymphocytes in B16 tumors.	Sunitinib	67-76	chemokine (C-X-C motif) ligand 10	Mus musculus	116-122
25361735-6	2015	Inhibition of VEGF signaling in B16 melanoma tumor-bearing mice by sunitinib treatment resulted in up-regulation of CXCL10 and CXCL11 in tumor vessels, accompanied by up to 18-fold increased infiltration of CD3(+) T-lymphocytes in B16 tumors.	Sunitinib	67-76	chemokine (C-X-C motif) ligand 11	Mus musculus	127-133
26788996-5	2015	Sunitinib inhibited PDGF-stimulated proliferation, migration, phosphorylation of MAPK and PI3K/Akt proteins and changes in the expression of cell-cycle regulatory proteins in vascular smooth-muscle cells as well as VEGF-stimulated endothelial cell proliferation in vitro.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	215-219
25381264-6	2015	Treatment with single-agent crizotinib reduced tumor vascularization but failed to inhibit tumor growth in either model, despite also a significant increase of c-met expression and phosphorylation in the sunitinib-resistant tumors.	Sunitinib	204-213	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	160-165
25100872-2	2015	Sunitinib malate (SU011248) is a small-molecule tyrosine kinase inhibitor that targets vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor, abundant in meningiomas.	Sunitinib	0-16	kinase insert domain receptor	Homo sapiens	87-130
25519698-4	2015	Axitinib, pazopanib, and sunitinib inhibited hENT1 at low micromolar concentrations.	Sunitinib	25-34	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	45-50
25519698-6	2015	Pazopanib &gt; axitinib &gt;= sunitinib inhibited hENT1 with IC50 values of 2, 7, and 29 mumol/L, respectively, leading to reduced intracellular gemcitabine and FLT accumulation.	Sunitinib	30-39	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	50-55
25100872-2	2015	Sunitinib malate (SU011248) is a small-molecule tyrosine kinase inhibitor that targets vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor, abundant in meningiomas.	Sunitinib	0-16	kinase insert domain receptor	Homo sapiens	132-137
25100872-2	2015	Sunitinib malate (SU011248) is a small-molecule tyrosine kinase inhibitor that targets vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor, abundant in meningiomas.	Sunitinib	18-26	kinase insert domain receptor	Homo sapiens	87-130
25100872-2	2015	Sunitinib malate (SU011248) is a small-molecule tyrosine kinase inhibitor that targets vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor, abundant in meningiomas.	Sunitinib	18-26	kinase insert domain receptor	Homo sapiens	132-137
24710685-5	2015	VEGFR-2 expression was associated significantly with initial and best overall responses to sunitinib, along with Karnofsky performance status and Memorial Sloan-Kettering Cancer Center prognostic risk group.	Sunitinib	91-100	kinase insert domain receptor	Homo sapiens	0-7
25575050-0	2015	[Inhibition of sunitinib on the expressions of PD-L1 and PD-L2 of mouse bone marrow-derived dendritic cells].	Sunitinib	15-24	CD274 antigen	Mus musculus	47-52
25575050-0	2015	[Inhibition of sunitinib on the expressions of PD-L1 and PD-L2 of mouse bone marrow-derived dendritic cells].	Sunitinib	15-24	programmed cell death 1 ligand 2	Mus musculus	57-62
25575050-1	2015	OBJECTIVE: To observe the changes of programmed death-1 ligand 1 (PD-L1) and PD-L2 expressions on mouse bone marrow-derived dendritic cells (DCs) stimulated by sunitinib.	Sunitinib	160-169	CD274 antigen	Mus musculus	37-64
24710685-9	2015	CONCLUSION: VEGFR-2 expression might be a useful biomarker for predicting the response to sunitinib by patients with metastatic RCC.	Sunitinib	90-99	kinase insert domain receptor	Homo sapiens	12-19
25575050-1	2015	OBJECTIVE: To observe the changes of programmed death-1 ligand 1 (PD-L1) and PD-L2 expressions on mouse bone marrow-derived dendritic cells (DCs) stimulated by sunitinib.	Sunitinib	160-169	CD274 antigen	Mus musculus	66-71
25575050-1	2015	OBJECTIVE: To observe the changes of programmed death-1 ligand 1 (PD-L1) and PD-L2 expressions on mouse bone marrow-derived dendritic cells (DCs) stimulated by sunitinib.	Sunitinib	160-169	programmed cell death 1 ligand 2	Mus musculus	77-82
25621299-9	2014	The lysosomal capacity reflected by LAMP-1 and -2 expression was higher in HT-29SUN compared to HT-29PAR tumors indicating an increased sequestration of sunitinib in lysosomes of resistant tumors.	Sunitinib	153-162	lysosomal associated membrane protein 1	Homo sapiens	36-49
25575050-4	2015	RESULTS: Compared with the control group, the expression of PD-L1 on mature DCs (mDCs) and all DCs [including mature DCs and immature DCs (imDCs)] was significantly down-regulated in sunitinib treatment groups.	Sunitinib	183-192	CD274 antigen	Mus musculus	60-65
25575050-5	2015	The PD-L1 expression percentages of imDCs, mDCs and DCs were significantly reduced in sunitinib treatment groups; the percentage of mDCs expressing PD-L2 also dropped in all treatment groups, and the percentage of DCs expressing PD-L2 decreased in 100 and 300 ng/mL sunitinib treatment groups.	Sunitinib	86-95	CD274 antigen	Mus musculus	4-9
25575050-6	2015	CONCLUSION: Sunitinib can significantly reduce the expressions of PD-L1 and PD-L2 on mouse DCs.	Sunitinib	12-21	CD274 antigen	Mus musculus	66-71
25575050-6	2015	CONCLUSION: Sunitinib can significantly reduce the expressions of PD-L1 and PD-L2 on mouse DCs.	Sunitinib	12-21	programmed cell death 1 ligand 2	Mus musculus	76-81
25540214-3	2014	When started on sunitinib he experienced improvement in his diabetes control with reduction in his insulin requirements, which later worsened when sunitinib was reduced or stopped.	Sunitinib	16-25	insulin	Homo sapiens	99-106
25515134-0	2014	Sunitinib-induced severe toxicities in a Japanese patient with the ABCG2 421 AA genotype.	Sunitinib	0-9	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	67-72
25515134-1	2014	BACKGROUND: Sunitinib is a multi-targeted receptor tyrosine kinase inhibitor that acts against receptors for vascular endothelial growth factor and platelet-derived growth factor.	Sunitinib	12-21	vascular endothelial growth factor A	Homo sapiens	109-143
25515134-10	2014	The patient"s genotype of ABCG2 (ATP-binding cassette, sub-family G (WHITE), member 2) 421C &gt; A was homozygous for the variant allele (AA), which was reported to be associated with high exposure to sunitinib.	Sunitinib	201-210	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	26-31
25515134-11	2014	Therefore, we speculated that the extremely high plasma concentrations of sunitinib and SU12662 caused by the ABCG2 421 AA genotype might have resulted in severe toxicities to the patient.	Sunitinib	74-83	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	110-115
25461627-8	2014	CONCLUSION: The orally-available XPO1 inhibitor, KPT-330, represents a novel target for RCC whose in vivo efficacy approaches that of sunitinib.	Sunitinib	134-143	exportin 1	Homo sapiens	33-37
25353068-5	2014	Our results demonstrated that a significantly higher amount of sunitinib could be delivered to the U87MG tumor by targeting VEGFR when compared with the non-targeted counterparts.	Sunitinib	63-72	kinase insert domain receptor	Homo sapiens	124-129
25117211-7	2014	KEY RESULTS: Among 12 different compounds, sunitinib inhibited CDK5 with an IC50 of 4.2 muM.	Sunitinib	43-52	cyclin dependent kinase 5	Homo sapiens	63-67
25117211-8	2014	In silico analysis revealed that, similarly to roscovitine, sunitinib fitted 6 of 10 features of the CDK5 pharmacophore.	Sunitinib	60-69	cyclin dependent kinase 5	Homo sapiens	101-105
25117211-9	2014	In a cell-based model, sunitinib reduced CDK5 phosphorylation (pCDK5), calpain-dependent p35/p25 conversion and protected neuronal cells from the toxic effects of gp120.	Sunitinib	23-32	cyclin dependent kinase 5	Homo sapiens	41-45
25117211-9	2014	In a cell-based model, sunitinib reduced CDK5 phosphorylation (pCDK5), calpain-dependent p35/p25 conversion and protected neuronal cells from the toxic effects of gp120.	Sunitinib	23-32	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	89-92
25117211-9	2014	In a cell-based model, sunitinib reduced CDK5 phosphorylation (pCDK5), calpain-dependent p35/p25 conversion and protected neuronal cells from the toxic effects of gp120.	Sunitinib	23-32	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	93-96
25117211-9	2014	In a cell-based model, sunitinib reduced CDK5 phosphorylation (pCDK5), calpain-dependent p35/p25 conversion and protected neuronal cells from the toxic effects of gp120.	Sunitinib	23-32	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	163-168
25117211-10	2014	In glial fibrillary acidic protein-gp120 transgenic (tg) mice, sunitinib reduced levels of pCDK5, p35/p25 and phosphorylated tau protein, along with amelioration of the neurodegenerative pathology.	Sunitinib	63-72	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	35-40
25117211-10	2014	In glial fibrillary acidic protein-gp120 transgenic (tg) mice, sunitinib reduced levels of pCDK5, p35/p25 and phosphorylated tau protein, along with amelioration of the neurodegenerative pathology.	Sunitinib	63-72	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	98-101
25117211-10	2014	In glial fibrillary acidic protein-gp120 transgenic (tg) mice, sunitinib reduced levels of pCDK5, p35/p25 and phosphorylated tau protein, along with amelioration of the neurodegenerative pathology.	Sunitinib	63-72	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	102-105
25151214-1	2014	Sunitinib malate (Sutent; Pfizer, Inc., New York, NY) is an oral multitargeted tyrosine kinase inhibitor that inhibits VEGF receptors (VEGFR-1, VEGFR-2, and VEGFR-3) among a family of kinase targets and have a central role in first-line treatment of metastatic renal cell carcinoma (mRCC).	Sunitinib	0-16	fms related receptor tyrosine kinase 1	Homo sapiens	135-142
25151214-1	2014	Sunitinib malate (Sutent; Pfizer, Inc., New York, NY) is an oral multitargeted tyrosine kinase inhibitor that inhibits VEGF receptors (VEGFR-1, VEGFR-2, and VEGFR-3) among a family of kinase targets and have a central role in first-line treatment of metastatic renal cell carcinoma (mRCC).	Sunitinib	0-16	kinase insert domain receptor	Homo sapiens	144-151
25151214-1	2014	Sunitinib malate (Sutent; Pfizer, Inc., New York, NY) is an oral multitargeted tyrosine kinase inhibitor that inhibits VEGF receptors (VEGFR-1, VEGFR-2, and VEGFR-3) among a family of kinase targets and have a central role in first-line treatment of metastatic renal cell carcinoma (mRCC).	Sunitinib	0-16	fms related receptor tyrosine kinase 4	Homo sapiens	157-164
25151214-1	2014	Sunitinib malate (Sutent; Pfizer, Inc., New York, NY) is an oral multitargeted tyrosine kinase inhibitor that inhibits VEGF receptors (VEGFR-1, VEGFR-2, and VEGFR-3) among a family of kinase targets and have a central role in first-line treatment of metastatic renal cell carcinoma (mRCC).	Sunitinib	18-24	fms related receptor tyrosine kinase 1	Homo sapiens	135-142
25151214-1	2014	Sunitinib malate (Sutent; Pfizer, Inc., New York, NY) is an oral multitargeted tyrosine kinase inhibitor that inhibits VEGF receptors (VEGFR-1, VEGFR-2, and VEGFR-3) among a family of kinase targets and have a central role in first-line treatment of metastatic renal cell carcinoma (mRCC).	Sunitinib	18-24	kinase insert domain receptor	Homo sapiens	144-151
25151214-1	2014	Sunitinib malate (Sutent; Pfizer, Inc., New York, NY) is an oral multitargeted tyrosine kinase inhibitor that inhibits VEGF receptors (VEGFR-1, VEGFR-2, and VEGFR-3) among a family of kinase targets and have a central role in first-line treatment of metastatic renal cell carcinoma (mRCC).	Sunitinib	18-24	fms related receptor tyrosine kinase 4	Homo sapiens	157-164
25299731-1	2014	A detailed atomistic description of the unbinding process of sorafenib and sunitinib, two known VEGFR2 inhibitors clinically used to treat renal cell carcinoma, was unraveled by using steered molecular dynamics (SMD) simulations.	Sunitinib	75-84	kinase insert domain receptor	Homo sapiens	96-102
24424564-1	2014	Sunitinib is a tyrosine kinase inhibitor with direct anti-tumor and anti-angiogenesis activity targeting VEGFR 1-2, PDGFR alpha-beta, c-kit, bFGF, (CSF-1), FLT3 and RET.	Sunitinib	0-9	fms related receptor tyrosine kinase 1	Homo sapiens	105-112
24424564-1	2014	Sunitinib is a tyrosine kinase inhibitor with direct anti-tumor and anti-angiogenesis activity targeting VEGFR 1-2, PDGFR alpha-beta, c-kit, bFGF, (CSF-1), FLT3 and RET.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	134-139
24424564-1	2014	Sunitinib is a tyrosine kinase inhibitor with direct anti-tumor and anti-angiogenesis activity targeting VEGFR 1-2, PDGFR alpha-beta, c-kit, bFGF, (CSF-1), FLT3 and RET.	Sunitinib	0-9	fibroblast growth factor 2	Homo sapiens	141-145
24424564-1	2014	Sunitinib is a tyrosine kinase inhibitor with direct anti-tumor and anti-angiogenesis activity targeting VEGFR 1-2, PDGFR alpha-beta, c-kit, bFGF, (CSF-1), FLT3 and RET.	Sunitinib	0-9	colony stimulating factor 1	Homo sapiens	148-153
24424564-1	2014	Sunitinib is a tyrosine kinase inhibitor with direct anti-tumor and anti-angiogenesis activity targeting VEGFR 1-2, PDGFR alpha-beta, c-kit, bFGF, (CSF-1), FLT3 and RET.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	156-160
24424564-1	2014	Sunitinib is a tyrosine kinase inhibitor with direct anti-tumor and anti-angiogenesis activity targeting VEGFR 1-2, PDGFR alpha-beta, c-kit, bFGF, (CSF-1), FLT3 and RET.	Sunitinib	0-9	ret proto-oncogene	Homo sapiens	165-168
25239608-2	2014	Imatinib, sunitinib, and regorafenib are approved therapies; however, efficacy is often limited by the acquisition of polyclonal secondary resistance mutations in KIT, with those located in the activation (A) loop (exons 17/18) being particularly problematic.	Sunitinib	10-19	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	163-166
24802849-0	2014	Fas/Fas ligand mediates keratinocyte death in sunitinib-induced hand-foot skin reaction.	Sunitinib	46-55	Fas ligand	Homo sapiens	4-14
24821582-13	2014	Array CGH profiles revealed sunitinib was associated with significant CA9 region loss.	Sunitinib	28-37	carbonic anhydrase 9	Homo sapiens	70-73
24821582-14	2014	RNAi CA9 silencing in two cell lines inhibited the antiproliferative effects of sunitinib.	Sunitinib	80-89	carbonic anhydrase 9	Homo sapiens	5-8
25691928-4	2014	The inhibitory effects of CEP701, imatinib, dasatinib, PKC412 and sunitinib were studied on cell proliferation and FLT3 tyrosine phosphorylation.	Sunitinib	66-75	fms related receptor tyrosine kinase 3	Homo sapiens	115-119
25691928-8	2014	FD-FLT3-ITD cells were three times more resistant to sunitinib than the FD-FLT3-WT cells.	Sunitinib	53-62	fms related receptor tyrosine kinase 3	Homo sapiens	3-7
25275248-1	2014	OBJECTIVES: The therapeutic use of the vascular endothelial growth factor (VEGF) antagonist sunitinib is limited by sunitinib-induced hypertension.	Sunitinib	92-101	vascular endothelial growth factor A	Rattus norvegicus	39-73
25275248-1	2014	OBJECTIVES: The therapeutic use of the vascular endothelial growth factor (VEGF) antagonist sunitinib is limited by sunitinib-induced hypertension.	Sunitinib	92-101	vascular endothelial growth factor A	Rattus norvegicus	75-79
25275248-1	2014	OBJECTIVES: The therapeutic use of the vascular endothelial growth factor (VEGF) antagonist sunitinib is limited by sunitinib-induced hypertension.	Sunitinib	116-125	vascular endothelial growth factor A	Rattus norvegicus	39-73
25275248-1	2014	OBJECTIVES: The therapeutic use of the vascular endothelial growth factor (VEGF) antagonist sunitinib is limited by sunitinib-induced hypertension.	Sunitinib	116-125	vascular endothelial growth factor A	Rattus norvegicus	75-79
24802849-9	2014	The skin biopsies of mice administered sunitinib exhibited increased expression of Fas and FasL in the apoptotic keratinocytes in the epidermis.	Sunitinib	39-48	Fas ligand (TNF superfamily, member 6)	Mus musculus	91-95
25275248-8	2014	CONCLUSION: Our data indicate that early sunitinib-induced hypertension is associated with modest alterations in renal vascular function, but markedly increased renal sodium reabsorption, probably due to direct actions of the VEGF antagonist on the collecting duct, suggesting that VEGF receptors regulate renal Na+ absorption.	Sunitinib	41-50	vascular endothelial growth factor A	Rattus norvegicus	226-230
25275248-8	2014	CONCLUSION: Our data indicate that early sunitinib-induced hypertension is associated with modest alterations in renal vascular function, but markedly increased renal sodium reabsorption, probably due to direct actions of the VEGF antagonist on the collecting duct, suggesting that VEGF receptors regulate renal Na+ absorption.	Sunitinib	41-50	vascular endothelial growth factor A	Rattus norvegicus	282-286
24802849-10	2014	Our data revealed that Fas/FasL interaction mediates keratinocyte death in sunitinib-induced HFSR.	Sunitinib	75-84	Fas ligand	Homo sapiens	27-31
25089810-7	2014	Compound 54 is more potent than sunitinib not only against FLT3-WT AML cells but also active against sunitinib-resistant FLT3-ITD AML cells.	Sunitinib	32-41	fms related receptor tyrosine kinase 3	Homo sapiens	59-63
25189542-5	2014	We observed in excess of 100 protein kinase targets plus various protein complexes involving, for instance, AMPK, TBK1 (sunitinib), and ILK (dasatinib).	Sunitinib	120-129	TANK-binding kinase 1	Mus musculus	114-118
25547700-0	2014	[Genetic polymorphisms of PDGFR associated with thrombocytopenia in Chinese patients with clear-cell metastatic renal cell carcinoma treated with sunitinib].	Sunitinib	146-155	platelet derived growth factor receptor beta	Homo sapiens	26-31
25547700-1	2014	OBJECTIVE: To explore the genetic polymorphisms of PDGFR associated with thrombocytopenia in Chinese patients with metastatic clear-cell renal cell carcinoma (mcc-RCC) treated with sunitinib.	Sunitinib	181-190	platelet derived growth factor receptor beta	Homo sapiens	51-56
25336977-9	2014	Among different VEGFR-TKIs, sorafenib and sunitinib had significant risk of death when compared with control arms, respectively.	Sunitinib	42-51	kinase insert domain receptor	Homo sapiens	16-21
25089810-7	2014	Compound 54 is more potent than sunitinib not only against FLT3-WT AML cells but also active against sunitinib-resistant FLT3-ITD AML cells.	Sunitinib	32-41	fms related receptor tyrosine kinase 3	Homo sapiens	121-125
25089810-7	2014	Compound 54 is more potent than sunitinib not only against FLT3-WT AML cells but also active against sunitinib-resistant FLT3-ITD AML cells.	Sunitinib	101-110	fms related receptor tyrosine kinase 3	Homo sapiens	121-125
25016061-5	2014	Assessment of tumoral neo-angiogenesis, assessed by morphometric analysis of the vascular network after CD31 immunolabeling, showed that both sunitinib and sorafenib reduced the microvessel area (-85% and -80%, respectively) and length (-80% and -78%, respectively) in treated compared to control tumors.	Sunitinib	142-151	platelet and endothelial cell adhesion molecule 1	Rattus norvegicus	104-108
25100134-9	2014	CONCLUSIONS: Serum Ang-2 and MMP-2 and tumor HIF-1alpha were identified as relevant baseline biomarkers of sunitinib activity in advanced RCC, warranting further research into their prognostic versus predictive value.	Sunitinib	107-116	angiopoietin 2	Homo sapiens	19-24
25100134-9	2014	CONCLUSIONS: Serum Ang-2 and MMP-2 and tumor HIF-1alpha were identified as relevant baseline biomarkers of sunitinib activity in advanced RCC, warranting further research into their prognostic versus predictive value.	Sunitinib	107-116	matrix metallopeptidase 2	Homo sapiens	29-34
25016061-9	2014	While sunitinib induced a rapid (4h) and pronounced (5-fold) increase in caspase-3/7-dependent apoptosis, sorafenib seems to exert its cytotoxic activity through a different mechanism.	Sunitinib	6-15	caspase 3	Rattus norvegicus	73-82
25228815-3	2014	In this study, we evaluate the changes in cell surface vascular endothelial growth factor receptor (VEGFR) expression on endothelial cells in culture treated with the antiangiogenic tyrosine kinase inhibitor drug sunitinib, using quantitative flow cytometry.	Sunitinib	213-222	kinase insert domain receptor	Homo sapiens	55-98
24612223-6	2014	Nilotinib, sunitinib, and imatinib were found to be potent CYP1A2 inhibitor.	Sunitinib	11-20	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	59-65
25109654-6	2014	The results demonstrated that sunitinib was able to reverse the multidrug resistance of A549/DDP lung cancer cells, which was possibly associated with the downregulation of multidrug resistance-associated gene expression and the inhibition of AKT and ERK phosphorylation.	Sunitinib	30-39	AKT serine/threonine kinase 1	Homo sapiens	243-246
25109654-6	2014	The results demonstrated that sunitinib was able to reverse the multidrug resistance of A549/DDP lung cancer cells, which was possibly associated with the downregulation of multidrug resistance-associated gene expression and the inhibition of AKT and ERK phosphorylation.	Sunitinib	30-39	mitogen-activated protein kinase 1	Homo sapiens	251-254
24800947-4	2014	We review evidence to evaluate whether sunitinib may have value as re-challenge therapy in patients who have progressed on prior targeted therapy with sunitinib and/or an alternative tyrosine kinase inhibitor or mammalian target of rapamycin inhibitor.	Sunitinib	39-48	mechanistic target of rapamycin kinase	Homo sapiens	212-241
25228815-3	2014	In this study, we evaluate the changes in cell surface vascular endothelial growth factor receptor (VEGFR) expression on endothelial cells in culture treated with the antiangiogenic tyrosine kinase inhibitor drug sunitinib, using quantitative flow cytometry.	Sunitinib	213-222	kinase insert domain receptor	Homo sapiens	100-105
25228815-4	2014	We find that proangiogenic VEGFR2 cell surface receptor numbers are increased with sunitinib treatment.	Sunitinib	83-92	kinase insert domain receptor	Homo sapiens	27-33
24927771-1	2014	We performed a systematic review and meta-analysis of thyroid function abnormalities associated with seven vascular endothelial growth factor receptor (VEGFR) targeted tyrosine kinase inhibitors (sorafenib, sunitinib, axitinib, cediranib, pazopanib, regorafenib and vandetanib).	Sunitinib	207-216	kinase insert domain receptor	Homo sapiens	152-157
25200065-0	2014	Twist1 expression induced by sunitinib accelerates tumor cell vasculogenic mimicry by increasing the population of CD133+ cells in triple-negative breast cancer.	Sunitinib	29-38	twist basic helix-loop-helix transcription factor 1	Mus musculus	0-6
25200065-0	2014	Twist1 expression induced by sunitinib accelerates tumor cell vasculogenic mimicry by increasing the population of CD133+ cells in triple-negative breast cancer.	Sunitinib	29-38	prominin 1	Mus musculus	115-120
25193011-6	2014	He was subsequently treated with immunochemotherapy, tyrosine kinase inhibitors (TKIs), and mTOR inhibitors (mTORIs) - that is sunitinib, everolimus, and sorafenib.	Sunitinib	127-136	mechanistic target of rapamycin kinase	Homo sapiens	92-96
25145356-0	2014	Blocking autocrine VEGF signaling by sunitinib, an anti-cancer drug, promotes embryonic stem cell self-renewal and somatic cell reprogramming.	Sunitinib	37-46	vascular endothelial growth factor A	Mus musculus	19-23
25145356-3	2014	Blocking VEGF signaling with sunitinib, an anti-cancer drug and a receptor tyrosine kinase (RTK) inhibitor mainly targeting VEGF receptors (VEGFRs), is capable of maintaining the mESCs in the undifferentiated state without the need for feeder cells or LIF.	Sunitinib	29-38	vascular endothelial growth factor A	Mus musculus	9-13
25145356-3	2014	Blocking VEGF signaling with sunitinib, an anti-cancer drug and a receptor tyrosine kinase (RTK) inhibitor mainly targeting VEGF receptors (VEGFRs), is capable of maintaining the mESCs in the undifferentiated state without the need for feeder cells or LIF.	Sunitinib	29-38	vascular endothelial growth factor A	Mus musculus	124-128
25145356-3	2014	Blocking VEGF signaling with sunitinib, an anti-cancer drug and a receptor tyrosine kinase (RTK) inhibitor mainly targeting VEGF receptors (VEGFRs), is capable of maintaining the mESCs in the undifferentiated state without the need for feeder cells or LIF.	Sunitinib	29-38	kinase insert domain protein receptor	Mus musculus	140-146
25145356-3	2014	Blocking VEGF signaling with sunitinib, an anti-cancer drug and a receptor tyrosine kinase (RTK) inhibitor mainly targeting VEGF receptors (VEGFRs), is capable of maintaining the mESCs in the undifferentiated state without the need for feeder cells or LIF.	Sunitinib	29-38	leukemia inhibitory factor	Mus musculus	252-255
25145356-5	2014	Sunitinib also promotes iPSC generation from MEFs with only Oct4.	Sunitinib	0-9	POU domain, class 5, transcription factor 1, related sequence 1	Mus musculus	60-64
25145356-6	2014	Knocking down VEGFR2 or blocking it with neutralizing antibody mimicks the effect of sunitinib, indicating that blocking VEGF/VEGFR signaling is indeed beneficial to the self-renewal of mESCs.	Sunitinib	85-94	kinase insert domain protein receptor	Mus musculus	14-20
25145356-6	2014	Knocking down VEGFR2 or blocking it with neutralizing antibody mimicks the effect of sunitinib, indicating that blocking VEGF/VEGFR signaling is indeed beneficial to the self-renewal of mESCs.	Sunitinib	85-94	vascular endothelial growth factor A	Mus musculus	14-18
25145356-11	2014	Blocking VEGF signaling with sunitinib or other small molecules help to maintain the mESCs in the ground state of pluripotency.	Sunitinib	29-38	vascular endothelial growth factor A	Mus musculus	9-13
25253994-3	2014	METHODS: PDGFR signaling was inhibited using Sunitinib malate, Imatinib mesylate or Regorafenib in murine and human luminal-like and claudin-low mammary tumor cell lines or Masitinib in only the human cell lines.	Sunitinib	45-61	platelet derived growth factor receptor, beta polypeptide	Mus musculus	9-14
25309777-4	2014	Vascular endothelial growth factor (VEGF)- and RET-directed therapies such as sorafenib, motesanib, and sunitinib have been shown to be the most effective at inducing clinical responses and stabilizing the disease process.	Sunitinib	104-113	vascular endothelial growth factor A	Homo sapiens	0-34
25309777-4	2014	Vascular endothelial growth factor (VEGF)- and RET-directed therapies such as sorafenib, motesanib, and sunitinib have been shown to be the most effective at inducing clinical responses and stabilizing the disease process.	Sunitinib	104-113	vascular endothelial growth factor A	Homo sapiens	36-40
25309777-4	2014	Vascular endothelial growth factor (VEGF)- and RET-directed therapies such as sorafenib, motesanib, and sunitinib have been shown to be the most effective at inducing clinical responses and stabilizing the disease process.	Sunitinib	104-113	ret proto-oncogene	Homo sapiens	47-50
24127298-11	2014	Treatment with VEGFR TKIs sorafenib, sunitinib and pazopanib is associated with a significant increase in the risk of GI events in patients with cancer, and frequent clinical monitoring should be emphasized when managing these three and newer VEGFR TKIs.	Sunitinib	37-46	kinase insert domain receptor	Homo sapiens	15-20
25068886-7	2014	Interestingly, sunitinib modulated tumor infiltration with bone marrow-derived cells (CD45+), recruitment of M2-like macrophages (CD163+) and activation of inflammatory pathways (phospho-STAT3) in a manner that was age-dependent.	Sunitinib	15-24	signal transducer and activator of transcription 3	Mus musculus	187-192
24127298-11	2014	Treatment with VEGFR TKIs sorafenib, sunitinib and pazopanib is associated with a significant increase in the risk of GI events in patients with cancer, and frequent clinical monitoring should be emphasized when managing these three and newer VEGFR TKIs.	Sunitinib	37-46	kinase insert domain receptor	Homo sapiens	243-248
25017943-6	2014	Interestingly, pharmacological lipogenesis inhibition with orlistat or fatty acid synthase downregulation with shRNA inhibited tumor regrowth and metastases after sunitinib treatment withdrawal.	Sunitinib	163-172	fatty acid synthase	Homo sapiens	71-90
25101168-10	2014	RESULTS: The window chamber model was useful to demonstrate the inhibition of angiogenesis using the VEGF pathway targeted agent Sunitinib.	Sunitinib	129-138	vascular endothelial growth factor A	Mus musculus	101-105
24423438-4	2014	Vascular endothelial growth factor related upstream Ras, Erk1/2 and STAT1 phosphorylation activity in Caki-1 and NGAL transfected Caki-1 cells after sunitinib treatment was analyzed using Western blot.	Sunitinib	149-158	lipocalin 2	Homo sapiens	113-117
24842548-1	2014	Our prior phase I study of the combination of vascular endothelial growth factor (VEGF) antibody, bevacizumab, and VEGF receptor (VEGFR) inhibitor, sunitinib, in advanced solid tumors identified an encouraging response evaluation.	Sunitinib	148-157	kinase insert domain receptor	Homo sapiens	115-128
24842548-1	2014	Our prior phase I study of the combination of vascular endothelial growth factor (VEGF) antibody, bevacizumab, and VEGF receptor (VEGFR) inhibitor, sunitinib, in advanced solid tumors identified an encouraging response evaluation.	Sunitinib	148-157	kinase insert domain receptor	Homo sapiens	130-135
24936559-4	2014	METHODS: We present a case report of a patient with a VIP-secreting malignant pheochromocytoma manifested as severe watery diarrhea, with an exquisite clinical response to sunitinib.	Sunitinib	172-181	vasoactive intestinal peptide	Homo sapiens	54-57
24936559-11	2014	CONCLUSION: To the best of our knowledge, this is the first report of a case of malignant VIP-producing pheochromocytoma that was responsive to sunitinib.	Sunitinib	144-153	vasoactive intestinal peptide	Homo sapiens	90-93
24423438-0	2014	NGAL can alternately mediate sunitinib resistance in renal cell carcinoma.	Sunitinib	29-38	lipocalin 2	Homo sapiens	0-4
24423438-1	2014	PURPOSE: Serum NGAL is highly expressed in patients with advanced renal cancer treated with sunitinib.	Sunitinib	92-101	lipocalin 2	Homo sapiens	15-19
24423438-2	2014	We investigated the role of NGAL in sunitinib resistance in renal cell carcinoma to identify potential tactics to overcome it.	Sunitinib	36-45	lipocalin 2	Homo sapiens	28-32
24423438-3	2014	MATERIALS AND METHODS: NGAL expression was correlated with sunitinib sensitivity.	Sunitinib	59-68	lipocalin 2	Homo sapiens	23-27
24423438-4	2014	Vascular endothelial growth factor related upstream Ras, Erk1/2 and STAT1 phosphorylation activity in Caki-1 and NGAL transfected Caki-1 cells after sunitinib treatment was analyzed using Western blot.	Sunitinib	149-158	signal transducer and activator of transcription 1	Homo sapiens	68-73
24974736-7	2014	Sunitinib or LY294002, but not erlotinib, significantly inhibited the platelet-induced proliferation of osteosarcoma cells, indicating that PDGF released from platelets plays an important role in the proliferation of osteosarcomas by activating the PDGFR and then Akt.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	249-254
24974736-7	2014	Sunitinib or LY294002, but not erlotinib, significantly inhibited the platelet-induced proliferation of osteosarcoma cells, indicating that PDGF released from platelets plays an important role in the proliferation of osteosarcomas by activating the PDGFR and then Akt.	Sunitinib	0-9	AKT serine/threonine kinase 1	Homo sapiens	264-267
25085632-0	2014	Next generation sequencing analysis of platinum refractory advanced germ cell tumor sensitive to Sunitinib (Sutent ) a VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor in a phase II trial.	Sunitinib	97-106	kinase insert domain receptor	Homo sapiens	119-125
25085632-0	2014	Next generation sequencing analysis of platinum refractory advanced germ cell tumor sensitive to Sunitinib (Sutent ) a VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor in a phase II trial.	Sunitinib	97-106	platelet derived growth factor receptor beta	Homo sapiens	126-135
25085632-0	2014	Next generation sequencing analysis of platinum refractory advanced germ cell tumor sensitive to Sunitinib (Sutent ) a VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor in a phase II trial.	Sunitinib	97-106	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	136-141
25085632-0	2014	Next generation sequencing analysis of platinum refractory advanced germ cell tumor sensitive to Sunitinib (Sutent ) a VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor in a phase II trial.	Sunitinib	97-106	fms related receptor tyrosine kinase 3	Homo sapiens	143-147
25085632-0	2014	Next generation sequencing analysis of platinum refractory advanced germ cell tumor sensitive to Sunitinib (Sutent ) a VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor in a phase II trial.	Sunitinib	97-106	ret proto-oncogene	Homo sapiens	148-151
25085632-0	2014	Next generation sequencing analysis of platinum refractory advanced germ cell tumor sensitive to Sunitinib (Sutent ) a VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor in a phase II trial.	Sunitinib	97-106	colony stimulating factor 1 receptor	Homo sapiens	152-157
25085632-0	2014	Next generation sequencing analysis of platinum refractory advanced germ cell tumor sensitive to Sunitinib (Sutent ) a VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor in a phase II trial.	Sunitinib	108-114	platelet derived growth factor receptor beta	Homo sapiens	126-135
25085632-4	2014	METHODS: Given the preclinical evidence implicating vascular endothelial growth factor (VEGF) signaling in the biology of germ cell tumors, we hypothesized that the vascular endothelial growth factor receptor (VEGFR) inhibitor sunitinib (Sutent) may possess important clinical activity in the treatment of this refractory disease.	Sunitinib	227-236	vascular endothelial growth factor A	Homo sapiens	52-86
25085632-4	2014	METHODS: Given the preclinical evidence implicating vascular endothelial growth factor (VEGF) signaling in the biology of germ cell tumors, we hypothesized that the vascular endothelial growth factor receptor (VEGFR) inhibitor sunitinib (Sutent) may possess important clinical activity in the treatment of this refractory disease.	Sunitinib	227-236	kinase insert domain receptor	Homo sapiens	165-208
25085632-4	2014	METHODS: Given the preclinical evidence implicating vascular endothelial growth factor (VEGF) signaling in the biology of germ cell tumors, we hypothesized that the vascular endothelial growth factor receptor (VEGFR) inhibitor sunitinib (Sutent) may possess important clinical activity in the treatment of this refractory disease.	Sunitinib	227-236	kinase insert domain receptor	Homo sapiens	210-215
25085632-4	2014	METHODS: Given the preclinical evidence implicating vascular endothelial growth factor (VEGF) signaling in the biology of germ cell tumors, we hypothesized that the vascular endothelial growth factor receptor (VEGFR) inhibitor sunitinib (Sutent) may possess important clinical activity in the treatment of this refractory disease.	Sunitinib	238-244	kinase insert domain receptor	Homo sapiens	165-208
25085632-4	2014	METHODS: Given the preclinical evidence implicating vascular endothelial growth factor (VEGF) signaling in the biology of germ cell tumors, we hypothesized that the vascular endothelial growth factor receptor (VEGFR) inhibitor sunitinib (Sutent) may possess important clinical activity in the treatment of this refractory disease.	Sunitinib	238-244	kinase insert domain receptor	Homo sapiens	210-215
25085632-9	2014	Next generation sequencing to understand this patient"s response to sunitinib revealed RET amplification, EGFR and KRAS amplification as relevant aberrations.	Sunitinib	68-77	ret proto-oncogene	Homo sapiens	87-90
25085632-9	2014	Next generation sequencing to understand this patient"s response to sunitinib revealed RET amplification, EGFR and KRAS amplification as relevant aberrations.	Sunitinib	68-77	epidermal growth factor receptor	Homo sapiens	106-110
25085632-9	2014	Next generation sequencing to understand this patient"s response to sunitinib revealed RET amplification, EGFR and KRAS amplification as relevant aberrations.	Sunitinib	68-77	KRAS proto-oncogene, GTPase	Homo sapiens	115-119
25085632-12	2014	Next generation sequencing of this "exceptional responder" identified the first reported case of a RET amplification as a potential basis of sensitivity to sunitinib (VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor) in a patient with refractory germ cell tumor.	Sunitinib	156-165	ret proto-oncogene	Homo sapiens	99-102
25085632-12	2014	Next generation sequencing of this "exceptional responder" identified the first reported case of a RET amplification as a potential basis of sensitivity to sunitinib (VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor) in a patient with refractory germ cell tumor.	Sunitinib	156-165	kinase insert domain receptor	Homo sapiens	167-173
25085632-12	2014	Next generation sequencing of this "exceptional responder" identified the first reported case of a RET amplification as a potential basis of sensitivity to sunitinib (VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor) in a patient with refractory germ cell tumor.	Sunitinib	156-165	platelet derived growth factor receptor beta	Homo sapiens	174-183
25085632-12	2014	Next generation sequencing of this "exceptional responder" identified the first reported case of a RET amplification as a potential basis of sensitivity to sunitinib (VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor) in a patient with refractory germ cell tumor.	Sunitinib	156-165	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	184-189
25085632-12	2014	Next generation sequencing of this "exceptional responder" identified the first reported case of a RET amplification as a potential basis of sensitivity to sunitinib (VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor) in a patient with refractory germ cell tumor.	Sunitinib	156-165	fms related receptor tyrosine kinase 3	Homo sapiens	191-195
25085632-12	2014	Next generation sequencing of this "exceptional responder" identified the first reported case of a RET amplification as a potential basis of sensitivity to sunitinib (VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor) in a patient with refractory germ cell tumor.	Sunitinib	156-165	ret proto-oncogene	Homo sapiens	196-199
25085632-12	2014	Next generation sequencing of this "exceptional responder" identified the first reported case of a RET amplification as a potential basis of sensitivity to sunitinib (VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor) in a patient with refractory germ cell tumor.	Sunitinib	156-165	colony stimulating factor 1 receptor	Homo sapiens	200-205
25091988-7	2014	Low-dose sunitinib blocked the PDGF-BB-induced cell proliferation and PDGFR-beta signaling.	Sunitinib	9-18	platelet derived growth factor receptor beta	Homo sapiens	70-80
25091988-10	2014	CONCLUSIONS: Sunitinib mesylate inhibited the proliferation of primary human colonic fibroblasts through target-inhibited PDGFR signaling in vitro and in vivo.	Sunitinib	13-22	platelet derived growth factor receptor beta	Homo sapiens	122-127
24423438-5	2014	NGAL and vascular endothelial growth factor-A interaction with sunitinib therapeutic efficacy was monitored in renal cell carcinoma tumor xenografted mice by tumor growth inhibition, serum NGAL and vascular endothelial growth factor-a levels, and microscopic examination of tumor microvascular density.	Sunitinib	63-72	vascular endothelial growth factor A	Mus musculus	9-45
24423438-6	2014	RESULTS: Sunitinib cytotoxicity in various renal cell carcinoma cell lines was reversibly related to NGAL expression.	Sunitinib	9-18	lipocalin 2	Homo sapiens	101-105
24423438-7	2014	Sunitinib showed the lowest 50% inhibitory concentration (5.53 muM) in Caki-1 cells, which had the lowest NGAL expression of these renal cell carcinoma cell lines.	Sunitinib	0-9	lipocalin 2	Homo sapiens	106-110
24423438-8	2014	After sunitinib treatment adding NGAL inhibited Ras and Erk1/2 phosphorylation but activated STAT1alpha phosphorylation in Caki-1 cells and Caki-1 cells transfected with NGAL.	Sunitinib	6-15	lipocalin 2	Homo sapiens	33-37
24423438-12	2014	CONCLUSIONS: NGAL in tumor cells may show crosstalk with vascular endothelial growth factor-a and alternative activation in stimulating tumor growth during sunitinib treatment.	Sunitinib	156-165	lipocalin 2	Homo sapiens	13-17
25013907-0	2014	Association of toxicity of sorafenib and sunitinib for human keratinocytes with inhibition of signal transduction and activator of transcription 3 (STAT3).	Sunitinib	41-50	signal transducer and activator of transcription 3	Homo sapiens	148-153
25130811-8	2014	The mRNA expression of C-MYC, hTERT and BCR-ABL was reduced significantly by SU11248 in a time-dependent manner (P &lt; 0.05).	Sunitinib	77-84	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	23-28
25130811-8	2014	The mRNA expression of C-MYC, hTERT and BCR-ABL was reduced significantly by SU11248 in a time-dependent manner (P &lt; 0.05).	Sunitinib	77-84	telomerase reverse transcriptase	Homo sapiens	30-35
25130811-8	2014	The mRNA expression of C-MYC, hTERT and BCR-ABL was reduced significantly by SU11248 in a time-dependent manner (P &lt; 0.05).	Sunitinib	77-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
25130811-9	2014	Western blot detection showed that the expression of p-Akt protein in K562 cells decreased in dose-and time-dependent manner after SU11248 treatment, but the expression of Akt was not significantly changed.	Sunitinib	131-138	AKT serine/threonine kinase 1	Homo sapiens	55-58
25130811-10	2014	It is concluded that SU11248 can inhibit the growth of K562 cells efficiently through inducing apoptosis, its mechanism may be closely relate with the expression down-regulation of C-MYC, hTERT, BCR-ABL and the inhibition of Akt phosphorylation.	Sunitinib	21-28	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	181-186
25130811-10	2014	It is concluded that SU11248 can inhibit the growth of K562 cells efficiently through inducing apoptosis, its mechanism may be closely relate with the expression down-regulation of C-MYC, hTERT, BCR-ABL and the inhibition of Akt phosphorylation.	Sunitinib	21-28	telomerase reverse transcriptase	Homo sapiens	188-193
25130811-10	2014	It is concluded that SU11248 can inhibit the growth of K562 cells efficiently through inducing apoptosis, its mechanism may be closely relate with the expression down-regulation of C-MYC, hTERT, BCR-ABL and the inhibition of Akt phosphorylation.	Sunitinib	21-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
25130811-10	2014	It is concluded that SU11248 can inhibit the growth of K562 cells efficiently through inducing apoptosis, its mechanism may be closely relate with the expression down-regulation of C-MYC, hTERT, BCR-ABL and the inhibition of Akt phosphorylation.	Sunitinib	21-28	AKT serine/threonine kinase 1	Homo sapiens	225-228
25076341-4	2014	New therapies focus on specific molecular targets such as sunitinib, angiogenesis inhibitor, that target vascular endothelial growth factor receptor (VEGFR) and other growth factor receptors and everolimus, an inhibitor of the mammalian target of rapamycin.	Sunitinib	58-67	kinase insert domain receptor	Homo sapiens	105-148
25076341-4	2014	New therapies focus on specific molecular targets such as sunitinib, angiogenesis inhibitor, that target vascular endothelial growth factor receptor (VEGFR) and other growth factor receptors and everolimus, an inhibitor of the mammalian target of rapamycin.	Sunitinib	58-67	kinase insert domain receptor	Homo sapiens	150-155
25013907-2	2014	This study aimed to examine whether the toxicity of sorafenib and sunitinib for human keratinocytes was associated with inhibiting signal transduction and activator of transcription 3 (STAT3).	Sunitinib	66-75	signal transducer and activator of transcription 3	Homo sapiens	185-190
25013907-3	2014	We studied whether STAT3 activity affects sorafenib- and sunitinib-induced cell growth inhibition in HaCaT cells by WST-8 assay.	Sunitinib	57-66	signal transducer and activator of transcription 3	Homo sapiens	19-24
25013907-5	2014	HaCaT cells transfected with constitutively-active STAT3 (STAT3C) were resistant to the sorafenib- and sunitinib-induced cell growth inhibition.	Sunitinib	103-112	signal transducer and activator of transcription 3	Homo sapiens	51-56
25013907-5	2014	HaCaT cells transfected with constitutively-active STAT3 (STAT3C) were resistant to the sorafenib- and sunitinib-induced cell growth inhibition.	Sunitinib	103-112	signal transducer and activator of transcription 3	Homo sapiens	58-64
25013907-6	2014	STAT3 activity decreased after short-term treatment with sorafenib and sunitinib in a dose-dependent manner and recovered after long-term treatment with sorafenib and sunitinib at low doses.	Sunitinib	71-80	signal transducer and activator of transcription 3	Homo sapiens	0-5
25013907-6	2014	STAT3 activity decreased after short-term treatment with sorafenib and sunitinib in a dose-dependent manner and recovered after long-term treatment with sorafenib and sunitinib at low doses.	Sunitinib	167-176	signal transducer and activator of transcription 3	Homo sapiens	0-5
25013907-7	2014	Moreover, the expression of survivin and bcl-2 decreased after treatment with sorafenib and sunitinib was concomitant with variations in STAT3 activity.	Sunitinib	92-101	BCL2 apoptosis regulator	Homo sapiens	41-46
25013907-8	2014	Sorafenib-induced STAT3 inhibition was mediated by regulation via MAPK pathways in HaCaT cells, while sunitinib-induced STAT3 inhibition was not.	Sunitinib	102-111	signal transducer and activator of transcription 3	Homo sapiens	120-125
25013907-9	2014	Thus, STAT3 activation mediating apoptosis suppressors may be a key factor in sorafenib and sunitinib-induced keratinocyte cytotoxicity.	Sunitinib	92-101	signal transducer and activator of transcription 3	Homo sapiens	6-11
24482243-3	2014	Encouragingly, VEGF pathway targeted drugs such as bevacizumab, sunitinib and aflibercept have shown activity in certain settings.	Sunitinib	64-73	vascular endothelial growth factor A	Homo sapiens	15-19
24566734-5	2014	From univariate analysis, we found that the SNPs in CYP3A4, CYP3A5, and ABCB1 were associated with the clearance of both sunitinib and SU12662.	Sunitinib	121-130	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	52-58
24215209-0	2014	Prognostic impact of baseline serum C-reactive protein in patients with metastatic renal cell carcinoma (RCC) treated with sunitinib.	Sunitinib	123-132	C-reactive protein	Homo sapiens	36-54
24215209-1	2014	OBJECTIVE: To evaluate the impact of baseline serum C-reactive protein (CRP) level on outcome in patients with metastatic renal cell carcinoma (mRCC) treated with sunitinib.	Sunitinib	163-172	C-reactive protein	Homo sapiens	52-70
24215209-1	2014	OBJECTIVE: To evaluate the impact of baseline serum C-reactive protein (CRP) level on outcome in patients with metastatic renal cell carcinoma (mRCC) treated with sunitinib.	Sunitinib	163-172	C-reactive protein	Homo sapiens	72-75
24215209-12	2014	CONCLUSION: Baseline serum CRP level is a strong independent variable linked with RR, PFS and OS in patients with mRCC treated with sunitinib.	Sunitinib	132-141	C-reactive protein	Homo sapiens	27-30
24566734-5	2014	From univariate analysis, we found that the SNPs in CYP3A4, CYP3A5, and ABCB1 were associated with the clearance of both sunitinib and SU12662.	Sunitinib	121-130	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	60-66
24566734-5	2014	From univariate analysis, we found that the SNPs in CYP3A4, CYP3A5, and ABCB1 were associated with the clearance of both sunitinib and SU12662.	Sunitinib	121-130	ATP binding cassette subfamily B member 1	Homo sapiens	72-77
24751611-7	2014	Sunitinib induced autophagy via upregulating beclin-1 expression which was blocked by chloroquine as evidenced by accumulated SQTSM1/p62 level.	Sunitinib	0-9	beclin 1	Homo sapiens	45-53
24562646-7	2014	Immunofluorescence staining and an enzyme-linked immunosorbent assay confirmed that sunitinib-induced changes in tumor uptake of CF680R-3PRGD2 and CF750-BevF(ab")2 were correlated with changes in the levels of integrin alphavbeta3 and VEGF.	Sunitinib	84-93	vascular endothelial growth factor A	Mus musculus	235-239
24976727-11	2014	Cells treated with sorafenib or sunitinib expressed less interleukin-6 mRNA as well as less collagen type 1 mRNA and protein.	Sunitinib	32-41	interleukin 6	Rattus norvegicus	57-70
24510251-4	2014	Two patients were treated with sunitinib at a standard dose (50 mg daily; 4 weeks on, 2 weeks off) after cyclophosphamide/vinblastine/dacarbazine chemotherapy, because vascular endothelial growth factor (VEGF)-positive cells were partly observed by immunohistochemical staining.	Sunitinib	31-40	vascular endothelial growth factor A	Homo sapiens	168-202
24510251-10	2014	In conclusion, sunitinib was effective in the treatment of malignant pheochromocytoma when VEGF-positive cells were observed in the tumor specimens.	Sunitinib	15-24	vascular endothelial growth factor A	Homo sapiens	91-95
24680659-3	2014	RESULTS: The baseline level of MMP-9 in nonresponders to sunitinib was significantly higher than that in responders, whereas the baseline level of TIMP-2 in nonresponders was significantly lower than that in responders.	Sunitinib	57-66	matrix metallopeptidase 9	Homo sapiens	31-36
24680659-8	2014	CONCLUSIONS: An imbalance between the serum MMP-9 and TIMP-2 levels could be a novel biomarker to predict disease progression in patients with mRCC under treatment with sunitinib.	Sunitinib	169-178	matrix metallopeptidase 9	Homo sapiens	44-49
24680659-8	2014	CONCLUSIONS: An imbalance between the serum MMP-9 and TIMP-2 levels could be a novel biomarker to predict disease progression in patients with mRCC under treatment with sunitinib.	Sunitinib	169-178	TIMP metallopeptidase inhibitor 2	Homo sapiens	54-60
24751611-7	2014	Sunitinib induced autophagy via upregulating beclin-1 expression which was blocked by chloroquine as evidenced by accumulated SQTSM1/p62 level.	Sunitinib	0-9	nucleoporin 62	Homo sapiens	133-136
24751611-8	2014	Furthermore, chloroquine augmented sunitinib-induced apoptosis by decreasing survivin level and increasing caspase 3 activity.	Sunitinib	35-44	caspase 3	Homo sapiens	107-116
24751611-9	2014	Chloroquine also enhanced the antiangiogenic capacity of sunitinib as indicated by decreased CD34 expression and peritoneal/skin angiogenesis.	Sunitinib	57-66	CD34 molecule	Homo sapiens	93-97
24185817-0	2014	Sunitinib--CLIO conjugate: a VEGFR/PDGFR-targeting active MR probe.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	29-34
24703573-13	2014	Among putative sunitinib targets, only RET was expressed and activated in analysed samples.	Sunitinib	15-24	ret proto-oncogene	Homo sapiens	39-42
25058995-1	2014	BACKGROUND: The VEGFR/PDGFR inhibitor sunitinib was approved in Israel in 2008 for the treatment of metastatic renal cell carcinoma (mRCC), based on an international trial.	Sunitinib	38-47	kinase insert domain receptor	Homo sapiens	16-21
25058995-1	2014	BACKGROUND: The VEGFR/PDGFR inhibitor sunitinib was approved in Israel in 2008 for the treatment of metastatic renal cell carcinoma (mRCC), based on an international trial.	Sunitinib	38-47	platelet derived growth factor receptor beta	Homo sapiens	22-27
24417304-1	2014	WHAT IS KNOWN AND OBJECTIVE: Sunitinib, a CYP3A4 substrate, is standard of care treatment in metastatic renal cell carcinoma (mRCC) and is administered orally as a single dose of 50 mg, in a 4 weeks on/2 weeks off regimen.	Sunitinib	29-38	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-48
24417304-16	2014	Due to adverse drug reactions and comorbidity, patients under sunitinib, a CYP3A4 substrate, took an average of 6 8 comedications provoking an important risk of major-to-moderate drug-drug interactions.	Sunitinib	62-71	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	75-81
24185817-0	2014	Sunitinib--CLIO conjugate: a VEGFR/PDGFR-targeting active MR probe.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	35-40
24185817-1	2014	PURPOSE: This study was conducted to evaluate feasibility of sunitinib-CLIO conjugate as a vascular endothelial growth factor receptor/platelet-derived growth factor receptor (VEGFR/PDGFR)-specific magnetic resonance (MR) probe.	Sunitinib	61-70	kinase insert domain receptor	Homo sapiens	176-181
24185817-1	2014	PURPOSE: This study was conducted to evaluate feasibility of sunitinib-CLIO conjugate as a vascular endothelial growth factor receptor/platelet-derived growth factor receptor (VEGFR/PDGFR)-specific magnetic resonance (MR) probe.	Sunitinib	61-70	platelet derived growth factor receptor beta	Homo sapiens	182-187
24185817-2	2014	PROCEDURE: VEGFR/PDGFR-targeting MR probe was synthesized by conjugating cross-linked iron-oxide (CLIO) with tyrosine-kinase inhibitor (sunitinib).	Sunitinib	136-145	kinase insert domain receptor	Homo sapiens	11-16
24185817-2	2014	PROCEDURE: VEGFR/PDGFR-targeting MR probe was synthesized by conjugating cross-linked iron-oxide (CLIO) with tyrosine-kinase inhibitor (sunitinib).	Sunitinib	136-145	platelet derived growth factor receptor beta	Homo sapiens	17-22
24185817-9	2014	CONCLUSIONS: Sunitinib-CLIO conjugate can be used as an active MR probe for quantifying VEGFR/PDGFR.	Sunitinib	13-22	kinase insert domain receptor	Homo sapiens	88-93
24185817-9	2014	CONCLUSIONS: Sunitinib-CLIO conjugate can be used as an active MR probe for quantifying VEGFR/PDGFR.	Sunitinib	13-22	platelet derived growth factor receptor beta	Homo sapiens	94-99
24825438-0	2014	The effect of ABCG2 genotype on the population pharmacokinetics of sunitinib in patients with renal cell carcinoma.	Sunitinib	67-76	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	14-19
24723451-1	2014	Sunitinib, an inhibitor of kinases, including VEGFR and platelet-derived growth factor receptor (PDGFR), efficiently induces apoptosis in vitro in glioblastoma (GBM) cells, but does not show any survival benefit in vivo.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	46-51
24723451-1	2014	Sunitinib, an inhibitor of kinases, including VEGFR and platelet-derived growth factor receptor (PDGFR), efficiently induces apoptosis in vitro in glioblastoma (GBM) cells, but does not show any survival benefit in vivo.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	56-95
24723451-1	2014	Sunitinib, an inhibitor of kinases, including VEGFR and platelet-derived growth factor receptor (PDGFR), efficiently induces apoptosis in vitro in glioblastoma (GBM) cells, but does not show any survival benefit in vivo.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	97-102
24825438-15	2014	CONCLUSIONS: This analysis provides a population PK model of sunitinib with the ABCG2 421C&gt;A genotype as a predictive covariate for CL/F.	Sunitinib	61-70	crooked neck pre-mRNA splicing factor 1	Homo sapiens	135-139
24825438-16	2014	It also suggests that IOV and change of CL/F over time need to be considered to predict the sunitinib PK more accurately.	Sunitinib	92-101	crooked neck pre-mRNA splicing factor 1	Homo sapiens	40-44
24825438-15	2014	CONCLUSIONS: This analysis provides a population PK model of sunitinib with the ABCG2 421C&gt;A genotype as a predictive covariate for CL/F.	Sunitinib	61-70	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	80-85
24877032-0	2014	Post-treatment neutrophil-to-lymphocyte ratio in predicting prognosis in patients with metastatic clear cell renal cell carcinoma receiving sunitinib as first line therapy.	Sunitinib	140-149	solute carrier family 35 member G1	Homo sapiens	0-4
24883179-4	2014	Early FLT3 inhibitors (including sunitinib, midostaurin, and lestaurtinib) demonstrated significant promise in preclinical models of FLT3 mutant AML.	Sunitinib	33-42	fms related receptor tyrosine kinase 3	Homo sapiens	6-10
24883179-4	2014	Early FLT3 inhibitors (including sunitinib, midostaurin, and lestaurtinib) demonstrated significant promise in preclinical models of FLT3 mutant AML.	Sunitinib	33-42	fms related receptor tyrosine kinase 3	Homo sapiens	133-137
24914410-6	2014	The effect of sunitinib on Notch-1 expression was determined by Western blot in cultured MDA-MB-468 cells.	Sunitinib	14-23	notch receptor 1	Homo sapiens	27-34
24914410-13	2014	Sunitinib significantly increased the expression of Notch-1 protein in cultured MDA-MB-468 or MDA-MB-231 cells.	Sunitinib	0-9	notch receptor 1	Homo sapiens	52-59
24914410-15	2014	These findings support the hypothesis that the possibility should be considered of sunitinib increasing breast CSCs though it inhibits TNBC tumor angiogenesis and growth/progression, and that effects of sunitinib on Notch expression and hypoxia may increase breast cancer stem cells.	Sunitinib	203-212	notch receptor 1	Homo sapiens	216-221
24819355-1	2014	We have investigated in vitro the metabolic capability of 3 extrahepatic cytochromes P-450, CYP1A1, 1B1 and 2J2, known to be over-expressed in various tumors, to biotransform 5 tyrosine kinase inhibitors (TKI): dasatinib, imatinib, nilotinib, sorafenib and sunitinib.	Sunitinib	257-266	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	92-103
24786599-9	2014	CONCLUSIONS: Our results suggest that the expression of phosphorylated (i.e., activated) KDR in tumour stroma might be used as predictive biomarker for the clinical outcome in renal cell carcinoma first-line sunitinib-treated patients.	Sunitinib	208-217	kinase insert domain receptor	Homo sapiens	89-92
24045439-8	2014	Similarly, sunitinib, a small-molecule inhibitor of RET, blocked GDNF-mediated activation of ERK and AKT.	Sunitinib	11-20	ret proto-oncogene	Homo sapiens	52-55
24310825-3	2014	METHODS: We report four pediatric patients with various malignancies (chronic myelogenous leukemia, acute lymphoblastic leukemia, and glioma/renal cell carcinoma) who developed nephrotic syndrome during treatment with TK inhibitors (imatinib, sunitinib, dasatinib, and quizartinib).	Sunitinib	243-252	TXK tyrosine kinase	Homo sapiens	218-220
23728343-3	2014	We found that the multi-kinase inhibitors midostaurin and sunitinib downregulate MITF protein levels.	Sunitinib	58-67	melanocyte inducing transcription factor	Homo sapiens	81-85
24816095-6	2014	Sunitinib forms nine preserved bond paths corresponding to hydrogen bonds and also to the C-H   O and C-H   pi contacts common to the VEGRF2, CDK2, G2, KIT and IT kinases.	Sunitinib	0-9	cyclin dependent kinase 2	Homo sapiens	142-146
24289201-1	2014	OBJECTIVES: The purpose of this study was to confirm the inhibitory effects of sunitinib, an angiogenesis inhibitor that targets tyrosine kinases of vascular endothelial growth factor receptor (VEGFR) family and platelet-derived growth factor receptor (PDGFR) family, on arthritis in mice with type II collagen-induced arthritis (CIA).	Sunitinib	79-88	platelet derived growth factor receptor, beta polypeptide	Mus musculus	212-251
24289201-1	2014	OBJECTIVES: The purpose of this study was to confirm the inhibitory effects of sunitinib, an angiogenesis inhibitor that targets tyrosine kinases of vascular endothelial growth factor receptor (VEGFR) family and platelet-derived growth factor receptor (PDGFR) family, on arthritis in mice with type II collagen-induced arthritis (CIA).	Sunitinib	79-88	platelet derived growth factor receptor, beta polypeptide	Mus musculus	253-258
24289201-1	2014	OBJECTIVES: The purpose of this study was to confirm the inhibitory effects of sunitinib, an angiogenesis inhibitor that targets tyrosine kinases of vascular endothelial growth factor receptor (VEGFR) family and platelet-derived growth factor receptor (PDGFR) family, on arthritis in mice with type II collagen-induced arthritis (CIA).	Sunitinib	79-88	nuclear receptor coactivator 5	Mus musculus	294-334
24759734-0	2014	Sunitinib suppress neuroblastoma growth through degradation of MYCN and inhibition of angiogenesis.	Sunitinib	0-9	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	63-67
24759734-7	2014	Treatment with sunitinib decreased MYCN protein levels by inhibition of PI3K/AKT signaling and GSK3beta.	Sunitinib	15-24	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	35-39
24759734-7	2014	Treatment with sunitinib decreased MYCN protein levels by inhibition of PI3K/AKT signaling and GSK3beta.	Sunitinib	15-24	glycogen synthase kinase 3 beta	Homo sapiens	95-103
24759734-9	2014	Sunitinib significantly inhibited the growth of established, subcutaneous MYCN-amplified neuroblastoma xenografts in nude mice and demonstrated an anti-angiogenic effect in vivo with a reduction of tumor vasculature and a decrease of MYCN expression.	Sunitinib	0-9	v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived	Mus musculus	74-78
24759734-9	2014	Sunitinib significantly inhibited the growth of established, subcutaneous MYCN-amplified neuroblastoma xenografts in nude mice and demonstrated an anti-angiogenic effect in vivo with a reduction of tumor vasculature and a decrease of MYCN expression.	Sunitinib	0-9	v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived	Mus musculus	234-238
24045439-8	2014	Similarly, sunitinib, a small-molecule inhibitor of RET, blocked GDNF-mediated activation of ERK and AKT.	Sunitinib	11-20	glial cell derived neurotrophic factor	Homo sapiens	65-69
24783183-2	2014	Several recent findings that there are activating mutations in the KIT and PDGFRA (platelet-derived growth factor receptor-alpha) genes of GISTs provide the rationale for using targeted therapies such as imatinib or sunitinib.	Sunitinib	216-225	platelet derived growth factor receptor alpha	Homo sapiens	83-128
24783183-3	2014	Sunitinib, an oral multitargeted receptor tyrosine kinase inhibitor that inhibits kinases such as KIT, PDGFR (platelet-derived growth factor recepter), and VEGFR (vascular endothelial growth factor receptor), was recently approved for the treatment of imatinib-refractory GIST.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-101
24783183-2	2014	Several recent findings that there are activating mutations in the KIT and PDGFRA (platelet-derived growth factor receptor-alpha) genes of GISTs provide the rationale for using targeted therapies such as imatinib or sunitinib.	Sunitinib	216-225	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-70
24783183-2	2014	Several recent findings that there are activating mutations in the KIT and PDGFRA (platelet-derived growth factor receptor-alpha) genes of GISTs provide the rationale for using targeted therapies such as imatinib or sunitinib.	Sunitinib	216-225	platelet derived growth factor receptor alpha	Homo sapiens	75-81
24045439-8	2014	Similarly, sunitinib, a small-molecule inhibitor of RET, blocked GDNF-mediated activation of ERK and AKT.	Sunitinib	11-20	mitogen-activated protein kinase 1	Homo sapiens	93-96
24783183-3	2014	Sunitinib, an oral multitargeted receptor tyrosine kinase inhibitor that inhibits kinases such as KIT, PDGFR (platelet-derived growth factor recepter), and VEGFR (vascular endothelial growth factor receptor), was recently approved for the treatment of imatinib-refractory GIST.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	103-108
24783183-3	2014	Sunitinib, an oral multitargeted receptor tyrosine kinase inhibitor that inhibits kinases such as KIT, PDGFR (platelet-derived growth factor recepter), and VEGFR (vascular endothelial growth factor receptor), was recently approved for the treatment of imatinib-refractory GIST.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	110-149
24045439-8	2014	Similarly, sunitinib, a small-molecule inhibitor of RET, blocked GDNF-mediated activation of ERK and AKT.	Sunitinib	11-20	AKT serine/threonine kinase 1	Homo sapiens	101-104
24783183-3	2014	Sunitinib, an oral multitargeted receptor tyrosine kinase inhibitor that inhibits kinases such as KIT, PDGFR (platelet-derived growth factor recepter), and VEGFR (vascular endothelial growth factor receptor), was recently approved for the treatment of imatinib-refractory GIST.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	156-161
24045439-9	2014	Inhibition of RET either by gene knockdown or by treatment with sunitinib or vandetanib reduced RET-dependent growth of luminal breast cancer cells.	Sunitinib	64-73	ret proto-oncogene	Homo sapiens	14-17
24783183-3	2014	Sunitinib, an oral multitargeted receptor tyrosine kinase inhibitor that inhibits kinases such as KIT, PDGFR (platelet-derived growth factor recepter), and VEGFR (vascular endothelial growth factor receptor), was recently approved for the treatment of imatinib-refractory GIST.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	163-206
24045439-9	2014	Inhibition of RET either by gene knockdown or by treatment with sunitinib or vandetanib reduced RET-dependent growth of luminal breast cancer cells.	Sunitinib	64-73	ret proto-oncogene	Homo sapiens	96-99
24045439-11	2014	Parallel experiments using treatment with tamoxifen and sunitinib confirmed the increased effectiveness of dual inhibition of the ER and RET pathways in regulating cell growth.	Sunitinib	56-65	ret proto-oncogene	Homo sapiens	137-140
24118906-0	2014	The evaluation of efficacy and safety of sunitinib on EGFR-TKI pretreated advanced non-small cell lung cancer patients in China.	Sunitinib	41-50	epidermal growth factor receptor	Homo sapiens	54-58
24612599-3	2014	This study aimed to assess the association between initial tumor size, involved organs, pre-treatment C-reactive protein (CRP) levels, and reduction in tumor size in patients with clear cell RCC (CCRCC) treated with sunitinib.	Sunitinib	216-225	C-reactive protein	Homo sapiens	102-120
24425345-3	2014	Sunitinib not only inhibits PDGFRs, KIT, and FLT3, it also blocks VEGFRs and thus serves as an antiangiogenic agent.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	36-39
24425345-3	2014	Sunitinib not only inhibits PDGFRs, KIT, and FLT3, it also blocks VEGFRs and thus serves as an antiangiogenic agent.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	45-49
24704536-6	2014	Plasma Ang2 decreased with sunitinib treatment and increased at time of disease progression.	Sunitinib	27-36	angiopoietin 2	Homo sapiens	7-11
24704536-7	2014	In the RCC mouse, dual Ang1/2 and Ang2 inhibition improved the activity of sunitinib.	Sunitinib	75-84	angiopoietin 1	Mus musculus	23-29
24704536-7	2014	In the RCC mouse, dual Ang1/2 and Ang2 inhibition improved the activity of sunitinib.	Sunitinib	75-84	angiopoietin 2	Homo sapiens	34-38
24704536-8	2014	Combined Ang1/2 and VEGFR inhibition prevented the resumption of blood flow associated with sunitinib resistance.	Sunitinib	92-101	angiopoietin 1	Homo sapiens	9-15
24704536-8	2014	Combined Ang1/2 and VEGFR inhibition prevented the resumption of blood flow associated with sunitinib resistance.	Sunitinib	92-101	kinase insert domain receptor	Homo sapiens	20-25
24704536-9	2014	Thus, Ang2 inhibition, independent of Ang1 inhibition, improves the activity of sunitinib and plasma Ang2 increases in the setting of progression on sunitinib possibly contributing to resistance.	Sunitinib	80-89	angiopoietin 2	Homo sapiens	6-10
24704536-9	2014	Thus, Ang2 inhibition, independent of Ang1 inhibition, improves the activity of sunitinib and plasma Ang2 increases in the setting of progression on sunitinib possibly contributing to resistance.	Sunitinib	149-158	angiopoietin 2	Homo sapiens	6-10
24704536-9	2014	Thus, Ang2 inhibition, independent of Ang1 inhibition, improves the activity of sunitinib and plasma Ang2 increases in the setting of progression on sunitinib possibly contributing to resistance.	Sunitinib	149-158	angiopoietin 2	Homo sapiens	101-105
24742865-9	2014	Sunitinib plus rapamycin markedly induced versican, IDO, arginase 1, IL-6, and TGF-beta expression in the lungs, whereas it reduced IDO and IL-10 expression in the primary tumor tissues.	Sunitinib	0-9	versican	Mus musculus	42-50
24742865-9	2014	Sunitinib plus rapamycin markedly induced versican, IDO, arginase 1, IL-6, and TGF-beta expression in the lungs, whereas it reduced IDO and IL-10 expression in the primary tumor tissues.	Sunitinib	0-9	indoleamine 2,3-dioxygenase 1	Mus musculus	52-55
24742865-9	2014	Sunitinib plus rapamycin markedly induced versican, IDO, arginase 1, IL-6, and TGF-beta expression in the lungs, whereas it reduced IDO and IL-10 expression in the primary tumor tissues.	Sunitinib	0-9	arginase, liver	Mus musculus	57-67
24742865-9	2014	Sunitinib plus rapamycin markedly induced versican, IDO, arginase 1, IL-6, and TGF-beta expression in the lungs, whereas it reduced IDO and IL-10 expression in the primary tumor tissues.	Sunitinib	0-9	interleukin 6	Mus musculus	69-73
24742865-9	2014	Sunitinib plus rapamycin markedly induced versican, IDO, arginase 1, IL-6, and TGF-beta expression in the lungs, whereas it reduced IDO and IL-10 expression in the primary tumor tissues.	Sunitinib	0-9	transforming growth factor, beta 1	Mus musculus	79-87
24742865-9	2014	Sunitinib plus rapamycin markedly induced versican, IDO, arginase 1, IL-6, and TGF-beta expression in the lungs, whereas it reduced IDO and IL-10 expression in the primary tumor tissues.	Sunitinib	0-9	indoleamine 2,3-dioxygenase 1	Mus musculus	132-135
24742865-9	2014	Sunitinib plus rapamycin markedly induced versican, IDO, arginase 1, IL-6, and TGF-beta expression in the lungs, whereas it reduced IDO and IL-10 expression in the primary tumor tissues.	Sunitinib	0-9	interleukin 10	Mus musculus	140-145
24744988-12	2014	Similarly, several marketed tyrosine kinase inhibitors (TKIs) in the US (sorafenib, sunitinib, vandetanib, cabozantinib, regorafenib) are potent RET inhibitors in vitro.	Sunitinib	84-93	ret proto-oncogene	Homo sapiens	145-148
24105638-4	2014	Mice immunized with recombinant alpha-lactalbumin, a lactation protein expressed on majority of breast tumors were treated with 1 mg of Sunitinib for seven consecutive days beginning (1) concurrently, on the day of alpha-lactalbumin immunization or (2) sequentially, on day 9 after immunization.	Sunitinib	136-145	lactalbumin, alpha	Mus musculus	32-49
24105638-5	2014	Ten-day lymph nodes or 21 day spleens were tested by ELISPOT assays and flow cytometry to evaluate responsiveness to alpha-lactalbumin immunization in presence of Sunitinib and distribution of cells involved in T cell antigen priming and proliferation in different lymphoid compartments.	Sunitinib	163-172	lactalbumin alpha	Homo sapiens	117-134
24105638-7	2014	Our studies reveal that concurrent administration of Sunitinib with active vaccination against a targeted tumor antigen inhibits priming to the immunogen due to a drastic decrease in CD11b+CD11c+ antigen presenting cells, leading to failure of vaccination.	Sunitinib	53-62	integrin subunit alpha M	Homo sapiens	183-188
24105638-7	2014	Our studies reveal that concurrent administration of Sunitinib with active vaccination against a targeted tumor antigen inhibits priming to the immunogen due to a drastic decrease in CD11b+CD11c+ antigen presenting cells, leading to failure of vaccination.	Sunitinib	53-62	integrin subunit alpha X	Homo sapiens	189-194
24612599-3	2014	This study aimed to assess the association between initial tumor size, involved organs, pre-treatment C-reactive protein (CRP) levels, and reduction in tumor size in patients with clear cell RCC (CCRCC) treated with sunitinib.	Sunitinib	216-225	C-reactive protein	Homo sapiens	122-125
24612599-11	2014	CONCLUSIONS: Patients with CCRCC with smaller lung metastatic lesions and lower CRP levels may achieve greater percent reductions in tumor size with sunitinib therapy than patients with extra-pulmonary lesions, large lung lesions, and/or higher CRP levels.	Sunitinib	149-158	C-reactive protein	Homo sapiens	80-83
23975598-5	2014	We found that PDGFR-beta expression in cell seems to be a protective factor against Sunitinib resistance formation.	Sunitinib	84-93	platelet derived growth factor receptor beta	Homo sapiens	14-24
24606768-1	2014	BACKGROUND: This phase II study evaluated the efficacy and safety/tolerability of sunitinib plus trastuzumab in patients with HER2-positive advanced breast cancer (ABC).	Sunitinib	82-91	erb-b2 receptor tyrosine kinase 2	Homo sapiens	126-130
24606768-15	2014	CONCLUSIONS: Sunitinib plus trastuzumab demonstrated antitumor activity in patients with HER2-positive ABC, particularly those who were treatment-naive or had only received prior adjuvant treatment.	Sunitinib	13-22	erb-b2 receptor tyrosine kinase 2	Homo sapiens	89-93
24606768-16	2014	Sunitinib plus trastuzumab had acceptable safety and tolerability in patients with HER2-positive ABC who had not received prior anthracycline therapy.	Sunitinib	0-9	erb-b2 receptor tyrosine kinase 2	Homo sapiens	83-87
24247421-0	2014	Development of cardiac hypertrophy by sunitinib in vivo and in vitro rat cardiomyocytes is influenced by the aryl hydrocarbon receptor signaling pathway.	Sunitinib	38-47	aryl hydrocarbon receptor	Rattus norvegicus	109-134
23975598-6	2014	In addition, we found that both SK1 and ERK were activated in Sunitinib-resistance cell lines and SK1 and ERK inhibitors could resensitize Sunitinib-resistant cell lines.	Sunitinib	62-71	sphingosine kinase 1	Homo sapiens	32-35
23975598-6	2014	In addition, we found that both SK1 and ERK were activated in Sunitinib-resistance cell lines and SK1 and ERK inhibitors could resensitize Sunitinib-resistant cell lines.	Sunitinib	62-71	EPH receptor B2	Homo sapiens	40-43
23975598-6	2014	In addition, we found that both SK1 and ERK were activated in Sunitinib-resistance cell lines and SK1 and ERK inhibitors could resensitize Sunitinib-resistant cell lines.	Sunitinib	139-148	sphingosine kinase 1	Homo sapiens	32-35
24414551-1	2014	BACKGROUND: Sunitinib treatment results in a compensatory increase in plasma VEGF levels.	Sunitinib	12-21	vascular endothelial growth factor A	Homo sapiens	77-81
23975598-6	2014	In addition, we found that both SK1 and ERK were activated in Sunitinib-resistance cell lines and SK1 and ERK inhibitors could resensitize Sunitinib-resistant cell lines.	Sunitinib	139-148	EPH receptor B2	Homo sapiens	40-43
24414551-2	2014	Acute withdrawal of sunitinib results in a proliferative withdrawal flare, primarily due to elevated VEGF levels.	Sunitinib	20-29	vascular endothelial growth factor A	Homo sapiens	101-105
24414551-14	2014	As predicted, VEGF levels increased during sunitinib exposure followed by a rapid decline after bevacizumab.	Sunitinib	43-52	vascular endothelial growth factor A	Homo sapiens	14-18
24414551-16	2014	The increase in VEGF at D42 was unexpected based on sunitinib alone and contrary to the hypothesis that we would block VEGF flare with low-dose bevacizumab.	Sunitinib	52-61	vascular endothelial growth factor A	Homo sapiens	16-20
23975598-6	2014	In addition, we found that both SK1 and ERK were activated in Sunitinib-resistance cell lines and SK1 and ERK inhibitors could resensitize Sunitinib-resistant cell lines.	Sunitinib	139-148	sphingosine kinase 1	Homo sapiens	98-101
23975598-6	2014	In addition, we found that both SK1 and ERK were activated in Sunitinib-resistance cell lines and SK1 and ERK inhibitors could resensitize Sunitinib-resistant cell lines.	Sunitinib	139-148	EPH receptor B2	Homo sapiens	106-109
23975598-7	2014	In conclusion, our observations suggest that SK1 and ERK activation is a feature of resistant cell lines, which serves as an alternative pathway evading anti-tumor activity of Sunitinib.	Sunitinib	176-185	sphingosine kinase 1	Homo sapiens	45-48
23975598-7	2014	In conclusion, our observations suggest that SK1 and ERK activation is a feature of resistant cell lines, which serves as an alternative pathway evading anti-tumor activity of Sunitinib.	Sunitinib	176-185	EPH receptor B2	Homo sapiens	53-56
24234588-0	2014	Predictive value of CYP3A and ABCB1 phenotyping probes for the pharmacokinetics of sunitinib: the ClearSun study.	Sunitinib	83-92	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	20-25
24234588-0	2014	Predictive value of CYP3A and ABCB1 phenotyping probes for the pharmacokinetics of sunitinib: the ClearSun study.	Sunitinib	83-92	ATP binding cassette subfamily B member 1	Homo sapiens	30-35
24393200-7	2014	In vitro NOS enzyme activity assay was used to determine the direct inhibition of nNOS by sunitinib.	Sunitinib	90-99	nitric oxide synthase 1	Homo sapiens	82-86
24234588-2	2014	In this prospective study cytochrome P450 (CYP) 3A and adenosine triphosphate binding cassette (ABC) B1 phenotypes were correlated to the pharmacokinetics of sunitinib and its active metabolite N-desethylsunitinib.	Sunitinib	158-167	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	26-50
24393200-10	2014	Sunitinib reversed the increase in NO levels, NOS activity, and nNOS expression induced by low potassium or MPP(+) .	Sunitinib	0-9	nitric oxide synthase 1	Homo sapiens	64-68
24234588-2	2014	In this prospective study cytochrome P450 (CYP) 3A and adenosine triphosphate binding cassette (ABC) B1 phenotypes were correlated to the pharmacokinetics of sunitinib and its active metabolite N-desethylsunitinib.	Sunitinib	158-167	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	55-94
24393200-11	2014	Knockdown of nNOS expression partially abolished the neuroprotective effects of sunitinib.	Sunitinib	80-89	nitric oxide synthase 1	Homo sapiens	13-17
24234588-2	2014	In this prospective study cytochrome P450 (CYP) 3A and adenosine triphosphate binding cassette (ABC) B1 phenotypes were correlated to the pharmacokinetics of sunitinib and its active metabolite N-desethylsunitinib.	Sunitinib	158-167	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	96-99
24393200-12	2014	Moreover, sunitinib directly inhibited nNOS enzyme activity.	Sunitinib	10-19	nitric oxide synthase 1	Homo sapiens	39-43
24025975-1	2014	Sunitinib is a multiple tyrosine kinase inhibitor of the vascular endothelial growth factor and platelet-derived growth factor pathway and inhibits angiogenesis, cell proliferation, and tumor cell invasion, and stimulates apoptosis.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	57-91
24393200-13	2014	CONCLUSIONS: Sunitinib exerts its neuroprotective effects by inhibiting NO overproduction, possibly via the inhibition of nNOS activity and the decrease in nNOS expression.	Sunitinib	13-22	nitric oxide synthase 1	Homo sapiens	122-126
24393200-13	2014	CONCLUSIONS: Sunitinib exerts its neuroprotective effects by inhibiting NO overproduction, possibly via the inhibition of nNOS activity and the decrease in nNOS expression.	Sunitinib	13-22	nitric oxide synthase 1	Homo sapiens	156-160
24277456-8	2014	Moreover, CDDP-resistant cells were more sensitive to incubation with PDGFRbeta inhibitors such as pazopanib or sunitinib than sensitive cells, a finding consistent with these cells being dependent on this signaling pathway.	Sunitinib	112-121	platelet derived growth factor receptor beta	Homo sapiens	70-79
24743196-3	2014	Sorafenib, sunitinib, axitinib, and pazopanib are kinase inhibitors that block vascular endothelial growth factor receptor(VEGFR).	Sunitinib	11-20	kinase insert domain receptor	Homo sapiens	123-128
24120473-11	2014	Sunitinib inhibited VEGF signaling in neoplastic cells and reduced weight and volume of xenograft tumors in mice.	Sunitinib	0-9	vascular endothelial growth factor A	Mus musculus	20-24
24120473-14	2014	Strategies to reduce autocrine VEGF signaling (eg, with sunitinib) might be used to prevent or treat cancer in patients with Barrett"s esophagus.	Sunitinib	56-65	vascular endothelial growth factor A	Homo sapiens	31-35
23421954-13	2014	mRCC patients with the CC-genotype in VEGFR1 SNP rs9582036 have a poorer response rate, PFS and OS when treated with sunitinib.	Sunitinib	117-126	fms related receptor tyrosine kinase 1	Homo sapiens	38-44
24276455-6	2014	RESULTS: Sunitinib and cisplatin synergistically inhibited the growth of MZ-CRC-1 cells harboring the RET M918T activating mutation.	Sunitinib	9-18	ret proto-oncogene	Homo sapiens	102-105
24276455-10	2014	CONCLUSIONS: Addition of cisplatin to sunitinib potentiates apoptotic cell death and has promising preclinical activity in MTCs harboring the RET M918T oncogene.	Sunitinib	38-47	ret proto-oncogene	Homo sapiens	142-145
24575017-6	2014	This report also documents the use of a novel drug combination based on sunitinib that was well tolerated and may warrant testing in other c-kit-dependent cancers.	Sunitinib	72-81	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	139-144
23421954-0	2014	VEGFR1 single nucleotide polymorphisms associated with outcome in patients with metastatic renal cell carcinoma treated with sunitinib - a multicentric retrospective analysis.	Sunitinib	125-134	fms related receptor tyrosine kinase 1	Homo sapiens	0-6
24475095-4	2014	In vitro experiments were conducted to study the role of miR-942 in sunitinib resistance.	Sunitinib	68-77	microRNA 942	Homo sapiens	57-64
24475095-7	2014	MiR-942 was the most accurate predictor of sunitinib efficacy (p = 0.0074).	Sunitinib	43-52	microRNA 942	Homo sapiens	0-7
24475095-10	2014	MiR-942 overexpression in Caki-2 up-regulates MMP-9 and VEGF secretion which, in turn, promote HBMEC endothelial migration and sunitinib resistance.	Sunitinib	127-136	microRNA 942	Homo sapiens	0-7
24475095-10	2014	MiR-942 overexpression in Caki-2 up-regulates MMP-9 and VEGF secretion which, in turn, promote HBMEC endothelial migration and sunitinib resistance.	Sunitinib	127-136	matrix metallopeptidase 9	Homo sapiens	46-51
24475095-10	2014	MiR-942 overexpression in Caki-2 up-regulates MMP-9 and VEGF secretion which, in turn, promote HBMEC endothelial migration and sunitinib resistance.	Sunitinib	127-136	vascular endothelial growth factor A	Homo sapiens	56-60
24475095-13	2014	We describe a novel paracrine mechanism through which high miR-942 levels in MRCC cells up-regulates MMP-9 and VEGF secretion to enhance endothelial migration and sunitinib resistance.	Sunitinib	163-172	microRNA 942	Homo sapiens	59-66
24475095-13	2014	We describe a novel paracrine mechanism through which high miR-942 levels in MRCC cells up-regulates MMP-9 and VEGF secretion to enhance endothelial migration and sunitinib resistance.	Sunitinib	163-172	matrix metallopeptidase 9	Homo sapiens	101-106
24475095-13	2014	We describe a novel paracrine mechanism through which high miR-942 levels in MRCC cells up-regulates MMP-9 and VEGF secretion to enhance endothelial migration and sunitinib resistance.	Sunitinib	163-172	vascular endothelial growth factor A	Homo sapiens	111-115
24967411-13	2014	CONCLUSION: The combination of sunitinib and telmisartan revealed an enhancement of the blockage of the VEGF pathway on renal tumor resulting in a decrease in neoangiogenesis and an increase in necrosis.	Sunitinib	31-40	vascular endothelial growth factor A	Mus musculus	104-108
24783204-1	2014	In the past few years, therapies targeted at the von Hippel-Lindau (VHL) and hypoxia-inducible factor (HIF) pathways, such as sunitinib and sorafenib, have been developed to treat clear cell renal cell carcinoma (ccRCC).	Sunitinib	126-135	von Hippel-Lindau tumor suppressor	Homo sapiens	49-66
24149944-2	2014	Since sunitinib is metabolized by cytochrome P450(CYP)3A4, variability in the activity of this enzyme may explain a considerable proportion of this inter-patient variability.	Sunitinib	6-15	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	34-57
24220935-6	2014	In multivariate analysis, baseline sVEGFR-3 and IL-8 remained independent predictors of OS in the sunitinib arm, while no independent predictors of outcome remained in the IFN-alpha arm.	Sunitinib	98-107	C-X-C motif chemokine ligand 8	Homo sapiens	48-52
24205792-4	2014	Although sunitinib malate, a multi-kinase inhibitor, has shown effectiveness against imatinib-resistant GISTs, recent studies have indicated that some imatinib-resistant GISTs harboring secondary mutations in the KIT activation loop were also resistant to sunitinib.	Sunitinib	9-25	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	213-216
24205792-4	2014	Although sunitinib malate, a multi-kinase inhibitor, has shown effectiveness against imatinib-resistant GISTs, recent studies have indicated that some imatinib-resistant GISTs harboring secondary mutations in the KIT activation loop were also resistant to sunitinib.	Sunitinib	9-18	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	213-216
24018642-6	2014	Combination of rapamycin with sunitinib resulted in enhanced cell cycle arrest in G1 phase, which was accompanied with enhanced suppression of mTOR signaling and disruption of the negative feedback loop that activate AKT upon mTORC1 inhibition.	Sunitinib	30-39	mechanistic target of rapamycin kinase	Homo sapiens	143-147
24018642-6	2014	Combination of rapamycin with sunitinib resulted in enhanced cell cycle arrest in G1 phase, which was accompanied with enhanced suppression of mTOR signaling and disruption of the negative feedback loop that activate AKT upon mTORC1 inhibition.	Sunitinib	30-39	AKT serine/threonine kinase 1	Homo sapiens	217-220
24018642-6	2014	Combination of rapamycin with sunitinib resulted in enhanced cell cycle arrest in G1 phase, which was accompanied with enhanced suppression of mTOR signaling and disruption of the negative feedback loop that activate AKT upon mTORC1 inhibition.	Sunitinib	30-39	CREB regulated transcription coactivator 1	Mus musculus	226-232
24018642-7	2014	Furthermore, sunitinib and rapamycin displayed synergistic activity against tube formation by human microvessel endothelial cells as well as outgrowth of endothelial tubes and microvessels both in vitro and in vivo, which is associated with down-regulation of VEGF secretion and HIF1alpha expression.	Sunitinib	13-22	vascular endothelial growth factor A	Homo sapiens	260-264
24018642-7	2014	Furthermore, sunitinib and rapamycin displayed synergistic activity against tube formation by human microvessel endothelial cells as well as outgrowth of endothelial tubes and microvessels both in vitro and in vivo, which is associated with down-regulation of VEGF secretion and HIF1alpha expression.	Sunitinib	13-22	hypoxia inducible factor 1 subunit alpha	Homo sapiens	279-288
25018885-3	2014	Autoimmune and neurological side effects have been linked to sunitinib"s inhibition of VEGF receptors with a corresponding increase in VEGF levels, which is associated with development of different neuropathies.	Sunitinib	61-70	vascular endothelial growth factor A	Homo sapiens	87-91
25018885-3	2014	Autoimmune and neurological side effects have been linked to sunitinib"s inhibition of VEGF receptors with a corresponding increase in VEGF levels, which is associated with development of different neuropathies.	Sunitinib	61-70	vascular endothelial growth factor A	Homo sapiens	135-139
24311637-13	2014	High endothelial c-KIT expression may define a subgroup of patients who will benefit from sunitinib treatment by achieving prolonged PFS.	Sunitinib	90-99	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-22
24384849-5	2014	Treatment with tyrosine kinase inhibitors (TKIs) such as imatinib, sunitinib, and regorafenib is effective in controlling unresectable disease; however, drug resistance caused by secondary KIT or PDGFRA mutations eventually develops in 90% of cases.	Sunitinib	67-76	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	189-192
24384849-5	2014	Treatment with tyrosine kinase inhibitors (TKIs) such as imatinib, sunitinib, and regorafenib is effective in controlling unresectable disease; however, drug resistance caused by secondary KIT or PDGFRA mutations eventually develops in 90% of cases.	Sunitinib	67-76	platelet derived growth factor receptor alpha	Homo sapiens	196-202
26168132-0	2014	HIF-1 Dimerization Inhibitor Acriflavine Enhances Antitumor Activity of Sunitinib in Breast Cancer Model.	Sunitinib	72-81	hypoxia inducible factor 1 subunit alpha	Homo sapiens	0-5
24685916-3	2014	She was successfully treated with daily administration of sunitinib malate, an oral multi-target tyrosine kinase inhibitor, which particularly targets vascular endothelial growth factor (VEGF) receptors.	Sunitinib	58-74	vascular endothelial growth factor A	Homo sapiens	151-185
24685916-3	2014	She was successfully treated with daily administration of sunitinib malate, an oral multi-target tyrosine kinase inhibitor, which particularly targets vascular endothelial growth factor (VEGF) receptors.	Sunitinib	58-74	vascular endothelial growth factor A	Homo sapiens	187-191
