PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
33012780-1	2021	OBJECTIVE: To determine why serum ferritin and reticulocyte hemoglobin (RET-He), drawn to assess neonatal iron sufficiency, sometimes have markedly discordant results.	Iron	106-110	ret proto-oncogene	Homo sapiens	72-75
33641722-0	2021	Selpercatinib Overcomes CCDC6-RET-Mediated Resistance to Osimertinib.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	30-33
33641722-0	2021	Selpercatinib Overcomes CCDC6-RET-Mediated Resistance to Osimertinib.	osimertinib	57-68	ret proto-oncogene	Homo sapiens	30-33
33161056-0	2021	Structural basis of acquired resistance to selpercatinib and pralsetinib mediated by non-gatekeeper RET mutations.	Selpercatinib	43-56	ret proto-oncogene	Homo sapiens	100-103
33637706-1	2021	Receptor tyrosine kinase (RTK) inhibitors, such as sunitinib and sorafenib, remain the first-line drugs for the treatment of mRCC.	sunitinib	51-60	ret proto-oncogene	Homo sapiens	0-24
33637706-1	2021	Receptor tyrosine kinase (RTK) inhibitors, such as sunitinib and sorafenib, remain the first-line drugs for the treatment of mRCC.	sunitinib	51-60	ret proto-oncogene	Homo sapiens	26-29
33637706-1	2021	Receptor tyrosine kinase (RTK) inhibitors, such as sunitinib and sorafenib, remain the first-line drugs for the treatment of mRCC.	sorafenib	65-74	ret proto-oncogene	Homo sapiens	0-24
33637706-1	2021	Receptor tyrosine kinase (RTK) inhibitors, such as sunitinib and sorafenib, remain the first-line drugs for the treatment of mRCC.	sorafenib	65-74	ret proto-oncogene	Homo sapiens	26-29
33673346-0	2021	Evidence for 2-Methoxyestradiol-Mediated Inhibition of Receptor Tyrosine Kinase RON in the Management of Prostate Cancer.	2-Methoxyestradiol	13-31	ret proto-oncogene	Homo sapiens	55-79
33161056-1	2021	BACKGROUND: Selpercatinib (LOXO-292) and pralsetinib (BLU-667) are highly potent RET-selective protein tyrosine kinase inhibitors (TKIs) for treating advanced RET-altered thyroid cancers and non-small cell lung cancer (NSCLC).	Selpercatinib	12-25	ret proto-oncogene	Homo sapiens	81-84
33161056-4	2021	Selpercatinib-resistant RET mutants were identified and cross-profiled with pralsetinib in cell cultures.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	24-27
33161056-7	2021	RETG810C mutant was detected in cfDNAs of a CCDC6-RET-fusion NSCLC patient who developed acquired resistance to selpercatinib.	Selpercatinib	112-125	ret proto-oncogene	Homo sapiens	0-3
33161056-8	2021	Five RET kinase domain mutations at three non-gatekeeper residues were identified from 39 selpercatinib-resistant cell lines.	Selpercatinib	90-103	ret proto-oncogene	Homo sapiens	5-8
33161056-9	2021	All five selpercatinib-resistant RET mutants were cross-resistant to pralsetinib.	Selpercatinib	9-22	ret proto-oncogene	Homo sapiens	33-36
33161056-10	2021	X-ray crystal structures of the RET-selpercatinib and RET-pralsetinib complexes reveal that, unlike other TKIs, these two RET TKIs anchor one end in the front cleft and wrap around the gate wall to access the back cleft.	Selpercatinib	36-49	ret proto-oncogene	Homo sapiens	32-35
33161056-12	2021	Selpercatinib and pralsetinib use an unconventional mode to bind RET that avoids the interference from gatekeeper mutations but is vulnerable to non-gatekeeper mutations.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	65-68
33450337-0	2021	Homozygosity for the pathogenic RET hotspot variant p.Cys634Trp: A consanguineous family with MEN2A.	cys634trp	54-63	ret proto-oncogene	Homo sapiens	32-35
33475524-7	2021	Our study highlights the predominant role of RET somatic mutations in MTC tumorigenesis.	Mitomycin	70-73	ret proto-oncogene	Homo sapiens	45-48