26168132-4	2014	The combination of sunitinib with acriflavine significantly decreased vascular endothelial growth factor and TGF-beta expression and reduced tumor vasculature followed by increased intratumor necrosis and apoptosis.	Sunitinib	19-28	vascular endothelial growth factor A	Homo sapiens	70-104
26168132-4	2014	The combination of sunitinib with acriflavine significantly decreased vascular endothelial growth factor and TGF-beta expression and reduced tumor vasculature followed by increased intratumor necrosis and apoptosis.	Sunitinib	19-28	transforming growth factor beta 1	Homo sapiens	109-117
24756791-1	2014	Sunitinib is an oral multikinase inhibitor that blocks the vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) alpha and beta, c-kit, and other receptors.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	59-102
24756791-1	2014	Sunitinib is an oral multikinase inhibitor that blocks the vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) alpha and beta, c-kit, and other receptors.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	104-109
24756791-1	2014	Sunitinib is an oral multikinase inhibitor that blocks the vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) alpha and beta, c-kit, and other receptors.	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	153-165
24756791-1	2014	Sunitinib is an oral multikinase inhibitor that blocks the vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) alpha and beta, c-kit, and other receptors.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	176-181
24324073-6	2013	AIM: This study sought to evaluate the expression of PDGFR alpha/beta and hypoxia-inducible factor-1alpha (HIF-1alpha) and their alterations induced by everolimus, sorafenib and sunitinib in chemonaive HPV-positive and HPV-negative HNSCC.	Sunitinib	178-187	platelet derived growth factor receptor alpha	Homo sapiens	53-64
25764782-7	2014	Systemic therapies regarding malignant insulinoma are: chemotherapy, somatostatin analogs, radiolabelled somatostatin analogs and the newly developed biological targeted therapies such as everolimus--oral inhibitor of the mammalian target of rapamycin, and sunitinib--the tyrosine kinase inhibitor.	Sunitinib	257-266	mechanistic target of rapamycin kinase	Homo sapiens	222-251
23848205-0	2013	Curcumin potentiates the ability of sunitinib to eliminate the VHL-lacking renal cancer cells 786-O: rapid inhibition of Rb phosphorylation as a preamble to cyclin D1 inhibition.	Sunitinib	36-45	cyclin D1	Homo sapiens	157-166
23848205-9	2013	Since curcumin is known to inhibit the cyclin D1-dependent G1/S-phase kinase CDK4 and the cyclin B-dependent G2/M-phase kinase CDK1 that catalyze phosphorylation-mediated inactivation of Rb, our results indicate that SunC containing a lower dose of sunitinib would be effective in restoring the tumor suppressor activity of Rb, thereby truncating cell cycle and triggering cell death.	Sunitinib	249-258	cyclin dependent kinase 1	Homo sapiens	127-131
24324073-6	2013	AIM: This study sought to evaluate the expression of PDGFR alpha/beta and hypoxia-inducible factor-1alpha (HIF-1alpha) and their alterations induced by everolimus, sorafenib and sunitinib in chemonaive HPV-positive and HPV-negative HNSCC.	Sunitinib	178-187	hypoxia inducible factor 1 subunit alpha	Homo sapiens	107-117
24324073-11	2013	Incubation with everolimus, sorafenib or sunitinib led to a decrease in PDGFR alpha/beta and HIF-1alpha expression, depending on the HPV status.	Sunitinib	41-50	platelet derived growth factor receptor alpha	Homo sapiens	72-83
24324073-11	2013	Incubation with everolimus, sorafenib or sunitinib led to a decrease in PDGFR alpha/beta and HIF-1alpha expression, depending on the HPV status.	Sunitinib	41-50	hypoxia inducible factor 1 subunit alpha	Homo sapiens	93-103
24295410-0	2013	Sunitinib in malignant melanoma: a treatment option only for KIT-mutated patients?	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-64
24061866-6	2013	Using specific human and mouse probes for genes encoding sunitinib targets, we showed a significant relation between apoptotic tumor cell numbers and human PDGFRBeta and RET mRNA expression in liver cancer and to human VEGFR2 expression in breast cancer xenografts.	Sunitinib	57-66	platelet derived growth factor receptor beta	Homo sapiens	156-165
24061866-6	2013	Using specific human and mouse probes for genes encoding sunitinib targets, we showed a significant relation between apoptotic tumor cell numbers and human PDGFRBeta and RET mRNA expression in liver cancer and to human VEGFR2 expression in breast cancer xenografts.	Sunitinib	57-66	ret proto-oncogene	Homo sapiens	170-173
24061866-6	2013	Using specific human and mouse probes for genes encoding sunitinib targets, we showed a significant relation between apoptotic tumor cell numbers and human PDGFRBeta and RET mRNA expression in liver cancer and to human VEGFR2 expression in breast cancer xenografts.	Sunitinib	57-66	kinase insert domain receptor	Homo sapiens	219-225
24122794-0	2013	Autotaxin-lysophosphatidic acid signaling axis mediates tumorigenesis and development of acquired resistance to sunitinib in renal cell carcinoma.	Sunitinib	112-121	ectonucleotide pyrophosphatase/phosphodiesterase 2	Homo sapiens	0-9
24122794-5	2013	RESULTS: Altered expression of autotaxin, an extracellular lysophospholipase D, was detected in sunitinib-treated tumor vasculature of human RCC and in the tumor endothelial cells of RCC xenograft models when adapting to sunitinib.	Sunitinib	96-105	ectonucleotide pyrophosphatase/phosphodiesterase 2	Homo sapiens	31-40
24122794-5	2013	RESULTS: Altered expression of autotaxin, an extracellular lysophospholipase D, was detected in sunitinib-treated tumor vasculature of human RCC and in the tumor endothelial cells of RCC xenograft models when adapting to sunitinib.	Sunitinib	96-105	ectonucleotide pyrophosphatase/phosphodiesterase 2	Homo sapiens	45-78
24122794-5	2013	RESULTS: Altered expression of autotaxin, an extracellular lysophospholipase D, was detected in sunitinib-treated tumor vasculature of human RCC and in the tumor endothelial cells of RCC xenograft models when adapting to sunitinib.	Sunitinib	221-230	ectonucleotide pyrophosphatase/phosphodiesterase 2	Homo sapiens	31-40
24122794-5	2013	RESULTS: Altered expression of autotaxin, an extracellular lysophospholipase D, was detected in sunitinib-treated tumor vasculature of human RCC and in the tumor endothelial cells of RCC xenograft models when adapting to sunitinib.	Sunitinib	221-230	ectonucleotide pyrophosphatase/phosphodiesterase 2	Homo sapiens	45-78
24122794-10	2013	In addition, coadministration of Ki16425 with sunitinib prolonged the sensitivity of RCC to sunitinib in xenograft models, suggesting that ATX-LPA signaling in part mediates the acquired resistance against sunitinib in RCC.	Sunitinib	46-55	ectonucleotide pyrophosphatase/phosphodiesterase 2	Homo sapiens	139-142
24122794-10	2013	In addition, coadministration of Ki16425 with sunitinib prolonged the sensitivity of RCC to sunitinib in xenograft models, suggesting that ATX-LPA signaling in part mediates the acquired resistance against sunitinib in RCC.	Sunitinib	92-101	ectonucleotide pyrophosphatase/phosphodiesterase 2	Homo sapiens	139-142
24122794-10	2013	In addition, coadministration of Ki16425 with sunitinib prolonged the sensitivity of RCC to sunitinib in xenograft models, suggesting that ATX-LPA signaling in part mediates the acquired resistance against sunitinib in RCC.	Sunitinib	92-101	ectonucleotide pyrophosphatase/phosphodiesterase 2	Homo sapiens	139-142
24122794-11	2013	CONCLUSIONS: Our results reveal that endothelial ATX acts through LPA signaling to promote renal tumorigenesis and is functionally involved in the acquired resistance of RCC to sunitinib.	Sunitinib	177-186	ectonucleotide pyrophosphatase/phosphodiesterase 2	Homo sapiens	49-52
24295410-1	2013	Sunitinib has previously been reported to be potentially effective in the treatment of malignant melanomas expressing c-KIT.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	118-123
24295410-4	2013	To our knowledge, this represents the first evidence of sunitinib activity in KIT wild-type melanoma.	Sunitinib	56-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	78-81
23812726-7	2013	The inhibition of kinase activation using multi-targeted kinase inhibitors, sorafenib and sunitinib led to significant cell growth inhibition and apoptosis induction via suppression of Erk1/2 and Akt activation, whereas drugs with specificity to a single kinase showed less potency.	Sunitinib	90-99	mitogen-activated protein kinase 3	Homo sapiens	185-191
24113148-5	2013	Furthermore, the distribution of sunitinib to the brain increased after administration of selective P-glycoprotein (P-gp) or breast cancer resistance protein (Bcrp) pharmacological inhibitors and a dual inhibitor, elacridar, comparable to that of the corresponding transgenic genotype.	Sunitinib	33-42	phosphoglycolate phosphatase	Mus musculus	100-114
24113148-5	2013	Furthermore, the distribution of sunitinib to the brain increased after administration of selective P-glycoprotein (P-gp) or breast cancer resistance protein (Bcrp) pharmacological inhibitors and a dual inhibitor, elacridar, comparable to that of the corresponding transgenic genotype.	Sunitinib	33-42	phosphoglycolate phosphatase	Mus musculus	116-120
24113148-5	2013	Furthermore, the distribution of sunitinib to the brain increased after administration of selective P-glycoprotein (P-gp) or breast cancer resistance protein (Bcrp) pharmacological inhibitors and a dual inhibitor, elacridar, comparable to that of the corresponding transgenic genotype.	Sunitinib	33-42	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	125-157
24113148-5	2013	Furthermore, the distribution of sunitinib to the brain increased after administration of selective P-glycoprotein (P-gp) or breast cancer resistance protein (Bcrp) pharmacological inhibitors and a dual inhibitor, elacridar, comparable to that of the corresponding transgenic genotype.	Sunitinib	33-42	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	159-163
24167056-5	2013	Among the differentially expressed proteins, heme oxygenase-1 (HO-1) was found in the sunitinib and imatinib mesylate treatment groups, which possibly acts as a specific target for synthetic lethality in combinational treatment.	Sunitinib	86-95	heme oxygenase 1	Homo sapiens	45-61
24167056-5	2013	Among the differentially expressed proteins, heme oxygenase-1 (HO-1) was found in the sunitinib and imatinib mesylate treatment groups, which possibly acts as a specific target for synthetic lethality in combinational treatment.	Sunitinib	86-95	heme oxygenase 1	Homo sapiens	63-67
23812726-7	2013	The inhibition of kinase activation using multi-targeted kinase inhibitors, sorafenib and sunitinib led to significant cell growth inhibition and apoptosis induction via suppression of Erk1/2 and Akt activation, whereas drugs with specificity to a single kinase showed less potency.	Sunitinib	90-99	AKT serine/threonine kinase 1	Homo sapiens	196-199
24222145-0	2013	VEGF expression and response to sunitinib in patients with metastatic clear cell renal cell carcinoma.	Sunitinib	32-41	vascular endothelial growth factor A	Homo sapiens	0-4
24107802-0	2013	Hyperbilirubinemia in pazopanib- or sunitinib-treated patients in COMPARZ is associated with UGT1A1 polymorphisms.	Sunitinib	36-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
24257372-0	2013	PKPD Modeling of VEGF, sVEGFR-2, sVEGFR-3, and sKIT as Predictors of Tumor Dynamics and Overall Survival Following Sunitinib Treatment in GIST.	Sunitinib	115-124	vascular endothelial growth factor A	Homo sapiens	17-21
24232460-0	2013	Sunitinib indirectly enhanced anti-tumor cytotoxicity of cytokine-induced killer cells and CD3+CD56+ subset through the co-culturing dendritic cells.	Sunitinib	0-9	neural cell adhesion molecule 1	Homo sapiens	95-99
24232460-5	2013	Sunitinib promoted Th1-inducing and pro-inflammatory phenotypes (IL-12, IFN-gamma and IL-6) in DCs at the expense of Th2 inducing phenotype (IL-13) and regulatory phenotype (PD-L1, IDO).	Sunitinib	0-9	negative elongation factor complex member C/D	Homo sapiens	19-22
24232460-5	2013	Sunitinib promoted Th1-inducing and pro-inflammatory phenotypes (IL-12, IFN-gamma and IL-6) in DCs at the expense of Th2 inducing phenotype (IL-13) and regulatory phenotype (PD-L1, IDO).	Sunitinib	0-9	interferon gamma	Homo sapiens	72-81
24232460-5	2013	Sunitinib promoted Th1-inducing and pro-inflammatory phenotypes (IL-12, IFN-gamma and IL-6) in DCs at the expense of Th2 inducing phenotype (IL-13) and regulatory phenotype (PD-L1, IDO).	Sunitinib	0-9	interleukin 6	Homo sapiens	86-90
24232460-5	2013	Sunitinib promoted Th1-inducing and pro-inflammatory phenotypes (IL-12, IFN-gamma and IL-6) in DCs at the expense of Th2 inducing phenotype (IL-13) and regulatory phenotype (PD-L1, IDO).	Sunitinib	0-9	CD274 molecule	Homo sapiens	174-179
24232460-5	2013	Sunitinib promoted Th1-inducing and pro-inflammatory phenotypes (IL-12, IFN-gamma and IL-6) in DCs at the expense of Th2 inducing phenotype (IL-13) and regulatory phenotype (PD-L1, IDO).	Sunitinib	0-9	indoleamine 2,3-dioxygenase 1	Homo sapiens	181-184
24232460-6	2013	Sunitinib-treated DCs subsequently induced the upregulation of Th1 phenotypic markers (IFN-gamma and T-bet) and the downregulation of the Th2 signature (GATA-3) and the Th17 marker (RORC) on the CD3+CD56+ subset of CIK cells.	Sunitinib	0-9	negative elongation factor complex member C/D	Homo sapiens	63-66
24232460-6	2013	Sunitinib-treated DCs subsequently induced the upregulation of Th1 phenotypic markers (IFN-gamma and T-bet) and the downregulation of the Th2 signature (GATA-3) and the Th17 marker (RORC) on the CD3+CD56+ subset of CIK cells.	Sunitinib	0-9	interferon gamma	Homo sapiens	87-96
24232460-6	2013	Sunitinib-treated DCs subsequently induced the upregulation of Th1 phenotypic markers (IFN-gamma and T-bet) and the downregulation of the Th2 signature (GATA-3) and the Th17 marker (RORC) on the CD3+CD56+ subset of CIK cells.	Sunitinib	0-9	T-box transcription factor 21	Homo sapiens	101-106
24232460-6	2013	Sunitinib-treated DCs subsequently induced the upregulation of Th1 phenotypic markers (IFN-gamma and T-bet) and the downregulation of the Th2 signature (GATA-3) and the Th17 marker (RORC) on the CD3+CD56+ subset of CIK cells.	Sunitinib	0-9	GATA binding protein 3	Homo sapiens	153-159
24232460-6	2013	Sunitinib-treated DCs subsequently induced the upregulation of Th1 phenotypic markers (IFN-gamma and T-bet) and the downregulation of the Th2 signature (GATA-3) and the Th17 marker (RORC) on the CD3+CD56+ subset of CIK cells.	Sunitinib	0-9	neural cell adhesion molecule 1	Homo sapiens	199-203
24232460-7	2013	It concluded that sunitinib-pretreated DCs drove the CD3+CD56+ subset toward Th1 phenotype with increased anti-tumor cytotoxicity.	Sunitinib	18-27	neural cell adhesion molecule 1	Homo sapiens	57-61
24232460-7	2013	It concluded that sunitinib-pretreated DCs drove the CD3+CD56+ subset toward Th1 phenotype with increased anti-tumor cytotoxicity.	Sunitinib	18-27	negative elongation factor complex member C/D	Homo sapiens	77-80
24223213-10	2013	Furthermore, treatment with two anti-proliferative, multi-receptor tyrosine kinase inhibitors-sunitinib and sorafenib-strongly upregulated biglycan expression.	Sunitinib	94-103	biglycan	Homo sapiens	139-147
24222145-5	2013	Patients with higher H-score and higher VEGF expression had a significantly shorter survival; OS after first-line sunitinib therapy and PFS correlated with MSKCC score and DMFS but not with VEGF expression and H score.	Sunitinib	114-123	vascular endothelial growth factor A	Homo sapiens	40-44
24222145-1	2013	AIM: To verify whether vascular endothelial growth factor (VEGF) is associated with distant metastasis free survival (DMFS) and Overall Survival (OS) of patients with renal cell carcinoma (RCC) treated with sunitinib.	Sunitinib	207-216	vascular endothelial growth factor A	Homo sapiens	23-57
24222145-1	2013	AIM: To verify whether vascular endothelial growth factor (VEGF) is associated with distant metastasis free survival (DMFS) and Overall Survival (OS) of patients with renal cell carcinoma (RCC) treated with sunitinib.	Sunitinib	207-216	vascular endothelial growth factor A	Homo sapiens	59-63
23969938-0	2013	Emergence of polyclonal FLT3 tyrosine kinase domain mutations during sequential therapy with sorafenib and sunitinib in FLT3-ITD-positive acute myeloid leukemia.	Sunitinib	107-116	fms related receptor tyrosine kinase 3	Homo sapiens	24-28
23471661-0	2013	Sunitinib reverse multidrug resistance in gastric cancer cells by modulating Stat3 and inhibiting P-gp function.	Sunitinib	0-9	signal transducer and activator of transcription 3	Homo sapiens	77-82
23471661-0	2013	Sunitinib reverse multidrug resistance in gastric cancer cells by modulating Stat3 and inhibiting P-gp function.	Sunitinib	0-9	phosphoglycolate phosphatase	Homo sapiens	98-102
23471661-6	2013	In addition, the present study revealed that Sunitinib inhibited Stat3 and down-regulated Bcl-2 in SGC7901/VCR cells, which might also contribute to the reversal of MDR.	Sunitinib	45-54	signal transducer and activator of transcription 3	Homo sapiens	65-70
23471661-6	2013	In addition, the present study revealed that Sunitinib inhibited Stat3 and down-regulated Bcl-2 in SGC7901/VCR cells, which might also contribute to the reversal of MDR.	Sunitinib	45-54	BCL2 apoptosis regulator	Homo sapiens	90-95
23471661-7	2013	In conclusion, Sunitinib reverses multidrug resistance in gastric cancer cells by inhibiting P-gp transporter function and modulating Stat3 and Bcl-2.	Sunitinib	15-24	phosphoglycolate phosphatase	Homo sapiens	93-97
23471661-7	2013	In conclusion, Sunitinib reverses multidrug resistance in gastric cancer cells by inhibiting P-gp transporter function and modulating Stat3 and Bcl-2.	Sunitinib	15-24	signal transducer and activator of transcription 3	Homo sapiens	134-139
23471661-7	2013	In conclusion, Sunitinib reverses multidrug resistance in gastric cancer cells by inhibiting P-gp transporter function and modulating Stat3 and Bcl-2.	Sunitinib	15-24	BCL2 apoptosis regulator	Homo sapiens	144-149
23659419-0	2013	Acute renal failure during the "off" period after sunitinib administration: possible mechanism of vascular endothelial growth factor cascade hyperactivation.	Sunitinib	50-59	vascular endothelial growth factor A	Homo sapiens	98-132
24204982-8	2013	We determined the 1.4 A co-crystal structure of PAK6 with the type II PAK inhibitor PF-3758309, and the 1.95 A co-crystal structure of PAK6 with sunitinib.	Sunitinib	145-154	p21 (RAC1) activated kinase 6	Mus musculus	135-139
23969938-1	2013	PURPOSE: To evaluate the clinical activity of sequential therapy with sorafenib and sunitinib in FMS-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD)-positive acute myelogenous leukemia (AML) and monitor the emergence of secondary FLT3 tyrosine kinase domain (TKD) mutations during treatment.	Sunitinib	84-93	fms related receptor tyrosine kinase 3	Homo sapiens	97-123
23969938-1	2013	PURPOSE: To evaluate the clinical activity of sequential therapy with sorafenib and sunitinib in FMS-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD)-positive acute myelogenous leukemia (AML) and monitor the emergence of secondary FLT3 tyrosine kinase domain (TKD) mutations during treatment.	Sunitinib	84-93	fms related receptor tyrosine kinase 3	Homo sapiens	125-129
23969938-13	2013	Cells expressing sorafenib-resistant FLT3 mutations were sensitive to sunitinib in vitro.	Sunitinib	70-79	fms related receptor tyrosine kinase 3	Homo sapiens	37-41
23969938-14	2013	CONCLUSIONS: Sunitinib has activity in patients that are resistant to sorafenib and harbor secondary FLT3 TKD mutations.	Sunitinib	13-22	fms related receptor tyrosine kinase 3	Homo sapiens	101-105
23716000-6	2013	Supplement with recombinant mouse IL-12b or restoration of IL-12b expression in the host by zoledronic acid, which was previously reported to enhance IL-12 expression in vitro and in vivo, alleviated the metastasis-promoting effects of sunitinib and sorafenib.	Sunitinib	236-245	interleukin 12b	Mus musculus	34-40
23716000-6	2013	Supplement with recombinant mouse IL-12b or restoration of IL-12b expression in the host by zoledronic acid, which was previously reported to enhance IL-12 expression in vitro and in vivo, alleviated the metastasis-promoting effects of sunitinib and sorafenib.	Sunitinib	236-245	interleukin 12b	Mus musculus	59-65
24123039-1	2013	BACKGROUND/AIM: We analyzed the efficacy and toxicity profile of sunitinib according to single nucleotide polymorphisms (SNPs) of vascular endothelial growth factor receptor (VEGFR) and Kinase insert domain receptor (KDR).	Sunitinib	65-74	kinase insert domain receptor	Homo sapiens	130-173
24123039-9	2013	CONCLUSION: Certain SNPs of KDR may affect treatment outcome and toxicity in patients treated with sunitinib.	Sunitinib	99-108	kinase insert domain receptor	Homo sapiens	28-31
24013576-8	2013	CONCLUSION: Among 12 genetic polymorphisms, polymorphism in the ABCG2 421C&gt;A gene may be mostly associated with the risk of sunitinib-related toxicity in mRCC patients.	Sunitinib	127-136	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	64-69
23707608-7	2013	The multi-targeted TKi sunitinib showed decreased cardiomyocyte viability, AMPK inhibition, increased lipid accumulation, disrupted beat pattern, and hERG block.	Sunitinib	23-32	ETS transcription factor ERG	Homo sapiens	150-154
23878397-0	2013	Platelet-derived growth factor/vascular endothelial growth factor receptor inactivation by sunitinib results in Tsc1/Tsc2-dependent inhibition of TORC1.	Sunitinib	91-100	vascular endothelial growth factor A	Homo sapiens	31-65
23878397-0	2013	Platelet-derived growth factor/vascular endothelial growth factor receptor inactivation by sunitinib results in Tsc1/Tsc2-dependent inhibition of TORC1.	Sunitinib	91-100	TSC complex subunit 1	Homo sapiens	112-116
23878397-0	2013	Platelet-derived growth factor/vascular endothelial growth factor receptor inactivation by sunitinib results in Tsc1/Tsc2-dependent inhibition of TORC1.	Sunitinib	91-100	TSC complex subunit 2	Homo sapiens	117-121
23878397-0	2013	Platelet-derived growth factor/vascular endothelial growth factor receptor inactivation by sunitinib results in Tsc1/Tsc2-dependent inhibition of TORC1.	Sunitinib	91-100	CREB regulated transcription coactivator 1	Homo sapiens	146-151
23878397-1	2013	Vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) receptors are implicated in development and tumorigenesis and dual inhibitors like sunitinib are prescribed for cancer treatment.	Sunitinib	167-176	vascular endothelial growth factor A	Homo sapiens	0-34
23878397-1	2013	Vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) receptors are implicated in development and tumorigenesis and dual inhibitors like sunitinib are prescribed for cancer treatment.	Sunitinib	167-176	vascular endothelial growth factor A	Homo sapiens	36-40
23878397-1	2013	Vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) receptors are implicated in development and tumorigenesis and dual inhibitors like sunitinib are prescribed for cancer treatment.	Sunitinib	167-176	PDGF- and VEGF-receptor related	Drosophila melanogaster	78-82
23878397-9	2013	Like its mammalian orthologs, PVR is inhibited by sunitinib, and sunitinib treatment phenocopies PVR loss in hemocytes.	Sunitinib	50-59	PVR cell adhesion molecule	Homo sapiens	30-33
23878397-9	2013	Like its mammalian orthologs, PVR is inhibited by sunitinib, and sunitinib treatment phenocopies PVR loss in hemocytes.	Sunitinib	65-74	PVR cell adhesion molecule	Homo sapiens	97-100
23878397-10	2013	Sunitinib inhibits TORC1 in insect cells, and sunitinib-mediated TORC1 inhibition requires an intact Tsc1/Tsc2 complex.	Sunitinib	0-9	CREB regulated transcription coactivator 1	Homo sapiens	19-24
23878397-10	2013	Sunitinib inhibits TORC1 in insect cells, and sunitinib-mediated TORC1 inhibition requires an intact Tsc1/Tsc2 complex.	Sunitinib	46-55	CREB regulated transcription coactivator 1	Homo sapiens	65-70
23878397-10	2013	Sunitinib inhibits TORC1 in insect cells, and sunitinib-mediated TORC1 inhibition requires an intact Tsc1/Tsc2 complex.	Sunitinib	46-55	TSC complex subunit 1	Homo sapiens	101-105
23878397-10	2013	Sunitinib inhibits TORC1 in insect cells, and sunitinib-mediated TORC1 inhibition requires an intact Tsc1/Tsc2 complex.	Sunitinib	46-55	TSC complex subunit 2	Homo sapiens	106-110
23878397-11	2013	Sunitinib similarly inhibited TORC1 in human endothelial cells in a Tsc1/Tsc2-dependent manner.	Sunitinib	0-9	CREB regulated transcription coactivator 1	Homo sapiens	30-35
23878397-11	2013	Sunitinib similarly inhibited TORC1 in human endothelial cells in a Tsc1/Tsc2-dependent manner.	Sunitinib	0-9	TSC complex subunit 1	Homo sapiens	68-72
23878397-11	2013	Sunitinib similarly inhibited TORC1 in human endothelial cells in a Tsc1/Tsc2-dependent manner.	Sunitinib	0-9	TSC complex subunit 2	Homo sapiens	73-77
23878397-12	2013	Our findings provide insight into the mechanism of action of PVR and may have implications for understanding sunitinib sensitivity and resistance in tumors.	Sunitinib	109-118	PVR cell adhesion molecule	Homo sapiens	61-64
24082917-2	2013	Currently available oral VEGF tyrosine kinase inhibitors (TKIs) approved for treatment of mRCC include sorafenib, sunitinib, pazopanib, and axitinib.	Sunitinib	114-123	vascular endothelial growth factor A	Homo sapiens	25-29
24086736-8	2013	RESULTS: Immunostaining of HIF-1alpha, CA9, Ki67, CD31, pVEGFR1, VEGFR1 and -2, pPDGFRalpha and -beta was significantly associated with the sunitinib response after 6 and 9 months as well as last report under therapy.	Sunitinib	140-149	hypoxia inducible factor 1 subunit alpha	Homo sapiens	27-37
24086736-8	2013	RESULTS: Immunostaining of HIF-1alpha, CA9, Ki67, CD31, pVEGFR1, VEGFR1 and -2, pPDGFRalpha and -beta was significantly associated with the sunitinib response after 6 and 9 months as well as last report under therapy.	Sunitinib	140-149	fms related receptor tyrosine kinase 1	Homo sapiens	65-78
23788753-5	2013	RESULTS: High expression of HIF2A and PDGFRB was associated with better sunitinib RECIST objective response (P = 0.024 and P = 0.026; respectively) and increased VEGFR3 expression was associated with longer progression-free survival (P = 0.012).	Sunitinib	72-81	endothelial PAS domain protein 1	Homo sapiens	28-33
24073208-0	2013	EMMPRIN promotes angiogenesis, proliferation, invasion and resistance to sunitinib in renal cell carcinoma, and its level predicts patient outcome.	Sunitinib	73-82	basigin (Ok blood group)	Homo sapiens	0-7
24073208-7	2013	EMMPRIN expression was evaluated in RCC patients who received sunitinib therapy and in sunitinib-resistant cells.	Sunitinib	62-71	basigin (Ok blood group)	Homo sapiens	0-7
24073208-7	2013	EMMPRIN expression was evaluated in RCC patients who received sunitinib therapy and in sunitinib-resistant cells.	Sunitinib	87-96	basigin (Ok blood group)	Homo sapiens	0-7
24073208-8	2013	Further, the relation between EMMPRIN expression and sensitivity to sunitinib was examined.	Sunitinib	68-77	basigin (Ok blood group)	Homo sapiens	30-37
24073208-12	2013	EMMPRIN expression was significantly increased in patients who received sunitinib therapy as well as in sunitinib-resistant 786-O cells (786-suni).	Sunitinib	72-81	basigin (Ok blood group)	Homo sapiens	0-7
24073208-12	2013	EMMPRIN expression was significantly increased in patients who received sunitinib therapy as well as in sunitinib-resistant 786-O cells (786-suni).	Sunitinib	104-113	basigin (Ok blood group)	Homo sapiens	0-7
24073208-13	2013	EMMPRIN-overexpressing RCC cells were resistant to sunitinib.	Sunitinib	51-60	basigin (Ok blood group)	Homo sapiens	0-7
24073208-14	2013	CONCLUSION: Our findings indicate that high expression of EMMPRIN in RCC plays important roles in tumor progression and sunitinib resistance.	Sunitinib	120-129	basigin (Ok blood group)	Homo sapiens	58-65
23788753-5	2013	RESULTS: High expression of HIF2A and PDGFRB was associated with better sunitinib RECIST objective response (P = 0.024 and P = 0.026; respectively) and increased VEGFR3 expression was associated with longer progression-free survival (P = 0.012).	Sunitinib	72-81	platelet derived growth factor receptor beta	Homo sapiens	38-44
23788753-6	2013	VEGFR3 overexpression showed a negative correlation with VEGFR3 polymorphism rs307826 (P = 0.002), a sunitinib resistance predictor.	Sunitinib	101-110	fms related receptor tyrosine kinase 4	Homo sapiens	0-6
23788753-6	2013	VEGFR3 overexpression showed a negative correlation with VEGFR3 polymorphism rs307826 (P = 0.002), a sunitinib resistance predictor.	Sunitinib	101-110	fms related receptor tyrosine kinase 4	Homo sapiens	57-63
23788753-10	2013	In addition, low VEGFR3 expression was associated with worse outcome and with VEGFR3 rs307826 variant allele, reinforcing VEGFR3 as a marker of sunitinib resistance.	Sunitinib	144-153	fms related receptor tyrosine kinase 4	Homo sapiens	17-23
25841679-10	2013	Biologic agents targeting the VEGF and mTOR signaling pathways, e.g., sunitinib, bevacizumab or everolimus are becoming integrated as treatments for PNET"s.	Sunitinib	70-79	vascular endothelial growth factor A	Homo sapiens	30-34
25841679-10	2013	Biologic agents targeting the VEGF and mTOR signaling pathways, e.g., sunitinib, bevacizumab or everolimus are becoming integrated as treatments for PNET"s.	Sunitinib	70-79	mechanistic target of rapamycin kinase	Homo sapiens	39-43
23475388-8	2013	CONCLUSIONS: Our findings showing constant expression levels of VEGFR2 in endothelial cells serve as a first indication that the use of small tyrosine kinase inhibitors such as Sunitinib directly targeting the VEGF-receptors might be worth testing, also in the clinical context in cases of therapy-refractory meningiomas.	Sunitinib	177-186	kinase insert domain receptor	Homo sapiens	64-70
23720233-4	2013	Inhibition of phosphoinositide 3-kinase (PI3K) by LY294002 treatment and application of sunitinib, a widely used anti-angiogenic compound, suppressed enhanced angiogenesis in Pten mutants.	Sunitinib	88-97	phosphatase and tensin homolog B	Danio rerio	175-179
23720233-8	2013	Surprisingly, sunitinib treatment dramatically enhanced vegfaa expression in Pten mutant embryos, which might account for tumor relapse in human patients who are treated with sunitinib.	Sunitinib	14-23	vascular endothelial growth factor Aa	Danio rerio	56-62
23720233-8	2013	Surprisingly, sunitinib treatment dramatically enhanced vegfaa expression in Pten mutant embryos, which might account for tumor relapse in human patients who are treated with sunitinib.	Sunitinib	14-23	phosphatase and tensin homolog	Homo sapiens	77-81
23720233-8	2013	Surprisingly, sunitinib treatment dramatically enhanced vegfaa expression in Pten mutant embryos, which might account for tumor relapse in human patients who are treated with sunitinib.	Sunitinib	175-184	vascular endothelial growth factor Aa	Danio rerio	56-62
23720233-8	2013	Surprisingly, sunitinib treatment dramatically enhanced vegfaa expression in Pten mutant embryos, which might account for tumor relapse in human patients who are treated with sunitinib.	Sunitinib	175-184	phosphatase and tensin homolog	Homo sapiens	77-81
23720233-9	2013	Combined treatment with suboptimal concentrations of sunitinib and LY294002 rescued enhanced angiogenesis in pten mutant embryos without the dramatic increase in vegfaa expression, suggesting a new approach for therapeutic intervention in VEGFR-signaling-dependent tumors.	Sunitinib	53-62	phosphatase and tensin homolog B	Danio rerio	109-113
23942298-8	2013	The role of KIT mutation and amplification in the development of ovarian dysgerminoma and the use of Sunitinib, a receptor tyrosine kinase inhibitor with an effect on vascular endothelial growth factor, platelet-derived growth factor and KIT receptors in patients with platinum-resistant GCT, are novel promising approaches.	Sunitinib	101-110	vascular endothelial growth factor A	Homo sapiens	167-201
23942298-8	2013	The role of KIT mutation and amplification in the development of ovarian dysgerminoma and the use of Sunitinib, a receptor tyrosine kinase inhibitor with an effect on vascular endothelial growth factor, platelet-derived growth factor and KIT receptors in patients with platinum-resistant GCT, are novel promising approaches.	Sunitinib	101-110	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	238-241
23767831-2	2013	Prior attempts to block vascular endothelial growth factor (VEGF) with sunitinib, sorafenib and thalidomide have obtained disappointing results.	Sunitinib	71-80	vascular endothelial growth factor A	Homo sapiens	24-58
23767831-2	2013	Prior attempts to block vascular endothelial growth factor (VEGF) with sunitinib, sorafenib and thalidomide have obtained disappointing results.	Sunitinib	71-80	vascular endothelial growth factor A	Homo sapiens	60-64
23475388-8	2013	CONCLUSIONS: Our findings showing constant expression levels of VEGFR2 in endothelial cells serve as a first indication that the use of small tyrosine kinase inhibitors such as Sunitinib directly targeting the VEGF-receptors might be worth testing, also in the clinical context in cases of therapy-refractory meningiomas.	Sunitinib	177-186	vascular endothelial growth factor A	Homo sapiens	64-68
23034406-1	2013	Sorafenib and sunitinib are oral tyrosine kinase inhibitors, commonly used in the treatment of metastatic renal cell carcinoma.	Sunitinib	14-23	TXK tyrosine kinase	Homo sapiens	33-48
23747315-4	2013	Analysis of cytokine milieu within TME revealed IL-10, TGFbeta, IL-6 rich type 2 characters was significantly switched to type 1 microenvironment with dominance of IFNgamma and IL-2 within NLGP-TME, which was not found in other cases; however Cisplatin-TME appeared better in type 2 to type 1 conversion than Sutent-TME as evidenced by RT-PCR, ELISA and immunohistochemical analysis.	Sunitinib	309-315	interleukin 10	Mus musculus	48-53
23747315-4	2013	Analysis of cytokine milieu within TME revealed IL-10, TGFbeta, IL-6 rich type 2 characters was significantly switched to type 1 microenvironment with dominance of IFNgamma and IL-2 within NLGP-TME, which was not found in other cases; however Cisplatin-TME appeared better in type 2 to type 1 conversion than Sutent-TME as evidenced by RT-PCR, ELISA and immunohistochemical analysis.	Sunitinib	309-315	interleukin 6	Mus musculus	64-68
23969186-0	2013	Antiproliferative and proapoptotic activity of sunitinib on endothelial and anaplastic thyroid cancer cells via inhibition of Akt and ERK1/2 phosphorylation and by down-regulation of cyclin-D1.	Sunitinib	47-56	AKT serine/threonine kinase 1	Homo sapiens	126-129
23969186-0	2013	Antiproliferative and proapoptotic activity of sunitinib on endothelial and anaplastic thyroid cancer cells via inhibition of Akt and ERK1/2 phosphorylation and by down-regulation of cyclin-D1.	Sunitinib	47-56	mitogen-activated protein kinase 3	Homo sapiens	134-140
23969186-0	2013	Antiproliferative and proapoptotic activity of sunitinib on endothelial and anaplastic thyroid cancer cells via inhibition of Akt and ERK1/2 phosphorylation and by down-regulation of cyclin-D1.	Sunitinib	47-56	cyclin D1	Homo sapiens	183-192
23969186-9	2013	Phospho-vascular endothelial growth factor receptor-2 levels significantly decreased after sunitinib treatment in activated endothelial cells.	Sunitinib	91-100	kinase insert domain receptor	Homo sapiens	8-53
23969186-10	2013	Phospho-epidermal growth factor receptor, ERK1/2, and Akt phosphorylation was significantly inhibited by sunitinib treatment in endothelial and cancer cells, and cyclin-D1 mRNA and protein expression was inhibited.	Sunitinib	105-114	mitogen-activated protein kinase 3	Homo sapiens	42-48
23969186-10	2013	Phospho-epidermal growth factor receptor, ERK1/2, and Akt phosphorylation was significantly inhibited by sunitinib treatment in endothelial and cancer cells, and cyclin-D1 mRNA and protein expression was inhibited.	Sunitinib	105-114	AKT serine/threonine kinase 1	Homo sapiens	54-57
23969186-12	2013	CONCLUSIONS: Sunitinib is active in vitro and in vivo against activated endothelial and ATC cells via the inhibition of Akt and ERK1/2 phosphorylation and through the down-regulation of cyclin-D1.	Sunitinib	13-22	AKT serine/threonine kinase 1	Homo sapiens	120-123
23969186-12	2013	CONCLUSIONS: Sunitinib is active in vitro and in vivo against activated endothelial and ATC cells via the inhibition of Akt and ERK1/2 phosphorylation and through the down-regulation of cyclin-D1.	Sunitinib	13-22	mitogen-activated protein kinase 3	Homo sapiens	128-134
23969186-12	2013	CONCLUSIONS: Sunitinib is active in vitro and in vivo against activated endothelial and ATC cells via the inhibition of Akt and ERK1/2 phosphorylation and through the down-regulation of cyclin-D1.	Sunitinib	13-22	cyclin D1	Homo sapiens	186-195
23931237-0	2013	Re: Cox-2 inhibition enhances the activity of sunitinib in human renal cell carcinoma xenografts.	Sunitinib	46-55	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	4-9
23843632-0	2013	Impact of P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) gene dosage on plasma pharmacokinetics and brain accumulation of dasatinib, sorafenib, and sunitinib.	Sunitinib	169-178	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	71-76
23732991-3	2013	Previously, we reported that the anticancer drug, sunitinib, an inhibitor of VEGF-R and PDGF-R, has off-target effects against both PKR and RNase L. Here we show that combining sunitinib treatments with infection by an oncolytic virus, vesicular stomatitis virus (VSV), led to the elimination of prostate, breast, and kidney malignant tumors in mice.	Sunitinib	50-59	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	132-135
23732991-3	2013	Previously, we reported that the anticancer drug, sunitinib, an inhibitor of VEGF-R and PDGF-R, has off-target effects against both PKR and RNase L. Here we show that combining sunitinib treatments with infection by an oncolytic virus, vesicular stomatitis virus (VSV), led to the elimination of prostate, breast, and kidney malignant tumors in mice.	Sunitinib	177-186	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	132-135
23732991-5	2013	In prostate tumors excised from treated mice, sunitinib decreased levels of the phosphorylated form of translation initiation factor, eIF2-alpha, a substrate of PKR, by 10-fold while increasing median viral titers by 23-fold.	Sunitinib	46-55	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	134-144
23732991-5	2013	In prostate tumors excised from treated mice, sunitinib decreased levels of the phosphorylated form of translation initiation factor, eIF2-alpha, a substrate of PKR, by 10-fold while increasing median viral titers by 23-fold.	Sunitinib	46-55	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	161-164
23578198-0	2013	Sunitinib induces cellular senescence via p53/Dec1 activation in renal cell carcinoma cells.	Sunitinib	0-9	tumor protein p53	Homo sapiens	42-45
24003340-14	2013	Although not fully evaluated in pNETs, biomarkers associated with response to sunitinib in several tumor types include soluble vascular endothelial growth factor receptor 2 and 3, interleukin 8, and stromal cell-derived factor 1alpha.	Sunitinib	78-87	C-X-C motif chemokine ligand 8	Homo sapiens	180-193
23964934-8	2013	Patients treated with sunitinib, as compared with those treated with pazopanib, had a higher incidence of fatigue (63% vs. 55%), the hand-foot syndrome (50% vs. 29%), and thrombocytopenia (78% vs. 41%); patients treated with pazopanib had a higher incidence of increased levels of alanine aminotransferase (60%, vs. 43% with sunitinib).	Sunitinib	22-31	glutamic--pyruvic transaminase	Homo sapiens	281-305
23887605-9	2013	RESULTS: We found that sunitinib treatment for 24 h triggers incomplete autophagy, impairs cathepsin B activation and stimulates a lysosomal-dependent necrosis.	Sunitinib	23-32	cathepsin B	Homo sapiens	91-102
23839492-3	2013	RESULTS: We demonstrated that, as single agents, sunitinib, sorafenib and everolimus share similar activity in inhibiting cell proliferation, signal transduction and vascular endothelial growth factor (VEGF) secretion in different RCC models, both in vitro and in tumour xenografts.	Sunitinib	49-58	vascular endothelial growth factor A	Homo sapiens	166-200
23839492-3	2013	RESULTS: We demonstrated that, as single agents, sunitinib, sorafenib and everolimus share similar activity in inhibiting cell proliferation, signal transduction and vascular endothelial growth factor (VEGF) secretion in different RCC models, both in vitro and in tumour xenografts.	Sunitinib	49-58	vascular endothelial growth factor A	Homo sapiens	202-206
23839492-5	2013	Inability by sunitinib to persistently inhibit HIF-1, VEGF and pMAPK anticipated treatment resistance in xenografted tumours.	Sunitinib	13-22	hypoxia inducible factor 1 subunit alpha	Homo sapiens	47-52
23839492-5	2013	Inability by sunitinib to persistently inhibit HIF-1, VEGF and pMAPK anticipated treatment resistance in xenografted tumours.	Sunitinib	13-22	vascular endothelial growth factor A	Homo sapiens	54-58
23839492-6	2013	After first-line sunitinib, second-line treatment with everolimus was more effective than either sorafenib or rechallenge with sunitinib in interfering with signalling proteins, VEGF and interleukin-8, translating into a significant advantage in tumour growth inhibition and mice survival.	Sunitinib	127-136	vascular endothelial growth factor A	Mus musculus	178-182
23839492-6	2013	After first-line sunitinib, second-line treatment with everolimus was more effective than either sorafenib or rechallenge with sunitinib in interfering with signalling proteins, VEGF and interleukin-8, translating into a significant advantage in tumour growth inhibition and mice survival.	Sunitinib	127-136	chemokine (C-X-C motif) ligand 15	Mus musculus	187-200
23898066-1	2013	The present study investigated the effect of the H2 antagonist cimetidine on the pharmacokinetics of a multi-targeted receptor tyrosine kinase (RTK) inhibitor, sunitinib, in Sprague-Dawley (SD) rats and Eisai hyperbilirubinemic mutant rats (EHBR) lacking the efflux transporter, ATP-binding cassette C2 protein (ABCC2).	Sunitinib	160-169	erb-b2 receptor tyrosine kinase 4	Rattus norvegicus	118-142
23898066-1	2013	The present study investigated the effect of the H2 antagonist cimetidine on the pharmacokinetics of a multi-targeted receptor tyrosine kinase (RTK) inhibitor, sunitinib, in Sprague-Dawley (SD) rats and Eisai hyperbilirubinemic mutant rats (EHBR) lacking the efflux transporter, ATP-binding cassette C2 protein (ABCC2).	Sunitinib	160-169	erb-b2 receptor tyrosine kinase 4	Rattus norvegicus	144-147
23898066-7	2013	Furthermore, the contribution of ABCC2 to the biliary excretion of sunitinib was also examined in SD rats and EHBR.	Sunitinib	67-76	ATP binding cassette subfamily C member 2	Rattus norvegicus	33-38
23898066-9	2013	These findings indicate that co-administration of cimetidine alters the pharmacokinetics of sunitinib probably due to inhibition of CYP3A4, suggesting the possibility that cimetidine should be used carefully for patients with cancer being treated with sunitinib therapy.	Sunitinib	92-101	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	132-138
23578198-0	2013	Sunitinib induces cellular senescence via p53/Dec1 activation in renal cell carcinoma cells.	Sunitinib	0-9	deleted in esophageal cancer 1	Homo sapiens	46-50
23578198-2	2013	Our present study revealed that sunitinib-treated RCC cells exhibit senescence characteristics including increased SA-beta-gal activity, DcR2 and Dec1 expression, and senescence-associated secretary phenotype (SASP) such as proinflammatory cytokines interleukin (IL)-1alpha, IL-6 and IL-8 secretion.	Sunitinib	32-41	C-C motif chemokine receptor 6	Homo sapiens	137-141
23578198-2	2013	Our present study revealed that sunitinib-treated RCC cells exhibit senescence characteristics including increased SA-beta-gal activity, DcR2 and Dec1 expression, and senescence-associated secretary phenotype (SASP) such as proinflammatory cytokines interleukin (IL)-1alpha, IL-6 and IL-8 secretion.	Sunitinib	32-41	deleted in esophageal cancer 1	Homo sapiens	146-150
23578198-2	2013	Our present study revealed that sunitinib-treated RCC cells exhibit senescence characteristics including increased SA-beta-gal activity, DcR2 and Dec1 expression, and senescence-associated secretary phenotype (SASP) such as proinflammatory cytokines interleukin (IL)-1alpha, IL-6 and IL-8 secretion.	Sunitinib	32-41	interleukin 1 alpha	Homo sapiens	250-273
23578198-2	2013	Our present study revealed that sunitinib-treated RCC cells exhibit senescence characteristics including increased SA-beta-gal activity, DcR2 and Dec1 expression, and senescence-associated secretary phenotype (SASP) such as proinflammatory cytokines interleukin (IL)-1alpha, IL-6 and IL-8 secretion.	Sunitinib	32-41	interleukin 6	Homo sapiens	275-279
23578198-2	2013	Our present study revealed that sunitinib-treated RCC cells exhibit senescence characteristics including increased SA-beta-gal activity, DcR2 and Dec1 expression, and senescence-associated secretary phenotype (SASP) such as proinflammatory cytokines interleukin (IL)-1alpha, IL-6 and IL-8 secretion.	Sunitinib	32-41	C-X-C motif chemokine ligand 8	Homo sapiens	284-288
23578198-4	2013	Mechanistic investigations indicated that therapy-induced senescence (TIS) following sunitinib treatment mainly attributed to p53/Dec1 signaling activation mediated by Raf-1/NF-kappaB inhibition in vitro.	Sunitinib	85-94	tumor protein p53	Homo sapiens	126-129
23578198-4	2013	Mechanistic investigations indicated that therapy-induced senescence (TIS) following sunitinib treatment mainly attributed to p53/Dec1 signaling activation mediated by Raf-1/NF-kappaB inhibition in vitro.	Sunitinib	85-94	deleted in esophageal cancer 1	Homo sapiens	130-134
23578198-4	2013	Mechanistic investigations indicated that therapy-induced senescence (TIS) following sunitinib treatment mainly attributed to p53/Dec1 signaling activation mediated by Raf-1/NF-kappaB inhibition in vitro.	Sunitinib	85-94	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	168-173
23578198-4	2013	Mechanistic investigations indicated that therapy-induced senescence (TIS) following sunitinib treatment mainly attributed to p53/Dec1 signaling activation mediated by Raf-1/NF-kappaB inhibition in vitro.	Sunitinib	85-94	nuclear factor kappa B subunit 1	Homo sapiens	174-183
23578198-5	2013	Importantly, in vivo study showed tumor growth inhibition and prolonged overall survival were associated with increased p53 and Dec1 expression, decreased Raf-1 and Ki67 staining, and upregulated SA-beta-gal activity after sunitinib treatment.	Sunitinib	223-232	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	155-160
23578198-7	2013	Taken together, our findings suggested that sunitinib treatment performance could be attributable to TIS, depending on p53/Dec1 activation via inhibited Raf-1/nuclear factor (NF)-kappaB activity.	Sunitinib	44-53	tumor protein p53	Homo sapiens	119-122
23578198-7	2013	Taken together, our findings suggested that sunitinib treatment performance could be attributable to TIS, depending on p53/Dec1 activation via inhibited Raf-1/nuclear factor (NF)-kappaB activity.	Sunitinib	44-53	deleted in esophageal cancer 1	Homo sapiens	123-127
23578198-7	2013	Taken together, our findings suggested that sunitinib treatment performance could be attributable to TIS, depending on p53/Dec1 activation via inhibited Raf-1/nuclear factor (NF)-kappaB activity.	Sunitinib	44-53	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	153-158
23674235-6	2013	Approximately 50 % of patients with malignant PHs and SPGs have been found to carry hereditary germline mutations in the succinate dehydrogenase subunit B gene (SDHB), and anti-angiogenic agents such as sunitinib have been found to potentially play a role in the treatment of malignant disease, especially in patients with SDHB mutations.	Sunitinib	203-212	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	161-165
23674235-6	2013	Approximately 50 % of patients with malignant PHs and SPGs have been found to carry hereditary germline mutations in the succinate dehydrogenase subunit B gene (SDHB), and anti-angiogenic agents such as sunitinib have been found to potentially play a role in the treatment of malignant disease, especially in patients with SDHB mutations.	Sunitinib	203-212	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	323-327
23305097-8	2013	After sunitinib treatment, the expression levels of phosphorylated Akt and p44/42 mitogen-activated protein kinase in ACHN/P, but not those in ACHN/R, were significantly inhibited.	Sunitinib	6-15	interferon induced protein 44	Homo sapiens	75-78
23880112-10	2013	The NF-kappaB inhibitors dicoumarol, SN50 and BAY11-7085 were employed to assess the role of NF-kappaB in sunitinib-mediated effects on neuronal survival as well as COX2 and NOS2 expression.	Sunitinib	106-115	nuclear factor kappa B subunit 1	Homo sapiens	93-102
23880112-12	2013	Exposure of neurons to sunitinib also induced an increase in the expression of NF-kappaB, COX2 and NOS2.	Sunitinib	23-32	nuclear factor kappa B subunit 1	Homo sapiens	79-88
23880112-12	2013	Exposure of neurons to sunitinib also induced an increase in the expression of NF-kappaB, COX2 and NOS2.	Sunitinib	23-32	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	90-94
23880112-12	2013	Exposure of neurons to sunitinib also induced an increase in the expression of NF-kappaB, COX2 and NOS2.	Sunitinib	23-32	nitric oxide synthase 2	Homo sapiens	99-103
23880112-13	2013	Inhibiting NF-kappaB blunted the increase in cell survival and decrease in cell death evoked by sunitinib.	Sunitinib	96-105	nuclear factor kappa B subunit 1	Homo sapiens	11-20
23880112-14	2013	Treatment of cell cultures with both sunitinib and NF-kappaB inhibitors mitigated the increase in COX2 and NOS2 caused by sunitinib.	Sunitinib	37-46	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	98-102
23880112-14	2013	Treatment of cell cultures with both sunitinib and NF-kappaB inhibitors mitigated the increase in COX2 and NOS2 caused by sunitinib.	Sunitinib	37-46	nitric oxide synthase 2	Homo sapiens	107-111
23880112-14	2013	Treatment of cell cultures with both sunitinib and NF-kappaB inhibitors mitigated the increase in COX2 and NOS2 caused by sunitinib.	Sunitinib	122-131	nuclear factor kappa B subunit 1	Homo sapiens	51-60
23880112-14	2013	Treatment of cell cultures with both sunitinib and NF-kappaB inhibitors mitigated the increase in COX2 and NOS2 caused by sunitinib.	Sunitinib	122-131	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	98-102
23880112-14	2013	Treatment of cell cultures with both sunitinib and NF-kappaB inhibitors mitigated the increase in COX2 and NOS2 caused by sunitinib.	Sunitinib	122-131	nitric oxide synthase 2	Homo sapiens	107-111
23880112-15	2013	CONCLUSIONS: Sunitinib increases neuronal survival and this neurotrophic effect is mediated by NF-kappaB.	Sunitinib	13-22	nuclear factor kappa B subunit 1	Homo sapiens	95-104
23880112-16	2013	Also, the inflammatory proteins COX2 and NOS2 are upregulated by sunitinib in an NF-kappaB-dependent manner.	Sunitinib	65-74	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	32-36
23880112-16	2013	Also, the inflammatory proteins COX2 and NOS2 are upregulated by sunitinib in an NF-kappaB-dependent manner.	Sunitinib	65-74	nitric oxide synthase 2	Homo sapiens	41-45
23880112-16	2013	Also, the inflammatory proteins COX2 and NOS2 are upregulated by sunitinib in an NF-kappaB-dependent manner.	Sunitinib	65-74	nuclear factor kappa B subunit 1	Homo sapiens	81-90
23842041-11	2013	CONCLUSION: In HCC, MRP may be a more sensitive biomarker in predicting early response and PFS following sunitinib than RECIST and mRECIST.	Sunitinib	105-114	ATP binding cassette subfamily C member 1	Homo sapiens	20-23
23749551-0	2013	Effect of P-glycoprotein and breast cancer resistance protein inhibition on the pharmacokinetics of sunitinib in rats.	Sunitinib	100-109	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	10-24
23749551-1	2013	The aim of this study was to elucidate the roles of P-glycoprotein (P-gp/ABCB1) and breast cancer resistance protein (BCRP/ABCG2) in the plasma concentration, biliary excretion, and distribution to the liver, kidney, and brain of sunitinib.	Sunitinib	230-239	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	52-66
23749551-1	2013	The aim of this study was to elucidate the roles of P-glycoprotein (P-gp/ABCB1) and breast cancer resistance protein (BCRP/ABCG2) in the plasma concentration, biliary excretion, and distribution to the liver, kidney, and brain of sunitinib.	Sunitinib	230-239	phosphoglycolate phosphatase	Rattus norvegicus	68-72
23749551-1	2013	The aim of this study was to elucidate the roles of P-glycoprotein (P-gp/ABCB1) and breast cancer resistance protein (BCRP/ABCG2) in the plasma concentration, biliary excretion, and distribution to the liver, kidney, and brain of sunitinib.	Sunitinib	230-239	ATP binding cassette subfamily B member 1A	Rattus norvegicus	73-78
23749551-1	2013	The aim of this study was to elucidate the roles of P-glycoprotein (P-gp/ABCB1) and breast cancer resistance protein (BCRP/ABCG2) in the plasma concentration, biliary excretion, and distribution to the liver, kidney, and brain of sunitinib.	Sunitinib	230-239	ATP binding cassette subfamily G member 2	Rattus norvegicus	123-128
23749551-7	2013	These results demonstrate that plasma concentrations of sunitinib and the biliary excretion and distribution to the kidney, liver, and brain of sunitinib are influenced by pharmacologic inhibition of P-gp and/or BCRP.	Sunitinib	56-65	phosphoglycolate phosphatase	Rattus norvegicus	200-204
23749551-7	2013	These results demonstrate that plasma concentrations of sunitinib and the biliary excretion and distribution to the kidney, liver, and brain of sunitinib are influenced by pharmacologic inhibition of P-gp and/or BCRP.	Sunitinib	144-153	phosphoglycolate phosphatase	Rattus norvegicus	200-204
23880112-0	2013	Sunitinib enhances neuronal survival in vitro via NF-kappaB-mediated signaling and expression of cyclooxygenase-2 and inducible nitric oxide synthase.	Sunitinib	0-9	nuclear factor kappa B subunit 1	Homo sapiens	50-59
23880112-0	2013	Sunitinib enhances neuronal survival in vitro via NF-kappaB-mediated signaling and expression of cyclooxygenase-2 and inducible nitric oxide synthase.	Sunitinib	0-9	prostaglandin-endoperoxide synthase 2	Homo sapiens	97-149
23880112-9	2013	The ability of sunitinib to affect NF-kappaB, COX2 and NOS2 expression was determined by western blot.	Sunitinib	15-24	nuclear factor kappa B subunit 1	Homo sapiens	35-44
23880112-9	2013	The ability of sunitinib to affect NF-kappaB, COX2 and NOS2 expression was determined by western blot.	Sunitinib	15-24	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	46-50
23880112-9	2013	The ability of sunitinib to affect NF-kappaB, COX2 and NOS2 expression was determined by western blot.	Sunitinib	15-24	nitric oxide synthase 2	Homo sapiens	55-59
23305097-8	2013	After sunitinib treatment, the expression levels of phosphorylated Akt and p44/42 mitogen-activated protein kinase in ACHN/P, but not those in ACHN/R, were significantly inhibited.	Sunitinib	6-15	La ribonucleoprotein 6, translational regulator	Homo sapiens	118-124
23601669-2	2013	Sunitinib, sorafenib and pazopanib were the first generation of vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) to have significant clinical activity in metastatic clear cell RCC.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	64-107
23811706-1	2013	BACKGROUND: Therapy for metastatic kidney cancer is actively evolving, particularly in the results of registration drug trials that have led to the approval of vascular endothelial growth factor pathway drugs such as sorafenib, sunitinib, pazopanib, bevacizumab, and axitinib, with focus on patients with good- or intermediate-risk criteria and clear cell histology.	Sunitinib	228-237	vascular endothelial growth factor A	Homo sapiens	160-194
23867518-4	2013	Although high-dose interleukin 2 immunotherapy has been superseded as first-line therapy for RCC by promiscuous receptor tyrosine kinase inhibitors (rTKIs) such as sunitinib, sunitinib itself is a potent immunoadjunct in animal tumor models.	Sunitinib	175-184	interleukin 2	Homo sapiens	19-32
23867518-8	2013	Although rTKIs like sunitinib have a remarkable capacity to deplete MDSCs and restore normal T-cell function in peripheral body compartments such as the bloodstream and the spleen, such rTKIs are effective only against MDSCs, which are engaged in phospho-STAT3-dependent programming (pSTAT3+).	Sunitinib	20-29	signal transducer and activator of transcription 3	Homo sapiens	255-260
23601669-2	2013	Sunitinib, sorafenib and pazopanib were the first generation of vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) to have significant clinical activity in metastatic clear cell RCC.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	109-114
23582185-6	2013	Sublines with an additional T670I c-Kit mutation showed resistance to imatinib, nilotinib and dasatinib, but responded to sunitinib.	Sunitinib	122-131	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-39
23840364-5	2013	Our results showed that SU more effectively inhibited mutant KIT with secondary exon 13 or 14 mutations than those with secondary exon 17 mutations, as clinically indicated.	Sunitinib	24-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-64
23818948-10	2013	The apoptosis-inducing effects of sunitinib, but not sorafenib, were enhanced when IGFR signaling activity was inhibited by NVP-AEW541 or IGFR knockdown.	Sunitinib	34-43	insulin like growth factor 1 receptor	Homo sapiens	83-87
23818948-10	2013	The apoptosis-inducing effects of sunitinib, but not sorafenib, were enhanced when IGFR signaling activity was inhibited by NVP-AEW541 or IGFR knockdown.	Sunitinib	34-43	insulin like growth factor 1 receptor	Homo sapiens	138-142
23576559-5	2013	Inhibition of VEGF signaling by anti-VEGF antibody or sunitinib in mice from the age of 14 to 17 weeks was accompanied by more intratumoral lymphatics, more tumor cells inside lymphatics, and more lymph node metastases.	Sunitinib	54-63	vascular endothelial growth factor A	Mus musculus	14-18
23818948-11	2013	Chk2 kinase activation was found contributory to the synergistic anti-tumor effects between sunitinib and IGFR inhibition.	Sunitinib	92-101	checkpoint kinase 2	Homo sapiens	0-4
23459719-3	2013	The results of clinical trials have further shown that the VEGF pathway inhibitor sunitinib and the mTOR inhibitor everolimus have efficacy in patients with advanced pancreatic NETs.	Sunitinib	82-91	vascular endothelial growth factor A	Homo sapiens	59-63
24396670-0	2013	Transformation of nonfunctioning pancreatic neuroendocrine carcinoma cells into insulin producing cells after treatment with sunitinib.	Sunitinib	125-134	insulin	Homo sapiens	80-87
24396670-6	2013	Immunohistochemical stain of the metastatic liver mass demonstrated that the initially nonfunctioning neuroendocrine carcinoma cells had changed into insulin-producing cells after sunitinib therapy.	Sunitinib	180-189	insulin	Homo sapiens	150-157
24396670-8	2013	A nonfunctioning pancreatic neuroendocrine carcinoma was transformed into an insulin-producing tumor after treatment with sunitinib, causing endogenous hyperinsulinemia and severe hypoglycemia.	Sunitinib	122-131	insulin	Homo sapiens	77-84
23455880-11	2013	Future studies will have to clarify whether KRAS can be used to guide sunitinib treatment or-in general-a treatment with a multityrosine kinase inhibitor in mCRC.	Sunitinib	70-79	KRAS proto-oncogene, GTPase	Homo sapiens	44-48
23705634-1	2013	INTRODUCTION: Some inhibitors of tyrosine kinase, as imatinib, erlotinib and sunitinib have antihyperglycemic effects but the mechanisms are not totally clear.	Sunitinib	77-86	TXK tyrosine kinase	Homo sapiens	33-48
23448320-11	2013	WHAT IS NEW AND CONCLUSION: P-glycoprotein inhibition by sunitinib has been demonstrated.	Sunitinib	57-66	ATP binding cassette subfamily B member 1	Homo sapiens	28-42
23455880-0	2013	KRAS allel-specific activity of sunitinib in an isogenic disease model of colorectal cancer.	Sunitinib	32-41	KRAS proto-oncogene, GTPase	Homo sapiens	0-4
23455880-1	2013	PURPOSE: To investigate the impact of different KRAS mutations on treatment with the tyrosine kinase inhibitor sunitinib in SW48 colorectal cancer cell line variants.	Sunitinib	111-120	KRAS proto-oncogene, GTPase	Homo sapiens	48-52
23455880-3	2013	In addition, the respective cell lines were tested for the effect of sunitinib on ERK/ELK phosphorylation, cell cycle, and cytotoxicity.	Sunitinib	69-78	EPH receptor B2	Homo sapiens	82-85
23455880-4	2013	RESULTS: Compared to KRAS wt cells, all KRAS mutant variants were associated with resistance to sunitinib treatment.	Sunitinib	96-105	KRAS proto-oncogene, GTPase	Homo sapiens	21-25
23455880-4	2013	RESULTS: Compared to KRAS wt cells, all KRAS mutant variants were associated with resistance to sunitinib treatment.	Sunitinib	96-105	KRAS proto-oncogene, GTPase	Homo sapiens	40-44
23455880-6	2013	The reduction in ERK phosphorylation due to treatment with sunitinib was highest in G12V (89 %) mutant cells and lowest in G12A (24 %) mutant cells.	Sunitinib	59-68	EPH receptor B2	Homo sapiens	17-20
23392356-0	2013	The secondary FLT3-ITD F691L mutation induces resistance to AC220 in FLT3-ITD+ AML but retains in vitro sensitivity to PKC412 and Sunitinib.	Sunitinib	130-139	fms related receptor tyrosine kinase 3	Homo sapiens	14-18
23455880-7	2013	ELK phosphorylation was less decreased in all KRAS mutant variants compared to KRAS wt cells following sunitinib treatment.	Sunitinib	103-112	KRAS proto-oncogene, GTPase	Homo sapiens	46-50
23455880-7	2013	ELK phosphorylation was less decreased in all KRAS mutant variants compared to KRAS wt cells following sunitinib treatment.	Sunitinib	103-112	KRAS proto-oncogene, GTPase	Homo sapiens	79-83
23455880-9	2013	CONCLUSION: Our isogenic cell culture model suggests that KRAS mutations in SW48 colorectal cancer cells are linked to resistance to the multityrosine kinase inhibitor sunitinib.	Sunitinib	168-177	KRAS proto-oncogene, GTPase	Homo sapiens	58-62
23730410-11	2013	CONCLUSION: Ang-2 could potentially identify a patient population that might have a better PFS when under anti-angiogenic treatment, like the tyrosine kinase inhibitor sunitinib.	Sunitinib	168-177	angiopoietin 2	Homo sapiens	12-17
23456621-0	2013	Secondary mutations of c-KIT contribute to acquired resistance to imatinib and decrease efficacy of sunitinib in Chinese patients with gastrointestinal stromal tumors.	Sunitinib	100-109	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-28
23456621-1	2013	The aim of this study was to investigate the associations between secondary mutations of c-KIT/PDGFRalpha and acquired imatinib resistance or efficacy of sunitinib in Chinese patients with gastrointestinal stromal tumors (GISTs).	Sunitinib	154-163	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	89-94
23456621-1	2013	The aim of this study was to investigate the associations between secondary mutations of c-KIT/PDGFRalpha and acquired imatinib resistance or efficacy of sunitinib in Chinese patients with gastrointestinal stromal tumors (GISTs).	Sunitinib	154-163	platelet derived growth factor receptor alpha	Homo sapiens	95-105
23456621-8	2013	Secondary mutations of c-KIT were significantly associated with acquired resistance to imatinib in Chinese GIST patients, and whether secondary mutations of c-KIT could influence the efficacy of sunitinib needed to be further investigated.	Sunitinib	195-204	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	157-162
23539200-6	2013	A significant decrease in the Th1/Th2 ratio was seen after sunitinib treatment only in the PFS-short group, suggesting a shift toward Th2 that down-regulates host immunity.	Sunitinib	59-68	negative elongation factor complex member C/D	Homo sapiens	30-33
23720580-6	2013	Sunitinib-induced pericyte depletion and coronary microvascular dysfunction are recapitulated by CP-673451, a structurally distinct PDGFR inhibitor, confirming the role of PDGFR in pericyte survival.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	132-137
23720580-6	2013	Sunitinib-induced pericyte depletion and coronary microvascular dysfunction are recapitulated by CP-673451, a structurally distinct PDGFR inhibitor, confirming the role of PDGFR in pericyte survival.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	172-177
23522954-11	2013	Finally, we checked whether compensatory activation of VEGF signaling occurred after sunitinib addition.	Sunitinib	85-94	vascular endothelial growth factor A	Homo sapiens	55-59
23492365-8	2013	Notably, JMJD1A inhibition enhanced the antitumor effects of the anti-VEGF compound bevacizumab and the VEGFR/KDR inhibitor sunitinib.	Sunitinib	124-133	lysine demethylase 3A	Homo sapiens	9-15
23492365-8	2013	Notably, JMJD1A inhibition enhanced the antitumor effects of the anti-VEGF compound bevacizumab and the VEGFR/KDR inhibitor sunitinib.	Sunitinib	124-133	kinase insert domain receptor	Homo sapiens	104-109
23492365-8	2013	Notably, JMJD1A inhibition enhanced the antitumor effects of the anti-VEGF compound bevacizumab and the VEGFR/KDR inhibitor sunitinib.	Sunitinib	124-133	kinase insert domain receptor	Homo sapiens	110-113
23288144-0	2013	Sunitinib, a tyrosine kinase inhibitor, induces cytochrome P450 1A1 gene in human breast cancer MCF7 cells through ligand-independent aryl hydrocarbon receptor activation.	Sunitinib	0-9	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	48-67
23288144-0	2013	Sunitinib, a tyrosine kinase inhibitor, induces cytochrome P450 1A1 gene in human breast cancer MCF7 cells through ligand-independent aryl hydrocarbon receptor activation.	Sunitinib	0-9	aryl hydrocarbon receptor	Homo sapiens	134-159
23580490-8	2013	Reduced F4/80+ cell infiltration was evidenced in sunitinib-treated mice and was associated to decreased VEGF-A (by 50%, P &lt; 0.01) and VEGF-C (by 35%, P &lt; 0.01) expressions, while VEGF-D and sVEGFR-2 expressions were not affected.	Sunitinib	50-59	vascular endothelial growth factor A	Mus musculus	105-111
23580490-8	2013	Reduced F4/80+ cell infiltration was evidenced in sunitinib-treated mice and was associated to decreased VEGF-A (by 50%, P &lt; 0.01) and VEGF-C (by 35%, P &lt; 0.01) expressions, while VEGF-D and sVEGFR-2 expressions were not affected.	Sunitinib	50-59	vascular endothelial growth factor C	Mus musculus	138-144
23580490-8	2013	Reduced F4/80+ cell infiltration was evidenced in sunitinib-treated mice and was associated to decreased VEGF-A (by 50%, P &lt; 0.01) and VEGF-C (by 35%, P &lt; 0.01) expressions, while VEGF-D and sVEGFR-2 expressions were not affected.	Sunitinib	50-59	vascular endothelial growth factor D	Mus musculus	186-192
23580490-8	2013	Reduced F4/80+ cell infiltration was evidenced in sunitinib-treated mice and was associated to decreased VEGF-A (by 50%, P &lt; 0.01) and VEGF-C (by 35%, P &lt; 0.01) expressions, while VEGF-D and sVEGFR-2 expressions were not affected.	Sunitinib	50-59	kinase insert domain protein receptor	Mus musculus	197-205
23580490-11	2013	Mechanistically, sunitinib blocked VEGFR-2 phosphorylation induced by VEGF-A released by macrophages.	Sunitinib	17-26	kinase insert domain protein receptor	Mus musculus	35-42
23580490-11	2013	Mechanistically, sunitinib blocked VEGFR-2 phosphorylation induced by VEGF-A released by macrophages.	Sunitinib	17-26	vascular endothelial growth factor A	Mus musculus	70-76
23206420-11	2013	CONCLUSIONS: In our study microRNA-141 down-regulation driven epithelial-to-mesenchymal transition in clear cell renal cell carcinoma was linked to an unfavorable response to sunitinib therapy.	Sunitinib	175-184	microRNA 141	Homo sapiens	26-38
23206420-13	2013	Future experiments should be done in vivo to see whether microRNA-141 driven reversal of epithelial-to-mesenchymal transition could affect the efficacy of sunitinib treatment.	Sunitinib	155-164	microRNA 141	Homo sapiens	57-69
23206420-0	2013	A possible role for microRNA-141 down-regulation in sunitinib resistant metastatic clear cell renal cell carcinoma through induction of epithelial-to-mesenchymal transition and hypoxia resistance.	Sunitinib	52-61	microRNA 141	Homo sapiens	20-32
21478036-0	2013	Expression level of vascular endothelial growth factor receptor-2 in radical nephrectomy specimens as a prognostic predictor in patients with metastatic renal cell carcinoma treated with sunitinib.	Sunitinib	187-196	kinase insert domain receptor	Homo sapiens	20-65
23206420-8	2013	RESULTS: Compared to good responders, microRNA-141 was significantly down-regulated in tumors of poor responders to sunitinib.	Sunitinib	116-125	microRNA 141	Homo sapiens	38-50
23819366-6	2013	Sunitinib was administered following Interferon alpha (IFN-alpha) therapy; however, the lung metastases became larger, so administration of everolimus at 10 mg/day was commenced.	Sunitinib	0-9	interferon alpha 1	Homo sapiens	55-64
21478036-4	2013	RESULTS: Of several factors examined, tumor grade and the expression level of VEGFR-2 were shown to have significant impacts on response to sunitinib in these 40 patients.	Sunitinib	140-149	kinase insert domain receptor	Homo sapiens	78-85
21478036-8	2013	CONCLUSIONS: Collectively, these findings suggest that it would be useful to consider expression levels of potential molecular markers, particularly VEGFR-2, as well as conventional clinical parameters to select metastatic RCC patients likely to benefit from treatment with sunitinib.	Sunitinib	274-283	kinase insert domain receptor	Homo sapiens	149-156
23180436-5	2013	Sunitinib induced G1 phase arrest associated with decreased cyclin D1, cyclin D3, and cyclin-dependent kinase (Cdk)2 and increased p27(Kip1), pRb1, and p130/Rb2 expression and phosphorylated activation of protein kinase C alpha and beta (PKCalpha/beta).	Sunitinib	0-9	cyclin dependent kinase inhibitor 1B	Homo sapiens	135-139
23454556-4	2013	We performed in vitro experiments to study whether Sunitinib, a platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) RTKs" inhibitor, could block both activated HSC functions and angiogenesis and thus prevent the progression of cirrhotic liver to hepatocellular carcinoma.	Sunitinib	51-60	vascular endothelial growth factor A	Homo sapiens	106-140
23454556-4	2013	We performed in vitro experiments to study whether Sunitinib, a platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) RTKs" inhibitor, could block both activated HSC functions and angiogenesis and thus prevent the progression of cirrhotic liver to hepatocellular carcinoma.	Sunitinib	51-60	vascular endothelial growth factor A	Homo sapiens	142-146
23454556-8	2013	In conclusion, the present study demonstrates that the RTK inhibitor Sunitinib blocks the activation of HSC and angiogenesis suggesting its potential as a drug candidate in pathological conditions like liver fibrosis and hepatocellular carcinoma.	Sunitinib	69-78	ret proto-oncogene	Homo sapiens	55-58
23544171-12	2013	Importantly, phospho-RTK arrays revealed novel targets for cediranib and sunitinib therapy.	Sunitinib	73-82	ret proto-oncogene	Homo sapiens	21-24
23511629-0	2013	VEGF and VEGFR polymorphisms affect clinical outcome in advanced renal cell carcinoma patients receiving first-line sunitinib.	Sunitinib	116-125	vascular endothelial growth factor A	Homo sapiens	0-4
23511629-0	2013	VEGF and VEGFR polymorphisms affect clinical outcome in advanced renal cell carcinoma patients receiving first-line sunitinib.	Sunitinib	116-125	kinase insert domain receptor	Homo sapiens	9-14
23378344-8	2013	Having identified PDGFR-beta to be regulated by FOXC2, we show that the U.S. Food and Drug Administration-approved PDGFR inhibitor, sunitinib, targets FOXC2-expressing tumor cells leading to reduced CSC and metastatic properties.	Sunitinib	132-141	platelet derived growth factor receptor beta	Homo sapiens	18-28
23378344-8	2013	Having identified PDGFR-beta to be regulated by FOXC2, we show that the U.S. Food and Drug Administration-approved PDGFR inhibitor, sunitinib, targets FOXC2-expressing tumor cells leading to reduced CSC and metastatic properties.	Sunitinib	132-141	forkhead box C2	Homo sapiens	48-53
23378344-8	2013	Having identified PDGFR-beta to be regulated by FOXC2, we show that the U.S. Food and Drug Administration-approved PDGFR inhibitor, sunitinib, targets FOXC2-expressing tumor cells leading to reduced CSC and metastatic properties.	Sunitinib	132-141	platelet derived growth factor receptor beta	Homo sapiens	18-23
23378344-8	2013	Having identified PDGFR-beta to be regulated by FOXC2, we show that the U.S. Food and Drug Administration-approved PDGFR inhibitor, sunitinib, targets FOXC2-expressing tumor cells leading to reduced CSC and metastatic properties.	Sunitinib	132-141	forkhead box C2	Homo sapiens	151-156
23462807-7	2013	CONCLUSION: Our results confirm former communications regarding the association between SNPs in ABCB1, NR1/2, NR1/3 and VEGFR3 and sunitinib outcome in clear-cell RCC.	Sunitinib	131-140	ATP binding cassette subfamily B member 1	Homo sapiens	96-101
23462807-7	2013	CONCLUSION: Our results confirm former communications regarding the association between SNPs in ABCB1, NR1/2, NR1/3 and VEGFR3 and sunitinib outcome in clear-cell RCC.	Sunitinib	131-140	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	103-108
23462807-7	2013	CONCLUSION: Our results confirm former communications regarding the association between SNPs in ABCB1, NR1/2, NR1/3 and VEGFR3 and sunitinib outcome in clear-cell RCC.	Sunitinib	131-140	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	110-115
23462807-7	2013	CONCLUSION: Our results confirm former communications regarding the association between SNPs in ABCB1, NR1/2, NR1/3 and VEGFR3 and sunitinib outcome in clear-cell RCC.	Sunitinib	131-140	fms related receptor tyrosine kinase 4	Homo sapiens	120-126
23497256-4	2013	RESULTS: Sunitinib treatment increased p53 levels in RCC xenografts and transiently induced the expression of p21(waf1), Noxa, and HDM2, the levels of which subsequently declined to baseline (or undetectable) with the emergence of sunitinib resistance.	Sunitinib	9-18	tumor protein p53	Homo sapiens	39-42
23497256-4	2013	RESULTS: Sunitinib treatment increased p53 levels in RCC xenografts and transiently induced the expression of p21(waf1), Noxa, and HDM2, the levels of which subsequently declined to baseline (or undetectable) with the emergence of sunitinib resistance.	Sunitinib	9-18	cyclin dependent kinase inhibitor 1A	Homo sapiens	110-113
23497256-4	2013	RESULTS: Sunitinib treatment increased p53 levels in RCC xenografts and transiently induced the expression of p21(waf1), Noxa, and HDM2, the levels of which subsequently declined to baseline (or undetectable) with the emergence of sunitinib resistance.	Sunitinib	9-18	cyclin dependent kinase inhibitor 1A	Homo sapiens	114-118
23497256-4	2013	RESULTS: Sunitinib treatment increased p53 levels in RCC xenografts and transiently induced the expression of p21(waf1), Noxa, and HDM2, the levels of which subsequently declined to baseline (or undetectable) with the emergence of sunitinib resistance.	Sunitinib	9-18	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	121-125
23497256-4	2013	RESULTS: Sunitinib treatment increased p53 levels in RCC xenografts and transiently induced the expression of p21(waf1), Noxa, and HDM2, the levels of which subsequently declined to baseline (or undetectable) with the emergence of sunitinib resistance.	Sunitinib	9-18	MDM2 proto-oncogene	Homo sapiens	131-135
23497256-7	2013	It also suppressed the expression of the chemokine SDF-1 (CXCL12) and the influx of CD11b+/Gr-1+ myeloid-derived suppressor cells (MDSC) otherwise induced by sunitinib.	Sunitinib	158-167	integrin subunit alpha M	Homo sapiens	84-89
23180436-5	2013	Sunitinib induced G1 phase arrest associated with decreased cyclin D1, cyclin D3, and cyclin-dependent kinase (Cdk)2 and increased p27(Kip1), pRb1, and p130/Rb2 expression and phosphorylated activation of protein kinase C alpha and beta (PKCalpha/beta).	Sunitinib	0-9	RB transcriptional corepressor like 2	Homo sapiens	152-156
23180436-5	2013	Sunitinib induced G1 phase arrest associated with decreased cyclin D1, cyclin D3, and cyclin-dependent kinase (Cdk)2 and increased p27(Kip1), pRb1, and p130/Rb2 expression and phosphorylated activation of protein kinase C alpha and beta (PKCalpha/beta).	Sunitinib	0-9	cyclin D1	Homo sapiens	60-69
23180436-5	2013	Sunitinib induced G1 phase arrest associated with decreased cyclin D1, cyclin D3, and cyclin-dependent kinase (Cdk)2 and increased p27(Kip1), pRb1, and p130/Rb2 expression and phosphorylated activation of protein kinase C alpha and beta (PKCalpha/beta).	Sunitinib	0-9	cyclin D3	Homo sapiens	71-80
23180436-5	2013	Sunitinib induced G1 phase arrest associated with decreased cyclin D1, cyclin D3, and cyclin-dependent kinase (Cdk)2 and increased p27(Kip1), pRb1, and p130/Rb2 expression and phosphorylated activation of protein kinase C alpha and beta (PKCalpha/beta).	Sunitinib	0-9	cyclin dependent kinase 2	Homo sapiens	111-116
23180436-5	2013	Sunitinib induced G1 phase arrest associated with decreased cyclin D1, cyclin D3, and cyclin-dependent kinase (Cdk)2 and increased p27(Kip1), pRb1, and p130/Rb2 expression and phosphorylated activation of protein kinase C alpha and beta (PKCalpha/beta).	Sunitinib	0-9	interferon alpha inducible protein 27	Homo sapiens	131-134
23375402-3	2013	Here, we present a case report of TC with c-Kit mutation, who has relapsed after exposure to multiple lines of combination chemotherapy, but he has shown an impressive and long lasting response to sunitinib after imatinib failure.	Sunitinib	197-206	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	42-47
23414694-15	2013	Responders to primary sunitinib who underwent CRN had better DSS and OS than patients who underwent primary CRN, followed by sunitinib.	Sunitinib	22-31	crooked neck pre-mRNA splicing factor 1	Homo sapiens	46-49
23180436-5	2013	Sunitinib induced G1 phase arrest associated with decreased cyclin D1, cyclin D3, and cyclin-dependent kinase (Cdk)2 and increased p27(Kip1), pRb1, and p130/Rb2 expression and phosphorylated activation of protein kinase C alpha and beta (PKCalpha/beta).	Sunitinib	0-9	proline rich protein BstNI subfamily 1	Homo sapiens	142-146
23180436-5	2013	Sunitinib induced G1 phase arrest associated with decreased cyclin D1, cyclin D3, and cyclin-dependent kinase (Cdk)2 and increased p27(Kip1), pRb1, and p130/Rb2 expression and phosphorylated activation of protein kinase C alpha and beta (PKCalpha/beta).	Sunitinib	0-9	RB transcriptional corepressor like 2	Homo sapiens	157-160
23180436-5	2013	Sunitinib induced G1 phase arrest associated with decreased cyclin D1, cyclin D3, and cyclin-dependent kinase (Cdk)2 and increased p27(Kip1), pRb1, and p130/Rb2 expression and phosphorylated activation of protein kinase C alpha and beta (PKCalpha/beta).	Sunitinib	0-9	protein kinase C alpha	Homo sapiens	205-227
23180436-5	2013	Sunitinib induced G1 phase arrest associated with decreased cyclin D1, cyclin D3, and cyclin-dependent kinase (Cdk)2 and increased p27(Kip1), pRb1, and p130/Rb2 expression and phosphorylated activation of protein kinase C alpha and beta (PKCalpha/beta).	Sunitinib	0-9	protein kinase C alpha	Homo sapiens	238-251
23180436-6	2013	Selective PKCalpha/beta inhibitor treatment abolished sunitinib-elicited AML differentiation, suggesting that PKCalpha/beta may underlie sunitinib-induced monocytic differentiation.	Sunitinib	54-63	protein kinase C alpha	Homo sapiens	10-23
23180436-6	2013	Selective PKCalpha/beta inhibitor treatment abolished sunitinib-elicited AML differentiation, suggesting that PKCalpha/beta may underlie sunitinib-induced monocytic differentiation.	Sunitinib	54-63	protein kinase C alpha	Homo sapiens	110-123
23180436-6	2013	Selective PKCalpha/beta inhibitor treatment abolished sunitinib-elicited AML differentiation, suggesting that PKCalpha/beta may underlie sunitinib-induced monocytic differentiation.	Sunitinib	137-146	protein kinase C alpha	Homo sapiens	10-23
23180436-6	2013	Selective PKCalpha/beta inhibitor treatment abolished sunitinib-elicited AML differentiation, suggesting that PKCalpha/beta may underlie sunitinib-induced monocytic differentiation.	Sunitinib	137-146	protein kinase C alpha	Homo sapiens	110-123
30349606-6	2013	Motesanib, sorafenib, vandetanib, sunitinib, lenvatinib, imatinib and cabozantinib are multi-kinase inhibitors that have the ability of inhibiting the rearranged during transection (RET) and vascular endothelial growth factor receptor (VEGFR), and other kinases, and have been used in advanced differentiated thyroid carcinoma.	Sunitinib	34-43	ret proto-oncogene	Homo sapiens	182-185
23507600-8	2013	Sunitinib is a tyrosine kinase inhibitor for multi-targets including VEGFR, PDGFR, c-kit et.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	69-74
23507600-8	2013	Sunitinib is a tyrosine kinase inhibitor for multi-targets including VEGFR, PDGFR, c-kit et.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	76-81
23507600-8	2013	Sunitinib is a tyrosine kinase inhibitor for multi-targets including VEGFR, PDGFR, c-kit et.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	83-88
23114714-8	2013	Overall, our results suggest a role for Cav-1 as a biomarker of response to both dasatinib and sunitinib treatment and as a therapeutic target in prostate cancer.	Sunitinib	95-104	caveolin 1, caveolae protein	Mus musculus	40-45
23201752-0	2013	MicroRNA-21 silencing enhances the cytotoxic effect of the antiangiogenic drug sunitinib in glioblastoma.	Sunitinib	79-88	microRNA 21	Homo sapiens	0-11
23201752-6	2013	Finally, we demonstrate for the first time that miR-21 silencing enhances the antitumoral effect of the tyrosine kinase inhibitor sunitinib, whereas no therapeutic benefit is observed when coupling miR-21 silencing with the first-line drug temozolomide.	Sunitinib	130-139	microRNA 21	Homo sapiens	48-54
23536339-12	2013	The sub-group analysis of two protocols of sunitinib administration showed that the incidence of diarrhea and hand-foot syndrome were higher in 50 mg/d (4/2) group than those in 37.5 mg/d CDD group (P=0.027, P=0.048).	Sunitinib	43-52	natriuretic peptide A	Homo sapiens	188-191
23536339-16	2013	The protocol of sunitinib 37.5 mg/d CDD possesses better safety.	Sunitinib	16-25	natriuretic peptide A	Homo sapiens	36-39
23626551-0	2013	Targeting VEGF-VEGFR Pathway by Sunitinib in Peripheral Primitive Neuroectodermal Tumor, Paraganglioma and Epithelioid Hemangioendothelioma: Three Case Reports.	Sunitinib	32-41	vascular endothelial growth factor A	Homo sapiens	10-14
23626551-0	2013	Targeting VEGF-VEGFR Pathway by Sunitinib in Peripheral Primitive Neuroectodermal Tumor, Paraganglioma and Epithelioid Hemangioendothelioma: Three Case Reports.	Sunitinib	32-41	kinase insert domain receptor	Homo sapiens	15-20
23179081-5	2013	Although the precise mechanism of these interactions is not well understood, cytochrome P450 mono-oxygenase 3A4 (CYP3A4) is a key enzyme to inactivate both glucocorticoids and sunitinib.	Sunitinib	176-185	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	77-111
23179081-5	2013	Although the precise mechanism of these interactions is not well understood, cytochrome P450 mono-oxygenase 3A4 (CYP3A4) is a key enzyme to inactivate both glucocorticoids and sunitinib.	Sunitinib	176-185	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	113-119
23114714-2	2013	Treatment of both cell lines with either dasatinib or sunitinib reduced phosphorylation of PDGFR, VEGFR2, Akt, FAK, Src (dasatinib only) and Cav-1, and reduced cellular and secreted levels of Cav-1.	Sunitinib	54-63	platelet derived growth factor receptor, beta polypeptide	Mus musculus	91-96
23114714-2	2013	Treatment of both cell lines with either dasatinib or sunitinib reduced phosphorylation of PDGFR, VEGFR2, Akt, FAK, Src (dasatinib only) and Cav-1, and reduced cellular and secreted levels of Cav-1.	Sunitinib	54-63	kinase insert domain protein receptor	Mus musculus	98-104
23114714-2	2013	Treatment of both cell lines with either dasatinib or sunitinib reduced phosphorylation of PDGFR, VEGFR2, Akt, FAK, Src (dasatinib only) and Cav-1, and reduced cellular and secreted levels of Cav-1.	Sunitinib	54-63	thymoma viral proto-oncogene 1	Mus musculus	106-109
23269235-2	2013	Previously, we demonstrated that sunitinib directly inhibited mTORC1 signaling in rat pheochromocytoma PC12 cells.	Sunitinib	33-42	CREB regulated transcription coactivator 1	Mus musculus	62-68
23114714-2	2013	Treatment of both cell lines with either dasatinib or sunitinib reduced phosphorylation of PDGFR, VEGFR2, Akt, FAK, Src (dasatinib only) and Cav-1, and reduced cellular and secreted levels of Cav-1.	Sunitinib	54-63	PTK2 protein tyrosine kinase 2	Mus musculus	111-114
23114714-2	2013	Treatment of both cell lines with either dasatinib or sunitinib reduced phosphorylation of PDGFR, VEGFR2, Akt, FAK, Src (dasatinib only) and Cav-1, and reduced cellular and secreted levels of Cav-1.	Sunitinib	54-63	Rous sarcoma oncogene	Mus musculus	116-119
23114714-2	2013	Treatment of both cell lines with either dasatinib or sunitinib reduced phosphorylation of PDGFR, VEGFR2, Akt, FAK, Src (dasatinib only) and Cav-1, and reduced cellular and secreted levels of Cav-1.	Sunitinib	54-63	caveolin 1, caveolae protein	Mus musculus	141-146
23114714-2	2013	Treatment of both cell lines with either dasatinib or sunitinib reduced phosphorylation of PDGFR, VEGFR2, Akt, FAK, Src (dasatinib only) and Cav-1, and reduced cellular and secreted levels of Cav-1.	Sunitinib	54-63	caveolin 1, caveolae protein	Mus musculus	192-197
23114714-6	2013	Serum Cav-1 levels were lower in dasatinib- and sunitinib-treated mice than they were in vehicle-treated mice, and correlated positively with tumor growth in dasatinib- and sunitinib-treated groups (r = 0.48, p = 0.031; r = 0.554, p = 0.0065, respectively), compared with vehicle controls.	Sunitinib	48-57	caveolin 1, caveolae protein	Mus musculus	6-11
23114714-6	2013	Serum Cav-1 levels were lower in dasatinib- and sunitinib-treated mice than they were in vehicle-treated mice, and correlated positively with tumor growth in dasatinib- and sunitinib-treated groups (r = 0.48, p = 0.031; r = 0.554, p = 0.0065, respectively), compared with vehicle controls.	Sunitinib	173-182	caveolin 1, caveolae protein	Mus musculus	6-11
23114714-7	2013	Cav-1 knockdown, in combination with dasatinib or sunitinib treatment in PC-3 cells, caused a greater reduction in the phosphorylation of PDGFR-beta and VEGFR2, and expression and secretion of PDGF-B and VEGF-A than that in PC-3 cells treated with dasatinib or sunitinib alone in control siRNA cells, suggesting that Cav-1 is involved in an autocrine pathway that is affected by these drugs.	Sunitinib	50-59	caveolin 1, caveolae protein	Mus musculus	0-5
23114714-7	2013	Cav-1 knockdown, in combination with dasatinib or sunitinib treatment in PC-3 cells, caused a greater reduction in the phosphorylation of PDGFR-beta and VEGFR2, and expression and secretion of PDGF-B and VEGF-A than that in PC-3 cells treated with dasatinib or sunitinib alone in control siRNA cells, suggesting that Cav-1 is involved in an autocrine pathway that is affected by these drugs.	Sunitinib	50-59	platelet derived growth factor receptor, beta polypeptide	Mus musculus	138-148
23114714-7	2013	Cav-1 knockdown, in combination with dasatinib or sunitinib treatment in PC-3 cells, caused a greater reduction in the phosphorylation of PDGFR-beta and VEGFR2, and expression and secretion of PDGF-B and VEGF-A than that in PC-3 cells treated with dasatinib or sunitinib alone in control siRNA cells, suggesting that Cav-1 is involved in an autocrine pathway that is affected by these drugs.	Sunitinib	50-59	kinase insert domain protein receptor	Mus musculus	153-159
23114714-7	2013	Cav-1 knockdown, in combination with dasatinib or sunitinib treatment in PC-3 cells, caused a greater reduction in the phosphorylation of PDGFR-beta and VEGFR2, and expression and secretion of PDGF-B and VEGF-A than that in PC-3 cells treated with dasatinib or sunitinib alone in control siRNA cells, suggesting that Cav-1 is involved in an autocrine pathway that is affected by these drugs.	Sunitinib	50-59	platelet derived growth factor, B polypeptide	Mus musculus	193-199
23114714-7	2013	Cav-1 knockdown, in combination with dasatinib or sunitinib treatment in PC-3 cells, caused a greater reduction in the phosphorylation of PDGFR-beta and VEGFR2, and expression and secretion of PDGF-B and VEGF-A than that in PC-3 cells treated with dasatinib or sunitinib alone in control siRNA cells, suggesting that Cav-1 is involved in an autocrine pathway that is affected by these drugs.	Sunitinib	50-59	vascular endothelial growth factor A	Mus musculus	204-210
23114714-7	2013	Cav-1 knockdown, in combination with dasatinib or sunitinib treatment in PC-3 cells, caused a greater reduction in the phosphorylation of PDGFR-beta and VEGFR2, and expression and secretion of PDGF-B and VEGF-A than that in PC-3 cells treated with dasatinib or sunitinib alone in control siRNA cells, suggesting that Cav-1 is involved in an autocrine pathway that is affected by these drugs.	Sunitinib	50-59	caveolin 1, caveolae protein	Mus musculus	317-322
23114714-7	2013	Cav-1 knockdown, in combination with dasatinib or sunitinib treatment in PC-3 cells, caused a greater reduction in the phosphorylation of PDGFR-beta and VEGFR2, and expression and secretion of PDGF-B and VEGF-A than that in PC-3 cells treated with dasatinib or sunitinib alone in control siRNA cells, suggesting that Cav-1 is involved in an autocrine pathway that is affected by these drugs.	Sunitinib	261-270	caveolin 1, caveolae protein	Mus musculus	0-5
23398161-1	2013	BACKGROUND: Thyroid dysfunction is a well-known adverse effect of sunitinib, a drug that targets multiple receptor tyrosine kinases, including vascular endothelial growth factor receptor (VEGFR).	Sunitinib	66-75	kinase insert domain receptor	Homo sapiens	143-186
23398161-1	2013	BACKGROUND: Thyroid dysfunction is a well-known adverse effect of sunitinib, a drug that targets multiple receptor tyrosine kinases, including vascular endothelial growth factor receptor (VEGFR).	Sunitinib	66-75	kinase insert domain receptor	Homo sapiens	188-193
23399884-7	2013	Some antiangiogenic drugs inhibiting the VEGFR2 receptor are successfully used in clinics for the treatment of several types of tumours in synergy with chemotherapy (e.g., Nexavar( ) from Bayer, Sutent( ) from Pfizer and Votrient( ) from GlaxoSmithKline, approved by the FDA in 2005, 2006 and 2009, respectively).	Sunitinib	195-201	kinase insert domain receptor	Homo sapiens	41-47
23127174-6	2013	The action of KIT kinase inhibitors, especially imatinib, sunitinib, dasatinib and PKC412, on different primary and secondary mutants is discussed.	Sunitinib	58-67	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
23613413-2	2013	METHODS: Three different doses of sutent (D1= 1 muM, D2= 5 muM, D3= 10 muM) were administered to cells for 72 h to determine the optimal dose.	Sunitinib	34-40	latexin	Homo sapiens	48-51
23613413-2	2013	METHODS: Three different doses of sutent (D1= 1 muM, D2= 5 muM, D3= 10 muM) were administered to cells for 72 h to determine the optimal dose.	Sunitinib	34-40	latexin	Homo sapiens	59-62
23613413-2	2013	METHODS: Three different doses of sutent (D1= 1 muM, D2= 5 muM, D3= 10 muM) were administered to cells for 72 h to determine the optimal dose.	Sunitinib	34-40	latexin	Homo sapiens	59-62
22995920-2	2013	Here, we describe a case of TFE3-positive RCC in which metastatic relapse to the mediastinal lymph nodes and pulmonary nodules was treated with single-agent sunitinib, a multitargeted tyrosine inhibitor.	Sunitinib	157-166	transcription factor binding to IGHM enhancer 3	Homo sapiens	28-32
23322198-0	2013	Cox-2 inhibition enhances the activity of sunitinib in human renal cell carcinoma xenografts.	Sunitinib	42-51	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
23322198-1	2013	BACKGROUND: Sunitinib (Su), a tyrosine kinase inhibitor of VEGFR, is effective at producing tumour response in clear cell renal cell carcinoma (cRCC), but resistance to therapy is inevitable.	Sunitinib	12-21	kinase insert domain receptor	Homo sapiens	59-64
23322198-1	2013	BACKGROUND: Sunitinib (Su), a tyrosine kinase inhibitor of VEGFR, is effective at producing tumour response in clear cell renal cell carcinoma (cRCC), but resistance to therapy is inevitable.	Sunitinib	12-14	kinase insert domain receptor	Homo sapiens	59-64
23322198-11	2013	Clinical trials combining Su and COX-2 inhibitors should be considered as a means delaying time to progression on sunitinib in patients with metastatic cRCC.	Sunitinib	114-123	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	33-38
23679326-14	2013	In our study, we observed second line sunitinib treatment following IFN-alpha to be effective and tolerable.	Sunitinib	38-47	interferon alpha 1	Homo sapiens	68-77
23331791-6	2013	However, HIF-1alpha knockdowns demonstrated relative final volumes that were significantly lower than unmodified tumors when both were treated with bevacizumab (35.88 +- 4.24 vs 53.57 +- 6.61, p=0.0544) or sunitinib (12.46 +- 2.59 vs 36.36 +- 4.82, p=0.0024).	Sunitinib	206-215	hypoxia inducible factor 1 subunit alpha	Homo sapiens	9-19
23269235-6	2013	Here, we demonstrated that sunitinib significantly increased the levels of LC3-II, concomitant with a decrease of p62 in PC12 cells.	Sunitinib	27-36	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	114-117
23269235-8	2013	Furthermore, Atg13 knockdown significantly reduced its protein level, which in turn abolished sunitinib-induced autophagy.	Sunitinib	94-103	autophagy related 13	Rattus norvegicus	13-18
23269235-9	2013	Moreover, inhibition of autophagy by siRNAs targeting Atg13 or by pharmacological inhibition with ammonium chloride, enhanced both sunitinib-induced apoptosis and anti-proliferation.	Sunitinib	131-140	autophagy related 13	Rattus norvegicus	54-59
23269235-10	2013	Thus, sunitinib-induced autophagy is dependent on the suppression of mTORC1 signaling and the formation of ULK1/2-Atg13-FIP200 complexes.	Sunitinib	6-15	CREB regulated transcription coactivator 1	Mus musculus	69-75
23269235-10	2013	Thus, sunitinib-induced autophagy is dependent on the suppression of mTORC1 signaling and the formation of ULK1/2-Atg13-FIP200 complexes.	Sunitinib	6-15	unc-51 like autophagy activating kinase 1	Rattus norvegicus	107-111
23269235-10	2013	Thus, sunitinib-induced autophagy is dependent on the suppression of mTORC1 signaling and the formation of ULK1/2-Atg13-FIP200 complexes.	Sunitinib	6-15	autophagy related 13	Rattus norvegicus	114-119
23329590-13	2013	Based upon the work presented including a 12.5 % discount for pazopanib, sunitinib was extendedly dominated by a combination of pazopanib and IFN-alpha.	Sunitinib	73-82	interferon alpha 1	Homo sapiens	142-151
24649132-0	2013	Successful treatment of erythropoietin-producing advanced renal cell carcinoma after targeted therapy using sunitinib: Case report and review of the literature.	Sunitinib	108-117	erythropoietin	Homo sapiens	24-38
24649132-3	2013	The present study aimed to report the first case of a patient demonstrating a therapeutic effect on EPO-producing advanced RCC, subsequent to targeted pre-surgical sunitinib therapy, with a review of the literature.	Sunitinib	164-173	erythropoietin	Homo sapiens	100-103
24649132-9	2013	The EPO-producing RCC was successfully treated following targeted presurgical therapy with sunitinib.	Sunitinib	91-100	erythropoietin	Homo sapiens	4-7
23555683-12	2013	The immunohistochemical analysis of sunitinib-treated metastatic renal cell carcinomas confirmed the correlation between RAB17, LGALS8, and EPCAM and overall survival.	Sunitinib	36-45	RAB17, member RAS oncogene family	Homo sapiens	121-126
23555683-12	2013	The immunohistochemical analysis of sunitinib-treated metastatic renal cell carcinomas confirmed the correlation between RAB17, LGALS8, and EPCAM and overall survival.	Sunitinib	36-45	galectin 8	Homo sapiens	128-134
23555683-12	2013	The immunohistochemical analysis of sunitinib-treated metastatic renal cell carcinomas confirmed the correlation between RAB17, LGALS8, and EPCAM and overall survival.	Sunitinib	36-45	epithelial cell adhesion molecule	Homo sapiens	140-145
23294714-5	2013	Moreover, SU11248 treatment concentration-dependently decreased cyclin G1 mRNA and protein expressions (P&lt;0.05), in contrast, it time-dependently increased P27(KIP1); mRNA and protein levels (P&lt;0.05).	Sunitinib	10-17	cyclin dependent kinase inhibitor 1B	Homo sapiens	163-167
23336010-1	2013	Current inhibitors of angiogenesis comprise either therapeutic antibodies (e.g. bevacicumab binding to VEGF-A) or small molecular inhibitors of receptor tyrosin kinases like e.g. sunitinib, which inhibits PDGFR and VEGFR.	Sunitinib	179-188	platelet derived growth factor receptor beta	Homo sapiens	205-210
23336010-1	2013	Current inhibitors of angiogenesis comprise either therapeutic antibodies (e.g. bevacicumab binding to VEGF-A) or small molecular inhibitors of receptor tyrosin kinases like e.g. sunitinib, which inhibits PDGFR and VEGFR.	Sunitinib	179-188	kinase insert domain receptor	Homo sapiens	215-220
23294714-5	2013	Moreover, SU11248 treatment concentration-dependently decreased cyclin G1 mRNA and protein expressions (P&lt;0.05), in contrast, it time-dependently increased P27(KIP1); mRNA and protein levels (P&lt;0.05).	Sunitinib	10-17	cyclin G1	Homo sapiens	64-73
24640739-7	2013	Currently, a number of VEGFR2 inhibitors are under clinical trials (ramucirumab, cediranib) and several were approved (sunitinib, sorafenib).	Sunitinib	119-128	kinase insert domain receptor	Homo sapiens	23-29
23294714-6	2013	CONCLUSION: SU11248 may significantly inhibit the proliferation of CNE-2 cells through up-regulating P27(KIP1); and down-regulating cyclin G1.	Sunitinib	12-19	cyclin dependent kinase inhibitor 1B	Homo sapiens	101-109
23294714-6	2013	CONCLUSION: SU11248 may significantly inhibit the proliferation of CNE-2 cells through up-regulating P27(KIP1); and down-regulating cyclin G1.	Sunitinib	12-19	cyclin G1	Homo sapiens	132-141
23294714-5	2013	Moreover, SU11248 treatment concentration-dependently decreased cyclin G1 mRNA and protein expressions (P&lt;0.05), in contrast, it time-dependently increased P27(KIP1); mRNA and protein levels (P&lt;0.05).	Sunitinib	10-17	zinc ribbon domain containing 2	Homo sapiens	159-162
22858558-2	2012	Hypertension (HTN), an on-target class effect of vascular endothelial growth factor signaling-pathway inhibitors, has been shown to correlate with clinical outcome in advanced renal cell carcinoma treated with sunitinib.	Sunitinib	210-219	vascular endothelial growth factor A	Homo sapiens	49-83
22868821-12	2012	Immunohistochemistry, Western blot, and quantitative polymerase chain reaction results showed both VEGFR-2 and PDGFR-beta expression in the control group was higher than that of the sunitinib-treated group.	Sunitinib	182-191	kinase insert domain protein receptor	Mus musculus	99-106
22700990-7	2012	In multivariable Cox regression, the skin toxicity was significantly associated with longer OS in the sunitinib cohort.	Sunitinib	102-111	cytochrome c oxidase subunit 8A	Homo sapiens	17-20
22289686-6	2012	Recent results of the AXIS phase 3 trial demonstrated improved efficacy with second-line axitinib compared with sorafenib in patients who progressed on a variety of first-line therapies, including the VEGFr-TKI sunitinib.	Sunitinib	211-220	kinase insert domain receptor	Homo sapiens	201-206
22959659-6	2012	Positive PTEN was related to good prognosis with sunitinib (PFS, 15.1 vs. 6.5 months; P = .003) and CKs (OS, 13.7 vs. 7.9 months; P = .039).	Sunitinib	49-58	phosphatase and tensin homolog	Homo sapiens	9-13
23231522-1	2012	AIM: Sunitinib is an orally active multi-targeted tyrosine kinase inhibitor that exerts its antitumor effects primarily through the selective inhibition of VEGF.	Sunitinib	5-14	vascular endothelial growth factor A	Homo sapiens	156-160
22644070-6	2012	PTEN demonstrated predictive value of response to sunitinib (70.8 vs. 34.1; p = 0.005).	Sunitinib	50-59	phosphatase and tensin homolog	Homo sapiens	0-4
22644070-7	2012	p21 was associated with a lower response to sunitinib (35.9 vs. 65.4; p = 0.025).	Sunitinib	44-53	H3 histone pseudogene 16	Homo sapiens	0-3
22644070-12	2012	PTEN and p21 may be important in predicting response to sunitinib.	Sunitinib	56-65	phosphatase and tensin homolog	Homo sapiens	0-4
22644070-12	2012	PTEN and p21 may be important in predicting response to sunitinib.	Sunitinib	56-65	H3 histone pseudogene 16	Homo sapiens	9-12
23022045-0	2012	An exploratory study of sunitinib in combination with docetaxel and trastuzumab as first-line therapy for HER2-positive metastatic breast cancer.	Sunitinib	24-33	erb-b2 receptor tyrosine kinase 2	Homo sapiens	106-110
23022045-2	2012	METHODS: Patients with unresectable, locally recurrent or metastatic human epidermal growth factor receptor 2 (HER2)+ breast cancer received sunitinib plus docetaxel and trastuzumab.	Sunitinib	141-150	erb-b2 receptor tyrosine kinase 2	Homo sapiens	75-109
23022045-2	2012	METHODS: Patients with unresectable, locally recurrent or metastatic human epidermal growth factor receptor 2 (HER2)+ breast cancer received sunitinib plus docetaxel and trastuzumab.	Sunitinib	141-150	erb-b2 receptor tyrosine kinase 2	Homo sapiens	111-115
23022045-14	2012	CONCLUSIONS: Sunitinib combined with docetaxel and trastuzumab had an acceptable toxicity profile and showed preliminary antitumor activity as first-line treatment for metastatic HER2+ breast cancer.	Sunitinib	13-22	erb-b2 receptor tyrosine kinase 2	Homo sapiens	179-183
22868821-12	2012	Immunohistochemistry, Western blot, and quantitative polymerase chain reaction results showed both VEGFR-2 and PDGFR-beta expression in the control group was higher than that of the sunitinib-treated group.	Sunitinib	182-191	platelet derived growth factor receptor, beta polypeptide	Mus musculus	111-121
23102636-5	2012	RESULTS: The minimum inhibitory concentrations (IC(min)) of sunitinib quenched its primary targets: FLT-3, VEGFR-2, and RET.	Sunitinib	60-69	fms related receptor tyrosine kinase 3	Homo sapiens	100-105
23102636-5	2012	RESULTS: The minimum inhibitory concentrations (IC(min)) of sunitinib quenched its primary targets: FLT-3, VEGFR-2, and RET.	Sunitinib	60-69	kinase insert domain receptor	Homo sapiens	107-114
23158184-4	2012	Autophagy protein 5 silencing diminished the antiproliferative effects of sunitinib and sorafenib by 44% (P &lt; .05) and 41% (P &lt; .05), respectively, in medullary thyroid cancer-1.1 cells and by 43% (P &lt; .01) and 39% (P &lt; .05), respectively, in TT cells.	Sunitinib	74-83	autophagy related 5	Homo sapiens	0-19
23102636-5	2012	RESULTS: The minimum inhibitory concentrations (IC(min)) of sunitinib quenched its primary targets: FLT-3, VEGFR-2, and RET.	Sunitinib	60-69	ret proto-oncogene	Homo sapiens	120-123
22869928-8	2012	In particular, phospholipase C-gamma1 phosphorylation in sunitinib-resistant tumors was up-regulated by 2.6-fold compared with that in sunitinib-sensitive tumors (p&lt;0.05).	Sunitinib	57-66	phospholipase C, gamma 1	Mus musculus	15-37
23047550-10	2012	The PDGFRbeta inhibitors gambogic acid, sunitinib, and tandutinib equally impaired the migration of meningioma cells.	Sunitinib	40-49	platelet derived growth factor receptor beta	Homo sapiens	4-13
22869928-8	2012	In particular, phospholipase C-gamma1 phosphorylation in sunitinib-resistant tumors was up-regulated by 2.6-fold compared with that in sunitinib-sensitive tumors (p&lt;0.05).	Sunitinib	135-144	phospholipase C, gamma 1	Mus musculus	15-37
22912364-1	2012	Sunitinib is an oral, small molecule multitargeted receptor tyrosine kinase inhibitor with antiangiogenic and antitumor activity that primarily targets vascular endothelial growth factor receptors (VEGFRs).	Sunitinib	0-9	kinase insert domain receptor	Rattus norvegicus	198-204
22912364-9	2012	Because Ser(40) phosphorylation significantly affects TH activity and is known to be regulated by PKC, sunitinib may inhibit Ser(40) phosphorylation via the VEGFR-2/PLC-gamma/PKC pathway.	Sunitinib	103-112	kinase insert domain receptor	Rattus norvegicus	157-164
22912364-10	2012	Additionally, sunitinib markedly decreased the activity of extracellular signal-regulated kinase (ERK), but not c-Jun NH(2)-terminal kinase or p38 mitogen-activated protein kinase.	Sunitinib	14-23	Eph receptor B1	Rattus norvegicus	59-96
22912364-10	2012	Additionally, sunitinib markedly decreased the activity of extracellular signal-regulated kinase (ERK), but not c-Jun NH(2)-terminal kinase or p38 mitogen-activated protein kinase.	Sunitinib	14-23	Eph receptor B1	Rattus norvegicus	98-101
22912364-11	2012	Therefore, sunitinib may reduce TH Ser(31) phosphorylation through inhibition of the VEGFR-2/PLC-gamma/PKC/Raf/mitogen-activated protein kinase/extracellular signal-regulated kinase kinase/ERK pathway.	Sunitinib	11-20	kinase insert domain receptor	Rattus norvegicus	85-92
22912364-11	2012	Therefore, sunitinib may reduce TH Ser(31) phosphorylation through inhibition of the VEGFR-2/PLC-gamma/PKC/Raf/mitogen-activated protein kinase/extracellular signal-regulated kinase kinase/ERK pathway.	Sunitinib	11-20	Eph receptor B1	Rattus norvegicus	144-181
22912364-11	2012	Therefore, sunitinib may reduce TH Ser(31) phosphorylation through inhibition of the VEGFR-2/PLC-gamma/PKC/Raf/mitogen-activated protein kinase/extracellular signal-regulated kinase kinase/ERK pathway.	Sunitinib	11-20	Eph receptor B1	Rattus norvegicus	189-192
22405734-5	2012	A variety of agents, including sorafenib, sunitinib, cediranib, axitinib, motesanib, linifinib and brivanib inhibit VEGF in addition to either platelet derived growth factor (PDGF), or fibroblast derived growth factor (FGF).	Sunitinib	42-51	vascular endothelial growth factor A	Homo sapiens	116-120
23036227-2	2012	Small molecule inhibitors such as imatinib and sunitinib are known to inhibit the aberrantly activated KIT and PDGFRA receptor signaling and can lead to excellent clinical outcomes for patients with GIST.	Sunitinib	47-56	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-106
23036227-2	2012	Small molecule inhibitors such as imatinib and sunitinib are known to inhibit the aberrantly activated KIT and PDGFRA receptor signaling and can lead to excellent clinical outcomes for patients with GIST.	Sunitinib	47-56	platelet derived growth factor receptor alpha	Homo sapiens	111-117
22955853-5	2012	RESULTS: The presence of EpCAM-positive, live CTCs predicts progression in individual mRCC patient, being associated with distant metastasis under first-line Sunitinib.	Sunitinib	158-167	epithelial cell adhesion molecule	Homo sapiens	25-30
23032654-11	2012	Although biopsy-proven cases of FSGS associated with sunitinib have been reported, this is, to our knowledge, the first reported case of biopsy-proven FSGS associated with sorafenib.	Sunitinib	53-62	actinin alpha 4	Homo sapiens	32-36
22868341-6	2012	The schedule of gemcitabine 800 mg/m(2) on days 1, 8, 15 and sunitinib 25 mg daily was considered to be a MTD.	Sunitinib	61-70	metallothionein 1E	Homo sapiens	106-109
22948895-0	2012	Polymorphisms in endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) predict sunitinib-induced hypertension.	Sunitinib	112-121	nitric oxide synthase 3	Homo sapiens	17-50
22948895-0	2012	Polymorphisms in endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) predict sunitinib-induced hypertension.	Sunitinib	112-121	nitric oxide synthase 3	Homo sapiens	52-56
22948895-0	2012	Polymorphisms in endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) predict sunitinib-induced hypertension.	Sunitinib	112-121	vascular endothelial growth factor A	Homo sapiens	62-96
22948895-0	2012	Polymorphisms in endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) predict sunitinib-induced hypertension.	Sunitinib	112-121	vascular endothelial growth factor A	Homo sapiens	98-102
22948895-7	2012	Genetic polymorphisms in VEGFA and eNOS independently predict rise in BP and/or development of severe hypertension in sunitinib-treated patients.	Sunitinib	118-127	vascular endothelial growth factor A	Homo sapiens	25-30
22819259-0	2012	Blockade of NFkappaB activity by Sunitinib increases cell death in Bortezomib-treated endometrial carcinoma cells.	Sunitinib	33-42	nuclear factor kappa B subunit 1	Homo sapiens	12-20
22948895-7	2012	Genetic polymorphisms in VEGFA and eNOS independently predict rise in BP and/or development of severe hypertension in sunitinib-treated patients.	Sunitinib	118-127	nitric oxide synthase 3	Homo sapiens	35-39
22327313-3	2012	Therapies targeting the VEGF pathway include bevacizumab, sorafenib, sunitinib, pazopanib, and axitinib, whereas temsirolimus and everolimus inhibit the mTOR pathway.	Sunitinib	69-78	vascular endothelial growth factor A	Homo sapiens	24-28
22837187-17	2012	Sunitinib serum levels might have been profoundly reduced by mitotane induced cytochrome P450-3A4 activity attenuating its antitumor activity and adverse effects.	Sunitinib	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	78-97
22744707-9	2012	PTC cell lines expressing PDGFR-alpha responded to PDGF-BB stimulation with increased invasive potential and this process can be blocked by the tyrosine kinase receptor inhibitor sunitinib (p &lt; 0.009).	Sunitinib	179-188	platelet derived growth factor receptor alpha	Homo sapiens	26-37
22671963-0	2012	C-reactive protein as a prognostic marker for advanced renal cell carcinoma treated with sunitinib.	Sunitinib	89-98	C-reactive protein	Homo sapiens	0-18
22671963-1	2012	OBJECTIVES: To investigate the prognostic role of C-reactive protein in patients with advanced renal cell carcinoma treated with sunitinib.	Sunitinib	129-138	C-reactive protein	Homo sapiens	50-68
22671963-8	2012	CONCLUSIONS: C-reactive protein is an independent prognostic indicator for patients with advanced renal cell carcinoma treated with sunitinib.	Sunitinib	132-141	C-reactive protein	Homo sapiens	13-31
22819259-3	2012	In the present study, we demonstrate that the tyrosine kinase receptor inhibitor Sunitinib reduces cell viability, proliferation, clonogenicity and induces apoptotic cell death in endometrial carcinoma cell lines, which is not due to its action through the most known targets like VEGFR, nor through EGFR as demonstrated in this work.	Sunitinib	81-90	kinase insert domain receptor	Homo sapiens	281-286
22819259-3	2012	In the present study, we demonstrate that the tyrosine kinase receptor inhibitor Sunitinib reduces cell viability, proliferation, clonogenicity and induces apoptotic cell death in endometrial carcinoma cell lines, which is not due to its action through the most known targets like VEGFR, nor through EGFR as demonstrated in this work.	Sunitinib	81-90	epidermal growth factor receptor	Homo sapiens	282-286
22819259-4	2012	Interestingly, Sunitinib reduces NFkappaB transcriptional activity either at basal level or activation by EGF or TNF-alpha.	Sunitinib	15-24	nuclear factor kappa B subunit 1	Homo sapiens	33-41
22819259-4	2012	Interestingly, Sunitinib reduces NFkappaB transcriptional activity either at basal level or activation by EGF or TNF-alpha.	Sunitinib	15-24	epidermal growth factor	Homo sapiens	106-109
22819259-4	2012	Interestingly, Sunitinib reduces NFkappaB transcriptional activity either at basal level or activation by EGF or TNF-alpha.	Sunitinib	15-24	tumor necrosis factor	Homo sapiens	113-122
22819259-5	2012	We observed that Sunitinib was able to inhibit the Bortezomib-induced NFkappaB transcriptional activity which correlates with a decrease of the phosphorylated levels of IKKalpha and beta, p65 and IkappaBalpha.	Sunitinib	17-26	nuclear factor kappa B subunit 1	Homo sapiens	70-78
22819259-5	2012	We observed that Sunitinib was able to inhibit the Bortezomib-induced NFkappaB transcriptional activity which correlates with a decrease of the phosphorylated levels of IKKalpha and beta, p65 and IkappaBalpha.	Sunitinib	17-26	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	169-186
22819259-5	2012	We observed that Sunitinib was able to inhibit the Bortezomib-induced NFkappaB transcriptional activity which correlates with a decrease of the phosphorylated levels of IKKalpha and beta, p65 and IkappaBalpha.	Sunitinib	17-26	RELA proto-oncogene, NF-kB subunit	Homo sapiens	188-191
22819259-5	2012	We observed that Sunitinib was able to inhibit the Bortezomib-induced NFkappaB transcriptional activity which correlates with a decrease of the phosphorylated levels of IKKalpha and beta, p65 and IkappaBalpha.	Sunitinib	17-26	NFKB inhibitor alpha	Homo sapiens	196-208
23275777-9	2012	The patient"s genotype was wild type for ABCG2 421C&gt;A, which is associated with increased sunitinib exposure.	Sunitinib	93-102	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	41-46
23073628-8	2012	Also other clinically used multiselective kinase inhibitors, for instance, sorafenib and sunitinib, have c-Kit included in their range of targets.	Sunitinib	89-98	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	105-110
22967802-3	2012	We have investigated the radiosensitizing effects of sunitinib, a potent, multi-tyrosine kinase inhibitor of the VEGFR and PDGFR receptors, on human prostate cancer cells.	Sunitinib	53-62	kinase insert domain receptor	Homo sapiens	113-118
22967802-3	2012	We have investigated the radiosensitizing effects of sunitinib, a potent, multi-tyrosine kinase inhibitor of the VEGFR and PDGFR receptors, on human prostate cancer cells.	Sunitinib	53-62	platelet derived growth factor receptor beta	Homo sapiens	123-128
22967802-4	2012	METHODS: The radiosensitizing effects of sunitinib were assessed on human prostate cancer cell lines DU145, PC3 and LNCaP by clonogenic assay.	Sunitinib	41-50	chromobox 8	Homo sapiens	108-111
22377563-3	2012	MATERIAL AND METHODS: The primary end point of this randomized phase II trial was the objective response rate according to RECIST criteria and/or Gynecologic Cancer InterGroup CA125 response criteria to sunitinib in patients with recurrent platinum-resistant ovarian cancer who were pretreated with up to three chemotherapies.	Sunitinib	203-212	mucin 16, cell surface associated	Homo sapiens	176-181
22993368-0	2012	Rapid relapse after resection of a sunitinib-resistant gastrointestinal stromal tumor harboring a secondary mutation in exon 13 of the c-KIT gene.	Sunitinib	35-44	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	135-140
22733151-10	2012	In vitro cell line study by immunowestern blotting found that sunitinib malate had an inhibitory effect on the PDGFA pathway by decreasing p-PDGFRA, AKT, and p-AKT expression.	Sunitinib	62-78	platelet derived growth factor subunit A	Homo sapiens	111-116
22733151-10	2012	In vitro cell line study by immunowestern blotting found that sunitinib malate had an inhibitory effect on the PDGFA pathway by decreasing p-PDGFRA, AKT, and p-AKT expression.	Sunitinib	62-78	platelet derived growth factor receptor alpha	Homo sapiens	141-147
22733151-10	2012	In vitro cell line study by immunowestern blotting found that sunitinib malate had an inhibitory effect on the PDGFA pathway by decreasing p-PDGFRA, AKT, and p-AKT expression.	Sunitinib	62-78	AKT serine/threonine kinase 1	Homo sapiens	149-152
22733151-10	2012	In vitro cell line study by immunowestern blotting found that sunitinib malate had an inhibitory effect on the PDGFA pathway by decreasing p-PDGFRA, AKT, and p-AKT expression.	Sunitinib	62-78	AKT serine/threonine kinase 1	Homo sapiens	160-163
22967802-7	2012	RESULTS: Clonogenic survival curve assays for both DU145 and PC3 cells showed that the surviving fraction at 2 Gy was reduced from 0.70 and 0.52 in controls to 0.44 and 0.38, respectively, by a 24 hr pretreatment with 100 nM sunitinib.	Sunitinib	225-234	chromobox 8	Homo sapiens	61-64
22967802-9	2012	Dose dependent decreases in VEGFR and PDGFR activation were also observed following sunitinib in both DU145 and PC3 cells.	Sunitinib	84-93	kinase insert domain receptor	Homo sapiens	28-33
22967802-9	2012	Dose dependent decreases in VEGFR and PDGFR activation were also observed following sunitinib in both DU145 and PC3 cells.	Sunitinib	84-93	chromobox 8	Homo sapiens	112-115
22967802-10	2012	We assessed the ability of sunitinib to radiosensitize PC3 xenograft tumors growing in the hind limb of nude mice.	Sunitinib	27-36	chromobox 8	Mus musculus	55-58
22317769-4	2012	We hypothesized that administration of sunitinib, a VEGFR inhibitor, following TAE would extend progression-free survival (PFS).	Sunitinib	39-48	kinase insert domain receptor	Homo sapiens	52-57
22317769-14	2012	Sunitinib, an oral VEGFR inhibitor, can be safely administered following embolization.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	19-24
20884251-9	2012	Bcl-2 apoptotic pathway induction by BCG and sunitinib treatment was evaluated by Western blotting method.	Sunitinib	45-54	BCL2 apoptosis regulator	Homo sapiens	0-5
22515521-3	2012	Sunitinib (targeting vascular endothelial growth factor), temsirolimus (an inhibitor of the mammalian target of rapamycin - mTOR) and pazopanib (a multi-targeted receptor tyrosine kinase inhibitor) are used in the first line of recurrent disease.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	21-55
22970046-7	2012	Sunitinib has been reported to inhibit platelet-derived growth factor receptor (PDGFR) phosphorylation at concentrations over the range of 50-100 ng/ml (sunitinib plus SU12662) in vivo.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	39-78
22970046-7	2012	Sunitinib has been reported to inhibit platelet-derived growth factor receptor (PDGFR) phosphorylation at concentrations over the range of 50-100 ng/ml (sunitinib plus SU12662) in vivo.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	80-85
22970046-7	2012	Sunitinib has been reported to inhibit platelet-derived growth factor receptor (PDGFR) phosphorylation at concentrations over the range of 50-100 ng/ml (sunitinib plus SU12662) in vivo.	Sunitinib	153-162	platelet derived growth factor receptor beta	Homo sapiens	39-78
22970046-7	2012	Sunitinib has been reported to inhibit platelet-derived growth factor receptor (PDGFR) phosphorylation at concentrations over the range of 50-100 ng/ml (sunitinib plus SU12662) in vivo.	Sunitinib	153-162	platelet derived growth factor receptor beta	Homo sapiens	80-85
22796529-3	2012	Use of 2 distinct approaches resulted in clinical efficacy in blocking the VEGF pathway: small molecule tyrosine kinase inhibitors (sunitinib, sorafenib, axitinib, pazopanib) and the humanized anti-VEGF monoclonal antibody bevacizumab that binds circulating VEGF and prevents activation of the VEGF receptor.	Sunitinib	132-141	vascular endothelial growth factor A	Homo sapiens	75-79
22129368-0	2012	Endothelial follicle stimulating hormone receptor in primary kidney cancer correlates with subsequent response to sunitinib.	Sunitinib	114-123	follicle stimulating hormone receptor	Homo sapiens	12-49
22129368-10	2012	The data suggest that FSHR expression levels in the blood vessels of CCRCC primary tumours can be used to predict, with high sensitivity and specificity, the patients who will respond to sunitinib therapy.	Sunitinib	187-196	follicle stimulating hormone receptor	Homo sapiens	22-26
21735145-5	2012	The mammalian target of rapamycin (mTOR) inhibitor everolimus was approved for use in patients who failed treatment with inhibitors of vascular endothelial growth factor (VEGF) and VEGF receptors (VEGFR) based on the results from a Phase III placebo-controlled study; however, until then, the only licensed agents across the spectrum of mRCC were VEGF(R) inhibitors (sorafenib, sunitinib and bevacizumab + interferon), and as such, a large body of evidence has accumulated regarding their use in sequence.	Sunitinib	378-387	mechanistic target of rapamycin kinase	Homo sapiens	4-33
21735145-5	2012	The mammalian target of rapamycin (mTOR) inhibitor everolimus was approved for use in patients who failed treatment with inhibitors of vascular endothelial growth factor (VEGF) and VEGF receptors (VEGFR) based on the results from a Phase III placebo-controlled study; however, until then, the only licensed agents across the spectrum of mRCC were VEGF(R) inhibitors (sorafenib, sunitinib and bevacizumab + interferon), and as such, a large body of evidence has accumulated regarding their use in sequence.	Sunitinib	378-387	mechanistic target of rapamycin kinase	Homo sapiens	35-39
22923165-3	2012	Recently, data from two large placebo-controlled phase III trials have demonstrated that targeted therapies directed against receptor of vascular endothelial growth factor (sunitinib) and mammalian target of rapamycin (mTOR) (everolimus) produced clinically significant improvement in patients with advanced PNETs, resulting in a doubling of progression free survival and leading to their FDA approval.	Sunitinib	173-182	vascular endothelial growth factor A	Homo sapiens	137-171
22676953-6	2012	The effects of sunitinib malate on angiogenesis and cellular proliferation were measured by immunostaining of CD31 and Ki-67.	Sunitinib	15-31	platelet/endothelial cell adhesion molecule 1	Mus musculus	110-114
22676953-10	2012	On targeted contrast-enhanced micro-ultrasound imaging, in vivo vascular endothelial growth factor receptor-2 expression was reduced in the sunitinib group and correlated with a decrease in microvessel density.	Sunitinib	140-149	kinase insert domain protein receptor	Mus musculus	64-109
20884251-15	2012	Furthermore, the bcl-2 expression was significant reduced in T24 cells in metachronous BCG and sunitinib combination treatment than single agent.	Sunitinib	95-104	BCL2 apoptosis regulator	Homo sapiens	17-22
22897944-0	2012	Soluble KIT correlates with clinical outcome in patients with metastatic breast cancer treated with sunitinib.	Sunitinib	100-109	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	8-11
22266184-0	2012	Sunitinib synergizes the antitumor effect of cisplatin via modulation of ERCC1 expression in models of gastric cancer.	Sunitinib	0-9	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	73-78
22266184-2	2012	Sunitinib showed antiproliferative effect in gastric cancer cells line with high PDGFRA expression.	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	81-87
22266184-3	2012	Knockdown of PDGFRA showed that sunitinib sensitivity was correlated with the basal expression of PDGFRA.	Sunitinib	32-41	platelet derived growth factor receptor alpha	Homo sapiens	13-19
22266184-3	2012	Knockdown of PDGFRA showed that sunitinib sensitivity was correlated with the basal expression of PDGFRA.	Sunitinib	32-41	platelet derived growth factor receptor alpha	Homo sapiens	98-104
22266184-6	2012	We found that sunitinib treatment resulted in the down-regulation of ERCC1 expression via the modulation of PDGFRA expression in gastric cancer cells.	Sunitinib	14-23	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	69-74
22266184-6	2012	We found that sunitinib treatment resulted in the down-regulation of ERCC1 expression via the modulation of PDGFRA expression in gastric cancer cells.	Sunitinib	14-23	platelet derived growth factor receptor alpha	Homo sapiens	108-114
21953673-2	2012	We here investigated whether inhibition of VEGFR signalin by sunitinib causes changes in plasma proteins associated with tumor endothelium.	Sunitinib	61-70	kinase insert domain receptor	Homo sapiens	43-48
22897944-1	2012	BACKGROUND: Sunitinib inhibits vascular endothelial growth factor receptors (VEGFRs), platelet-derived growth factor receptors, and stem cell factor receptor (KIT).	Sunitinib	12-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	159-162
21953673-9	2012	During sunitinib treatment, circulating Ang-2 and sTie-2 significantly decreased (p &lt; 0.001 for both), plasma levels of sVCAM-1 and VEGF significantly increased (p = 0.022 and p &lt; 0.001), whereas those of sICAM-1 and vWF remained stable.	Sunitinib	7-16	angiopoietin 2	Homo sapiens	40-45
21953673-9	2012	During sunitinib treatment, circulating Ang-2 and sTie-2 significantly decreased (p &lt; 0.001 for both), plasma levels of sVCAM-1 and VEGF significantly increased (p = 0.022 and p &lt; 0.001), whereas those of sICAM-1 and vWF remained stable.	Sunitinib	7-16	vascular endothelial growth factor A	Homo sapiens	135-139
22897944-10	2012	CONCLUSIONS: This exploratory analysis suggests that changes in sKIT and possibly VEGF-A early during sunitinib treatment may be predictive of clinical outcome in MBC.	Sunitinib	102-111	vascular endothelial growth factor A	Homo sapiens	82-88
21953673-9	2012	During sunitinib treatment, circulating Ang-2 and sTie-2 significantly decreased (p &lt; 0.001 for both), plasma levels of sVCAM-1 and VEGF significantly increased (p = 0.022 and p &lt; 0.001), whereas those of sICAM-1 and vWF remained stable.	Sunitinib	7-16	von Willebrand factor	Homo sapiens	223-226
21953673-13	2012	In conclusion, sunitinib-induced changes in Ang-2, sTie-2, sVCAM-1 and VEGF are related to the administration schedule, while reduction in Ang-2 is also associated with decrease in tumor burden.	Sunitinib	15-24	angiopoietin 2	Homo sapiens	44-49
22391574-0	2012	Sunitinib targets PDGF-receptor and Flt3 and reduces survival and migration of human meningioma cells.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	36-40
21953673-13	2012	In conclusion, sunitinib-induced changes in Ang-2, sTie-2, sVCAM-1 and VEGF are related to the administration schedule, while reduction in Ang-2 is also associated with decrease in tumor burden.	Sunitinib	15-24	vascular endothelial growth factor A	Homo sapiens	71-75
21953673-13	2012	In conclusion, sunitinib-induced changes in Ang-2, sTie-2, sVCAM-1 and VEGF are related to the administration schedule, while reduction in Ang-2 is also associated with decrease in tumor burden.	Sunitinib	15-24	angiopoietin 2	Homo sapiens	139-144
22207048-8	2012	The effect of VEGF, bevacizumab, and sunitinib on the phosphorylation of VEGFR-2 and downstream effecter molecules, MAPK and PI3K, was examined by western blot.	Sunitinib	37-46	kinase insert domain receptor	Homo sapiens	73-80
22207048-8	2012	The effect of VEGF, bevacizumab, and sunitinib on the phosphorylation of VEGFR-2 and downstream effecter molecules, MAPK and PI3K, was examined by western blot.	Sunitinib	37-46	mitogen-activated protein kinase 1	Homo sapiens	116-120
22207048-12	2012	VEGF/VEGFR inhibitors, bevacizumab and sunitinib, significantly decreased the motility of pancreas cancer cells.	Sunitinib	39-48	vascular endothelial growth factor A	Homo sapiens	0-4
22207048-12	2012	VEGF/VEGFR inhibitors, bevacizumab and sunitinib, significantly decreased the motility of pancreas cancer cells.	Sunitinib	39-48	kinase insert domain receptor	Homo sapiens	5-10
22207048-14	2012	Bevacizumab and sunitinib decreased the level of VEGFR-2 phosphorylation, p-ERK, and p-Akt expression.	Sunitinib	16-25	kinase insert domain receptor	Homo sapiens	49-56
22207048-14	2012	Bevacizumab and sunitinib decreased the level of VEGFR-2 phosphorylation, p-ERK, and p-Akt expression.	Sunitinib	16-25	mitogen-activated protein kinase 1	Homo sapiens	76-79
22532265-2	2012	Multiple VEGF inhibiting orally administered tyrosine kinase inhibitors (TKIs) have been approved including sunitinib, sorafenib, pazopanib and most recently, axitinib.	Sunitinib	108-117	vascular endothelial growth factor A	Homo sapiens	9-13
22336056-1	2012	BACKGROUND: This exploratory study examined the pharmacokinetics, safety, and antitumor activity of sunitinib plus docetaxel in patients with HER-2-negative advanced breast cancer.	Sunitinib	100-109	erb-b2 receptor tyrosine kinase 2	Homo sapiens	142-147
22391574-9	2012	Western blot analyses showed abolished platelet derived growth factor receptor (PDGFR)-autophosphorylation after sunitinib.	Sunitinib	113-122	platelet derived growth factor receptor beta	Homo sapiens	39-78
22391574-9	2012	Western blot analyses showed abolished platelet derived growth factor receptor (PDGFR)-autophosphorylation after sunitinib.	Sunitinib	113-122	platelet derived growth factor receptor beta	Homo sapiens	80-85
22572725-3	2012	RECENT FINDINGS: Recent studies with oral vascular endothelial growth factor receptor (VEGFR) inhibitors such as sunitinib, sorafenib and cediranib have shown disease stabilization in patients with advanced synovial sarcoma.	Sunitinib	113-122	kinase insert domain receptor	Homo sapiens	42-85
22611036-7	2012	Consistent with these results, sunitinib treatment resulted in an up-regulation of the hypoxia marker GLUT1 in PNETs, whereas anti-VEGF did not.	Sunitinib	31-40	solute carrier family 2 (facilitated glucose transporter), member 1	Mus musculus	102-107
22665524-7	2012	Notably our data indicate that sorafenib is more effective than imatinib or sunitinib for inhibiting the kinase activity of drug-resistant KIT mutants (as assessed by biochemical IC(50)).	Sunitinib	76-85	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	139-142
22463589-10	2012	Moreover, Fuhrman grading and concomitant, CXCR4 and Fuhrman grading, strongly predicted sunitinib first line therapy responsiveness on progression-free survival and overall survival.	Sunitinib	89-98	C-X-C motif chemokine receptor 4	Homo sapiens	43-48
22463589-11	2012	CONCLUSIONS: High CXCR4 expression correlates with sunitinib poor response in metastatic renal cancer.	Sunitinib	51-60	C-X-C motif chemokine receptor 4	Homo sapiens	18-23
22560921-2	2012	Sunitinib, an oral agent that inhibits the VEGF signaling pathway, may delay progression in sequence with chemotherapy.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	43-47
22020623-0	2012	PRKX, TTBK2 and RSK4 expression causes Sunitinib resistance in kidney carcinoma- and melanoma-cell lines.	Sunitinib	39-48	protein kinase X-linked	Homo sapiens	0-4
22020623-0	2012	PRKX, TTBK2 and RSK4 expression causes Sunitinib resistance in kidney carcinoma- and melanoma-cell lines.	Sunitinib	39-48	tau tubulin kinase 2	Homo sapiens	6-11
22020623-0	2012	PRKX, TTBK2 and RSK4 expression causes Sunitinib resistance in kidney carcinoma- and melanoma-cell lines.	Sunitinib	39-48	ribosomal protein S6 kinase A6	Homo sapiens	16-20
22020623-7	2012	Therefore, development of specific or multi-targeted inhibitors for these kinases for combinatorial therapy with e.g., an IL-8 neutralizing antibody might circumvent or substantially delay Sunitinib resistance formation and enhance survival prognosis.	Sunitinib	189-198	C-X-C motif chemokine ligand 8	Homo sapiens	122-126
22020623-10	2012	In line with the elevated expression of PRKX, TTBK2 or RSK4, this sensitization effect was strikingly higher in the Sunitinib resistant cell lines, suggesting an expression-based mechanism of these genes to trigger Sunitinib resistance.	Sunitinib	116-125	protein kinase X-linked	Homo sapiens	40-44
22020623-10	2012	In line with the elevated expression of PRKX, TTBK2 or RSK4, this sensitization effect was strikingly higher in the Sunitinib resistant cell lines, suggesting an expression-based mechanism of these genes to trigger Sunitinib resistance.	Sunitinib	116-125	tau tubulin kinase 2	Homo sapiens	46-51
22020623-10	2012	In line with the elevated expression of PRKX, TTBK2 or RSK4, this sensitization effect was strikingly higher in the Sunitinib resistant cell lines, suggesting an expression-based mechanism of these genes to trigger Sunitinib resistance.	Sunitinib	116-125	ribosomal protein S6 kinase A6	Homo sapiens	55-59
22020623-10	2012	In line with the elevated expression of PRKX, TTBK2 or RSK4, this sensitization effect was strikingly higher in the Sunitinib resistant cell lines, suggesting an expression-based mechanism of these genes to trigger Sunitinib resistance.	Sunitinib	215-224	protein kinase X-linked	Homo sapiens	40-44
22020623-10	2012	In line with the elevated expression of PRKX, TTBK2 or RSK4, this sensitization effect was strikingly higher in the Sunitinib resistant cell lines, suggesting an expression-based mechanism of these genes to trigger Sunitinib resistance.	Sunitinib	215-224	tau tubulin kinase 2	Homo sapiens	46-51
22020623-10	2012	In line with the elevated expression of PRKX, TTBK2 or RSK4, this sensitization effect was strikingly higher in the Sunitinib resistant cell lines, suggesting an expression-based mechanism of these genes to trigger Sunitinib resistance.	Sunitinib	215-224	ribosomal protein S6 kinase A6	Homo sapiens	55-59
22020623-11	2012	Hence, we propose that PRKX, TTBK2 and RSK4 are potential resistance markers in Sunitinib therapy and might therefore represent targets for the development of novel strategies to overcome resistance.	Sunitinib	80-89	protein kinase X-linked	Homo sapiens	23-27
22020623-11	2012	Hence, we propose that PRKX, TTBK2 and RSK4 are potential resistance markers in Sunitinib therapy and might therefore represent targets for the development of novel strategies to overcome resistance.	Sunitinib	80-89	tau tubulin kinase 2	Homo sapiens	29-34
22020623-11	2012	Hence, we propose that PRKX, TTBK2 and RSK4 are potential resistance markers in Sunitinib therapy and might therefore represent targets for the development of novel strategies to overcome resistance.	Sunitinib	80-89	ribosomal protein S6 kinase A6	Homo sapiens	39-43
22269210-0	2012	HGF/c-Met pathway is one of the mediators of sunitinib-induced tumor cell type-dependent metastasis.	Sunitinib	45-54	hepatocyte growth factor	Mus musculus	0-3
22269210-0	2012	HGF/c-Met pathway is one of the mediators of sunitinib-induced tumor cell type-dependent metastasis.	Sunitinib	45-54	met proto-oncogene	Mus musculus	4-9
22269210-7	2012	In conclusion, our findings indicate that sunitinib-induced metastasis is tumor cell-type dependent and further supports a rationale for combination of anti-angiogenics and c-Met inhibition in the clinic.	Sunitinib	42-51	met proto-oncogene	Mus musculus	173-178
22463589-0	2012	High CXCR4 expression correlates with sunitinib poor response in metastatic renal cancer.	Sunitinib	38-47	C-X-C motif chemokine receptor 4	Homo sapiens	5-10
22463589-3	2012	It was hypothesized that CXCR4 expression in primary renal cancer could predict sunitinib responsiveness.	Sunitinib	80-89	C-X-C motif chemokine receptor 4	Homo sapiens	25-30
22463589-9	2012	Low or absent CXCR4 expression predicted response to sunitinib therapy.	Sunitinib	53-62	C-X-C motif chemokine receptor 4	Homo sapiens	14-19
22572725-3	2012	RECENT FINDINGS: Recent studies with oral vascular endothelial growth factor receptor (VEGFR) inhibitors such as sunitinib, sorafenib and cediranib have shown disease stabilization in patients with advanced synovial sarcoma.	Sunitinib	113-122	kinase insert domain receptor	Homo sapiens	87-92
22213155-0	2012	Sunitinib inhibits the phosphorylation of platelet-derived growth factor receptor beta in the skin of mice with scleroderma-like features and prevents the development of the disease.	Sunitinib	0-9	platelet derived growth factor receptor, beta polypeptide	Mus musculus	42-86
23264850-6	2012	Pimozide shows a combinatorial effect with the tyrosine kinase inhibitors midostaurin (PKC412) and sunitinib in the inhibition of STAT5 tyrosine phosphorylation and the induction of apoptosis.	Sunitinib	99-108	signal transducer and activator of transcription 5A	Mus musculus	130-135
22904678-6	2012	Small-molecule tyrosine kinase inhibitor, sunitinib, caused an inhibition of VEGFR2 phosphorylation in WM239 but not in WM115 cells.	Sunitinib	42-51	kinase insert domain receptor	Homo sapiens	77-83
22080184-2	2012	This study aimed to assess the antitumor activity of sunitinib, a multi-targeted inhibitor of vascular endothelial growth factor receptor, c-kit, platelet-derived growth factor receptor, ret proto-oncogene (RET) and FMS-like tyrosine kinase 3 (FLT3), in ACC of the salivary gland.	Sunitinib	53-62	vascular endothelial growth factor A	Homo sapiens	94-128
22080184-2	2012	This study aimed to assess the antitumor activity of sunitinib, a multi-targeted inhibitor of vascular endothelial growth factor receptor, c-kit, platelet-derived growth factor receptor, ret proto-oncogene (RET) and FMS-like tyrosine kinase 3 (FLT3), in ACC of the salivary gland.	Sunitinib	53-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	139-144
22080184-2	2012	This study aimed to assess the antitumor activity of sunitinib, a multi-targeted inhibitor of vascular endothelial growth factor receptor, c-kit, platelet-derived growth factor receptor, ret proto-oncogene (RET) and FMS-like tyrosine kinase 3 (FLT3), in ACC of the salivary gland.	Sunitinib	53-62	ret proto-oncogene	Homo sapiens	187-190
22080184-2	2012	This study aimed to assess the antitumor activity of sunitinib, a multi-targeted inhibitor of vascular endothelial growth factor receptor, c-kit, platelet-derived growth factor receptor, ret proto-oncogene (RET) and FMS-like tyrosine kinase 3 (FLT3), in ACC of the salivary gland.	Sunitinib	53-62	ret proto-oncogene	Homo sapiens	207-210
22080184-2	2012	This study aimed to assess the antitumor activity of sunitinib, a multi-targeted inhibitor of vascular endothelial growth factor receptor, c-kit, platelet-derived growth factor receptor, ret proto-oncogene (RET) and FMS-like tyrosine kinase 3 (FLT3), in ACC of the salivary gland.	Sunitinib	53-62	fms related receptor tyrosine kinase 3	Homo sapiens	216-242
22080184-2	2012	This study aimed to assess the antitumor activity of sunitinib, a multi-targeted inhibitor of vascular endothelial growth factor receptor, c-kit, platelet-derived growth factor receptor, ret proto-oncogene (RET) and FMS-like tyrosine kinase 3 (FLT3), in ACC of the salivary gland.	Sunitinib	53-62	fms related receptor tyrosine kinase 3	Homo sapiens	244-248
22532600-0	2012	Modulation of Akt/mTOR signaling overcomes sunitinib resistance in renal and prostate cancer cells.	Sunitinib	43-52	AKT serine/threonine kinase 1	Homo sapiens	14-17
22532600-0	2012	Modulation of Akt/mTOR signaling overcomes sunitinib resistance in renal and prostate cancer cells.	Sunitinib	43-52	mechanistic target of rapamycin kinase	Homo sapiens	18-22
22532600-4	2012	Our experiments showed that PTEN expression inversely correlates with sunitinib resistance in renal and prostate cancer cells.	Sunitinib	70-79	phosphatase and tensin homolog	Homo sapiens	28-32
22532600-5	2012	Restoration of PTEN expression markedly increases sensitivity of tumor cells to sunitinib both in vitro and in vivo.	Sunitinib	80-89	phosphatase and tensin homolog	Homo sapiens	15-19
22532600-6	2012	In addition, pharmacologic manipulation of PI3K/Akt/mTOR signaling with PI3K/mTOR inhibitor, GDC-0980, mTOR inhibitor, temsirolimus, or pan-Akt inhibitor, GSK690693, was able to overcome sunitinib resistance in cancer cells.	Sunitinib	187-196	mechanistic target of rapamycin kinase	Homo sapiens	52-56
22532600-7	2012	Our findings underscore the importance of PTEN expression in relation to sunitinib resistance and imply a direct cytotoxic effect by sunitinib on tumor cells in addition to its antiangiogenic actions.	Sunitinib	73-82	phosphatase and tensin homolog	Homo sapiens	42-46
21956360-8	2012	Patients presented with a mean elevation of parathyroid hormone after 2.2 cycles of sunitinib.	Sunitinib	84-93	parathyroid hormone	Homo sapiens	44-63
21956360-11	2012	Parathyroid hormone elevation usually persisted but did not progress during long-term therapy with sunitinib.	Sunitinib	99-108	parathyroid hormone	Homo sapiens	0-19
22213155-12	2012	Sunitinib significantly reduced the phosphorylation of both PDGF and VEGF receptors.	Sunitinib	0-9	vascular endothelial growth factor A	Mus musculus	69-73
22213155-13	2012	CONCLUSION: Inhibition of the hyperactivated PDGF and VEGF pathways by sunitinib prevented the development of fibrosis in HOCl-induced murine SSc and may represent a new SSc treatment for testing in clinical trials.	Sunitinib	71-80	vascular endothelial growth factor A	Mus musculus	54-58
22442268-0	2012	Activation of the RAS/RAF/ERK signaling pathway contributes to resistance to sunitinib in thyroid carcinoma cell lines.	Sunitinib	77-86	zinc fingers and homeoboxes 2	Homo sapiens	22-25
22607009-2	2012	Sunitinib is an oral, small-molecule, multi-targeted receptor tyrosine kinase inhibitor (TKI) that targets a number of receptors, including vascular endothelial growth factor receptors (VEGFR) and platelet-derived growth factor receptors (PDGFR).	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	140-184
22607009-2	2012	Sunitinib is an oral, small-molecule, multi-targeted receptor tyrosine kinase inhibitor (TKI) that targets a number of receptors, including vascular endothelial growth factor receptors (VEGFR) and platelet-derived growth factor receptors (PDGFR).	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	186-191
22442268-4	2012	RESULTS: Sunitinib was found to selectively inhibit cell proliferation, induce cell accumulation in the G0-G1 phase, and inhibit the phosphorylation of ERK1/2 in both KRAS/BRAF wild-type thyroid cancer cells and in tumor cells harboring the RET/PTC rearrangement, whereas it was completely ineffective in KRAS- or BRAF-mutated thyroid carcinoma cells.	Sunitinib	9-18	mitogen-activated protein kinase 3	Homo sapiens	152-158
22442268-4	2012	RESULTS: Sunitinib was found to selectively inhibit cell proliferation, induce cell accumulation in the G0-G1 phase, and inhibit the phosphorylation of ERK1/2 in both KRAS/BRAF wild-type thyroid cancer cells and in tumor cells harboring the RET/PTC rearrangement, whereas it was completely ineffective in KRAS- or BRAF-mutated thyroid carcinoma cells.	Sunitinib	9-18	KRAS proto-oncogene, GTPase	Homo sapiens	167-171
21792888-7	2012	Molecular studies in Caki-1 showed that saracatinib alone and in combination with sunitinib inhibited phosphorylation of the cell progression regulator c-Myc in a dose-dependent manner.	Sunitinib	82-91	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	152-157
21792888-8	2012	Sunitinib alone or in combination suppressed cyclin-D1 expression with the combination showing greater dose-dependent effect.	Sunitinib	0-9	cyclin D1	Homo sapiens	45-54
21792888-9	2012	Sunitinib inhibited vascular endothelial growth factor (VEGF) secretion through the inhibition of STAT3 signaling and VEGF biosynthesis.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	56-60
21792888-9	2012	Sunitinib inhibited vascular endothelial growth factor (VEGF) secretion through the inhibition of STAT3 signaling and VEGF biosynthesis.	Sunitinib	0-9	signal transducer and activator of transcription 3	Homo sapiens	98-103
21792888-9	2012	Sunitinib inhibited vascular endothelial growth factor (VEGF) secretion through the inhibition of STAT3 signaling and VEGF biosynthesis.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	118-122
21792888-10	2012	HIF1-alpha expression in normoxic and hypoxic conditions in Caki-1 cells was inhibited by either saracatinib or sunitinib when administered alone, however, a greater reduction occurred when these compounds were given in combination.	Sunitinib	112-121	hypoxia inducible factor 1 subunit alpha	Homo sapiens	0-10
22442268-4	2012	RESULTS: Sunitinib was found to selectively inhibit cell proliferation, induce cell accumulation in the G0-G1 phase, and inhibit the phosphorylation of ERK1/2 in both KRAS/BRAF wild-type thyroid cancer cells and in tumor cells harboring the RET/PTC rearrangement, whereas it was completely ineffective in KRAS- or BRAF-mutated thyroid carcinoma cells.	Sunitinib	9-18	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	172-176
22442268-4	2012	RESULTS: Sunitinib was found to selectively inhibit cell proliferation, induce cell accumulation in the G0-G1 phase, and inhibit the phosphorylation of ERK1/2 in both KRAS/BRAF wild-type thyroid cancer cells and in tumor cells harboring the RET/PTC rearrangement, whereas it was completely ineffective in KRAS- or BRAF-mutated thyroid carcinoma cells.	Sunitinib	9-18	ret proto-oncogene	Homo sapiens	241-244
22442268-4	2012	RESULTS: Sunitinib was found to selectively inhibit cell proliferation, induce cell accumulation in the G0-G1 phase, and inhibit the phosphorylation of ERK1/2 in both KRAS/BRAF wild-type thyroid cancer cells and in tumor cells harboring the RET/PTC rearrangement, whereas it was completely ineffective in KRAS- or BRAF-mutated thyroid carcinoma cells.	Sunitinib	9-18	ret proto-oncogene	Homo sapiens	245-248
22442268-4	2012	RESULTS: Sunitinib was found to selectively inhibit cell proliferation, induce cell accumulation in the G0-G1 phase, and inhibit the phosphorylation of ERK1/2 in both KRAS/BRAF wild-type thyroid cancer cells and in tumor cells harboring the RET/PTC rearrangement, whereas it was completely ineffective in KRAS- or BRAF-mutated thyroid carcinoma cells.	Sunitinib	9-18	KRAS proto-oncogene, GTPase	Homo sapiens	305-310
22442268-4	2012	RESULTS: Sunitinib was found to selectively inhibit cell proliferation, induce cell accumulation in the G0-G1 phase, and inhibit the phosphorylation of ERK1/2 in both KRAS/BRAF wild-type thyroid cancer cells and in tumor cells harboring the RET/PTC rearrangement, whereas it was completely ineffective in KRAS- or BRAF-mutated thyroid carcinoma cells.	Sunitinib	9-18	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	314-318
22442268-0	2012	Activation of the RAS/RAF/ERK signaling pathway contributes to resistance to sunitinib in thyroid carcinoma cell lines.	Sunitinib	77-86	mitogen-activated protein kinase 1	Homo sapiens	26-29
22442268-6	2012	Of note, the constitutive activation of RAS/RAF/ERK signaling in KRAS/BRAF wild-type cells by transfection of the R12 HRAS or V600E BRAF mutants or stimulation with epithelial growth factor resulted in the loss of responsiveness to sunitinib, whereas pharmacological inhibition of MAPK kinase activity resulted in the resensitization of KRAS- or BRAF-mutated cells to the multikinase inhibitor.	Sunitinib	232-241	zinc fingers and homeoboxes 2	Homo sapiens	44-47
22442268-6	2012	Of note, the constitutive activation of RAS/RAF/ERK signaling in KRAS/BRAF wild-type cells by transfection of the R12 HRAS or V600E BRAF mutants or stimulation with epithelial growth factor resulted in the loss of responsiveness to sunitinib, whereas pharmacological inhibition of MAPK kinase activity resulted in the resensitization of KRAS- or BRAF-mutated cells to the multikinase inhibitor.	Sunitinib	232-241	mitogen-activated protein kinase 1	Homo sapiens	48-51
22442268-1	2012	CONTEXT: Sunitinib is currently being evaluated in advanced human thyroid carcinomas, based on the rationale that the vascular endothelial growth factor and platelet-derived growth factor receptors and the RET/PTC rearrangement are valuable targets for the treatment of this malignancy.	Sunitinib	9-18	vascular endothelial growth factor A	Homo sapiens	118-152
22442268-6	2012	Of note, the constitutive activation of RAS/RAF/ERK signaling in KRAS/BRAF wild-type cells by transfection of the R12 HRAS or V600E BRAF mutants or stimulation with epithelial growth factor resulted in the loss of responsiveness to sunitinib, whereas pharmacological inhibition of MAPK kinase activity resulted in the resensitization of KRAS- or BRAF-mutated cells to the multikinase inhibitor.	Sunitinib	232-241	KRAS proto-oncogene, GTPase	Homo sapiens	65-69
22442268-1	2012	CONTEXT: Sunitinib is currently being evaluated in advanced human thyroid carcinomas, based on the rationale that the vascular endothelial growth factor and platelet-derived growth factor receptors and the RET/PTC rearrangement are valuable targets for the treatment of this malignancy.	Sunitinib	9-18	ret proto-oncogene	Homo sapiens	206-209
22442268-6	2012	Of note, the constitutive activation of RAS/RAF/ERK signaling in KRAS/BRAF wild-type cells by transfection of the R12 HRAS or V600E BRAF mutants or stimulation with epithelial growth factor resulted in the loss of responsiveness to sunitinib, whereas pharmacological inhibition of MAPK kinase activity resulted in the resensitization of KRAS- or BRAF-mutated cells to the multikinase inhibitor.	Sunitinib	232-241	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	70-74
22442268-6	2012	Of note, the constitutive activation of RAS/RAF/ERK signaling in KRAS/BRAF wild-type cells by transfection of the R12 HRAS or V600E BRAF mutants or stimulation with epithelial growth factor resulted in the loss of responsiveness to sunitinib, whereas pharmacological inhibition of MAPK kinase activity resulted in the resensitization of KRAS- or BRAF-mutated cells to the multikinase inhibitor.	Sunitinib	232-241	mitogen-activated protein kinase 3	Homo sapiens	281-285
22442268-1	2012	CONTEXT: Sunitinib is currently being evaluated in advanced human thyroid carcinomas, based on the rationale that the vascular endothelial growth factor and platelet-derived growth factor receptors and the RET/PTC rearrangement are valuable targets for the treatment of this malignancy.	Sunitinib	9-18	ret proto-oncogene	Homo sapiens	210-213
22442268-6	2012	Of note, the constitutive activation of RAS/RAF/ERK signaling in KRAS/BRAF wild-type cells by transfection of the R12 HRAS or V600E BRAF mutants or stimulation with epithelial growth factor resulted in the loss of responsiveness to sunitinib, whereas pharmacological inhibition of MAPK kinase activity resulted in the resensitization of KRAS- or BRAF-mutated cells to the multikinase inhibitor.	Sunitinib	232-241	KRAS proto-oncogene, GTPase	Homo sapiens	337-342
22442268-7	2012	CONCLUSIONS: The constitutive activation of the RAS/RAF/ERK pathway may favor resistance to sunitinib in thyroid carcinoma cells.	Sunitinib	92-101	zinc fingers and homeoboxes 2	Homo sapiens	52-55
22442268-3	2012	DESIGN: The effect of activating somatic mutations in the KRAS and BRAF genes on the responsiveness to sunitinib was evaluated in a panel of thyroid cancer cell lines harboring wild-type KRAS and BRAF genes, the RET/PTC1 rearrangement, the G12R KRAS, or the V600E BRAF mutation.	Sunitinib	103-112	KRAS proto-oncogene, GTPase	Homo sapiens	58-62
22442268-7	2012	CONCLUSIONS: The constitutive activation of the RAS/RAF/ERK pathway may favor resistance to sunitinib in thyroid carcinoma cells.	Sunitinib	92-101	mitogen-activated protein kinase 1	Homo sapiens	56-59
22442268-3	2012	DESIGN: The effect of activating somatic mutations in the KRAS and BRAF genes on the responsiveness to sunitinib was evaluated in a panel of thyroid cancer cell lines harboring wild-type KRAS and BRAF genes, the RET/PTC1 rearrangement, the G12R KRAS, or the V600E BRAF mutation.	Sunitinib	103-112	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	67-71
22442268-3	2012	DESIGN: The effect of activating somatic mutations in the KRAS and BRAF genes on the responsiveness to sunitinib was evaluated in a panel of thyroid cancer cell lines harboring wild-type KRAS and BRAF genes, the RET/PTC1 rearrangement, the G12R KRAS, or the V600E BRAF mutation.	Sunitinib	103-112	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	196-200
22442268-3	2012	DESIGN: The effect of activating somatic mutations in the KRAS and BRAF genes on the responsiveness to sunitinib was evaluated in a panel of thyroid cancer cell lines harboring wild-type KRAS and BRAF genes, the RET/PTC1 rearrangement, the G12R KRAS, or the V600E BRAF mutation.	Sunitinib	103-112	ret proto-oncogene	Homo sapiens	212-215
22442268-3	2012	DESIGN: The effect of activating somatic mutations in the KRAS and BRAF genes on the responsiveness to sunitinib was evaluated in a panel of thyroid cancer cell lines harboring wild-type KRAS and BRAF genes, the RET/PTC1 rearrangement, the G12R KRAS, or the V600E BRAF mutation.	Sunitinib	103-112	patched 1	Homo sapiens	216-220
22442268-3	2012	DESIGN: The effect of activating somatic mutations in the KRAS and BRAF genes on the responsiveness to sunitinib was evaluated in a panel of thyroid cancer cell lines harboring wild-type KRAS and BRAF genes, the RET/PTC1 rearrangement, the G12R KRAS, or the V600E BRAF mutation.	Sunitinib	103-112	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	196-200
22932406-10	2012	CONCLUSION: The c-kit/PDGFRalpha genotypes after imatinib mesylate resistance may both relate to primary mutations and efficacy of sunitinib treatment.	Sunitinib	131-140	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	16-21
22579211-0	2012	Re: Targeting PIM kinase enhances the activity of sunitinib in renal cell carcinoma.	Sunitinib	50-59	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	14-17
21455800-9	2012	Both docetaxel and sunitinib malate had no effect on each other in inhibiting ERK1/2 phosphorylation in sequential treatments, while docetaxel eliminated inhibitory activity of sunitinib malate on ERK1/2 phosphorylation in concurrent treatment.	Sunitinib	177-193	mitogen-activated protein kinase 3	Homo sapiens	197-203
21455800-11	2012	Combined treatment with sunitinib malate and docetaxel had a greater therapeutic effect than monotherapy, and the first sequential scheduling was more effective than concurrent scheduling, which partly due to the effect of docetaxel on receptor tyrosine kinase (RTK) signaling pathway.	Sunitinib	24-40	ret proto-oncogene	Homo sapiens	236-260
21455800-11	2012	Combined treatment with sunitinib malate and docetaxel had a greater therapeutic effect than monotherapy, and the first sequential scheduling was more effective than concurrent scheduling, which partly due to the effect of docetaxel on receptor tyrosine kinase (RTK) signaling pathway.	Sunitinib	24-40	ret proto-oncogene	Homo sapiens	262-265
22783417-8	2012	There was a tendency for a positive correlation between the sensitivity to sunitinib and platelet-derived growth factor beta (PDGFR-beta) expression levels, which were examined by reverse transcription polymerase chain reaction.	Sunitinib	75-84	platelet derived growth factor receptor beta	Homo sapiens	126-136
22585430-3	2012	When exposed to vascular endothelial growth factor (VEGFR) inhibitors such as sunitinib, target lesions display few if any variation in tumor size, but rather detectable modifications in tumor density.	Sunitinib	78-87	vascular endothelial growth factor A	Homo sapiens	16-50
22585430-3	2012	When exposed to vascular endothelial growth factor (VEGFR) inhibitors such as sunitinib, target lesions display few if any variation in tumor size, but rather detectable modifications in tumor density.	Sunitinib	78-87	vascular endothelial growth factor A	Homo sapiens	52-57
22585430-7	2012	Choi criteria have been recently proposed as a surrogate endpoint for efficacy and to identify patients that are good responders to VEGFR inhibitors such as sunitinib and sorafenib in advanced hepatocellular carcinoma, another disease highly addicted to angiogenesis.	Sunitinib	157-166	vascular endothelial growth factor A	Homo sapiens	132-137
22592949-3	2012	Therefore, several antiangiogenic compounds have been tested in these malignancies, and among these, sunitinib has demonstrated activity in pancreatic NET patients by dually targeting the VEGFR and PDGFR pathways.	Sunitinib	101-110	kinase insert domain receptor	Homo sapiens	188-193
22592949-3	2012	Therefore, several antiangiogenic compounds have been tested in these malignancies, and among these, sunitinib has demonstrated activity in pancreatic NET patients by dually targeting the VEGFR and PDGFR pathways.	Sunitinib	101-110	platelet derived growth factor receptor beta	Homo sapiens	198-203
22932406-0	2012	[Secondary mutation of c-kit/PDGFRalpha genotypes after imatinib mesylate therapy and its relationship with efficacy of sunitinib].	Sunitinib	120-129	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-28
22932406-0	2012	[Secondary mutation of c-kit/PDGFRalpha genotypes after imatinib mesylate therapy and its relationship with efficacy of sunitinib].	Sunitinib	120-129	platelet derived growth factor receptor alpha	Homo sapiens	29-39
22932406-1	2012	OBJECTIVE: To investigate the relationship between secondary mutations of c-kit/PDGFRalpha resistance to imatinib mesylate and the efficacy of sunitinib in patients with gastrointestinal stromal tumor (GIST).	Sunitinib	143-152	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	74-79
22932406-10	2012	CONCLUSION: The c-kit/PDGFRalpha genotypes after imatinib mesylate resistance may both relate to primary mutations and efficacy of sunitinib treatment.	Sunitinib	131-140	platelet derived growth factor receptor alpha	Homo sapiens	22-32
22932406-1	2012	OBJECTIVE: To investigate the relationship between secondary mutations of c-kit/PDGFRalpha resistance to imatinib mesylate and the efficacy of sunitinib in patients with gastrointestinal stromal tumor (GIST).	Sunitinib	143-152	platelet derived growth factor receptor alpha	Homo sapiens	80-90
22344606-0	2012	Sunitinib enhances antitumor effects against chemotherapy-resistant             bladder cancer through suppression of ERK1/2 phosphorylation.	Sunitinib	0-9	mitogen-activated protein kinase 3	Homo sapiens	118-124
22568998-0	2012	Q-TWiST analysis to estimate overall benefit for patients with metastatic renal cell carcinoma treated in a phase III trial of sunitinib vs interferon-alpha.	Sunitinib	127-136	twist family bHLH transcription factor 1	Homo sapiens	0-7
22568998-6	2012	RESULTS: Q-TWiST scores showed that quality-adjusted survival time was greater with sunitinib than with IFN-alpha, even though certain grade 3/4 toxicities occurred more frequently with sunitinib.	Sunitinib	84-93	twist family bHLH transcription factor 1	Homo sapiens	11-16
22568998-9	2012	CONCLUSION: Patients randomised to sunitinib had longer clinical benefit, defined as Q-TWiST scores, than patients randomised to IFN-alpha.	Sunitinib	35-44	twist family bHLH transcription factor 1	Homo sapiens	85-92
22969964-6	2012	Combination therapy using the multi-tyrosine kinase inhibitors, sorafenib or sunitinib, with S-1 against breast cancer (MX-1 cell line) and NSCLC (NCI-H460 cell line) was significantly superior to either monotherapy (P&lt;0.01).	Sunitinib	77-86	proteasome 26S subunit, non-ATPase 1	Homo sapiens	93-96
22314934-0	2012	Antitumor effect of vascular endothelial growth factor inhibitor sunitinib in preclinical models of hepatocellular carcinoma.	Sunitinib	65-74	vascular endothelial growth factor A	Homo sapiens	20-54
22314934-4	2012	Recently, another VEGF inhibitor, sunitinib, showed survival benefits in HCC hepatitis B-positive patients, but failed to improve survival in HCC hepatitis C-positive patients.	Sunitinib	34-43	vascular endothelial growth factor A	Homo sapiens	18-22
22314934-9	2012	RESULTS: Sunitinib has the potential to moderately inhibit proliferation in the Huh7.5 cell line, induce p53 in the p53-wild-type cell line SK-hep-1, and to increase the S-phase and the sub-G1 component of the cell cycle in the Hep3B cell line.	Sunitinib	9-18	tumor protein p53	Homo sapiens	105-108
22314934-9	2012	RESULTS: Sunitinib has the potential to moderately inhibit proliferation in the Huh7.5 cell line, induce p53 in the p53-wild-type cell line SK-hep-1, and to increase the S-phase and the sub-G1 component of the cell cycle in the Hep3B cell line.	Sunitinib	9-18	tumor protein p53	Homo sapiens	116-119
22314934-9	2012	RESULTS: Sunitinib has the potential to moderately inhibit proliferation in the Huh7.5 cell line, induce p53 in the p53-wild-type cell line SK-hep-1, and to increase the S-phase and the sub-G1 component of the cell cycle in the Hep3B cell line.	Sunitinib	9-18	DNL-type zinc finger	Homo sapiens	143-148
22344606-4	2012	We hypothesized that sunitinib would             be effective in bladder cancer as it is an oral inhibitor of multiple receptor             tyrosine kinases, including VEGF receptors, platelet derived growth factor (PDGF)             receptors and stem cell factor receptor (c-KIT), and is a standard first-line             treatment of advanced clear cell renal carcinoma.	Sunitinib	21-30	vascular endothelial growth factor A	Homo sapiens	168-172
22344606-4	2012	We hypothesized that sunitinib would             be effective in bladder cancer as it is an oral inhibitor of multiple receptor             tyrosine kinases, including VEGF receptors, platelet derived growth factor (PDGF)             receptors and stem cell factor receptor (c-KIT), and is a standard first-line             treatment of advanced clear cell renal carcinoma.	Sunitinib	21-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	275-280
22437942-4	2012	(Function of activation loop tyrosine phosphorylation in the mechanism of c-Kit autoactivation and its implication in sunitinib resistance.	Sunitinib	118-127	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	74-79
22344606-5	2012	In the present study, the antiproliferative             effects of sunitinib were clearly demonstrated in KK47, KK47/DDP20 and KK47/ADR             cell lines in vitro due to the suppression of ERK1/2 phosphorylation.	Sunitinib	67-76	mitogen-activated protein kinase 3	Homo sapiens	194-200
22444679-1	2012	Sunitinib  (SU11248) is a highly potent tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor (VEGFR).	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	76-119
22484816-4	2012	Here, we show that semaphorin 3A (Sema3A) expression overcomes the proinvasive and prometastatic resistance observed upon angiogenesis reduction by the small-molecule tyrosine inhibitor sunitinib in both pancreatic neuroendocrine tumors (PNETs) in RIP-Tag2 mice and cervical carcinomas in HPV16/E2 mice.	Sunitinib	186-195	sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3A	Mus musculus	19-32
22484816-4	2012	Here, we show that semaphorin 3A (Sema3A) expression overcomes the proinvasive and prometastatic resistance observed upon angiogenesis reduction by the small-molecule tyrosine inhibitor sunitinib in both pancreatic neuroendocrine tumors (PNETs) in RIP-Tag2 mice and cervical carcinomas in HPV16/E2 mice.	Sunitinib	186-195	sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3A	Mus musculus	34-40
22484816-5	2012	By improving cancer tissue oxygenation and extending the normalization window, Sema3A counteracted sunitinib-induced activation of HIF-1alpha, Met tyrosine kinase receptor, epithelial-mesenchymal transition (EMT), and other hypoxia-dependent signaling pathways.	Sunitinib	99-108	sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3A	Mus musculus	79-85
22484816-5	2012	By improving cancer tissue oxygenation and extending the normalization window, Sema3A counteracted sunitinib-induced activation of HIF-1alpha, Met tyrosine kinase receptor, epithelial-mesenchymal transition (EMT), and other hypoxia-dependent signaling pathways.	Sunitinib	99-108	hypoxia inducible factor 1, alpha subunit	Mus musculus	131-141
22048125-3	2012	Injection of sunitinib malate, AMPK inhibitor, to the mice lowered AV formation in their brains.	Sunitinib	13-29	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	31-35
22326847-2	2012	We tested, if the cytotoxic cancer therapy doxorubicin (Doxo) or the anti-angiogenic therapy sunitinib alters viability and VEGF signaling in primary cardiac microvascular endothelial cells (CMEC) and adult rat ventricular myocytes (ARVM).	Sunitinib	93-102	vascular endothelial growth factor A	Rattus norvegicus	124-128
22326847-14	2012	VEGF receptor 2 amounts were reduced by Doxo and by sunitinib in a dose-dependent manner in both CMEC and ARVM.	Sunitinib	52-61	vascular endothelial growth factor A	Rattus norvegicus	0-4
22444679-1	2012	Sunitinib  (SU11248) is a highly potent tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor (VEGFR).	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	121-126
21633954-5	2012	In vitro, sunitinib inhibited PDGFR phosphorylation on MC38-CEA cells at concentrations similar to those biologically available during human treatment.	Sunitinib	10-19	CEA cell adhesion molecule 3	Homo sapiens	60-63
22444679-1	2012	Sunitinib  (SU11248) is a highly potent tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor (VEGFR).	Sunitinib	12-19	kinase insert domain receptor	Homo sapiens	76-119
21633954-7	2012	In a model using CEA-Tg mice bearing CEA(+)  tumors, continuous sunitinib followed by vaccine increased intratumoral infiltration of antigen-specific T lymphocytes, decreased immunosuppressant T regulatory cells and myeloid-derived suppressor cells, reduced tumor volumes and increased survival.	Sunitinib	64-73	carcinoembryonic antigen gene family	Mus musculus	17-20
21633954-7	2012	In a model using CEA-Tg mice bearing CEA(+)  tumors, continuous sunitinib followed by vaccine increased intratumoral infiltration of antigen-specific T lymphocytes, decreased immunosuppressant T regulatory cells and myeloid-derived suppressor cells, reduced tumor volumes and increased survival.	Sunitinib	64-73	carcinoembryonic antigen gene family	Mus musculus	37-40
22444679-1	2012	Sunitinib  (SU11248) is a highly potent tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor (VEGFR).	Sunitinib	12-19	kinase insert domain receptor	Homo sapiens	121-126
21882181-5	2012	RESULTS: VEGF SNP -634 genotype was associated with the prevalence and duration of sunitinib-induced hypertension (as defined by systolic pressure &gt;=150 mmHg and/or diastolic pressure &gt;=90 mmHg) in both univariable analysis (P = .03 and .01, respectively) and multivariable analysis, which adjusted for baseline BP and use of antihypertension medication (P = .05 and .02, respectively).	Sunitinib	83-92	vascular endothelial growth factor A	Homo sapiens	9-13
21882181-9	2012	CONCLUSIONS: In MCCRCC patients treated with sunitinib, VEGF SNP -634 is associated with hypertension and a combination of VEGF SNP 936 and VEGFR2 SNP 889 genotypes is associated with overall survival.	Sunitinib	45-54	vascular endothelial growth factor A	Homo sapiens	56-60
21898375-2	2012	Everolimus, an oral mTOR inhibitor, and sunitinib, an oral tyrosine kinase inhibitor targeting VEGF, are standard agents in the management of metastatic RCC.	Sunitinib	40-49	vascular endothelial growth factor A	Homo sapiens	95-99
22179104-1	2012	PURPOSE: Sunitinib is an oral tyrosine kinase inhibitor of VEGF, PDGF, c-KIT, and flt-3 receptors.	Sunitinib	9-18	vascular endothelial growth factor A	Homo sapiens	59-63
22338018-4	2012	And, recent phase III studies showed both everolimus and sunitinib improved progression-free survival in pancreatic NETs, validating the phosphoinositide 3-kinase/Akt/mTOR pathway and angiogenesis as important targets for further advances.	Sunitinib	57-66	AKT serine/threonine kinase 1	Homo sapiens	163-166
22338018-4	2012	And, recent phase III studies showed both everolimus and sunitinib improved progression-free survival in pancreatic NETs, validating the phosphoinositide 3-kinase/Akt/mTOR pathway and angiogenesis as important targets for further advances.	Sunitinib	57-66	mechanistic target of rapamycin kinase	Homo sapiens	167-171
22238213-0	2012	P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) restrict brain accumulation of the active sunitinib metabolite N-desethyl sunitinib.	Sunitinib	110-119	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	16-21
20960028-1	2012	BACKGROUND: Sunitinib is an oral multitargeted tyrosine kinase inhibitor of vascular endothelial growth factor and platelet-derived growth factor receptors, as well as of other receptor types.	Sunitinib	12-21	vascular endothelial growth factor A	Homo sapiens	76-110
21104107-7	2012	The superior efficacy of sunitinib against GISTs with KIT exon 9 mutations appears to be similar in Korean patients to Western experience although statistical significance was not secured.	Sunitinib	25-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	54-57
22237457-11	2012	CONCLUSIONS: VEGFR TKIs, especially sunitinib, are active and tolerated by mRCC patients with poor risk features.	Sunitinib	36-45	kinase insert domain receptor	Homo sapiens	13-18
22238213-0	2012	P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) restrict brain accumulation of the active sunitinib metabolite N-desethyl sunitinib.	Sunitinib	110-119	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	61-66
22238213-7	2012	In the absence of the ABCB1 and ABCG2 inhibitor elacridar, brain concentrations of N-desethyl sunitinib were detectable only in Abcb1a/1b(-/-)/Abcg2(-/-) mice after sunitinib administration.	Sunitinib	94-103	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	128-134
22238213-7	2012	In the absence of the ABCB1 and ABCG2 inhibitor elacridar, brain concentrations of N-desethyl sunitinib were detectable only in Abcb1a/1b(-/-)/Abcg2(-/-) mice after sunitinib administration.	Sunitinib	94-103	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	143-148
21878661-0	2012	Sunitinib induces apoptosis in pheochromocytoma tumor cells by inhibiting VEGFR2/Akt/mTOR/S6K1 pathways through modulation of Bcl-2 and BAD.	Sunitinib	0-9	kinase insert domain receptor	Rattus norvegicus	74-80
22331954-1	2012	PURPOSE: To investigate whether sunitinib plus docetaxel improves clinical outcomes for patients with human epidermal growth factor receptor 2 (HER2)/neu-negative advanced breast cancer (ABC) versus docetaxel alone.	Sunitinib	32-41	erb-b2 receptor tyrosine kinase 2	Homo sapiens	108-142
22331954-1	2012	PURPOSE: To investigate whether sunitinib plus docetaxel improves clinical outcomes for patients with human epidermal growth factor receptor 2 (HER2)/neu-negative advanced breast cancer (ABC) versus docetaxel alone.	Sunitinib	32-41	erb-b2 receptor tyrosine kinase 2	Homo sapiens	144-148
21878661-0	2012	Sunitinib induces apoptosis in pheochromocytoma tumor cells by inhibiting VEGFR2/Akt/mTOR/S6K1 pathways through modulation of Bcl-2 and BAD.	Sunitinib	0-9	AKT serine/threonine kinase 1	Rattus norvegicus	81-84
21878661-0	2012	Sunitinib induces apoptosis in pheochromocytoma tumor cells by inhibiting VEGFR2/Akt/mTOR/S6K1 pathways through modulation of Bcl-2 and BAD.	Sunitinib	0-9	mechanistic target of rapamycin kinase	Rattus norvegicus	85-89
21878661-0	2012	Sunitinib induces apoptosis in pheochromocytoma tumor cells by inhibiting VEGFR2/Akt/mTOR/S6K1 pathways through modulation of Bcl-2 and BAD.	Sunitinib	0-9	ribosomal protein S6 kinase B1	Rattus norvegicus	90-94
21878661-0	2012	Sunitinib induces apoptosis in pheochromocytoma tumor cells by inhibiting VEGFR2/Akt/mTOR/S6K1 pathways through modulation of Bcl-2 and BAD.	Sunitinib	0-9	BCL2, apoptosis regulator	Rattus norvegicus	126-131
21878661-1	2012	Sunitinib is an oral multitargeted receptor tyrosine kinase inhibitor with antiangiogenic and antitumor activity that mainly targets vascular endothelial growth factor receptors (VEGFRs).	Sunitinib	0-9	kinase insert domain receptor	Rattus norvegicus	179-185
21878661-5	2012	Furthermore, in support of these findings, we found that sunitinib induced a reduction in the expression of the antiapoptotic molecule Bcl-2 as well as dephosphorylation of the proapoptotic molecule BAD, which results in the activation of BAD in these cells.	Sunitinib	57-66	BCL2, apoptosis regulator	Rattus norvegicus	135-140
21878661-6	2012	Consistent with these apoptotic effects, our results showed that sunitinib inhibited phosphorylation of Akt and mTOR and was followed by a reduction of S6K1, which is a well-known target of mTOR.	Sunitinib	65-74	AKT serine/threonine kinase 1	Rattus norvegicus	104-107
21878661-6	2012	Consistent with these apoptotic effects, our results showed that sunitinib inhibited phosphorylation of Akt and mTOR and was followed by a reduction of S6K1, which is a well-known target of mTOR.	Sunitinib	65-74	mechanistic target of rapamycin kinase	Rattus norvegicus	112-116
21878661-6	2012	Consistent with these apoptotic effects, our results showed that sunitinib inhibited phosphorylation of Akt and mTOR and was followed by a reduction of S6K1, which is a well-known target of mTOR.	Sunitinib	65-74	ribosomal protein S6 kinase B1	Rattus norvegicus	152-156
21878661-6	2012	Consistent with these apoptotic effects, our results showed that sunitinib inhibited phosphorylation of Akt and mTOR and was followed by a reduction of S6K1, which is a well-known target of mTOR.	Sunitinib	65-74	mechanistic target of rapamycin kinase	Rattus norvegicus	190-194
21878661-7	2012	Knockdown of VEGFR-2 attenuated the sunitinib-induced effects, including apoptosis and inhibition of signaling pathways such as the phosphorylation of Akt as well as mTOR, and Bcl-2, which confirmed that these effects could be mediated by VEGFR-2.	Sunitinib	36-45	kinase insert domain receptor	Rattus norvegicus	13-20
21878661-7	2012	Knockdown of VEGFR-2 attenuated the sunitinib-induced effects, including apoptosis and inhibition of signaling pathways such as the phosphorylation of Akt as well as mTOR, and Bcl-2, which confirmed that these effects could be mediated by VEGFR-2.	Sunitinib	36-45	AKT serine/threonine kinase 1	Rattus norvegicus	151-154
21878661-7	2012	Knockdown of VEGFR-2 attenuated the sunitinib-induced effects, including apoptosis and inhibition of signaling pathways such as the phosphorylation of Akt as well as mTOR, and Bcl-2, which confirmed that these effects could be mediated by VEGFR-2.	Sunitinib	36-45	mechanistic target of rapamycin kinase	Rattus norvegicus	166-170
21878661-7	2012	Knockdown of VEGFR-2 attenuated the sunitinib-induced effects, including apoptosis and inhibition of signaling pathways such as the phosphorylation of Akt as well as mTOR, and Bcl-2, which confirmed that these effects could be mediated by VEGFR-2.	Sunitinib	36-45	BCL2, apoptosis regulator	Rattus norvegicus	176-181
21878661-7	2012	Knockdown of VEGFR-2 attenuated the sunitinib-induced effects, including apoptosis and inhibition of signaling pathways such as the phosphorylation of Akt as well as mTOR, and Bcl-2, which confirmed that these effects could be mediated by VEGFR-2.	Sunitinib	36-45	kinase insert domain receptor	Rattus norvegicus	239-246
21878661-8	2012	In addition, silencing of S6K1 induced apoptosis accompanied by a decrease in the phosphorylation of BAD and Bcl-2, similar to that observed with sunitinib treatment.	Sunitinib	146-155	ribosomal protein S6 kinase B1	Rattus norvegicus	26-30
21878661-9	2012	Thus, these results together suggest that sunitinib initially exerts its apoptotic effect through the inhibition of VEGFR-2, which, when followed by reduction of its downstream effectors, including Akt/mTOR/S6K1, may lead to inhibition of the antiapoptotic molecule Bcl-2 and activation of the proapoptotic molecule BAD in PC12 cells.	Sunitinib	42-51	kinase insert domain receptor	Rattus norvegicus	116-123
21878661-9	2012	Thus, these results together suggest that sunitinib initially exerts its apoptotic effect through the inhibition of VEGFR-2, which, when followed by reduction of its downstream effectors, including Akt/mTOR/S6K1, may lead to inhibition of the antiapoptotic molecule Bcl-2 and activation of the proapoptotic molecule BAD in PC12 cells.	Sunitinib	42-51	AKT serine/threonine kinase 1	Rattus norvegicus	198-201
21878661-9	2012	Thus, these results together suggest that sunitinib initially exerts its apoptotic effect through the inhibition of VEGFR-2, which, when followed by reduction of its downstream effectors, including Akt/mTOR/S6K1, may lead to inhibition of the antiapoptotic molecule Bcl-2 and activation of the proapoptotic molecule BAD in PC12 cells.	Sunitinib	42-51	mechanistic target of rapamycin kinase	Rattus norvegicus	202-206
21878661-9	2012	Thus, these results together suggest that sunitinib initially exerts its apoptotic effect through the inhibition of VEGFR-2, which, when followed by reduction of its downstream effectors, including Akt/mTOR/S6K1, may lead to inhibition of the antiapoptotic molecule Bcl-2 and activation of the proapoptotic molecule BAD in PC12 cells.	Sunitinib	42-51	ribosomal protein S6 kinase B1	Rattus norvegicus	207-211
21878661-9	2012	Thus, these results together suggest that sunitinib initially exerts its apoptotic effect through the inhibition of VEGFR-2, which, when followed by reduction of its downstream effectors, including Akt/mTOR/S6K1, may lead to inhibition of the antiapoptotic molecule Bcl-2 and activation of the proapoptotic molecule BAD in PC12 cells.	Sunitinib	42-51	BCL2, apoptosis regulator	Rattus norvegicus	266-271
22585997-5	2012	A similar benefit was found in orthotopic Panc-1 pancreatic carcinomas treated with sunitinib plus PF-04217903 and in RIP-Tag2 tumors treated with XL184 (cabozantinib), which simultaneously blocks VEGF and c-Met signaling.	Sunitinib	84-93	pancreas protein 1	Mus musculus	42-48