33475524-9	2021	Based on these results, we can conclude that RET mutated C-cells"s growth and proliferation are more rapid than those of non-mutated cells and give origin to bigger and more aggressive MTC.	Mitomycin	185-188	ret proto-oncogene	Homo sapiens	45-48
33477006-0	2021	Rethinking treatment for RET-altered lung and thyroid cancers: selpercatinib approval by the EMA.	Selpercatinib	63-76	ret proto-oncogene	Homo sapiens	25-28
33565728-3	2021	Starting with the synthesized Room temperature Ionic Liquid (RT-IL) [nBu3 MeN][B(OMe)3 (CN)], we were able to crystallize the double salt [nBu3 MeN]2 [B(OMe)3 (CN)](CN).	Salts	133-137	ret proto-oncogene	Homo sapiens	144-158
33450337-0	2021	Homozygosity for the pathogenic RET hotspot variant p.Cys634Trp: A consanguineous family with MEN2A.	cys634trp	54-63	ret proto-oncogene	Homo sapiens	94-99
33450337-4	2021	Here we describe a consanguineous family with MEN2A that includes two children homozygous for the established pathogenic variant p.Cys634Trp.	cys634trp	131-140	ret proto-oncogene	Homo sapiens	46-51
33450337-7	2021	We present the first report of individuals homozygous for the highly activating RET p.Cys634Trp pathogenic variant and discuss disease severity and onset in this rare occurrence.	cys634trp	86-95	ret proto-oncogene	Homo sapiens	80-83
33525725-5	2021	A number of RET kinase inhibitors have been approved by the FDA for the treatment of cancer, such as cabozantinib, vandetanib, lenvatinib, and sorafenib.	cabozantinib	101-113	ret proto-oncogene	Homo sapiens	12-15
33348023-5	2021	The results from real-time PCR (qPCR) confirmed overexpression of targets of anlotinib activity, including receptor tyrosine kinase or the MPAK/PI3K-AKT pathway kinases, in LSCC tissues.	anlotinib	77-86	ret proto-oncogene	Homo sapiens	107-131
33525725-5	2021	A number of RET kinase inhibitors have been approved by the FDA for the treatment of cancer, such as cabozantinib, vandetanib, lenvatinib, and sorafenib.	vandetanib	115-125	ret proto-oncogene	Homo sapiens	12-15
33525725-5	2021	A number of RET kinase inhibitors have been approved by the FDA for the treatment of cancer, such as cabozantinib, vandetanib, lenvatinib, and sorafenib.	lenvatinib	127-137	ret proto-oncogene	Homo sapiens	12-15
33525725-5	2021	A number of RET kinase inhibitors have been approved by the FDA for the treatment of cancer, such as cabozantinib, vandetanib, lenvatinib, and sorafenib.	Sorafenib	143-152	ret proto-oncogene	Homo sapiens	12-15
33525725-8	2021	In this work, we have performed various molecular modelling studies, such as molecular docking and dynamics simulation for the most active compound of the pyrazole series as RET kinase inhibitors.	pyrazole	155-163	ret proto-oncogene	Homo sapiens	174-177
33471819-2	2021	Our study was designed to determine the effect of cabozantinib, a multi-targeted tyrosine kinase inhibitor that inhibits VEGFR2, MET and RET on SCNPC.	cabozantinib	50-62	ret proto-oncogene	Homo sapiens	137-140
33471819-6	2021	Notably, MET+/RET+ LuCaP 93 and MET-/RET- LuCaP 173.1 tumor volumes were significantly decreased with cabozantinib treatment in vivo, and this activity was independent of MET or RET expression in LuCaP 173.1.	cabozantinib	102-114	ret proto-oncogene	Homo sapiens	14-17
33471819-6	2021	Notably, MET+/RET+ LuCaP 93 and MET-/RET- LuCaP 173.1 tumor volumes were significantly decreased with cabozantinib treatment in vivo, and this activity was independent of MET or RET expression in LuCaP 173.1.	cabozantinib	102-114	ret proto-oncogene	Homo sapiens	37-40
33471819-6	2021	Notably, MET+/RET+ LuCaP 93 and MET-/RET- LuCaP 173.1 tumor volumes were significantly decreased with cabozantinib treatment in vivo, and this activity was independent of MET or RET expression in LuCaP 173.1.	cabozantinib	102-114	ret proto-oncogene	Homo sapiens	37-40