22369443-8	2012	However, the decision to use either high-dose imatinib or sunitinib should be based on the underlying cause of failure on imatinib, KIT mutational status and on whether the patient is intolerant of or has developed a resistance to imatinib.	Sunitinib	58-67	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	132-135
22399609-4	2012	RESULTS: Mono-Mac 1 cells had inhibited proliferation and extracellular-signal regulated kinase activity as a result of CSF-1R inhibition and a dose-dependent increase in CSF-1R expression with both sunitinib and cFMS-I.	Sunitinib	199-208	integrin subunit alpha M	Homo sapiens	14-19
22399609-4	2012	RESULTS: Mono-Mac 1 cells had inhibited proliferation and extracellular-signal regulated kinase activity as a result of CSF-1R inhibition and a dose-dependent increase in CSF-1R expression with both sunitinib and cFMS-I.	Sunitinib	199-208	colony stimulating factor 1 receptor	Homo sapiens	171-177
22399609-5	2012	CONCLUSION: Our results suggest potential for CSF-1R as an important target of sunitinib or other similar drugs.	Sunitinib	79-88	colony stimulating factor 1 receptor	Homo sapiens	46-52
22261812-0	2012	Sunitinib therapy for melanoma patients with KIT mutations.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-48
22261812-2	2012	We aimed to assess the predictive role of KIT mutation, amplification, or overexpression for response to treatment with the kinase inhibitor sunitinib.	Sunitinib	141-150	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	42-45
22261812-4	2012	Patients with mutations, amplifications, or overexpression of KIT were treated with sunitinib and responses measured by Response Evaluation Criteria in Solid Tumors (RECIST).	Sunitinib	84-93	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-65
22261812-11	2012	CONCLUSIONS: Sunitinib may have activity in patients with melanoma and KIT mutations; more study is needed.	Sunitinib	13-22	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-74
22369324-9	2012	presented retrospective data showing that retreatment with VEGF-directed targeted agents, including sunitinib, bevacizumab/interferon, dovitinib and sorafenib, was associated with a progression-free survival time of approximately 5 months.	Sunitinib	100-109	vascular endothelial growth factor A	Homo sapiens	59-63
21445973-5	2012	Examination of intracellular signaling found that Akt/ mammalian target of rapamycin (mTOR) signaling remained activated in GIST-T1R but not in parental GIST-T1 cells, after exposure of these cells to sunitinib, as measured by immunoblotting.	Sunitinib	201-210	mechanistic target of rapamycin kinase	Homo sapiens	55-84
22115851-0	2012	RhoB mediates antitumor synergy of combined ixabepilone and sunitinib in human ovarian serous cancer.	Sunitinib	60-69	ras homolog family member B	Homo sapiens	0-4
22115851-6	2012	The GTPase, RhoB, was synergistically upregulated in cells treated with ixabepilone and sunitinib.	Sunitinib	88-97	ras homolog family member B	Homo sapiens	12-16
22115851-9	2012	CONCLUSIONS: Ixabepilone plus sunitinib demonstrated antitumor synergy via RhoB in naive and paclitaxel-resistant cells resulting in apoptosis.	Sunitinib	30-39	ras homolog family member B	Homo sapiens	75-79
22115851-11	2012	RhoB could be envisioned as an early biomarker of response to therapy in a planned Phase II clinical trial to assess the efficacy of ixabepilone combined with a receptor tyrosine kinase inhibitor such as sunitinib.	Sunitinib	204-213	ras homolog family member B	Homo sapiens	0-4
25806151-3	2012	Thus, this system has become the focus of therapeutic interventions, which led to the approval of the anti-VEGF blocking antibody bevacizumab and the VEGFR-2 pathway inhibitors pazopanib, sorafenib and sunitinib.	Sunitinib	202-211	vascular endothelial growth factor A	Homo sapiens	107-111
25806151-3	2012	Thus, this system has become the focus of therapeutic interventions, which led to the approval of the anti-VEGF blocking antibody bevacizumab and the VEGFR-2 pathway inhibitors pazopanib, sorafenib and sunitinib.	Sunitinib	202-211	kinase insert domain receptor	Homo sapiens	150-157
22308314-6	2012	We further show that the Akt/beta-catenin cancer stem cell regulatory pathway is activated in breast cancer cells under hypoxic conditions in vitro and in sunitinib-treated mouse xenografts.	Sunitinib	155-164	thymoma viral proto-oncogene 1	Mus musculus	25-28
22308314-6	2012	We further show that the Akt/beta-catenin cancer stem cell regulatory pathway is activated in breast cancer cells under hypoxic conditions in vitro and in sunitinib-treated mouse xenografts.	Sunitinib	155-164	catenin (cadherin associated protein), beta 1	Mus musculus	29-41
21445973-0	2012	Long-term exposure of gastrointestinal stromal tumor cells to sunitinib induces epigenetic silencing of the PTEN gene.	Sunitinib	62-71	phosphatase and tensin homolog	Homo sapiens	108-112
21445973-5	2012	Examination of intracellular signaling found that Akt/ mammalian target of rapamycin (mTOR) signaling remained activated in GIST-T1R but not in parental GIST-T1 cells, after exposure of these cells to sunitinib, as measured by immunoblotting.	Sunitinib	201-210	AKT serine/threonine kinase 1	Homo sapiens	50-53
21445973-5	2012	Examination of intracellular signaling found that Akt/ mammalian target of rapamycin (mTOR) signaling remained activated in GIST-T1R but not in parental GIST-T1 cells, after exposure of these cells to sunitinib, as measured by immunoblotting.	Sunitinib	201-210	mechanistic target of rapamycin kinase	Homo sapiens	86-90
21445973-7	2012	Notably, forced-expression of PTEN in GIST-T1R cells negatively regulated the Akt/mTOR pathways and sensitized these cells to sunitinib-mediated growth arrest and apoptosis.	Sunitinib	126-135	phosphatase and tensin homolog	Homo sapiens	30-34
21445974-0	2012	Inhibition of activated receptor tyrosine kinases by Sunitinib induces growth arrest and sensitizes melanoma cells to Bortezomib by blocking Akt pathway.	Sunitinib	53-62	AKT serine/threonine kinase 1	Homo sapiens	141-144
21445974-6	2012	Moreover, the two metastatic melanoma cell lines harbored an activated receptor (PDGFRalpha and VEGFR, respectively), and Sunitinib suppressed the phosphorylation of the RTKs and their downstream targets Akt and ribosomal protein S6, in these two cell lines.	Sunitinib	122-131	kinase insert domain receptor	Homo sapiens	96-101
21445974-6	2012	Moreover, the two metastatic melanoma cell lines harbored an activated receptor (PDGFRalpha and VEGFR, respectively), and Sunitinib suppressed the phosphorylation of the RTKs and their downstream targets Akt and ribosomal protein S6, in these two cell lines.	Sunitinib	122-131	AKT serine/threonine kinase 1	Homo sapiens	204-207
21445974-6	2012	Moreover, the two metastatic melanoma cell lines harbored an activated receptor (PDGFRalpha and VEGFR, respectively), and Sunitinib suppressed the phosphorylation of the RTKs and their downstream targets Akt and ribosomal protein S6, in these two cell lines.	Sunitinib	122-131	ribosomal protein S6	Homo sapiens	212-232
21445974-10	2012	Moreover, LY294002, a PI3K inhibitor, sensitized melanoma cells to Bortezomib treatment, suggesting that downregulation of phospho-Akt by Sunitinib mediates the synergy obtained by Bortezomib + Sunitinib cotreatment.	Sunitinib	138-147	AKT serine/threonine kinase 1	Homo sapiens	131-134
21445974-10	2012	Moreover, LY294002, a PI3K inhibitor, sensitized melanoma cells to Bortezomib treatment, suggesting that downregulation of phospho-Akt by Sunitinib mediates the synergy obtained by Bortezomib + Sunitinib cotreatment.	Sunitinib	194-203	AKT serine/threonine kinase 1	Homo sapiens	131-134
22395469-8	2012	After PTK/ZK or sunitinib treatment, no-VEGFR-methylation cancer cells showed dose- or time-dependent decreases in proliferation.	Sunitinib	16-25	kinase insert domain receptor	Homo sapiens	40-45
22866542-0	2012	Structural and functional analysis of KIT gene encoding receptor tyrosine kinase and its interaction with sunitinib and HDAC inhibitors: an in silico approach.	Sunitinib	106-115	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	38-41
22078005-2	2012	Since then, vascular endothelial growth factor (VEGF) has been identified as the most potent cytokine to induce angiogenesis and drugs targeting VEGF, principally the humanized monoclonal antibody bevacizumab and the tyrosine kinase inhibitors sunitinib and sorafenib, have proven therapeutic benefit.	Sunitinib	244-253	vascular endothelial growth factor A	Homo sapiens	12-46
22078005-2	2012	Since then, vascular endothelial growth factor (VEGF) has been identified as the most potent cytokine to induce angiogenesis and drugs targeting VEGF, principally the humanized monoclonal antibody bevacizumab and the tyrosine kinase inhibitors sunitinib and sorafenib, have proven therapeutic benefit.	Sunitinib	244-253	vascular endothelial growth factor A	Homo sapiens	48-52
22450834-6	2012	After one course of sunitinib, mental status was altered due to hypercalcemia (serum calcium level was 18.6 mg/dl and PTH-rP was 3.7 pmol/l).	Sunitinib	20-29	parathyroid hormone like hormone	Homo sapiens	118-124
22866542-0	2012	Structural and functional analysis of KIT gene encoding receptor tyrosine kinase and its interaction with sunitinib and HDAC inhibitors: an in silico approach.	Sunitinib	106-115	ret proto-oncogene	Homo sapiens	56-80
22866542-4	2012	In this study, a computational analysis to detect the most deleterious nonsynonymous SNPs of KIT gene was performed and investigated its binding affinity to native and predicted mutant protein structure (D816V) with sunitinib and HDAC (Trichostatin A and Panobinostat) inhibitors was investigated.	Sunitinib	216-225	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-96
24451769-4	2012	Further, vascular endothelial growth factor receptor (VEGF-R) inhibitory agents including sorafenib, sunitinib, pazopanib, and axitinib that are already approved in the United States for use in advanced renal cell carcinoma have shown high response rates in treating advanced DTCs in multiple phase II trials, and have become commonly used in progressive radioiodine-refractory metastatic DTC.	Sunitinib	101-110	kinase insert domain receptor	Homo sapiens	9-52
22497103-15	2012	Sunitinib, recommended by NICE, is administered orally and acts by inhibiting the VEGF receptor.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	82-86
22191389-2	2012	The multikinase inhibitor Sunitinib has been shown to inhibit the kinase activity of the RET oncogene and reduce proliferation in differentiated thyroid cancer cells harboring the RET/PTC rearrangement.	Sunitinib	26-35	ret proto-oncogene	Homo sapiens	89-92
22191389-2	2012	The multikinase inhibitor Sunitinib has been shown to inhibit the kinase activity of the RET oncogene and reduce proliferation in differentiated thyroid cancer cells harboring the RET/PTC rearrangement.	Sunitinib	26-35	ret proto-oncogene	Homo sapiens	180-183
22191389-5	2012	RESULTS: Exposure to nanomolar concentrations of Sunitinib significantly reduced cell viability in only TPC-1 cells, and this effect was paralleled by reduction of cyclin D1 levels.	Sunitinib	49-58	two pore segment channel 1	Homo sapiens	104-109
22191389-5	2012	RESULTS: Exposure to nanomolar concentrations of Sunitinib significantly reduced cell viability in only TPC-1 cells, and this effect was paralleled by reduction of cyclin D1 levels.	Sunitinib	49-58	cyclin D1	Homo sapiens	164-173
21933194-7	2012	Spleen cells from sunitinib-treated mice contained smaller numbers of antigen-specific IgG-producing cells and secreted lower amounts of both Th1 and Th2 cytokines than those of the control mice, whereas the levels of antigen-specific antibodies in serum were not decreased.	Sunitinib	18-27	negative elongation factor complex member C/D, Th1l	Mus musculus	142-145
21933194-7	2012	Spleen cells from sunitinib-treated mice contained smaller numbers of antigen-specific IgG-producing cells and secreted lower amounts of both Th1 and Th2 cytokines than those of the control mice, whereas the levels of antigen-specific antibodies in serum were not decreased.	Sunitinib	18-27	heart and neural crest derivatives expressed 2	Mus musculus	150-153
21933194-8	2012	The reactions and MMCP-1 release in oral antigen-induced anaphylaxis and passive systemic anaphylaxis were attenuated even by a single predose of sunitinib.	Sunitinib	146-155	mast cell protease 9	Mus musculus	18-24
24451769-4	2012	Further, vascular endothelial growth factor receptor (VEGF-R) inhibitory agents including sorafenib, sunitinib, pazopanib, and axitinib that are already approved in the United States for use in advanced renal cell carcinoma have shown high response rates in treating advanced DTCs in multiple phase II trials, and have become commonly used in progressive radioiodine-refractory metastatic DTC.	Sunitinib	101-110	kinase insert domain receptor	Homo sapiens	54-60
21699503-2	2012	Indolinones (e.g. SU5416 and Sutent) and anilinophthalazines (e.g. PTK787) are potent small molecule inhibitors of VEGFR2 and other tyrosine kinases, but their effects on VEGF-A- and bFGF-stimulated endothelial responses are unclear.	Sunitinib	29-35	kinase insert domain receptor	Homo sapiens	115-121
21699503-2	2012	Indolinones (e.g. SU5416 and Sutent) and anilinophthalazines (e.g. PTK787) are potent small molecule inhibitors of VEGFR2 and other tyrosine kinases, but their effects on VEGF-A- and bFGF-stimulated endothelial responses are unclear.	Sunitinib	29-35	vascular endothelial growth factor A	Homo sapiens	171-177
21699503-2	2012	Indolinones (e.g. SU5416 and Sutent) and anilinophthalazines (e.g. PTK787) are potent small molecule inhibitors of VEGFR2 and other tyrosine kinases, but their effects on VEGF-A- and bFGF-stimulated endothelial responses are unclear.	Sunitinib	29-35	fibroblast growth factor 2	Homo sapiens	183-187
21699503-7	2012	Sutent is a potent inhibitor of both VEGFR2 and FGFR1 tyrosine kinase activity in vitro.	Sunitinib	0-6	kinase insert domain receptor	Homo sapiens	37-43
21699503-7	2012	Sutent is a potent inhibitor of both VEGFR2 and FGFR1 tyrosine kinase activity in vitro.	Sunitinib	0-6	fibroblast growth factor receptor 1	Homo sapiens	48-53
22673043-0	2012	Impact of genetic variation in breast cancer resistance protein (BCRP/ABCG2) on sunitinib pharmacokinetics.	Sunitinib	80-89	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	31-63
22814298-6	2012	A 48 h exposure to sunitinib (10 microM) significantly decreased forward scatter and increased annexin-V-binding, effects paralleled by significant increase of [Ca(2+)](i).	Sunitinib	19-28	annexin A5	Homo sapiens	95-104
22814298-8	2012	Sunitinib induced annexin-V-binding was slightly, but significantly blunted by removal of extracellular Ca(2+), by p38 kinase inhibitor SB203580 (10 microM) and by the pancaspase inhibitor zVAD (10 microM).	Sunitinib	0-9	annexin A5	Homo sapiens	18-27
22814298-8	2012	Sunitinib induced annexin-V-binding was slightly, but significantly blunted by removal of extracellular Ca(2+), by p38 kinase inhibitor SB203580 (10 microM) and by the pancaspase inhibitor zVAD (10 microM).	Sunitinib	0-9	mitogen-activated protein kinase 14	Homo sapiens	115-118
22015552-10	2012	More recently, sunitinib (Sutent, Pfizer, New York, NY), which inhibits vascular endothelial growth factor receptor (VEGFR) in addition to KIT and PDGFRA, has proven efficacious in patients who are intolerant or refractory to imatinib.	Sunitinib	15-24	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	139-142
22015552-10	2012	More recently, sunitinib (Sutent, Pfizer, New York, NY), which inhibits vascular endothelial growth factor receptor (VEGFR) in addition to KIT and PDGFRA, has proven efficacious in patients who are intolerant or refractory to imatinib.	Sunitinib	15-24	platelet derived growth factor receptor alpha	Homo sapiens	147-153
22015552-10	2012	More recently, sunitinib (Sutent, Pfizer, New York, NY), which inhibits vascular endothelial growth factor receptor (VEGFR) in addition to KIT and PDGFRA, has proven efficacious in patients who are intolerant or refractory to imatinib.	Sunitinib	26-32	kinase insert domain receptor	Homo sapiens	72-115
22015552-10	2012	More recently, sunitinib (Sutent, Pfizer, New York, NY), which inhibits vascular endothelial growth factor receptor (VEGFR) in addition to KIT and PDGFRA, has proven efficacious in patients who are intolerant or refractory to imatinib.	Sunitinib	26-32	kinase insert domain receptor	Homo sapiens	117-122
22015552-10	2012	More recently, sunitinib (Sutent, Pfizer, New York, NY), which inhibits vascular endothelial growth factor receptor (VEGFR) in addition to KIT and PDGFRA, has proven efficacious in patients who are intolerant or refractory to imatinib.	Sunitinib	26-32	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	139-142
22015552-10	2012	More recently, sunitinib (Sutent, Pfizer, New York, NY), which inhibits vascular endothelial growth factor receptor (VEGFR) in addition to KIT and PDGFRA, has proven efficacious in patients who are intolerant or refractory to imatinib.	Sunitinib	26-32	platelet derived growth factor receptor alpha	Homo sapiens	147-153
22855636-2	2012	Early events in GIST development are activating mutations in KIT or PDGFRA, which occur in most GISTs and encode for mutated tyrosine receptor kinases that are therapeutic targets for tyrosine kinase inhibitors, including imatinib and sunitinib.	Sunitinib	235-244	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-64
22855636-2	2012	Early events in GIST development are activating mutations in KIT or PDGFRA, which occur in most GISTs and encode for mutated tyrosine receptor kinases that are therapeutic targets for tyrosine kinase inhibitors, including imatinib and sunitinib.	Sunitinib	235-244	platelet derived growth factor receptor alpha	Homo sapiens	68-74
22015552-10	2012	More recently, sunitinib (Sutent, Pfizer, New York, NY), which inhibits vascular endothelial growth factor receptor (VEGFR) in addition to KIT and PDGFRA, has proven efficacious in patients who are intolerant or refractory to imatinib.	Sunitinib	15-24	kinase insert domain receptor	Homo sapiens	72-115
22015552-10	2012	More recently, sunitinib (Sutent, Pfizer, New York, NY), which inhibits vascular endothelial growth factor receptor (VEGFR) in addition to KIT and PDGFRA, has proven efficacious in patients who are intolerant or refractory to imatinib.	Sunitinib	15-24	kinase insert domain receptor	Homo sapiens	117-122
22673043-0	2012	Impact of genetic variation in breast cancer resistance protein (BCRP/ABCG2) on sunitinib pharmacokinetics.	Sunitinib	80-89	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	65-69
22673043-0	2012	Impact of genetic variation in breast cancer resistance protein (BCRP/ABCG2) on sunitinib pharmacokinetics.	Sunitinib	80-89	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	70-75
22673043-1	2012	To elucidate the impact of genetic variations in breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (MDR1/ABCB1) on the pharmacokinetics of sunitinib, we carried out a pharmacogenetic study in a clinical setting and pharmacokinetic analysis using Abcg2(-/-), Abcb1a/1b(-/-) and Abcb1a/1b;Abcg2(-/-) mice.	Sunitinib	154-163	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	49-81
22673043-1	2012	To elucidate the impact of genetic variations in breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (MDR1/ABCB1) on the pharmacokinetics of sunitinib, we carried out a pharmacogenetic study in a clinical setting and pharmacokinetic analysis using Abcg2(-/-), Abcb1a/1b(-/-) and Abcb1a/1b;Abcg2(-/-) mice.	Sunitinib	154-163	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	83-87
22673043-1	2012	To elucidate the impact of genetic variations in breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (MDR1/ABCB1) on the pharmacokinetics of sunitinib, we carried out a pharmacogenetic study in a clinical setting and pharmacokinetic analysis using Abcg2(-/-), Abcb1a/1b(-/-) and Abcb1a/1b;Abcg2(-/-) mice.	Sunitinib	154-163	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	88-93
22673043-1	2012	To elucidate the impact of genetic variations in breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (MDR1/ABCB1) on the pharmacokinetics of sunitinib, we carried out a pharmacogenetic study in a clinical setting and pharmacokinetic analysis using Abcg2(-/-), Abcb1a/1b(-/-) and Abcb1a/1b;Abcg2(-/-) mice.	Sunitinib	154-163	ATP binding cassette subfamily B member 1	Homo sapiens	99-113
22673043-1	2012	To elucidate the impact of genetic variations in breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (MDR1/ABCB1) on the pharmacokinetics of sunitinib, we carried out a pharmacogenetic study in a clinical setting and pharmacokinetic analysis using Abcg2(-/-), Abcb1a/1b(-/-) and Abcb1a/1b;Abcg2(-/-) mice.	Sunitinib	154-163	ATP binding cassette subfamily B member 1	Homo sapiens	115-119
22673043-1	2012	To elucidate the impact of genetic variations in breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (MDR1/ABCB1) on the pharmacokinetics of sunitinib, we carried out a pharmacogenetic study in a clinical setting and pharmacokinetic analysis using Abcg2(-/-), Abcb1a/1b(-/-) and Abcb1a/1b;Abcg2(-/-) mice.	Sunitinib	154-163	ATP binding cassette subfamily B member 1	Homo sapiens	120-125
22673043-1	2012	To elucidate the impact of genetic variations in breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (MDR1/ABCB1) on the pharmacokinetics of sunitinib, we carried out a pharmacogenetic study in a clinical setting and pharmacokinetic analysis using Abcg2(-/-), Abcb1a/1b(-/-) and Abcb1a/1b;Abcg2(-/-) mice.	Sunitinib	154-163	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	261-266
22673043-1	2012	To elucidate the impact of genetic variations in breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (MDR1/ABCB1) on the pharmacokinetics of sunitinib, we carried out a pharmacogenetic study in a clinical setting and pharmacokinetic analysis using Abcg2(-/-), Abcb1a/1b(-/-) and Abcb1a/1b;Abcg2(-/-) mice.	Sunitinib	154-163	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	273-279
22673043-1	2012	To elucidate the impact of genetic variations in breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (MDR1/ABCB1) on the pharmacokinetics of sunitinib, we carried out a pharmacogenetic study in a clinical setting and pharmacokinetic analysis using Abcg2(-/-), Abcb1a/1b(-/-) and Abcb1a/1b;Abcg2(-/-) mice.	Sunitinib	154-163	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	292-298
22673043-1	2012	To elucidate the impact of genetic variations in breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (MDR1/ABCB1) on the pharmacokinetics of sunitinib, we carried out a pharmacogenetic study in a clinical setting and pharmacokinetic analysis using Abcg2(-/-), Abcb1a/1b(-/-) and Abcb1a/1b;Abcg2(-/-) mice.	Sunitinib	154-163	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	302-307
22673043-5	2012	The dose-adjusted AUC(0-24) of sunitinib was significantly higher in patients with a heterozygous variant for ABCG2 421C&gt;A than in wild-type patients (p = 0.02), and one homozygous patient showed the highest dose-adjusted AUC(0-24).	Sunitinib	31-40	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	110-115
22673043-7	2012	The maximum concentration and AUC(0-4) of sunitinib were significantly higher in Abcg2(-/-), Abcb1a/1b(-/-) and Abcb1a/1b;Abcg2(-/-) mice than wild-type mice when sunitinib was given orally but not intraperitoneally.	Sunitinib	42-51	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	81-86
22673043-7	2012	The maximum concentration and AUC(0-4) of sunitinib were significantly higher in Abcg2(-/-), Abcb1a/1b(-/-) and Abcb1a/1b;Abcg2(-/-) mice than wild-type mice when sunitinib was given orally but not intraperitoneally.	Sunitinib	42-51	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	93-99
22673043-7	2012	The maximum concentration and AUC(0-4) of sunitinib were significantly higher in Abcg2(-/-), Abcb1a/1b(-/-) and Abcb1a/1b;Abcg2(-/-) mice than wild-type mice when sunitinib was given orally but not intraperitoneally.	Sunitinib	42-51	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	112-118
22673043-7	2012	The maximum concentration and AUC(0-4) of sunitinib were significantly higher in Abcg2(-/-), Abcb1a/1b(-/-) and Abcb1a/1b;Abcg2(-/-) mice than wild-type mice when sunitinib was given orally but not intraperitoneally.	Sunitinib	42-51	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	122-127
22673043-9	2012	These results suggest that the loss of protein expression of ABCG2 by genetic polymorphism is associated with an increase in the systemic exposure to sunitinib and sunitinib-induced toxicity.	Sunitinib	150-159	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	61-66
22673043-9	2012	These results suggest that the loss of protein expression of ABCG2 by genetic polymorphism is associated with an increase in the systemic exposure to sunitinib and sunitinib-induced toxicity.	Sunitinib	164-173	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	61-66
21898502-10	2012	In addition, sunitinib treatment of tumor-bearing mice was associated with suppression of STAT3 and a block in T-cell tolerance.	Sunitinib	13-22	signal transducer and activator of transcription 3	Mus musculus	90-95
21898502-11	2012	CONCLUSION: These findings indicate that sunitinib inhibits HCC tumor growth directly through the STAT3 pathway and prevents tumor antigen-specific CD8(+) T-cell tolerance, thus defining a synergistic chemoimmunotherapeutic approach for HCC.	Sunitinib	41-50	signal transducer and activator of transcription 3	Mus musculus	98-103
22677881-8	2012	Predominantly the superiority of sunitinib regarding PFS2 contributed to the longer combined PFS in sequential use.	Sunitinib	33-42	GINS complex subunit 2	Homo sapiens	53-57
23017141-1	2012	The receptor tyrosine kinase inhibitor, sunitinib, is astonishingly effective in its capacity to reduce MDSCs in peripheral tissues such as blood (human) and spleen (mouse), restoring responsiveness of bystander T lymphocytes to TcR stimulation.	Sunitinib	40-49	T cell receptor alpha variable 6-3	Mus musculus	229-232
23017141-5	2012	The presence or absence of GM-CSF is likely the major determinant in each compartment, given that GM-CSF"s capacity to preempt STAT3-dependent with dominant STAT5-dependent hematopoietic programming confers sunitinib resistance and redirects differentiation from the n-MDSC lineage to the more versatile monocytoid (m-MDSC) lineage.	Sunitinib	207-216	colony stimulating factor 2	Homo sapiens	98-104
21351087-0	2012	Brain accumulation of sunitinib is restricted by P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) and can be enhanced by oral elacridar and sunitinib coadministration.	Sunitinib	22-31	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	65-70
21351087-0	2012	Brain accumulation of sunitinib is restricted by P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) and can be enhanced by oral elacridar and sunitinib coadministration.	Sunitinib	22-31	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	110-115
21351087-2	2012	We aimed to investigate the in vivo roles of the ATP-binding cassette drug efflux transporters ABCB1 and ABCG2 in plasma pharmacokinetics and brain accumulation of oral sunitinib, and the feasibility of improving sunitinib kinetics using oral coadministration of the dual ABCB1/ABCG2 inhibitor elacridar.	Sunitinib	169-178	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	95-100
21351087-2	2012	We aimed to investigate the in vivo roles of the ATP-binding cassette drug efflux transporters ABCB1 and ABCG2 in plasma pharmacokinetics and brain accumulation of oral sunitinib, and the feasibility of improving sunitinib kinetics using oral coadministration of the dual ABCB1/ABCG2 inhibitor elacridar.	Sunitinib	169-178	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	105-110
21351087-2	2012	We aimed to investigate the in vivo roles of the ATP-binding cassette drug efflux transporters ABCB1 and ABCG2 in plasma pharmacokinetics and brain accumulation of oral sunitinib, and the feasibility of improving sunitinib kinetics using oral coadministration of the dual ABCB1/ABCG2 inhibitor elacridar.	Sunitinib	213-222	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	95-100
21351087-2	2012	We aimed to investigate the in vivo roles of the ATP-binding cassette drug efflux transporters ABCB1 and ABCG2 in plasma pharmacokinetics and brain accumulation of oral sunitinib, and the feasibility of improving sunitinib kinetics using oral coadministration of the dual ABCB1/ABCG2 inhibitor elacridar.	Sunitinib	213-222	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	105-110
21351087-2	2012	We aimed to investigate the in vivo roles of the ATP-binding cassette drug efflux transporters ABCB1 and ABCG2 in plasma pharmacokinetics and brain accumulation of oral sunitinib, and the feasibility of improving sunitinib kinetics using oral coadministration of the dual ABCB1/ABCG2 inhibitor elacridar.	Sunitinib	213-222	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	272-277
21351087-2	2012	We aimed to investigate the in vivo roles of the ATP-binding cassette drug efflux transporters ABCB1 and ABCG2 in plasma pharmacokinetics and brain accumulation of oral sunitinib, and the feasibility of improving sunitinib kinetics using oral coadministration of the dual ABCB1/ABCG2 inhibitor elacridar.	Sunitinib	213-222	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	278-283
21351087-4	2012	In vitro, sunitinib was a good substrate of murine (mu)ABCG2 and a moderate substrate of human (hu)ABCB1 and huABCG2.	Sunitinib	10-19	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	55-60
21351087-4	2012	In vitro, sunitinib was a good substrate of murine (mu)ABCG2 and a moderate substrate of human (hu)ABCB1 and huABCG2.	Sunitinib	10-19	ATP binding cassette subfamily B member 1	Homo sapiens	99-104
21351087-6	2012	Brain accumulation of sunitinib was markedly (23-fold) increased in Abcb1a/b/Abcg2(-/-)  mice, but only slightly (2.3-fold) in Abcb1a/b(-/-)  mice, and not in Abcg2(-/-)  mice.	Sunitinib	22-31	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	68-74
21351087-6	2012	Brain accumulation of sunitinib was markedly (23-fold) increased in Abcb1a/b/Abcg2(-/-)  mice, but only slightly (2.3-fold) in Abcb1a/b(-/-)  mice, and not in Abcg2(-/-)  mice.	Sunitinib	22-31	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	77-82
21351087-6	2012	Brain accumulation of sunitinib was markedly (23-fold) increased in Abcb1a/b/Abcg2(-/-)  mice, but only slightly (2.3-fold) in Abcb1a/b(-/-)  mice, and not in Abcg2(-/-)  mice.	Sunitinib	22-31	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	159-164
21351087-7	2012	Importantly, a clinically realistic coadministration of oral elacridar and oral sunitinib to wild-type mice resulted in markedly increased sunitinib brain accumulation, equaling levels in Abcb1a/1b/Abcg2(-/-)  mice.	Sunitinib	80-89	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	188-194
21351087-7	2012	Importantly, a clinically realistic coadministration of oral elacridar and oral sunitinib to wild-type mice resulted in markedly increased sunitinib brain accumulation, equaling levels in Abcb1a/1b/Abcg2(-/-)  mice.	Sunitinib	80-89	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	198-203
21876693-4	2012	Research on angiogenesis in general, and vascular endothelial growth factor in particular, is a major focus in biomedicine and has led to the clinical approval of several antiangiogenic agents including thalidomide, bevacizumab, sorafenib, sunitinib, pazopanib, temesirolimus, and everolimus.	Sunitinib	240-249	vascular endothelial growth factor A	Homo sapiens	41-75
21961001-3	2012	On this basis, agents rendering VEGF ineffective by neutralizing VEGF (bevacizumab), blocking its receptors (aflibercept), or interfering with the postreceptor signaling pathways (sunitinib) provide us with the rational treatment options.	Sunitinib	180-189	vascular endothelial growth factor A	Homo sapiens	32-36
22357730-5	2012	Specifically, phase III studies indicate that pharmacologic inhibition of the vascular endothelial growth factor pathway with sunitinib, and of the mammalian target of rapamycin pathway with everolimus, appears to have altered the natural history of these diseases.	Sunitinib	126-135	vascular endothelial growth factor A	Homo sapiens	78-112
21880693-5	2012	Binding analysis of the inhibitors to the two different phosphorylation forms of CSF-1R, using surface plasmon resonance spectrometry, revealed that staurosporine bound to both forms with similar affinity, but sunitinib bound to the dephosphorylated form with higher affinity.	Sunitinib	210-219	colony stimulating factor 1 receptor	Homo sapiens	81-87
21880693-6	2012	Thus, these observations suggest that sunitinib binds preferentially to the inactive form, preventing the activation of CSF-1R.	Sunitinib	38-47	colony stimulating factor 1 receptor	Homo sapiens	120-126
22677881-6	2012	In second-line treatment, sunitinib showed a significantly longer PFS2 than sorafenib (average increase 2.66 months, 95% CI 1.02-4.3, p = 0.003).	Sunitinib	26-35	GINS complex subunit 2	Homo sapiens	66-70
23028796-7	2012	Sunitinib could induce more apoptotic cells in 786-0 cells with knockdown EpoR expression.	Sunitinib	0-9	erythropoietin receptor	Homo sapiens	74-78
23056179-8	2012	However, the in vivo efficacy testing of the gefitinib and sunitinib combination in an EGFR amplified/PTEN wild type GBM xenograft model revealed that gefitinib alone could significantly improve survival in animals whereas sunitinib did not show any survival benefit.	Sunitinib	59-68	epidermal growth factor receptor	Homo sapiens	87-91
23056179-8	2012	However, the in vivo efficacy testing of the gefitinib and sunitinib combination in an EGFR amplified/PTEN wild type GBM xenograft model revealed that gefitinib alone could significantly improve survival in animals whereas sunitinib did not show any survival benefit.	Sunitinib	59-68	phosphatase and tensin homolog	Homo sapiens	102-106
23028796-8	2012	Our results suggested that Epo/EpoR pathway was involved in cell growth, invasion, survival, and sensitivity to the multi-kinases inhibitor Sunitinib in RCC cells.	Sunitinib	140-149	erythropoietin	Homo sapiens	27-30
23028796-8	2012	Our results suggested that Epo/EpoR pathway was involved in cell growth, invasion, survival, and sensitivity to the multi-kinases inhibitor Sunitinib in RCC cells.	Sunitinib	140-149	erythropoietin receptor	Homo sapiens	31-35
22723862-6	2012	In endothelial HUVECs, gemcitabine, bevacizumab, sunitinib and EMAP caused 70, 41, 86 and 67 percent inhibition, while combination of gemcitabine with bevacizumab, sunitinib or EMAP had additive effects.	Sunitinib	49-58	EMAP like 1	Homo sapiens	177-181
22723862-6	2012	In endothelial HUVECs, gemcitabine, bevacizumab, sunitinib and EMAP caused 70, 41, 86 and 67 percent inhibition, while combination of gemcitabine with bevacizumab, sunitinib or EMAP had additive effects.	Sunitinib	164-173	EMAP like 1	Homo sapiens	63-67
22412884-9	2012	The marginal cost-effectiveness (cost per additional QALY) gained via the sunitinib strategy compared with the conventional strategy was $220,384 (without SPAP, interleukin-2 plus interferon-alfa and bevacizumab plus interferon-alfa were dominated) and $16,993 (with SPAP, interferon-alfa, interleukin-2 plus interferon-alfa and bevacizumab plus interferon-alfa were dominated).	Sunitinib	74-83	interleukin 2	Homo sapiens	290-303
22662219-7	2012	P53 reactivation substantially improved the apoptotic response after effective KIT inhibition with sunitinib and 17-AAG in IM-resistant cell lines.	Sunitinib	99-108	tumor protein p53	Homo sapiens	0-3
22745791-3	2012	We investigated the renal effects of the administration, during 45 days, of sunitinib (Su), a VEGF receptor inhibitor, to rats with 5/6 renal ablation (Nx).	Sunitinib	76-85	vascular endothelial growth factor A	Rattus norvegicus	94-98
22229044-1	2012	Based on preclinical data available in the RIP1-Tag2 transgenic mouse model, sunitinib is an inhibitor of angiogenesis in pancreatic neuroendocrine tumors blocking vascular endothelial growth factor receptors and platelet-derived growth factor receptors in endothelial cells and pericytes, respectively.	Sunitinib	77-86	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	43-47
22084065-3	2011	We evaluated sunitinib, an angiogenesis inhibitor that targets VEGF and PDGF receptor signaling, in two GEMMs of pancreatic cancer.	Sunitinib	13-22	vascular endothelial growth factor A	Mus musculus	63-67
23650573-0	2012	IGF-1 receptor is down-regulated by sunitinib induces MDM2-dependent ubiquitination.	Sunitinib	36-45	insulin like growth factor 1	Homo sapiens	0-5
23650573-2	2012	The aim is to investigate the effects of sunitinib on IGF-1R cell signaling transduction, especially on receptor phosphorylation and ubiquitination.	Sunitinib	41-50	insulin like growth factor 1 receptor	Homo sapiens	54-60
23650573-4	2012	However, the phosphorylations of receptor tyrosine, Akt and ERK were significant inhibited by sunitinib.	Sunitinib	94-103	AKT serine/threonine kinase 1	Homo sapiens	52-55
23650573-4	2012	However, the phosphorylations of receptor tyrosine, Akt and ERK were significant inhibited by sunitinib.	Sunitinib	94-103	mitogen-activated protein kinase 1	Homo sapiens	60-63
23650573-5	2012	We found that both IGF-1 and sunitinib obviously down regulated the IGF-1R expression.	Sunitinib	29-38	insulin like growth factor 1 receptor	Homo sapiens	68-74
23650573-6	2012	For analysis the ubiquitination, HEK293 cells were simulated with 100 ng/ml IGF-1 or 10 nM sunitinib for 10 min after serum starvation for 24 h. Both IGF-1 and sunitinib could obviously induce the IGF-1R ubiquitination at 10 min compared with control (only serum free, no stimulation), indicating IGF-1 and sunitinib down-regulate the IGF-1R by increasing the receptor degradation through ubiquitination dependent proteasome pathway.	Sunitinib	91-100	insulin like growth factor 1	Homo sapiens	150-155
23650573-6	2012	For analysis the ubiquitination, HEK293 cells were simulated with 100 ng/ml IGF-1 or 10 nM sunitinib for 10 min after serum starvation for 24 h. Both IGF-1 and sunitinib could obviously induce the IGF-1R ubiquitination at 10 min compared with control (only serum free, no stimulation), indicating IGF-1 and sunitinib down-regulate the IGF-1R by increasing the receptor degradation through ubiquitination dependent proteasome pathway.	Sunitinib	91-100	insulin like growth factor 1 receptor	Homo sapiens	197-203
23650573-6	2012	For analysis the ubiquitination, HEK293 cells were simulated with 100 ng/ml IGF-1 or 10 nM sunitinib for 10 min after serum starvation for 24 h. Both IGF-1 and sunitinib could obviously induce the IGF-1R ubiquitination at 10 min compared with control (only serum free, no stimulation), indicating IGF-1 and sunitinib down-regulate the IGF-1R by increasing the receptor degradation through ubiquitination dependent proteasome pathway.	Sunitinib	91-100	insulin like growth factor 1	Homo sapiens	150-169
23650573-6	2012	For analysis the ubiquitination, HEK293 cells were simulated with 100 ng/ml IGF-1 or 10 nM sunitinib for 10 min after serum starvation for 24 h. Both IGF-1 and sunitinib could obviously induce the IGF-1R ubiquitination at 10 min compared with control (only serum free, no stimulation), indicating IGF-1 and sunitinib down-regulate the IGF-1R by increasing the receptor degradation through ubiquitination dependent proteasome pathway.	Sunitinib	91-100	insulin like growth factor 1 receptor	Homo sapiens	335-341
23650573-6	2012	For analysis the ubiquitination, HEK293 cells were simulated with 100 ng/ml IGF-1 or 10 nM sunitinib for 10 min after serum starvation for 24 h. Both IGF-1 and sunitinib could obviously induce the IGF-1R ubiquitination at 10 min compared with control (only serum free, no stimulation), indicating IGF-1 and sunitinib down-regulate the IGF-1R by increasing the receptor degradation through ubiquitination dependent proteasome pathway.	Sunitinib	160-169	insulin like growth factor 1	Homo sapiens	76-81
23650573-6	2012	For analysis the ubiquitination, HEK293 cells were simulated with 100 ng/ml IGF-1 or 10 nM sunitinib for 10 min after serum starvation for 24 h. Both IGF-1 and sunitinib could obviously induce the IGF-1R ubiquitination at 10 min compared with control (only serum free, no stimulation), indicating IGF-1 and sunitinib down-regulate the IGF-1R by increasing the receptor degradation through ubiquitination dependent proteasome pathway.	Sunitinib	160-169	insulin like growth factor 1 receptor	Homo sapiens	197-203
23650573-6	2012	For analysis the ubiquitination, HEK293 cells were simulated with 100 ng/ml IGF-1 or 10 nM sunitinib for 10 min after serum starvation for 24 h. Both IGF-1 and sunitinib could obviously induce the IGF-1R ubiquitination at 10 min compared with control (only serum free, no stimulation), indicating IGF-1 and sunitinib down-regulate the IGF-1R by increasing the receptor degradation through ubiquitination dependent proteasome pathway.	Sunitinib	160-169	insulin like growth factor 1 receptor	Homo sapiens	335-341
23650573-7	2012	We also found that MDM2 combined to IGF-1R in response to sunitinib stimulation.	Sunitinib	58-67	MDM2 proto-oncogene	Homo sapiens	19-23
23650573-7	2012	We also found that MDM2 combined to IGF-1R in response to sunitinib stimulation.	Sunitinib	58-67	insulin like growth factor 1 receptor	Homo sapiens	36-42
23650573-11	2012	These results mean that sunitinib mediates ubiquitination of IGF-1R dependent on MDM2.	Sunitinib	24-33	insulin like growth factor 1 receptor	Homo sapiens	61-67
23650573-11	2012	These results mean that sunitinib mediates ubiquitination of IGF-1R dependent on MDM2.	Sunitinib	24-33	MDM2 proto-oncogene	Homo sapiens	81-85
23650573-12	2012	In summary, sunitinib could block signaling transduction and mediate degradation of IGF-1R.	Sunitinib	12-21	insulin like growth factor 1 receptor	Homo sapiens	84-90
22038997-10	2011	Sunitinib PK and VEGF ligand levels increased during sunitinib exposure and returned toward baseline during the treatment withdrawal.	Sunitinib	53-62	vascular endothelial growth factor A	Homo sapiens	17-21
22038997-11	2011	CONCLUSIONS: The increase of cellular proliferation during sunitinib withdrawal in patients with renal cell carcinoma and other solid malignancies is consistent with a VEGF receptor (VEGFR) tyrosine kinase inhibitor (TKI) withdrawal flare.	Sunitinib	59-68	kinase insert domain receptor	Homo sapiens	168-181
22038997-11	2011	CONCLUSIONS: The increase of cellular proliferation during sunitinib withdrawal in patients with renal cell carcinoma and other solid malignancies is consistent with a VEGF receptor (VEGFR) tyrosine kinase inhibitor (TKI) withdrawal flare.	Sunitinib	59-68	kinase insert domain receptor	Homo sapiens	183-188
22014215-11	2011	In addition, Zt/c9-Dox-IL in combination with small molecule inhibitors lapatinib, sunitinib, or dasatinib further reduced the viability of CSCs(+24/44/ESA).	Sunitinib	83-92	paraoxonase 1	Homo sapiens	140-156
21415240-4	2011	RESULTS: Sunitinib demonstrated comparable dose-dependent growth inhibition in cisplatin-sensitive and cisplatin-resistant cell lines, with IC(50) between 3.0 and 3.8 muM.	Sunitinib	9-18	latexin	Homo sapiens	167-170
21826469-5	2011	This review discusses the relevant translational data from animal models of heart failure, focusing on three key pathways that are inhibited by sunitinib: AMP-activated protein kinase (AMPK), platelet-derived growth factor receptors (PDGFRs), and the vascular endothelial growth factor receptors (VEGFRs) 1, 2, and 3.	Sunitinib	144-153	fms related receptor tyrosine kinase 1	Homo sapiens	251-316
22199315-2	2011	We investigated the IDH1 gene mutation status by nested PCR and denaturing gradient gel electrophoresis (DGGE) on DNA extracted from archival tumor blocks of 63 glioma patients who were treated following recurrence with the epidermal growth factor receptor (EGFR)-targeted blocking monoclonal antibody cetuximab, or the vascular endothelial growth factor (receptor) (VEGF(R))-targeted agents sunitinib malate and bevacizumab.	Sunitinib	392-408	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	20-24
22199315-4	2011	Patients with IDH1 mutation also had a superior OS from the time of recurrence when treated with sunitinib or bevacizumab but a worse OS when treated with cetuximab.	Sunitinib	97-106	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	14-18
21931979-4	2011	Initially developed for its inhibition of the vascular endothelial growth factor (VEGF) signaling pathway, sunitinib has been associated with hypertension and heart failure.	Sunitinib	107-116	vascular endothelial growth factor A	Homo sapiens	46-80
21931979-4	2011	Initially developed for its inhibition of the vascular endothelial growth factor (VEGF) signaling pathway, sunitinib has been associated with hypertension and heart failure.	Sunitinib	107-116	vascular endothelial growth factor A	Homo sapiens	82-86
20467883-1	2011	PURPOSE: Sunitinib is a multi-target receptor tyrosine kinase (RTK) inhibitor against vascular endothelial growth factor receptors, platelet-derived growth factor receptors (PDGFR), c-kit and RET.	Sunitinib	9-18	TYRO3 protein tyrosine kinase 3	Mus musculus	37-61
22098229-2	2011	Currently available oral multitargeted VEGF tyrosine kinase inhibitors (TKIs) that have been approved by the US Food and Drug Administration for advanced RCC, include sunitinib, sorafenib and pazopanib.	Sunitinib	167-176	vascular endothelial growth factor A	Homo sapiens	39-43
20676744-0	2011	VEGF pathway inhibition by anticancer agent sunitinib and susceptibility to atherosclerosis plaque disruption.	Sunitinib	44-53	vascular endothelial growth factor A	Homo sapiens	0-4
20676744-3	2011	We report on a case of bowel infarction in a renal cancer patient treated with the anti-VEGF agent sunitinib.	Sunitinib	99-108	vascular endothelial growth factor A	Homo sapiens	88-92
20467883-1	2011	PURPOSE: Sunitinib is a multi-target receptor tyrosine kinase (RTK) inhibitor against vascular endothelial growth factor receptors, platelet-derived growth factor receptors (PDGFR), c-kit and RET.	Sunitinib	9-18	TYRO3 protein tyrosine kinase 3	Mus musculus	63-66
20467883-1	2011	PURPOSE: Sunitinib is a multi-target receptor tyrosine kinase (RTK) inhibitor against vascular endothelial growth factor receptors, platelet-derived growth factor receptors (PDGFR), c-kit and RET.	Sunitinib	9-18	platelet derived growth factor receptor, beta polypeptide	Mus musculus	132-172
20467883-1	2011	PURPOSE: Sunitinib is a multi-target receptor tyrosine kinase (RTK) inhibitor against vascular endothelial growth factor receptors, platelet-derived growth factor receptors (PDGFR), c-kit and RET.	Sunitinib	9-18	platelet derived growth factor receptor, beta polypeptide	Mus musculus	174-179
20467883-1	2011	PURPOSE: Sunitinib is a multi-target receptor tyrosine kinase (RTK) inhibitor against vascular endothelial growth factor receptors, platelet-derived growth factor receptors (PDGFR), c-kit and RET.	Sunitinib	9-18	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	182-187
20467883-1	2011	PURPOSE: Sunitinib is a multi-target receptor tyrosine kinase (RTK) inhibitor against vascular endothelial growth factor receptors, platelet-derived growth factor receptors (PDGFR), c-kit and RET.	Sunitinib	9-18	ret proto-oncogene	Mus musculus	192-195
22027642-6	2011	Sunitinib is a multikinase inhibitor that targets the PDGF-alpha- and ?beta-, VEGF-1-3-, KIT-, FLT3-, CSF-1- and RET-receptor, thereby impairing tumour proliferation, pathological angiogenesis and metastasation.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	95-99
21906609-2	2011	Although the precise mechanism of sunitinib cardiotoxicity is not known, both the key metabolic energy regulator, AMP-activated protein kinase (AMPK), and ribosomal S 6 kinase (RSK) have been hypothesized as causative, albeit based on rodent models.	Sunitinib	34-43	ribosomal protein S6 kinase A2	Homo sapiens	177-180
21744079-1	2011	We determined the maximum tolerated dose (MTD) and dose-limiting toxicities (DLT) of the oral vascular endothelial growth factor receptor (VEGFR) inhibitor, sunitinib, when administered with irinotecan among recurrent malignant glioma (MG) patients.	Sunitinib	157-166	kinase insert domain receptor	Homo sapiens	94-137
21744079-1	2011	We determined the maximum tolerated dose (MTD) and dose-limiting toxicities (DLT) of the oral vascular endothelial growth factor receptor (VEGFR) inhibitor, sunitinib, when administered with irinotecan among recurrent malignant glioma (MG) patients.	Sunitinib	157-166	kinase insert domain receptor	Homo sapiens	139-144
22027642-6	2011	Sunitinib is a multikinase inhibitor that targets the PDGF-alpha- and ?beta-, VEGF-1-3-, KIT-, FLT3-, CSF-1- and RET-receptor, thereby impairing tumour proliferation, pathological angiogenesis and metastasation.	Sunitinib	0-9	colony stimulating factor 1	Homo sapiens	102-125
21954449-12	2011	DISCUSSION: Sunitinib is a small molecule that inhibits multiple receptor tyrosine kinases such as stem cell factor receptor, vascular endothelial growth factor, and platelet-derived growth factor.	Sunitinib	12-21	vascular endothelial growth factor A	Homo sapiens	126-160
22015557-6	2011	SGI-1776 in combination with sunitinib induced a further reduction in c-Myc levels, which was associated with enhanced anticancer activity.	Sunitinib	29-38	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	70-75
22015557-7	2011	siRNA-mediated knockdown of c-Myc demonstrated that its expression has a key role in regulating the sensitivity to the combination of SGI-1776 and sunitinib.	Sunitinib	147-156	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	28-33
21952069-18	2011	A preliminary report of the investigational VEGF receptorinhibitor axitinib gave superior PFS to sorafenib after either prior cytokine or prior sunitinib treatment.	Sunitinib	144-153	vascular endothelial growth factor A	Homo sapiens	44-48
21933109-1	2011	Research on the formation of new blood vessels (angiogenesis) in general and vascular endothelial growth factor (VEGF) in particular is a major focus in biomedicine and has led to the clinical approval of the monoclonal anti- VEGF antibody bevazicumab; and the second-generation multitargeted receptor kinase inhibitors (RTKIs) sorafenib, sunitinib, and pazopanib.	Sunitinib	339-348	vascular endothelial growth factor A	Homo sapiens	226-230
22166826-7	2011	The chemotherapy (gemcitabine and cisplatin) and the molecular target therapy (sunitinib) were administerd but the primary lesion and metastases was progressive and serum G-CSF concentration was elevated to 229 pg/ml.	Sunitinib	79-88	colony stimulating factor 3	Homo sapiens	171-176
21965162-1	2011	We report the case of a patient with metastatic renal cell carcinoma with Xp11.2 translocation/transcription factor E3 (TFE3) gene fusion who had presented with sunitinib-induced nephrotic syndrome in association with favorable and durable treatment response.	Sunitinib	161-170	transcription factor binding to IGHM enhancer 3	Homo sapiens	81-118
21965162-1	2011	We report the case of a patient with metastatic renal cell carcinoma with Xp11.2 translocation/transcription factor E3 (TFE3) gene fusion who had presented with sunitinib-induced nephrotic syndrome in association with favorable and durable treatment response.	Sunitinib	161-170	transcription factor binding to IGHM enhancer 3	Homo sapiens	120-124
22029859-5	2011	This correlated with viral NS1 expression levels and was enhanced by combination with chemotherapeutic agents or sunitinib.	Sunitinib	113-122	influenza virus NS1A binding protein	Homo sapiens	27-30
21883349-4	2011	Recently, sunitinib, a multityrosine kinase inhibitor (TKI), has been found to be rapidly metabolized by CYP3A4 during mitotane treatment, indicating clinically relevant drug interactions with mitotane.	Sunitinib	10-19	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	105-111
22005473-5	2011	METHODS: This open-labeled phase II trial evaluated single-agent sunitinib, an inhibitor of multiple receptor tyrosine kinases including the vascular endothelial growth factor receptors, given at 50 mg daily orally for 4 weeks followed by a 2-week rest, in patients with advanced MPM.	Sunitinib	65-74	vascular endothelial growth factor A	Homo sapiens	141-175
22015057-10	2011	Two VEGFR3 missense polymorphisms were associated with reduced PFS with sunitinib on multivariable analysis: rs307826 (hazard ratio [HR] per allele 3 57, 1 75-7 30; p(unadjusted)=0 00049, p(adjusted)=0 0079) and rs307821 (3 31, 1 64-6 68; p(unadjusted)=0 00085, p(adjusted)=0 014).	Sunitinib	72-81	fms related receptor tyrosine kinase 4	Homo sapiens	4-10
22015057-13	2011	INTERPRETATION: Polymorphisms in VEGFR3 and CYP3A5*1 might be able to define a subset of patients with renal-cell carcinoma with decreased sunitinib response and tolerability.	Sunitinib	139-148	fms related receptor tyrosine kinase 4	Homo sapiens	33-39
22015057-13	2011	INTERPRETATION: Polymorphisms in VEGFR3 and CYP3A5*1 might be able to define a subset of patients with renal-cell carcinoma with decreased sunitinib response and tolerability.	Sunitinib	139-148	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	44-50
21456006-9	2011	The objective response rate was 3%, comprising 1 PR in a patient with a GIST possessing both a KIT exon 11 mutation, and an imatinib-resistant and sunitinib-resistant KIT exon 17 mutation.	Sunitinib	147-156	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	167-170
21951737-2	2011	Four agents antagonizing vascular endothelial growth factor-mediated signaling have been approved for the treatment of metastatic RCC, including the monoclonal antibody bevacizumab and the small molecular inhibitors sunitinib, sorafenib, and pazopanib.	Sunitinib	216-225	vascular endothelial growth factor A	Homo sapiens	25-59
21970485-2	2011	They harbor specific activating mutations in the KIT or platelet-derived growth factor receptor alpha ( PDGFRA ) receptor tyrosine kinases, which makes them responsive to pharmacologic inhibitors, such as imatinib mesylate and sunitinib malate.	Sunitinib	227-243	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
21970485-2	2011	They harbor specific activating mutations in the KIT or platelet-derived growth factor receptor alpha ( PDGFRA ) receptor tyrosine kinases, which makes them responsive to pharmacologic inhibitors, such as imatinib mesylate and sunitinib malate.	Sunitinib	227-243	platelet derived growth factor receptor alpha	Homo sapiens	56-101
21970485-2	2011	They harbor specific activating mutations in the KIT or platelet-derived growth factor receptor alpha ( PDGFRA ) receptor tyrosine kinases, which makes them responsive to pharmacologic inhibitors, such as imatinib mesylate and sunitinib malate.	Sunitinib	227-243	platelet derived growth factor receptor alpha	Homo sapiens	104-110
22654799-0	2011	Sunitinib Inhibits Cell Proliferation and Alters Steroidogenesis by Down-Regulation of HSD3B2 in Adrenocortical Carcinoma Cells.	Sunitinib	0-9	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 2	Homo sapiens	87-93
22654799-14	2011	Sunitinib exhibits anti-proliferative effects in vitro, and appears to specifically block adrenal steroidogenesis by down-regulation of HSD3B2, rendering it a promising option for treatment of ACC.	Sunitinib	0-9	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 2	Homo sapiens	136-142
21771900-6	2011	Treatment with the Flt3 inhibitor sunitinib was started together with mBSA immunization or together with the induction of arthritis.	Sunitinib	34-43	fms related receptor tyrosine kinase 3	Homo sapiens	19-23
21128230-8	2011	The administration of sunitinib, a drug known to inhibit PDGFR, was associated in murine models and in cancer patients with an increase of apoptotic/necrotic circulating PPC, suggesting a direct targeting of these cells.	Sunitinib	22-31	platelet derived growth factor receptor, beta polypeptide	Mus musculus	57-62
22654799-11	2011	Sunitinib induced down-regulation of HSD3B2 mRNA and protein in ACC cell lines (mRNA: 1 muM 44 +- 16%*; 5 muM 22 +- 2%*; 10 muM 19 +- 4%*; protein: 1 muM 82 +- 8%; 5 muM 63 +- 8%*; 10 muM 55 +- 9%*).	Sunitinib	0-9	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 2	Homo sapiens	37-43
21725210-0	2011	Sunitinib inhibits papillary thyroid carcinoma with RET/PTC rearrangement but not BRAF mutation.	Sunitinib	0-9	ret proto-oncogene	Homo sapiens	52-55
21265994-4	2011	RESULTS:   Sunitinib was more effective and less costly than sorafenib (gains of 0.52 PFLYs, 0.16 LYs and 0.17 QALYs and savings/patient of $13,576 in the US) and bevacizumab plus IFN-alpha (gains of 0.19 PFLYs, 0.23 LYs and 0.16 QALYs in both countries and savings/patient of $67,798 and $47,264 in the US and Sweden, respectively).	Sunitinib	11-20	interferon alpha 1	Homo sapiens	180-189
21725210-0	2011	Sunitinib inhibits papillary thyroid carcinoma with RET/PTC rearrangement but not BRAF mutation.	Sunitinib	0-9	ret proto-oncogene	Homo sapiens	56-59
21725210-4	2011	Cell growth of papillary thyroid cancer cells with RET/PTC rearrangement was effectively inhibited at low doses of sunitinib (IC50=0.658 muM), whereas that of BRAF mutated cells required higher doses.	Sunitinib	115-124	ret proto-oncogene	Homo sapiens	51-54
21725210-4	2011	Cell growth of papillary thyroid cancer cells with RET/PTC rearrangement was effectively inhibited at low doses of sunitinib (IC50=0.658 muM), whereas that of BRAF mutated cells required higher doses.	Sunitinib	115-124	ret proto-oncogene	Homo sapiens	55-58
21725210-7	2011	In vivo orthotopic thyroid cancer mouse model demonstrated statistically significant tumor growth inhibition by sunitinib in RET/PTC rearrangement cancer cells.	Sunitinib	112-121	ret proto-oncogene	Mus musculus	125-128
21737509-2	2011	Imatinib (IMA) and sunitinib (SUN) are very effective KIT-inhibitors in patients with advanced GIST but have no curative potential.	Sunitinib	19-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	54-57
21725210-7	2011	In vivo orthotopic thyroid cancer mouse model demonstrated statistically significant tumor growth inhibition by sunitinib in RET/PTC rearrangement cancer cells.	Sunitinib	112-121	ret proto-oncogene	Mus musculus	129-132
21725210-8	2011	We conclude that sunitinib effectively inhibits RET/PTC rearrangement cells but not BRAF mutated cells.	Sunitinib	17-26	ret proto-oncogene	Homo sapiens	48-51
21725210-8	2011	We conclude that sunitinib effectively inhibits RET/PTC rearrangement cells but not BRAF mutated cells.	Sunitinib	17-26	ret proto-oncogene	Homo sapiens	52-55
21725210-9	2011	These data suggest that sunitinib exerts its effect by inhibiting the upstream MAPK signaling cascade.	Sunitinib	24-33	mitogen-activated protein kinase 1	Homo sapiens	79-83
21796416-0	2011	Synergistic interaction between sunitinib and docetaxel is sequence dependent in human non-small lung cancer with EGFR TKIs-resistant mutation.	Sunitinib	32-41	epidermal growth factor receptor	Homo sapiens	114-118
21817899-0	2011	VEGF expression is related to good response and long progression-free survival in gastrointestinal stromal tumor patients treated with Sunitinib.	Sunitinib	135-144	vascular endothelial growth factor A	Homo sapiens	0-4
21817899-8	2011	In the sunitinib treatment, VEGF expression was related to a favorable response (P=0.002) and long PFS (P=0.020) in univariate analysis.	Sunitinib	7-16	vascular endothelial growth factor A	Homo sapiens	28-32
21817899-9	2011	CD34 (P=0.023) and PDGFR (P=0.022) expressions were also related to long sunitinib PFS in univariate analysis.	Sunitinib	73-82	CD34 molecule	Homo sapiens	0-4
21817899-9	2011	CD34 (P=0.023) and PDGFR (P=0.022) expressions were also related to long sunitinib PFS in univariate analysis.	Sunitinib	73-82	platelet derived growth factor receptor beta	Homo sapiens	19-24
21817899-11	2011	In conclusion, expressions of VEGF, PDGFR, and CD34 may have predictive value in sunitinib treatments.	Sunitinib	81-90	vascular endothelial growth factor A	Homo sapiens	30-34
21817899-11	2011	In conclusion, expressions of VEGF, PDGFR, and CD34 may have predictive value in sunitinib treatments.	Sunitinib	81-90	platelet derived growth factor receptor beta	Homo sapiens	36-41
21817899-11	2011	In conclusion, expressions of VEGF, PDGFR, and CD34 may have predictive value in sunitinib treatments.	Sunitinib	81-90	CD34 molecule	Homo sapiens	47-51
21843259-9	2011	Su increased apoptosis, as evidenced by the cleavage of caspase-3 and PARP-1 proteins.	Sunitinib	0-2	caspase 3	Mus musculus	56-65
21843259-9	2011	Su increased apoptosis, as evidenced by the cleavage of caspase-3 and PARP-1 proteins.	Sunitinib	0-2	poly (ADP-ribose) polymerase family, member 1	Mus musculus	70-76
22040503-1	2011	BACKGROUND: The tyrosine kinase inhibitors (TKIs) sunitinib, the first targeted agent for the first line treatment of metastatic renal cell carcinoma (RCC), targets the vascular endothelial growth factor (VEGF) pathway.	Sunitinib	50-59	vascular endothelial growth factor A	Homo sapiens	169-203
22040503-1	2011	BACKGROUND: The tyrosine kinase inhibitors (TKIs) sunitinib, the first targeted agent for the first line treatment of metastatic renal cell carcinoma (RCC), targets the vascular endothelial growth factor (VEGF) pathway.	Sunitinib	50-59	vascular endothelial growth factor A	Homo sapiens	205-209
21796416-10	2011	CONCLUSIONS: Sunitinib as a single agent exhibits anti-proliferative effects in vitro in NSCLC cell lines with EGFR T790M and K-ras mutations but the sequential administration of docetaxel followed by sunitinib is superior to sunitinib followed by docetaxel and concurrent administration.	Sunitinib	13-22	epidermal growth factor receptor	Homo sapiens	111-115
21796416-10	2011	CONCLUSIONS: Sunitinib as a single agent exhibits anti-proliferative effects in vitro in NSCLC cell lines with EGFR T790M and K-ras mutations but the sequential administration of docetaxel followed by sunitinib is superior to sunitinib followed by docetaxel and concurrent administration.	Sunitinib	13-22	KRAS proto-oncogene, GTPase	Homo sapiens	126-131
21508896-6	2011	Sunitinib, a kinase inhibitor, blocked several receptors, including vascular endothelial growth factor receptor 3 (VEGFR3), the major growth factor receptor for lymphatic endothelial cells.	Sunitinib	0-9	FMS-like tyrosine kinase 4	Mus musculus	68-113
21316102-8	2011	In addition, both PD173074 and sunitinib inhibited the activation of FGFR3 in t(4;14)-positive MM cells.	Sunitinib	31-40	fibroblast growth factor receptor 3	Homo sapiens	69-74
21316102-10	2011	CONCLUSIONS: These data demonstrate that PD173074 and sunitinib are inhibitors of FGFR3 in MM cell lines, and that sunitinib has in vivo activity in a human MM tumour xenograft model.	Sunitinib	54-63	fibroblast growth factor receptor 3	Homo sapiens	82-87
21636578-0	2011	Inhibition of RNase L and RNA-dependent protein kinase (PKR) by sunitinib impairs antiviral innate immunity.	Sunitinib	64-73	ribonuclease L (2', 5'-oligoisoadenylate synthetase-dependent)	Mus musculus	14-21
21636578-0	2011	Inhibition of RNase L and RNA-dependent protein kinase (PKR) by sunitinib impairs antiviral innate immunity.	Sunitinib	64-73	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	56-59
21636578-2	2011	Sunitinib is an orally available, ATP-competitive inhibitor of VEGF and PDGF receptors used clinically to suppress angiogenesis and tumor growth.	Sunitinib	0-9	vascular endothelial growth factor A	Mus musculus	63-67
21636578-3	2011	Sunitinib also impacts IRE1, an endoplasmic reticulum protein involved in the unfolded protein response that is closely related to RNase L.	Sunitinib	0-9	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	23-27
21636578-3	2011	Sunitinib also impacts IRE1, an endoplasmic reticulum protein involved in the unfolded protein response that is closely related to RNase L.	Sunitinib	0-9	ribonuclease L (2', 5'-oligoisoadenylate synthetase-dependent)	Mus musculus	131-138
21636578-4	2011	Here, we report that sunitinib is a potent inhibitor of both RNase L and PKR with IC(50) values of 1.4 and 0.3 muM, respectively.	Sunitinib	21-30	ribonuclease L (2', 5'-oligoisoadenylate synthetase-dependent)	Mus musculus	61-68
21636578-4	2011	Here, we report that sunitinib is a potent inhibitor of both RNase L and PKR with IC(50) values of 1.4 and 0.3 muM, respectively.	Sunitinib	21-30	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	73-76
21636578-8	2011	Furthermore, oral delivery of sunitinib in WT mice resulted in 10-fold higher viral titers in heart tissues while suppressing by about 2-fold the IFN-beta levels.	Sunitinib	30-39	interferon beta 1, fibroblast	Mus musculus	146-154
21636578-11	2011	Results indicate that sunitinib treatments prevent antiviral innate immune responses mediated by RNase L and PKR.	Sunitinib	22-31	ribonuclease L (2', 5'-oligoisoadenylate synthetase-dependent)	Mus musculus	97-104
21636578-11	2011	Results indicate that sunitinib treatments prevent antiviral innate immune responses mediated by RNase L and PKR.	Sunitinib	22-31	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	109-112
21705501-2	2011	We report here 2 male patients with ETV6-FLT3(+) myeloid/lymphoid neoplasms with eosinophilia who were treated with the multitargeted TK inhibitors sunitinib and sorafenib.	Sunitinib	148-157	ETS variant transcription factor 6	Homo sapiens	36-40
21705501-2	2011	We report here 2 male patients with ETV6-FLT3(+) myeloid/lymphoid neoplasms with eosinophilia who were treated with the multitargeted TK inhibitors sunitinib and sorafenib.	Sunitinib	148-157	fms related receptor tyrosine kinase 3	Homo sapiens	41-45
21705501-2	2011	We report here 2 male patients with ETV6-FLT3(+) myeloid/lymphoid neoplasms with eosinophilia who were treated with the multitargeted TK inhibitors sunitinib and sorafenib.	Sunitinib	148-157	TXK tyrosine kinase	Homo sapiens	134-136
21787417-2	2011	Sunitinib has antiangiogenic activity and is an oral multitargeted inhibitor of vascular endothelial growth factor receptors (VEGFRs)-1, -2, and -3, platelet-derived growth factor receptors (PDGFRs)-alpha and -beta, stem-cell factor receptor (KIT), and other tyrosine kinases.	Sunitinib	0-9	fms related receptor tyrosine kinase 1	Homo sapiens	80-147
21787417-2	2011	Sunitinib has antiangiogenic activity and is an oral multitargeted inhibitor of vascular endothelial growth factor receptors (VEGFRs)-1, -2, and -3, platelet-derived growth factor receptors (PDGFRs)-alpha and -beta, stem-cell factor receptor (KIT), and other tyrosine kinases.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	243-246
21787417-11	2011	CONCLUSIONS: Baseline plasma VEGF-C levels predicted disease control (based on RECIST) and were positively associated with both TTP and OS in this exploratory analysis, suggesting that this VEGF family member may have utility in predicting clinical outcome in patients with HCC who receive sunitinib.	Sunitinib	290-299	vascular endothelial growth factor C	Homo sapiens	29-35
21787417-11	2011	CONCLUSIONS: Baseline plasma VEGF-C levels predicted disease control (based on RECIST) and were positively associated with both TTP and OS in this exploratory analysis, suggesting that this VEGF family member may have utility in predicting clinical outcome in patients with HCC who receive sunitinib.	Sunitinib	290-299	vascular endothelial growth factor A	Homo sapiens	29-33
21508896-6	2011	Sunitinib, a kinase inhibitor, blocked several receptors, including vascular endothelial growth factor receptor 3 (VEGFR3), the major growth factor receptor for lymphatic endothelial cells.	Sunitinib	0-9	FMS-like tyrosine kinase 4	Mus musculus	115-121
21508896-6	2011	Sunitinib, a kinase inhibitor, blocked several receptors, including vascular endothelial growth factor receptor 3 (VEGFR3), the major growth factor receptor for lymphatic endothelial cells.	Sunitinib	0-9	receptor-like tyrosine kinase	Mus musculus	89-111
21242589-10	2011	Antiproliferative assays and biochemistry on short-term culture showed that sunitinib is able to markedly impair ASPS cells growth and switch-off PDGFRB.	Sunitinib	76-85	platelet derived growth factor receptor beta	Homo sapiens	146-152
21242589-13	2011	CONCLUSIONS: We confirm the clinical efficacy of sunitinib in ASPS, mediated by PDGFRB, VEGFR2, and RET, which are all expressed in tumor cells.	Sunitinib	49-58	platelet derived growth factor receptor beta	Homo sapiens	80-86
21242589-13	2011	CONCLUSIONS: We confirm the clinical efficacy of sunitinib in ASPS, mediated by PDGFRB, VEGFR2, and RET, which are all expressed in tumor cells.	Sunitinib	49-58	kinase insert domain receptor	Homo sapiens	88-94
21242589-13	2011	CONCLUSIONS: We confirm the clinical efficacy of sunitinib in ASPS, mediated by PDGFRB, VEGFR2, and RET, which are all expressed in tumor cells.	Sunitinib	49-58	ret proto-oncogene	Homo sapiens	100-103
21519258-4	2011	RECENT FINDINGS: The major mechanism of resistance toward imatinib and sunitinib is the development of secondary resistance mutations in the kinase domain of KIT.	Sunitinib	71-80	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	158-161
21693010-0	2011	Sunitinib inhibits lymphatic endothelial cell functions and lymph node metastasis in a breast cancer model through inhibition of vascular endothelial growth factor receptor 3.	Sunitinib	0-9	fms related receptor tyrosine kinase 4	Homo sapiens	129-174
21315783-3	2011	Sunitinib also targets myeloid derived suppressor cells (MDSCs) significantly reducing their accumulation in the peripheral blood and reversing T cell (IFNgamma) suppression in both mRCC patients and in murine tumor models.	Sunitinib	0-9	interferon gamma	Homo sapiens	152-160
21315783-9	2011	Additionally, in vitro and in vivo experiments showed that GM-CSF prolongs survival of MDSCs, thus protecting them from the effects of sunitinib via a pSTAT5-dependent pathway.	Sunitinib	135-144	colony stimulating factor 2	Homo sapiens	59-65
21315783-15	2011	GM-CSF"s role in promoting MDSC survival in patient tumors is supported by the observation that GM-CSF is produced in short-term RCC cultures at levels capable of protecting MDSCs from sunitinib-induced cell death.	Sunitinib	185-194	colony stimulating factor 2	Homo sapiens	0-6
21315783-15	2011	GM-CSF"s role in promoting MDSC survival in patient tumors is supported by the observation that GM-CSF is produced in short-term RCC cultures at levels capable of protecting MDSCs from sunitinib-induced cell death.	Sunitinib	185-194	colony stimulating factor 2	Homo sapiens	96-102
20872043-2	2011	The KIT, PDGFR-alpha, and VEGFR2 genes are frequently amplified and expressed in HGG and are molecular targets for therapeutic inhibition by the small-molecule kinase inhibitor sunitinib malate.	Sunitinib	177-193	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-7
20872043-2	2011	The KIT, PDGFR-alpha, and VEGFR2 genes are frequently amplified and expressed in HGG and are molecular targets for therapeutic inhibition by the small-molecule kinase inhibitor sunitinib malate.	Sunitinib	177-193	platelet derived growth factor receptor alpha	Homo sapiens	9-20
20872043-2	2011	The KIT, PDGFR-alpha, and VEGFR2 genes are frequently amplified and expressed in HGG and are molecular targets for therapeutic inhibition by the small-molecule kinase inhibitor sunitinib malate.	Sunitinib	177-193	kinase insert domain receptor	Homo sapiens	26-32
21577109-4	2011	Inhibition of CSF1R using small molecule inhibitors such as imatinib, nilotinib or sunitinib can result in clinical, radiological and functional improvement in the affected joint.	Sunitinib	83-92	colony stimulating factor 1 receptor	Homo sapiens	14-19
21772092-7	2011	Those patients who presented low serum VEGF showed prolonged progression-free survival when treated with sunitinib.	Sunitinib	105-114	vascular endothelial growth factor A	Homo sapiens	39-43
21693010-9	2011	Furthermore, sunitinib attenuated the cell-proliferation activity induced by VEGF-C/D and prevented VEGF-C-induced migration and tube formation of the LECs; however, anti-VEGFR2 treatment shows only a partial effect on the growth and functions of the LECs.	Sunitinib	13-22	vascular endothelial growth factor C	Homo sapiens	77-83
21693010-9	2011	Furthermore, sunitinib attenuated the cell-proliferation activity induced by VEGF-C/D and prevented VEGF-C-induced migration and tube formation of the LECs; however, anti-VEGFR2 treatment shows only a partial effect on the growth and functions of the LECs.	Sunitinib	13-22	vascular endothelial growth factor C	Homo sapiens	100-106
21693010-9	2011	Furthermore, sunitinib attenuated the cell-proliferation activity induced by VEGF-C/D and prevented VEGF-C-induced migration and tube formation of the LECs; however, anti-VEGFR2 treatment shows only a partial effect on the growth and functions of the LECs.	Sunitinib	13-22	kinase insert domain receptor	Homo sapiens	171-177
21693010-13	2011	This effect of sunitinib was more potent than that of DC101, an anti-mouse VEGFR-2 antibody.	Sunitinib	15-24	kinase insert domain receptor	Homo sapiens	75-82
21693010-14	2011	CONCLUSIONS: The results suggest that sunitinib might be beneficial for the treatment of breast cancer by suppressing lymphangiogenesis and lymph node metastasis, through inhibition, particularly important, of VEGFR-3.	Sunitinib	38-47	fms related receptor tyrosine kinase 4	Homo sapiens	210-217
21693010-5	2011	The purpose of this study was to investigate the effects of sunitinib on vascular endothelial growth factor receptor 3 (VEGFR-3) and a related event, lymphangiogenesis.	Sunitinib	60-69	fms related receptor tyrosine kinase 4	Homo sapiens	73-118
21693010-5	2011	The purpose of this study was to investigate the effects of sunitinib on vascular endothelial growth factor receptor 3 (VEGFR-3) and a related event, lymphangiogenesis.	Sunitinib	60-69	fms related receptor tyrosine kinase 4	Homo sapiens	120-127
21693010-6	2011	METHODS: The effects of sunitinib on the degree of phosphorylation of VEGFR-2/3 and other signaling molecules was examined in lymphatic endothelial cells (LECs) treated with the drug; VEGF-induced LEC growth, migration, and tube formation were also examined.	Sunitinib	24-33	kinase insert domain receptor	Homo sapiens	70-79
21693010-6	2011	METHODS: The effects of sunitinib on the degree of phosphorylation of VEGFR-2/3 and other signaling molecules was examined in lymphatic endothelial cells (LECs) treated with the drug; VEGF-induced LEC growth, migration, and tube formation were also examined.	Sunitinib	24-33	vascular endothelial growth factor A	Homo sapiens	70-74
21693010-6	2011	METHODS: The effects of sunitinib on the degree of phosphorylation of VEGFR-2/3 and other signaling molecules was examined in lymphatic endothelial cells (LECs) treated with the drug; VEGF-induced LEC growth, migration, and tube formation were also examined.	Sunitinib	24-33	C-C motif chemokine ligand 16	Homo sapiens	155-158
21693010-8	2011	RESULTS: First, in human LECs, sunitinib blocked both VEGFR-2 and VEGFR-3 phosphorylation induced by VEGF-C or VEGF-D, and abrogated the activation of the downstream molecules extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt.	Sunitinib	31-40	kinase insert domain receptor	Homo sapiens	54-61
21693010-8	2011	RESULTS: First, in human LECs, sunitinib blocked both VEGFR-2 and VEGFR-3 phosphorylation induced by VEGF-C or VEGF-D, and abrogated the activation of the downstream molecules extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt.	Sunitinib	31-40	fms related receptor tyrosine kinase 4	Homo sapiens	66-73
21693010-8	2011	RESULTS: First, in human LECs, sunitinib blocked both VEGFR-2 and VEGFR-3 phosphorylation induced by VEGF-C or VEGF-D, and abrogated the activation of the downstream molecules extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt.	Sunitinib	31-40	vascular endothelial growth factor C	Homo sapiens	101-107
21693010-8	2011	RESULTS: First, in human LECs, sunitinib blocked both VEGFR-2 and VEGFR-3 phosphorylation induced by VEGF-C or VEGF-D, and abrogated the activation of the downstream molecules extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt.	Sunitinib	31-40	vascular endothelial growth factor D	Homo sapiens	111-117
21693010-8	2011	RESULTS: First, in human LECs, sunitinib blocked both VEGFR-2 and VEGFR-3 phosphorylation induced by VEGF-C or VEGF-D, and abrogated the activation of the downstream molecules extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt.	Sunitinib	31-40	mitogen-activated protein kinase 1	Homo sapiens	176-217
21693010-8	2011	RESULTS: First, in human LECs, sunitinib blocked both VEGFR-2 and VEGFR-3 phosphorylation induced by VEGF-C or VEGF-D, and abrogated the activation of the downstream molecules extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt.	Sunitinib	31-40	mitogen-activated protein kinase 3	Homo sapiens	219-225
21693010-8	2011	RESULTS: First, in human LECs, sunitinib blocked both VEGFR-2 and VEGFR-3 phosphorylation induced by VEGF-C or VEGF-D, and abrogated the activation of the downstream molecules extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt.	Sunitinib	31-40	AKT serine/threonine kinase 1	Homo sapiens	231-234
21704235-11	2011	An indirect comparison suggests that sunitinib is likely to demonstrate greater clinical benefit than sorafenib in terms of PFS (HR = 0.47; 95% CI, 0.316-0.713; P &lt; 0.001), using IFN-alpha as the comparator.	Sunitinib	37-46	interferon alpha 1	Homo sapiens	182-191
21672194-7	2011	A number of biologically targeted agents targeting the VEGF and mTOR signaling pathways have recently shown promise, with recent trials showing treatment with the VEGFR tyrosine kinase inhibitor sunitinib or the mTOR inhibitor everolimus improves progression-free survival in patients with advanced NET.	Sunitinib	195-204	vascular endothelial growth factor A	Homo sapiens	55-59
21672194-7	2011	A number of biologically targeted agents targeting the VEGF and mTOR signaling pathways have recently shown promise, with recent trials showing treatment with the VEGFR tyrosine kinase inhibitor sunitinib or the mTOR inhibitor everolimus improves progression-free survival in patients with advanced NET.	Sunitinib	195-204	mechanistic target of rapamycin kinase	Homo sapiens	64-68
21481584-2	2011	Everolimus is an orally administered inhibitor of the mammalian target of rapamycin that recently received approval from the European Medicines Agency for the treatment of advanced RCC that has progressed on or after treatment with vascular endothelial growth factor (VEGF)-targeted therapy, and from the United States Food and Drug Administration for treatment of advanced RCC after failure of sorafenib or sunitinib.	Sunitinib	408-417	vascular endothelial growth factor A	Homo sapiens	268-272
21334201-10	2011	The influence of Imatinib and Sunitinib therapy in metastasized GISTs with wild type genotype and c-kit exon 9 mutations needs further investigation.	Sunitinib	30-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-103
21566429-9	2011	More recently, sunitinib, a new KIT/PDGFRA kinase inhibitor, has been tested in patients with GIST resistant to imatinib with promising results.	Sunitinib	15-24	platelet derived growth factor receptor alpha	Homo sapiens	36-42
21677482-4	2011	Sunitinib malate, a multi-targeted tyrosine kinase inhibitor that shows activity against KIT and other receptor tyrosine kinases, including PDGFR and vascular endothelial growth factor receptor, is the only treatment for imatinib-resistant GISTs that is covered by national health insurance in Japan as ofthis writing.	Sunitinib	0-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	89-92
21677482-4	2011	Sunitinib malate, a multi-targeted tyrosine kinase inhibitor that shows activity against KIT and other receptor tyrosine kinases, including PDGFR and vascular endothelial growth factor receptor, is the only treatment for imatinib-resistant GISTs that is covered by national health insurance in Japan as ofthis writing.	Sunitinib	0-16	platelet derived growth factor receptor beta	Homo sapiens	140-145
21527770-1	2011	BACKGROUND: Hypertension (HTN) is an on-target effect of the vascular endothelial growth factor pathway inhibitor, sunitinib.	Sunitinib	115-124	vascular endothelial growth factor A	Homo sapiens	61-95
21266595-6	2011	In contrast, midazolam 1"-hydroxylation catalyzed by recombinant CYP3A5 was enhanced by the coexistence of sorafenib or sunitinib in a concentration-dependent manner, with saturation occurring at approximately 10 muM.	Sunitinib	120-129	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	65-71
21266595-6	2011	In contrast, midazolam 1"-hydroxylation catalyzed by recombinant CYP3A5 was enhanced by the coexistence of sorafenib or sunitinib in a concentration-dependent manner, with saturation occurring at approximately 10 muM.	Sunitinib	120-129	latexin	Homo sapiens	213-216
21266595-8	2011	Sorafenib N-oxidation and sunitinib N-deethylation, the primary routes of metabolism, were predominantly catalyzed by CYP3A4 but not by CYP3A5.	Sunitinib	26-35	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	118-124
21266595-11	2011	Our results thus showed that sorafenib and sunitinib activated midazolam 1"-hydroxylation by CYP3A5 but inhibited that by CYP3A4.	Sunitinib	43-52	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	93-99
21266595-11	2011	Our results thus showed that sorafenib and sunitinib activated midazolam 1"-hydroxylation by CYP3A5 but inhibited that by CYP3A4.	Sunitinib	43-52	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	122-128
21266595-12	2011	Unexpected drug interactions involving sorafenib and sunitinib might occur via heterotropic cooperativity of CYP3A5.	Sunitinib	53-62	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	109-115
21584715-2	2011	Small molecule tyrosine kinase inhibitors such as sorafenib, sunitinib, and pazopanib inhibit the downstream pathways of all three of the vascular endothelial growth factor receptors (VEGFR 1, 2, and 3).	Sunitinib	61-70	fms related receptor tyrosine kinase 1	Homo sapiens	184-201
21480952-1	2011	AIMS: Reversible posterior leucoencephalopathy syndrome (RPLS) has been reported following the use of anti-vascular endothelial growth factor (VEGF) agents such as bevacizumab, sorafinib and sunitinib.	Sunitinib	191-200	vascular endothelial growth factor A	Homo sapiens	102-141
21480952-1	2011	AIMS: Reversible posterior leucoencephalopathy syndrome (RPLS) has been reported following the use of anti-vascular endothelial growth factor (VEGF) agents such as bevacizumab, sorafinib and sunitinib.	Sunitinib	191-200	vascular endothelial growth factor A	Homo sapiens	143-147
21469976-2	2011	Sunitinib is an oral multitargeted inhibitor of vascular endothelial growth factor receptors (VEGFRs-1, -2, and -3), platelet-derived growth factor receptors (PDGFRs-alpha and -beta), stem-cell factor receptor (KIT), FMS-like tyrosine kinase 3 (FLT3), colony-stimulating factor 1 receptor (CSF-1R), and glial cell line-derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	0-9	fms related receptor tyrosine kinase 1	Homo sapiens	94-114
21469976-2	2011	Sunitinib is an oral multitargeted inhibitor of vascular endothelial growth factor receptors (VEGFRs-1, -2, and -3), platelet-derived growth factor receptors (PDGFRs-alpha and -beta), stem-cell factor receptor (KIT), FMS-like tyrosine kinase 3 (FLT3), colony-stimulating factor 1 receptor (CSF-1R), and glial cell line-derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	159-181
21469976-2	2011	Sunitinib is an oral multitargeted inhibitor of vascular endothelial growth factor receptors (VEGFRs-1, -2, and -3), platelet-derived growth factor receptors (PDGFRs-alpha and -beta), stem-cell factor receptor (KIT), FMS-like tyrosine kinase 3 (FLT3), colony-stimulating factor 1 receptor (CSF-1R), and glial cell line-derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	211-214
21469976-2	2011	Sunitinib is an oral multitargeted inhibitor of vascular endothelial growth factor receptors (VEGFRs-1, -2, and -3), platelet-derived growth factor receptors (PDGFRs-alpha and -beta), stem-cell factor receptor (KIT), FMS-like tyrosine kinase 3 (FLT3), colony-stimulating factor 1 receptor (CSF-1R), and glial cell line-derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	217-243
21469976-2	2011	Sunitinib is an oral multitargeted inhibitor of vascular endothelial growth factor receptors (VEGFRs-1, -2, and -3), platelet-derived growth factor receptors (PDGFRs-alpha and -beta), stem-cell factor receptor (KIT), FMS-like tyrosine kinase 3 (FLT3), colony-stimulating factor 1 receptor (CSF-1R), and glial cell line-derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	245-249
21469976-2	2011	Sunitinib is an oral multitargeted inhibitor of vascular endothelial growth factor receptors (VEGFRs-1, -2, and -3), platelet-derived growth factor receptors (PDGFRs-alpha and -beta), stem-cell factor receptor (KIT), FMS-like tyrosine kinase 3 (FLT3), colony-stimulating factor 1 receptor (CSF-1R), and glial cell line-derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	0-9	colony stimulating factor 1 receptor	Homo sapiens	252-288
21469976-2	2011	Sunitinib is an oral multitargeted inhibitor of vascular endothelial growth factor receptors (VEGFRs-1, -2, and -3), platelet-derived growth factor receptors (PDGFRs-alpha and -beta), stem-cell factor receptor (KIT), FMS-like tyrosine kinase 3 (FLT3), colony-stimulating factor 1 receptor (CSF-1R), and glial cell line-derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	0-9	colony stimulating factor 1 receptor	Homo sapiens	290-296
21469976-2	2011	Sunitinib is an oral multitargeted inhibitor of vascular endothelial growth factor receptors (VEGFRs-1, -2, and -3), platelet-derived growth factor receptors (PDGFRs-alpha and -beta), stem-cell factor receptor (KIT), FMS-like tyrosine kinase 3 (FLT3), colony-stimulating factor 1 receptor (CSF-1R), and glial cell line-derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	0-9	ret proto-oncogene	Homo sapiens	389-392
21266595-0	2011	Sorafenib and sunitinib, two anticancer drugs, inhibit CYP3A4-mediated and activate CY3A5-mediated midazolam 1"-hydroxylation.	Sunitinib	14-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	55-61
21266595-3	2011	The effects of sorafenib and sunitinib on midazolam 1"-hydroxylation catalyzed by human CYP3A4 or CYP3A5 were investigated.	Sunitinib	29-38	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	88-94
21266595-4	2011	Sorafenib and sunitinib inhibited metabolic reactions catalyzed by recombinant CYP3A4.	Sunitinib	14-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	79-85
21240876-13	2011	SUT significantly improved overexpression of dialysate transforming growth factor-ss1, monocyte chemoattractant protein-1 and vascular endothelial growth factor (VEGF) levels as compared with resting group.	Sunitinib	0-3	C-C motif chemokine ligand 2	Rattus norvegicus	87-121
20809412-0	2011	Role of sorafenib and sunitinib in the induction of expressions of NKG2D ligands in nasopharyngeal carcinoma with high expression of ABCG2.	Sunitinib	22-31	killer cell lectin like receptor K1	Homo sapiens	67-72
20809412-0	2011	Role of sorafenib and sunitinib in the induction of expressions of NKG2D ligands in nasopharyngeal carcinoma with high expression of ABCG2.	Sunitinib	22-31	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	133-138
20809412-6	2011	FCM was used to evaluate the expressions of NKG2D ligands (NKG2DLs,) on target cells before and after incubated with sorafenib and sunitinib.	Sunitinib	131-140	killer cell lectin like receptor K1	Homo sapiens	44-49
20809412-8	2011	RESULTS: The results revealed that target cells" cytotoxic sensitivity to natural killer (NK) cells increased in association with up-regulation of NKG2DLs on tumor cells after incubation with sorafenib and sunitinib.	Sunitinib	206-215	killer cell lectin like receptor C1	Homo sapiens	147-151
20809412-9	2011	Furthermore, up-regulation in sunitinib group was much higher than in sorafenib group when it came to the expressions of NKG2DLs on tumor cells.	Sunitinib	30-39	killer cell lectin like receptor C1	Homo sapiens	121-125
20809412-11	2011	CONCLUSIONS: Our research revealed for the first time that sorafenib and sunitinib could up-regulate NKG2DLs on tumor cells resulting in markedly increased tumor cells cytotoxic sensitivity to NK cells, which suggested that combining usage of molecular targeted agents and ACI may result in great benefits in clinical practice for the therapy-resistant cases and drug-resistant relapse.	Sunitinib	73-82	killer cell lectin like receptor C1	Homo sapiens	101-105
21240876-13	2011	SUT significantly improved overexpression of dialysate transforming growth factor-ss1, monocyte chemoattractant protein-1 and vascular endothelial growth factor (VEGF) levels as compared with resting group.	Sunitinib	0-3	vascular endothelial growth factor A	Rattus norvegicus	126-160
21240876-13	2011	SUT significantly improved overexpression of dialysate transforming growth factor-ss1, monocyte chemoattractant protein-1 and vascular endothelial growth factor (VEGF) levels as compared with resting group.	Sunitinib	0-3	vascular endothelial growth factor A	Rattus norvegicus	162-166
21463120-2	2011	We conducted a phase II trial of the multi-targeted vascular endothelial growth factor receptor (VEGFR) kinase inhibitor, sunitinib, 37.5 mg given orally once daily in adult patients with relapsed or refractory DLBCL.	Sunitinib	122-131	kinase insert domain receptor	Homo sapiens	52-95
21463120-2	2011	We conducted a phase II trial of the multi-targeted vascular endothelial growth factor receptor (VEGFR) kinase inhibitor, sunitinib, 37.5 mg given orally once daily in adult patients with relapsed or refractory DLBCL.	Sunitinib	122-131	kinase insert domain receptor	Homo sapiens	97-102
20943595-12	2011	A concurrent fall in HPCs and growth factor expression (IGF-1) with sunitinib occurs.	Sunitinib	68-77	insulin like growth factor 1	Homo sapiens	56-61
21343371-0	2011	IL6-STAT3-HIF signaling and therapeutic response to the angiogenesis inhibitor sunitinib in ovarian clear cell cancer.	Sunitinib	79-88	interleukin 6	Homo sapiens	0-3
21343371-0	2011	IL6-STAT3-HIF signaling and therapeutic response to the angiogenesis inhibitor sunitinib in ovarian clear cell cancer.	Sunitinib	79-88	signal transducer and activator of transcription 3	Homo sapiens	4-9
21309545-8	2011	Furthermore, sunitinib was transported equally by ABCB1 and ABCG2 at low concentrations, but ABCG2-mediated transport became saturated at lower concentrations than ABCB1-mediated transport.	Sunitinib	13-22	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	50-55
21309545-8	2011	Furthermore, sunitinib was transported equally by ABCB1 and ABCG2 at low concentrations, but ABCG2-mediated transport became saturated at lower concentrations than ABCB1-mediated transport.	Sunitinib	13-22	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	60-65
20943595-2	2011	We investigate their expression in mRCC patients treated with sunitinib and correlate their expression with plasma growth factor levels [insulin-like growth factor (IGF)-1].	Sunitinib	62-71	insulin like growth factor 1	Homo sapiens	137-171
21325074-2	2011	Sunitinib, a potent inhibitor of RET, VEGF receptor (VEGFR)-1, VEGFR-2, VEGFR-3, and platelet-derived growth factor receptor (PDGFR)alpha/beta, has been reported as clinically effective in some patients with advanced MTC.	Sunitinib	0-9	ret proto-oncogene	Homo sapiens	33-36
20943595-8	2011	Both HPC and IGF-1 levels fell with sunitinib (61% and 14% fall, respectively, P &lt;0.05 for both).	Sunitinib	36-45	insulin like growth factor 1	Homo sapiens	13-18
21508369-11	2011	The amounts of p-VEGFR-2 and p-Tyr, as determined by immunohistochemistry, were greatly reduced in sunitinib-treated mice.	Sunitinib	99-108	kinase insert domain protein receptor	Mus musculus	17-24
21508369-12	2011	CONCLUSION: In a mouse model of mammary cancer, sunitinib inhibited tumor growth and metastasis (with the exception of lymph node metastasis), angiogenesis, and cell proliferation possibly due to reduced levels of p-VEGFR-2 and p-Tyr.	Sunitinib	48-57	kinase insert domain protein receptor	Mus musculus	216-223
21447721-2	2011	Sorafenib and sunitinib are small molecule inhibitors of multiple kinases including VEGF receptor (VEGFR) kinases.	Sunitinib	14-23	kinase insert domain receptor	Homo sapiens	84-97
21325074-2	2011	Sunitinib, a potent inhibitor of RET, VEGF receptor (VEGFR)-1, VEGFR-2, VEGFR-3, and platelet-derived growth factor receptor (PDGFR)alpha/beta, has been reported as clinically effective in some patients with advanced MTC.	Sunitinib	0-9	fms related receptor tyrosine kinase 1	Homo sapiens	53-61
21447721-2	2011	Sorafenib and sunitinib are small molecule inhibitors of multiple kinases including VEGF receptor (VEGFR) kinases.	Sunitinib	14-23	kinase insert domain receptor	Homo sapiens	99-104
21325074-2	2011	Sunitinib, a potent inhibitor of RET, VEGF receptor (VEGFR)-1, VEGFR-2, VEGFR-3, and platelet-derived growth factor receptor (PDGFR)alpha/beta, has been reported as clinically effective in some patients with advanced MTC.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	63-70
21325074-2	2011	Sunitinib, a potent inhibitor of RET, VEGF receptor (VEGFR)-1, VEGFR-2, VEGFR-3, and platelet-derived growth factor receptor (PDGFR)alpha/beta, has been reported as clinically effective in some patients with advanced MTC.	Sunitinib	0-9	fms related receptor tyrosine kinase 4	Homo sapiens	72-79
21325074-2	2011	Sunitinib, a potent inhibitor of RET, VEGF receptor (VEGFR)-1, VEGFR-2, VEGFR-3, and platelet-derived growth factor receptor (PDGFR)alpha/beta, has been reported as clinically effective in some patients with advanced MTC.	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	126-137
21325074-4	2011	EXPERIMENTAL DESIGN: Both in vitro and in vivo assays, using the human TT RET(C634W) MTC cell line, were done to assess the activity of sunitinib.	Sunitinib	136-145	ret proto-oncogene	Homo sapiens	74-77
21325074-6	2011	RESULTS: Sunitinib displayed antiproliferative and antiangiogenic activities and inhibited RET autophosphorylation and activation of downstream signaling pathways.	Sunitinib	9-18	ret proto-oncogene	Homo sapiens	91-94
21325074-7	2011	We showed that sunitinib treatment induced major changes in the expression of genes involved in tissue invasion and metastasis including vimentin (VIM), urokinase plasminogen (PLAU), tenascin-C (TN-C), SPARC, and CD44.	Sunitinib	15-24	vimentin	Homo sapiens	137-145
21325074-7	2011	We showed that sunitinib treatment induced major changes in the expression of genes involved in tissue invasion and metastasis including vimentin (VIM), urokinase plasminogen (PLAU), tenascin-C (TN-C), SPARC, and CD44.	Sunitinib	15-24	vimentin	Homo sapiens	147-150
21325074-7	2011	We showed that sunitinib treatment induced major changes in the expression of genes involved in tissue invasion and metastasis including vimentin (VIM), urokinase plasminogen (PLAU), tenascin-C (TN-C), SPARC, and CD44.	Sunitinib	15-24	plasminogen activator, urokinase	Homo sapiens	176-180
21325074-7	2011	We showed that sunitinib treatment induced major changes in the expression of genes involved in tissue invasion and metastasis including vimentin (VIM), urokinase plasminogen (PLAU), tenascin-C (TN-C), SPARC, and CD44.	Sunitinib	15-24	tenascin C	Homo sapiens	183-193
21325074-7	2011	We showed that sunitinib treatment induced major changes in the expression of genes involved in tissue invasion and metastasis including vimentin (VIM), urokinase plasminogen (PLAU), tenascin-C (TN-C), SPARC, and CD44.	Sunitinib	15-24	tenascin C	Homo sapiens	195-199
21325074-7	2011	We showed that sunitinib treatment induced major changes in the expression of genes involved in tissue invasion and metastasis including vimentin (VIM), urokinase plasminogen (PLAU), tenascin-C (TN-C), SPARC, and CD44.	Sunitinib	15-24	secreted protein acidic and cysteine rich	Homo sapiens	202-207
21325074-7	2011	We showed that sunitinib treatment induced major changes in the expression of genes involved in tissue invasion and metastasis including vimentin (VIM), urokinase plasminogen (PLAU), tenascin-C (TN-C), SPARC, and CD44.	Sunitinib	15-24	CD44 molecule (Indian blood group)	Homo sapiens	213-217
21325074-8	2011	Analyzing downregulated genes, we identified those encoding secreted proteins and, among them, interleukin (IL)-8 was found to be modulated in the serum of xenografted mice under sunitinib treatment.	Sunitinib	179-188	chemokine (C-X-C motif) ligand 15	Mus musculus	95-113
21540050-8	2011	Additional broad-spectrum VEGF receptor tyrosine kinase inhibitors, such as sunitinib and sorafenib, are used in monotherapy for metastatic renal carcinoma, while sunitinib is also approved for imatinib resistant gastrointestinal stromal tumors and sorafenib for advanced stage hepatocellular carcinoma.	Sunitinib	76-85	vascular endothelial growth factor A	Homo sapiens	26-30
21220434-5	2011	The sunitinib PK study was designed to determine the relationship between CYP3A4 activity and sunitinib exposure using 7.5 mg midazolam orally as a phenotypic probe.	Sunitinib	4-13	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	74-80
21220434-5	2011	The sunitinib PK study was designed to determine the relationship between CYP3A4 activity and sunitinib exposure using 7.5 mg midazolam orally as a phenotypic probe.	Sunitinib	94-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	74-80
21097529-5	2011	We further present evidence that L1-CAM was involved in the resistance against therapeutic reagents like rapamycin, sunitinib and cisplatin.	Sunitinib	116-125	L1 cell adhesion molecule	Homo sapiens	33-39
21057538-0	2011	Fibroblast growth factor 2 regulates endothelial cell sensitivity to sunitinib.	Sunitinib	69-78	fibroblast growth factor 2	Homo sapiens	0-26
21057538-1	2011	The vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor sunitinib has been approved for first-line treatment of patients with metastatic renal cancer and is currently being trialled in other cancers.	Sunitinib	81-90	vascular endothelial growth factor A	Homo sapiens	4-38
21057538-1	2011	The vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor sunitinib has been approved for first-line treatment of patients with metastatic renal cancer and is currently being trialled in other cancers.	Sunitinib	81-90	vascular endothelial growth factor A	Homo sapiens	40-44
21057538-3	2011	By screening a panel of candidate growth factors we identified fibroblast growth factor 2 (FGF2) as a potent regulator of endothelial cell sensitivity to sunitinib.	Sunitinib	154-163	fibroblast growth factor 2	Homo sapiens	63-89
21057538-3	2011	By screening a panel of candidate growth factors we identified fibroblast growth factor 2 (FGF2) as a potent regulator of endothelial cell sensitivity to sunitinib.	Sunitinib	154-163	fibroblast growth factor 2	Homo sapiens	91-95
21057538-4	2011	We show that FGF2 supports endothelial proliferation and de novo tubule formation in the presence of sunitinib and that FGF2 can suppress sunitinib-induced retraction of tubules.	Sunitinib	101-110	fibroblast growth factor 2	Homo sapiens	13-17
21057538-4	2011	We show that FGF2 supports endothelial proliferation and de novo tubule formation in the presence of sunitinib and that FGF2 can suppress sunitinib-induced retraction of tubules.	Sunitinib	138-147	fibroblast growth factor 2	Homo sapiens	120-124
21317875-4	2011	We show that the Xbp1-specific ribonuclease activity depends on autophosphorylation, and that ATP-competitive inhibitors staurosporin and sunitinib, which inhibit autophosphorylation in vitro, also inhibit Xbp1 splicing in vivo.	Sunitinib	138-147	X-box binding protein 1	Homo sapiens	17-21
21317875-4	2011	We show that the Xbp1-specific ribonuclease activity depends on autophosphorylation, and that ATP-competitive inhibitors staurosporin and sunitinib, which inhibit autophosphorylation in vitro, also inhibit Xbp1 splicing in vivo.	Sunitinib	138-147	X-box binding protein 1	Homo sapiens	206-210
20437403-5	2011	The activation of this pathway explains the use of both VEGF and VEGF-receptor inhibitors (bevacizumab, sunitinib and sorafenib) in the therapy of advanced CCRCC.	Sunitinib	104-113	vascular endothelial growth factor A	Homo sapiens	65-69
21308478-2	2011	Recently, data from a phase III trial demonstrated that sunitinib produces a clinically significant improvement in progression-free survival in patients with unresectable, advanced, or metastatic GEP-NETs.	Sunitinib	56-65	granulin precursor	Homo sapiens	196-199
21308478-3	2011	Based on this finding, sunitinib became the first targeted drug approved for the treatment of GEP-NETs, paving the way for the approval of other anticancer agents in this drug-orphan disease.	Sunitinib	23-32	granulin precursor	Homo sapiens	94-97
21233403-10	2011	When combined with sunitinib, sorafenib, bevacizumab, irinotecan, or docetaxel, Ang2 CovX-Bodies produced even greater efficacy (~80% TGI, P &lt; 0.01).	Sunitinib	19-28	angiopoietin 2	Homo sapiens	80-84
20437403-5	2011	The activation of this pathway explains the use of both VEGF and VEGF-receptor inhibitors (bevacizumab, sunitinib and sorafenib) in the therapy of advanced CCRCC.	Sunitinib	104-113	vascular endothelial growth factor A	Homo sapiens	56-60
21097719-3	2011	PDGFRbeta was found to be the main tyrosine kinase target of sunitinib expressed in BM stromal ST-2 and MC3T3-E1 preosteoblastic cells.	Sunitinib	61-70	platelet derived growth factor receptor, beta polypeptide	Mus musculus	0-9
20708948-3	2011	Despite the initial unimpressive clinical performance of anti-VEGF antibody (bevacizumab) as cancer monotherapy, clear improvements in clinical outcomes following combination bevacizumab and chemotherapy regimens and multi-targeted VEGF receptor tyrosine kinase inhibitors (sorafenib and sunitinib) in select tumor types have established VEGF-targeted agents as an effective means of controlling cancer growth.	Sunitinib	288-297	vascular endothelial growth factor A	Homo sapiens	232-236
20708948-3	2011	Despite the initial unimpressive clinical performance of anti-VEGF antibody (bevacizumab) as cancer monotherapy, clear improvements in clinical outcomes following combination bevacizumab and chemotherapy regimens and multi-targeted VEGF receptor tyrosine kinase inhibitors (sorafenib and sunitinib) in select tumor types have established VEGF-targeted agents as an effective means of controlling cancer growth.	Sunitinib	288-297	vascular endothelial growth factor A	Homo sapiens	232-236
21273619-2	2011	Limited clinical trial data have shown minimal activity with cytokines and chemotherapy, although small-molecule inhibitors of the vascular endothelial growth factor and platelet-derived growth factor pathways such as sunitinib and sorafenib, which are associated with significant clinical activity in clear-cell RCC (ccRCC), have been associated with a 25% response rate in chRCC.	Sunitinib	218-227	vascular endothelial growth factor A	Homo sapiens	131-165
21084271-0	2011	VEGF-PET imaging is a noninvasive biomarker showing differential changes in the tumor during sunitinib treatment.	Sunitinib	93-102	vascular endothelial growth factor A	Homo sapiens	0-4
21084271-2	2011	In this study, we evaluated the role of VEGF-PET as a biomarker of dynamic angiogenic changes in tumors following treatment with the kinase inhibitor sunitinib.	Sunitinib	150-159	vascular endothelial growth factor A	Homo sapiens	40-44
21484496-2	2011	The first category, vascular endothelial growth factor (VEGF)-directed therapies, includes sunitinib, pazopanib, sorafenib and bevacizumab.	Sunitinib	91-100	vascular endothelial growth factor A	Homo sapiens	20-54
21484496-2	2011	The first category, vascular endothelial growth factor (VEGF)-directed therapies, includes sunitinib, pazopanib, sorafenib and bevacizumab.	Sunitinib	91-100	vascular endothelial growth factor A	Homo sapiens	56-60
22130231-14	2011	VEGFR tyrosine kinase inhibitors such as sunitinib and sorafenib are also effective in antiangiogenic tumor therapy by inhibiting VEGFR signaling.	Sunitinib	41-50	kinase insert domain receptor	Homo sapiens	0-5
22130231-14	2011	VEGFR tyrosine kinase inhibitors such as sunitinib and sorafenib are also effective in antiangiogenic tumor therapy by inhibiting VEGFR signaling.	Sunitinib	41-50	kinase insert domain receptor	Homo sapiens	130-135
25819130-3	2011	For sunitinib, sorafenib, and pazopanib: potential drug interactions are possible with inducers/inhibitors of CYP3A4, anti-hypertensive drugs, antidiabetic drugs, thyroid hormones, and anticoagulant treatments.	Sunitinib	4-13	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	110-116
21116624-15	2011	The mechanism of resistance to sunitinib is unknown at this time but is also appears related to growth of clones with secondary mutations in KIT.	Sunitinib	31-40	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	141-144
21084271-5	2011	In contrast to (18)F-FDG and (15)O-water PET, VEGF-PET demonstrated dynamic changes during sunitinib treatment within the tumor with a strong decline in signal in the tumor center and only minimal reduction in tumor rim, with a pronounced rebound after sunitinib discontinuation.	Sunitinib	91-100	vascular endothelial growth factor A	Homo sapiens	46-50
21097719-3	2011	PDGFRbeta was found to be the main tyrosine kinase target of sunitinib expressed in BM stromal ST-2 and MC3T3-E1 preosteoblastic cells.	Sunitinib	61-70	interleukin 1 receptor-like 1	Mus musculus	95-99
21097719-5	2011	Incubation of ST-2 and human BM endothelial cells with sunitinib led to potent cell growth inhibition and induction of apoptosis in a dose-dependent manner.	Sunitinib	55-64	ST2	Homo sapiens	14-18
21181476-7	2011	Sunitinib malate, a second-generation KIT inhibitor is active in imatinib-resistant disease and is FDA-approved for use in this setting.	Sunitinib	0-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	38-41
21097719-6	2011	Similarly, sunitinib induced a robust proapoptotic effect in vivo on BM stromal PDGFRbeta(+) cells and produced extensive disruption of tissue architecture and vessel leakage in the BM cavity.	Sunitinib	11-20	platelet derived growth factor receptor, beta polypeptide	Mus musculus	80-89
21097719-7	2011	Pretreatment of ST-2 cells with sunitinib also hindered heterotypic adhesion to lung cancer cell lines.	Sunitinib	32-41	interleukin 1 receptor-like 1	Mus musculus	16-20
21627339-2	2011	Immunotherapy with interferon-alpha (IFNalpha) and interleukin-2 (IL-2) has been the historical therapy of choice for the treatment of locally advanced or metastatic RCC prior to the more recent development of targeted therapies, including sunitinib and bevacizumab (combined with IFNalpha).	Sunitinib	240-249	interleukin 2	Homo sapiens	66-70
22050750-9	2011	Other small molecule inhibitors of VEGF tyrosine kinase activity (TKIs) such as sunitinib, vandetanib and sorafenib are being tested in MBC.	Sunitinib	80-89	vascular endothelial growth factor A	Homo sapiens	35-39
21717054-2	2011	Sunitinib is able to inhibit RTKs such as receptors for platelet-derived growth factor (PDGF-Ralpha and beta) and for vascular endothelial growth factor (VEGFRs).	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	118-152
20304669-7	2011	Since c-kit can be readily inhibited by several small molecule inhibitors including imatinib, sunitinib and dasatinib, targeting immune suppressing cells can be readily accomplished in the clinic.	Sunitinib	94-103	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	6-11
20524040-0	2011	Sunitinib induces PTEN expression and inhibits PDGFR signaling and migration of medulloblastoma cells.	Sunitinib	0-9	phosphatase and tensin homolog	Homo sapiens	18-22
20524040-0	2011	Sunitinib induces PTEN expression and inhibits PDGFR signaling and migration of medulloblastoma cells.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	47-52
20524040-3	2011	In this study, we investigated whether the multi-tyrosine kinase inhibitor sunitinib, effectively inhibits PDGFR signaling required for medulloblastoma cell migration.	Sunitinib	75-84	platelet derived growth factor receptor beta	Homo sapiens	107-112
20524040-4	2011	Daoy and D556 human medulloblastoma cells pre-treated for 1 h with 0.2 muM sunitinib demonstrated induction of PTEN expression and significant inhibition of PDGFR signaling activity and transactivation of EGFR, in a RAS-independent manner, in response to PDGF-BB stimulation.	Sunitinib	75-84	phosphatase and tensin homolog	Homo sapiens	111-115
20524040-4	2011	Daoy and D556 human medulloblastoma cells pre-treated for 1 h with 0.2 muM sunitinib demonstrated induction of PTEN expression and significant inhibition of PDGFR signaling activity and transactivation of EGFR, in a RAS-independent manner, in response to PDGF-BB stimulation.	Sunitinib	75-84	platelet derived growth factor receptor beta	Homo sapiens	157-162
20524040-4	2011	Daoy and D556 human medulloblastoma cells pre-treated for 1 h with 0.2 muM sunitinib demonstrated induction of PTEN expression and significant inhibition of PDGFR signaling activity and transactivation of EGFR, in a RAS-independent manner, in response to PDGF-BB stimulation.	Sunitinib	75-84	epidermal growth factor receptor	Homo sapiens	205-209
20524040-8	2011	Sunitinib similarly inhibited PDGFR signaling and migration of primary murine Smo/Smo medulloblastoma cells, suggesting that the Smo/Smo mouse is an appropriate model for preclinical testing of sunitinib.	Sunitinib	0-9	platelet derived growth factor receptor, beta polypeptide	Mus musculus	30-35
20524040-8	2011	Sunitinib similarly inhibited PDGFR signaling and migration of primary murine Smo/Smo medulloblastoma cells, suggesting that the Smo/Smo mouse is an appropriate model for preclinical testing of sunitinib.	Sunitinib	0-9	smoothened, frizzled class receptor	Mus musculus	78-81
20524040-8	2011	Sunitinib similarly inhibited PDGFR signaling and migration of primary murine Smo/Smo medulloblastoma cells, suggesting that the Smo/Smo mouse is an appropriate model for preclinical testing of sunitinib.	Sunitinib	0-9	smoothened, frizzled class receptor	Mus musculus	82-85
20524040-8	2011	Sunitinib similarly inhibited PDGFR signaling and migration of primary murine Smo/Smo medulloblastoma cells, suggesting that the Smo/Smo mouse is an appropriate model for preclinical testing of sunitinib.	Sunitinib	0-9	smoothened, frizzled class receptor	Mus musculus	82-85
20524040-8	2011	Sunitinib similarly inhibited PDGFR signaling and migration of primary murine Smo/Smo medulloblastoma cells, suggesting that the Smo/Smo mouse is an appropriate model for preclinical testing of sunitinib.	Sunitinib	0-9	smoothened, frizzled class receptor	Mus musculus	82-85
21187670-10	2011	The activity of PI3K/Akt signal pathway was inhibited, which could be the potential mechanisms that account for the enhanced radiation response induced by sunitinib.	Sunitinib	155-164	AKT serine/threonine kinase 1	Homo sapiens	21-24
21980525-10	2011	In agreement, we observed that the binding of VEGFR2 to DNA requires VEGF activation, being blocked by Bevacizumab and Sunitinib, two anti-angiogenic agents that inhibit VEGFR2 activation.	Sunitinib	119-128	kinase insert domain receptor	Homo sapiens	46-52
21344032-9	2011	Sunitinib suppressed the expression of cyclin B1, p-Akt, and t-Akt while augmenting the expression of cyclin D and pro-apoptotic Bax and Bad in HTB5 cells.	Sunitinib	0-9	cyclin B1	Homo sapiens	39-48
21344032-9	2011	Sunitinib suppressed the expression of cyclin B1, p-Akt, and t-Akt while augmenting the expression of cyclin D and pro-apoptotic Bax and Bad in HTB5 cells.	Sunitinib	0-9	AKT serine/threonine kinase 1	Homo sapiens	52-55
21344032-9	2011	Sunitinib suppressed the expression of cyclin B1, p-Akt, and t-Akt while augmenting the expression of cyclin D and pro-apoptotic Bax and Bad in HTB5 cells.	Sunitinib	0-9	AKT serine/threonine kinase 1	Homo sapiens	63-66
21344032-9	2011	Sunitinib suppressed the expression of cyclin B1, p-Akt, and t-Akt while augmenting the expression of cyclin D and pro-apoptotic Bax and Bad in HTB5 cells.	Sunitinib	0-9	BCL2 associated X, apoptosis regulator	Homo sapiens	129-132
21625184-0	2011	Efficacy of sunitinib re-exposure after failure of an mTOR inhibitor in patients with metastatic RCC.	Sunitinib	12-21	mechanistic target of rapamycin kinase	Homo sapiens	54-58
21245940-5	2011	Sunitinib (40 mg/kg, once daily), a receptor tyrosine kinase inhibitor of VEGFR2 and other growth factor receptors, also caused significant loss of tumor blood vessels in RCC models but had weaker effects than DC101 on pericytes and lymphatic vessels.	Sunitinib	0-9	kinase insert domain protein receptor	Mus musculus	74-80
21980525-10	2011	In agreement, we observed that the binding of VEGFR2 to DNA requires VEGF activation, being blocked by Bevacizumab and Sunitinib, two anti-angiogenic agents that inhibit VEGFR2 activation.	Sunitinib	119-128	vascular endothelial growth factor A	Homo sapiens	46-50
21980525-10	2011	In agreement, we observed that the binding of VEGFR2 to DNA requires VEGF activation, being blocked by Bevacizumab and Sunitinib, two anti-angiogenic agents that inhibit VEGFR2 activation.	Sunitinib	119-128	kinase insert domain receptor	Homo sapiens	170-176
20975250-7	2011	RESULTS: Sunitinib was associated with significant declines in total leucocyte (-48%), neutrophil (-62%), CD3 total T cell (-31%) and CD4 counts (32%; p &lt; 0.05).	Sunitinib	9-18	CD4 molecule	Homo sapiens	134-137
20818610-2	2010	Small molecule kinase inhibitors have been developed for the treatment of certain cancers, and some antioncogenic agents such as sunitinib, may nonspecifically inhibit LRRK2.	Sunitinib	129-138	leucine rich repeat kinase 2	Homo sapiens	168-173
21187479-1	2010	OBJECTIVE: The aim of this study was to assess the antitumour effect of an anti-VEGFR (sunitinib) and the anti-EGFR multi-targeted agent (lapatinib), applied either alone or in combination on the migration capacity of two glioma cell lines.	Sunitinib	87-96	kinase insert domain receptor	Homo sapiens	80-85
21187479-1	2010	OBJECTIVE: The aim of this study was to assess the antitumour effect of an anti-VEGFR (sunitinib) and the anti-EGFR multi-targeted agent (lapatinib), applied either alone or in combination on the migration capacity of two glioma cell lines.	Sunitinib	87-96	epidermal growth factor receptor	Homo sapiens	81-85
21187479-2	2010	Furthermore, this study sought to evaluate the effect of lapatinib in the formation of EGFR-integrin beta(1) complex, as well as the effect of sunitinib in the VEGFR-integrin beta(3) and PDGFR-integrin beta(3) complexes formation.	Sunitinib	143-152	kinase insert domain receptor	Homo sapiens	160-165
21187479-9	2010	Likewise, sunitinib inhibited complex formation of VEGFR-integrin beta(3) complex within two h after its application without affecting PDGFR-integrin beta(3) complex.	Sunitinib	10-19	kinase insert domain receptor	Homo sapiens	51-56
21187479-11	2010	CONCLUSION: The preliminary results of this study are the first to support the implication of a dual anti-EGFR/HER-2 agent, lapatinib and a multi-targeted agent, sunitinib in glioma cell migration, through a mechanism implying interruption of growth factor receptor integrin complexes formation.	Sunitinib	162-171	epidermal growth factor receptor	Homo sapiens	106-110
21118964-6	2010	Sunitinib inhibited Stat3 in dendritic cells and T cells and reduced conversion of transferred FoxP3(-) T cells to tumor-associated regulatory T cells while increasing transferred CD8(+) T-cell infiltration and activation at the tumor site, leading to inhibition of primary tumor growth.	Sunitinib	0-9	signal transducer and activator of transcription 3	Homo sapiens	20-25
21118964-6	2010	Sunitinib inhibited Stat3 in dendritic cells and T cells and reduced conversion of transferred FoxP3(-) T cells to tumor-associated regulatory T cells while increasing transferred CD8(+) T-cell infiltration and activation at the tumor site, leading to inhibition of primary tumor growth.	Sunitinib	0-9	forkhead box P3	Homo sapiens	95-100
21118964-6	2010	Sunitinib inhibited Stat3 in dendritic cells and T cells and reduced conversion of transferred FoxP3(-) T cells to tumor-associated regulatory T cells while increasing transferred CD8(+) T-cell infiltration and activation at the tumor site, leading to inhibition of primary tumor growth.	Sunitinib	0-9	CD8a molecule	Homo sapiens	180-183
20952508-0	2010	HGF/c-Met acts as an alternative angiogenic pathway in sunitinib-resistant tumors.	Sunitinib	55-64	hepatocyte growth factor	Homo sapiens	0-3
20952508-0	2010	HGF/c-Met acts as an alternative angiogenic pathway in sunitinib-resistant tumors.	Sunitinib	55-64	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-9
20952508-6	2010	Combination of sunitinib and a selective c-Met inhibitor significantly inhibited tumor growth compared with sunitinib or c-Met inhibitor alone in resistant tumors.	Sunitinib	108-117	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	41-46
20952508-8	2010	Conversely, systemic injection of HGF in the sensitive tumor models conferred resistance to sunitinib through maintenance of tumor angiogenesis.	Sunitinib	92-101	hepatocyte growth factor	Homo sapiens	34-37
20142724-1	2010	OBJECTIVES: Sunitinib is an oral, multitargeted tyrosine kinase inhibitor of vascular endothelial growth factor and platelet-derived growth factor receptors with proven clinical benefit in patients with metastatic renal cell carcinoma (RCC).	Sunitinib	12-21	vascular endothelial growth factor A	Homo sapiens	77-111
21095547-4	2010	Recently, sunitinib demonstrating efficacy in pancreatic islet cell carcinomas has opened a new avenue for the treatment of NETs, and further trials shall be considered in NET types such as carcinoids, poorly differentiated neuroendocrine carcinomas, and several other endocrine tumors that depend on vascular endothelial growth factor (VEGF)/VEGF receptor for angiogenesis.	Sunitinib	10-19	vascular endothelial growth factor A	Homo sapiens	301-335
21095547-4	2010	Recently, sunitinib demonstrating efficacy in pancreatic islet cell carcinomas has opened a new avenue for the treatment of NETs, and further trials shall be considered in NET types such as carcinoids, poorly differentiated neuroendocrine carcinomas, and several other endocrine tumors that depend on vascular endothelial growth factor (VEGF)/VEGF receptor for angiogenesis.	Sunitinib	10-19	vascular endothelial growth factor A	Homo sapiens	337-341
21095547-4	2010	Recently, sunitinib demonstrating efficacy in pancreatic islet cell carcinomas has opened a new avenue for the treatment of NETs, and further trials shall be considered in NET types such as carcinoids, poorly differentiated neuroendocrine carcinomas, and several other endocrine tumors that depend on vascular endothelial growth factor (VEGF)/VEGF receptor for angiogenesis.	Sunitinib	10-19	vascular endothelial growth factor A	Homo sapiens	343-347
21030045-0	2010	The immunocytokine F8-IL2 improves the therapeutic performance of sunitinib in a mouse model of renal cell carcinoma.	Sunitinib	66-75	interleukin-2	Cricetulus griseus	22-25
21030045-6	2010	CONCLUSIONS: Considering that recombinant interleukin-2 based immunocytokines are now being investigated in several clinical trials in patients with cancer alone or combined with chemotherapy our preclinical results provide a motivation to study F8-IL2 combined with sunitinib in clinical trials in patients with kidney cancer.	Sunitinib	267-276	interleukin 2	Homo sapiens	42-55
20948437-5	2010	We observed a decrease in the number of peripheral blood Foxp3+ regulatory T cells after each cycle of sunitinib-based therapy.	Sunitinib	103-112	forkhead box P3	Homo sapiens	57-62
20950441-7	2010	After paracetamol coadministration with low sunitinib doses (group-D), ALT and AST concentrations ranged 182.79-221.03 U/L and 259.7-264.4 U/L respectively, lower than group-B.	Sunitinib	44-53	glutamic pyruvic transaminase, soluble	Mus musculus	71-74
20471160-0	2010	mTOR inhibition by everolimus counteracts VEGF induction by sunitinib and improves anti-tumor activity against gastric cancer in vivo.	Sunitinib	60-69	mechanistic target of rapamycin kinase	Homo sapiens	0-4
20471160-0	2010	mTOR inhibition by everolimus counteracts VEGF induction by sunitinib and improves anti-tumor activity against gastric cancer in vivo.	Sunitinib	60-69	vascular endothelial growth factor A	Homo sapiens	42-46
20471160-2	2010	We hypothesized that mTOR inhibition by everolimus counteracts VEGF induction by sunitinib resulting in an improved anti-tumor activity of sunitinib.	Sunitinib	81-90	mechanistic target of rapamycin kinase	Homo sapiens	21-25
20471160-2	2010	We hypothesized that mTOR inhibition by everolimus counteracts VEGF induction by sunitinib resulting in an improved anti-tumor activity of sunitinib.	Sunitinib	81-90	vascular endothelial growth factor A	Homo sapiens	63-67
20471160-2	2010	We hypothesized that mTOR inhibition by everolimus counteracts VEGF induction by sunitinib resulting in an improved anti-tumor activity of sunitinib.	Sunitinib	139-148	mechanistic target of rapamycin kinase	Homo sapiens	21-25
20471160-2	2010	We hypothesized that mTOR inhibition by everolimus counteracts VEGF induction by sunitinib resulting in an improved anti-tumor activity of sunitinib.	Sunitinib	139-148	vascular endothelial growth factor A	Homo sapiens	63-67
20471160-6	2010	In conclusion mTOR inhibition by everolimus counteracts VEGF induction by sunitinib and results in significant reduction of tumor burden and long-lasting tumor growth control.	Sunitinib	74-83	mechanistic target of rapamycin kinase	Homo sapiens	14-18
20471160-6	2010	In conclusion mTOR inhibition by everolimus counteracts VEGF induction by sunitinib and results in significant reduction of tumor burden and long-lasting tumor growth control.	Sunitinib	74-83	vascular endothelial growth factor A	Homo sapiens	56-60
20950441-8	2010	Paracetamol coadministration with high sunitinib doses showed higher ALT and AST values (range 269.6-349.2 U/L and 430.2-540.3 U/L respectively), p &lt; 0.05.	Sunitinib	39-48	glutamic pyruvic transaminase, soluble	Mus musculus	69-72
20950441-8	2010	Paracetamol coadministration with high sunitinib doses showed higher ALT and AST values (range 269.6-349.2 U/L and 430.2-540.3 U/L respectively), p &lt; 0.05.	Sunitinib	39-48	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	77-80
20686367-1	2010	SU11248 is a selective inhibitor of certain protein kinases including VEGFR types 1-3 that are expressed in human breast cancer.	Sunitinib	0-7	kinase insert domain receptor	Homo sapiens	70-75
20591397-16	2010	Blocking both VEGF and platelet-derived growth factor pathways using sunitinib was 3-fold more effective.	Sunitinib	69-78	vascular endothelial growth factor A	Oryctolagus cuniculus	14-18
20943646-9	2010	The vascular endothelial growth factor inhibitor sunitinib has demonstrated antitumor effects in pancreatic NETs.	Sunitinib	49-58	vascular endothelial growth factor A	Homo sapiens	4-38
20686367-10	2010	VEGF (10 ng/ml) caused a 42% increase in proliferation of E0771 cells, compared to the control (p &lt; 0.01; n = 8), and there was a significant decrease in proliferation of E0771 cells treated with VEGF plus SU11248 (10 mumol/L) vs. the control (65%, p &lt; 0.01).	Sunitinib	209-216	vascular endothelial growth factor A	Homo sapiens	0-4
20686367-11	2010	VEGF caused a 2-fold increase in the proliferation of HUVEC vs. the control (p &lt; 0.01; n = 8), but its action was completely eradicated by SU11248.	Sunitinib	142-149	vascular endothelial growth factor A	Homo sapiens	0-4
20686367-15	2010	These findings support the hypothesis that the antitumor activity of SU11248 on breast cancer is possibly mediated by targeting the paracrine and autocrine effects of VEGF on breast cancer to suppress tumor angiogenesis, proliferation and migration.	Sunitinib	69-76	vascular endothelial growth factor A	Homo sapiens	167-171
20133148-3	2010	Sunitinib is an oral multitargeted inhibitor of the VEGF, platelet-derived growth factor (PDGF), and c-KIT, among others, tyrosine kinase receptors.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	52-56
20133148-3	2010	Sunitinib is an oral multitargeted inhibitor of the VEGF, platelet-derived growth factor (PDGF), and c-KIT, among others, tyrosine kinase receptors.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-106
21090521-3	2010	Sunitinib and sorafenib are small molecule tyrosine kinase inhibitors that target vascular endothelial growth factor receptor, platelet-derived growth factor receptor, C-Kit and others.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	168-173
20733093-0	2010	Hypertension induced by the tyrosine kinase inhibitor sunitinib is associated with increased circulating endothelin-1 levels.	Sunitinib	54-63	endothelin 1	Homo sapiens	105-117
20733093-7	2010	In rats, 8 days of sunitinib administration induced an  30-mm Hg rise in BP, an attenuation of the circadian BP rhythm, and a 3-fold rise in serum endothelin-1 and creatinine, of which all but the rise in creatinine reversed after sunitinib withdrawal.	Sunitinib	19-28	endothelin 1	Rattus norvegicus	147-159
20733093-8	2010	Coronary microvascular function studies after 8 days of sunitinib administration showed decreased responses to bradykinin, angiotensin II, and sodium nitroprusside, all normalizing after sunitinib withdrawal.	Sunitinib	56-65	kininogen 1	Homo sapiens	111-121
20733093-8	2010	Coronary microvascular function studies after 8 days of sunitinib administration showed decreased responses to bradykinin, angiotensin II, and sodium nitroprusside, all normalizing after sunitinib withdrawal.	Sunitinib	56-65	angiotensinogen	Homo sapiens	123-137
20733093-10	2010	In conclusion, sunitinib induces a reversible rise in BP in patients and in rats associated with activation of the endothelin-1 system, suppression of the renin-angiotensin system, and generalized microvascular dysfunction.	Sunitinib	15-24	endothelin 1	Rattus norvegicus	115-127
20733093-10	2010	In conclusion, sunitinib induces a reversible rise in BP in patients and in rats associated with activation of the endothelin-1 system, suppression of the renin-angiotensin system, and generalized microvascular dysfunction.	Sunitinib	15-24	renin	Rattus norvegicus	155-160
19603143-11	2010	However, MMP-9 and MMP-2 levels were decreased 48 h after treatment of M059K cells with sunitinib either alone or in combination with lapatinib.	Sunitinib	88-97	matrix metallopeptidase 9	Homo sapiens	9-14
19603143-11	2010	However, MMP-9 and MMP-2 levels were decreased 48 h after treatment of M059K cells with sunitinib either alone or in combination with lapatinib.	Sunitinib	88-97	matrix metallopeptidase 2	Homo sapiens	19-24
20699227-6	2010	Sunitinib administration led to an early downmodulation of IFNgamma levels as well as reduction of IFNgamma receptor and downstream angiostatic chemokines CXCL9 to 11 within the tumor.	Sunitinib	0-9	interferon gamma	Homo sapiens	59-67
19649772-1	2010	BACKGROUND: Sunitinib is an orally administered multitargeted tyrosine kinase inhibitor of RET, VEGFR, PDGFR, and c-KIT.	Sunitinib	12-21	ret proto-oncogene	Homo sapiens	91-94
19649772-1	2010	BACKGROUND: Sunitinib is an orally administered multitargeted tyrosine kinase inhibitor of RET, VEGFR, PDGFR, and c-KIT.	Sunitinib	12-21	kinase insert domain receptor	Homo sapiens	96-101
19649772-1	2010	BACKGROUND: Sunitinib is an orally administered multitargeted tyrosine kinase inhibitor of RET, VEGFR, PDGFR, and c-KIT.	Sunitinib	12-21	platelet derived growth factor receptor beta	Homo sapiens	103-108
19649772-1	2010	BACKGROUND: Sunitinib is an orally administered multitargeted tyrosine kinase inhibitor of RET, VEGFR, PDGFR, and c-KIT.	Sunitinib	12-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	114-119
19649772-22	2010	Sunitinib was well tolerated in PS 2 patients.	Sunitinib	0-9	taste 2 receptor member 64 pseudogene	Homo sapiens	32-36
20699227-6	2010	Sunitinib administration led to an early downmodulation of IFNgamma levels as well as reduction of IFNgamma receptor and downstream angiostatic chemokines CXCL9 to 11 within the tumor.	Sunitinib	0-9	interferon gamma	Homo sapiens	99-107
20699227-6	2010	Sunitinib administration led to an early downmodulation of IFNgamma levels as well as reduction of IFNgamma receptor and downstream angiostatic chemokines CXCL9 to 11 within the tumor.	Sunitinib	0-9	C-X-C motif chemokine ligand 9	Homo sapiens	155-160
20699227-7	2010	Intratumoral injection of CXCL9, although producing minimal effects by itself, when combined with sunitinib resulted in delayed resistance in vivo accompanied by a prolonged reduction of microvascular density and tumor perfusion as measured by perfusion imaging relative to sunitinib alone.	Sunitinib	98-107	C-X-C motif chemokine ligand 9	Homo sapiens	26-31
20699227-7	2010	Intratumoral injection of CXCL9, although producing minimal effects by itself, when combined with sunitinib resulted in delayed resistance in vivo accompanied by a prolonged reduction of microvascular density and tumor perfusion as measured by perfusion imaging relative to sunitinib alone.	Sunitinib	274-283	C-X-C motif chemokine ligand 9	Homo sapiens	26-31
20039326-6	2010	The addition of sunitinib to VEGF-stimulated NCI-N87 cells was associated with a reduction in MAPK phosphorylation (pMAPK) but not Akt phosphorylation (pAkt), whereas the addition of vandetanib was associated with reductions in both VEGF- and EGF-mediated VEGFR2 phosphorylation, pMAPK and pAkt.	Sunitinib	16-25	vascular endothelial growth factor A	Homo sapiens	29-33
20652398-2	2010	The method involves a two-arm open-label (2:1 randomization) multicenter, randomized phase II trial evaluating the efficacy of sunitinib (arm A) versus no therapy (arm B) in patients with HER-2-negative metastatic breast cancer who achieved an objective response to taxane-based chemotherapy.	Sunitinib	127-136	erb-b2 receptor tyrosine kinase 2	Homo sapiens	188-193
20625300-4	2010	Sunitinib, sorafenib, bevacizumab with interferon-alpha, pazopanib, temsirolimus, and everolimus have improved clinical outcomes in randomized phase III clinical trials by inhibiting vascular endothelial growth factors, other tyrosine kinases, the mammalian target of rapamycin pathway, and other related pathways.	Sunitinib	0-9	mechanistic target of rapamycin kinase	Homo sapiens	248-277
20922699-7	2010	Inhibitors of vascular endothelial growth factor (VEGF), such as bevacizumab, sunitinib, and sorafenib, interfere with angiogenesis.	Sunitinib	78-87	vascular endothelial growth factor A	Homo sapiens	14-48
20922699-7	2010	Inhibitors of vascular endothelial growth factor (VEGF), such as bevacizumab, sunitinib, and sorafenib, interfere with angiogenesis.	Sunitinib	78-87	vascular endothelial growth factor A	Homo sapiens	50-54
20922699-9	2010	Sunitinib and sorafenib are small molecules inhibiting tyrosine kinase of the intracellular domain of the VEGF receptor.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	106-110
20637791-4	2010	But apoptotic markers (PARP cleavage, caspase 3 cleavage and chromatin condensation) were uniformly negative in H9c2 cells after Sunitinib treatment for 48 h, indicating that another cell death pathway may be involved in Sunitinib-induced cardiotoxicity.	Sunitinib	129-138	caspase 3	Rattus norvegicus	38-47
20637791-7	2010	Furthermore, knocking down Beclin 1 by RNA-interference to block autophagy in H9c2 cells revealed that the death rate was decreased when treated with Sunitinib in comparison to control cells.	Sunitinib	150-159	beclin 1	Rattus norvegicus	27-35
20659021-6	2010	Our results suggest that H-1152 and sunitinib induce dephosphorylation of Ser910 and Ser935 by inhibiting LRRK2 kinase activity, as these compounds failed to induce significant dephosphorylation of a drug-resistant LRRK2(A2016T) mutant.	Sunitinib	36-45	leucine rich repeat kinase 2	Homo sapiens	106-111
20659021-6	2010	Our results suggest that H-1152 and sunitinib induce dephosphorylation of Ser910 and Ser935 by inhibiting LRRK2 kinase activity, as these compounds failed to induce significant dephosphorylation of a drug-resistant LRRK2(A2016T) mutant.	Sunitinib	36-45	leucine rich repeat kinase 2	Homo sapiens	215-220
20840755-0	2010	Brain natriuretic peptide precursor (NT-pro-BNP) levels predict for clinical benefit to sunitinib treatment in patients with metastatic renal cell carcinoma.	Sunitinib	88-97	natriuretic peptide B	Homo sapiens	44-47
20230385-5	2010	RESULTS: There was heterogeneity in tumour responsiveness to sunitinib or sorafenib according to CAIX status; the mean shrinkage was -17% vs -25% for sunitinib-treated patients with high vs low tumour CAIX expression, compared to -13% vs +9% for sorafenib-treated patients (P interaction, 0.05).	Sunitinib	61-70	carbonic anhydrase 9	Homo sapiens	97-101
20230385-5	2010	RESULTS: There was heterogeneity in tumour responsiveness to sunitinib or sorafenib according to CAIX status; the mean shrinkage was -17% vs -25% for sunitinib-treated patients with high vs low tumour CAIX expression, compared to -13% vs +9% for sorafenib-treated patients (P interaction, 0.05).	Sunitinib	61-70	carbonic anhydrase 9	Homo sapiens	201-205
20230385-5	2010	RESULTS: There was heterogeneity in tumour responsiveness to sunitinib or sorafenib according to CAIX status; the mean shrinkage was -17% vs -25% for sunitinib-treated patients with high vs low tumour CAIX expression, compared to -13% vs +9% for sorafenib-treated patients (P interaction, 0.05).	Sunitinib	150-159	carbonic anhydrase 9	Homo sapiens	97-101
20230385-5	2010	RESULTS: There was heterogeneity in tumour responsiveness to sunitinib or sorafenib according to CAIX status; the mean shrinkage was -17% vs -25% for sunitinib-treated patients with high vs low tumour CAIX expression, compared to -13% vs +9% for sorafenib-treated patients (P interaction, 0.05).	Sunitinib	150-159	carbonic anhydrase 9	Homo sapiens	201-205
20039326-5	2010	Both EGF and VEGF were shown to stimulate tumor cell growth, and both sunitinib and vandetanib were found to be associated with significant dose-dependent inhibition of proliferation and an enhancement of apoptosis, as determined by MTT and propidium iodide/Annexin V labeling assays, respectively.	Sunitinib	70-79	annexin A5	Homo sapiens	258-267
20039326-6	2010	The addition of sunitinib to VEGF-stimulated NCI-N87 cells was associated with a reduction in MAPK phosphorylation (pMAPK) but not Akt phosphorylation (pAkt), whereas the addition of vandetanib was associated with reductions in both VEGF- and EGF-mediated VEGFR2 phosphorylation, pMAPK and pAkt.	Sunitinib	16-25	vascular endothelial growth factor A	Homo sapiens	233-237
20039326-6	2010	The addition of sunitinib to VEGF-stimulated NCI-N87 cells was associated with a reduction in MAPK phosphorylation (pMAPK) but not Akt phosphorylation (pAkt), whereas the addition of vandetanib was associated with reductions in both VEGF- and EGF-mediated VEGFR2 phosphorylation, pMAPK and pAkt.	Sunitinib	16-25	kinase insert domain receptor	Homo sapiens	256-262
20133077-13	2010	CONCLUSIONS: These preliminary results suggest that sunitinib and helical tomotherapy yield high Response Evaluation Criteria in Solid Tumors (RECIST) and AFP response rates in advanced HCC with an acceptable safety profile.	Sunitinib	52-61	alpha fetoprotein	Homo sapiens	155-158
20629553-0	2010	Sunitinib inhibits MEK/ERK and SAPK/JNK pathways and increases sodium/iodide symporter expression in papillary thyroid cancer.	Sunitinib	0-9	mitogen-activated protein kinase kinase 7	Homo sapiens	19-22
20629553-1	2010	BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET.	Sunitinib	12-28	vascular endothelial growth factor A	Homo sapiens	174-178
20629553-0	2010	Sunitinib inhibits MEK/ERK and SAPK/JNK pathways and increases sodium/iodide symporter expression in papillary thyroid cancer.	Sunitinib	0-9	mitogen-activated protein kinase 1	Homo sapiens	23-26
20629553-1	2010	BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET.	Sunitinib	12-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	186-189
20629553-1	2010	BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET.	Sunitinib	12-28	fms related receptor tyrosine kinase 3	Homo sapiens	191-195
20629553-0	2010	Sunitinib inhibits MEK/ERK and SAPK/JNK pathways and increases sodium/iodide symporter expression in papillary thyroid cancer.	Sunitinib	0-9	mitogen-activated protein kinase 9	Homo sapiens	31-35
20629553-1	2010	BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET.	Sunitinib	12-28	ret proto-oncogene	Homo sapiens	201-204
20629553-1	2010	BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET.	Sunitinib	30-36	vascular endothelial growth factor A	Homo sapiens	174-178
20629553-1	2010	BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET.	Sunitinib	30-36	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	186-189
20629553-1	2010	BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET.	Sunitinib	30-36	fms related receptor tyrosine kinase 3	Homo sapiens	191-195
20629553-0	2010	Sunitinib inhibits MEK/ERK and SAPK/JNK pathways and increases sodium/iodide symporter expression in papillary thyroid cancer.	Sunitinib	0-9	mitogen-activated protein kinase 8	Homo sapiens	36-39
20629553-1	2010	BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET.	Sunitinib	30-36	ret proto-oncogene	Homo sapiens	201-204
20686603-3	2010	Sunitinib is a drug targeting receptor tyrosine kinases (RTK) like PDGFRalpha, c-Kit and VEGFR-2.	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	67-77
20629553-1	2010	BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET.	Sunitinib	52-59	vascular endothelial growth factor A	Homo sapiens	174-178
20629553-1	2010	BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET.	Sunitinib	52-59	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	186-189
20629553-1	2010	BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET.	Sunitinib	52-59	fms related receptor tyrosine kinase 3	Homo sapiens	191-195
20629553-1	2010	BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET.	Sunitinib	52-59	ret proto-oncogene	Homo sapiens	201-204
20629553-2	2010	The objective of this study was to determine the effects of sunitinib on signal transduction pathways and on gene expression of iodide-metabolizing proteins in papillary cancer cells with the RET/PTC1 rearrangement.	Sunitinib	60-69	ret proto-oncogene	Homo sapiens	192-195
20629553-2	2010	The objective of this study was to determine the effects of sunitinib on signal transduction pathways and on gene expression of iodide-metabolizing proteins in papillary cancer cells with the RET/PTC1 rearrangement.	Sunitinib	60-69	patched 1	Homo sapiens	196-200
20629553-4	2010	RESULTS: Sunitinib inhibited proliferation of RET/PTC1 subclones in a time- and dose-related manner.	Sunitinib	9-18	ret proto-oncogene	Homo sapiens	46-49
20629553-4	2010	RESULTS: Sunitinib inhibited proliferation of RET/PTC1 subclones in a time- and dose-related manner.	Sunitinib	9-18	patched 1	Homo sapiens	50-54
20629553-6	2010	Incubation of RET/PTC1 cells with 1 microM sunitinib inhibited their migration potential and transformed their morphology.	Sunitinib	43-52	ret proto-oncogene	Homo sapiens	14-17
20629553-6	2010	Incubation of RET/PTC1 cells with 1 microM sunitinib inhibited their migration potential and transformed their morphology.	Sunitinib	43-52	patched 1	Homo sapiens	18-22
20629553-7	2010	Sunitinib inhibited RET autophosphorylation at Y1062 and the activation of signal transducer and activator of transcription 3 by blocking Y705 phosphorylation.	Sunitinib	0-9	ret proto-oncogene	Homo sapiens	20-23
20629553-7	2010	Sunitinib inhibited RET autophosphorylation at Y1062 and the activation of signal transducer and activator of transcription 3 by blocking Y705 phosphorylation.	Sunitinib	0-9	signal transducer and activator of transcription 3	Homo sapiens	75-125
20629553-9	2010	Western blot analysis of the p38, MEK/ERK, and SAPK/JNK mitogen-activated protein kinase signal transduction pathways showed that sunitinib blocked ERK 1/2 and JNK phosphorylation in the cytoplasm.	Sunitinib	130-139	mitogen-activated protein kinase 1	Homo sapiens	29-32
20629553-9	2010	Western blot analysis of the p38, MEK/ERK, and SAPK/JNK mitogen-activated protein kinase signal transduction pathways showed that sunitinib blocked ERK 1/2 and JNK phosphorylation in the cytoplasm.	Sunitinib	130-139	mitogen-activated protein kinase kinase 7	Homo sapiens	34-37
20629553-9	2010	Western blot analysis of the p38, MEK/ERK, and SAPK/JNK mitogen-activated protein kinase signal transduction pathways showed that sunitinib blocked ERK 1/2 and JNK phosphorylation in the cytoplasm.	Sunitinib	130-139	mitogen-activated protein kinase 1	Homo sapiens	38-41
20629553-9	2010	Western blot analysis of the p38, MEK/ERK, and SAPK/JNK mitogen-activated protein kinase signal transduction pathways showed that sunitinib blocked ERK 1/2 and JNK phosphorylation in the cytoplasm.	Sunitinib	130-139	mitogen-activated protein kinase 9	Homo sapiens	47-51
20629553-9	2010	Western blot analysis of the p38, MEK/ERK, and SAPK/JNK mitogen-activated protein kinase signal transduction pathways showed that sunitinib blocked ERK 1/2 and JNK phosphorylation in the cytoplasm.	Sunitinib	130-139	mitogen-activated protein kinase 8	Homo sapiens	52-55
20629553-9	2010	Western blot analysis of the p38, MEK/ERK, and SAPK/JNK mitogen-activated protein kinase signal transduction pathways showed that sunitinib blocked ERK 1/2 and JNK phosphorylation in the cytoplasm.	Sunitinib	130-139	mitogen-activated protein kinase 3	Homo sapiens	148-155
20629553-9	2010	Western blot analysis of the p38, MEK/ERK, and SAPK/JNK mitogen-activated protein kinase signal transduction pathways showed that sunitinib blocked ERK 1/2 and JNK phosphorylation in the cytoplasm.	Sunitinib	130-139	mitogen-activated protein kinase 8	Homo sapiens	160-163
20629553-10	2010	Sunitinib treatment of RET/PTC1 cell lines, in combination, with forskolin induced expression of the sodium (Na)/iodide (I) symporter (NIS) and the transcription factors that bind the NIS upstream enhancer.	Sunitinib	0-9	ret proto-oncogene	Homo sapiens	23-26
20629553-10	2010	Sunitinib treatment of RET/PTC1 cell lines, in combination, with forskolin induced expression of the sodium (Na)/iodide (I) symporter (NIS) and the transcription factors that bind the NIS upstream enhancer.	Sunitinib	0-9	patched 1	Homo sapiens	27-31
20629553-12	2010	CONCLUSION: Sunitinib appears to target the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell lines, suggesting that blocking these pathways is at least part of the mechanism by which sunitinib inhibits cell proliferation and causes stimulation of NIS gene expression in RET/PTC1 cells.	Sunitinib	12-21	mitogen-activated protein kinase kinase 7	Homo sapiens	54-57
20629553-12	2010	CONCLUSION: Sunitinib appears to target the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell lines, suggesting that blocking these pathways is at least part of the mechanism by which sunitinib inhibits cell proliferation and causes stimulation of NIS gene expression in RET/PTC1 cells.	Sunitinib	12-21	mitogen-activated protein kinase 1	Homo sapiens	58-61
20629553-12	2010	CONCLUSION: Sunitinib appears to target the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell lines, suggesting that blocking these pathways is at least part of the mechanism by which sunitinib inhibits cell proliferation and causes stimulation of NIS gene expression in RET/PTC1 cells.	Sunitinib	12-21	mitogen-activated protein kinase 9	Homo sapiens	66-70
20629553-12	2010	CONCLUSION: Sunitinib appears to target the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell lines, suggesting that blocking these pathways is at least part of the mechanism by which sunitinib inhibits cell proliferation and causes stimulation of NIS gene expression in RET/PTC1 cells.	Sunitinib	12-21	mitogen-activated protein kinase 8	Homo sapiens	71-74
20629553-12	2010	CONCLUSION: Sunitinib appears to target the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell lines, suggesting that blocking these pathways is at least part of the mechanism by which sunitinib inhibits cell proliferation and causes stimulation of NIS gene expression in RET/PTC1 cells.	Sunitinib	12-21	ret proto-oncogene	Homo sapiens	91-94
20629553-12	2010	CONCLUSION: Sunitinib appears to target the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell lines, suggesting that blocking these pathways is at least part of the mechanism by which sunitinib inhibits cell proliferation and causes stimulation of NIS gene expression in RET/PTC1 cells.	Sunitinib	12-21	patched 1	Homo sapiens	95-99
20629553-12	2010	CONCLUSION: Sunitinib appears to target the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell lines, suggesting that blocking these pathways is at least part of the mechanism by which sunitinib inhibits cell proliferation and causes stimulation of NIS gene expression in RET/PTC1 cells.	Sunitinib	12-21	ret proto-oncogene	Homo sapiens	282-285
20629553-12	2010	CONCLUSION: Sunitinib appears to target the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell lines, suggesting that blocking these pathways is at least part of the mechanism by which sunitinib inhibits cell proliferation and causes stimulation of NIS gene expression in RET/PTC1 cells.	Sunitinib	12-21	patched 1	Homo sapiens	286-290
20013807-9	2010	However, imatinib and sunitinib did induce secretion of anti-inflammatory IL-10 in macrophage cultures, indicating that treatment with these inhibitors might contribute to an immune suppressive microenvironment in GIST.	Sunitinib	22-31	interleukin 10	Homo sapiens	74-79
20545945-2	2010	By applying high-throughput protein engineering and crystallization, we have determined the X-ray crystal structures of IL-2-inducible T cell kinase in complex with its selective inhibitor BMS-509744 and the broad-spectrum kinase inhibitors sunitinib and RO5191614.	Sunitinib	241-250	interleukin 2	Homo sapiens	120-124
20545945-3	2010	Sunitinib uniquely stabilizes IL-2-inducible T cell kinase in the helix C-in conformation by inducing side chain conformational changes in the ATP-binding site.	Sunitinib	0-9	IL2 inducible T cell kinase	Homo sapiens	30-58
19547919-2	2010	We conducted a single-institution phase II trial of sunitinib, an oral inhibitor of the VEGF receptor, in patients with relapsed or refractory GCT.	Sunitinib	52-61	vascular endothelial growth factor A	Homo sapiens	88-92
20520641-0	2010	Identification of a secondary FLT3/A848P mutation in a patient with FLT3-ITD-positive blast phase CMML and response to sunitinib and sorafenib.	Sunitinib	119-128	fms related receptor tyrosine kinase 3	Homo sapiens	30-34
20520641-0	2010	Identification of a secondary FLT3/A848P mutation in a patient with FLT3-ITD-positive blast phase CMML and response to sunitinib and sorafenib.	Sunitinib	119-128	fms related receptor tyrosine kinase 3	Homo sapiens	68-72
20179017-9	2010	Our study is the first to show a direct link between MGMT expression and decreased angiogenicity and tumorigenicity of GBM cells and suggests the combination of sunitinib and standard therapy as an alternative strategy for GBM patients with MGMT-positive tumors.	Sunitinib	161-170	O-6-methylguanine-DNA methyltransferase	Homo sapiens	53-57
20137855-1	2010	The present data showed that sunitinib potentiated the in vitro and in vivo anticancer capabilities of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), also known as Apo2 ligand.	Sunitinib	29-38	TNF superfamily member 10	Homo sapiens	103-158
20137855-1	2010	The present data showed that sunitinib potentiated the in vitro and in vivo anticancer capabilities of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), also known as Apo2 ligand.	Sunitinib	29-38	TNF superfamily member 10	Homo sapiens	160-165
20137855-1	2010	The present data showed that sunitinib potentiated the in vitro and in vivo anticancer capabilities of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), also known as Apo2 ligand.	Sunitinib	29-38	TNF superfamily member 10	Homo sapiens	182-193
20163917-5	2010	In contrast, non-VEGF-related side effects are observed with agents inhibiting multiple receptor tyrosine kinases (sunitinib, sorafenib, axitinib and pazopanib) and mammalian target of rapamycin inhibitors (temsirolimus and everolimus); these include diarrhoea, skin rash, stomatitis, hand-foot skin reaction, hypothyroidism, and haematological and metabolic abnormalities.	Sunitinib	115-124	vascular endothelial growth factor A	Homo sapiens	17-21
20179017-0	2010	MGMT modulates glioblastoma angiogenesis and response to the tyrosine kinase inhibitor sunitinib.	Sunitinib	87-96	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-4
20179017-3	2010	We showed that the addition of sunitinib to standard therapy (temozolomide [TMZ] and radiation therapy [RT]) significantly improved the response of MGMT-positive but not of MGMT-negative cells.	Sunitinib	31-40	O-6-methylguanine-DNA methyltransferase	Homo sapiens	148-152
20179017-3	2010	We showed that the addition of sunitinib to standard therapy (temozolomide [TMZ] and radiation therapy [RT]) significantly improved the response of MGMT-positive but not of MGMT-negative cells.	Sunitinib	31-40	O-6-methylguanine-DNA methyltransferase	Homo sapiens	173-177
20137855-6	2010	Furthermore, treatment of colon cancer SW620-bearing nude mice with sunitinib plus TRAIL resulted in more significant tumor growth inhibition (52.8%), comparing with the moderate inhibition in TRAIL-treated (35.3%) or sunitinib-treated groups (26.7%) (p&lt;0.05).	Sunitinib	68-77	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	193-198
20137855-6	2010	Furthermore, treatment of colon cancer SW620-bearing nude mice with sunitinib plus TRAIL resulted in more significant tumor growth inhibition (52.8%), comparing with the moderate inhibition in TRAIL-treated (35.3%) or sunitinib-treated groups (26.7%) (p&lt;0.05).	Sunitinib	218-227	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	83-88
20686603-3	2010	Sunitinib is a drug targeting receptor tyrosine kinases (RTK) like PDGFRalpha, c-Kit and VEGFR-2.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	79-84
20686603-3	2010	Sunitinib is a drug targeting receptor tyrosine kinases (RTK) like PDGFRalpha, c-Kit and VEGFR-2.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	89-96
20599738-0	2010	Sunitinib deregulates tumor adaptation to hypoxia by inhibiting HIF-1alpha synthesis in HT-29 colon cancer cells.	Sunitinib	0-9	hypoxia inducible factor 1 subunit alpha	Homo sapiens	64-74
20686603-10	2010	Moreover, sunitinib induced apoptosis and prevented PDGF-AA induced signaling via PDGFRalpha as determined by western blotting.	Sunitinib	10-19	platelet derived growth factor receptor alpha	Homo sapiens	82-92
20599738-2	2010	Preclinical studies demonstrated that the sunitinib effects are attributed to inhibition of VEGFR and PDGFR phosphorylation.	Sunitinib	42-51	kinase insert domain receptor	Homo sapiens	92-97
20599738-2	2010	Preclinical studies demonstrated that the sunitinib effects are attributed to inhibition of VEGFR and PDGFR phosphorylation.	Sunitinib	42-51	platelet derived growth factor receptor beta	Homo sapiens	102-107
20599738-5	2010	First we found that sunitinib limits the colony growth of HT-29, which is a colon adenocarcinoma cell line lacking the RTKs, and that HIF-1alpha in the colonies is decreased by sunitinib.	Sunitinib	177-186	hypoxia inducible factor 1 subunit alpha	Homo sapiens	134-144
20686603-12	2010	We show that VEGF triggered signal transduction via the MAPK pathway, which could be blocked by sunitinib.	Sunitinib	96-105	vascular endothelial growth factor A	Homo sapiens	13-17
20599738-6	2010	In cultured HT-29 cells, sunitinib suppressed HIF-1alpha under hypoxic conditions.	Sunitinib	25-34	hypoxia inducible factor 1 subunit alpha	Homo sapiens	46-56
20599738-7	2010	Moreover, sunitinib repressed the activity of HIF-1alpha and subsequently decreased the expressions of HIF-1 downstream genes.	Sunitinib	10-19	hypoxia inducible factor 1 subunit alpha	Homo sapiens	46-56
20686603-14	2010	Presence of the 4q12 amplicon and subsequent over-expression of PDGFRA might serve as predictive markers for efficacy of sunitinib.	Sunitinib	121-130	platelet derived growth factor receptor alpha	Homo sapiens	64-70
20599738-7	2010	Moreover, sunitinib repressed the activity of HIF-1alpha and subsequently decreased the expressions of HIF-1 downstream genes.	Sunitinib	10-19	hypoxia inducible factor 1 subunit alpha	Homo sapiens	46-51
20599738-8	2010	Mechanistically, sunitinib blocked the 5"-UTR-dependent translation of HIF-1alpha.	Sunitinib	17-26	hypoxia inducible factor 1 subunit alpha	Homo sapiens	71-81
20601807-7	2010	Sunitinib, which targets VEGF-1, 2 and 3 and PDGF seems to be a well tolerated treatment for advanced tumors.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	25-29
20599738-9	2010	The HIF-1alpha suppression by sunitinib was also reproduced in a VHL-null renal cell carcinoma cell line, where HIF-1alpha is not degradable.	Sunitinib	30-39	hypoxia inducible factor 1 subunit alpha	Homo sapiens	4-14
20599738-9	2010	The HIF-1alpha suppression by sunitinib was also reproduced in a VHL-null renal cell carcinoma cell line, where HIF-1alpha is not degradable.	Sunitinib	30-39	hypoxia inducible factor 1 subunit alpha	Homo sapiens	112-122
20599738-10	2010	In conclusion, the sunitinib inhibition of HIF-1 signaling could restrain tumor progression in hypoxic regions, which may contribute to anticancer effect of sunitinib.	Sunitinib	19-28	hypoxia inducible factor 1 subunit alpha	Homo sapiens	43-48
20599738-10	2010	In conclusion, the sunitinib inhibition of HIF-1 signaling could restrain tumor progression in hypoxic regions, which may contribute to anticancer effect of sunitinib.	Sunitinib	157-166	hypoxia inducible factor 1 subunit alpha	Homo sapiens	43-48
20558072-4	2010	Remarkably, dimethylation of both the 4-N and N7 afford whole cell EGFR inhibitors that are more cytotoxic than clinically used erlotinib and mono-methylation at the 4-N or N7 affords more cytotoxic whole cell PDGFR-beta inhibitors than clinically used sunitinib.	Sunitinib	253-262	epidermal growth factor receptor	Homo sapiens	67-71
20204363-3	2010	Sunitinib malate is a VEGFR inhibitor approved for the treatment of advanced renal cell carcinoma.	Sunitinib	0-16	kinase insert domain receptor	Homo sapiens	22-27
20345483-0	2010	Pharmacological interaction with sunitinib is abolished by a germ-line mutation (1291T&gt;C) of BCRP/ABCG2 gene.	Sunitinib	33-42	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	96-100
20495370-0	2010	SU11248 (sunitinib) directly inhibits the activity of mammalian 5"-AMP-activated protein kinase (AMPK).	Sunitinib	0-7	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	97-101
20495370-0	2010	SU11248 (sunitinib) directly inhibits the activity of mammalian 5"-AMP-activated protein kinase (AMPK).	Sunitinib	9-18	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	97-101
20495370-6	2010	Here we report that the chemotherapeutic drug SU11248 (sunitinib) is at least as potent an inhibitor of AMPK as compound C, which is a commonly used experimental direct inhibitor of the enzyme.	Sunitinib	46-53	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	104-108
20495370-6	2010	Here we report that the chemotherapeutic drug SU11248 (sunitinib) is at least as potent an inhibitor of AMPK as compound C, which is a commonly used experimental direct inhibitor of the enzyme.	Sunitinib	55-64	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	104-108
20495370-8	2010	The ability of SU11248 to inhibit AMPK has potential clinical significance--there may be populations of SU11248-treated patients in which AMPK activity is inhibited in normal as well as in tumor tissue.	Sunitinib	15-22	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	34-38
20495370-8	2010	The ability of SU11248 to inhibit AMPK has potential clinical significance--there may be populations of SU11248-treated patients in which AMPK activity is inhibited in normal as well as in tumor tissue.	Sunitinib	15-22	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	138-142
20495370-8	2010	The ability of SU11248 to inhibit AMPK has potential clinical significance--there may be populations of SU11248-treated patients in which AMPK activity is inhibited in normal as well as in tumor tissue.	Sunitinib	104-111	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	34-38
20495370-8	2010	The ability of SU11248 to inhibit AMPK has potential clinical significance--there may be populations of SU11248-treated patients in which AMPK activity is inhibited in normal as well as in tumor tissue.	Sunitinib	104-111	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	138-142
20571071-4	2010	Small molecule tyrosine kinase inhibitors (TKI) targeting the VEGF receptor (i.e., sunitinib, sorafenib, and vandetanib) show activity in phase II clinical studies.	Sunitinib	83-92	vascular endothelial growth factor A	Homo sapiens	62-66
20509775-2	2010	The efforts in this area have been greatly enhanced by the approval of tyrosine kinase inhibitors with PDGFR inhibitory activity such as imatinib, sunitinib and sorafenib.	Sunitinib	147-156	platelet derived growth factor receptor beta	Homo sapiens	103-108
20533592-4	2010	Imatinib and sunitinib, both tyrosine kinase inhibitors directed to KIT, were approved for first- and second-line treatment of metastatic and unresectable GISTs.	Sunitinib	13-22	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-71
20345483-0	2010	Pharmacological interaction with sunitinib is abolished by a germ-line mutation (1291T&gt;C) of BCRP/ABCG2 gene.	Sunitinib	33-42	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	101-106
20345483-4	2010	Sunitinib remarkably reversed BCRP-mediated and partially reversed P-gp-mediated drug resistance in the respective transfectants.	Sunitinib	0-9	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	30-34
20345483-4	2010	Sunitinib remarkably reversed BCRP-mediated and partially reversed P-gp-mediated drug resistance in the respective transfectants.	Sunitinib	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	67-71
20345483-5	2010	The in vitro vesicle transport assay indicated that sunitinib competitively inhibited BCRP-mediated estrone 3-sulfate transport and P-gp-mediated vincristine transport.	Sunitinib	52-61	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	86-90
20345483-5	2010	The in vitro vesicle transport assay indicated that sunitinib competitively inhibited BCRP-mediated estrone 3-sulfate transport and P-gp-mediated vincristine transport.	Sunitinib	52-61	ATP binding cassette subfamily B member 1	Homo sapiens	132-136
20345483-9	2010	Thus, residue Phe-431 of BCRP is important for the pharmacological interaction with sunitinib and FTC.	Sunitinib	84-93	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	25-29
19444655-1	2010	Sunitinib is a recently approved tyrosine-kinase inhibitor that targets the vascular endothelial growth factor receptors (VEGFR).	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	76-120
20733555-4	2010	Sorafenib and sunitinib were the first FLT3 inhibitors to be studied in the clinic and have the most clinically relevant data.	Sunitinib	14-23	fms related receptor tyrosine kinase 3	Homo sapiens	39-43
20484434-0	2010	Molecular imaging of changes in the prevalence of vascular endothelial growth factor receptor in sunitinib-treated murine mammary tumors.	Sunitinib	97-106	vascular endothelial growth factor A	Mus musculus	50-84
19444655-1	2010	Sunitinib is a recently approved tyrosine-kinase inhibitor that targets the vascular endothelial growth factor receptors (VEGFR).	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	122-127
20067776-7	2010	Many of these drugs, including emetine, fluorosalan, sunitinib malate, bithionol, narasin, tribromsalan, and lestaurtinib, inhibited NF-kappaB signaling via inhibition of IkappaBalpha phosphorylation.	Sunitinib	53-69	nuclear factor kappa B subunit 1	Homo sapiens	133-142
20231424-2	2010	We studied whether sunitinib, a multityrosine kinase inhibitor that inhibits KIT, enhances engraftment after bone marrow transplantation (BMT) in mice.	Sunitinib	19-28	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	77-80
20231424-7	2010	Sunitinib did not increase engraftment in mice with deficient KIT signaling, and the pattern of more potent effects on T cell compared with HSC engraftment observed in sunitinib-treated hosts was also observed after BMT into KIT(W/Wv) mice.	Sunitinib	168-177	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	225-228
20502715-0	2010	Soluble isoforms of vascular endothelial growth factor are predictors of response to sunitinib in metastatic renal cell carcinomas.	Sunitinib	85-94	vascular endothelial growth factor A	Homo sapiens	20-54
20502715-8	2010	Among transcripts analyzed, only the levels of vascular endothelial growth factor (VEGF) soluble isoforms (VEGF(121) and VEGF(165)) were associated with the response to sunitinib (P = 0.04 for both).	Sunitinib	169-178	vascular endothelial growth factor A	Homo sapiens	47-81
20502715-8	2010	Among transcripts analyzed, only the levels of vascular endothelial growth factor (VEGF) soluble isoforms (VEGF(121) and VEGF(165)) were associated with the response to sunitinib (P = 0.04 for both).	Sunitinib	169-178	vascular endothelial growth factor A	Homo sapiens	83-87
20502715-8	2010	Among transcripts analyzed, only the levels of vascular endothelial growth factor (VEGF) soluble isoforms (VEGF(121) and VEGF(165)) were associated with the response to sunitinib (P = 0.04 for both).	Sunitinib	169-178	vascular endothelial growth factor A	Homo sapiens	107-111
20502715-8	2010	Among transcripts analyzed, only the levels of vascular endothelial growth factor (VEGF) soluble isoforms (VEGF(121) and VEGF(165)) were associated with the response to sunitinib (P = 0.04 for both).	Sunitinib	169-178	vascular endothelial growth factor A	Homo sapiens	107-111
20208561-9	2010	In a neuroblastoma xenograft model, tumor growth inhibition by sunitinib was associated with inhibition of angiogenesis and reduced HIF-1alpha levels.	Sunitinib	63-72	hypoxia inducible factor 1 subunit alpha	Homo sapiens	132-142
20067776-7	2010	Many of these drugs, including emetine, fluorosalan, sunitinib malate, bithionol, narasin, tribromsalan, and lestaurtinib, inhibited NF-kappaB signaling via inhibition of IkappaBalpha phosphorylation.	Sunitinib	53-69	NFKB inhibitor alpha	Homo sapiens	171-183
20147887-7	2010	Our study shows that serum levels of VEGF and NGAL are significant predictors of progression-free survival in patients with renal cell carcinoma treated with sunitinib.	Sunitinib	158-167	lipocalin 2	Homo sapiens	46-50
20406969-6	2010	Proteomic analyses comparing tumor to peripheral compartments showed that granulocyte macrophage colony-stimulating factor (GM-CSF) predicted sunitinib resistance and recombinant GM-CSF conferred sunitinib resistance to MDSC in vivo and in vitro.	Sunitinib	142-151	colony stimulating factor 2	Homo sapiens	74-122
20406969-6	2010	Proteomic analyses comparing tumor to peripheral compartments showed that granulocyte macrophage colony-stimulating factor (GM-CSF) predicted sunitinib resistance and recombinant GM-CSF conferred sunitinib resistance to MDSC in vivo and in vitro.	Sunitinib	142-151	colony stimulating factor 2	Homo sapiens	124-130
20406969-6	2010	Proteomic analyses comparing tumor to peripheral compartments showed that granulocyte macrophage colony-stimulating factor (GM-CSF) predicted sunitinib resistance and recombinant GM-CSF conferred sunitinib resistance to MDSC in vivo and in vitro.	Sunitinib	196-205	colony stimulating factor 2	Homo sapiens	179-185
20406969-8	2010	STAT5ab(null/null) MDSC were rendered sensitive to sunitinib in the presence of GM-CSF in vitro.	Sunitinib	51-60	signal transducer and activator of transcription 5A	Homo sapiens	0-5
20406969-8	2010	STAT5ab(null/null) MDSC were rendered sensitive to sunitinib in the presence of GM-CSF in vitro.	Sunitinib	51-60	colony stimulating factor 2	Homo sapiens	80-86
20406969-9	2010	We conclude that compartment-dependent GM-CSF exposure in resistant tumors may account for the regionalized effect of sunitinib upon host MDSC modulation and hypothesize that ancillary strategies to decrease such regionalized escape will enhance the potency of sunitinib as an immunomodulator and a cancer therapy.	Sunitinib	118-127	colony stimulating factor 2	Homo sapiens	39-45
20406969-9	2010	We conclude that compartment-dependent GM-CSF exposure in resistant tumors may account for the regionalized effect of sunitinib upon host MDSC modulation and hypothesize that ancillary strategies to decrease such regionalized escape will enhance the potency of sunitinib as an immunomodulator and a cancer therapy.	Sunitinib	261-270	colony stimulating factor 2	Homo sapiens	39-45
20335444-7	2010	VEGF receptor (VEGFR) tyrosine kinase inhibition (through exposure to sunitinib and 676475) blocked vhl(-/-)-induced angiogenesis in all affected tissues, demonstrating that Vegfaa, Vegfab and Vegfb are key effectors of the vhl(-/-) angiogenic phenotype through Flt1, Kdr and Kdr-like signaling.	Sunitinib	70-79	vascular endothelial growth factor Aa	Danio rerio	0-4
20335444-7	2010	VEGF receptor (VEGFR) tyrosine kinase inhibition (through exposure to sunitinib and 676475) blocked vhl(-/-)-induced angiogenesis in all affected tissues, demonstrating that Vegfaa, Vegfab and Vegfb are key effectors of the vhl(-/-) angiogenic phenotype through Flt1, Kdr and Kdr-like signaling.	Sunitinib	70-79	von Hippel-Lindau tumor suppressor	Danio rerio	100-103
20351323-1	2010	PURPOSE: Sunitinib and sorafenib are oral vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) used in a vast range of cancers.	Sunitinib	9-18	kinase insert domain receptor	Homo sapiens	42-85
20351323-1	2010	PURPOSE: Sunitinib and sorafenib are oral vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) used in a vast range of cancers.	Sunitinib	9-18	kinase insert domain receptor	Homo sapiens	87-92
20351323-11	2010	CONCLUSION: Treatment with VEGFR TKIs sunitinib and sorafenib is associated with a significant increase in the risk of ATEs.	Sunitinib	38-47	kinase insert domain receptor	Homo sapiens	27-32
20147887-0	2010	Predictive value of baseline serum vascular endothelial growth factor and neutrophil gelatinase-associated lipocalin in advanced kidney cancer patients receiving sunitinib.	Sunitinib	162-171	vascular endothelial growth factor A	Homo sapiens	35-69
20147887-0	2010	Predictive value of baseline serum vascular endothelial growth factor and neutrophil gelatinase-associated lipocalin in advanced kidney cancer patients receiving sunitinib.	Sunitinib	162-171	lipocalin 2	Homo sapiens	74-116
20147887-7	2010	Our study shows that serum levels of VEGF and NGAL are significant predictors of progression-free survival in patients with renal cell carcinoma treated with sunitinib.	Sunitinib	158-167	vascular endothelial growth factor A	Homo sapiens	37-41
20339913-0	2010	Phase III randomized trial of sunitinib versus capecitabine in patients with previously treated HER2-negative advanced breast cancer.	Sunitinib	30-39	erb-b2 receptor tyrosine kinase 2	Homo sapiens	96-100
20064605-5	2010	The molecularly targeted cancer therapeutics, sunitinib and imatinib, exhibited profound effects on Ca(i)(2+), combining effects of cytotoxic chemotherapeutics, TdP inducers and potent hERG channel blockers.	Sunitinib	46-55	ETS transcription factor ERG	Homo sapiens	185-189
20234089-6	2010	However, preconditioning by short-term Sm treatment proved to be successful as an adjunct therapy, increasing the frequency of IFN-gamma+ and IFN-gamma+TNF+CD4+ T cells, enhancing NO production by splenic macrophages, and providing dose-sparing effects when combined with a first-line immune-dependent anti-leishmanial drug.	Sunitinib	39-41	interferon gamma	Mus musculus	127-136
20234089-6	2010	However, preconditioning by short-term Sm treatment proved to be successful as an adjunct therapy, increasing the frequency of IFN-gamma+ and IFN-gamma+TNF+CD4+ T cells, enhancing NO production by splenic macrophages, and providing dose-sparing effects when combined with a first-line immune-dependent anti-leishmanial drug.	Sunitinib	39-41	interferon gamma	Mus musculus	142-151
20234089-6	2010	However, preconditioning by short-term Sm treatment proved to be successful as an adjunct therapy, increasing the frequency of IFN-gamma+ and IFN-gamma+TNF+CD4+ T cells, enhancing NO production by splenic macrophages, and providing dose-sparing effects when combined with a first-line immune-dependent anti-leishmanial drug.	Sunitinib	39-41	tumor necrosis factor	Mus musculus	152-155
20368728-5	2010	Drugs that modulate the downstream targets of the pVHL/HIF pathway, including sunitinib, sorafenib, temsirolimus and bevacizumab, have proven benefit in treating ccRCC.	Sunitinib	78-87	von Hippel-Lindau tumor suppressor	Homo sapiens	50-54
20015695-5	2010	In addition, sunitinib led to accumulation in G(0)/G(1) phase of the cell cycle, inhibition of cytokine production, downregulation of activation markers expression and blockade of Zap-70 signaling in the T cells.	Sunitinib	13-22	zeta chain of T cell receptor associated protein kinase 70	Homo sapiens	180-186
20446917-4	2010	In these conditions, abrogating specifically Pgp-mediated efflux in vitro revealed the remarkable and statistically significant cellular accumulation of imatinib (difference in cellular levels between Pgp-expressing and silenced cells, at high and low incubation concentration, respectively: 6.1 and 6.6), dasatinib (4.9 and 5.6), sunitinib (3.7 and 7.3) and sorafenib (1.2 and 1.4), confirming that these TKIs are all substrates of Pgp.	Sunitinib	331-340	ATP binding cassette subfamily B member 1	Homo sapiens	45-48
20147452-0	2010	Function of activation loop tyrosine phosphorylation in the mechanism of c-Kit auto-activation and its implication in sunitinib resistance.	Sunitinib	118-127	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-78
20658715-2	2010	Vascular endothelial growth factor (VEGF) pathway is the principle target for drugs like sunitinib, sorafenib and bevacizumab.	Sunitinib	89-98	vascular endothelial growth factor A	Homo sapiens	0-34
20658715-2	2010	Vascular endothelial growth factor (VEGF) pathway is the principle target for drugs like sunitinib, sorafenib and bevacizumab.	Sunitinib	89-98	vascular endothelial growth factor A	Homo sapiens	36-40
20095048-2	2010	Biophysical, biochemical, and structural studies have provided insight into the molecular basis of resistance to the KIT inhibitors, imatinib and sunitinib.	Sunitinib	146-155	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	117-120
20095048-3	2010	Here, solution-phase hydrogen/deuterium exchange (HDX) and direct binding mass spectrometry experiments provide a link between static structure models and the dynamic equilibrium of the multiple states of KIT, supporting that sunitinib targets the autoinhibited conformation of WT-KIT.	Sunitinib	226-235	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	205-208
20095048-3	2010	Here, solution-phase hydrogen/deuterium exchange (HDX) and direct binding mass spectrometry experiments provide a link between static structure models and the dynamic equilibrium of the multiple states of KIT, supporting that sunitinib targets the autoinhibited conformation of WT-KIT.	Sunitinib	226-235	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	281-284
20095048-6	2010	This result correlates with the V560D mutant exhibiting a sensitivity to sunitinib that is less than for WT KIT but greater than for KIT D816H.	Sunitinib	73-82	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	108-111
19626587-0	2010	Rlip76 transports sunitinib and sorafenib and mediates drug resistance in kidney cancer.	Sunitinib	18-27	ralA binding protein 1	Homo sapiens	0-6
19626587-6	2010	Results of these studies show that sorafenib as well as sunitinib are substrates for transport by RLIP76 thus are competitive inhibitors of GS-E transport.	Sunitinib	56-65	ralA binding protein 1	Homo sapiens	98-104
20019017-4	2010	The renal biopsy revealed focal segmental glomerulosclerosis (FSGS) in addition to thrombotic microangiopathy (TMA), and the complete syndrome disappeared 6 months after sunitinib withdrawal.	Sunitinib	170-179	actinin alpha 4	Homo sapiens	62-66
20019017-5	2010	To our knowledge, this is the first case of FSGS associated to TMA secondary to sunitinib treatment.	Sunitinib	80-89	actinin alpha 4	Homo sapiens	44-48
19949796-1	2010	The discovery of activating oncogenic C-KIT and PDGFRA mutations in gastrointestinal stromal tumors (GIST) represented the key for the development of innovative targeted molecular therapy using the tyrosine kinase inhibitors (TKI) Imatinib (Glivec(R)), Sunitinib and other substances.	Sunitinib	253-262	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	38-43
19949796-1	2010	The discovery of activating oncogenic C-KIT and PDGFRA mutations in gastrointestinal stromal tumors (GIST) represented the key for the development of innovative targeted molecular therapy using the tyrosine kinase inhibitors (TKI) Imatinib (Glivec(R)), Sunitinib and other substances.	Sunitinib	253-262	platelet derived growth factor receptor alpha	Homo sapiens	48-54
20103651-0	2010	Interleukin-8 mediates resistance to antiangiogenic agent sunitinib in renal cell carcinoma.	Sunitinib	58-67	C-X-C motif chemokine ligand 8	Homo sapiens	0-13
20187785-1	2010	BACKGROUND: Sunitinib is a small molecule that inhibits receptor tyrosine kinases, including the vascular endothelial growth factor receptors, and exhibits antiangiogenic and antitumor activity.	Sunitinib	12-21	vascular endothelial growth factor A	Homo sapiens	97-131
19952730-2	2010	This is the first report of sorafenib and sunitinib, both small molecule tyrosine kinase inhibitors of vascular endothelial growth factor and platelet-derived growth factor receptors, triggering radiation recall dermatitis.	Sunitinib	42-51	vascular endothelial growth factor A	Homo sapiens	103-137
20103629-4	2010	Microarray expression profiling and Western blot analysis revealed that among known sunitinib targets, only platelet-derived growth factor receptor-beta and vascular endothelial growth factor receptor-2 (VEGFR-2) were overexpressed in ccRCCs relative to normal tissues.	Sunitinib	84-93	platelet derived growth factor receptor beta	Homo sapiens	108-152
20103629-4	2010	Microarray expression profiling and Western blot analysis revealed that among known sunitinib targets, only platelet-derived growth factor receptor-beta and vascular endothelial growth factor receptor-2 (VEGFR-2) were overexpressed in ccRCCs relative to normal tissues.	Sunitinib	84-93	kinase insert domain receptor	Homo sapiens	157-202
20103651-6	2010	Notably, escape coincided with increased secretion of interleukin-8 (IL-8) from tumors into the plasma, and coadministration of an IL-8 neutralizing antibody resensitized tumors to sunitinib treatment.	Sunitinib	181-190	C-X-C motif chemokine ligand 8	Homo sapiens	131-135
20103629-4	2010	Microarray expression profiling and Western blot analysis revealed that among known sunitinib targets, only platelet-derived growth factor receptor-beta and vascular endothelial growth factor receptor-2 (VEGFR-2) were overexpressed in ccRCCs relative to normal tissues.	Sunitinib	84-93	kinase insert domain receptor	Homo sapiens	204-211
20103629-6	2010	In contrast, sunitinib inhibited endothelial cell proliferation and motility at the same concentrations by suppressing VEGFR-2 signaling.	Sunitinib	13-22	kinase insert domain receptor	Homo sapiens	119-126
20103651-7	2010	In patients who were refractory to sunitinib treatment, IL-8 expression was elevated in ccRCC tumors, supporting the concept that IL-8 levels might predict clinical response to sunitinib.	Sunitinib	177-186	C-X-C motif chemokine ligand 8	Homo sapiens	56-60
20103651-7	2010	In patients who were refractory to sunitinib treatment, IL-8 expression was elevated in ccRCC tumors, supporting the concept that IL-8 levels might predict clinical response to sunitinib.	Sunitinib	177-186	C-X-C motif chemokine ligand 8	Homo sapiens	130-134
20103651-8	2010	Our results reveal IL-8 as an important contributor to sunitinib resistance in ccRCC and a candidate therapeutic target to reverse acquired or intrinsic resistance to sunitinib in this malignancy.	Sunitinib	55-64	C-X-C motif chemokine ligand 8	Homo sapiens	19-23