34036231-0	2021	Complete Response to Selective RET Inhibition With Selpercatinib (LOXO-292) in a Patient With RET Fusion-Positive Breast Cancer.	Selpercatinib	51-64	ret proto-oncogene	Homo sapiens	31-34
34036231-0	2021	Complete Response to Selective RET Inhibition With Selpercatinib (LOXO-292) in a Patient With RET Fusion-Positive Breast Cancer.	Selpercatinib	51-64	ret proto-oncogene	Homo sapiens	94-97
33419162-0	2021	Characterization of LDD-2633 as a Novel RET Kinase Inhibitor with Anti-Tumor Effects in Thyroid Cancer.	ldd-2633	20-28	ret proto-oncogene	Homo sapiens	40-43
33419162-7	2021	In vitro, LDD-2633 showed potent inhibition of RET kinase activity, with an IC50 of 4.42 nM.	ldd-2633	10-18	ret proto-oncogene	Homo sapiens	47-50
33419162-8	2021	The growth of TT thyroid carcinoma cells harboring an RET mutation was suppressed by LDD-2633 treatment via the proliferation suppression and the induction of apoptosis.	ldd-2633	85-93	ret proto-oncogene	Homo sapiens	54-57
33419162-9	2021	The effects of LDD-2633 on the RET signaling pathway were examined; LDD-2633 inhibited the phosphorylation of the RET protein and the downstream molecules Shc and ERK1/2.	ldd-2633	68-76	ret proto-oncogene	Homo sapiens	31-34
33419162-9	2021	The effects of LDD-2633 on the RET signaling pathway were examined; LDD-2633 inhibited the phosphorylation of the RET protein and the downstream molecules Shc and ERK1/2.	ldd-2633	68-76	ret proto-oncogene	Homo sapiens	114-117
33082208-0	2021	Overcoming MET-dependent resistance to selective RET inhibition in patients with RET fusion-positive lung cancer by combining selpercatinib with crizotinib.	Selpercatinib	126-139	ret proto-oncogene	Homo sapiens	49-52
32778510-0	2021	A Case of Resistance to Selective RET-TKI Therapy With Pleural-Genotyped MET Amplification and Response to Crizotinib.	Crizotinib	107-117	ret proto-oncogene	Homo sapiens	34-37
33082208-0	2021	Overcoming MET-dependent resistance to selective RET inhibition in patients with RET fusion-positive lung cancer by combining selpercatinib with crizotinib.	Selpercatinib	126-139	ret proto-oncogene	Homo sapiens	81-84
33082208-6	2021	RESULTS: MET amplification was identified in post-treatment biopsies in four patients with RET fusion-positive NSCLC treated with selpercatinib.	Selpercatinib	130-143	ret proto-oncogene	Homo sapiens	91-94
33082208-8	2021	We demonstrate that increased MET expression in RET fusion-positive tumor cells causes resistance to selpercatinib, and this can be overcome by combining selpercatinib with crizotinib.	Selpercatinib	101-114	ret proto-oncogene	Homo sapiens	48-51
33082208-0	2021	Overcoming MET-dependent resistance to selective RET inhibition in patients with RET fusion-positive lung cancer by combining selpercatinib with crizotinib.	Crizotinib	145-155	ret proto-oncogene	Homo sapiens	49-52
33082208-8	2021	We demonstrate that increased MET expression in RET fusion-positive tumor cells causes resistance to selpercatinib, and this can be overcome by combining selpercatinib with crizotinib.	Selpercatinib	154-167	ret proto-oncogene	Homo sapiens	48-51
33082208-8	2021	We demonstrate that increased MET expression in RET fusion-positive tumor cells causes resistance to selpercatinib, and this can be overcome by combining selpercatinib with crizotinib.	Crizotinib	173-183	ret proto-oncogene	Homo sapiens	48-51
33082208-0	2021	Overcoming MET-dependent resistance to selective RET inhibition in patients with RET fusion-positive lung cancer by combining selpercatinib with crizotinib.	Crizotinib	145-155	ret proto-oncogene	Homo sapiens	81-84
33082208-2	2021	Selpercatinib is a highly selective RET kinase inhibitor that has recently been approved by the FDA in lung and thyroid cancers with activating RET gene fusions and mutations.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	36-39