20103651-8	2010	Our results reveal IL-8 as an important contributor to sunitinib resistance in ccRCC and a candidate therapeutic target to reverse acquired or intrinsic resistance to sunitinib in this malignancy.	Sunitinib	167-176	C-X-C motif chemokine ligand 8	Homo sapiens	19-23
19940466-5	2010	Sunitinib, a small molecule blocking intracellular VEGF, KIT, Flt3 and PDGF receptors, which regulate angiogenesis and cell growth, is approved for the treatment of advanced renal cell cancer (RCC) and malignant gastrointestinal stromal tumor.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	51-55
20721275-2	2010	These include the immunotherapeutics, alfa-interferon, and interleukin-2, and agents that target the vascular endothelial growth factor receptor (VEGFR) via its tyrosine kinase, such as sorafenib, sunitinib, and pazopanib, or the mammalian target of rapamycin (mTOR), such as temsirolimus and everolimus.	Sunitinib	197-206	kinase insert domain receptor	Homo sapiens	101-144
21067536-6	2010	While, the role of sunitinib and inhibitors of mammalian target of rapamycin (mTOR) in breast cancer has to be defined.	Sunitinib	19-28	mechanistic target of rapamycin kinase	Homo sapiens	78-82
19996579-3	2010	Recently 12 cases of metastatic melanoma and KIT-activating mutations have been published to be successfully treated with c-KIT blockers such as imatinib, sunitinib, dasatinib or sorafenib.	Sunitinib	155-164	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-48
19996579-3	2010	Recently 12 cases of metastatic melanoma and KIT-activating mutations have been published to be successfully treated with c-KIT blockers such as imatinib, sunitinib, dasatinib or sorafenib.	Sunitinib	155-164	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	122-127
20696054-6	2010	Genes whose protein products are targeted by the RET inhibitors sunitinib and sorafenib correlated with being amplified and or highly expressed.	Sunitinib	64-73	ret proto-oncogene	Homo sapiens	49-52
20103668-4	2010	It is likely that the multikinase inhibitors, sorafenib, sunitinib, axitinib, and motesanib, whose targets include VEGFR-2, exert their effects primarily through inhibition of endothelial cells.	Sunitinib	57-66	kinase insert domain receptor	Homo sapiens	115-122
19740535-2	2010	Sunitinib malate is an oral, multi-targeted tyrosine kinase inhibitor that inhibits receptors for VEGF, c-Kit and platelet-derived growth factor.	Sunitinib	0-16	vascular endothelial growth factor A	Homo sapiens	98-102
19740535-2	2010	Sunitinib malate is an oral, multi-targeted tyrosine kinase inhibitor that inhibits receptors for VEGF, c-Kit and platelet-derived growth factor.	Sunitinib	0-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	104-109
20031962-8	2010	However, clinical development of small molecule multi-kinase inhibitors including those targeting vascular endothelial growth factor receptors, such as vandetanib, sunitinib and sorafenib, has not been very successful.	Sunitinib	164-173	vascular endothelial growth factor A	Homo sapiens	98-132
20165865-6	2010	Although, KIT (CD117) immunohistochemistry is a reliable diagnostic tool in the diagnosis of GIST, KIT-negative GISTs, GISTs showing unusual morphology as well as GISTs which progress during or after treatment with imatinib/sunitinib can be a challenge for pathologists and clinicians.	Sunitinib	224-233	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-13
19900123-2	2010	The receptor tyrosine kinase (RTK) inhibitor imatinib mesylate has been approved as the first-line choice of therapy for this group of patients, while the RTK inhibitor, sunitinib malate, has been approved for the treatment of GIST after disease progression or intolerance to imatinib.	Sunitinib	170-186	ret proto-oncogene	Homo sapiens	155-158
20721275-2	2010	These include the immunotherapeutics, alfa-interferon, and interleukin-2, and agents that target the vascular endothelial growth factor receptor (VEGFR) via its tyrosine kinase, such as sorafenib, sunitinib, and pazopanib, or the mammalian target of rapamycin (mTOR), such as temsirolimus and everolimus.	Sunitinib	197-206	kinase insert domain receptor	Homo sapiens	146-151
20949248-2	2010	Sunitinib is able to inhibit RTKs such as receptors for platelet-derived growth factor (PDGF-R alpha and beta) and for vascular endothelial growth factor (VEGFRs).	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	88-100
20949248-2	2010	Sunitinib is able to inhibit RTKs such as receptors for platelet-derived growth factor (PDGF-R alpha and beta) and for vascular endothelial growth factor (VEGFRs).	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	119-153
21158731-4	2010	The initial pessimism about the usefulness of the antiangiogenic therapeutic approach for cancer, derived from the poor results obtained in clinical trials, turned into euphoria after the approvals of the anti-VEGF monoclonal antibody bevacizumab and the multitargeted tyrosine kinase inhibitors sunitinib, sorafenib and pazopanib.	Sunitinib	296-305	vascular endothelial growth factor A	Homo sapiens	210-214
19940466-5	2010	Sunitinib, a small molecule blocking intracellular VEGF, KIT, Flt3 and PDGF receptors, which regulate angiogenesis and cell growth, is approved for the treatment of advanced renal cell cancer (RCC) and malignant gastrointestinal stromal tumor.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-60
20102396-9	2010	In vitro, addition of sunitinib prevented the release of endocan in human umbilical vascular endothelial cells when induced by vascular endothelial growth factor.	Sunitinib	22-31	endothelial cell specific molecule 1	Homo sapiens	57-64
20102396-9	2010	In vitro, addition of sunitinib prevented the release of endocan in human umbilical vascular endothelial cells when induced by vascular endothelial growth factor.	Sunitinib	22-31	vascular endothelial growth factor A	Homo sapiens	127-161
19940466-5	2010	Sunitinib, a small molecule blocking intracellular VEGF, KIT, Flt3 and PDGF receptors, which regulate angiogenesis and cell growth, is approved for the treatment of advanced renal cell cancer (RCC) and malignant gastrointestinal stromal tumor.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	62-66
19833232-0	2010	Therapeutic activity of sunitinib for Her2/neu induced mammary cancer in FVB mice.	Sunitinib	24-33	erb-b2 receptor tyrosine kinase 2	Mus musculus	38-42
19833232-0	2010	Therapeutic activity of sunitinib for Her2/neu induced mammary cancer in FVB mice.	Sunitinib	24-33	erb-b2 receptor tyrosine kinase 2	Mus musculus	43-46
19833232-5	2010	In association with its therapeutic activity, sunitinib reduced the absolute number of splenic T-reg cells (CD4(+)CD25(+)CD62L(+)) and MDSCs (CD11b(+)Gr1(+)) that were increased during tumor progression with less activity in mice with gross tumors.	Sunitinib	46-55	integrin alpha M	Mus musculus	142-147
19833232-8	2010	Additionally immune-regulatory cytokines and enzymes were down regulated by sunitinib treatment, including TGFbeta and NOS2 in the spleen cells of sunitinib treated mice as compared to untreated tumor bearing (TB) mice.	Sunitinib	76-85	transforming growth factor, beta 1	Mus musculus	107-114
19833232-8	2010	Additionally immune-regulatory cytokines and enzymes were down regulated by sunitinib treatment, including TGFbeta and NOS2 in the spleen cells of sunitinib treated mice as compared to untreated tumor bearing (TB) mice.	Sunitinib	76-85	nitric oxide synthase 2, inducible	Mus musculus	119-123
19833232-8	2010	Additionally immune-regulatory cytokines and enzymes were down regulated by sunitinib treatment, including TGFbeta and NOS2 in the spleen cells of sunitinib treated mice as compared to untreated tumor bearing (TB) mice.	Sunitinib	147-156	transforming growth factor, beta 1	Mus musculus	107-114
19833232-8	2010	Additionally immune-regulatory cytokines and enzymes were down regulated by sunitinib treatment, including TGFbeta and NOS2 in the spleen cells of sunitinib treated mice as compared to untreated tumor bearing (TB) mice.	Sunitinib	147-156	nitric oxide synthase 2, inducible	Mus musculus	119-123
20215359-3	2010	These include the vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors sunitinib and sorafenib, which inhibit angiogenic signaling in endothelial cells and vascular pericytes predominantly through VEGFR and platelet-derived growth factor receptor beta.	Sunitinib	97-106	kinase insert domain receptor	Homo sapiens	18-61
20053726-10	2010	Expression of a constitutively activated STAT3 mutant or myristoylated AKT partially blocked the effects of sunitinib in these tumor cells.	Sunitinib	108-117	signal transducer and activator of transcription 3	Homo sapiens	41-46
20053726-10	2010	Expression of a constitutively activated STAT3 mutant or myristoylated AKT partially blocked the effects of sunitinib in these tumor cells.	Sunitinib	108-117	AKT serine/threonine kinase 1	Homo sapiens	71-74
20215359-3	2010	These include the vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors sunitinib and sorafenib, which inhibit angiogenic signaling in endothelial cells and vascular pericytes predominantly through VEGFR and platelet-derived growth factor receptor beta.	Sunitinib	97-106	kinase insert domain receptor	Homo sapiens	223-228
20215359-3	2010	These include the vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors sunitinib and sorafenib, which inhibit angiogenic signaling in endothelial cells and vascular pericytes predominantly through VEGFR and platelet-derived growth factor receptor beta.	Sunitinib	97-106	platelet derived growth factor receptor beta	Homo sapiens	233-277
20053726-0	2010	Sunitinib induces apoptosis and growth arrest of medulloblastoma tumor cells by inhibiting STAT3 and AKT signaling pathways.	Sunitinib	0-9	signal transducer and activator of transcription 3	Homo sapiens	91-96
20053726-0	2010	Sunitinib induces apoptosis and growth arrest of medulloblastoma tumor cells by inhibiting STAT3 and AKT signaling pathways.	Sunitinib	0-9	AKT serine/threonine kinase 1	Homo sapiens	101-104
20053726-4	2010	Sunitinib treatment resulted in the activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase and upregulation of proapoptotic genes, Bak and Bim, and inhibited the expression of survivin, an antiapoptotic protein.	Sunitinib	0-9	caspase 3	Homo sapiens	50-59
20053726-4	2010	Sunitinib treatment resulted in the activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase and upregulation of proapoptotic genes, Bak and Bim, and inhibited the expression of survivin, an antiapoptotic protein.	Sunitinib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	76-103
20053726-5	2010	Sunitinib treatment also downregulated cyclin E, cyclin D2, and cyclin D3 and upregulated p21Cip1, all of which are involved in regulating cell cycle.	Sunitinib	0-9	cyclin D2	Homo sapiens	49-58
20053726-5	2010	Sunitinib treatment also downregulated cyclin E, cyclin D2, and cyclin D3 and upregulated p21Cip1, all of which are involved in regulating cell cycle.	Sunitinib	0-9	cyclin D3	Homo sapiens	64-73
20053726-5	2010	Sunitinib treatment also downregulated cyclin E, cyclin D2, and cyclin D3 and upregulated p21Cip1, all of which are involved in regulating cell cycle.	Sunitinib	0-9	cyclin dependent kinase inhibitor 1A	Homo sapiens	90-97
20053726-7	2010	Dephosphorylation of STAT3 (Tyr(705)) induced by sunitinib was helped by a reduction in activities of Janus-activated kinase 2 and Src.	Sunitinib	49-58	signal transducer and activator of transcription 3	Homo sapiens	21-26
20053726-7	2010	Dephosphorylation of STAT3 (Tyr(705)) induced by sunitinib was helped by a reduction in activities of Janus-activated kinase 2 and Src.	Sunitinib	49-58	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	131-134
20053726-8	2010	Additionally, sodium vanadate, an inhibitor of protein tyrosine phosphatases, partially blocked the inhibition of phosphorylated STAT3 by sunitinib.	Sunitinib	138-147	signal transducer and activator of transcription 3	Homo sapiens	129-134
20053726-9	2010	Loss of phosphorylated AKT after sunitinib treatment was accompanied by decreased phosphorylation of downstream proteins glycogen synthase kinase-3beta and mammalian target of rapamycin.	Sunitinib	33-42	AKT serine/threonine kinase 1	Homo sapiens	23-26
20053726-9	2010	Loss of phosphorylated AKT after sunitinib treatment was accompanied by decreased phosphorylation of downstream proteins glycogen synthase kinase-3beta and mammalian target of rapamycin.	Sunitinib	33-42	glycogen synthase kinase 3 beta	Homo sapiens	121-151
20053726-9	2010	Loss of phosphorylated AKT after sunitinib treatment was accompanied by decreased phosphorylation of downstream proteins glycogen synthase kinase-3beta and mammalian target of rapamycin.	Sunitinib	33-42	mechanistic target of rapamycin kinase	Homo sapiens	156-185
20215359-3	2010	These include the vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors sunitinib and sorafenib, which inhibit angiogenic signaling in endothelial cells and vascular pericytes predominantly through VEGFR and platelet-derived growth factor receptor beta.	Sunitinib	97-106	kinase insert domain receptor	Homo sapiens	63-68
20072832-1	2010	Sunitinib is an oral multikinase inhibitor that blocks the vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) alpha and beta, c-kit, and other receptors.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	176-181
20173383-0	2010	Plasma N-terminal pro-brain natriuretic peptide as prognostic marker in fatal cardial decompensation with sunitinib malate therapy.	Sunitinib	106-122	natriuretic peptide B	Homo sapiens	18-47
20072832-1	2010	Sunitinib is an oral multikinase inhibitor that blocks the vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) alpha and beta, c-kit, and other receptors.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	59-102
20072832-1	2010	Sunitinib is an oral multikinase inhibitor that blocks the vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) alpha and beta, c-kit, and other receptors.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	104-109
20072832-1	2010	Sunitinib is an oral multikinase inhibitor that blocks the vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) alpha and beta, c-kit, and other receptors.	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	153-165
21789125-2	2010	Based on available phase III randomized trials, anti-VEGF agents such as sunitinib, sorafenib, bevacizumab-based therapy, and mTOR-targeted agents such as temsirolimus and everolimus have been used in the treatment armamentarium for this disease.	Sunitinib	73-82	vascular endothelial growth factor A	Homo sapiens	53-57
20980789-1	2010	INTRODUCTION: We describe our experience with sorafenib and sunitinib in the treatment of chemotherapy-refractory advanced penile squamous cell carcinoma (SCC).	Sunitinib	60-69	serpin family B member 3	Homo sapiens	155-158
20980789-10	2010	The patient who achieved partial response had an SCC antigen reduction of nearly 95% after treatment with sunitinib.	Sunitinib	106-115	serpin family B member 3	Homo sapiens	49-52
20044640-1	2009	BACKGROUND: The tyrosine kinase inhibitors (TKI) sunitinib and imatinib were shown to induce macrocytosis in patients with renal cell cancer (RCC) and gastrointestinal stromal tumors (GIST), presumably through inhibition of the c-KIT dependent signaling pathway of erythroid progenitor cells of the bone marrow.	Sunitinib	49-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	228-233
20980789-12	2010	CONCLUSIONS: The feasibility and activity of sorafenib and sunitinib in our series suggest that this approach may be a promising alternative in chemotherapy-refractory advanced penile SCC.	Sunitinib	59-68	serpin family B member 3	Homo sapiens	184-187
19911111-1	2009	Sunitinib demonstrating efficacy in pancreatic islet cell carcinomas will pave the way for further trials in other neuroendocrine tumor types such as carcinoid, poorly differentiated neuroendocrine disease, and several other endocrine tumors that are dependent on VEGF/VEGFR for angiogenesis.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	264-268
19904265-0	2009	Identification of TNF-alpha and MMP-9 as potential baseline predictive serum markers of sunitinib activity in patients with renal cell carcinoma using a human cytokine array.	Sunitinib	88-97	tumor necrosis factor	Homo sapiens	18-27
19904265-0	2009	Identification of TNF-alpha and MMP-9 as potential baseline predictive serum markers of sunitinib activity in patients with renal cell carcinoma using a human cytokine array.	Sunitinib	88-97	matrix metallopeptidase 9	Homo sapiens	32-37
19904265-9	2009	The area under the ROC curves for TNF-alpha and MMP-9 as predictive markers of sunitinib activity were 0.83 and 0.77.	Sunitinib	79-88	tumor necrosis factor	Homo sapiens	34-43
19904265-9	2009	The area under the ROC curves for TNF-alpha and MMP-9 as predictive markers of sunitinib activity were 0.83 and 0.77.	Sunitinib	79-88	matrix metallopeptidase 9	Homo sapiens	48-53
19954293-7	2009	Multiple new agents targeting the VEGF pathway have been tested and approved, including sunitinib, sorafenib and bevacizumab, with others waiting in the wings.	Sunitinib	88-97	vascular endothelial growth factor A	Homo sapiens	34-38
19904265-10	2009	CONCLUSION: Baseline levels of TNF-alpha and MMP-9 warrant further study as predictive markers of sunitinib activity in MRCC.	Sunitinib	98-107	tumor necrosis factor	Homo sapiens	31-40
19904265-10	2009	CONCLUSION: Baseline levels of TNF-alpha and MMP-9 warrant further study as predictive markers of sunitinib activity in MRCC.	Sunitinib	98-107	matrix metallopeptidase 9	Homo sapiens	45-50
19911111-1	2009	Sunitinib demonstrating efficacy in pancreatic islet cell carcinomas will pave the way for further trials in other neuroendocrine tumor types such as carcinoid, poorly differentiated neuroendocrine disease, and several other endocrine tumors that are dependent on VEGF/VEGFR for angiogenesis.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	269-274
19767240-0	2009	Risk of bleeding with vascular endothelial growth factor receptor tyrosine-kinase inhibitors sunitinib and sorafenib: a systematic review and meta-analysis of clinical trials.	Sunitinib	93-102	kinase insert domain receptor	Homo sapiens	22-65
19887629-6	2009	Inhibition of VEGF receptor signaling pathways by sunitinib or VEGFR2 morpholinos virtually completely ablated VEGF-induced tumor cell dissemination and metastasis.	Sunitinib	50-59	vascular endothelial growth factor Aa	Danio rerio	14-18
19861442-3	2009	The clinical benefit of sunitinib is genotype-dependent in regards to both primary and secondary mutations, with GIST patients harboring the KIT(AY502-3ins) exon 9 mutation being the most sensitive.	Sunitinib	24-33	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	141-144
19861442-6	2009	RESULTS: Tumors from patients who developed sunitinib resistance after at least 1 year of radiographic response were analyzed, showing similar findings of a primary KIT(AY502-3ins) mutation and a secondary mutation in the KIT activation loop.	Sunitinib	44-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	165-168
19861442-6	2009	RESULTS: Tumors from patients who developed sunitinib resistance after at least 1 year of radiographic response were analyzed, showing similar findings of a primary KIT(AY502-3ins) mutation and a secondary mutation in the KIT activation loop.	Sunitinib	44-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	222-225
19755855-5	2009	Treatment of NCI-H1703 cells with PDGFRA-specific shRNAs or with the PDGFRalpha/KIT small molecule inhibitors imatinib or sunitinib leads to cell growth inhibition.	Sunitinib	122-131	platelet derived growth factor receptor alpha	Homo sapiens	69-79
19755855-5	2009	Treatment of NCI-H1703 cells with PDGFRA-specific shRNAs or with the PDGFRalpha/KIT small molecule inhibitors imatinib or sunitinib leads to cell growth inhibition.	Sunitinib	122-131	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	80-83
19811659-9	2009	The potential targets for other kinase inhibitors (sunitinib and sorafenib) in ChRCC seem to be VEGFR and PDGFR.	Sunitinib	51-60	kinase insert domain receptor	Homo sapiens	96-101
19811659-9	2009	The potential targets for other kinase inhibitors (sunitinib and sorafenib) in ChRCC seem to be VEGFR and PDGFR.	Sunitinib	51-60	platelet derived growth factor receptor beta	Homo sapiens	106-111
19844230-6	2009	RESULTS: Sunitinib inhibited more kinases than pazopanib and sorafenib, at potencies within 10-fold of VEGFR-2.	Sunitinib	9-18	kinase insert domain receptor	Homo sapiens	103-110
19844230-9	2009	Addition of stem cell factor and/or Flt-3 ligand with granulocyte-macrophage colony stimulating factor resulted in significant shifts in potency for sorafenib and sunitinib but less so for pazopanib.	Sunitinib	163-172	KIT ligand	Homo sapiens	12-28
19844230-9	2009	Addition of stem cell factor and/or Flt-3 ligand with granulocyte-macrophage colony stimulating factor resulted in significant shifts in potency for sorafenib and sunitinib but less so for pazopanib.	Sunitinib	163-172	fms related receptor tyrosine kinase 3	Homo sapiens	36-41
19773375-1	2009	PURPOSE: Bevacizumab is an antibody against vascular endothelial growth factor; sunitinib is an inhibitor of vascular endothelial growth factor and related receptors.	Sunitinib	80-89	vascular endothelial growth factor A	Homo sapiens	109-143
19773380-6	2009	Sorafenib and sunitinib showed concentration-dependent (1 and 10 micromol/L), low to moderate affinity for ABCB1 but were not affected by the other ABC transporters.	Sunitinib	14-23	ATP binding cassette subfamily B member 1	Homo sapiens	107-112
19767240-1	2009	BACKGROUND: Sunitinib and sorafenib are oral vascular endothelial growth factor receptor (VEGFR) tyrosine-kinase inhibitors used in various cancers.	Sunitinib	12-21	kinase insert domain receptor	Homo sapiens	45-88
19767240-1	2009	BACKGROUND: Sunitinib and sorafenib are oral vascular endothelial growth factor receptor (VEGFR) tyrosine-kinase inhibitors used in various cancers.	Sunitinib	12-21	kinase insert domain receptor	Homo sapiens	90-95
19767240-11	2009	INTERPRETATION: Treatment with the VEGFR tyrosine-kinase inhibitors sunitinib and sorafenib is associated with a significant increase in risk of bleeding.	Sunitinib	68-77	kinase insert domain receptor	Homo sapiens	35-40
19481151-1	2009	Several antiangiogenic agents, including bevacizumab, sunitinib, and sorafenib, which mainly target the VEGF signaling system, have been approved for the treatment of human cancers.	Sunitinib	54-63	vascular endothelial growth factor A	Homo sapiens	104-108
19774211-2	2009	This breakthrough in science led to the development of a variety of small molecules inhibiting the VEGF-dependent angiogenic pathway, such as sunitinib and sorafenib.	Sunitinib	142-151	vascular endothelial growth factor A	Homo sapiens	99-103
19754358-2	2009	Since HCC is a particularly vascular solid tumor, we determined the antitumor and antiangiogenic activities of sunitinib malate, a potent inhibitor of two receptors involved in angiogenesis - vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR).	Sunitinib	111-127	kinase insert domain receptor	Homo sapiens	192-235
19737946-7	2009	Sunitinib treatment was associated with reduced tumor cell proliferation by &gt;25% in 52% of cases analyzed and reduced levels of phospho-KIT in tumor biopsies (indicating target modulation).	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	139-142
19737946-11	2009	CONCLUSION: Cellular and molecular analyses showed that sunitinib clinical activity is associated with inhibition of KIT in GIST following imatinib failure, illustrating the rational approach used to develop a therapy aimed at the underlying oncogenic signaling pathway aberrancy.	Sunitinib	56-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	117-120
19737953-0	2009	Circulating levels of soluble KIT serve as a biomarker for clinical outcome in gastrointestinal stromal tumor patients receiving sunitinib following imatinib failure.	Sunitinib	129-138	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-33
19737953-1	2009	PURPOSE: To evaluate changes in circulating levels of soluble KIT (sKIT) extracellular domain as a potential biomarker for clinical outcome in gastrointestinal stromal tumor patients treated with the multitargeted tyrosine kinase inhibitor sunitinib following imatinib failure in a previously reported phase III study.	Sunitinib	240-249	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-65
19754358-2	2009	Since HCC is a particularly vascular solid tumor, we determined the antitumor and antiangiogenic activities of sunitinib malate, a potent inhibitor of two receptors involved in angiogenesis - vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR).	Sunitinib	111-127	kinase insert domain receptor	Homo sapiens	237-242
19754358-2	2009	Since HCC is a particularly vascular solid tumor, we determined the antitumor and antiangiogenic activities of sunitinib malate, a potent inhibitor of two receptors involved in angiogenesis - vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR).	Sunitinib	111-127	platelet derived growth factor receptor beta	Homo sapiens	248-287
19754358-2	2009	Since HCC is a particularly vascular solid tumor, we determined the antitumor and antiangiogenic activities of sunitinib malate, a potent inhibitor of two receptors involved in angiogenesis - vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR).	Sunitinib	111-127	platelet derived growth factor receptor beta	Homo sapiens	289-294
19754358-4	2009	Sunitinib inhibited phosphorylation of VEGFR-2 at Tyr951 and PDGFR-beta at Tyr1021 both in vitro and in vivo.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	39-46
19754358-4	2009	Sunitinib inhibited phosphorylation of VEGFR-2 at Tyr951 and PDGFR-beta at Tyr1021 both in vitro and in vivo.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	61-71
19724685-9	2009	KCI-18 cells and tumors expressed vascular endothelial growth factor receptor 2 and platelet-derived growth factor receptor beta molecular targets of sunitinib that were modulated by the drug treatment.	Sunitinib	150-159	kinase insert domain protein receptor	Mus musculus	34-128
19672141-2	2009	Sunitinib malate is an oral, multitargeted inhibitor of vascular endothelial growth factor receptor-1, -2, and -3, platelet-derived growth factor receptor-alpha and -beta, and other kinases implicated in tumor growth, angiogenesis, and metastasis.	Sunitinib	0-16	platelet derived growth factor receptor alpha	Homo sapiens	115-170
19726307-3	2009	The inhibitory activity of Sunitinib, a standard PTK inhibitor, on vascular endothelia growth factor receptor 2 (VEGFR-2) kinase activity was investigated.	Sunitinib	27-36	kinase insert domain receptor	Homo sapiens	67-111
19726307-3	2009	The inhibitory activity of Sunitinib, a standard PTK inhibitor, on vascular endothelia growth factor receptor 2 (VEGFR-2) kinase activity was investigated.	Sunitinib	27-36	kinase insert domain receptor	Homo sapiens	113-120
19726307-6	2009	Sunitinib inhibited VEGFR-2 kinase activity with an IC50 value of 86.7 nmol/L, which was close to the values tested using other methods.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	20-27
19672141-2	2009	Sunitinib malate is an oral, multitargeted inhibitor of vascular endothelial growth factor receptor-1, -2, and -3, platelet-derived growth factor receptor-alpha and -beta, and other kinases implicated in tumor growth, angiogenesis, and metastasis.	Sunitinib	0-16	fms related receptor tyrosine kinase 1	Homo sapiens	56-113
19617296-5	2009	Receptor tyrosine-kinase inhibitors (imatinib, dasatinib, sunitinib) may have a role in treatment of patients with melanoma harbouring c-Kit mutations.	Sunitinib	58-67	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	135-140
19568242-14	2009	CONCLUSION: There is evidence to suggest that treatment with sunitinib and treatment with bevacizumab plus IFN has clinically relevant and statistically significant advantages over treatment with IFN alone in patients with metastatic RCC.	Sunitinib	61-70	interferon alpha 1	Homo sapiens	196-199
19689244-6	2009	In contrast, folliculitis is not common during administration of sorafenib and sunitinib, which target VEGFR, PDGFR, FLT3, and others, whereas both agents have been associated with subungual splinter hemorrhages.	Sunitinib	79-88	kinase insert domain receptor	Homo sapiens	103-108
19232821-0	2009	Sensitization of ABCG2-overexpressing cells to conventional chemotherapeutic agent by sunitinib was associated with inhibiting the function of ABCG2.	Sunitinib	86-95	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	17-22
19326424-1	2009	BACKGROUND: Sunitinib inhibits KIT and other members of the split-kinase-domain family of receptor tyrosine kinases.	Sunitinib	12-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	31-34
21789110-3	2009	Bevacizumab is directed against the vascular endothelial growth factor (VEGF), a key mediator of angiogenesis, whilst sorafenib and sunitinib inhibit a number of targets including the VEGF and platelet-derived growth factor (PDGFR) receptor tyrosine kinases.	Sunitinib	132-141	vascular endothelial growth factor A	Homo sapiens	184-188
21789110-3	2009	Bevacizumab is directed against the vascular endothelial growth factor (VEGF), a key mediator of angiogenesis, whilst sorafenib and sunitinib inhibit a number of targets including the VEGF and platelet-derived growth factor (PDGFR) receptor tyrosine kinases.	Sunitinib	132-141	platelet derived growth factor receptor beta	Homo sapiens	193-223
18534874-1	2009	PURPOSE: Sunitinib malate (Pfizer, Inc.) is a multitargeted kinase inhibitor that inhibits vascular endothelial growth factor (VEGF) receptor (R)-1, 2 and 3, platelet-derived growth factor receptors (PDGFR)-alpha and beta, Flt3, RET, and Kit.	Sunitinib	9-25	vascular endothelial growth factor A	Homo sapiens	127-131
18534874-1	2009	PURPOSE: Sunitinib malate (Pfizer, Inc.) is a multitargeted kinase inhibitor that inhibits vascular endothelial growth factor (VEGF) receptor (R)-1, 2 and 3, platelet-derived growth factor receptors (PDGFR)-alpha and beta, Flt3, RET, and Kit.	Sunitinib	9-25	platelet derived growth factor receptor alpha	Homo sapiens	200-212
18534874-1	2009	PURPOSE: Sunitinib malate (Pfizer, Inc.) is a multitargeted kinase inhibitor that inhibits vascular endothelial growth factor (VEGF) receptor (R)-1, 2 and 3, platelet-derived growth factor receptors (PDGFR)-alpha and beta, Flt3, RET, and Kit.	Sunitinib	9-25	fms related receptor tyrosine kinase 3	Homo sapiens	223-227
18534874-1	2009	PURPOSE: Sunitinib malate (Pfizer, Inc.) is a multitargeted kinase inhibitor that inhibits vascular endothelial growth factor (VEGF) receptor (R)-1, 2 and 3, platelet-derived growth factor receptors (PDGFR)-alpha and beta, Flt3, RET, and Kit.	Sunitinib	9-25	ret proto-oncogene	Homo sapiens	229-232
19232821-0	2009	Sensitization of ABCG2-overexpressing cells to conventional chemotherapeutic agent by sunitinib was associated with inhibiting the function of ABCG2.	Sunitinib	86-95	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	143-148
19232821-2	2009	In this study, we evaluated the possible interaction of sunitinib with P-glycoprotein (P-gp, ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), breast cancer resistance protein (BCRP, ABCG2) and lung-resistance protein (LRP) in vitro.	Sunitinib	56-65	ATP binding cassette subfamily B member 1	Homo sapiens	71-85
19232821-2	2009	In this study, we evaluated the possible interaction of sunitinib with P-glycoprotein (P-gp, ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), breast cancer resistance protein (BCRP, ABCG2) and lung-resistance protein (LRP) in vitro.	Sunitinib	56-65	ATP binding cassette subfamily B member 1	Homo sapiens	87-91
19232821-2	2009	In this study, we evaluated the possible interaction of sunitinib with P-glycoprotein (P-gp, ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), breast cancer resistance protein (BCRP, ABCG2) and lung-resistance protein (LRP) in vitro.	Sunitinib	56-65	ATP binding cassette subfamily B member 1	Homo sapiens	93-98
19232821-2	2009	In this study, we evaluated the possible interaction of sunitinib with P-glycoprotein (P-gp, ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), breast cancer resistance protein (BCRP, ABCG2) and lung-resistance protein (LRP) in vitro.	Sunitinib	56-65	ATP binding cassette subfamily B member 1	Homo sapiens	101-131
19232821-2	2009	In this study, we evaluated the possible interaction of sunitinib with P-glycoprotein (P-gp, ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), breast cancer resistance protein (BCRP, ABCG2) and lung-resistance protein (LRP) in vitro.	Sunitinib	56-65	ATP binding cassette subfamily B member 1	Homo sapiens	133-137
19232821-2	2009	In this study, we evaluated the possible interaction of sunitinib with P-glycoprotein (P-gp, ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), breast cancer resistance protein (BCRP, ABCG2) and lung-resistance protein (LRP) in vitro.	Sunitinib	56-65	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	181-185
19232821-2	2009	In this study, we evaluated the possible interaction of sunitinib with P-glycoprotein (P-gp, ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), breast cancer resistance protein (BCRP, ABCG2) and lung-resistance protein (LRP) in vitro.	Sunitinib	56-65	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	187-192
19232821-2	2009	In this study, we evaluated the possible interaction of sunitinib with P-glycoprotein (P-gp, ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), breast cancer resistance protein (BCRP, ABCG2) and lung-resistance protein (LRP) in vitro.	Sunitinib	56-65	major vault protein	Homo sapiens	198-221
19232821-2	2009	In this study, we evaluated the possible interaction of sunitinib with P-glycoprotein (P-gp, ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), breast cancer resistance protein (BCRP, ABCG2) and lung-resistance protein (LRP) in vitro.	Sunitinib	56-65	major vault protein	Homo sapiens	223-226
19232821-3	2009	Our results showed that sunitinib completely reverse drug resistance mediated by ABCG2 at a non-toxic concentration of 2.5muM and has no significant reversal effect on ABCB1-, ABCC1- and LRP-mediated drug resistance, although a small synergetic effect was observed in combining sunitinib and conventional chemotherapeutic agents in ABCB1 overexpressing MCF-7/adr and parental sensitive MCF-7 cells, ABCC1 overexpressing C-A120 and parental sensitive KB-3-1 cells.	Sunitinib	24-33	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	81-86
19232821-4	2009	Sunitinib significantly increased intracellular accumulation of rhodamine 123 and doxorubicin and remarkably inhibited the efflux of rhodamine 123 and methotrexate by ABCG2 in ABCG2-overexpressing cells, and also profoundly inhibited the transport of [(3)H]-methotrexate by ABCG2.	Sunitinib	0-9	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	167-172
19232821-4	2009	Sunitinib significantly increased intracellular accumulation of rhodamine 123 and doxorubicin and remarkably inhibited the efflux of rhodamine 123 and methotrexate by ABCG2 in ABCG2-overexpressing cells, and also profoundly inhibited the transport of [(3)H]-methotrexate by ABCG2.	Sunitinib	0-9	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	176-181
19232821-4	2009	Sunitinib significantly increased intracellular accumulation of rhodamine 123 and doxorubicin and remarkably inhibited the efflux of rhodamine 123 and methotrexate by ABCG2 in ABCG2-overexpressing cells, and also profoundly inhibited the transport of [(3)H]-methotrexate by ABCG2.	Sunitinib	0-9	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	176-181
19232821-7	2009	Overall, we conclude that sunitinib reverses ABCG2-mediated MDR through inhibiting the drug efflux function of ABCG2.	Sunitinib	26-35	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	45-50
19232821-7	2009	Overall, we conclude that sunitinib reverses ABCG2-mediated MDR through inhibiting the drug efflux function of ABCG2.	Sunitinib	26-35	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	111-116
19453268-3	2009	Sunitinib is a multi-kinase inhibitor of VEGFR-2, PDGFR (alpha,beta), FLT-3, KIT, CSF-1 and RET.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	41-48
19467916-5	2009	We discuss how the cross-talk between major downstream signaling pathways, such as PI3K/PTEN/Akt/mTOR, RAS/Raf/MEK/ERK, and Jak/STAT, can be exploited for therapeutic purposes by targeting key signaling molecules with selective inhibitors, such as mTOR inhibitors, HSP90 inhibitors, or farnesyltransferase inhibitors, and identifying those agents with the ability to positively combine with inhibitors of FLT3, such as PKC412 and sunitinib.	Sunitinib	430-439	phosphatase and tensin homolog	Homo sapiens	88-92
19467916-5	2009	We discuss how the cross-talk between major downstream signaling pathways, such as PI3K/PTEN/Akt/mTOR, RAS/Raf/MEK/ERK, and Jak/STAT, can be exploited for therapeutic purposes by targeting key signaling molecules with selective inhibitors, such as mTOR inhibitors, HSP90 inhibitors, or farnesyltransferase inhibitors, and identifying those agents with the ability to positively combine with inhibitors of FLT3, such as PKC412 and sunitinib.	Sunitinib	430-439	AKT serine/threonine kinase 1	Homo sapiens	93-96
19467916-5	2009	We discuss how the cross-talk between major downstream signaling pathways, such as PI3K/PTEN/Akt/mTOR, RAS/Raf/MEK/ERK, and Jak/STAT, can be exploited for therapeutic purposes by targeting key signaling molecules with selective inhibitors, such as mTOR inhibitors, HSP90 inhibitors, or farnesyltransferase inhibitors, and identifying those agents with the ability to positively combine with inhibitors of FLT3, such as PKC412 and sunitinib.	Sunitinib	430-439	mechanistic target of rapamycin kinase	Homo sapiens	97-101
19467916-5	2009	We discuss how the cross-talk between major downstream signaling pathways, such as PI3K/PTEN/Akt/mTOR, RAS/Raf/MEK/ERK, and Jak/STAT, can be exploited for therapeutic purposes by targeting key signaling molecules with selective inhibitors, such as mTOR inhibitors, HSP90 inhibitors, or farnesyltransferase inhibitors, and identifying those agents with the ability to positively combine with inhibitors of FLT3, such as PKC412 and sunitinib.	Sunitinib	430-439	zinc fingers and homeoboxes 2	Homo sapiens	107-110
19467916-5	2009	We discuss how the cross-talk between major downstream signaling pathways, such as PI3K/PTEN/Akt/mTOR, RAS/Raf/MEK/ERK, and Jak/STAT, can be exploited for therapeutic purposes by targeting key signaling molecules with selective inhibitors, such as mTOR inhibitors, HSP90 inhibitors, or farnesyltransferase inhibitors, and identifying those agents with the ability to positively combine with inhibitors of FLT3, such as PKC412 and sunitinib.	Sunitinib	430-439	mitogen-activated protein kinase kinase 7	Homo sapiens	111-114
19467916-5	2009	We discuss how the cross-talk between major downstream signaling pathways, such as PI3K/PTEN/Akt/mTOR, RAS/Raf/MEK/ERK, and Jak/STAT, can be exploited for therapeutic purposes by targeting key signaling molecules with selective inhibitors, such as mTOR inhibitors, HSP90 inhibitors, or farnesyltransferase inhibitors, and identifying those agents with the ability to positively combine with inhibitors of FLT3, such as PKC412 and sunitinib.	Sunitinib	430-439	EPH receptor B2	Homo sapiens	115-118
19467916-5	2009	We discuss how the cross-talk between major downstream signaling pathways, such as PI3K/PTEN/Akt/mTOR, RAS/Raf/MEK/ERK, and Jak/STAT, can be exploited for therapeutic purposes by targeting key signaling molecules with selective inhibitors, such as mTOR inhibitors, HSP90 inhibitors, or farnesyltransferase inhibitors, and identifying those agents with the ability to positively combine with inhibitors of FLT3, such as PKC412 and sunitinib.	Sunitinib	430-439	mechanistic target of rapamycin kinase	Homo sapiens	248-252
19467916-5	2009	We discuss how the cross-talk between major downstream signaling pathways, such as PI3K/PTEN/Akt/mTOR, RAS/Raf/MEK/ERK, and Jak/STAT, can be exploited for therapeutic purposes by targeting key signaling molecules with selective inhibitors, such as mTOR inhibitors, HSP90 inhibitors, or farnesyltransferase inhibitors, and identifying those agents with the ability to positively combine with inhibitors of FLT3, such as PKC412 and sunitinib.	Sunitinib	430-439	heat shock protein 90 alpha family class A member 1	Homo sapiens	265-270
19467916-5	2009	We discuss how the cross-talk between major downstream signaling pathways, such as PI3K/PTEN/Akt/mTOR, RAS/Raf/MEK/ERK, and Jak/STAT, can be exploited for therapeutic purposes by targeting key signaling molecules with selective inhibitors, such as mTOR inhibitors, HSP90 inhibitors, or farnesyltransferase inhibitors, and identifying those agents with the ability to positively combine with inhibitors of FLT3, such as PKC412 and sunitinib.	Sunitinib	430-439	fms related receptor tyrosine kinase 3	Homo sapiens	405-409
19496707-5	2009	It has been tested in patients with progressive disease after therapy with tyrosine kinase receptor inhibitors (sunitinib, sorafenib or both), which interfere with signaling pathways, such as the VEGF pathway.	Sunitinib	112-121	vascular endothelial growth factor A	Homo sapiens	196-200
19318229-3	2009	GI50 values were determined: ZD6474 and SU11248, mainly VEGFR2 inhibitors, gave the lowest GI50 across all cell lines (3.5-6.9 microM) whereas ZD1839 gave a GI50 in this range only in H28 cells.	Sunitinib	40-47	kinase insert domain receptor	Homo sapiens	56-62
19318229-5	2009	ZD6474 and ZD1839 inhibited EGF-induced phosphorylation of EGFR, AKT and ERK, whereas VEGF-induced phosphorylation of VEGFR2 was completely inhibited with 0.1 microM SU11248.	Sunitinib	166-173	vascular endothelial growth factor A	Homo sapiens	86-90
19318229-5	2009	ZD6474 and ZD1839 inhibited EGF-induced phosphorylation of EGFR, AKT and ERK, whereas VEGF-induced phosphorylation of VEGFR2 was completely inhibited with 0.1 microM SU11248.	Sunitinib	166-173	kinase insert domain receptor	Homo sapiens	118-124
19453268-3	2009	Sunitinib is a multi-kinase inhibitor of VEGFR-2, PDGFR (alpha,beta), FLT-3, KIT, CSF-1 and RET.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	50-55
19453268-3	2009	Sunitinib is a multi-kinase inhibitor of VEGFR-2, PDGFR (alpha,beta), FLT-3, KIT, CSF-1 and RET.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	70-75
19453268-3	2009	Sunitinib is a multi-kinase inhibitor of VEGFR-2, PDGFR (alpha,beta), FLT-3, KIT, CSF-1 and RET.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-80
19453268-3	2009	Sunitinib is a multi-kinase inhibitor of VEGFR-2, PDGFR (alpha,beta), FLT-3, KIT, CSF-1 and RET.	Sunitinib	0-9	colony stimulating factor 1	Homo sapiens	82-87
19453268-3	2009	Sunitinib is a multi-kinase inhibitor of VEGFR-2, PDGFR (alpha,beta), FLT-3, KIT, CSF-1 and RET.	Sunitinib	0-9	ret proto-oncogene	Homo sapiens	92-95
19171421-4	2009	Both Sorafenib and Sunitinib with Enzastaurin at concentrations feasible in vivo showed a synergistic reduction of viable RCC cells by inhibiting cell growth through inhibition of phospho-S6-kinase and GSK3-beta.	Sunitinib	19-28	glycogen synthase kinase 3 beta	Homo sapiens	202-211
19493441-0	2009	Inhibitory effects of sunitinib on ovalbumin-induced chronic experimental asthma in mice.	Sunitinib	22-31	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	35-44
19402059-2	2009	Sunitinib malate, sorafenib tosylate, bevacizumab with interferon alpha, temsirolimus, and everolimus have improved clinical outcomes in randomized phase 3 trials by inhibiting the vascular endothelial growth factor and related pathways.	Sunitinib	0-16	vascular endothelial growth factor A	Homo sapiens	181-215
19402073-3	2009	Approaches to bind circulating VEGF protein (eg, bevacizumab) and small molecule inhibitors of the receptor on which the VEGF ligand binds (eg, sunitinib, sorafenib, axitinib, and pazopanib) have been tested.	Sunitinib	144-153	vascular endothelial growth factor A	Homo sapiens	121-125
19403935-10	2009	Significant changes following sunitinib treatment were observed in serum-soluble biomarkers including soluble vascular endothelial growth factor receptor-2, platelet-derived growth factor aa, placental growth factor and leptin.	Sunitinib	30-39	placental growth factor	Homo sapiens	192-215
19366796-2	2009	Sunitinib is a clinically approved multitargeted tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor, c-KIT, and PDGFR, and has shown clinical activity in various solid tumors.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	134-139
19366796-2	2009	Sunitinib is a clinically approved multitargeted tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor, c-KIT, and PDGFR, and has shown clinical activity in various solid tumors.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	145-150
19366796-3	2009	Activation of PDGFR signaling has been described in gastrointestinal stromal tumors (PDGFRA mutations) as well as in chronic myeloid leukemia (BCR-PDGFRA translocation), and sunitinib can yield clinical benefit in both settings.	Sunitinib	174-183	platelet derived growth factor receptor beta	Homo sapiens	14-19
19366796-4	2009	However, the discovery of PDGFR activating mutations or gene rearrangements in other tumor types could reveal additional patient populations who might benefit from treatment with anti-PDGFR therapies, such as sunitinib.	Sunitinib	209-218	platelet derived growth factor receptor beta	Homo sapiens	26-31
19458500-0	2009	Sunitinib and PF-562,271 (FAK/Pyk2 inhibitor) effectively block  growth and recovery of human hepatocellular carcinoma in a rat  xenograft model.	Sunitinib	0-9	protein tyrosine kinase 2	Homo sapiens	26-29
19366796-4	2009	However, the discovery of PDGFR activating mutations or gene rearrangements in other tumor types could reveal additional patient populations who might benefit from treatment with anti-PDGFR therapies, such as sunitinib.	Sunitinib	209-218	platelet derived growth factor receptor beta	Homo sapiens	184-189
19458500-0	2009	Sunitinib and PF-562,271 (FAK/Pyk2 inhibitor) effectively block  growth and recovery of human hepatocellular carcinoma in a rat  xenograft model.	Sunitinib	0-9	protein tyrosine kinase 2 beta	Homo sapiens	30-34
19366796-7	2009	In the sunitinib-sensitive adenosquamous NSCLC cell line, PDGFRA expression was associated with focal PFGRA gene amplification, which was similarly detected in a small fraction of squamous cell NSCLC primary tumor specimens.	Sunitinib	7-16	platelet derived growth factor receptor alpha	Homo sapiens	58-64
19366796-9	2009	A similar codependency on PDGFRA and PDGFC was observed in the sunitinib-sensitive rhabdomyosarcoma cell line.	Sunitinib	63-72	platelet derived growth factor receptor alpha	Homo sapiens	26-32
19366796-9	2009	A similar codependency on PDGFRA and PDGFC was observed in the sunitinib-sensitive rhabdomyosarcoma cell line.	Sunitinib	63-72	platelet derived growth factor C	Homo sapiens	37-42
19435875-7	2009	We found that disruption of HIF-1alpha, HIF-2alpha, or both HIF-1alpha and HIF-2alpha genes led to improved tumor response to sunitinib.	Sunitinib	126-135	hypoxia inducible factor 1 subunit alpha	Homo sapiens	28-38
19336014-2	2009	Dissection of the molecular pathways that regulate proliferation, apoptosis, and angiogenesis has led to the development of targeted therapies such as the receptor tyrosine kinase inhibitors sunitinib and sorafenib, the anti-vascular endothelial growth factor antibody bevacizumab, and a class of rapamycin analogues including everolimus and temsirolimus.	Sunitinib	191-200	vascular endothelial growth factor A	Homo sapiens	225-259
19435875-7	2009	We found that disruption of HIF-1alpha, HIF-2alpha, or both HIF-1alpha and HIF-2alpha genes led to improved tumor response to sunitinib.	Sunitinib	126-135	endothelial PAS domain protein 1	Homo sapiens	40-50
19435875-8	2009	For xenografts in which both HIF-1alpha and HIF-2alpha genes were disrupted, there was prolonged complete remission with sunitinib treatment in 50% of mice.	Sunitinib	121-130	hypoxia inducible factor 1, alpha subunit	Mus musculus	29-39
19435875-8	2009	For xenografts in which both HIF-1alpha and HIF-2alpha genes were disrupted, there was prolonged complete remission with sunitinib treatment in 50% of mice.	Sunitinib	121-130	endothelial PAS domain protein 1	Mus musculus	44-54
19435875-10	2009	First, tumor angiogenesis and perfusion were almost completely inhibited by sunitinib when both HIF-1alpha and HIF-2alpha genes were disrupted.	Sunitinib	76-85	hypoxia inducible factor 1 subunit alpha	Homo sapiens	96-106
19435875-10	2009	First, tumor angiogenesis and perfusion were almost completely inhibited by sunitinib when both HIF-1alpha and HIF-2alpha genes were disrupted.	Sunitinib	76-85	endothelial PAS domain protein 1	Homo sapiens	111-121
19277038-2	2009	Bevacizumab, sorafenib and sunitinib target VEGF-mediated angiogenesis and are active against several types of cancer, but their effects on the immune system are poorly understood.	Sunitinib	27-36	vascular endothelial growth factor A	Homo sapiens	44-48
19412427-11	2009	Low-dose sunitinib (20 mg/kg) demonstrates synergistic cytotoxicity with an mTOR inhibitor, rapamycin, which is more effective than the traditional chemotherapeutic drug, cyclophosphamide.	Sunitinib	9-18	mechanistic target of rapamycin kinase	Homo sapiens	76-80
19336729-5	2009	We showed that daily treatment with sunitinib reduced tumor size, caused tumor necrosis, blocked tumor progression, and prolonged median survival in both the metastatic (Lkb1/Kras) and nonmetastatic (Kras) mouse models; median survival was not reached in the nonmetastatic model after 1 year.	Sunitinib	36-45	serine/threonine kinase 11	Mus musculus	170-174
19318574-9	2009	TK1 mutations exhibited a differential response to SU5614, sorafenib, and sunitinib but strongly impaired response to PKC412.	Sunitinib	74-83	thymidine kinase 1	Homo sapiens	0-3
19336729-5	2009	We showed that daily treatment with sunitinib reduced tumor size, caused tumor necrosis, blocked tumor progression, and prolonged median survival in both the metastatic (Lkb1/Kras) and nonmetastatic (Kras) mouse models; median survival was not reached in the nonmetastatic model after 1 year.	Sunitinib	36-45	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	175-179
19318574-10	2009	TK2 exchanges identified with SU5614 were sensitive to PKC412, sunitinib, or sorafenib, with the exception of Y842D, which caused a strong resistance to sorafenib.	Sunitinib	63-72	thymidine kinase 2	Homo sapiens	0-3
19336729-5	2009	We showed that daily treatment with sunitinib reduced tumor size, caused tumor necrosis, blocked tumor progression, and prolonged median survival in both the metastatic (Lkb1/Kras) and nonmetastatic (Kras) mouse models; median survival was not reached in the nonmetastatic model after 1 year.	Sunitinib	36-45	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	200-204
19335275-4	2009	In this situation the second-line TKI sunitinib is well suited to patients with KIT exon 9 mutations, or for patients without KIT/PDGFRA mutations (wild-type GIST).	Sunitinib	38-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	80-83
19258444-2	2009	Following administration, sunitinib is metabolized by cytochrome P450 3A4 to an active metabolite (SU12662).	Sunitinib	26-35	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	54-73
19335275-4	2009	In this situation the second-line TKI sunitinib is well suited to patients with KIT exon 9 mutations, or for patients without KIT/PDGFRA mutations (wild-type GIST).	Sunitinib	38-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	126-129
19335275-4	2009	In this situation the second-line TKI sunitinib is well suited to patients with KIT exon 9 mutations, or for patients without KIT/PDGFRA mutations (wild-type GIST).	Sunitinib	38-47	platelet derived growth factor receptor alpha	Homo sapiens	130-136
19224847-1	2009	PURPOSE: Both bevacizumab and sunitinib target the vascular endothelial growth factor pathway and demonstrate activity against advanced renal cell carcinoma (RCC).	Sunitinib	30-39	vascular endothelial growth factor A	Homo sapiens	51-85
19381023-3	2009	However, cis-mutations in the activation loop of the KIT gene tend to develop Sunitinib-resistant GIST.	Sunitinib	78-87	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-56
19390946-0	2009	Sunitinib-resistant gastrointestinal stromal tumors harbor cis-mutations in the activation loop of the KIT gene.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-106
19390946-4	2009	RESULTS: All imatinib- as well as sunitinib-resistant lesions showed viable tumor cells strongly re-expressing the KIT protein.	Sunitinib	34-43	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-118
19390946-7	2009	A tumor with mutations in exon 11 and 13 of the KIT gene, and showing partial response to sunitinib, harbored a third mutation in the activation loop when sunitinib resistance was shown.	Sunitinib	90-99	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-51
19390946-7	2009	A tumor with mutations in exon 11 and 13 of the KIT gene, and showing partial response to sunitinib, harbored a third mutation in the activation loop when sunitinib resistance was shown.	Sunitinib	155-164	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-51
19390946-9	2009	CONCLUSION: These findings indicate that an additional cis-mutation in the activation loop of the KIT gene could be a potential cause of sunitinib resistance in gastrointestinal stromal tumors.	Sunitinib	137-146	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-101
19244102-0	2009	Sunitinib inhibition of Stat3 induces renal cell carcinoma tumor cell apoptosis and reduces immunosuppressive cells.	Sunitinib	0-9	signal transducer and activator of transcription 3	Mus musculus	24-29
19244102-4	2009	We show that sunitinib induces tumor cell apoptosis and growth arrest in RCC tumor cells, which correlates with signal transducer and activator of transcription 3 (Stat3) activity inhibition.	Sunitinib	13-22	signal transducer and activator of transcription 3	Mus musculus	112-162
19244102-4	2009	We show that sunitinib induces tumor cell apoptosis and growth arrest in RCC tumor cells, which correlates with signal transducer and activator of transcription 3 (Stat3) activity inhibition.	Sunitinib	13-22	signal transducer and activator of transcription 3	Mus musculus	164-169
19244102-6	2009	Reduction of Stat3 activity enhances the antitumor effects of sunitinib, whereas expression of a constitutively activated Stat3 mutant rescues tumor cell death.	Sunitinib	62-71	signal transducer and activator of transcription 3	Mus musculus	13-18
19276342-6	2009	Interestingly, sunitinib treatment resulted in reduced expression of interleukin (IL)-10, transforming growth factor-beta, and Foxp3 but enhanced expression of Th1 cytokine IFN-gamma and increased CTL responses in isolated tumor-infiltrating leukocytes.	Sunitinib	15-24	interleukin 10	Mus musculus	69-88
19244102-8	2009	Sunitinib also inhibits Stat3 in Renca tumor-associated myeloid-derived suppressor cells (MDSC), down-regulates angiogenic gene expression, and reduces MDSCs and tumor T regulatory cells.	Sunitinib	0-9	signal transducer and activator of transcription 3	Mus musculus	24-29
19276342-6	2009	Interestingly, sunitinib treatment resulted in reduced expression of interleukin (IL)-10, transforming growth factor-beta, and Foxp3 but enhanced expression of Th1 cytokine IFN-gamma and increased CTL responses in isolated tumor-infiltrating leukocytes.	Sunitinib	15-24	forkhead box P3	Mus musculus	127-132
19276342-6	2009	Interestingly, sunitinib treatment resulted in reduced expression of interleukin (IL)-10, transforming growth factor-beta, and Foxp3 but enhanced expression of Th1 cytokine IFN-gamma and increased CTL responses in isolated tumor-infiltrating leukocytes.	Sunitinib	15-24	negative elongation factor complex member C/D, Th1l	Mus musculus	160-163
19276342-6	2009	Interestingly, sunitinib treatment resulted in reduced expression of interleukin (IL)-10, transforming growth factor-beta, and Foxp3 but enhanced expression of Th1 cytokine IFN-gamma and increased CTL responses in isolated tumor-infiltrating leukocytes.	Sunitinib	15-24	interferon gamma	Mus musculus	173-182
19276342-7	2009	A significantly higher percentage and infiltration of CD8 and CD4 cells was detected in tumors of sunitinib-treated mice when compared with control-treated mice.	Sunitinib	98-107	CD4 molecule	Sus scrofa	62-65
19244102-9	2009	These results suggest that Stat3 activity is important for RCC response to sunitinib, and Stat3 inhibition permits the direct proapoptotic activity of sunitinib on tumor cells and positive effects on tumor immunologic microenvironment.	Sunitinib	75-84	signal transducer and activator of transcription 3	Mus musculus	27-32
19276342-8	2009	More importantly, the expression of negative costimulatory molecules CTLA4 and PD-1 in both CD4 and CD8 T cells, and PDL-1 expression on MDSC and plasmacytoid dendritic cells, was also significantly decreased by sunitinib treatment.	Sunitinib	212-221	cytotoxic T-lymphocyte protein 4	Sus scrofa	69-74
19276342-8	2009	More importantly, the expression of negative costimulatory molecules CTLA4 and PD-1 in both CD4 and CD8 T cells, and PDL-1 expression on MDSC and plasmacytoid dendritic cells, was also significantly decreased by sunitinib treatment.	Sunitinib	212-221	CD4 molecule	Sus scrofa	92-95
19244102-9	2009	These results suggest that Stat3 activity is important for RCC response to sunitinib, and Stat3 inhibition permits the direct proapoptotic activity of sunitinib on tumor cells and positive effects on tumor immunologic microenvironment.	Sunitinib	151-160	signal transducer and activator of transcription 3	Mus musculus	90-95
19276342-8	2009	More importantly, the expression of negative costimulatory molecules CTLA4 and PD-1 in both CD4 and CD8 T cells, and PDL-1 expression on MDSC and plasmacytoid dendritic cells, was also significantly decreased by sunitinib treatment.	Sunitinib	212-221	CD274 molecule	Sus scrofa	117-122
19017755-6	2009	Patient was treated with sunitinib, a potent tyrosine kinase inhibitor of vascular endothelial growth factor, platelet-derived growth factor, RET, c-KIT, and FLT-3 receptors.	Sunitinib	25-34	vascular endothelial growth factor A	Homo sapiens	74-108
19035443-10	2009	Finally, we found significant growth suppressive effects of sunitinib in two acral melanoma cell lines; one harboring the D820Y mutation and one showing SCF-dependent KIT activation.	Sunitinib	60-69	KIT ligand	Homo sapiens	153-156
19035443-10	2009	Finally, we found significant growth suppressive effects of sunitinib in two acral melanoma cell lines; one harboring the D820Y mutation and one showing SCF-dependent KIT activation.	Sunitinib	60-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	167-170
19035443-11	2009	These results show pathological activation of KIT in a substantial number of metastatic tumors of acral and mucosal melanomas, and suggest a potential therapeutic benefit of sunitinib for these melanomas.	Sunitinib	174-183	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	46-49
19164557-0	2009	KIT kinase mutants show unique mechanisms of drug resistance to imatinib and sunitinib in gastrointestinal stromal tumor patients.	Sunitinib	77-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
19164557-2	2009	The efficacy of the inhibitors imatinib mesylate and sunitinib malate in GIST patients has been linked to their inhibition of these mutant KIT proteins.	Sunitinib	53-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	139-142
19164557-6	2009	Our results show that sunitinib targets the autoinhibited conformation of WT KIT and that the D816H mutant undergoes a shift in conformational equilibrium toward the active state.	Sunitinib	22-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-80
18971320-0	2009	Sunitinib (Sutent, SU11248), a small-molecule receptor tyrosine kinase inhibitor, blocks function of the ATP-binding cassette (ABC) transporters P-glycoprotein (ABCB1) and ABCG2.	Sunitinib	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	145-159
18971320-0	2009	Sunitinib (Sutent, SU11248), a small-molecule receptor tyrosine kinase inhibitor, blocks function of the ATP-binding cassette (ABC) transporters P-glycoprotein (ABCB1) and ABCG2.	Sunitinib	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	161-166
18971320-0	2009	Sunitinib (Sutent, SU11248), a small-molecule receptor tyrosine kinase inhibitor, blocks function of the ATP-binding cassette (ABC) transporters P-glycoprotein (ABCB1) and ABCG2.	Sunitinib	0-9	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	172-177
19284623-1	2009	BACKGROUND: Sunitinib is a protein tyrosine kinase-inhibitor targeting VEGFR, c-kit and PDGFR.	Sunitinib	12-21	kinase insert domain receptor	Homo sapiens	71-76
19284623-1	2009	BACKGROUND: Sunitinib is a protein tyrosine kinase-inhibitor targeting VEGFR, c-kit and PDGFR.	Sunitinib	12-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	78-83
19284623-1	2009	BACKGROUND: Sunitinib is a protein tyrosine kinase-inhibitor targeting VEGFR, c-kit and PDGFR.	Sunitinib	12-21	platelet derived growth factor receptor beta	Homo sapiens	88-93
19127560-11	2009	CONCLUSIONS: The introduction of first-line sunitinib was associated with a doubling of overall survival compared with patients treated with IFN alone.	Sunitinib	44-53	interferon alpha 1	Homo sapiens	141-144
18971320-0	2009	Sunitinib (Sutent, SU11248), a small-molecule receptor tyrosine kinase inhibitor, blocks function of the ATP-binding cassette (ABC) transporters P-glycoprotein (ABCB1) and ABCG2.	Sunitinib	11-17	ATP binding cassette subfamily B member 1	Homo sapiens	145-159
18971320-0	2009	Sunitinib (Sutent, SU11248), a small-molecule receptor tyrosine kinase inhibitor, blocks function of the ATP-binding cassette (ABC) transporters P-glycoprotein (ABCB1) and ABCG2.	Sunitinib	11-17	ATP binding cassette subfamily B member 1	Homo sapiens	161-166
18971320-0	2009	Sunitinib (Sutent, SU11248), a small-molecule receptor tyrosine kinase inhibitor, blocks function of the ATP-binding cassette (ABC) transporters P-glycoprotein (ABCB1) and ABCG2.	Sunitinib	11-17	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	172-177
18971320-0	2009	Sunitinib (Sutent, SU11248), a small-molecule receptor tyrosine kinase inhibitor, blocks function of the ATP-binding cassette (ABC) transporters P-glycoprotein (ABCB1) and ABCG2.	Sunitinib	19-26	ATP binding cassette subfamily B member 1	Homo sapiens	145-159
18971320-0	2009	Sunitinib (Sutent, SU11248), a small-molecule receptor tyrosine kinase inhibitor, blocks function of the ATP-binding cassette (ABC) transporters P-glycoprotein (ABCB1) and ABCG2.	Sunitinib	19-26	ATP binding cassette subfamily B member 1	Homo sapiens	161-166
18971320-0	2009	Sunitinib (Sutent, SU11248), a small-molecule receptor tyrosine kinase inhibitor, blocks function of the ATP-binding cassette (ABC) transporters P-glycoprotein (ABCB1) and ABCG2.	Sunitinib	19-26	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	172-177
18971320-3	2009	bioavailability and brain penetration of chemotherapy drugs in animal models, we sought to examine the effect of sunitinib on the ATP-binding cassette (ABC) drug transporters P-glycoprotein (P-gp, ABCB1), the multidrug resistance-associated protein 1 (ABCC1), and ABCG2, which are known to transport a wide variety of anticancer drugs.	Sunitinib	113-122	ATP binding cassette subfamily B member 1	Homo sapiens	175-189
18971320-3	2009	bioavailability and brain penetration of chemotherapy drugs in animal models, we sought to examine the effect of sunitinib on the ATP-binding cassette (ABC) drug transporters P-glycoprotein (P-gp, ABCB1), the multidrug resistance-associated protein 1 (ABCC1), and ABCG2, which are known to transport a wide variety of anticancer drugs.	Sunitinib	113-122	ATP binding cassette subfamily B member 1	Homo sapiens	191-195
18971320-3	2009	bioavailability and brain penetration of chemotherapy drugs in animal models, we sought to examine the effect of sunitinib on the ATP-binding cassette (ABC) drug transporters P-glycoprotein (P-gp, ABCB1), the multidrug resistance-associated protein 1 (ABCC1), and ABCG2, which are known to transport a wide variety of anticancer drugs.	Sunitinib	113-122	ATP binding cassette subfamily B member 1	Homo sapiens	197-202
18971320-4	2009	In this study, we show that sunitinib inhibits P-gp- and ABCG2-mediated efflux of fluorescent substrates in cells overexpressing these transporters.	Sunitinib	28-37	ATP binding cassette subfamily B member 1	Homo sapiens	47-51
18971320-4	2009	In this study, we show that sunitinib inhibits P-gp- and ABCG2-mediated efflux of fluorescent substrates in cells overexpressing these transporters.	Sunitinib	28-37	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	57-62
18971320-5	2009	In 4-day cytotoxicity assays, at a nontoxic concentration (2 microM) sunitinib was able to partially reverse drug resistance mediated by P-gp and completely reverse resistance mediated by ABCG2.	Sunitinib	69-78	ATP binding cassette subfamily B member 1	Homo sapiens	137-141
18971320-5	2009	In 4-day cytotoxicity assays, at a nontoxic concentration (2 microM) sunitinib was able to partially reverse drug resistance mediated by P-gp and completely reverse resistance mediated by ABCG2.	Sunitinib	69-78	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	188-193
18971320-6	2009	We further show a direct interaction of sunitinib with the substrate binding pocket of these transporters as it inhibited binding of the photoaffinity substrate [(125)I]iodoarylazidoprazosin to P-gp (IC(50) = 14.2 microM) and ABCG2 (IC(50) = 1.33 microM).	Sunitinib	40-49	ATP binding cassette subfamily B member 1	Homo sapiens	194-198
18971320-6	2009	We further show a direct interaction of sunitinib with the substrate binding pocket of these transporters as it inhibited binding of the photoaffinity substrate [(125)I]iodoarylazidoprazosin to P-gp (IC(50) = 14.2 microM) and ABCG2 (IC(50) = 1.33 microM).	Sunitinib	40-49	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	226-231
18971320-8	2009	Conformation-sensitive antibody binding assays with the P-gp- and ABCG2-specific antibodies, UIC2 and 5D3, respectively, also confirmed the interaction of sunitinib with these transporters.	Sunitinib	155-164	phosphoglycolate phosphatase	Homo sapiens	56-61
18971320-8	2009	Conformation-sensitive antibody binding assays with the P-gp- and ABCG2-specific antibodies, UIC2 and 5D3, respectively, also confirmed the interaction of sunitinib with these transporters.	Sunitinib	155-164	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	66-71
19017755-6	2009	Patient was treated with sunitinib, a potent tyrosine kinase inhibitor of vascular endothelial growth factor, platelet-derived growth factor, RET, c-KIT, and FLT-3 receptors.	Sunitinib	25-34	ret proto-oncogene	Homo sapiens	142-145
19017755-6	2009	Patient was treated with sunitinib, a potent tyrosine kinase inhibitor of vascular endothelial growth factor, platelet-derived growth factor, RET, c-KIT, and FLT-3 receptors.	Sunitinib	25-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	147-152
19017755-6	2009	Patient was treated with sunitinib, a potent tyrosine kinase inhibitor of vascular endothelial growth factor, platelet-derived growth factor, RET, c-KIT, and FLT-3 receptors.	Sunitinib	25-34	fms related receptor tyrosine kinase 3	Homo sapiens	158-163
19213665-1	2009	BACKGROUND: Sunitinib malate is an oral, multitargeted tyrosine kinase inhibitor that has demonstrated superior efficacy over interferon (IFN)-alpha in a phase III trial in first-line, metastatic renal cell carcinoma (RCC).	Sunitinib	12-28	interferon alpha 1	Homo sapiens	126-148
19173737-11	2009	Using indirect comparisons with interferon-alpha as the common comparator, we found that sunitinib was superior to both sorafenib (HR 0.58, 95% CI, 0.38-0.86, P = &lt; 0.001) and bevacizumab + IFN-a (HR 0.75, 95% CI, 0.60-0.93, P = 0.001).	Sunitinib	89-98	interferon alpha 2	Homo sapiens	193-198
21686655-3	2009	Treatment with the novel multi-targeted tyrosine kinase inhibitor sunitinib resulted in a sustained partial response and reduced the level of the angiogenic marker PIGF.	Sunitinib	66-75	phosphatidylinositol glycan anchor biosynthesis class F	Homo sapiens	164-168
19054798-0	2009	Thrombotic microangiopathy secondary to VEGF pathway inhibition by sunitinib.	Sunitinib	67-76	vascular endothelial growth factor A	Homo sapiens	40-44
19054798-3	2009	It was shown recently that sunitinib, a small molecule inhibiting several tyrosine kinase receptors, including VEGF receptors, can also induce proteinuria, hypertension and biological features of TMA.	Sunitinib	27-36	vascular endothelial growth factor A	Homo sapiens	111-115
19212818-9	2009	In conclusion, opposite kinetics of two circulating CD34(bright) cell populations, HPCs and small CECs, were observed in sunitinib-treated RCC patients.	Sunitinib	121-130	CD34 molecule	Homo sapiens	52-56
19894779-0	2009	Sunitinib: a multitargeted receptor tyrosine kinase inhibitor in the era of molecular cancer therapies.	Sunitinib	0-9	ret proto-oncogene	Homo sapiens	27-51
20877672-10	2009	Sunitinib inhibits the vascular endothelial growth factor receptor (VEGFR), the platelet-derived growth factor receptor (PDGFR), c-kit and the colony-stimulating factor 1 (CSF-1) receptor.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	23-66
20877672-10	2009	Sunitinib inhibits the vascular endothelial growth factor receptor (VEGFR), the platelet-derived growth factor receptor (PDGFR), c-kit and the colony-stimulating factor 1 (CSF-1) receptor.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	68-73
20877672-10	2009	Sunitinib inhibits the vascular endothelial growth factor receptor (VEGFR), the platelet-derived growth factor receptor (PDGFR), c-kit and the colony-stimulating factor 1 (CSF-1) receptor.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	80-119
20877672-10	2009	Sunitinib inhibits the vascular endothelial growth factor receptor (VEGFR), the platelet-derived growth factor receptor (PDGFR), c-kit and the colony-stimulating factor 1 (CSF-1) receptor.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	121-126
20877672-10	2009	Sunitinib inhibits the vascular endothelial growth factor receptor (VEGFR), the platelet-derived growth factor receptor (PDGFR), c-kit and the colony-stimulating factor 1 (CSF-1) receptor.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	129-134
20877672-10	2009	Sunitinib inhibits the vascular endothelial growth factor receptor (VEGFR), the platelet-derived growth factor receptor (PDGFR), c-kit and the colony-stimulating factor 1 (CSF-1) receptor.	Sunitinib	0-9	colony stimulating factor 1	Homo sapiens	143-170
20877672-10	2009	Sunitinib inhibits the vascular endothelial growth factor receptor (VEGFR), the platelet-derived growth factor receptor (PDGFR), c-kit and the colony-stimulating factor 1 (CSF-1) receptor.	Sunitinib	0-9	colony stimulating factor 1 receptor	Homo sapiens	172-187
19096396-2	2009	In 2007, a pivotal phase III trial randomly allocated 750 patients with advanced renal cell carcinoma to receive either the VEGF-receptor tyrosine kinase inhibitor sunitinib or interferon alpha, and showed that sunitinib led to improved response rates, progression-free and overall survival.	Sunitinib	211-220	vascular endothelial growth factor A	Homo sapiens	124-128
19105714-1	2009	Sunitinib malate is an oral, multitargeted receptor tyrosine kinase inhibitor of VEGF receptors 1, 2 and 3; PDGF receptors alpha and beta, and other receptor tyrosine kinases implicated in tumor growth, angiogenesis and metastasis.	Sunitinib	0-16	vascular endothelial growth factor A	Homo sapiens	81-85
19096396-2	2009	In 2007, a pivotal phase III trial randomly allocated 750 patients with advanced renal cell carcinoma to receive either the VEGF-receptor tyrosine kinase inhibitor sunitinib or interferon alpha, and showed that sunitinib led to improved response rates, progression-free and overall survival.	Sunitinib	164-173	vascular endothelial growth factor A	Homo sapiens	124-128
19468197-6	2009	While such tyrosine kinase inhibitors, particularly those affecting RET activity such as vandetanib, sorafenib and sunitinib, are promising, the low rate of partial responses and absence of complete responses in all of the various trials of monotherapy emphasize the need for new and more effective single agents or combinations of therapeutic agents with acceptable toxicity.	Sunitinib	115-124	ret proto-oncogene	Homo sapiens	68-71
18618496-1	2008	BACKGROUND: Sunitinib and sorafenib are small molecules that inhibit the vascular endothelial growth factor and related receptors with substantial clinical activity reported in metastatic renal cell carcinoma (RCC).	Sunitinib	12-21	vascular endothelial growth factor A	Homo sapiens	73-107
19891126-5	2008	This review will summarize the major clinical trials and practical recommendations for the most studied VEGF inhibitors, including sunitinib, sorafenib, and bevacizumab; introduce novel VEGF inhibitor agents; outline side effects and toxicities; and discuss sequential and combination therapy with these agents.	Sunitinib	131-140	vascular endothelial growth factor A	Homo sapiens	104-108
18815214-3	2008	Sunitinib potently inhibited the enzyme activity of both AMP-activated protein kinase (AMPK) and the ribosomal S6 kinase RSK1 at therapeutically relevant concentrations.	Sunitinib	0-9	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	57-85
18815214-3	2008	Sunitinib potently inhibited the enzyme activity of both AMP-activated protein kinase (AMPK) and the ribosomal S6 kinase RSK1 at therapeutically relevant concentrations.	Sunitinib	0-9	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	87-91
18815214-3	2008	Sunitinib potently inhibited the enzyme activity of both AMP-activated protein kinase (AMPK) and the ribosomal S6 kinase RSK1 at therapeutically relevant concentrations.	Sunitinib	0-9	ribosomal protein S6 kinase A1	Rattus norvegicus	121-125
18815214-6	2008	Sunitinib treatment also caused a dose-dependent reduction in myocyte protein levels of the phosphorylated alpha and beta isoforms of the AMPK phosphorylation target acetyl-Coenzyme A carboxylase.	Sunitinib	0-9	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	138-142
18815214-11	2008	In conclusion, even though sunitinib potently inhibits AMPK and RSK1, given the extreme lack of kinase selectivity that sunitinib exhibits, it is likely that inhibition of other kinases or combinations of kinases are responsible for the cardiotoxic effects of sunitinib.	Sunitinib	27-36	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	55-59
18815214-11	2008	In conclusion, even though sunitinib potently inhibits AMPK and RSK1, given the extreme lack of kinase selectivity that sunitinib exhibits, it is likely that inhibition of other kinases or combinations of kinases are responsible for the cardiotoxic effects of sunitinib.	Sunitinib	27-36	ribosomal protein S6 kinase A1	Rattus norvegicus	64-68
18981453-0	2008	Nonclinical safety evaluation of sunitinib: a potent inhibitor of VEGF, PDGF, KIT, FLT3, and RET receptors.	Sunitinib	33-42	vascular endothelial growth factor A	Rattus norvegicus	66-70
18981453-0	2008	Nonclinical safety evaluation of sunitinib: a potent inhibitor of VEGF, PDGF, KIT, FLT3, and RET receptors.	Sunitinib	33-42	KIT proto-oncogene receptor tyrosine kinase	Rattus norvegicus	78-81
18981453-0	2008	Nonclinical safety evaluation of sunitinib: a potent inhibitor of VEGF, PDGF, KIT, FLT3, and RET receptors.	Sunitinib	33-42	Fms related receptor tyrosine kinase 3	Rattus norvegicus	83-87
18932293-1	2008	The molecular targets of sunitinib are receptor tyrosine kinases (RTKs), and this drug has also been known to exert blocking effects on the activation of KIT, which is similar to the mechanism of action of imatinib.	Sunitinib	25-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	154-157
18927310-4	2008	EXPERIMENTAL DESIGN: Type-1 (IFNgamma) and type-2 (interleukin-4) responses were assessed in T cells at baseline and day 28 of treatment with sunitinib (50 mg/d) by measuring intracellular cytokines after in vitro stimulation with anti-CD3/anti-CD28 antibodies.	Sunitinib	142-151	interferon gamma	Homo sapiens	29-37
18927310-4	2008	EXPERIMENTAL DESIGN: Type-1 (IFNgamma) and type-2 (interleukin-4) responses were assessed in T cells at baseline and day 28 of treatment with sunitinib (50 mg/d) by measuring intracellular cytokines after in vitro stimulation with anti-CD3/anti-CD28 antibodies.	Sunitinib	142-151	interleukin 4	Homo sapiens	51-64
20020657-4	2009	We were the first to demonstrate that endothelial cell incubation was followed by increase in 5"-nucleotidase activity in the presence of sutent while celecoxib did not produce such effect.	Sunitinib	138-144	5'-nucleotidase ecto	Homo sapiens	94-109
19075590-4	2008	Both sunitinib and sorafenib target VEGF and PDGF receptor tyrosine kinases while bevacizumab is a monoclonal antibody to VEGF.	Sunitinib	5-14	vascular endothelial growth factor A	Homo sapiens	36-40
18955458-2	2008	Sunitinib, which targets KIT, PDGFRs, and several other kinases, has demonstrated efficacy in patients with GIST after they experience imatinib failure.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	25-28
18955458-7	2008	RESULTS: Clinical benefit (partial response or stable disease for &gt; or = 6 months) with sunitinib was observed for the three most common primary GIST genotypes: KIT exon 9 (58%), KIT exon 11 (34%), and wild-type KIT/PDGFRA (56%).	Sunitinib	91-100	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	164-167
18955458-7	2008	RESULTS: Clinical benefit (partial response or stable disease for &gt; or = 6 months) with sunitinib was observed for the three most common primary GIST genotypes: KIT exon 9 (58%), KIT exon 11 (34%), and wild-type KIT/PDGFRA (56%).	Sunitinib	91-100	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	182-185
18955458-7	2008	RESULTS: Clinical benefit (partial response or stable disease for &gt; or = 6 months) with sunitinib was observed for the three most common primary GIST genotypes: KIT exon 9 (58%), KIT exon 11 (34%), and wild-type KIT/PDGFRA (56%).	Sunitinib	91-100	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	182-185
18955458-7	2008	RESULTS: Clinical benefit (partial response or stable disease for &gt; or = 6 months) with sunitinib was observed for the three most common primary GIST genotypes: KIT exon 9 (58%), KIT exon 11 (34%), and wild-type KIT/PDGFRA (56%).	Sunitinib	91-100	platelet derived growth factor receptor alpha	Homo sapiens	219-225
18922106-2	2008	Sunitinib malate, sorafenib tosylate, bevacizumab +/- interferon-alfa, temsirolimus, and everolimus have improved clinical outcomes in randomized Phase III trials by inhibiting the VEGF and related pathways.	Sunitinib	0-16	vascular endothelial growth factor A	Homo sapiens	181-185
18374947-1	2008	OBJECTIVE: To determine the effects of sunitinib, a vascular endothelial growth factor receptor 2 (VEGFR-2) antagonist, on intra-abdominal adhesions.	Sunitinib	39-48	kinase insert domain protein receptor	Mus musculus	52-97
18794101-0	2008	Sunitinib-induced myeloid lineage redistribution in renal cell cancer patients: CD1c+ dendritic cell frequency predicts progression-free survival.	Sunitinib	0-9	CD1c molecule	Homo sapiens	80-84
18794101-9	2008	Subsequent to sunitinib treatment, an increase to high levels of myeloid DC (MDC) subset frequencies relative to other myeloid subsets, was specifically observed in patients experiencing tumor regression.	Sunitinib	14-23	C-C motif chemokine ligand 22	Homo sapiens	65-75
18794101-9	2008	Subsequent to sunitinib treatment, an increase to high levels of myeloid DC (MDC) subset frequencies relative to other myeloid subsets, was specifically observed in patients experiencing tumor regression.	Sunitinib	14-23	C-C motif chemokine ligand 22	Homo sapiens	77-80
18374947-1	2008	OBJECTIVE: To determine the effects of sunitinib, a vascular endothelial growth factor receptor 2 (VEGFR-2) antagonist, on intra-abdominal adhesions.	Sunitinib	39-48	kinase insert domain protein receptor	Mus musculus	99-106
18374947-4	2008	Sunitinib, a tyrosine kinase inhibitor with antiangiogenic and antitumor properties, may prevent or reduce postoperative abdominal adhesions by VEGFR-2 inhibition.	Sunitinib	0-9	kinase insert domain protein receptor	Mus musculus	144-151
18374947-14	2008	Sunitinib, a VEGFR-2 antagonist, significantly reduces adhesion formation in a murine model.	Sunitinib	0-9	kinase insert domain protein receptor	Mus musculus	13-20
18669461-8	2008	Mean plasma VEGF-A and PlGF levels significantly increased whereas VEGF-C and sVEGFR-3 levels decreased with sunitinib treatment.	Sunitinib	109-118	vascular endothelial growth factor C	Homo sapiens	67-73
18711190-7	2008	RESULTS: Treatment with sunitinib is associated with a gain in progression-free years of 0.41 and 0.35 over IFN-alpha and IL-2.	Sunitinib	24-33	interferon alpha 1	Homo sapiens	108-117
18711190-7	2008	RESULTS: Treatment with sunitinib is associated with a gain in progression-free years of 0.41 and 0.35 over IFN-alpha and IL-2.	Sunitinib	24-33	interleukin 2	Homo sapiens	122-126
18711190-9	2008	Both IFN-alpha and sunitinib treatments dominate IL-2 treatment; the incremental cost-effectiveness ratio of sunitinib versus IFN-alpha was $18,611 per progression-free year gained and $67,215 per LY gained, and the cost-utility ratio is $52,593 per QALY gained (at a 5% discount rate).	Sunitinib	109-118	interferon alpha 1	Homo sapiens	5-14
18082353-10	2008	FINDINGS: Sunitinib (SU11248) is a novel multi-targeted tyrosine kinase inhibitor with activity not only against the receptor tyrosine kinase product of c-KIT but also other cell-signalling pathways that may be relevant in GIST; FLT3, platelet-derived growth receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR).	Sunitinib	10-19	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	153-158
18082353-10	2008	FINDINGS: Sunitinib (SU11248) is a novel multi-targeted tyrosine kinase inhibitor with activity not only against the receptor tyrosine kinase product of c-KIT but also other cell-signalling pathways that may be relevant in GIST; FLT3, platelet-derived growth receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR).	Sunitinib	10-19	fms related receptor tyrosine kinase 3	Homo sapiens	229-233
18082353-10	2008	FINDINGS: Sunitinib (SU11248) is a novel multi-targeted tyrosine kinase inhibitor with activity not only against the receptor tyrosine kinase product of c-KIT but also other cell-signalling pathways that may be relevant in GIST; FLT3, platelet-derived growth receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR).	Sunitinib	10-19	platelet derived growth factor receptor beta	Homo sapiens	269-274
18082353-10	2008	FINDINGS: Sunitinib (SU11248) is a novel multi-targeted tyrosine kinase inhibitor with activity not only against the receptor tyrosine kinase product of c-KIT but also other cell-signalling pathways that may be relevant in GIST; FLT3, platelet-derived growth receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR).	Sunitinib	10-19	kinase insert domain receptor	Homo sapiens	280-323
18082353-10	2008	FINDINGS: Sunitinib (SU11248) is a novel multi-targeted tyrosine kinase inhibitor with activity not only against the receptor tyrosine kinase product of c-KIT but also other cell-signalling pathways that may be relevant in GIST; FLT3, platelet-derived growth receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR).	Sunitinib	10-19	kinase insert domain receptor	Homo sapiens	325-330
18082353-10	2008	FINDINGS: Sunitinib (SU11248) is a novel multi-targeted tyrosine kinase inhibitor with activity not only against the receptor tyrosine kinase product of c-KIT but also other cell-signalling pathways that may be relevant in GIST; FLT3, platelet-derived growth receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR).	Sunitinib	21-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	153-158
18082353-10	2008	FINDINGS: Sunitinib (SU11248) is a novel multi-targeted tyrosine kinase inhibitor with activity not only against the receptor tyrosine kinase product of c-KIT but also other cell-signalling pathways that may be relevant in GIST; FLT3, platelet-derived growth receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR).	Sunitinib	21-28	fms related receptor tyrosine kinase 3	Homo sapiens	229-233
18082353-10	2008	FINDINGS: Sunitinib (SU11248) is a novel multi-targeted tyrosine kinase inhibitor with activity not only against the receptor tyrosine kinase product of c-KIT but also other cell-signalling pathways that may be relevant in GIST; FLT3, platelet-derived growth receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR).	Sunitinib	21-28	platelet derived growth factor receptor beta	Homo sapiens	269-274
18082353-10	2008	FINDINGS: Sunitinib (SU11248) is a novel multi-targeted tyrosine kinase inhibitor with activity not only against the receptor tyrosine kinase product of c-KIT but also other cell-signalling pathways that may be relevant in GIST; FLT3, platelet-derived growth receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR).	Sunitinib	21-28	kinase insert domain receptor	Homo sapiens	280-323
18082353-10	2008	FINDINGS: Sunitinib (SU11248) is a novel multi-targeted tyrosine kinase inhibitor with activity not only against the receptor tyrosine kinase product of c-KIT but also other cell-signalling pathways that may be relevant in GIST; FLT3, platelet-derived growth receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR).	Sunitinib	21-28	kinase insert domain receptor	Homo sapiens	325-330
18669461-11	2008	CONCLUSION: Sunitinib has substantial antitumor activity in patients with bevacizumab-refractory mRCC and modulates circulating VEGF pathway biomarkers.	Sunitinib	12-21	vascular endothelial growth factor A	Homo sapiens	128-132
18525301-13	2008	Further development of the thalidomide plus IL-2 combination therapy will address patients who have received molecular-targeted agents, such as sunitinib and sorafenib, as first- or second-line therapy.	Sunitinib	144-153	interleukin 2	Homo sapiens	44-48
18648503-5	2008	Orally active anti-VEGF agents including sunitinib and ZM323881 effectively block hypoxia-induced retinal neovascularization.	Sunitinib	41-50	vascular endothelial growth factor Aa	Danio rerio	19-23
19296000-5	2008	Multi-kinase ihibitors (sorafenib and sunitinib) are orally administered small-molecules, that inhibit different receptors (essentials in the neoplastic angiogenesis), such as the VEGFR or PDGFR.	Sunitinib	38-47	kinase insert domain receptor	Homo sapiens	180-185
19296000-5	2008	Multi-kinase ihibitors (sorafenib and sunitinib) are orally administered small-molecules, that inhibit different receptors (essentials in the neoplastic angiogenesis), such as the VEGFR or PDGFR.	Sunitinib	38-47	platelet derived growth factor receptor beta	Homo sapiens	189-194
18514780-1	2008	PURPOSE: SU11248 (sunitinib) is a small-molecule tyrosine kinase inhibitor which targets VEGFR and PDGFR isoforms.	Sunitinib	9-16	kinase insert domain receptor	Homo sapiens	89-94
18514780-1	2008	PURPOSE: SU11248 (sunitinib) is a small-molecule tyrosine kinase inhibitor which targets VEGFR and PDGFR isoforms.	Sunitinib	9-16	platelet derived growth factor receptor beta	Homo sapiens	99-104
18514780-1	2008	PURPOSE: SU11248 (sunitinib) is a small-molecule tyrosine kinase inhibitor which targets VEGFR and PDGFR isoforms.	Sunitinib	18-27	kinase insert domain receptor	Homo sapiens	89-94
18514780-1	2008	PURPOSE: SU11248 (sunitinib) is a small-molecule tyrosine kinase inhibitor which targets VEGFR and PDGFR isoforms.	Sunitinib	18-27	platelet derived growth factor receptor beta	Homo sapiens	99-104
18514780-7	2008	RESULTS: SU11248 attenuated radiation-induced phosphorylation of Akt and ERK at 0, 5, 15, and 30 min.	Sunitinib	9-16	AKT serine/threonine kinase 1	Homo sapiens	65-68
18514780-7	2008	RESULTS: SU11248 attenuated radiation-induced phosphorylation of Akt and ERK at 0, 5, 15, and 30 min.	Sunitinib	9-16	EPH receptor B2	Homo sapiens	73-76
18293383-1	2008	BACKGROUND: Sunitinib is an orally bioavailable, multi-targeted tyrosine kinase inhibitor with selectivity for PDGF receptors, VEGF receptors, FLT3, and KIT.	Sunitinib	12-21	FMS-like tyrosine kinase 3	Mus musculus	143-147
18293383-1	2008	BACKGROUND: Sunitinib is an orally bioavailable, multi-targeted tyrosine kinase inhibitor with selectivity for PDGF receptors, VEGF receptors, FLT3, and KIT.	Sunitinib	12-21	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	153-156
18612155-3	2008	Sunitinib malate, an oral tyrosine kinase inhibitor, has activity against VEGFRs as well as platelet-derived growth factor receptors, stem-cell factor receptor, glial cell line-derived neurotrophic factor, and FMS-like tyrosine kinase-3.	Sunitinib	0-16	fms related receptor tyrosine kinase 3	Homo sapiens	210-236
18418222-3	2008	Sunitinib is active against the RET kinase and has both antineoplastic and antiangiogenic properties.	Sunitinib	0-9	ret proto-oncogene	Homo sapiens	32-35
17983653-0	2008	Blockade of MEK/ERK signaling enhances sunitinib-induced growth inhibition and apoptosis of leukemia cells possessing activating mutations of the FLT3 gene.	Sunitinib	39-48	mitogen-activated protein kinase kinase 7	Homo sapiens	12-15
17983653-0	2008	Blockade of MEK/ERK signaling enhances sunitinib-induced growth inhibition and apoptosis of leukemia cells possessing activating mutations of the FLT3 gene.	Sunitinib	39-48	fms related receptor tyrosine kinase 3	Homo sapiens	146-150
17983653-7	2008	Interestingly, when AZD6244 was combined with sunitinib, a FLT3 kinase inhibitor, growth inhibition and apoptosis of both MV4-11 and MOLM13 cells were synergistically enhanced in association with further down-regulation of phospho-ERK1/2 and p-p70S6K in these cells.	Sunitinib	46-55	fms related receptor tyrosine kinase 3	Homo sapiens	59-63
17983653-7	2008	Interestingly, when AZD6244 was combined with sunitinib, a FLT3 kinase inhibitor, growth inhibition and apoptosis of both MV4-11 and MOLM13 cells were synergistically enhanced in association with further down-regulation of phospho-ERK1/2 and p-p70S6K in these cells.	Sunitinib	46-55	ribosomal protein S6 kinase B1	Homo sapiens	244-250
18537751-7	2008	Currently, the sole approved second-line drug is sunitinib--a multitargeted agent, an inhibitor of tyrosine kinase, of KIT and PDGFRA/B and of the vascular endothelial growth factor receptors (VEGFRs)-1, -2 and 3, FMS-like tyrosine kinase-3 (FLT3), colony stimulating factor 1 receptor (CSF-1R), and glial cell-line derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	49-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	119-122
18537751-7	2008	Currently, the sole approved second-line drug is sunitinib--a multitargeted agent, an inhibitor of tyrosine kinase, of KIT and PDGFRA/B and of the vascular endothelial growth factor receptors (VEGFRs)-1, -2 and 3, FMS-like tyrosine kinase-3 (FLT3), colony stimulating factor 1 receptor (CSF-1R), and glial cell-line derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	49-58	platelet derived growth factor receptor alpha	Homo sapiens	127-133
18537751-7	2008	Currently, the sole approved second-line drug is sunitinib--a multitargeted agent, an inhibitor of tyrosine kinase, of KIT and PDGFRA/B and of the vascular endothelial growth factor receptors (VEGFRs)-1, -2 and 3, FMS-like tyrosine kinase-3 (FLT3), colony stimulating factor 1 receptor (CSF-1R), and glial cell-line derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	49-58	fms related receptor tyrosine kinase 1	Homo sapiens	147-212
18537751-7	2008	Currently, the sole approved second-line drug is sunitinib--a multitargeted agent, an inhibitor of tyrosine kinase, of KIT and PDGFRA/B and of the vascular endothelial growth factor receptors (VEGFRs)-1, -2 and 3, FMS-like tyrosine kinase-3 (FLT3), colony stimulating factor 1 receptor (CSF-1R), and glial cell-line derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	49-58	fms related receptor tyrosine kinase 3	Homo sapiens	214-240
18537751-7	2008	Currently, the sole approved second-line drug is sunitinib--a multitargeted agent, an inhibitor of tyrosine kinase, of KIT and PDGFRA/B and of the vascular endothelial growth factor receptors (VEGFRs)-1, -2 and 3, FMS-like tyrosine kinase-3 (FLT3), colony stimulating factor 1 receptor (CSF-1R), and glial cell-line derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	49-58	fms related receptor tyrosine kinase 3	Homo sapiens	242-246
18537751-7	2008	Currently, the sole approved second-line drug is sunitinib--a multitargeted agent, an inhibitor of tyrosine kinase, of KIT and PDGFRA/B and of the vascular endothelial growth factor receptors (VEGFRs)-1, -2 and 3, FMS-like tyrosine kinase-3 (FLT3), colony stimulating factor 1 receptor (CSF-1R), and glial cell-line derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	49-58	colony stimulating factor 1 receptor	Homo sapiens	249-285
18537751-7	2008	Currently, the sole approved second-line drug is sunitinib--a multitargeted agent, an inhibitor of tyrosine kinase, of KIT and PDGFRA/B and of the vascular endothelial growth factor receptors (VEGFRs)-1, -2 and 3, FMS-like tyrosine kinase-3 (FLT3), colony stimulating factor 1 receptor (CSF-1R), and glial cell-line derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	49-58	colony stimulating factor 1 receptor	Homo sapiens	287-293
18537751-7	2008	Currently, the sole approved second-line drug is sunitinib--a multitargeted agent, an inhibitor of tyrosine kinase, of KIT and PDGFRA/B and of the vascular endothelial growth factor receptors (VEGFRs)-1, -2 and 3, FMS-like tyrosine kinase-3 (FLT3), colony stimulating factor 1 receptor (CSF-1R), and glial cell-line derived neurotrophic factor receptor (REarranged during Transfection; RET).	Sunitinib	49-58	ret proto-oncogene	Homo sapiens	386-389
18506667-9	2008	Small-molecule inhibitors of the VEGF receptor tyrosine kinase, such as sunitinib and sorafenib, have also shown promise in phase II trials and are being further investigated in phase III studies.	Sunitinib	72-81	vascular endothelial growth factor A	Homo sapiens	33-37
18483389-9	2008	In vitro studies showed that nilotinib, sunitinib, dasatinib, and sorafenib are more effective than imatinib against WT KIT.	Sunitinib	40-49	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	120-123
18483300-3	2008	Sorafenib and sunitinib were potent inhibitors of cells with fms-like tyrosine kinase 3 internal tandem duplication (IC50, 2 and 7 nmol/L) and c-KIT N822K mutations (IC50, 23 and 40 nmol/L).	Sunitinib	14-23	fms related receptor tyrosine kinase 3	Homo sapiens	61-87
18472378-2	2008	Among them, the major are those targeting the VEGF pathway, including anti-VEGF antibodies (bevacizumab) and VEGF receptor tyrosine kinase inhibitors (vatalanib, sorafenib, sunitinib...).	Sunitinib	173-182	vascular endothelial growth factor A	Homo sapiens	46-50
18483300-3	2008	Sorafenib and sunitinib were potent inhibitors of cells with fms-like tyrosine kinase 3 internal tandem duplication (IC50, 2 and 7 nmol/L) and c-KIT N822K mutations (IC50, 23 and 40 nmol/L).	Sunitinib	14-23	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	143-148
18474019-4	2008	Sunitinib is a multitarget receptor tyrosine-kinase (TK) inhibitor, acting on VEGF receptor (VEGFR) and platelet-derived growth factor receptors (PDGFR).	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	78-91
18474019-4	2008	Sunitinib is a multitarget receptor tyrosine-kinase (TK) inhibitor, acting on VEGF receptor (VEGFR) and platelet-derived growth factor receptors (PDGFR).	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	93-98
18474019-4	2008	Sunitinib is a multitarget receptor tyrosine-kinase (TK) inhibitor, acting on VEGF receptor (VEGFR) and platelet-derived growth factor receptors (PDGFR).	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	104-144
18474019-4	2008	Sunitinib is a multitarget receptor tyrosine-kinase (TK) inhibitor, acting on VEGF receptor (VEGFR) and platelet-derived growth factor receptors (PDGFR).	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	146-151
17505827-1	2008	PURPOSE: Sunitinib, an oral multitargeted tyrosine kinase inhibitor that inhibits VEGFR, PDGFR, FLT3, KIT, and RET, is currently approved for the treatment of imatinib-refractory GIST and advanced renal cell carcinoma at a dose of 50 mg daily for 4 weeks followed by a 2-week off period (4/2 schedule).	Sunitinib	9-18	kinase insert domain receptor	Homo sapiens	82-87
18347007-1	2008	PURPOSE: Sunitinib is an oral, multitargeted tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor, stem cell factor receptor (KIT), and colony-stimulating factor-1 receptor.	Sunitinib	9-18	kinase insert domain receptor	Homo sapiens	85-128
18347007-1	2008	PURPOSE: Sunitinib is an oral, multitargeted tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor, stem cell factor receptor (KIT), and colony-stimulating factor-1 receptor.	Sunitinib	9-18	kinase insert domain receptor	Homo sapiens	130-135
18347007-1	2008	PURPOSE: Sunitinib is an oral, multitargeted tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor, stem cell factor receptor (KIT), and colony-stimulating factor-1 receptor.	Sunitinib	9-18	colony stimulating factor 1 receptor	Homo sapiens	179-252
18265991-3	2008	Two tyrosine kinase inhibitors targeting the vascular endothelial growth factor (VEGF) receptor have been shown to improve the progression-free survival of patients in first-line (Sunitinib vs. interferon-alpha) or second-line treatment (Sorafenib vs. placebo).	Sunitinib	180-189	vascular endothelial growth factor A	Homo sapiens	81-85
18035517-3	2008	Two inhibitors targeting several protein kinases, including the VEGF receptor, have increased progression-free survival in patients with metastatic RCC and are now commercially available: sunitinib (Sutent) as first-line treatment and sorafenib (Nexavar) as second-line treatment.	Sunitinib	188-197	vascular endothelial growth factor A	Homo sapiens	64-68
18035517-3	2008	Two inhibitors targeting several protein kinases, including the VEGF receptor, have increased progression-free survival in patients with metastatic RCC and are now commercially available: sunitinib (Sutent) as first-line treatment and sorafenib (Nexavar) as second-line treatment.	Sunitinib	199-205	vascular endothelial growth factor A	Homo sapiens	64-68
17505827-1	2008	PURPOSE: Sunitinib, an oral multitargeted tyrosine kinase inhibitor that inhibits VEGFR, PDGFR, FLT3, KIT, and RET, is currently approved for the treatment of imatinib-refractory GIST and advanced renal cell carcinoma at a dose of 50 mg daily for 4 weeks followed by a 2-week off period (4/2 schedule).	Sunitinib	9-18	platelet derived growth factor receptor beta	Homo sapiens	89-94
17505827-1	2008	PURPOSE: Sunitinib, an oral multitargeted tyrosine kinase inhibitor that inhibits VEGFR, PDGFR, FLT3, KIT, and RET, is currently approved for the treatment of imatinib-refractory GIST and advanced renal cell carcinoma at a dose of 50 mg daily for 4 weeks followed by a 2-week off period (4/2 schedule).	Sunitinib	9-18	fms related receptor tyrosine kinase 3	Homo sapiens	96-100
17505827-1	2008	PURPOSE: Sunitinib, an oral multitargeted tyrosine kinase inhibitor that inhibits VEGFR, PDGFR, FLT3, KIT, and RET, is currently approved for the treatment of imatinib-refractory GIST and advanced renal cell carcinoma at a dose of 50 mg daily for 4 weeks followed by a 2-week off period (4/2 schedule).	Sunitinib	9-18	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	102-105
17505827-1	2008	PURPOSE: Sunitinib, an oral multitargeted tyrosine kinase inhibitor that inhibits VEGFR, PDGFR, FLT3, KIT, and RET, is currently approved for the treatment of imatinib-refractory GIST and advanced renal cell carcinoma at a dose of 50 mg daily for 4 weeks followed by a 2-week off period (4/2 schedule).	Sunitinib	9-18	ret proto-oncogene	Homo sapiens	111-114
18316579-6	2008	Furthermore, both sunitinib-treated groups maintained the molecular balance between angiopoietins Ang-1 and Ang-2, suggesting a critical role of angiopoietins in vascular normalization.	Sunitinib	18-27	angiopoietin 1	Homo sapiens	98-103
18316579-6	2008	Furthermore, both sunitinib-treated groups maintained the molecular balance between angiopoietins Ang-1 and Ang-2, suggesting a critical role of angiopoietins in vascular normalization.	Sunitinib	18-27	angiopoietin 2	Homo sapiens	108-113
17962201-2	2008	Sunitinib, also a VEGFR inhibitor, induces biochemical hypothyroidism in 85% of metastatic RCC patients, the majority of whom have signs or symptoms of hypothyroidism.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	18-23
18287850-0	2008	F-18 FDG PET/CT assessment of gastrointestinal stromal tumor response to sunitinib malate therapy.	Sunitinib	73-89	mastermind like domain containing 1	Homo sapiens	0-12
18366295-2	2008	In study populations comprising primarily good- and intermediate-risk patients with clear cell renal cell carcinoma and prior nephrectomy, prolonged progression-free survival was demonstrated for three angiogenesis-targeted agents: sunitinib (compared with interferon [IFN]), bevacizumab plus IFN (vs IFN alone) and sorafenib (vs placebo in cytokine-refractory patients).	Sunitinib	232-241	interferon alpha 1	Homo sapiens	293-296
18366295-2	2008	In study populations comprising primarily good- and intermediate-risk patients with clear cell renal cell carcinoma and prior nephrectomy, prolonged progression-free survival was demonstrated for three angiogenesis-targeted agents: sunitinib (compared with interferon [IFN]), bevacizumab plus IFN (vs IFN alone) and sorafenib (vs placebo in cytokine-refractory patients).	Sunitinib	232-241	interferon alpha 1	Homo sapiens	293-296
18230576-6	2008	Sunitinib is another approved drug and an inhibitor of multiple tyrosine kinases including KIT, PDGFR alpha as well as PDGFR beta and VEGFRs which are associated with angiogenesis.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	91-94
17945482-1	2008	SU11248 sunitinib malate sutent is a selective inhibitor of certain protein tyrosine kinases including VEGF-R types 1-3 PDGF-R-a and -b, c-kit, and RET.	Sunitinib	0-7	ret proto-oncogene	Homo sapiens	148-151
18235126-2	2008	We evaluated the clinical activity and tolerability of sunitinib malate (SU11248), an oral, multitargeted tyrosine kinase inhibitor that blocks the activity of receptors for VEGF and PDGF, as well as related tyrosine kinases in patients with previously treated, advanced NSCLC.	Sunitinib	55-71	vascular endothelial growth factor A	Homo sapiens	174-178
18235126-2	2008	We evaluated the clinical activity and tolerability of sunitinib malate (SU11248), an oral, multitargeted tyrosine kinase inhibitor that blocks the activity of receptors for VEGF and PDGF, as well as related tyrosine kinases in patients with previously treated, advanced NSCLC.	Sunitinib	73-80	vascular endothelial growth factor A	Homo sapiens	174-178
18192256-2	2008	SUMMARY: Sunitinib malate is a potent inhibitor of vascular endothelial growth factor (VEGF) receptors, FMS-like tyrosine kinase 3 (FLT3), c-KIT, and platelet-derived growth factor (PDGF), which give the drug its direct antitumor and antiangiogenic properties.	Sunitinib	9-25	vascular endothelial growth factor A	Homo sapiens	51-85
18192256-2	2008	SUMMARY: Sunitinib malate is a potent inhibitor of vascular endothelial growth factor (VEGF) receptors, FMS-like tyrosine kinase 3 (FLT3), c-KIT, and platelet-derived growth factor (PDGF), which give the drug its direct antitumor and antiangiogenic properties.	Sunitinib	9-25	vascular endothelial growth factor A	Homo sapiens	87-91
18192256-2	2008	SUMMARY: Sunitinib malate is a potent inhibitor of vascular endothelial growth factor (VEGF) receptors, FMS-like tyrosine kinase 3 (FLT3), c-KIT, and platelet-derived growth factor (PDGF), which give the drug its direct antitumor and antiangiogenic properties.	Sunitinib	9-25	fms related receptor tyrosine kinase 3	Homo sapiens	104-130
18192256-2	2008	SUMMARY: Sunitinib malate is a potent inhibitor of vascular endothelial growth factor (VEGF) receptors, FMS-like tyrosine kinase 3 (FLT3), c-KIT, and platelet-derived growth factor (PDGF), which give the drug its direct antitumor and antiangiogenic properties.	Sunitinib	9-25	fms related receptor tyrosine kinase 3	Homo sapiens	132-136
18192256-2	2008	SUMMARY: Sunitinib malate is a potent inhibitor of vascular endothelial growth factor (VEGF) receptors, FMS-like tyrosine kinase 3 (FLT3), c-KIT, and platelet-derived growth factor (PDGF), which give the drug its direct antitumor and antiangiogenic properties.	Sunitinib	9-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	139-144
18230576-6	2008	Sunitinib is another approved drug and an inhibitor of multiple tyrosine kinases including KIT, PDGFR alpha as well as PDGFR beta and VEGFRs which are associated with angiogenesis.	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	96-107
18230576-6	2008	Sunitinib is another approved drug and an inhibitor of multiple tyrosine kinases including KIT, PDGFR alpha as well as PDGFR beta and VEGFRs which are associated with angiogenesis.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	119-129
17942672-3	2007	However, here we report that an identical pattern of change is observed in normal nontumor-bearing mice treated with SU11248/sunitinib, a small-molecule inhibitor of VEGF and PDGF RTKs.	Sunitinib	117-124	vascular endothelial growth factor A	Mus musculus	166-170
18288997-10	2008	With the recent approval by FDA of Sorafenib and Sunitinib--targeting VEGFR, PDGFR, FLT-3 and c-Kit--a different scenario has been emerging, where a new generation of anti-cancer drugs, able to inhibit more than one pathway, would probably play a major role.	Sunitinib	49-58	platelet derived growth factor receptor beta	Homo sapiens	77-82
18288997-10	2008	With the recent approval by FDA of Sorafenib and Sunitinib--targeting VEGFR, PDGFR, FLT-3 and c-Kit--a different scenario has been emerging, where a new generation of anti-cancer drugs, able to inhibit more than one pathway, would probably play a major role.	Sunitinib	49-58	fms related receptor tyrosine kinase 3	Homo sapiens	84-89
18288997-10	2008	With the recent approval by FDA of Sorafenib and Sunitinib--targeting VEGFR, PDGFR, FLT-3 and c-Kit--a different scenario has been emerging, where a new generation of anti-cancer drugs, able to inhibit more than one pathway, would probably play a major role.	Sunitinib	49-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	94-99
17593391-10	2008	There were significantly higher pro-apoptotic effects (caspase-3 cleavage) observed for the sunitinib-docetaxel and sunitinib-docetaxel-cetuximab as compared to the other conditions.	Sunitinib	92-101	caspase 3	Mus musculus	55-64
17593391-10	2008	There were significantly higher pro-apoptotic effects (caspase-3 cleavage) observed for the sunitinib-docetaxel and sunitinib-docetaxel-cetuximab as compared to the other conditions.	Sunitinib	116-125	caspase 3	Mus musculus	55-64
18615363-3	2008	The new multitargeted kinase inhibitors sorafenib (Nexavar/BAY 43-9006) and sunitinib (Sutent/SUO 11248) interfere mainly with vascular endothelial growth factor and platelet-derived growth factor pathways.	Sunitinib	76-85	vascular endothelial growth factor A	Homo sapiens	127-161
18615363-3	2008	The new multitargeted kinase inhibitors sorafenib (Nexavar/BAY 43-9006) and sunitinib (Sutent/SUO 11248) interfere mainly with vascular endothelial growth factor and platelet-derived growth factor pathways.	Sunitinib	87-93	vascular endothelial growth factor A	Homo sapiens	127-161
17935226-5	2007	The in vivo effects of SU11248 treatment were monitored in the livers of cirrhotic rats by measuring angiogenesis, inflammatory infiltrate, fibrosis, alpha-smooth muscle actin (alpha-SMA) accumulation, differential gene expression by microarrays, and portal pressure.	Sunitinib	23-30	actin gamma 2, smooth muscle	Rattus norvegicus	150-175
17935226-5	2007	The in vivo effects of SU11248 treatment were monitored in the livers of cirrhotic rats by measuring angiogenesis, inflammatory infiltrate, fibrosis, alpha-smooth muscle actin (alpha-SMA) accumulation, differential gene expression by microarrays, and portal pressure.	Sunitinib	23-30	actin gamma 2, smooth muscle	Rattus norvegicus	177-186
17935226-9	2007	SU11248 treatment resulted in a significant decrease in hepatic vascular density, inflammatory infiltrate, alpha-SMA abundance, LX-2 viability, collagen expression, and portal pressure.	Sunitinib	0-7	actin gamma 2, smooth muscle	Rattus norvegicus	107-116
18165617-7	2007	Small-molecule multikinase inhibitors that target VEGF receptors (sunitinib and sorafenib) have a favorable toxicity profile and can prolong time to progression and preserve quality of life when used in newly diagnosed or previously treated patients.	Sunitinib	66-75	vascular endothelial growth factor A	Homo sapiens	50-54
18165647-10	2008	Two (4.8%) of 41 PRCC patients achieved a response (both patients were treated with sunitinib).	Sunitinib	84-93	proline rich mitotic checkpoint control factor	Homo sapiens	17-21
18165647-12	2008	Sunitinib-treated PRCC patients had a PFS of 11.9 months compared with 5.1 months for sorafenib-treated patients (P &lt; .001).	Sunitinib	0-9	proline rich mitotic checkpoint control factor	Homo sapiens	18-22
18165647-13	2008	CONCLUSION: Patients with PRCC and ChRCC may have prolonged PFS from sunitinib and sorafenib, although clinical responses remain overall low in PRCC.	Sunitinib	69-78	proline rich mitotic checkpoint control factor	Homo sapiens	26-30
18272027-1	2007	Sunitinib is a tyrosine kinase inhibitor with activity against vascular endothelial growth factor (VEGF) receptor and platelet-derived growth factor receptor recently approved by the FDA for the treatment of advanced renal cell carcinoma (RCC).	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	99-103
17942672-3	2007	However, here we report that an identical pattern of change is observed in normal nontumor-bearing mice treated with SU11248/sunitinib, a small-molecule inhibitor of VEGF and PDGF RTKs.	Sunitinib	125-134	vascular endothelial growth factor A	Mus musculus	166-170
17622648-9	2007	Sunitinib treatment caused a 74% reduction in microvessel density (p &lt; 0.05), an increase in tumor necrosis, and a decrease in number of GBM cells positive for MIB antibody.	Sunitinib	0-9	MIB E3 ubiquitin protein ligase 1	Homo sapiens	163-166
17889720-0	2007	Sensitivity toward sorafenib and sunitinib varies between different activating and drug-resistant FLT3-ITD mutations.	Sunitinib	33-42	fms related receptor tyrosine kinase 3	Homo sapiens	98-102
17889720-6	2007	Here we tested the efficacy of sunitinib and sorafenib to inhibit primary FLT3 activating mutations (ITD and D835Y) and of secondary resistance mutations.	Sunitinib	31-40	fms related receptor tyrosine kinase 3	Homo sapiens	74-78
17889720-11	2007	Importantly, sensitivity toward sorafenib and sunitinib varies between the different secondary FLT3-ITD resistance mutations.	Sunitinib	46-55	fms related receptor tyrosine kinase 3	Homo sapiens	95-99
17889720-12	2007	CONCLUSIONS: These results establish sensitivity profiles for the FLT3 inhibitors sunitinib and sorafenib.	Sunitinib	82-91	fms related receptor tyrosine kinase 3	Homo sapiens	66-70
17761721-1	2007	Sunitinib malate is an oral, multitargeted tyrosine kinase inhibitor that targets both angiogenic pathways (i.e., vascular endothelial growth factor receptor and platelet-derived growth factor receptor) and direct pro-oncogenic pathways (e.g., stem-cell factor receptor and FMS-like tyrosine kinase-3).	Sunitinib	0-16	fms related receptor tyrosine kinase 3	Homo sapiens	274-300
17701051-11	2007	Very recently, it has been shown that sunitinib may be especially effective in GISTs with KIT exon 9 mutation, whereas these tumors show only an intermediate response to imatinib.	Sunitinib	38-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-93
17671153-2	2007	Most clinical trial data generated to date have been with either bevacizumab, a monoclonal antibody to VEGF, or small-molecule inhibitors of VEGF receptor (VEGFR) tyrosine kinase activity (sunitinib, sorafenib, and ZD6474).	Sunitinib	189-198	kinase insert domain receptor	Homo sapiens	156-161
17704140-1	2007	Two recent clinical trials have shown that the placenta growth factor (PlGF) is up-regulated after bevacizumab treatment in colorectal cancer and after SU11248 treatment in metastatic renal cell carcinoma.	Sunitinib	152-159	placental growth factor	Homo sapiens	47-69
17704140-1	2007	Two recent clinical trials have shown that the placenta growth factor (PlGF) is up-regulated after bevacizumab treatment in colorectal cancer and after SU11248 treatment in metastatic renal cell carcinoma.	Sunitinib	152-159	placental growth factor	Homo sapiens	71-75
17136543-2	2007	Sunitinib (sunitinib malate; SU11248; SUTENT; Pfizer Inc, New York, NY, USA) is a novel, orally bio-available, oxindole, multi-targeted tyrosine kinase inhibitor with high binding affinity for VEGFR and PDGFR which has shown anti-tumor and anti-angiogenic activities.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	193-198
17136543-2	2007	Sunitinib (sunitinib malate; SU11248; SUTENT; Pfizer Inc, New York, NY, USA) is a novel, orally bio-available, oxindole, multi-targeted tyrosine kinase inhibitor with high binding affinity for VEGFR and PDGFR which has shown anti-tumor and anti-angiogenic activities.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	203-208
17136543-2	2007	Sunitinib (sunitinib malate; SU11248; SUTENT; Pfizer Inc, New York, NY, USA) is a novel, orally bio-available, oxindole, multi-targeted tyrosine kinase inhibitor with high binding affinity for VEGFR and PDGFR which has shown anti-tumor and anti-angiogenic activities.	Sunitinib	11-27	kinase insert domain receptor	Homo sapiens	193-198
17136543-2	2007	Sunitinib (sunitinib malate; SU11248; SUTENT; Pfizer Inc, New York, NY, USA) is a novel, orally bio-available, oxindole, multi-targeted tyrosine kinase inhibitor with high binding affinity for VEGFR and PDGFR which has shown anti-tumor and anti-angiogenic activities.	Sunitinib	11-27	platelet derived growth factor receptor beta	Homo sapiens	203-208
17935273-7	2007	Sorafenib and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor.	Sunitinib	14-23	kinase insert domain receptor	Homo sapiens	86-140
17935273-7	2007	Sorafenib and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor.	Sunitinib	14-23	kinase insert domain receptor	Homo sapiens	142-149
17935273-7	2007	Sorafenib and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor.	Sunitinib	14-23	fms related receptor tyrosine kinase 4	Homo sapiens	151-158
17935273-7	2007	Sorafenib and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor.	Sunitinib	14-23	platelet derived growth factor receptor beta	Homo sapiens	164-208
17935273-7	2007	Sorafenib and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor.	Sunitinib	14-23	platelet derived growth factor receptor beta	Homo sapiens	210-220
17935273-7	2007	Sorafenib and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor.	Sunitinib	14-23	mechanistic target of rapamycin kinase	Homo sapiens	248-252
17605814-0	2007	Circulating protein biomarkers of pharmacodynamic activity of sunitinib in patients with metastatic renal cell carcinoma: modulation of VEGF and VEGF-related proteins.	Sunitinib	62-71	vascular endothelial growth factor A	Homo sapiens	136-140
17710208-1	2007	Sunitinib (SU11248) is an orally bioavailable inhibitor that affects the receptor tyrosine kinases involved in tumour proliferation and angiogenesis, including vascular endothelial growth factor (VEGF) receptors 1, 2, 3, and platelet-derived growth factor receptors alpha (PDGFRA) and beta (PDGFRB).	Sunitinib	0-9	fms related receptor tyrosine kinase 1	Homo sapiens	160-219
17710208-1	2007	Sunitinib (SU11248) is an orally bioavailable inhibitor that affects the receptor tyrosine kinases involved in tumour proliferation and angiogenesis, including vascular endothelial growth factor (VEGF) receptors 1, 2, 3, and platelet-derived growth factor receptors alpha (PDGFRA) and beta (PDGFRB).	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	273-279
17710208-1	2007	Sunitinib (SU11248) is an orally bioavailable inhibitor that affects the receptor tyrosine kinases involved in tumour proliferation and angiogenesis, including vascular endothelial growth factor (VEGF) receptors 1, 2, 3, and platelet-derived growth factor receptors alpha (PDGFRA) and beta (PDGFRB).	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	291-297
17710208-1	2007	Sunitinib (SU11248) is an orally bioavailable inhibitor that affects the receptor tyrosine kinases involved in tumour proliferation and angiogenesis, including vascular endothelial growth factor (VEGF) receptors 1, 2, 3, and platelet-derived growth factor receptors alpha (PDGFRA) and beta (PDGFRB).	Sunitinib	11-18	fms related receptor tyrosine kinase 1	Homo sapiens	160-219
17710208-1	2007	Sunitinib (SU11248) is an orally bioavailable inhibitor that affects the receptor tyrosine kinases involved in tumour proliferation and angiogenesis, including vascular endothelial growth factor (VEGF) receptors 1, 2, 3, and platelet-derived growth factor receptors alpha (PDGFRA) and beta (PDGFRB).	Sunitinib	11-18	platelet derived growth factor receptor alpha	Homo sapiens	273-279
17710208-1	2007	Sunitinib (SU11248) is an orally bioavailable inhibitor that affects the receptor tyrosine kinases involved in tumour proliferation and angiogenesis, including vascular endothelial growth factor (VEGF) receptors 1, 2, 3, and platelet-derived growth factor receptors alpha (PDGFRA) and beta (PDGFRB).	Sunitinib	11-18	platelet derived growth factor receptor beta	Homo sapiens	291-297
17710208-2	2007	Because angiogenesis is necessary for the growth and metastasis of solid tumours, and VEGF is believed to have a pivotal role in that process, SUNITINIB treatment may have broad-spectrum clinical utility.	Sunitinib	143-152	vascular endothelial growth factor A	Homo sapiens	86-90
17687201-4	2007	Meanwhile, sunitinib malate,which inhibits three VEGF-Rs and FLT 3 in addition to KIT as well as PDGF-R, was clinically evaluated in the phase II clinical trials for imatinib-resistant or intolerant GIST, and advanced renal cell carcinoma in Japan.	Sunitinib	11-27	fms related receptor tyrosine kinase 3	Homo sapiens	61-66
17687201-4	2007	Meanwhile, sunitinib malate,which inhibits three VEGF-Rs and FLT 3 in addition to KIT as well as PDGF-R, was clinically evaluated in the phase II clinical trials for imatinib-resistant or intolerant GIST, and advanced renal cell carcinoma in Japan.	Sunitinib	11-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-85
17657252-5	2007	Sunitinib, sorafenib and axitinib are kinase inhibitors that inhibit the VEGF, platelet-derived growth factor and c-kit receptor tyrosine kinases.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	73-77
17655513-6	2007	Sorafenib and sunitinib are novel therapies that target growth factor receptors known to be activated by the hypoxia-inducible factor and the Ras-Raf/MEK/ERK pathways.	Sunitinib	14-23	zinc fingers and homeoboxes 2	Homo sapiens	146-149
17655513-6	2007	Sorafenib and sunitinib are novel therapies that target growth factor receptors known to be activated by the hypoxia-inducible factor and the Ras-Raf/MEK/ERK pathways.	Sunitinib	14-23	mitogen-activated protein kinase kinase 7	Homo sapiens	150-153
17655513-6	2007	Sorafenib and sunitinib are novel therapies that target growth factor receptors known to be activated by the hypoxia-inducible factor and the Ras-Raf/MEK/ERK pathways.	Sunitinib	14-23	mitogen-activated protein kinase 1	Homo sapiens	154-157
17605814-0	2007	Circulating protein biomarkers of pharmacodynamic activity of sunitinib in patients with metastatic renal cell carcinoma: modulation of VEGF and VEGF-related proteins.	Sunitinib	62-71	vascular endothelial growth factor A	Homo sapiens	145-149
17605814-9	2007	CONCLUSION: Sunitinib treatment in advanced RCC patients leads to modulation of plasma levels of circulating proteins involved in VEGF signaling, including soluble forms of two VEGF receptors.	Sunitinib	12-21	vascular endothelial growth factor A	Homo sapiens	130-134
17605814-9	2007	CONCLUSION: Sunitinib treatment in advanced RCC patients leads to modulation of plasma levels of circulating proteins involved in VEGF signaling, including soluble forms of two VEGF receptors.	Sunitinib	12-21	vascular endothelial growth factor A	Homo sapiens	177-181
17588358-2	2007	Sunitinib is a tyrosine kinase inhibitor with a wide range of kinase inhibition, including KIT, platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor (VEGF), and FLT3.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	91-94
17588358-2	2007	Sunitinib is a tyrosine kinase inhibitor with a wide range of kinase inhibition, including KIT, platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor (VEGF), and FLT3.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	96-135
17825686-8	2007	Sunitinib is metabolized by cytochrome P450 (CYP) 3A4 to an active metabolite, SU12662, which is further metabolized by CYP3A4 to an inactive moiety.	Sunitinib	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	120-126
17588358-2	2007	Sunitinib is a tyrosine kinase inhibitor with a wide range of kinase inhibition, including KIT, platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor (VEGF), and FLT3.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	137-142
17588358-2	2007	Sunitinib is a tyrosine kinase inhibitor with a wide range of kinase inhibition, including KIT, platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor (VEGF), and FLT3.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	145-179
17588358-2	2007	Sunitinib is a tyrosine kinase inhibitor with a wide range of kinase inhibition, including KIT, platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor (VEGF), and FLT3.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	181-185
17588358-2	2007	Sunitinib is a tyrosine kinase inhibitor with a wide range of kinase inhibition, including KIT, platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor (VEGF), and FLT3.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	192-196
17552016-0	2007	Effect of sunitinib on metastatic gastrointestinal stromal tumor in patients with neurofibromatosis type 1: a case report.	Sunitinib	10-19	neurofibromin 1	Homo sapiens	82-106
17545799-8	2007	Patients with gastrointestinal stromal tumor with KIT exon 9 mutation may benefit more from sunitinib than those with exon 11 mutation.	Sunitinib	92-101	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-53
17591808-8	2007	More recently Sunitinib, a new KIT/PDGFRA kinase inhibitor, has been tested in patients with GIST resistant to imatinib, with promising results.	Sunitinib	14-23	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	31-34
17591808-8	2007	More recently Sunitinib, a new KIT/PDGFRA kinase inhibitor, has been tested in patients with GIST resistant to imatinib, with promising results.	Sunitinib	14-23	platelet derived growth factor receptor alpha	Homo sapiens	35-41
17591828-6	2007	Sunitinib targets selectively vascular endothelial growth factor, KIT, Flt3 and platelet-derived growth factor receptors and the receptor encoded by the ret proto-oncogene.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	66-69
17591828-6	2007	Sunitinib targets selectively vascular endothelial growth factor, KIT, Flt3 and platelet-derived growth factor receptors and the receptor encoded by the ret proto-oncogene.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	71-75
17552016-14	2007	The metastatic lesions in the liver and omentum were decreased in size after four courses, suggesting that sunitinib is also an effective treatment modality for metastatic GIST in NF patients.	Sunitinib	107-116	neurofascin	Homo sapiens	180-182
17355219-3	2007	One of the most clear examples is the identification of KIT and platelet-derived growth factor receptor-alpha kinase mutations in gastrointestinal stromal tumours, a subset of sarcomas arising from precursors of the interstitial cells of Cajal in the digestive tract, which led to the development of imatinib, sunitinib and other tyrosine kinase inhibitors for the treatment of solid tumours.	Sunitinib	310-319	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	56-59
17392388-3	2007	Several anti-VEGF agents, including ligand-binding agents such as bevacizumab and the small molecule inhibitors of VEGF and related receptors such as sunitinib and sorafenib, have demonstrated clinical activity in patients with metastatic RCC.	Sunitinib	150-159	vascular endothelial growth factor A	Homo sapiens	13-17
17392388-3	2007	Several anti-VEGF agents, including ligand-binding agents such as bevacizumab and the small molecule inhibitors of VEGF and related receptors such as sunitinib and sorafenib, have demonstrated clinical activity in patients with metastatic RCC.	Sunitinib	150-159	vascular endothelial growth factor A	Homo sapiens	115-119
17272980-6	2007	Sunitinib is a vascular endothelial growth factor receptor 1, 2, and 3, c-KIT, and platelet-derived growth factor receptor alpha and beta tyrosine kinase inhibitor.	Sunitinib	0-9	fms related receptor tyrosine kinase 1	Homo sapiens	15-70
17272980-6	2007	Sunitinib is a vascular endothelial growth factor receptor 1, 2, and 3, c-KIT, and platelet-derived growth factor receptor alpha and beta tyrosine kinase inhibitor.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-77
17272980-6	2007	Sunitinib is a vascular endothelial growth factor receptor 1, 2, and 3, c-KIT, and platelet-derived growth factor receptor alpha and beta tyrosine kinase inhibitor.	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	83-128
17367763-0	2007	Sunitinib: a VEGF and PDGF receptor protein kinase and angiogenesis inhibitor.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	13-17
17367763-1	2007	Sunitinib (SU-11248, Sutent) inhibits at least eight receptor protein-tyrosine kinases including vascular endothelial growth factor receptors 1-3 (VEGFR1-VEGFR3), platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta), stem cell factor receptor (Kit), Flt-3, and colony-stimulating factor-1 receptor (CSF-1R).	Sunitinib	0-9	fms related receptor tyrosine kinase 1	Homo sapiens	97-145
17367763-1	2007	Sunitinib (SU-11248, Sutent) inhibits at least eight receptor protein-tyrosine kinases including vascular endothelial growth factor receptors 1-3 (VEGFR1-VEGFR3), platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta), stem cell factor receptor (Kit), Flt-3, and colony-stimulating factor-1 receptor (CSF-1R).	Sunitinib	0-9	fms related receptor tyrosine kinase 1	Homo sapiens	147-153
17367763-1	2007	Sunitinib (SU-11248, Sutent) inhibits at least eight receptor protein-tyrosine kinases including vascular endothelial growth factor receptors 1-3 (VEGFR1-VEGFR3), platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta), stem cell factor receptor (Kit), Flt-3, and colony-stimulating factor-1 receptor (CSF-1R).	Sunitinib	0-9	fms related receptor tyrosine kinase 4	Homo sapiens	154-160
17367763-1	2007	Sunitinib (SU-11248, Sutent) inhibits at least eight receptor protein-tyrosine kinases including vascular endothelial growth factor receptors 1-3 (VEGFR1-VEGFR3), platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta), stem cell factor receptor (Kit), Flt-3, and colony-stimulating factor-1 receptor (CSF-1R).	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	205-215
17367763-1	2007	Sunitinib (SU-11248, Sutent) inhibits at least eight receptor protein-tyrosine kinases including vascular endothelial growth factor receptors 1-3 (VEGFR1-VEGFR3), platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta), stem cell factor receptor (Kit), Flt-3, and colony-stimulating factor-1 receptor (CSF-1R).	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	220-229
17367763-1	2007	Sunitinib (SU-11248, Sutent) inhibits at least eight receptor protein-tyrosine kinases including vascular endothelial growth factor receptors 1-3 (VEGFR1-VEGFR3), platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta), stem cell factor receptor (Kit), Flt-3, and colony-stimulating factor-1 receptor (CSF-1R).	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	259-262
17367763-1	2007	Sunitinib (SU-11248, Sutent) inhibits at least eight receptor protein-tyrosine kinases including vascular endothelial growth factor receptors 1-3 (VEGFR1-VEGFR3), platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta), stem cell factor receptor (Kit), Flt-3, and colony-stimulating factor-1 receptor (CSF-1R).	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	265-270
17367763-1	2007	Sunitinib (SU-11248, Sutent) inhibits at least eight receptor protein-tyrosine kinases including vascular endothelial growth factor receptors 1-3 (VEGFR1-VEGFR3), platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta), stem cell factor receptor (Kit), Flt-3, and colony-stimulating factor-1 receptor (CSF-1R).	Sunitinib	0-9	colony stimulating factor 1 receptor	Homo sapiens	276-312
17367763-1	2007	Sunitinib (SU-11248, Sutent) inhibits at least eight receptor protein-tyrosine kinases including vascular endothelial growth factor receptors 1-3 (VEGFR1-VEGFR3), platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta), stem cell factor receptor (Kit), Flt-3, and colony-stimulating factor-1 receptor (CSF-1R).	Sunitinib	0-9	colony stimulating factor 1 receptor	Homo sapiens	314-321
17367763-1	2007	Sunitinib (SU-11248, Sutent) inhibits at least eight receptor protein-tyrosine kinases including vascular endothelial growth factor receptors 1-3 (VEGFR1-VEGFR3), platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta), stem cell factor receptor (Kit), Flt-3, and colony-stimulating factor-1 receptor (CSF-1R).	Sunitinib	11-19	fms related receptor tyrosine kinase 1	Homo sapiens	97-145
17367763-1	2007	Sunitinib (SU-11248, Sutent) inhibits at least eight receptor protein-tyrosine kinases including vascular endothelial growth factor receptors 1-3 (VEGFR1-VEGFR3), platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta), stem cell factor receptor (Kit), Flt-3, and colony-stimulating factor-1 receptor (CSF-1R).	Sunitinib	11-19	fms related receptor tyrosine kinase 1	Homo sapiens	147-153
17367763-1	2007	Sunitinib (SU-11248, Sutent) inhibits at least eight receptor protein-tyrosine kinases including vascular endothelial growth factor receptors 1-3 (VEGFR1-VEGFR3), platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta), stem cell factor receptor (Kit), Flt-3, and colony-stimulating factor-1 receptor (CSF-1R).	Sunitinib	21-27	fms related receptor tyrosine kinase 1	Homo sapiens	97-145
17367763-1	2007	Sunitinib (SU-11248, Sutent) inhibits at least eight receptor protein-tyrosine kinases including vascular endothelial growth factor receptors 1-3 (VEGFR1-VEGFR3), platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta), stem cell factor receptor (Kit), Flt-3, and colony-stimulating factor-1 receptor (CSF-1R).	Sunitinib	21-27	fms related receptor tyrosine kinase 1	Homo sapiens	147-153
17367763-1	2007	Sunitinib (SU-11248, Sutent) inhibits at least eight receptor protein-tyrosine kinases including vascular endothelial growth factor receptors 1-3 (VEGFR1-VEGFR3), platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta), stem cell factor receptor (Kit), Flt-3, and colony-stimulating factor-1 receptor (CSF-1R).	Sunitinib	21-27	fms related receptor tyrosine kinase 4	Homo sapiens	154-160
17367763-4	2007	Sunitinib inhibits angiogenesis by diminishing signaling through VEGFR1, VEGFR2, and PDGFRbeta.	Sunitinib	0-9	fms related receptor tyrosine kinase 1	Homo sapiens	65-71
17367763-4	2007	Sunitinib inhibits angiogenesis by diminishing signaling through VEGFR1, VEGFR2, and PDGFRbeta.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	73-79
17367763-4	2007	Sunitinib inhibits angiogenesis by diminishing signaling through VEGFR1, VEGFR2, and PDGFRbeta.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	85-94
17367763-7	2007	Sunitinib is approved for the treatment of those tumors that are resistant to imatinib (STI-571, Gleevec), another Kit and PDGFRalpha protein-tyrosine kinase inhibitor.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-118
17367763-7	2007	Sunitinib is approved for the treatment of those tumors that are resistant to imatinib (STI-571, Gleevec), another Kit and PDGFRalpha protein-tyrosine kinase inhibitor.	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	123-133
17573273-2	2007	This article will review the pathology of GISTs, the molecular pathology related to c-kit, and disease management and will discuss a new drug approved in the management of GISTs, sunitinib malate.	Sunitinib	179-195	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-89
17619763-3	2007	Sutent and sorafenib are orally available inhibitors of the VEGFR and platelet derived growth factor receptor (PDGFR).	Sunitinib	0-6	kinase insert domain receptor	Homo sapiens	60-65
17619763-3	2007	Sutent and sorafenib are orally available inhibitors of the VEGFR and platelet derived growth factor receptor (PDGFR).	Sunitinib	0-6	platelet derived growth factor receptor beta	Homo sapiens	70-109
17619763-3	2007	Sutent and sorafenib are orally available inhibitors of the VEGFR and platelet derived growth factor receptor (PDGFR).	Sunitinib	0-6	platelet derived growth factor receptor beta	Homo sapiens	111-116
17355219-3	2007	One of the most clear examples is the identification of KIT and platelet-derived growth factor receptor-alpha kinase mutations in gastrointestinal stromal tumours, a subset of sarcomas arising from precursors of the interstitial cells of Cajal in the digestive tract, which led to the development of imatinib, sunitinib and other tyrosine kinase inhibitors for the treatment of solid tumours.	Sunitinib	310-319	platelet derived growth factor receptor alpha	Homo sapiens	64-109
17327610-2	2007	Tyrosine kinase inhibitors such as SU6668 and SU5416 (semaxanib) demonstrated poor pharmacologic properties and limited efficacy; therefore, sunitinib was rationally designed and chosen for its high bioavailability and its nanomolar-range potency against the antiangiogenic receptor tyrosine kinases (RTKs)--vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR).	Sunitinib	141-150	kinase insert domain receptor	Homo sapiens	353-358
17327610-2	2007	Tyrosine kinase inhibitors such as SU6668 and SU5416 (semaxanib) demonstrated poor pharmacologic properties and limited efficacy; therefore, sunitinib was rationally designed and chosen for its high bioavailability and its nanomolar-range potency against the antiangiogenic receptor tyrosine kinases (RTKs)--vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR).	Sunitinib	141-150	platelet derived growth factor receptor beta	Homo sapiens	364-403
17327610-2	2007	Tyrosine kinase inhibitors such as SU6668 and SU5416 (semaxanib) demonstrated poor pharmacologic properties and limited efficacy; therefore, sunitinib was rationally designed and chosen for its high bioavailability and its nanomolar-range potency against the antiangiogenic receptor tyrosine kinases (RTKs)--vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR).	Sunitinib	141-150	platelet derived growth factor receptor beta	Homo sapiens	405-410
17327610-3	2007	Sunitinib inhibits other tyrosine kinases including, KIT, FLT3, colony-stimulating factor 1 (CSF-1), and RET, which are involved in a number of malignancies including small-cell lung cancer, GI stromal tumors (GISTs), breast cancer, acute myelogenous leukemia, multiple endocrine neoplasia types 2A and 2B, and familial medullary thyroid carcinoma.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-56
17327610-3	2007	Sunitinib inhibits other tyrosine kinases including, KIT, FLT3, colony-stimulating factor 1 (CSF-1), and RET, which are involved in a number of malignancies including small-cell lung cancer, GI stromal tumors (GISTs), breast cancer, acute myelogenous leukemia, multiple endocrine neoplasia types 2A and 2B, and familial medullary thyroid carcinoma.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	58-62
17327610-3	2007	Sunitinib inhibits other tyrosine kinases including, KIT, FLT3, colony-stimulating factor 1 (CSF-1), and RET, which are involved in a number of malignancies including small-cell lung cancer, GI stromal tumors (GISTs), breast cancer, acute myelogenous leukemia, multiple endocrine neoplasia types 2A and 2B, and familial medullary thyroid carcinoma.	Sunitinib	0-9	colony stimulating factor 1	Homo sapiens	64-91
17327610-3	2007	Sunitinib inhibits other tyrosine kinases including, KIT, FLT3, colony-stimulating factor 1 (CSF-1), and RET, which are involved in a number of malignancies including small-cell lung cancer, GI stromal tumors (GISTs), breast cancer, acute myelogenous leukemia, multiple endocrine neoplasia types 2A and 2B, and familial medullary thyroid carcinoma.	Sunitinib	0-9	colony stimulating factor 1	Homo sapiens	93-98
17327610-3	2007	Sunitinib inhibits other tyrosine kinases including, KIT, FLT3, colony-stimulating factor 1 (CSF-1), and RET, which are involved in a number of malignancies including small-cell lung cancer, GI stromal tumors (GISTs), breast cancer, acute myelogenous leukemia, multiple endocrine neoplasia types 2A and 2B, and familial medullary thyroid carcinoma.	Sunitinib	0-9	ret proto-oncogene	Homo sapiens	105-108
17327610-4	2007	Sunitinib demonstrated robust antitumor activity in preclinical studies resulting not only in tumor growth inhibition, but tumor regression in models of colon cancer, non-small-cell lung cancer, melanoma, renal carcinoma, and squamous cell carcinoma, which were associated with inhibition of VEGFR and PDGFR phosphorylation.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	292-297
17327610-4	2007	Sunitinib demonstrated robust antitumor activity in preclinical studies resulting not only in tumor growth inhibition, but tumor regression in models of colon cancer, non-small-cell lung cancer, melanoma, renal carcinoma, and squamous cell carcinoma, which were associated with inhibition of VEGFR and PDGFR phosphorylation.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	302-307
17208434-2	2007	These rare neoplasms are remarkably sensitive to the KIT and PDGFRA kinase inhibitors imatinib (also known as Gleevec) and sunitinib (Sutent), which have recently been approved as the standard therapeutic courses for patients with inoperable GIST.	Sunitinib	134-140	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-56
17621562-6	2007	A recent Phase III study evaluating sunitinib as first-line therapy showed a significant difference when compared to interferonalfa (IFN-alpha) for a progression-free survival of 11 months in the sunitinib arm and 5 months in the IFN-alpha arm (hazard ratio 0.42; 95% CI 0.32-0.54; P50.001).	Sunitinib	36-45	interferon alpha 1	Homo sapiens	230-239
17317817-3	2007	Three agents targeting the VEGF pathway have shown clinical activity as monotherapy in metastatic renal cell carcinoma: the anti-VEGF monoclonal antibody, bevacizumab, and small-molecule VEGF receptor tyrosine kinase inhibitors, sorafenib and sunitinib.	Sunitinib	243-252	vascular endothelial growth factor A	Homo sapiens	27-31
17208434-2	2007	These rare neoplasms are remarkably sensitive to the KIT and PDGFRA kinase inhibitors imatinib (also known as Gleevec) and sunitinib (Sutent), which have recently been approved as the standard therapeutic courses for patients with inoperable GIST.	Sunitinib	134-140	platelet derived growth factor receptor alpha	Homo sapiens	61-67
17208434-4	2007	Imatinib and sunitinib resistance generally result from secondary mutations in the KIT and/or PDGFRA kinase domains.	Sunitinib	13-22	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	83-86
17208434-4	2007	Imatinib and sunitinib resistance generally result from secondary mutations in the KIT and/or PDGFRA kinase domains.	Sunitinib	13-22	platelet derived growth factor receptor alpha	Homo sapiens	94-100
17202116-1	2007	Sunitinib is an inhibitor of the vascular endothelial growth factor and platelet-derived growth factor receptors, and it has antitumor activity in metastatic renal cell carcinoma and gastrointestinal stromal tumors.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	33-67
17296815-7	2007	Sunitinib is a multitargeted inhibitor of PDGFR, KIT, fms-like tyrosine kinase 3, and VEGFR.	Sunitinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	42-47
17296815-7	2007	Sunitinib is a multitargeted inhibitor of PDGFR, KIT, fms-like tyrosine kinase 3, and VEGFR.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
17296815-7	2007	Sunitinib is a multitargeted inhibitor of PDGFR, KIT, fms-like tyrosine kinase 3, and VEGFR.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	54-80
17296815-7	2007	Sunitinib is a multitargeted inhibitor of PDGFR, KIT, fms-like tyrosine kinase 3, and VEGFR.	Sunitinib	0-9	kinase insert domain receptor	Homo sapiens	86-91
17255305-5	2007	In contrast, two multitargeted receptor tyrosine kinase inhibitors that target both VEGF and PDGF receptors (sunitinib and AG013736) have shown &gt; or =40% objective responses with clinically important duration.	Sunitinib	109-118	vascular endothelial growth factor A	Homo sapiens	84-88
17189392-4	2006	We review here the biology of RCC and how a combination of proximal and distal block of VHL/hypoxia-inducible factor alpha pathway by novel targeted agents, including sunitinib, sorafenib, bevacizumab, everolimus, and temsirolimus, has led to significant improvements in progression-free survival.	Sunitinib	167-176	von Hippel-Lindau tumor suppressor	Homo sapiens	88-91
17607922-8	2007	Sunitinib, another tyrosine kinase inhibitor, seems to be useful especially in patients with exon 9 mutations of c-kit, who usually have a worse response to imatinib.	Sunitinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	113-118
16995874-5	2006	Interestingly, when ZD6474 was combined with sunitinib (SU11248; Sutent, Pfizer, Kalamazoo, MI, USA), a class III and V receptor tyrosine kinase inhibitor, the ZD6474-mediated growth inhibition was potentiated in association with further down-regulation of the mTOR targets p-p70S6K and p-4E-BP-1.	Sunitinib	45-54	mechanistic target of rapamycin kinase	Homo sapiens	261-265
16995874-5	2006	Interestingly, when ZD6474 was combined with sunitinib (SU11248; Sutent, Pfizer, Kalamazoo, MI, USA), a class III and V receptor tyrosine kinase inhibitor, the ZD6474-mediated growth inhibition was potentiated in association with further down-regulation of the mTOR targets p-p70S6K and p-4E-BP-1.	Sunitinib	45-54	ribosomal protein S6 kinase B1	Homo sapiens	276-282
16860997-3	2006	Sunitinib, sorafenib and axitinib are new agents which belong to a class of drugs called kinase inhibitors and inhibit the VEGF, platelet-derived growth factor (PDGF) and c-KIT receptor tyrosine kinases.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	123-127
16990784-0	2006	FLT3 K663Q is a novel AML-associated oncogenic kinase: Determination of biochemical properties and sensitivity to Sunitinib (SU11248).	Sunitinib	114-123	FMS-like tyrosine kinase 3	Mus musculus	0-4
17064223-6	2006	So far, three anti-VEGF inhibitors, bevacizumab, sunitinib and sorafenib, have been approved for the treatment of solid human malignancies including colorectal cancer, gastrointestinal stromal tumours and renal cell carcinoma.	Sunitinib	49-58	vascular endothelial growth factor A	Homo sapiens	19-23
16990784-0	2006	FLT3 K663Q is a novel AML-associated oncogenic kinase: Determination of biochemical properties and sensitivity to Sunitinib (SU11248).	Sunitinib	125-132	FMS-like tyrosine kinase 3	Mus musculus	0-4
16990784-8	2006	Of note, this mutation was potently inhibited by Sunitinib (SU11248), a previously described FLT3 kinase inhibitor.	Sunitinib	49-58	FMS-like tyrosine kinase 3	Mus musculus	93-97
16990784-8	2006	Of note, this mutation was potently inhibited by Sunitinib (SU11248), a previously described FLT3 kinase inhibitor.	Sunitinib	60-67	FMS-like tyrosine kinase 3	Mus musculus	93-97
16990784-9	2006	Sunitinib reduced the proliferation and induced apoptosis of transformed Ba/F3 cells expressing FLT3 K663Q.	Sunitinib	0-9	FMS-like tyrosine kinase 3	Mus musculus	96-100
16990784-10	2006	The potency of Sunitinib against FLT3 K663Q was similar to its potency against FLT3 ITD mutations.	Sunitinib	15-24	FMS-like tyrosine kinase 3	Mus musculus	33-37
17041096-2	2006	Thymidine uptake studies showed that sunitinib was active against EOL-1, MV4-11, and Kasumi-1 cells, which possessed activating mutations of the PDGFRalpha, FLT-3, and c-KIT genes, respectively, with IC(50)s of &lt;30 nmol/L.	Sunitinib	37-46	platelet derived growth factor receptor alpha	Homo sapiens	145-155
16849418-0	2006	An orally administered multitarget tyrosine kinase inhibitor, SU11248, is a novel potent inhibitor of thyroid oncogenic RET/papillary thyroid cancer kinases.	Sunitinib	62-69	ret proto-oncogene	Homo sapiens	120-123
16849418-3	2006	OBJECTIVE: The objective of the study was to evaluate the efficacies of the recently developed kinase inhibitors SU11248, SU5416, and SU6668 in inhibition of RET/PTC.	Sunitinib	113-120	ret proto-oncogene	Homo sapiens	158-161
16849418-3	2006	OBJECTIVE: The objective of the study was to evaluate the efficacies of the recently developed kinase inhibitors SU11248, SU5416, and SU6668 in inhibition of RET/PTC.	Sunitinib	113-120	ret proto-oncogene	Homo sapiens	162-165
16849418-4	2006	DESIGN: SU11248, SU5416, and SU6668 were synthesized, and their inhibitory potencies were evaluated using an in vitro RET/PTC kinase assay.	Sunitinib	8-15	ret proto-oncogene	Homo sapiens	122-125
16849418-6	2006	RESULTS: An in vitro kinase assay revealed that SU5416, SU6668, and SU11248 inhibited phosphorylation of the synthetic tyrosine kinase substrate peptide E4Y by RET/PTC3 in a dose-dependent manner with IC(50) of approximately 944 nm for SU5416, 562 nm for SU6668, and 224 nm for SU11248.	Sunitinib	68-75	ret proto-oncogene	Homo sapiens	160-163
16849418-6	2006	RESULTS: An in vitro kinase assay revealed that SU5416, SU6668, and SU11248 inhibited phosphorylation of the synthetic tyrosine kinase substrate peptide E4Y by RET/PTC3 in a dose-dependent manner with IC(50) of approximately 944 nm for SU5416, 562 nm for SU6668, and 224 nm for SU11248.	Sunitinib	68-75	nuclear receptor coactivator 4	Homo sapiens	164-168
16849418-6	2006	RESULTS: An in vitro kinase assay revealed that SU5416, SU6668, and SU11248 inhibited phosphorylation of the synthetic tyrosine kinase substrate peptide E4Y by RET/PTC3 in a dose-dependent manner with IC(50) of approximately 944 nm for SU5416, 562 nm for SU6668, and 224 nm for SU11248.	Sunitinib	278-285	ret proto-oncogene	Homo sapiens	160-163
16849418-7	2006	Thus, SU11248 effectively inhibits the kinase activity of RET/PTC3.	Sunitinib	6-13	ret proto-oncogene	Homo sapiens	58-61
16849418-7	2006	Thus, SU11248 effectively inhibits the kinase activity of RET/PTC3.	Sunitinib	6-13	nuclear receptor coactivator 4	Homo sapiens	62-66
16849418-8	2006	RET/PTC-mediated Y705 phosphorylation of STAT3 was inhibited by addition of SU11248, and the inhibitory effects of SU11248 on the tyrosine phosphorylation and transcriptional activation of STAT3 were very closely correlated with decreased autophosphorylation of RET/PTC.	Sunitinib	76-83	ret proto-oncogene	Homo sapiens	0-3
16849418-8	2006	RET/PTC-mediated Y705 phosphorylation of STAT3 was inhibited by addition of SU11248, and the inhibitory effects of SU11248 on the tyrosine phosphorylation and transcriptional activation of STAT3 were very closely correlated with decreased autophosphorylation of RET/PTC.	Sunitinib	76-83	ret proto-oncogene	Homo sapiens	4-7
16849418-8	2006	RET/PTC-mediated Y705 phosphorylation of STAT3 was inhibited by addition of SU11248, and the inhibitory effects of SU11248 on the tyrosine phosphorylation and transcriptional activation of STAT3 were very closely correlated with decreased autophosphorylation of RET/PTC.	Sunitinib	76-83	signal transducer and activator of transcription 3	Homo sapiens	41-46
16849418-8	2006	RET/PTC-mediated Y705 phosphorylation of STAT3 was inhibited by addition of SU11248, and the inhibitory effects of SU11248 on the tyrosine phosphorylation and transcriptional activation of STAT3 were very closely correlated with decreased autophosphorylation of RET/PTC.	Sunitinib	115-122	ret proto-oncogene	Homo sapiens	0-3
16849418-8	2006	RET/PTC-mediated Y705 phosphorylation of STAT3 was inhibited by addition of SU11248, and the inhibitory effects of SU11248 on the tyrosine phosphorylation and transcriptional activation of STAT3 were very closely correlated with decreased autophosphorylation of RET/PTC.	Sunitinib	115-122	ret proto-oncogene	Homo sapiens	4-7
16849418-8	2006	RET/PTC-mediated Y705 phosphorylation of STAT3 was inhibited by addition of SU11248, and the inhibitory effects of SU11248 on the tyrosine phosphorylation and transcriptional activation of STAT3 were very closely correlated with decreased autophosphorylation of RET/PTC.	Sunitinib	115-122	signal transducer and activator of transcription 3	Homo sapiens	189-194
16849418-8	2006	RET/PTC-mediated Y705 phosphorylation of STAT3 was inhibited by addition of SU11248, and the inhibitory effects of SU11248 on the tyrosine phosphorylation and transcriptional activation of STAT3 were very closely correlated with decreased autophosphorylation of RET/PTC.	Sunitinib	115-122	ret proto-oncogene	Homo sapiens	262-265
16849418-8	2006	RET/PTC-mediated Y705 phosphorylation of STAT3 was inhibited by addition of SU11248, and the inhibitory effects of SU11248 on the tyrosine phosphorylation and transcriptional activation of STAT3 were very closely correlated with decreased autophosphorylation of RET/PTC.	Sunitinib	115-122	ret proto-oncogene	Homo sapiens	266-269
16849418-9	2006	SU11248 caused a complete morphological reversion of transformed NIH-RET/PTC3 cells and inhibited the growth of TPC-1 cells that have an endogenous RET/PTC1.	Sunitinib	0-7	ret proto-oncogene	Homo sapiens	69-72
16849418-9	2006	SU11248 caused a complete morphological reversion of transformed NIH-RET/PTC3 cells and inhibited the growth of TPC-1 cells that have an endogenous RET/PTC1.	Sunitinib	0-7	nuclear receptor coactivator 4	Homo sapiens	73-77
16849418-9	2006	SU11248 caused a complete morphological reversion of transformed NIH-RET/PTC3 cells and inhibited the growth of TPC-1 cells that have an endogenous RET/PTC1.	Sunitinib	0-7	ret proto-oncogene	Homo sapiens	148-151
16849418-9	2006	SU11248 caused a complete morphological reversion of transformed NIH-RET/PTC3 cells and inhibited the growth of TPC-1 cells that have an endogenous RET/PTC1.	Sunitinib	0-7	patched 1	Homo sapiens	152-156
16849418-10	2006	CONCLUSION: SU11248 is a highly effective tyrosine kinase inhibitor of the RET/PTC oncogenic kinase.	Sunitinib	12-19	ret proto-oncogene	Homo sapiens	75-78
16849418-10	2006	CONCLUSION: SU11248 is a highly effective tyrosine kinase inhibitor of the RET/PTC oncogenic kinase.	Sunitinib	12-19	ret proto-oncogene	Homo sapiens	79-82
17041096-2	2006	Thymidine uptake studies showed that sunitinib was active against EOL-1, MV4-11, and Kasumi-1 cells, which possessed activating mutations of the PDGFRalpha, FLT-3, and c-KIT genes, respectively, with IC(50)s of &lt;30 nmol/L.	Sunitinib	37-46	fms related receptor tyrosine kinase 3	Homo sapiens	157-162
17041096-2	2006	Thymidine uptake studies showed that sunitinib was active against EOL-1, MV4-11, and Kasumi-1 cells, which possessed activating mutations of the PDGFRalpha, FLT-3, and c-KIT genes, respectively, with IC(50)s of &lt;30 nmol/L.	Sunitinib	37-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	168-173
17041096-3	2006	In addition, sunitinib inhibited the proliferation of freshly isolated leukemia cells from patients possessing mutations in FLT3 gene.	Sunitinib	13-22	fms related receptor tyrosine kinase 3	Homo sapiens	124-128
17041096-4	2006	Annexin V staining showed that sunitinib induced apoptosis of these cells.	Sunitinib	31-40	annexin A5	Homo sapiens	0-9
17041096-5	2006	Sunitinib inhibited phosphorylation of FLT3 and PDGFRalpha in conjunction with blockade of mammalian target of rapamycin signaling in MV4-11 and EOL-1 cells, respectively.	Sunitinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	39-43
17041096-5	2006	Sunitinib inhibited phosphorylation of FLT3 and PDGFRalpha in conjunction with blockade of mammalian target of rapamycin signaling in MV4-11 and EOL-1 cells, respectively.	Sunitinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	48-58
16974118-8	2006	This opens interesting new treatment strategies including blockade of VEGF with the monoclonal antibody bevacizumab (Avastin) and inhibition of VEGF receptor tyrosine kinases with small oral molecules such as sunitinib (SU11248, Sutent) or PTK787.	Sunitinib	209-218	vascular endothelial growth factor A	Homo sapiens	144-148
16916320-0	2006	Effect of SU11248 on gastrointestinal stromal tumor-T1 cells: enhancement of growth inhibition via inhibition of 3-kinase/Akt/mammalian target of rapamycin signaling.	Sunitinib	10-17	AKT serine/threonine kinase 1	Homo sapiens	122-125
16916320-0	2006	Effect of SU11248 on gastrointestinal stromal tumor-T1 cells: enhancement of growth inhibition via inhibition of 3-kinase/Akt/mammalian target of rapamycin signaling.	Sunitinib	10-17	mechanistic target of rapamycin kinase	Homo sapiens	126-155
16916320-3	2006	Taking advantage of GIST-T1 cells, which possess an activating mutation in exon 11 of the c-KIT gene, we examined the medicinal action of SU11248 in GIST cells.	Sunitinib	138-145	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-95
16916320-5	2006	SU11248 (10 or 20 nM, 48 h) activated caspase-3 and induced apoptosis of GIST-T1 cells as measured by caspase assay, annexin V staining and cleavage of poly (ADP-ribose) polymerase.	Sunitinib	0-7	caspase 3	Homo sapiens	38-47
16916320-5	2006	SU11248 (10 or 20 nM, 48 h) activated caspase-3 and induced apoptosis of GIST-T1 cells as measured by caspase assay, annexin V staining and cleavage of poly (ADP-ribose) polymerase.	Sunitinib	0-7	annexin A5	Homo sapiens	117-126
16916320-5	2006	SU11248 (10 or 20 nM, 48 h) activated caspase-3 and induced apoptosis of GIST-T1 cells as measured by caspase assay, annexin V staining and cleavage of poly (ADP-ribose) polymerase.	Sunitinib	0-7	poly(ADP-ribose) polymerase 1	Homo sapiens	152-180
16916320-6	2006	Western blot analyses found that SU11248 blocked autophosphorylation of c-KIT in association with inhibition of its downstream effectors, including Akt and extracellular signal-regulated kinase, but not signal transducers and activators of transcription.	Sunitinib	33-40	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-77
16916320-6	2006	Western blot analyses found that SU11248 blocked autophosphorylation of c-KIT in association with inhibition of its downstream effectors, including Akt and extracellular signal-regulated kinase, but not signal transducers and activators of transcription.	Sunitinib	33-40	AKT serine/threonine kinase 1	Homo sapiens	148-151
16916320-7	2006	Interestingly, when phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin signaling was blocked simultaneously by either LY294002 or rapamycin, growth inhibition mediated by SU11248 was potentiated.	Sunitinib	184-191	AKT serine/threonine kinase 1	Homo sapiens	50-53
16916320-7	2006	Interestingly, when phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin signaling was blocked simultaneously by either LY294002 or rapamycin, growth inhibition mediated by SU11248 was potentiated.	Sunitinib	184-191	mechanistic target of rapamycin kinase	Homo sapiens	54-83
16685460-3	2006	Bevacizumab (Avastin), Sunitinib (Sutent) and Sorafenib (Nexavar) are anti-cancer drugs targeted to VEGF signaling pathway.	Sunitinib	23-32	vascular endothelial growth factor A	Homo sapiens	100-104
16859583-1	2006	Sunitinib and sorafenib are multitargeted receptor tyrosine kinase inhibitors of the vascular endothelial growth factor and platelet-derived growth factor receptor families with antiangiogenic and antitumor activity in metastatic renal cell carcinoma.	Sunitinib	0-9	vascular endothelial growth factor A	Homo sapiens	85-119
16910860-0	2006	A novel vascular endothelial growth factor receptor 2 inhibitor, SU11248, suppresses choroidal neovascularization in vivo.	Sunitinib	65-72	kinase insert domain protein receptor	Mus musculus	8-53
16910860-1	2006	AIM: An oral, multitargeted receptor tyrosine kinase inhibitor, SU11248, inhibits vascular endothelial growth factor receptor 2 (VEG FR2, kinase domain receptor F1K1), platelet-derived growth factor receptor, stem cell factor receptor (Kit), and fetal liver tyrosine kinase 3.	Sunitinib	64-71	kinase insert domain protein receptor	Mus musculus	82-127
16910860-1	2006	AIM: An oral, multitargeted receptor tyrosine kinase inhibitor, SU11248, inhibits vascular endothelial growth factor receptor 2 (VEG FR2, kinase domain receptor F1K1), platelet-derived growth factor receptor, stem cell factor receptor (Kit), and fetal liver tyrosine kinase 3.	Sunitinib	64-71	kinase insert domain protein receptor	Mus musculus	129-136
16910860-1	2006	AIM: An oral, multitargeted receptor tyrosine kinase inhibitor, SU11248, inhibits vascular endothelial growth factor receptor 2 (VEG FR2, kinase domain receptor F1K1), platelet-derived growth factor receptor, stem cell factor receptor (Kit), and fetal liver tyrosine kinase 3.	Sunitinib	64-71	receptor-like tyrosine kinase	Mus musculus	103-125
16850127-3	2006	To date, the vascular endothelial growth factor receptor (VEGFR) pathway has been the most promising target, and two agents (BAY 43-9006 and SU 11248) that inhibit not only VEGFR but also other receptors, including platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), KIT, and Raf kinase, were recently approved by the FDA for advanced RCC.	Sunitinib	141-149	kinase insert domain receptor	Homo sapiens	173-178
16850127-3	2006	To date, the vascular endothelial growth factor receptor (VEGFR) pathway has been the most promising target, and two agents (BAY 43-9006 and SU 11248) that inhibit not only VEGFR but also other receptors, including platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), KIT, and Raf kinase, were recently approved by the FDA for advanced RCC.	Sunitinib	141-149	platelet derived growth factor receptor beta	Homo sapiens	215-254
16850127-3	2006	To date, the vascular endothelial growth factor receptor (VEGFR) pathway has been the most promising target, and two agents (BAY 43-9006 and SU 11248) that inhibit not only VEGFR but also other receptors, including platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), KIT, and Raf kinase, were recently approved by the FDA for advanced RCC.	Sunitinib	141-149	platelet derived growth factor receptor beta	Homo sapiens	256-261
16850127-3	2006	To date, the vascular endothelial growth factor receptor (VEGFR) pathway has been the most promising target, and two agents (BAY 43-9006 and SU 11248) that inhibit not only VEGFR but also other receptors, including platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), KIT, and Raf kinase, were recently approved by the FDA for advanced RCC.	Sunitinib	141-149	fms related receptor tyrosine kinase 3	Homo sapiens	264-290
16850127-3	2006	To date, the vascular endothelial growth factor receptor (VEGFR) pathway has been the most promising target, and two agents (BAY 43-9006 and SU 11248) that inhibit not only VEGFR but also other receptors, including platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), KIT, and Raf kinase, were recently approved by the FDA for advanced RCC.	Sunitinib	141-149	fms related receptor tyrosine kinase 3	Homo sapiens	292-296
16850127-3	2006	To date, the vascular endothelial growth factor receptor (VEGFR) pathway has been the most promising target, and two agents (BAY 43-9006 and SU 11248) that inhibit not only VEGFR but also other receptors, including platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), KIT, and Raf kinase, were recently approved by the FDA for advanced RCC.	Sunitinib	141-149	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	299-302
16685460-3	2006	Bevacizumab (Avastin), Sunitinib (Sutent) and Sorafenib (Nexavar) are anti-cancer drugs targeted to VEGF signaling pathway.	Sunitinib	34-40	vascular endothelial growth factor A	Homo sapiens	100-104
16731761-2	2006	SU11248, a small-molecule inhibitor targeting class III/V receptor tyrosine kinases, including the platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) receptors, KIT and FLT3, exhibits direct effects on cancer cells as well as antiangiogenic activity.	Sunitinib	0-7	vascular endothelial growth factor A	Homo sapiens	141-175
16731761-5	2006	To elucidate the specific contributions of inhibition of PDGF and VEGF receptors to the in vivo efficacy of SU11248, we employed two selective inhibitors, SU10944 (VEGF receptor inhibitor) and Gleevec (PDGF receptor inhibitor).	Sunitinib	108-115	vascular endothelial growth factor A	Homo sapiens	66-70
16731761-9	2006	The one exception was a model driven by an activated mutant of FLT3, in which the activity of SU11248, which targets FLT3, was greater than that of SU10944 plus Gleevec.	Sunitinib	94-101	fms related receptor tyrosine kinase 3	Homo sapiens	63-67
16731761-9	2006	The one exception was a model driven by an activated mutant of FLT3, in which the activity of SU11248, which targets FLT3, was greater than that of SU10944 plus Gleevec.	Sunitinib	94-101	fms related receptor tyrosine kinase 3	Homo sapiens	117-121
16638875-10	2006	In agreement with these results, two of the three imatinib-resistant patients with the KIT-V654A mutation responded to SU11248 treatment.	Sunitinib	119-126	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-90
16638875-11	2006	CONCLUSIONS: These studies suggest that SU11248 may be a useful therapeutic agent to treat gastrointestinal stromal tumors harboring the imatinib-resistant KIT-V654A or KIT-T670I mutations, but it has no effect on the activity of the PDGFRA-D842V mutant.	Sunitinib	40-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	156-159
16638875-4	2006	We tested the activity of SU11248, an orally active small-molecule tyrosine kinase inhibitor, to inhibit important imatinib-resistant KIT and PDGFRA mutants.	Sunitinib	26-33	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	134-137
16638875-11	2006	CONCLUSIONS: These studies suggest that SU11248 may be a useful therapeutic agent to treat gastrointestinal stromal tumors harboring the imatinib-resistant KIT-V654A or KIT-T670I mutations, but it has no effect on the activity of the PDGFRA-D842V mutant.	Sunitinib	40-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	169-172
16638875-4	2006	We tested the activity of SU11248, an orally active small-molecule tyrosine kinase inhibitor, to inhibit important imatinib-resistant KIT and PDGFRA mutants.	Sunitinib	26-33	platelet derived growth factor receptor alpha	Homo sapiens	142-148
16638875-6	2006	Three patients with the KIT-V654A mutation were treated with SU11248.	Sunitinib	61-68	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-27
16638875-11	2006	CONCLUSIONS: These studies suggest that SU11248 may be a useful therapeutic agent to treat gastrointestinal stromal tumors harboring the imatinib-resistant KIT-V654A or KIT-T670I mutations, but it has no effect on the activity of the PDGFRA-D842V mutant.	Sunitinib	40-47	platelet derived growth factor receptor alpha	Homo sapiens	234-240
16638875-7	2006	RESULTS: Based on ex vivo assays, SU11248 potently inhibits KIT kinase activity of V654A and T670I mutants and suppresses proliferation of the cells expressing these mutations.	Sunitinib	34-41	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-63
16638875-8	2006	Sensitivity of KIT-V654A and KIT-T670I mutants to SU11248 was confirmed using cell lines expressing these mutants.	Sunitinib	50-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	15-18
16638875-8	2006	Sensitivity of KIT-V654A and KIT-T670I mutants to SU11248 was confirmed using cell lines expressing these mutants.	Sunitinib	50-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-32
16556328-3	2006	For example Imatinib/Gleevec (primarily a bcr/abl kinase inhibitor) or SU11248 (mainly a VEGFR inhibitor) are also potent inhibitors of PDGFR and other kinases.	Sunitinib	71-78	kinase insert domain receptor	Homo sapiens	89-94
16648572-6	2006	SU11248 is a potent inhibitor of CSF-1R in the enzyme assay (IC50 = 7 nmol/L) and inhibits receptor phosphorylation in the cellular assay (IC50 = 61 nmol/L).	Sunitinib	0-7	colony stimulating factor 1 receptor	Homo sapiens	33-39
16556328-3	2006	For example Imatinib/Gleevec (primarily a bcr/abl kinase inhibitor) or SU11248 (mainly a VEGFR inhibitor) are also potent inhibitors of PDGFR and other kinases.	Sunitinib	71-78	platelet derived growth factor receptor beta	Homo sapiens	136-141
16425985-2	2005	SU11248 and AG013736 are small-molecule inhibitors of the tyrosine kinase portion of the VEGF and PDGF receptors.	Sunitinib	0-7	vascular endothelial growth factor A	Homo sapiens	89-93
16640800-2	2006	These include the small-molecule receptor tyrosine kinase (TK) inhibitors ZD6474, sorafenib, sunitinib malate, and AG-013736, all of which inhibit VEGF receptor TK activity.	Sunitinib	93-109	vascular endothelial growth factor A	Homo sapiens	147-151
18393778-6	2006	In addition, other KIT tyrosine kinase inhibitors with anti-VEGF receptor inhibitory activity, such as SU11248, PTK787/ZK787 and AMG 706, are currently being explored as second line monotherapy for imatinib mesylate-resistant GIST.	Sunitinib	103-110	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	19-22
16330672-2	2006	SU11248 (sunitinib malate), a small molecule inhibitor with high binding affinity for VEGF and PDGF receptors, was tested for clinical activity in patients with metastatic RCC.	Sunitinib	0-7	vascular endothelial growth factor A	Homo sapiens	86-90
16330672-9	2006	CONCLUSION: SU11248, a multitargeted receptor tyrosine kinase inhibitor of VEGF and PDGF receptors, demonstrates antitumor activity in metastatic RCC as second-line therapy, a setting where no effective systemic therapy is presently recognized.	Sunitinib	12-19	vascular endothelial growth factor A	Homo sapiens	75-79
16425993-2	2005	Significant advances in the treatment of clear-cell RCC have been derived from agents that target these pathways, including the multiple-kinase inhibitors (MKIs) sorafenib, sunitinib, and AG013736, which target multiple VEGFRs as well as PDGFR-beta.	Sunitinib	173-182	kinase insert domain receptor	Homo sapiens	220-226
15459012-1	2005	Fifteen patients with refractory AML were treated in a phase 1 study with SU11248, an oral kinase inhibitor of fms-like tyrosine kinase 3 (Flt3), Kit, vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF) receptors.	Sunitinib	74-81	fms related receptor tyrosine kinase 3	Homo sapiens	111-137
16185167-4	2005	Results using small-molecule inhibitors of VEGF, FLT3, KIT and platelet-derived growth factor receptor tyrosine kinases, such as sunitinib, show a 40% objective response rate.	Sunitinib	129-138	vascular endothelial growth factor A	Homo sapiens	43-47
15557593-4	2005	MATERIALS AND METHODS: Seeking to improve efficacy against otherwise intractable end-stage pancreatic islet tumors, two receptor tyrosine kinase inhibitors, imatinib and SU11248, were used to disrupt PDGFR-mediated pericyte support of tumor endothelial cells in concert with maximum-tolerated dose (MTD) or metronomic chemotherapy and/or VEGFR inhibition.	Sunitinib	170-177	platelet derived growth factor receptor, beta polypeptide	Mus musculus	200-205
16115922-1	2005	PURPOSE: To compare two dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) techniques in terms of their ability in assessing the early antiangiogenic effect of SU11248, a novel selective multitargeted tyrosine kinase inhibitor, that exhibits direct antitumor and antiangiogenic activity via inhibition of the receptor tyrosine kinases platelet-derived growth factor receptor, vascular endothelial growth factor receptor, KIT, and FLT3.	Sunitinib	172-179	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	433-436
16115922-1	2005	PURPOSE: To compare two dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) techniques in terms of their ability in assessing the early antiangiogenic effect of SU11248, a novel selective multitargeted tyrosine kinase inhibitor, that exhibits direct antitumor and antiangiogenic activity via inhibition of the receptor tyrosine kinases platelet-derived growth factor receptor, vascular endothelial growth factor receptor, KIT, and FLT3.	Sunitinib	172-179	fms related receptor tyrosine kinase 3	Homo sapiens	442-446
16046538-6	2005	The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase.	Sunitinib	23-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-7
16046538-6	2005	The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase.	Sunitinib	23-31	fms related receptor tyrosine kinase 3	Homo sapiens	8-12
16046538-6	2005	The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase.	Sunitinib	23-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
16046538-6	2005	The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase.	Sunitinib	23-31	epidermal growth factor receptor	Homo sapiens	208-212
16046538-6	2005	The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase.	Sunitinib	23-31	epidermal growth factor receptor	Homo sapiens	332-336
16046538-6	2005	The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase.	Sunitinib	139-147	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-7
16046538-6	2005	The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase.	Sunitinib	139-147	fms related receptor tyrosine kinase 3	Homo sapiens	8-12
15304385-0	2004	Synergistic effect of SU11248 with cytarabine or daunorubicin on FLT3 ITD-positive leukemic cells.	Sunitinib	22-29	fms related receptor tyrosine kinase 3	Homo sapiens	65-69
15304385-4	2004	SU11248 had additive-to-synergistic inhibitory effects on FLT3-dependent leukemic cell proliferation when combined with cytarabine or daunorubicin.	Sunitinib	0-7	fms related receptor tyrosine kinase 3	Homo sapiens	58-62
14985702-8	2004	One such potential biomarker, cadherin-11, was further evaluated at the protein level and was found to have increased expression in xenograft tumors after SU11248 treatment.	Sunitinib	155-162	cadherin 11	Homo sapiens	30-41
15304385-6	2004	SU11248 inhibited the proliferation of primary AML myeloblasts expressing mutant FLT3 ITD but not WT FLT3 protein.	Sunitinib	0-7	fms related receptor tyrosine kinase 3	Homo sapiens	81-85
15304385-7	2004	Combining SU11248 and cytarabine synergistically inhibited the proliferation of primary AML myeloblasts expressing FLT3 ITD but not WT FLT3 protein.	Sunitinib	10-17	fms related receptor tyrosine kinase 3	Homo sapiens	115-119
15304385-8	2004	These data suggest that the addition of potent FLT3 inhibitors such as SU11248 to AML chemotherapy regimens could result in improved treatment results.	Sunitinib	71-78	fms related receptor tyrosine kinase 3	Homo sapiens	47-51
15648955-1	2004	SUGEN is developing SU-11248, an orally active inhibitor of platelet-derived growth factor tyrosine kinase (TK) and other TK signaling pathways, as a potential anticancer agent.	Sunitinib	20-28	TXK tyrosine kinase	Homo sapiens	91-106
15648955-1	2004	SUGEN is developing SU-11248, an orally active inhibitor of platelet-derived growth factor tyrosine kinase (TK) and other TK signaling pathways, as a potential anticancer agent.	Sunitinib	20-28	TXK tyrosine kinase	Homo sapiens	108-110
15648955-1	2004	SUGEN is developing SU-11248, an orally active inhibitor of platelet-derived growth factor tyrosine kinase (TK) and other TK signaling pathways, as a potential anticancer agent.	Sunitinib	20-28	TXK tyrosine kinase	Homo sapiens	122-124
14985702-10	2004	Importantly, SU11248 treatment also resulted in increased expression of cadherin-11 protein in human tumor biopsies in three out of seven patients examined and confirms the feasibility of using transcriptional profiling of preclinical models to identify clinically translatable biomarkers.	Sunitinib	13-20	cadherin 11	Homo sapiens	72-83
14753710-1	2004	SU11248 is a potent inhibitor of PDGFR, VEGFR, KIT, and Flt3, and is currently under Phase I clinical evaluation as an anticancer drug.	Sunitinib	0-7	platelet derived growth factor receptor beta	Homo sapiens	33-38
14753710-1	2004	SU11248 is a potent inhibitor of PDGFR, VEGFR, KIT, and Flt3, and is currently under Phase I clinical evaluation as an anticancer drug.	Sunitinib	0-7	kinase insert domain receptor	Homo sapiens	40-45
14753710-1	2004	SU11248 is a potent inhibitor of PDGFR, VEGFR, KIT, and Flt3, and is currently under Phase I clinical evaluation as an anticancer drug.	Sunitinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-50
14753710-1	2004	SU11248 is a potent inhibitor of PDGFR, VEGFR, KIT, and Flt3, and is currently under Phase I clinical evaluation as an anticancer drug.	Sunitinib	0-7	fms related receptor tyrosine kinase 3	Homo sapiens	56-60
15609077-0	2004	The receptor tyrosine kinase inhibitor SU11248 impedes endothelial cell migration, tubule formation, and blood vessel formation in vivo, but has little effect on existing tumor vessels.	Sunitinib	39-46	ret proto-oncogene	Homo sapiens	4-28
15609077-2	2004	To determine whether the vascular endothelial growth factor (VEGF) receptor is a molecular target to prevent metastatic disease, we utilized a non-specific inhibitor of the VEGF receptor, SU11248.	Sunitinib	188-195	vascular endothelial growth factor A	Homo sapiens	61-65
15609077-2	2004	To determine whether the vascular endothelial growth factor (VEGF) receptor is a molecular target to prevent metastatic disease, we utilized a non-specific inhibitor of the VEGF receptor, SU11248.	Sunitinib	188-195	vascular endothelial growth factor A	Homo sapiens	173-177
15000426-2	2004	SU011248 is an oral, multitargeted receptor tyrosine kinase inhibitor (anti PDGFR, VEGFR, Kit, and Flt3) for the treatment of solid tumors.	Sunitinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	76-81
15000426-2	2004	SU011248 is an oral, multitargeted receptor tyrosine kinase inhibitor (anti PDGFR, VEGFR, Kit, and Flt3) for the treatment of solid tumors.	Sunitinib	0-8	kinase insert domain receptor	Homo sapiens	83-88
15000426-2	2004	SU011248 is an oral, multitargeted receptor tyrosine kinase inhibitor (anti PDGFR, VEGFR, Kit, and Flt3) for the treatment of solid tumors.	Sunitinib	0-8	fms related receptor tyrosine kinase 3	Homo sapiens	99-103
12748309-4	2003	The biological significance of KIT inhibition was evaluated in vivo by treating mice bearing s.c. NCI-H526 tumors with SU11248 or another structurally unrelated KIT inhibitor, STI571 (Gleevec), which is also known to inhibit Bcr-Abl and PDGFRbeta.	Sunitinib	119-126	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	31-34
14654525-0	2003	An innovative phase I clinical study demonstrates inhibition of FLT3 phosphorylation by SU11248 in acute myeloid leukemia patients.	Sunitinib	88-95	fms related receptor tyrosine kinase 3	Homo sapiens	64-68
14654525-2	2003	SU11248 is an oral multitargeted kinase inhibitor with selectivity for fms-related tyrosine kinase 3/Flk2 (FLT3), platelet-derived growth factor receptor alpha/beta, vascular endothelial growth factor receptor 1/2, and KIT receptor tyrosine kinases.	Sunitinib	0-7	fms related receptor tyrosine kinase 3	Homo sapiens	71-100
14654525-2	2003	SU11248 is an oral multitargeted kinase inhibitor with selectivity for fms-related tyrosine kinase 3/Flk2 (FLT3), platelet-derived growth factor receptor alpha/beta, vascular endothelial growth factor receptor 1/2, and KIT receptor tyrosine kinases.	Sunitinib	0-7	fms related receptor tyrosine kinase 3	Homo sapiens	101-105
14654525-2	2003	SU11248 is an oral multitargeted kinase inhibitor with selectivity for fms-related tyrosine kinase 3/Flk2 (FLT3), platelet-derived growth factor receptor alpha/beta, vascular endothelial growth factor receptor 1/2, and KIT receptor tyrosine kinases.	Sunitinib	0-7	fms related receptor tyrosine kinase 3	Homo sapiens	107-111