33082208-2	2021	Selpercatinib is a highly selective RET kinase inhibitor that has recently been approved by the FDA in lung and thyroid cancers with activating RET gene fusions and mutations.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	144-147
33260286-0	2021	EGFR-mutated pulmonary adenocarcinoma with concurrent PIK3CA mutation, and with acquired RET fusion and EGFR T790M mutation after afatinib therapy.	Afatinib	130-138	ret proto-oncogene	Homo sapiens	89-92
33169506-4	2021	METHODS: We report the first published case of neoadjuvant selpercatinib followed by surgery for a patient with initially unresectable, widely metastatic, RET-mutated MTC who was treated on a single patient protocol.	Selpercatinib	59-72	ret proto-oncogene	Homo sapiens	155-158
33318047-1	2020	Multi-kinase RET inhibitors, such as cabozantinib and RXDX-105, are active in lung cancer patients with RET fusions; however, the overall response rates to these two drugs are unsatisfactory compared to other targeted therapy paradigms.	cabozantinib	37-49	ret proto-oncogene	Homo sapiens	13-16
33129112-4	2021	We found that EGF and tumor growth factor alpha (TGFalpha) significantly decreased the antiproliferative activity of the RET inhibitor BLU-667 in CCDC6-RET cells and brigatinib, alectinib and crizotinib in EML4-ALK translocated cells.	alectinib	178-187	ret proto-oncogene	Homo sapiens	121-124
33011620-1	2020	A ratiometric electrochemiluminescence resonance energy transfer (ECL-RET) platform depended on novel dye BODIPY derivatives was proposed for rapid detection of lactoferrin.	4,4-difluoro-4-bora-3a,4a-diaza-s-indacene	106-112	ret proto-oncogene	Homo sapiens	70-73
33011620-2	2020	This ECL-RET platform is composed of aptamer decorated BODIPY composites and C60@BSA, in which BODIPY derivative is the ECL probe and can generate significant resonance energy transfer with K2S2O8.	potassium persulfate	190-196	ret proto-oncogene	Homo sapiens	9-12
33028660-0	2021	Heparan sulfate synthesized by Ext1 regulates receptor tyrosine kinase signaling and promotes resistance to EGFR inhibitors in GBM.	Heparitin Sulfate	0-15	ret proto-oncogene	Homo sapiens	46-70
33569315-0	2021	Phase 1/2 study of alectinib in RET-rearranged previously-treated non-small cell lung cancer (ALL-RET).	alectinib	19-28	ret proto-oncogene	Homo sapiens	32-35
33569315-0	2021	Phase 1/2 study of alectinib in RET-rearranged previously-treated non-small cell lung cancer (ALL-RET).	alectinib	19-28	ret proto-oncogene	Homo sapiens	98-101
33569315-10	2021	The primary endpoint was the objective response rate (ORR) in RET inhibitor-naive patients treated with the RD of alectinib.	alectinib	114-123	ret proto-oncogene	Homo sapiens	62-65
33569315-19	2021	Conclusions: Alectinib exerts limited activity against RET-rearranged NSCLC.	alectinib	13-22	ret proto-oncogene	Homo sapiens	55-58
33318047-1	2020	Multi-kinase RET inhibitors, such as cabozantinib and RXDX-105, are active in lung cancer patients with RET fusions; however, the overall response rates to these two drugs are unsatisfactory compared to other targeted therapy paradigms.	cabozantinib	37-49	ret proto-oncogene	Homo sapiens	104-107
33318047-1	2020	Multi-kinase RET inhibitors, such as cabozantinib and RXDX-105, are active in lung cancer patients with RET fusions; however, the overall response rates to these two drugs are unsatisfactory compared to other targeted therapy paradigms.	agerafenib	54-62	ret proto-oncogene	Homo sapiens	13-16
33318047-1	2020	Multi-kinase RET inhibitors, such as cabozantinib and RXDX-105, are active in lung cancer patients with RET fusions; however, the overall response rates to these two drugs are unsatisfactory compared to other targeted therapy paradigms.	agerafenib	54-62	ret proto-oncogene	Homo sapiens	104-107