14654525-2	2003	SU11248 is an oral multitargeted kinase inhibitor with selectivity for fms-related tyrosine kinase 3/Flk2 (FLT3), platelet-derived growth factor receptor alpha/beta, vascular endothelial growth factor receptor 1/2, and KIT receptor tyrosine kinases.	Sunitinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	219-222
14654525-4	2003	We conducted an innovative single-dose clinical study with a primary objective to demonstrate inhibition of FLT3 phosphorylation by SU11248 in AML.	Sunitinib	132-139	fms related receptor tyrosine kinase 3	Homo sapiens	108-112
14578466-1	2003	SU11248 is an oral multitargeted tyrosine kinase inhibitor with antitumor and antiangiogenic activities through targeting platelet-derived growth factor receptor, vascular endothelial growth factor receptor, KIT, and FLT3, the first three of which are expressed in human breast cancer and/or its supporting tissues.	Sunitinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	208-211
14578466-1	2003	SU11248 is an oral multitargeted tyrosine kinase inhibitor with antitumor and antiangiogenic activities through targeting platelet-derived growth factor receptor, vascular endothelial growth factor receptor, KIT, and FLT3, the first three of which are expressed in human breast cancer and/or its supporting tissues.	Sunitinib	0-7	fms related receptor tyrosine kinase 3	Homo sapiens	217-221
14578466-3	2003	SU11248 was administered as a monotherapy to (1) mouse mammary tumor virus-v-Ha-ras mice and 7,12-dimethylbenz(a)anthracene-treated rats bearing mammary tumors and (2) mice bearing human breast cancer xenografts of s.c. MX-1 tumors and osseous metastasis of a MDA-MB-435-derived cell line (435/HAL-Luc).	Sunitinib	0-7	histidine ammonia-lyase	Homo sapiens	294-297
14578466-7	2003	SU11248 treatment in combination with docetaxel effectively prolonged survival of mice, with 435/HAL-Luc cancer xenografts established in bone compared with either agent alone (P &lt; 0.05).	Sunitinib	0-7	histidine ammonia lyase	Mus musculus	97-100
12748309-0	2003	SU11248 inhibits KIT and platelet-derived growth factor receptor beta in preclinical models of human small cell lung cancer.	Sunitinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-20
12748309-0	2003	SU11248 inhibits KIT and platelet-derived growth factor receptor beta in preclinical models of human small cell lung cancer.	Sunitinib	0-7	platelet derived growth factor receptor beta	Homo sapiens	25-69
12748309-1	2003	The purpose of this study was to evaluate the activity of the indolinone kinase inhibitor SU11248 against the receptor tyrosine kinase KIT in vitro and in vivo, examine the role of KIT in small cell lung cancer (SCLC), and anticipate clinical utility of SU11248 in SCLC.	Sunitinib	90-97	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	135-138
12748309-2	2003	SU11248 is an oral, multitargeted tyrosine kinase inhibitor with direct antitumor and antiangiogenic activity through targeting platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor receptor, KIT, and FLT3 receptors.	Sunitinib	0-7	platelet derived growth factor receptor beta	Homo sapiens	128-167
12748309-2	2003	SU11248 is an oral, multitargeted tyrosine kinase inhibitor with direct antitumor and antiangiogenic activity through targeting platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor receptor, KIT, and FLT3 receptors.	Sunitinib	0-7	platelet derived growth factor receptor beta	Homo sapiens	169-174
12748309-2	2003	SU11248 is an oral, multitargeted tyrosine kinase inhibitor with direct antitumor and antiangiogenic activity through targeting platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor receptor, KIT, and FLT3 receptors.	Sunitinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	222-225
12748309-2	2003	SU11248 is an oral, multitargeted tyrosine kinase inhibitor with direct antitumor and antiangiogenic activity through targeting platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor receptor, KIT, and FLT3 receptors.	Sunitinib	0-7	fms related receptor tyrosine kinase 3	Homo sapiens	231-235
12748309-3	2003	Treatment of the KIT-expressing SCLC-derived NCI-H526 cell line in vitro with SU11248 resulted in dose-dependent inhibition of stem cell factor-stimulated KIT phosphotyrosine levels and proliferation.	Sunitinib	78-85	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-20
12748309-3	2003	Treatment of the KIT-expressing SCLC-derived NCI-H526 cell line in vitro with SU11248 resulted in dose-dependent inhibition of stem cell factor-stimulated KIT phosphotyrosine levels and proliferation.	Sunitinib	78-85	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	155-158
12873999-2	2003	The novel broad spectrum receptor tyrosine kinase inhibitor, SU11248, inhibits vascular endothelial growth factor receptor 2, platelet-derived growth factor receptor, c-kit, and fetal liver tyrosine kinase 3.	Sunitinib	61-68	kinase insert domain protein receptor	Mus musculus	79-124
12873999-2	2003	The novel broad spectrum receptor tyrosine kinase inhibitor, SU11248, inhibits vascular endothelial growth factor receptor 2, platelet-derived growth factor receptor, c-kit, and fetal liver tyrosine kinase 3.	Sunitinib	61-68	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	167-172
12531805-0	2003	SU11248 is a novel FLT3 tyrosine kinase inhibitor with potent activity in vitro and in vivo.	Sunitinib	0-7	fms related receptor tyrosine kinase 3	Homo sapiens	19-23
12531805-5	2003	SU11248 is a recently described selective inhibitor with selectivity for split kinase domain RTKs, including platelet-derived growth factor receptors, vascular endothelial growth factor receptors, and KIT.	Sunitinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	151-204
12531805-6	2003	We show that SU11248 also has potent activity against wild-type FLT3 (FLT3-WT), FLT3-ITD, and FLT3 activation loop (FLT3-Asp835) mutants in phosphorylation assays.	Sunitinib	13-20	fms related receptor tyrosine kinase 3	Homo sapiens	64-68
12531805-6	2003	We show that SU11248 also has potent activity against wild-type FLT3 (FLT3-WT), FLT3-ITD, and FLT3 activation loop (FLT3-Asp835) mutants in phosphorylation assays.	Sunitinib	13-20	fms related receptor tyrosine kinase 3	Homo sapiens	70-77
12531805-6	2003	We show that SU11248 also has potent activity against wild-type FLT3 (FLT3-WT), FLT3-ITD, and FLT3 activation loop (FLT3-Asp835) mutants in phosphorylation assays.	Sunitinib	13-20	fms related receptor tyrosine kinase 3	Homo sapiens	70-74
12531805-6	2003	We show that SU11248 also has potent activity against wild-type FLT3 (FLT3-WT), FLT3-ITD, and FLT3 activation loop (FLT3-Asp835) mutants in phosphorylation assays.	Sunitinib	13-20	fms related receptor tyrosine kinase 3	Homo sapiens	70-74
12531805-6	2003	We show that SU11248 also has potent activity against wild-type FLT3 (FLT3-WT), FLT3-ITD, and FLT3 activation loop (FLT3-Asp835) mutants in phosphorylation assays.	Sunitinib	13-20	fms related receptor tyrosine kinase 3	Homo sapiens	70-74
12531805-7	2003	SU11248 inhibits FLT3-driven phosphorylation and induces apoptosis in vitro.	Sunitinib	0-7	fms related receptor tyrosine kinase 3	Homo sapiens	17-21
12531805-8	2003	In addition, SU11248 inhibits FLT3-induced VEGF production.	Sunitinib	13-20	fms related receptor tyrosine kinase 3	Homo sapiens	30-34
12531805-8	2003	In addition, SU11248 inhibits FLT3-induced VEGF production.	Sunitinib	13-20	vascular endothelial growth factor A	Homo sapiens	43-47
12748309-7	2003	Likewise, phospho-PDGFRbeta levels contributed by tumor stroma and with known involvement in angiogenesis were strongly inhibited by SU11248 and less so by STI571.	Sunitinib	133-140	platelet derived growth factor receptor beta	Homo sapiens	18-27
12748309-9	2003	These results expand the profile of SU11248 as a KIT signaling inhibitor and suggest that SU11248 may have clinical potential in the treatment of SCLC via direct antitumor activity mediated via KIT as well as tumor angiogenesis via vascular endothelial growth factor receptor FLK1/KDR and PDGFRbeta.	Sunitinib	36-43	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
12748309-9	2003	These results expand the profile of SU11248 as a KIT signaling inhibitor and suggest that SU11248 may have clinical potential in the treatment of SCLC via direct antitumor activity mediated via KIT as well as tumor angiogenesis via vascular endothelial growth factor receptor FLK1/KDR and PDGFRbeta.	Sunitinib	90-97	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	194-197
12748309-9	2003	These results expand the profile of SU11248 as a KIT signaling inhibitor and suggest that SU11248 may have clinical potential in the treatment of SCLC via direct antitumor activity mediated via KIT as well as tumor angiogenesis via vascular endothelial growth factor receptor FLK1/KDR and PDGFRbeta.	Sunitinib	90-97	kinase insert domain receptor	Homo sapiens	276-280
12748309-9	2003	These results expand the profile of SU11248 as a KIT signaling inhibitor and suggest that SU11248 may have clinical potential in the treatment of SCLC via direct antitumor activity mediated via KIT as well as tumor angiogenesis via vascular endothelial growth factor receptor FLK1/KDR and PDGFRbeta.	Sunitinib	90-97	kinase insert domain receptor	Homo sapiens	281-284
12748309-9	2003	These results expand the profile of SU11248 as a KIT signaling inhibitor and suggest that SU11248 may have clinical potential in the treatment of SCLC via direct antitumor activity mediated via KIT as well as tumor angiogenesis via vascular endothelial growth factor receptor FLK1/KDR and PDGFRbeta.	Sunitinib	90-97	platelet derived growth factor receptor beta	Homo sapiens	289-298
14713109-0	2003	SU11248 inhibits tumor growth and CSF-1R-dependent osteolysis in an experimental breast cancer bone metastasis model.	Sunitinib	0-7	colony stimulating factor 1 receptor	Mus musculus	34-40
12538485-0	2003	In vivo antitumor activity of SU11248, a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor and platelet-derived growth factor receptors: determination of a pharmacokinetic/pharmacodynamic relationship.	Sunitinib	30-37	vascular endothelial growth factor A	Homo sapiens	83-117
12538485-3	2003	SU11248, a novel small molecule receptor tyrosine kinase inhibitor with direct antitumor as well as antiangiogenic activity via targeting the vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), KIT, and FLT3 receptor tyrosine kinases, was used as the pharmacological agent in these studies.	Sunitinib	0-7	vascular endothelial growth factor A	Homo sapiens	142-176
12538485-3	2003	SU11248, a novel small molecule receptor tyrosine kinase inhibitor with direct antitumor as well as antiangiogenic activity via targeting the vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), KIT, and FLT3 receptor tyrosine kinases, was used as the pharmacological agent in these studies.	Sunitinib	0-7	vascular endothelial growth factor A	Homo sapiens	178-182
14713109-1	2003	The aim of the study was to investigate inhibitory effects of the receptor tyrosine kinase (RTK) inhibitor SU11248 against CSF-1R and osteoclast (OC) formation.	Sunitinib	107-114	colony stimulating factor 1 receptor	Mus musculus	123-129
12538485-3	2003	SU11248, a novel small molecule receptor tyrosine kinase inhibitor with direct antitumor as well as antiangiogenic activity via targeting the vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), KIT, and FLT3 receptor tyrosine kinases, was used as the pharmacological agent in these studies.	Sunitinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	224-227
12538485-3	2003	SU11248, a novel small molecule receptor tyrosine kinase inhibitor with direct antitumor as well as antiangiogenic activity via targeting the vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), KIT, and FLT3 receptor tyrosine kinases, was used as the pharmacological agent in these studies.	Sunitinib	0-7	fms related receptor tyrosine kinase 3	Homo sapiens	233-237
14713109-3	2003	The in vitro effects of SU11248 on CSF-1R phosphorylation, OC formation and function were evaluated.	Sunitinib	24-31	colony stimulating factor 1 (macrophage)	Mus musculus	35-40
12538485-6	2003	In target modulation studies in vivo, SU11248 selectively inhibited Flk-1/KDR (VEGF receptor 2) and PDGF receptor beta phosphorylation (in a time- and dose-dependent manner) when plasma concentrations of inhibitor reached or exceeded 50-100 ng/ml.	Sunitinib	38-45	kinase insert domain receptor	Homo sapiens	68-73
14713109-5	2003	Phosphorylation of the receptor for M-CSF (CSF-1R) expressed by NIH3T3 cells was inhibited by SU11248 with an IC50 of 50-100 nM, consistent with CSF-1R belonging to the class III split kinase domain RTK family.	Sunitinib	94-101	colony stimulating factor 1 (macrophage)	Mus musculus	36-41
12538485-6	2003	In target modulation studies in vivo, SU11248 selectively inhibited Flk-1/KDR (VEGF receptor 2) and PDGF receptor beta phosphorylation (in a time- and dose-dependent manner) when plasma concentrations of inhibitor reached or exceeded 50-100 ng/ml.	Sunitinib	38-45	kinase insert domain receptor	Homo sapiens	74-77
12538485-6	2003	In target modulation studies in vivo, SU11248 selectively inhibited Flk-1/KDR (VEGF receptor 2) and PDGF receptor beta phosphorylation (in a time- and dose-dependent manner) when plasma concentrations of inhibitor reached or exceeded 50-100 ng/ml.	Sunitinib	38-45	vascular endothelial growth factor A	Homo sapiens	79-83
14713109-5	2003	Phosphorylation of the receptor for M-CSF (CSF-1R) expressed by NIH3T3 cells was inhibited by SU11248 with an IC50 of 50-100 nM, consistent with CSF-1R belonging to the class III split kinase domain RTK family.	Sunitinib	94-101	colony stimulating factor 1 receptor	Mus musculus	43-49
14713109-5	2003	Phosphorylation of the receptor for M-CSF (CSF-1R) expressed by NIH3T3 cells was inhibited by SU11248 with an IC50 of 50-100 nM, consistent with CSF-1R belonging to the class III split kinase domain RTK family.	Sunitinib	94-101	colony stimulating factor 1 receptor	Mus musculus	145-151
14713109-6	2003	The early M-CSF-dependent phase of in vitro murine OC development and function were inhibited by SU11248 at 10-100 nM.	Sunitinib	97-104	colony stimulating factor 1 (macrophage)	Mus musculus	10-15
14988747-8	2003	Although very preliminary, a phase I trial found tumor regressions that were caused by an oral VEGF receptor tyrosine kinase inhibitor, SU11248.	Sunitinib	136-143	vascular endothelial growth factor A	Homo sapiens	95-99
33972682-5	2021	TKI sunitinib resistance was rescued by DPP4 inhibition using sitagliptin or specific siRNAs in RCC cells and tumors.	Sunitinib	4-13	dipeptidyl peptidase 4	Homo sapiens	40-44
33799686-6	2021	Compared with control cells transduced with scrambled vector (UMRC3-SC cells), PHD3-knockdown cells (UMRC3-PHD3KD cells) showed increased cell invasion, tumor growth, and response to sunitinib.	Sunitinib	183-192	egl-9 family hypoxia inducible factor 3	Homo sapiens	79-83
33799686-8	2021	However, following sunitinib treatment, expression of HIF2alpha and phosphorylated EGFR were equivalent in both PHD3 knockdown and control tumors.	Sunitinib	19-28	endothelial PAS domain protein 1	Homo sapiens	54-63
33799686-8	2021	However, following sunitinib treatment, expression of HIF2alpha and phosphorylated EGFR were equivalent in both PHD3 knockdown and control tumors.	Sunitinib	19-28	epidermal growth factor	Homo sapiens	83-87
33762959-9	2021	Compared with the C allele, the ABCB1 rs1128503 T allele was associated with a decreased risk of sunitinib-induced hypertension but worse progression-free survival (PFS) (ES = 0.44, 95% CI = 0.26-0.77, p = 0.004; ES = 1.36, 95% CI = 1.07-1.73, p = 0.011).	Sunitinib	97-106	ATP binding cassette subfamily B member 1	Homo sapiens	32-37
33762959-0	2021	Meta-Analysis of ABCG2 and ABCB1 Polymorphisms With Sunitinib-Induced Toxicity and Efficacy in Renal Cell Carcinoma.	Sunitinib	52-61	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	17-22
33762959-0	2021	Meta-Analysis of ABCG2 and ABCB1 Polymorphisms With Sunitinib-Induced Toxicity and Efficacy in Renal Cell Carcinoma.	Sunitinib	52-61	ATP binding cassette subfamily B member 1	Homo sapiens	27-32
33762959-12	2021	Conclusion: The results indicate that the ABCG2 rs2231142 polymorphism may serve as a predictor of sunitinib-induced thrombocytopenia and HFS in Asians, while the ABCB1 rs1128503 polymorphism may serve as a predictor of sunitinib-induced hypertension, and both the ABCB1 rs1128503 and rs2032582 polymorphisms may serve as predictors of PFS in RCC.	Sunitinib	99-108	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	42-47
33762959-1	2021	Background: ABCG2 and ABCB1 are genes related to the pharmacokinetics of sunitinib and have been associated with its toxicity and efficacy.	Sunitinib	73-82	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	12-17
33762959-1	2021	Background: ABCG2 and ABCB1 are genes related to the pharmacokinetics of sunitinib and have been associated with its toxicity and efficacy.	Sunitinib	73-82	ATP binding cassette subfamily B member 1	Homo sapiens	22-27
33762959-3	2021	This study aimed to evaluate the associations of ABCG2 and ABCB1 polymorphisms with sunitinib-induced toxicity and efficacy in renal cell carcinoma (RCC) by meta-analysis.	Sunitinib	84-93	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	49-54
33762959-3	2021	This study aimed to evaluate the associations of ABCG2 and ABCB1 polymorphisms with sunitinib-induced toxicity and efficacy in renal cell carcinoma (RCC) by meta-analysis.	Sunitinib	84-93	ATP binding cassette subfamily B member 1	Homo sapiens	59-64
33762959-7	2021	The ABCG2 rs2231142 A allele was associated with an increased risk of sunitinib-induced thrombocytopenia and hand-foot syndrome (HFS) in Asians (ES = 1.65, 95% CI = 1.15-2.36, p = 0.006; ES = 1.52, 95% CI = 1.02-2.27, p = 0.041).	Sunitinib	70-79	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	4-9
33762959-12	2021	Conclusion: The results indicate that the ABCG2 rs2231142 polymorphism may serve as a predictor of sunitinib-induced thrombocytopenia and HFS in Asians, while the ABCB1 rs1128503 polymorphism may serve as a predictor of sunitinib-induced hypertension, and both the ABCB1 rs1128503 and rs2032582 polymorphisms may serve as predictors of PFS in RCC.	Sunitinib	99-108	ATP binding cassette subfamily B member 1	Homo sapiens	265-270
33762959-12	2021	Conclusion: The results indicate that the ABCG2 rs2231142 polymorphism may serve as a predictor of sunitinib-induced thrombocytopenia and HFS in Asians, while the ABCB1 rs1128503 polymorphism may serve as a predictor of sunitinib-induced hypertension, and both the ABCB1 rs1128503 and rs2032582 polymorphisms may serve as predictors of PFS in RCC.	Sunitinib	220-229	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	42-47
33812180-4	2021	As a result of the inhibition that is caused by sunitinib malate agent at the receptor level, vascular endothelial growth factor (VEGF) level increases.	Sunitinib	48-57	vascular endothelial growth factor A	Homo sapiens	94-128
33812180-4	2021	As a result of the inhibition that is caused by sunitinib malate agent at the receptor level, vascular endothelial growth factor (VEGF) level increases.	Sunitinib	48-57	vascular endothelial growth factor A	Homo sapiens	130-134
34949839-5	2022	Several other Food and Drug Administration (FDA)-approved inhibitors, such erlotinib and sunitinib, also bound and activated GCN2.	Sunitinib	89-98	eukaryotic translation initiation factor 2 alpha kinase 4	Homo sapiens	125-129
24874929-0	2014	Efflux pump ABCB1 single nucleotide polymorphisms and dose reductions in patients with metastatic renal cell carcinoma treated with sunitinib.	Sunitinib	132-141	ATP binding cassette subfamily B member 1	Homo sapiens	12-17
24874929-4	2014	We genotyped 11 key SNPs, respectively, in ABCB1, NR1/2, NR1/3 and CYP3A5, involved in sunitinib pharmacokinetics as well as VEGFR1 and VEGFR3, which have been suggested as regulators of sunitinib pharmacodynamics.	Sunitinib	87-96	ATP binding cassette subfamily B member 1	Homo sapiens	43-48
24874929-4	2014	We genotyped 11 key SNPs, respectively, in ABCB1, NR1/2, NR1/3 and CYP3A5, involved in sunitinib pharmacokinetics as well as VEGFR1 and VEGFR3, which have been suggested as regulators of sunitinib pharmacodynamics.	Sunitinib	87-96	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	50-55
24874929-4	2014	We genotyped 11 key SNPs, respectively, in ABCB1, NR1/2, NR1/3 and CYP3A5, involved in sunitinib pharmacokinetics as well as VEGFR1 and VEGFR3, which have been suggested as regulators of sunitinib pharmacodynamics.	Sunitinib	87-96	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	50-53
24874929-4	2014	We genotyped 11 key SNPs, respectively, in ABCB1, NR1/2, NR1/3 and CYP3A5, involved in sunitinib pharmacokinetics as well as VEGFR1 and VEGFR3, which have been suggested as regulators of sunitinib pharmacodynamics.	Sunitinib	87-96	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	67-73
24874929-4	2014	We genotyped 11 key SNPs, respectively, in ABCB1, NR1/2, NR1/3 and CYP3A5, involved in sunitinib pharmacokinetics as well as VEGFR1 and VEGFR3, which have been suggested as regulators of sunitinib pharmacodynamics.	Sunitinib	187-196	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	67-73
25639617-0	2015	Refractory angiosarcoma of the breast with VEGFR2 upregulation successfully treated with sunitinib.	Sunitinib	89-98	kinase insert domain receptor	Homo sapiens	43-49
34826699-2	2022	As interleukin-6 (IL-6) is overexpressed in sunitinib-resistant cells, the purpose of this study was to explore the potential of IL-6 inhibition with tocilizumab, an IL-6 receptor inhibitor, to overcome resistance.	Sunitinib	44-53	interleukin 6	Mus musculus	3-16
34826699-2	2022	As interleukin-6 (IL-6) is overexpressed in sunitinib-resistant cells, the purpose of this study was to explore the potential of IL-6 inhibition with tocilizumab, an IL-6 receptor inhibitor, to overcome resistance.	Sunitinib	44-53	interleukin 6	Mus musculus	18-22
34826699-2	2022	As interleukin-6 (IL-6) is overexpressed in sunitinib-resistant cells, the purpose of this study was to explore the potential of IL-6 inhibition with tocilizumab, an IL-6 receptor inhibitor, to overcome resistance.	Sunitinib	44-53	interleukin 6	Mus musculus	129-133
34826699-7	2022	In vitro, tocilizumab induced significant cell death, and reduced the expression of IL-6, VEGF, and Bcl-2 in sunitinib-resistant cells.	Sunitinib	109-118	interleukin 6	Mus musculus	84-88
34826699-7	2022	In vitro, tocilizumab induced significant cell death, and reduced the expression of IL-6, VEGF, and Bcl-2 in sunitinib-resistant cells.	Sunitinib	109-118	vascular endothelial growth factor A	Mus musculus	90-94
34826699-7	2022	In vitro, tocilizumab induced significant cell death, and reduced the expression of IL-6, VEGF, and Bcl-2 in sunitinib-resistant cells.	Sunitinib	109-118	B cell leukemia/lymphoma 2	Mus musculus	100-105
34868230-9	2021	Finally, drugs including arsenic trioxide, cisplatin, Jinfukang, and sunitinib were mined for the treatment of the eight hub genes.	Sunitinib	69-78	ELAV like RNA binding protein 2	Homo sapiens	121-124
34158245-2	2022	We hypothesized that adding sunitinib, a tyrosine kinase inhibitor with antitumor and antiangiogenic activity, to an anthracycline and taxane regimen would improve pathologic complete response (pCR) rates to a prespecified endpoint of 45% in patients with HER2-negative LABC or IBC.	Sunitinib	28-37	erb-b2 receptor tyrosine kinase 2	Homo sapiens	256-260
34158245-3	2022	METHODS: We conducted a multicenter, phase II trial of neoadjuvant sunitinib with paclitaxel (S+T) followed by doxorubicin and cyclophosphamide plus G-CSF for patients with HER2-negative LABC or IBC.	Sunitinib	67-76	erb-b2 receptor tyrosine kinase 2	Homo sapiens	173-177
34158245-14	2022	The addition of sunitinib to neoadjuvant chemotherapy may provide promising incremental benefit for patients with ER positive LABC.	Sunitinib	16-25	estrogen receptor 1	Homo sapiens	114-116
34626691-0	2021	Circular RNA circSNX6 promotes sunitinib resistance in renal cell carcinoma through the miR-1184/GPCPD1/ lysophosphatidic acid axis.	Sunitinib	31-40	microRNA 1184-1	Homo sapiens	88-96
34626691-7	2021	circSNX6 acts as a molecular "sponge" to relieve the suppressive effect of microRNA (miR)-1184 on its target gene, glycerophosphocholine phosphodiesterase 1 (GPCPD1), which increases intracellular lysophosphatidic acid (LPA) levels and, ultimately, promotes sunitinib resistance in RCC cells.	Sunitinib	258-267	microRNA 1184-1	Homo sapiens	75-94
34626691-7	2021	circSNX6 acts as a molecular "sponge" to relieve the suppressive effect of microRNA (miR)-1184 on its target gene, glycerophosphocholine phosphodiesterase 1 (GPCPD1), which increases intracellular lysophosphatidic acid (LPA) levels and, ultimately, promotes sunitinib resistance in RCC cells.	Sunitinib	258-267	glycerophosphocholine phosphodiesterase 1	Homo sapiens	115-156
34626691-7	2021	circSNX6 acts as a molecular "sponge" to relieve the suppressive effect of microRNA (miR)-1184 on its target gene, glycerophosphocholine phosphodiesterase 1 (GPCPD1), which increases intracellular lysophosphatidic acid (LPA) levels and, ultimately, promotes sunitinib resistance in RCC cells.	Sunitinib	258-267	glycerophosphocholine phosphodiesterase 1	Homo sapiens	158-164
34626691-8	2021	Our findings demonstrated that the circSNX6/miR-1184/GPCPD1 axis had a critical role in regulation of intracellular LPA levels and sunitinib resistance in RCC; they also provide a novel prognostic indicator and promising therapeutic targets.	Sunitinib	131-140	microRNA 1184-1	Homo sapiens	44-52
34626691-8	2021	Our findings demonstrated that the circSNX6/miR-1184/GPCPD1 axis had a critical role in regulation of intracellular LPA levels and sunitinib resistance in RCC; they also provide a novel prognostic indicator and promising therapeutic targets.	Sunitinib	131-140	glycerophosphocholine phosphodiesterase 1	Homo sapiens	53-59
34875133-12	2022	Interestingly, the PDGFRA protein fusions can be targeted by tyrosine kinase inhibitors such as imatinib, sunitinib and sorafenib.	Sunitinib	106-115	platelet derived growth factor receptor alpha	Homo sapiens	19-25
34838486-3	2022	Vascular Endothelial Growth Factor inhibitors have different mechanisms of action, targeting either the ligand (e.g. bevacizumab, anti-Vascular Endothelial Growth Factor monoclonal antibody; aflibercept, recombinant anti-Vascular Endothelial Growth Factor fusion protein), or its receptors such as tyrosine kinase inhibitors (e.g. sunitinib or sorafenib).	Sunitinib	331-340	vascular endothelial growth factor A	Homo sapiens	0-34
34461182-0	2022	Sunitinib increases the cancer stem cells and vasculogenic mimicry formation via modulating the lncRNA-ECVSR/ERbeta/Hif2-alpha signaling.	Sunitinib	0-9	estrogen receptor 1	Homo sapiens	109-115
34461182-0	2022	Sunitinib increases the cancer stem cells and vasculogenic mimicry formation via modulating the lncRNA-ECVSR/ERbeta/Hif2-alpha signaling.	Sunitinib	0-9	endothelial PAS domain protein 1	Homo sapiens	116-126
34461182-4	2022	Mechanism dissection revealed that sunitinib can increase the expression of a long non-coding RNA (lncRNA), lncRNA-ECVSR, thereby enhancing the stability of estrogen receptor beta (ERbeta) mRNA.	Sunitinib	35-44	estrogen receptor 1	Homo sapiens	157-179
34461182-4	2022	Mechanism dissection revealed that sunitinib can increase the expression of a long non-coding RNA (lncRNA), lncRNA-ECVSR, thereby enhancing the stability of estrogen receptor beta (ERbeta) mRNA.	Sunitinib	35-44	estrogen receptor 1	Homo sapiens	181-187
34461182-6	2022	Notably, sunitinib-increased lncRNA-ECVSR/ERbeta/Hif2-alpha signaling resulted in an increased cancer stem cell (CSC) phenotype, thereby promoting VM formation.	Sunitinib	9-18	estrogen receptor 1	Homo sapiens	42-48
34461182-6	2022	Notably, sunitinib-increased lncRNA-ECVSR/ERbeta/Hif2-alpha signaling resulted in an increased cancer stem cell (CSC) phenotype, thereby promoting VM formation.	Sunitinib	9-18	endothelial PAS domain protein 1	Homo sapiens	49-59
34461182-7	2022	Furthermore, the sunitinib/lncRNA-ECVSR-increased ERbeta expression can transcriptionally regulate lncRNA-ECVSR expression via a positive-feedback loop.	Sunitinib	17-26	estrogen receptor 1	Homo sapiens	50-56
34881630-0	2022	Blocking stanniocalcin 2 reduces sunitinib resistance in clear cell renal cell carcinoma.	Sunitinib	33-42	stanniocalcin 2	Homo sapiens	9-24
34881630-3	2022	In this study, we investigated the relationship between high expression of STC2 and sunitinib resistance in cells and the underlying mechanism.	Sunitinib	84-93	stanniocalcin 2	Homo sapiens	75-79
34881630-7	2022	The sunitinib resistance could be significantly reduced by STC2 neutralizing antibody but aggravated by the addition of recombinant human STC2 in ccRCC cells.	Sunitinib	4-13	stanniocalcin 2	Homo sapiens	59-63
34881630-7	2022	The sunitinib resistance could be significantly reduced by STC2 neutralizing antibody but aggravated by the addition of recombinant human STC2 in ccRCC cells.	Sunitinib	4-13	stanniocalcin 2	Homo sapiens	138-142
34881630-8	2022	Sunitinib suppressed STC2 expression and secretion, destroyed lysosomal acidic pH, and accumulated in the cells.	Sunitinib	0-9	stanniocalcin 2	Homo sapiens	21-25
34881630-9	2022	However, STC2 neutralizing antibody can reduce the accumulation of sunitinib in cells to improve the inhibitory efficiency of sunitinib on cell proliferation.	Sunitinib	67-76	stanniocalcin 2	Homo sapiens	9-13
34881630-9	2022	However, STC2 neutralizing antibody can reduce the accumulation of sunitinib in cells to improve the inhibitory efficiency of sunitinib on cell proliferation.	Sunitinib	126-135	stanniocalcin 2	Homo sapiens	9-13
34857034-0	2021	Correction to: PFKFB4 is overexpressed in clear-cell renal cell carcinoma promoting pentose phosphate pathway that mediates Sunitinib resistance.	Sunitinib	124-133	6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4	Homo sapiens	15-21
34912710-9	2021	Moreover, drug sensitivity analysis revealed that subgroup C2(SC-A) had the highest sensitivity to immunotherapy CTLA-4 blockade and the vascular endothelial growth factor receptor (VEGFR) inhibitor sunitinib.	Sunitinib	199-208	complement C2	Homo sapiens	59-66
34912710-9	2021	Moreover, drug sensitivity analysis revealed that subgroup C2(SC-A) had the highest sensitivity to immunotherapy CTLA-4 blockade and the vascular endothelial growth factor receptor (VEGFR) inhibitor sunitinib.	Sunitinib	199-208	kinase insert domain receptor	Homo sapiens	137-180
34912710-9	2021	Moreover, drug sensitivity analysis revealed that subgroup C2(SC-A) had the highest sensitivity to immunotherapy CTLA-4 blockade and the vascular endothelial growth factor receptor (VEGFR) inhibitor sunitinib.	Sunitinib	199-208	kinase insert domain receptor	Homo sapiens	182-187
34610839-9	2021	The extent of nuclear localization of YAP1 was significantly reduced after sunitinib stimulation and tended to return to normal levels after drug washout.	Sunitinib	75-84	Yes1 associated transcriptional regulator	Homo sapiens	38-42
34775465-8	2021	Sunitinib inhibited MamBo38HER2loss tumor growth in vivo and reduced stemness and IL6 production in vitro.	Sunitinib	0-9	interleukin 6	Homo sapiens	82-85
34669974-11	2022	In addition, the estimated sunitinib apparent oral clearance (CL/F) was significantly lower in the severe adverse effects group.	Sunitinib	27-36	crooked neck pre-mRNA splicing factor 1	Homo sapiens	62-66
34681859-12	2021	Dasatinib, fostamatinib, sunitinib, and pazopanib interfered in early collagen receptor-induced molecular-signaling compared with cabozantinib and vatalanib.	Sunitinib	25-34	integrin subunit alpha 2	Homo sapiens	70-87
34722286-2	2021	In this study, we reported a novel GNAS mutation and 1p/22q co-deletion responding to sunitinib in a patient with multiple recurrent meningiomas.	Sunitinib	86-95	GNAS complex locus	Homo sapiens	35-39
34763724-2	2021	In recent years, pneumatosis intestinalis was reported in patients undergoing cancer treatment, and some case reports exist that report that pneumatosis intestinalis occurs during administration of vascular endothelial growth factor inhibitors, such as bevacizumab and sunitinib.	Sunitinib	269-278	vascular endothelial growth factor A	Homo sapiens	198-232
34634226-0	2022	Expression of Concern: Depletion of lncRNA MALAT1 inhibited sunitinib resistance through regulating miR-362-3p-mediated G3BP1 in renal cell carcinoma.	Sunitinib	60-69	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	43-49
34634226-0	2022	Expression of Concern: Depletion of lncRNA MALAT1 inhibited sunitinib resistance through regulating miR-362-3p-mediated G3BP1 in renal cell carcinoma.	Sunitinib	60-69	G3BP stress granule assembly factor 1	Homo sapiens	120-125
34413312-5	2021	A saFRET biosensor-based high-throughput drug screening (saFRET-HTDS) assay further enables the identification of an FDA-approved cancer drug, Sunitinib, that can be repurposed to inhibit ZAP70 activity and autoimmune-disease-related T-cell activation.	Sunitinib	143-152	zeta chain of T cell receptor associated protein kinase 70	Homo sapiens	188-193
34402193-6	2021	RESULTS: We refined immature dendritic cells and central memory CD4 T cells which showed associations with sunitinib and ccRCC.	Sunitinib	107-116	CD4 molecule	Homo sapiens	64-67
34402193-7	2021	Following, five hub genes (CRYBB1, RIMBP3C, CEACAM4, HAMP, and LYL1) were identified for their strong relationships with sunitinib and immune infiltration in ccRCC.	Sunitinib	121-130	crystallin beta B1	Homo sapiens	27-33
34402193-7	2021	Following, five hub genes (CRYBB1, RIMBP3C, CEACAM4, HAMP, and LYL1) were identified for their strong relationships with sunitinib and immune infiltration in ccRCC.	Sunitinib	121-130	RIMS binding protein 3C	Homo sapiens	35-42
34402193-7	2021	Following, five hub genes (CRYBB1, RIMBP3C, CEACAM4, HAMP, and LYL1) were identified for their strong relationships with sunitinib and immune infiltration in ccRCC.	Sunitinib	121-130	CEA cell adhesion molecule 4	Homo sapiens	44-51
34402193-7	2021	Following, five hub genes (CRYBB1, RIMBP3C, CEACAM4, HAMP, and LYL1) were identified for their strong relationships with sunitinib and immune infiltration in ccRCC.	Sunitinib	121-130	hepcidin antimicrobial peptide	Homo sapiens	53-57
34402193-7	2021	Following, five hub genes (CRYBB1, RIMBP3C, CEACAM4, HAMP, and LYL1) were identified for their strong relationships with sunitinib and immune infiltration in ccRCC.	Sunitinib	121-130	LYL1 basic helix-loop-helix family member	Homo sapiens	63-67
34402193-8	2021	Further validations in external data refined CRYBB1, CEACAM4, and HAMP which play a vital role in sunitinib resistance, immune infiltrations in ccRCC, and the development and progression of ccRCC.	Sunitinib	98-107	crystallin beta B1	Homo sapiens	45-51
34402193-8	2021	Further validations in external data refined CRYBB1, CEACAM4, and HAMP which play a vital role in sunitinib resistance, immune infiltrations in ccRCC, and the development and progression of ccRCC.	Sunitinib	98-107	CEA cell adhesion molecule 4	Homo sapiens	53-60
34765076-5	2021	We found that S6 activation was more common in poor risk NC-RCC tumors and S6/Akt activation was associated with worse PFS and OS outcomes with both everolimus and sunitinib, while c-kit was commonly expressed in chromophobe tumors and associated with improved outcomes with both agents.	Sunitinib	164-173	AKT serine/threonine kinase 1	Homo sapiens	78-81
34549873-14	2021	Within the translational endpoints, pre-surgical Sunitinib significantly increased necrosis, and reduced CD31, Ki67, circulating VEGF-C, and Ktrans (measured using DCE-MRI) (all p<0.05).	Sunitinib	49-58	platelet and endothelial cell adhesion molecule 1	Homo sapiens	105-109
34549873-14	2021	Within the translational endpoints, pre-surgical Sunitinib significantly increased necrosis, and reduced CD31, Ki67, circulating VEGF-C, and Ktrans (measured using DCE-MRI) (all p<0.05).	Sunitinib	49-58	vascular endothelial growth factor C	Homo sapiens	129-135
34545713-8	2021	RESULTS: Four kinase inhibitors (lapatinib, PD169316, sunitinib, gefitinib) significantly increased ALA-PpIX fluorescence and PDT response in TNBC cells with ABCG2 activity, but not in MCF10A nontumor breast epithelial cell line without ABCG2 activity.	Sunitinib	54-63	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	158-163
34236401-2	2021	KIT inhibitors commonly used to treat GIST (eg, imatinib and sunitinib) are inactive-state (type II) inhibitors.	Sunitinib	61-70	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
34216806-5	2021	RESULTS: Our study showed that treatment with sunitinib and photoirradiation at 8 mW/cm2 for 30 min resulted in the production intracellular reactive oxygen species (ROS), which is indicated by the increase in mRNA expression levels of PAI-1, NF-kappabeta, and Caspase-3.	Sunitinib	46-55	serpin family E member 1	Homo sapiens	236-241
34216806-5	2021	RESULTS: Our study showed that treatment with sunitinib and photoirradiation at 8 mW/cm2 for 30 min resulted in the production intracellular reactive oxygen species (ROS), which is indicated by the increase in mRNA expression levels of PAI-1, NF-kappabeta, and Caspase-3.	Sunitinib	46-55	nuclear factor kappa B subunit 1	Homo sapiens	243-255
34216806-5	2021	RESULTS: Our study showed that treatment with sunitinib and photoirradiation at 8 mW/cm2 for 30 min resulted in the production intracellular reactive oxygen species (ROS), which is indicated by the increase in mRNA expression levels of PAI-1, NF-kappabeta, and Caspase-3.	Sunitinib	46-55	caspase 3	Homo sapiens	261-270
34503211-7	2021	The immunotherapy target PD-L1 was consistently up-regulated in resistant cells, and we demonstrated that the silencing of this gene resulted in an increase in sensitivity to sunitinib treatment only in 786-O-resistant cells, suggesting that some ccRCC patients might benefit from combination therapy with PD-L1 checkpoint inhibitors.	Sunitinib	175-184	CD274 molecule	Homo sapiens	25-30
34593435-0	2021	CD44 Is Involved in Sunitinib Resistance and Poor Progression-free Survival After Sunitinib Treatment of Renal Cell Carcinoma.	Sunitinib	20-29	CD44 molecule (Indian blood group)	Homo sapiens	0-4
34593435-0	2021	CD44 Is Involved in Sunitinib Resistance and Poor Progression-free Survival After Sunitinib Treatment of Renal Cell Carcinoma.	Sunitinib	82-91	CD44 molecule (Indian blood group)	Homo sapiens	0-4
34593435-2	2021	This study aimed to examine the role of CD44 in sunitinib resistance and as a predictive marker in mRCC.	Sunitinib	48-57	CD44 molecule (Indian blood group)	Homo sapiens	40-44
34593435-3	2021	MATERIALS AND METHODS: We analyzed the effect of CD44 knockdown on sunitinib resistance in RCC cell lines using WST-1 assays.	Sunitinib	67-76	CD44 molecule (Indian blood group)	Homo sapiens	49-53
34593435-4	2021	CD44 expression in mRCC patients treated with first-line sunitinib was determined by immunohistochemistry.	Sunitinib	57-66	CD44 molecule (Indian blood group)	Homo sapiens	0-4
34593435-6	2021	RESULTS: CD44 knockdown increased sensitivity to sunitinib.	Sunitinib	49-58	CD44 molecule (Indian blood group)	Homo sapiens	9-13
34593435-8	2021	CD44-positive cases were associated with poor progression-free survival (PFS) after first-line sunitinib treatment.	Sunitinib	95-104	CD44 molecule (Indian blood group)	Homo sapiens	0-4
34593435-9	2021	In the JAVELIN 101 study, high CD44 expression was significantly associated with poor PFS after sunitinib but not after avelumab + axitinib therapy.	Sunitinib	96-105	CD44 molecule (Indian blood group)	Homo sapiens	31-35
34593435-10	2021	CONCLUSION: CD44 is involved in sunitinib resistance and may be a promising marker for sunitinib treatment in mRCC.	Sunitinib	32-41	CD44 molecule (Indian blood group)	Homo sapiens	12-16
34593435-10	2021	CONCLUSION: CD44 is involved in sunitinib resistance and may be a promising marker for sunitinib treatment in mRCC.	Sunitinib	87-96	CD44 molecule (Indian blood group)	Homo sapiens	12-16
34402193-8	2021	Further validations in external data refined CRYBB1, CEACAM4, and HAMP which play a vital role in sunitinib resistance, immune infiltrations in ccRCC, and the development and progression of ccRCC.	Sunitinib	98-107	hepcidin antimicrobial peptide	Homo sapiens	66-70
34593007-0	2021	PFKFB4 is overexpressed in clear-cell renal cell carcinoma promoting pentose phosphate pathway that mediates Sunitinib resistance.	Sunitinib	109-118	6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4	Mus musculus	0-6
34593007-11	2021	PFKFB4-knockdown overcame resistance to Sunitinib in vitro and in vivo both in xenograft and tail-vein injection murine models.	Sunitinib	40-49	6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4	Mus musculus	0-6
34593007-13	2021	Targeting PFKFB4 held promise to combat resistance to Sunitinib.	Sunitinib	54-63	6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4	Mus musculus	10-16
34568318-5	2021	We found that the MEK inhibitor trametinib and the multi-target tyrosine kinase inhibitor sunitinib exquisitely increased apoptotic priming in an NRAS-mutant and in a KMT2A-rearranged cell line presenting a high expression of FLT3, respectively.	Sunitinib	90-99	NRAS proto-oncogene, GTPase	Homo sapiens	146-150
34568318-5	2021	We found that the MEK inhibitor trametinib and the multi-target tyrosine kinase inhibitor sunitinib exquisitely increased apoptotic priming in an NRAS-mutant and in a KMT2A-rearranged cell line presenting a high expression of FLT3, respectively.	Sunitinib	90-99	lysine methyltransferase 2A	Homo sapiens	167-172
34568318-5	2021	We found that the MEK inhibitor trametinib and the multi-target tyrosine kinase inhibitor sunitinib exquisitely increased apoptotic priming in an NRAS-mutant and in a KMT2A-rearranged cell line presenting a high expression of FLT3, respectively.	Sunitinib	90-99	fms related receptor tyrosine kinase 3	Homo sapiens	226-230
34568318-10	2021	Similar observations were made in BCP-ALL KMT2A-rearranged PDX cells in response to sunitinib, showing an analogous DBP profile to the SEM cell line.	Sunitinib	84-93	lysine methyltransferase 2A	Homo sapiens	42-47
34572331-0	2021	Transgelin Contributes to a Poor Response of Metastatic Renal Cell Carcinoma to Sunitinib Treatment.	Sunitinib	80-89	transgelin	Homo sapiens	0-10
34572331-9	2021	Our data indicate that transgelin is an essential protein supporting RCC cell proliferation, which could contribute to intrinsic sunitinib resistance.	Sunitinib	129-138	transgelin	Homo sapiens	23-33
34319001-0	2021	RRM2 Regulates Sensitivity to Sunitinib and PD-1 Blockade in Renal Cancer by Stabilizing ANXA1 and Activating the AKT Pathway.	Sunitinib	30-39	ribonucleotide reductase regulatory subunit M2	Homo sapiens	0-4
34319001-8	2021	In this study, the authors have demonstrated that RRM2 is upregulated in sunitinib-resistant RCC cells and patient tissues.	Sunitinib	73-82	ribonucleotide reductase regulatory subunit M2	Homo sapiens	50-54
34319001-9	2021	They also find that RRM2 stabilizes ANXA1 and activates the AKT pathway independent of its ribonucleotide reductase activity, promoting sunitinib resistance in RCC.	Sunitinib	136-145	ribonucleotide reductase regulatory subunit M2	Homo sapiens	20-24
34475048-0	2021	P53 Is Involved in Sunitinib Resistance and Poor Progression-free Survival After Sunitinib Treatment of Renal Cell Carcinoma.	Sunitinib	19-28	tumor protein p53	Homo sapiens	0-3
34475048-0	2021	P53 Is Involved in Sunitinib Resistance and Poor Progression-free Survival After Sunitinib Treatment of Renal Cell Carcinoma.	Sunitinib	81-90	tumor protein p53	Homo sapiens	0-3
34475048-3	2021	MATERIALS AND METHODS: We analysed the effects of p53 knockout on sunitinib resistance.	Sunitinib	66-75	tumor protein p53	Homo sapiens	50-53
34475048-4	2021	p53 expression in 53 mRCC patients receiving first-line sunitinib was determined immunohistochemically.	Sunitinib	56-65	tumor protein p53	Homo sapiens	0-3
34475048-6	2021	RESULTS: WST-1 assays showed that p53 knockout decreased sensitivity to sunitinib.	Sunitinib	72-81	tumor protein p53	Homo sapiens	34-37
34475048-9	2021	Kaplan-Meier analysis showed that p53-positive cases tended to be associated with poor progression-free survival (PFS) after first-line sunitinib treatment.	Sunitinib	136-145	tumor protein p53	Homo sapiens	34-37
34475048-10	2021	In the JAVELIN 101 study, TP53 mutation was significantly associated with poor PFS after sunitinib treatment.	Sunitinib	89-98	tumor protein p53	Homo sapiens	26-30
34475048-11	2021	CONCLUSION: p53 may be involved in sunitinib resistance and represent a valuable marker for sunitinib treatment in mRCC.	Sunitinib	35-44	tumor protein p53	Homo sapiens	12-15
34475048-11	2021	CONCLUSION: p53 may be involved in sunitinib resistance and represent a valuable marker for sunitinib treatment in mRCC.	Sunitinib	92-101	tumor protein p53	Homo sapiens	12-15
34243074-6	2021	Kinase inhibitory properties support their multi-targeted inhibitory activities against VEGFR-2 and c-kit in similar behavior to that of Sunitinib.	Sunitinib	137-146	kinase insert domain receptor	Homo sapiens	88-95
34243074-6	2021	Kinase inhibitory properties support their multi-targeted inhibitory activities against VEGFR-2 and c-kit in similar behavior to that of Sunitinib.	Sunitinib	137-146	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	100-105
34432562-0	2021	Autophagic degradation of CCN2 (cellular communication network factor 2) causes cardiotoxicity of sunitinib.	Sunitinib	98-107	cellular communication network factor 2	Mus musculus	26-30
34432562-0	2021	Autophagic degradation of CCN2 (cellular communication network factor 2) causes cardiotoxicity of sunitinib.	Sunitinib	98-107	cellular communication network factor 2	Mus musculus	32-71
34432562-3	2021	Here, we found that sunitinib-induced autophagy leads to apoptosis of cardiomyocyte and cardiac dysfunction as the cardiomyocyte-specific Atg7-/+ heterozygous mice are resistant to sunitinib.	Sunitinib	20-29	autophagy related 7	Mus musculus	138-142
34432562-5	2021	Remarkably, deletion of Hmgb1 (high mobility group box 1) inhibited sunitinib-induced cardiomyocyte autophagy and apoptosis, and the HMGB1-specific inhibitor glycyrrhizic acid (GA) significantly mitigated sunitinib-induced autophagy, cardiomyocyte death and cardiotoxicity.	Sunitinib	68-77	high mobility group box 1	Mus musculus	24-29
34432562-6	2021	Our study reveals a novel target protein of autophagic degradation in the regulation of cardiomyocyte death and highlights the pharmacological inhibitor of HMGB1 as an attractive approach for improving the safety of sunitinib-based cancer therapy.	Sunitinib	216-225	high mobility group box 1	Mus musculus	156-161
34367125-10	2021	We found that Sunitinib significantly decreased the endometriotic lesion size and weight after 1 and 3 weeks, and decreased p-STAT3 activation in MDSCs after 1 week of treatment.	Sunitinib	14-23	signal transducer and activator of transcription 3	Homo sapiens	126-131
34363384-0	2021	Lefty A is involved in sunitinib resistance of renal cell carcinoma cells via regulation of IL-8.	Sunitinib	23-32	left-right determination factor 2	Homo sapiens	0-7
34363384-8	2021	Knockdown of IL-8 abolished Lefty-regulated sunitinib sensitivity of RCC cells.	Sunitinib	44-53	C-X-C motif chemokine ligand 8	Homo sapiens	13-17
34363384-10	2021	Collectively, our present revealed that Lefty A can regulate sunitinib sensitivity of RCC cells of via NF-kappaB/IL-8 signals.	Sunitinib	61-70	left-right determination factor 2	Homo sapiens	40-47
34363384-10	2021	Collectively, our present revealed that Lefty A can regulate sunitinib sensitivity of RCC cells of via NF-kappaB/IL-8 signals.	Sunitinib	61-70	nuclear factor kappa B subunit 1	Homo sapiens	103-112
34380680-5	2021	Cessation of sunitinib led to reduction in anti-PLA2R antibody IgG titres while resumption, due to concern for cancer progression, led to worsening symptoms.	Sunitinib	13-22	phospholipase A2 receptor 1	Homo sapiens	48-53
34367125-11	2021	In the first week, Sunitinib specifically increased the G-MDSC population in peritoneal fluid but the isolated CD11b+Ly6G+Ly6Clo MDSCs after Sunitinib treatment were presented as mature polynuclear MDSCs, while the control group had immature mononuclear MDSCs.	Sunitinib	141-150	integrin subunit alpha M	Homo sapiens	111-116
34298757-0	2021	New Target for Precision Medicine Treatment of Giant-Cell Tumor of Bone: Sunitinib Is Effective in the Treatment of Neoplastic Stromal Cells with Activated PDGFRbeta Signaling.	Sunitinib	73-82	platelet derived growth factor receptor beta	Homo sapiens	156-165
34116693-0	2021	Retraction Note to: Effects of HDM2 antagonism on sunitinib resistance, p53 activation, SDF-1 induction, and tumor infiltration by CD11b+/Gr-1+ myeloid derived suppressor cells.	Sunitinib	50-59	MDM2 proto-oncogene	Homo sapiens	31-35
34306023-0	2021	Identification of MX2 as a Novel Prognostic Biomarker for Sunitinib Resistance in Clear Cell Renal Cell Carcinoma.	Sunitinib	58-67	MX dynamin like GTPase 2	Homo sapiens	18-21
34306023-1	2021	Background: Antiangiogenic agents that specifically target vascular endothelial growth factor receptor (VEGFR), such as sunitinib, have been utilized as the standard therapy for metastatic clear cell renal cell carcinoma (ccRCC) patients.	Sunitinib	120-129	kinase insert domain receptor	Homo sapiens	59-102
34306023-1	2021	Background: Antiangiogenic agents that specifically target vascular endothelial growth factor receptor (VEGFR), such as sunitinib, have been utilized as the standard therapy for metastatic clear cell renal cell carcinoma (ccRCC) patients.	Sunitinib	120-129	kinase insert domain receptor	Homo sapiens	104-109
34306023-10	2021	Sunitinib-resistant cell lines were constructed, and loss-of-function experiments were conducted by knocking down MX2.	Sunitinib	0-9	MX dynamin like GTPase 2	Homo sapiens	114-117
34306023-12	2021	Results: A total of 760 DEGs were derived from two datasets in GEO database, and five hub genes were identified, among which high-level MX2 exhibited a pronounced correlation with poor overall survival (OS) in sunitinib-resistant ccRCC patients.	Sunitinib	210-219	MX dynamin like GTPase 2	Homo sapiens	136-139
34306023-14	2021	qRT-PCR and Western blotting revealed that MX2 was distinctly upregulated in sunitinib-resistant RCC cell lines.	Sunitinib	77-86	MX dynamin like GTPase 2	Homo sapiens	43-46
34306023-15	2021	Colony formation assay and Cell Counting Kit-8 (CCK8) assay showed that MX2 strongly promoted resistant capability to sunitinib of ccRCC cells.	Sunitinib	118-127	MX dynamin like GTPase 2	Homo sapiens	72-75
34306023-16	2021	Conclusion: MX2 is a potent indicator for sunitinib resistance and a therapeutic target in ccRCC patients.	Sunitinib	42-51	MX dynamin like GTPase 2	Homo sapiens	12-15
34220265-9	2021	However, hypermethylated seed genes HMGA1 and PSAT1 showcased a good interaction affinity with drugs cisplatin, cyclosporin, bisphenol A, progesterone, and sunitinib, and are crucial in the proliferation of ovarian cancer.	Sunitinib	156-165	high mobility group AT-hook 1	Homo sapiens	36-41
34220265-9	2021	However, hypermethylated seed genes HMGA1 and PSAT1 showcased a good interaction affinity with drugs cisplatin, cyclosporin, bisphenol A, progesterone, and sunitinib, and are crucial in the proliferation of ovarian cancer.	Sunitinib	156-165	phosphoserine aminotransferase 1	Homo sapiens	46-51
34220265-10	2021	Conclusion: Our study reveals that HMGA1 and PSAT1 can be deployed for initial screening of ovarian cancer and drugs cisplatin, bisphenol A, cyclosporin, progesterone, and sunitinib are effective in curbing the epigenetic alteration.	Sunitinib	172-181	high mobility group AT-hook 1	Homo sapiens	35-40
34220265-10	2021	Conclusion: Our study reveals that HMGA1 and PSAT1 can be deployed for initial screening of ovarian cancer and drugs cisplatin, bisphenol A, cyclosporin, progesterone, and sunitinib are effective in curbing the epigenetic alteration.	Sunitinib	172-181	phosphoserine aminotransferase 1	Homo sapiens	45-50
34221997-0	2021	Sunitinib Treatment for Advanced Paraganglioma: Case Report of a Novel SDHD Gene Mutation Variant and Systematic Review of the Literature.	Sunitinib	0-9	succinate dehydrogenase complex subunit D	Homo sapiens	71-75
34221997-4	2021	We describe the case of a man with Familial Paraganglioma Syndrome type 1 (FPGL) related to a novel mutation in SDHD gene treated with sunitinib.	Sunitinib	135-144	succinate dehydrogenase complex subunit D	Homo sapiens	112-116
34178667-0	2021	Polydatin Reduces Cardiotoxicity and Enhances the Anticancer Effects of Sunitinib by Decreasing Pro-Oxidative Stress, Pro-Inflammatory Cytokines, and NLRP3 Inflammasome Expression.	Sunitinib	72-81	NLR family pyrin domain containing 3	Homo sapiens	150-155
34853223-5	2021	We assessed 24 cases who received VEGFR-TKI monotherapy (sunitinib, sorafenib, pazopanib, axitinib) with left ventricular ejection fraction (LVEF) above 50% during the therapy at the Osaka University Hospital from January 2008 to June 2019.	Sunitinib	57-66	kinase insert domain receptor	Homo sapiens	34-39
34200459-12	2021	In conclusion, high plasma HGF, CXCL11, CXCL10 and IL-6 levels are associated with worse outcome in mRCC patients treated with sunitinib or pazopanib.	Sunitinib	127-136	hepatocyte growth factor	Homo sapiens	27-30
34200459-12	2021	In conclusion, high plasma HGF, CXCL11, CXCL10 and IL-6 levels are associated with worse outcome in mRCC patients treated with sunitinib or pazopanib.	Sunitinib	127-136	C-X-C motif chemokine ligand 11	Homo sapiens	32-38
34200459-12	2021	In conclusion, high plasma HGF, CXCL11, CXCL10 and IL-6 levels are associated with worse outcome in mRCC patients treated with sunitinib or pazopanib.	Sunitinib	127-136	C-X-C motif chemokine ligand 10	Homo sapiens	40-46
34200459-12	2021	In conclusion, high plasma HGF, CXCL11, CXCL10 and IL-6 levels are associated with worse outcome in mRCC patients treated with sunitinib or pazopanib.	Sunitinib	127-136	interleukin 6	Homo sapiens	51-55
34190510-4	2021	MATERIALS AND METHODS: We analyzed the expression levels of tumor miR-99b, -144, -155, -210, -222, -302a, -377 in 93 RCC patients who received pazopanib or sunitinib in neoadjuvant regimen using RT-PCR.	Sunitinib	156-165	microRNA 99b	Homo sapiens	66-104
34190510-8	2021	Similarly, the characteristic expression profile of miR-210, -222, -302a and -377 was suggested for sunitinib responders.	Sunitinib	100-109	microRNA 210	Homo sapiens	52-59
34121685-2	2021	This study evaluates ezrin expression in sunitinib-treated metastatic clear cell renal cell carcinoma (ccRCC) patients and elucidates its role as a possible marker for survival.	Sunitinib	41-50	ezrin	Homo sapiens	21-26
34121685-3	2021	Materials and Methods: The expression of ezrin was measured by immunohistochemistry in 80 patients with ccRCC treated by first-line sunitinib between January 2007 and June 2012.	Sunitinib	132-141	ezrin	Homo sapiens	41-46
34473615-6	2021	RESULTS: Imatinib exhibited the strongest inhibitory effect towards CYP3A, while the inhibitory potential of gefitinib and sunitinib were comparable to each other but weaker than imatinib.	Sunitinib	123-132	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	68-73
34473615-12	2021	Therefore, caution should be taken when CYP3A-metabolizing drugs are co-administrated with imatinib, sunitinib, or gefitinib.	Sunitinib	101-110	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	40-45
34285770-10	2021	While Sunitinib has already been known to inhibit LRRK2, Crizotinib is a novel LRRK2 binder.	Sunitinib	6-15	leucine rich repeat kinase 2	Homo sapiens	50-55
35500680-2	2022	Systemic chemotherapy such as cisplatin and multi-targeted receptor tyrosine kinase inhibitors, including sunitinib, has marginal activity and frequent toxicity.	Sunitinib	106-115	ret proto-oncogene	Homo sapiens	59-83
35500680-9	2022	Low concentrations of 4 mug/ml cisplatin and 2.8 mug/ml sunitinib showed significant Bcl-2 down-regulation and Bax up-regulation.	Sunitinib	56-65	BCL2 apoptosis regulator	Homo sapiens	85-90
35443205-0	2022	Pharmacological PDGFRbeta inhibitors imatinib and sunitinib cause human brain pericyte death in vitro.	Sunitinib	50-59	platelet derived growth factor receptor beta	Homo sapiens	16-25
35500680-9	2022	Low concentrations of 4 mug/ml cisplatin and 2.8 mug/ml sunitinib showed significant Bcl-2 down-regulation and Bax up-regulation.	Sunitinib	56-65	BCL2 associated X, apoptosis regulator	Homo sapiens	111-114
35358627-1	2022	The efficacy/safety of combining palbociclib (a CDK4/6 inhibitor) and sunitinib (a multi-targeted receptor tyrosine kinase inhibitor) was evaluated, using patient-derived xenograft (PDX) models.	Sunitinib	70-79	ret proto-oncogene	Homo sapiens	98-122
35266920-1	2022	ABSTRACT: Sunitinib is associated with cardiotoxicity through inhibition of AMP-protein kinase (AMPK) signalling.	Sunitinib	10-19	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	76-94
35266920-1	2022	ABSTRACT: Sunitinib is associated with cardiotoxicity through inhibition of AMP-protein kinase (AMPK) signalling.	Sunitinib	10-19	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	96-100
35266920-11	2022	The MTT assay demonstrated an increase in the EC50-value during co-administration of metformin with sunitinib compared to sunitinib mono-therapy in HepG2 and HL-60 cell lines, demonstrating the impact and complexity of metformin co-administration and the possible role of AMPK signalling.	Sunitinib	100-109	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	272-276
35443205-7	2022	Imatinib and sunitinib, but not orantinib, inhibited PDGFRbeta phosphorylation in pericytes.	Sunitinib	13-22	platelet derived growth factor receptor beta	Homo sapiens	53-62
35585158-1	2022	Although KIT-mutant GISTs can be effectively treated with tyrosine kinase inhibitors (TKIs), many patients develop resistance to imatinib mesylate (IM) as well as the FDA-approved later-line agents sunitinib, regorafenib and ripretinib.	Sunitinib	198-207	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	9-12
35623140-3	2022	Docking studies in the active site of CDK2, one of the key checkpoints enzymes, revealed that the binding scores of the designed molecules are comparable to the reference enzyme"s inhibitors Sunitinib, Nintedanib, and Semaxanib.	Sunitinib	191-200	cyclin dependent kinase 2	Homo sapiens	38-42
35538475-0	2022	N6-methyladenosine-modified TRAF1 promotes sunitinib resistance by regulating apoptosis and angiogenesis in a METTL14-dependent manner in renal cell carcinoma.	Sunitinib	43-52	TNF receptor associated factor 1	Homo sapiens	28-33
35562668-0	2022	RNF7 inhibits apoptosis and sunitinib sensitivity and promotes glycolysis in renal cell carcinoma via the SOCS1/JAK/STAT3 feedback loop.	Sunitinib	28-37	ring finger protein 7	Homo sapiens	0-4
35562668-7	2022	Moreover, RNF7 overexpression affected the sensitivity of RCC cells to sunitinib.	Sunitinib	71-80	ring finger protein 7	Homo sapiens	10-14
35562668-9	2022	CONCLUSION: These results demonstrate that RNF7 inhibited apoptosis, promoted glycolysis, and inhibited sunitinib sensitivity in RCC cells via ubiquitination of SOCS1, thus activating STAT3 signaling.	Sunitinib	104-113	ring finger protein 7	Homo sapiens	43-47
35562668-9	2022	CONCLUSION: These results demonstrate that RNF7 inhibited apoptosis, promoted glycolysis, and inhibited sunitinib sensitivity in RCC cells via ubiquitination of SOCS1, thus activating STAT3 signaling.	Sunitinib	104-113	suppressor of cytokine signaling 1	Homo sapiens	161-166
35562668-9	2022	CONCLUSION: These results demonstrate that RNF7 inhibited apoptosis, promoted glycolysis, and inhibited sunitinib sensitivity in RCC cells via ubiquitination of SOCS1, thus activating STAT3 signaling.	Sunitinib	104-113	signal transducer and activator of transcription 3	Homo sapiens	184-189
35538475-8	2022	Moreover, in vivo adeno-associated virus 9 (AAV9) -mediated transduction of TRAF1 suppressed the sunitinib-induced apoptotic and antiangiogenic effects in the CDX models, whereas knockdown of TRAF1 effectively resensitized the sunitinib-resistant CDXs to sunitinib treatment.	Sunitinib	97-106	TNF receptor associated factor 1	Homo sapiens	76-81
35538475-8	2022	Moreover, in vivo adeno-associated virus 9 (AAV9) -mediated transduction of TRAF1 suppressed the sunitinib-induced apoptotic and antiangiogenic effects in the CDX models, whereas knockdown of TRAF1 effectively resensitized the sunitinib-resistant CDXs to sunitinib treatment.	Sunitinib	97-106	TNF receptor associated factor 1	Homo sapiens	192-197
35538475-8	2022	Moreover, in vivo adeno-associated virus 9 (AAV9) -mediated transduction of TRAF1 suppressed the sunitinib-induced apoptotic and antiangiogenic effects in the CDX models, whereas knockdown of TRAF1 effectively resensitized the sunitinib-resistant CDXs to sunitinib treatment.	Sunitinib	227-236	TNF receptor associated factor 1	Homo sapiens	76-81
35562342-5	2022	Consequently, this axis activates VEGFA/VEGFR2 signaling pathway, resulting in angiogenesis and resistance of tumor cells to sunitinib in ccRCC.	Sunitinib	125-134	vascular endothelial growth factor A	Homo sapiens	34-39
35562342-5	2022	Consequently, this axis activates VEGFA/VEGFR2 signaling pathway, resulting in angiogenesis and resistance of tumor cells to sunitinib in ccRCC.	Sunitinib	125-134	kinase insert domain receptor	Homo sapiens	40-46
35538475-8	2022	Moreover, in vivo adeno-associated virus 9 (AAV9) -mediated transduction of TRAF1 suppressed the sunitinib-induced apoptotic and antiangiogenic effects in the CDX models, whereas knockdown of TRAF1 effectively resensitized the sunitinib-resistant CDXs to sunitinib treatment.	Sunitinib	227-236	TNF receptor associated factor 1	Homo sapiens	192-197
35538475-0	2022	N6-methyladenosine-modified TRAF1 promotes sunitinib resistance by regulating apoptosis and angiogenesis in a METTL14-dependent manner in renal cell carcinoma.	Sunitinib	43-52	methyltransferase 14, N6-adenosine-methyltransferase subunit	Homo sapiens	110-117
35538475-8	2022	Moreover, in vivo adeno-associated virus 9 (AAV9) -mediated transduction of TRAF1 suppressed the sunitinib-induced apoptotic and antiangiogenic effects in the CDX models, whereas knockdown of TRAF1 effectively resensitized the sunitinib-resistant CDXs to sunitinib treatment.	Sunitinib	255-264	TNF receptor associated factor 1	Homo sapiens	76-81
35538475-8	2022	Moreover, in vivo adeno-associated virus 9 (AAV9) -mediated transduction of TRAF1 suppressed the sunitinib-induced apoptotic and antiangiogenic effects in the CDX models, whereas knockdown of TRAF1 effectively resensitized the sunitinib-resistant CDXs to sunitinib treatment.	Sunitinib	255-264	TNF receptor associated factor 1	Homo sapiens	192-197
35538475-5	2022	RESULTS: We identified a tumor necrosis factor receptor-associated factor, TRAF1, that was significantly increased in sunitinib-resistant cells, resistant cell-derived xenograft (CDX-R) models and clinical patients with sunitinib resistance.	Sunitinib	118-127	TNF receptor associated factor 1	Homo sapiens	75-80
35538475-9	2022	CONCLUSIONS: Overexpression of TRAF1 promotes sunitinib resistance by modulating apoptotic and angiogenic pathways in a METTL14-dependent manner.	Sunitinib	46-55	TNF receptor associated factor 1	Homo sapiens	31-36
35538475-5	2022	RESULTS: We identified a tumor necrosis factor receptor-associated factor, TRAF1, that was significantly increased in sunitinib-resistant cells, resistant cell-derived xenograft (CDX-R) models and clinical patients with sunitinib resistance.	Sunitinib	220-229	TNF receptor associated factor 1	Homo sapiens	75-80
35538475-9	2022	CONCLUSIONS: Overexpression of TRAF1 promotes sunitinib resistance by modulating apoptotic and angiogenic pathways in a METTL14-dependent manner.	Sunitinib	46-55	methyltransferase 14, N6-adenosine-methyltransferase subunit	Homo sapiens	120-127
35538475-6	2022	Silencing TRAF1 increased sunitinib-induced apoptotic and antiangiogenic effects.	Sunitinib	26-35	TNF receptor associated factor 1	Homo sapiens	10-15
35538475-10	2022	Targeting TRAF1 and its pathways may be a novel pharmaceutical intervention for sunitinib-treated patients.	Sunitinib	80-89	TNF receptor associated factor 1	Homo sapiens	10-15
35538475-7	2022	Mechanistically, the upregulated level of TRAF1 in sunitinib-resistant cells was derived from increased TRAF1 RNA stability, which was caused by an increased level of N6-methyladenosine (m6A) in a METTL14-dependent manner.	Sunitinib	51-60	TNF receptor associated factor 1	Homo sapiens	42-47
35538475-7	2022	Mechanistically, the upregulated level of TRAF1 in sunitinib-resistant cells was derived from increased TRAF1 RNA stability, which was caused by an increased level of N6-methyladenosine (m6A) in a METTL14-dependent manner.	Sunitinib	51-60	TNF receptor associated factor 1	Homo sapiens	104-109
35538475-7	2022	Mechanistically, the upregulated level of TRAF1 in sunitinib-resistant cells was derived from increased TRAF1 RNA stability, which was caused by an increased level of N6-methyladenosine (m6A) in a METTL14-dependent manner.	Sunitinib	51-60	methyltransferase 14, N6-adenosine-methyltransferase subunit	Homo sapiens	197-204
35412955-0	2022	Circular RNA Eps15-homology domain-containing protein 2 induce resistance of renal cell carcinoma to sunitinib via microRNA-4731-5p/ABCF2 axis.	Sunitinib	101-110	EH domain containing 2	Homo sapiens	13-55
35476809-0	2022	Role of Sam68 in Sunitinib induced renal cell carcinoma apoptosis.	Sunitinib	17-26	KH RNA binding domain containing, signal transduction associated 1	Homo sapiens	8-13
35476809-3	2022	This article reveals that Sam68 impacts the sensitivity to sunitinib by mediating the apoptosis of RCC cells.	Sunitinib	59-68	KH RNA binding domain containing, signal transduction associated 1	Homo sapiens	26-31
35476809-4	2022	Immunohistochemical staining indicated that the Sam68 expression levels in sunitinib sensitive tumor tissues were markedly higher than those in sunitinib resistant tumor tissues.	Sunitinib	75-84	KH RNA binding domain containing, signal transduction associated 1	Homo sapiens	48-53
35476809-5	2022	Sunitinib induced RCC cell apoptosis in a concentration-dependent manner and inhibited the expression of total and phosphorylated Sam68 (p-Sam68).	Sunitinib	0-9	KH RNA binding domain containing, signal transduction associated 1	Homo sapiens	130-135
35476809-5	2022	Sunitinib induced RCC cell apoptosis in a concentration-dependent manner and inhibited the expression of total and phosphorylated Sam68 (p-Sam68).	Sunitinib	0-9	KH RNA binding domain containing, signal transduction associated 1	Homo sapiens	139-144
35476809-6	2022	Downregulation of Sam68 expression inhibited RCC cell apoptosis induced by sunitinib.	Sunitinib	75-84	KH RNA binding domain containing, signal transduction associated 1	Homo sapiens	18-23
35476809-7	2022	While upregulation of Sam68 expression could enhance apoptosis induced by sunitinib.	Sunitinib	74-83	KH RNA binding domain containing, signal transduction associated 1	Homo sapiens	22-27
35476809-8	2022	Xenograft models showed that tumors in the Sam68-knockdown group did not shrink as much as those in the control group after treatment with sunitinib for 4 weeks.	Sunitinib	139-148	KH RNA binding domain containing, signal transduction associated 1	Homo sapiens	43-48
35476809-9	2022	Together, our results suggest that Sam68 expression is associated with the sensitivity of ccRCC patients to sunitinib.	Sunitinib	108-117	KH RNA binding domain containing, signal transduction associated 1	Homo sapiens	35-40
35476809-10	2022	Sam68 may promote cell apoptosis induced by sunitinib, and the Sam68 expression level may be a biomarker for predicting sunitinib sensitivity in ccRCC patients.	Sunitinib	44-53	KH RNA binding domain containing, signal transduction associated 1	Homo sapiens	0-5
35476809-10	2022	Sam68 may promote cell apoptosis induced by sunitinib, and the Sam68 expression level may be a biomarker for predicting sunitinib sensitivity in ccRCC patients.	Sunitinib	44-53	KH RNA binding domain containing, signal transduction associated 1	Homo sapiens	63-68
35476809-10	2022	Sam68 may promote cell apoptosis induced by sunitinib, and the Sam68 expression level may be a biomarker for predicting sunitinib sensitivity in ccRCC patients.	Sunitinib	120-129	KH RNA binding domain containing, signal transduction associated 1	Homo sapiens	63-68
35216667-6	2022	Functionally, re-expressing wild-type FH or PTEN C211S phenocopies an AKT inhibitor in suppressing tumor growth and sensitizing PRCC2 to sunitinib.	Sunitinib	137-146	fumarate hydratase	Homo sapiens	38-40
35216667-6	2022	Functionally, re-expressing wild-type FH or PTEN C211S phenocopies an AKT inhibitor in suppressing tumor growth and sensitizing PRCC2 to sunitinib.	Sunitinib	137-146	phosphatase and tensin homolog	Homo sapiens	44-48
35216667-6	2022	Functionally, re-expressing wild-type FH or PTEN C211S phenocopies an AKT inhibitor in suppressing tumor growth and sensitizing PRCC2 to sunitinib.	Sunitinib	137-146	AKT serine/threonine kinase 1	Homo sapiens	70-73
35216667-8	2022	Collectively, these findings elucidate a non-metabolic, oncogenic role of fumarate in PRCC2 via direct post-translational modification of PTEN and further reveal potential stratification strategies for patients with FH loss by combinatorial AKTi and sunitinib therapy.	Sunitinib	250-259	phosphatase and tensin homolog	Homo sapiens	138-142
35629359-0	2022	Endothelial EphrinB2 Regulates Sunitinib Therapy Response in Murine Glioma.	Sunitinib	31-40	ephrin B2	Mus musculus	12-20
35290929-7	2022	Interestingly, among the identified lead molecules, compound 17 displayed remarkable VEGFR2 inhibition activity with IC50 value of 19.8 nM compared to Sunitinib (IC50 = 75 nM) and Sorafenib (IC50 = 30 nM).	Sunitinib	151-160	kinase insert domain receptor	Homo sapiens	85-91
35313079-5	2022	To validate the potential of KDR as a therapeutic target for thyroid cancers, we used the KDR RTK inhibitor sunitinib.	Sunitinib	108-117	kinase insert domain receptor	Homo sapiens	90-93
35165100-6	2022	pTyr-phosphoproteomic profiles of tumor samples from 4 sunitinib-treated versus 7 control patients revealed 108 significantly up- and 23 downregulated (p<0.05) phosphopeptides for sunitinib-treatment, resulting in an EGFR-centered signaling network.	Sunitinib	180-189	epidermal growth factor receptor	Homo sapiens	217-221
35387658-0	2022	Correction to: Sunitinib-suppressed miR-452-5p facilitates renal cancer cell invasion and metastasis through modulating SMAD4/SMAD7 signals.	Sunitinib	15-24	microRNA 452	Homo sapiens	36-43
35387658-0	2022	Correction to: Sunitinib-suppressed miR-452-5p facilitates renal cancer cell invasion and metastasis through modulating SMAD4/SMAD7 signals.	Sunitinib	15-24	SMAD family member 4	Homo sapiens	120-125
35387658-0	2022	Correction to: Sunitinib-suppressed miR-452-5p facilitates renal cancer cell invasion and metastasis through modulating SMAD4/SMAD7 signals.	Sunitinib	15-24	SMAD family member 7	Homo sapiens	126-131
35409367-0	2022	Sunitinib and Pterostilbene Combination Treatment Exerts Antitumor Effects in Gastric Cancer via Suppression of PDZD8.	Sunitinib	0-9	PDZ domain containing 8	Homo sapiens	112-117
35412955-0	2022	Circular RNA Eps15-homology domain-containing protein 2 induce resistance of renal cell carcinoma to sunitinib via microRNA-4731-5p/ABCF2 axis.	Sunitinib	101-110	ATP binding cassette subfamily F member 2	Homo sapiens	132-137
35412955-3	2022	This research assessed the role and mechanism of circular RNA circ Eps15-homology domain-containing protein 2 (EHD2) in the resistance of sunitinib (SU) to RCC.	Sunitinib	138-147	EH domain containing 2	Homo sapiens	67-109
35412955-3	2022	This research assessed the role and mechanism of circular RNA circ Eps15-homology domain-containing protein 2 (EHD2) in the resistance of sunitinib (SU) to RCC.	Sunitinib	138-147	EH domain containing 2	Homo sapiens	111-115
35412955-3	2022	This research assessed the role and mechanism of circular RNA circ Eps15-homology domain-containing protein 2 (EHD2) in the resistance of sunitinib (SU) to RCC.	Sunitinib	149-151	EH domain containing 2	Homo sapiens	67-109
35412955-3	2022	This research assessed the role and mechanism of circular RNA circ Eps15-homology domain-containing protein 2 (EHD2) in the resistance of sunitinib (SU) to RCC.	Sunitinib	149-151	EH domain containing 2	Homo sapiens	111-115
35412955-14	2022	In conclusion, circEHD2 enhances RCC resistance to SU via acting as a miR-4731-5p sponge to mediate ABCF2.	Sunitinib	51-53	microRNA 4731	Homo sapiens	70-78
35412955-14	2022	In conclusion, circEHD2 enhances RCC resistance to SU via acting as a miR-4731-5p sponge to mediate ABCF2.	Sunitinib	51-53	ATP binding cassette subfamily F member 2	Homo sapiens	100-105
35456602-7	2022	As demonstrated by the results of inhibition on multi-receptors by Sunitinib, we confirmed that SN-38/Sunitinib co-loaded micelles to be a treatment modality that could inhibit VEGF and PDGF receptors and enhance the antitumor effect of SN-38 (p < 0.05).	Sunitinib	102-111	vascular endothelial growth factor A	Homo sapiens	177-181
35370676-4	2022	Molecular dynamics (MD) simulations were performed to delve into the interaction of sunitinib and the identified compound M074-2865 with the kinase domain of HPK1.	Sunitinib	84-93	mitogen-activated protein kinase kinase kinase kinase 1	Homo sapiens	158-162
35419359-12	2022	As for therapeutic correlations, SLC1A5 was related to the efficacy of dasatinib, sunitinib, sorafenib, and imatinib but may not predict that of radiotherapy, chemotherapeutic drugs, and immune checkpoints inhibitors (ICIs).	Sunitinib	82-91	solute carrier family 1 (neutral amino acid transporter), member 5	Mus musculus	33-39
35386213-3	2022	Methods: In this systematic review and network meta-analysis, we searched PubMed, Embase, and Cochrane Library databases for randomized controlled trials (RCTs) with the time set from database establishment to December 10, 2021, using programmed death factor 1 (PD-1) inhibitors, nivolumab, and sunitinib in the treatment of mRCC.	Sunitinib	295-304	programmed cell death 1	Homo sapiens	235-260
35386213-3	2022	Methods: In this systematic review and network meta-analysis, we searched PubMed, Embase, and Cochrane Library databases for randomized controlled trials (RCTs) with the time set from database establishment to December 10, 2021, using programmed death factor 1 (PD-1) inhibitors, nivolumab, and sunitinib in the treatment of mRCC.	Sunitinib	295-304	programmed cell death 1	Homo sapiens	262-266
35406411-4	2022	We have also found evidence that sunitinib induces RCC VM formation by up-regulating ERbeta expression.	Sunitinib	33-42	estrogen receptor 1	Homo sapiens	85-91
35406411-5	2022	In this study, we further demonstrated that treatment with sunitinib, as well as axitinib, another TKI, could induce ERbeta expression in RCC cell lines.	Sunitinib	59-68	estrogen receptor 1	Homo sapiens	117-123
35318312-0	2022	Single-cell RNA-sequencing analysis reveals MYH9 promotes renal cell carcinoma development and sunitinib resistance via AKT signaling pathway.	Sunitinib	95-104	myosin heavy chain 9	Homo sapiens	44-48
35318312-0	2022	Single-cell RNA-sequencing analysis reveals MYH9 promotes renal cell carcinoma development and sunitinib resistance via AKT signaling pathway.	Sunitinib	95-104	AKT serine/threonine kinase 1	Homo sapiens	120-123
35318312-9	2022	Furthermore, MYH9/AKT axis determined the responses of ccRCC cells to sunitinib treatment and might serve as a biomarker for sunitinib benefits in ccRCC patients.	Sunitinib	70-79	myosin heavy chain 9	Homo sapiens	13-17
35318312-9	2022	Furthermore, MYH9/AKT axis determined the responses of ccRCC cells to sunitinib treatment and might serve as a biomarker for sunitinib benefits in ccRCC patients.	Sunitinib	70-79	AKT serine/threonine kinase 1	Homo sapiens	18-21
35318312-9	2022	Furthermore, MYH9/AKT axis determined the responses of ccRCC cells to sunitinib treatment and might serve as a biomarker for sunitinib benefits in ccRCC patients.	Sunitinib	125-134	myosin heavy chain 9	Homo sapiens	13-17
35318312-9	2022	Furthermore, MYH9/AKT axis determined the responses of ccRCC cells to sunitinib treatment and might serve as a biomarker for sunitinib benefits in ccRCC patients.	Sunitinib	125-134	AKT serine/threonine kinase 1	Homo sapiens	18-21
35238167-0	2022	A novel role of TCAIM: suppressing renal carcinoma growth and enhancing its sensitivity to sunitinib.	Sunitinib	91-100	T cell activation inhibitor, mitochondrial	Homo sapiens	16-21
35241735-0	2022	miR-96-5p targets PTEN to mediate sunitinib resistance in clear cell renal cell carcinoma.	Sunitinib	34-43	microRNA 96	Homo sapiens	0-6
35241735-0	2022	miR-96-5p targets PTEN to mediate sunitinib resistance in clear cell renal cell carcinoma.	Sunitinib	34-43	phosphatase and tensin homolog	Homo sapiens	18-22
35241735-4	2022	Using miRNA profiling, we identified miR-96-5p upregulation in tumors from sunitinib-resistant CCRCC patients.	Sunitinib	75-84	microRNA 96	Homo sapiens	37-43
35241735-5	2022	By bioinformatic analysis, PTEN was selected as a potential target of miR-96-5p, which showed low levels in tumors from sunitinib-resistant CCRCC patients.	Sunitinib	120-129	phosphatase and tensin homolog	Homo sapiens	27-31
35241735-5	2022	By bioinformatic analysis, PTEN was selected as a potential target of miR-96-5p, which showed low levels in tumors from sunitinib-resistant CCRCC patients.	Sunitinib	120-129	microRNA 96	Homo sapiens	70-76
35241735-7	2022	Additionally, four-week sunitinib treatment increased miR-96-5p and decreased PTEN only in tumors from a sunitinib-resistant patient-derived xenograft model.	Sunitinib	24-33	microRNA 96	Homo sapiens	54-60
35328529-0	2022	LPPR5 Expression in Glioma Affects Growth, Vascular Architecture, and Sunitinib Resistance.	Sunitinib	70-79	phospholipid phosphatase related 5	Mus musculus	0-5
35311121-17	2022	In addition, CTD database analysis identified abrine, Benzo (A) Pyrene, bisphenol A, Soman, Sunitinib, Tetrachloroethylene, Valproic Acid as seven targeted therapy drugs that may be effective treatments for seven targeted therapeutics.	Sunitinib	92-101	CTD	Homo sapiens	13-16
35238167-6	2022	Additionally, TCAIM also enhanced their sensitivity to sunitinib by aggravating apoptosis.	Sunitinib	55-64	T cell activation inhibitor, mitochondrial	Homo sapiens	14-19
35241735-7	2022	Additionally, four-week sunitinib treatment increased miR-96-5p and decreased PTEN only in tumors from a sunitinib-resistant patient-derived xenograft model.	Sunitinib	24-33	phosphatase and tensin homolog	Homo sapiens	78-82
35241735-7	2022	Additionally, four-week sunitinib treatment increased miR-96-5p and decreased PTEN only in tumors from a sunitinib-resistant patient-derived xenograft model.	Sunitinib	105-114	phosphatase and tensin homolog	Homo sapiens	78-82
35281041-0	2022	Elevated SNRPA1, as a Promising Predictor Reflecting Severe Clinical Outcome via Effecting Tumor Immunity for ccRCC, Is Related to Cell Invasion, Metastasis, and Sunitinib Sensitivity.	Sunitinib	162-171	small nuclear ribonucleoprotein polypeptide A'	Homo sapiens	9-15
35241735-9	2022	Furthermore, we demonstrated that repression of PTEN by miR-96-5p increased cell proliferation and migration in sunitinib-treated cell lines.	Sunitinib	112-121	phosphatase and tensin homolog	Homo sapiens	48-52
35241735-9	2022	Furthermore, we demonstrated that repression of PTEN by miR-96-5p increased cell proliferation and migration in sunitinib-treated cell lines.	Sunitinib	112-121	microRNA 96	Homo sapiens	56-62
35241735-10	2022	These results highlight the direct suppression of PTEN by miR-96-5p and that high miR-96-5p and low PTEN are partially responsible for sunitinib resistance and poor prognosis in CCRCC.	Sunitinib	135-144	microRNA 96	Homo sapiens	82-88
35241735-10	2022	These results highlight the direct suppression of PTEN by miR-96-5p and that high miR-96-5p and low PTEN are partially responsible for sunitinib resistance and poor prognosis in CCRCC.	Sunitinib	135-144	phosphatase and tensin homolog	Homo sapiens	100-104
35091290-12	2022	Furthermore, inhibitory activity of compounds 5a, 5b, 5e1, 5m, 6f and 6j on CDK2 enzyme were tested and revealed that compound 6f, with the N-4-flourobenzyl- 2-oxindole and 3-p-chlorobenzylidene moieties, has a comparable inhibitory activity to the reference drug sunitinib.	Sunitinib	264-273	cyclin dependent kinase 2	Homo sapiens	76-80
35281041-6	2022	The knockout expression of SNRPA by sgRNA plasmid inhibited the cell proliferation, migration, and metastasis ability and significantly increased the sensitivity of sunitinib treatment.	Sunitinib	165-174	small nuclear ribonucleoprotein polypeptide A	Homo sapiens	27-32
35155225-8	2022	Crizotinib and sunitinib induced apoptosis via the mitochondrial pathway, which was characterized by decreasing Bcl2/Bax ratio to dissipate the mitochondrial membrane potential, and increasing apoptotic markers levels.	Sunitinib	15-24	BCL2 apoptosis regulator	Homo sapiens	112-116
35157045-0	2022	Sunitinib inhibits STAT3 phosphorylation in cardiac muscle and prevents cardiomyopathy in the mdx mouse model of Duchenne muscular dystrophy.	Sunitinib	0-9	signal transducer and activator of transcription 3	Mus musculus	19-24
35157045-8	2022	Recently, we have shown that a Food and Drug Administration (FDA)-approved small molecule, sunitinib, a multi-targeted tyrosine kinase inhibitor can mitigate skeletal muscle disease through an increase in myogenic capacity, cell membrane integrity, and improvement of skeletal muscle function via regulation of STAT3-related signaling pathway.	Sunitinib	91-100	signal transducer and activator of transcription 3	Homo sapiens	311-316
35157045-11	2022	Our results showed sunitinib treatment reduced STAT3 phosphorylation in the heart muscle of mdx mice, improved cardiac electrical function, increased cardiac output and stroke volume, decreased ventricular hypertrophy, reduced cardiomyocytes membrane damage, fibrotic tissue deposition, and slightly decreased cardiac inflammation.	Sunitinib	19-28	signal transducer and activator of transcription 3	Mus musculus	47-52
35123514-13	2022	The gene-drug interaction network stated that CENPF inhibitors, such as Cisplatin, Sunitinib, and Etoposide, might serve as potential drugs for the therapy of ACC.	Sunitinib	83-92	centromere protein F	Homo sapiens	46-51
34974812-4	2022	In the present study, Sunitinib and Everolimus treatment, respectively, downregulated nc886 expression in a dose-dependent manner in all four renal cancer cell lines.	Sunitinib	22-31	vault RNA 2-1	Homo sapiens	86-91
34974812-5	2022	Nc886 overexpression in 786-O cells and ACHN cells significantly reduced the sensitivity of cancer cells to both Sunitinib and Everolimus treatment, respectively, by promoting cell viability and inhibiting cell apoptosis, whereas nc886 silencing increased cancer cell sensitivity.	Sunitinib	113-122	vault RNA 2-1	Homo sapiens	0-5
34974812-6	2022	In renal cancer cell line with the highest drug-resistance, 786-O cells, Sunitinib, or Everolimus treatment enhanced the cellular EMT and was further enhanced by nc886 overexpression while attenuated by nc886 silencing.	Sunitinib	73-82	IL2 inducible T cell kinase	Homo sapiens	130-133
34974812-6	2022	In renal cancer cell line with the highest drug-resistance, 786-O cells, Sunitinib, or Everolimus treatment enhanced the cellular EMT and was further enhanced by nc886 overexpression while attenuated by nc886 silencing.	Sunitinib	73-82	vault RNA 2-1	Homo sapiens	162-167
34974812-7	2022	In 786-O cells, nc886 overexpression significantly promoted EMT, ROCK2 phosphorylation, and beta-catenin nucleus translocation under Sunitinib or Everolimus treatment.	Sunitinib	133-142	vault RNA 2-1	Homo sapiens	16-21
34974812-7	2022	In 786-O cells, nc886 overexpression significantly promoted EMT, ROCK2 phosphorylation, and beta-catenin nucleus translocation under Sunitinib or Everolimus treatment.	Sunitinib	133-142	catenin beta 1	Homo sapiens	92-104
34974812-10	2022	nc886 also promotes renal cancer cell drug-resistance to Sunitinib or Everolimus by promoting EMT through Rock2 phosphorylation-mediated nuclear translocation of beta-catenin.	Sunitinib	57-66	vault RNA 2-1	Homo sapiens	0-5
34974812-10	2022	nc886 also promotes renal cancer cell drug-resistance to Sunitinib or Everolimus by promoting EMT through Rock2 phosphorylation-mediated nuclear translocation of beta-catenin.	Sunitinib	57-66	IL2 inducible T cell kinase	Homo sapiens	94-97
34974812-10	2022	nc886 also promotes renal cancer cell drug-resistance to Sunitinib or Everolimus by promoting EMT through Rock2 phosphorylation-mediated nuclear translocation of beta-catenin.	Sunitinib	57-66	catenin beta 1	Homo sapiens	162-174
35209964-8	2022	In the supernatant of FLC-4 cells with sunitinib, the heat shock protein (HSP) 90 was significantly increased.	Sunitinib	39-48	heat shock protein 90 alpha family class A member 1	Homo sapiens	54-81
35155225-8	2022	Crizotinib and sunitinib induced apoptosis via the mitochondrial pathway, which was characterized by decreasing Bcl2/Bax ratio to dissipate the mitochondrial membrane potential, and increasing apoptotic markers levels.	Sunitinib	15-24	BCL2 associated X, apoptosis regulator	Homo sapiens	117-120
35155225-10	2022	Taken together, this study demonstrated that crizotinib- and sunitinib-caused oxidative stress and apoptosis finally impaired hepatic function, which was strongly supported by the histopathological lesions and markedly increased levels of serum alanine aminotransferase, alkaline phosphatase and lactate dehydrogenase.	Sunitinib	61-70	glutamic--pyruvic transaminase	Homo sapiens	245-269
35066605-0	2022	The multitargeted receptor tyrosine kinase inhibitor sunitinib induces resistance of HER2 positive breast cancer cells to trastuzumab-mediated ADCC.	Sunitinib	53-62	erb-b2 receptor tyrosine kinase 2	Homo sapiens	85-89
35153769-4	2021	Our screening revealed that both the bromodomain and extra-terminal domain (BET) inhibitor, I-BET151, and kinase inhibitor, sunitinib, decreased the BCL-2 family protein expression and significantly synergized with venetoclax, enhancing KMT2A-r AML cell line death.	Sunitinib	124-133	BCL2 apoptosis regulator	Homo sapiens	149-154
35153769-4	2021	Our screening revealed that both the bromodomain and extra-terminal domain (BET) inhibitor, I-BET151, and kinase inhibitor, sunitinib, decreased the BCL-2 family protein expression and significantly synergized with venetoclax, enhancing KMT2A-r AML cell line death.	Sunitinib	124-133	lysine methyltransferase 2A	Homo sapiens	237-242
35066605-7	2022	Moreover, sunitinib induced downregulation of HER2 on the target cells" surface, changed the morphology and increased adherence of the target cells.	Sunitinib	10-19	erb-b2 receptor tyrosine kinase 2	Homo sapiens	46-50
35066605-9	2022	Sunitinib-induced ADCC resistance has been confirmed in a 3D tumor model revealing the prevention of apoptotic cell death (Annexin V staining) in JIMT-1 spheroids co-incubated with NK cells and trastuzumab.	Sunitinib	0-9	annexin A5	Homo sapiens	123-132
34983047-8	2022	In contranst, the multi-tyrosine kinase inhibitor sunitinib displays better activity in KIT-exon 9 mutant GISTs compared to others.	Sunitinib	50-59	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	88-91
35154527-0	2022	The expression of long non-coding RNA HOTAIR in advanced hepatocellular carcinoma and its prognostic correlation with sunitinib therapy.	Sunitinib	118-127	HOX transcript antisense RNA	Homo sapiens	38-44
35154527-2	2022	In addition, we also investigated the prognostic correlation between the expression level of lncRNA HOTAIR in tumour tissues and peripheral blood of patients with advanced HCC and sunitinib monotherapy.	Sunitinib	180-189	HOX transcript antisense RNA	Homo sapiens	100-106
35154527-12	2022	Cox regression analysis indicated that the expression level of lncRNA HOTAIR in tumour tissue and peripheral blood was an independent predictive factor of OS and PFS in patients with advanced HCC treated by sunitinib.	Sunitinib	207-216	HOX transcript antisense RNA	Homo sapiens	70-76
35154527-14	2022	In addition, the expression level of lncRNA HOTAIR was one of the indicators predicting the effectiveness of sunitinib therapy.	Sunitinib	109-118	HOX transcript antisense RNA	Homo sapiens	44-50