33318047-5	2020	Using these models, we re-examined the efficacy and mechanism of action of cabozantinib and found that this RET inhibitor was effective at blocking growth of cell lines, activating caspase 3/7 and inhibiting activation of ERK and AKT.	cabozantinib	75-87	ret proto-oncogene	Homo sapiens	108-111
33007380-2	2020	RET-selective inhibitors selpercatinib (LOXO-292) and pralsetinib (BLU-667) recently demonstrated favorable antitumor activity and safety profiles in advanced RET fusion-positive NSCLC, and both have received approval by the US Food and Drug Administration for this indication.	Selpercatinib	25-38	ret proto-oncogene	Homo sapiens	0-3
33007380-2	2020	RET-selective inhibitors selpercatinib (LOXO-292) and pralsetinib (BLU-667) recently demonstrated favorable antitumor activity and safety profiles in advanced RET fusion-positive NSCLC, and both have received approval by the US Food and Drug Administration for this indication.	Selpercatinib	25-38	ret proto-oncogene	Homo sapiens	159-162
33231049-3	2020	The reticulocyte hemoglobin equivalent (RET-He) is a marker that is not altered by inflammatory conditions and directly reflects iron availability in the bone marrow.	Iron	129-133	ret proto-oncogene	Homo sapiens	40-43
32665298-5	2020	New selective RET inhibitors selpercatinib and pralsetinib are showing promising activities, improved response rates and more favorable toxicity profiles in early clinical trials.	Selpercatinib	29-42	ret proto-oncogene	Homo sapiens	14-17
33104871-4	2020	The RET-He is a cost-effective parameter for the diagnosis and monitoring of the iron supply for erythropoiesis.	Iron	81-85	ret proto-oncogene	Homo sapiens	4-7
32964492-0	2020	GDNF/RET Signaling Pathway Activation Eliminates Lewy Body Pathology in Midbrain Dopamine Neurons.	Dopamine	81-89	ret proto-oncogene	Homo sapiens	5-8
32777409-7	2020	The protein remained dimeric even after cleavage of the tag via the cysteine disulfide, as in full-length RET in the context of MEN 2A and related pathologies.	Cystine	68-86	ret proto-oncogene	Homo sapiens	128-134
32777409-7	2020	The protein remained dimeric even after cleavage of the tag via the cysteine disulfide, as in full-length RET in the context of MEN 2A and related pathologies.	Cystine	68-86	ret proto-oncogene	Homo sapiens	106-109
33175529-4	2020	The C, E-N-CNT/carbon black (C, E-N-CNT/C) demonstrates exciting oxygen reduction reaction (ORR) electrocatalysis with exceptionally low-onset potential (E0, 913 mV versus RHE) and satisfactory half-wave potential (E1/2, merely -7.3 mV shift compared with that of commercial 20% platinum/C (Pt/C)).	Carbon	15-21	ret proto-oncogene	Homo sapiens	291-295
33489819-5	2020	In 2020, the US Food and Drug Administration approved selpercatinib, a selective RET inhibitor, for adults with lung and thyroid cancers with RET rearrangements or mutations, making it the first targeted therapy to be approved for RET-altered cancers.	Selpercatinib	54-67	ret proto-oncogene	Homo sapiens	81-84
33489819-5	2020	In 2020, the US Food and Drug Administration approved selpercatinib, a selective RET inhibitor, for adults with lung and thyroid cancers with RET rearrangements or mutations, making it the first targeted therapy to be approved for RET-altered cancers.	Selpercatinib	54-67	ret proto-oncogene	Homo sapiens	142-145
33479704-6	2020	RET is the signalling receptor for a known survival factor for dopamine neurons called glial cell line-derived neurotrophic factor (GDNF).	Dopamine	63-71	ret proto-oncogene	Homo sapiens	0-3
33161982-1	2020	A signal "off-on" electrochemiluminescence resonance energy transfer (ECL-RET) sensor based on carboxylated graphene-like carbon nitride (C-g-C3N4) as donor and CuO nanoneedles as acceptor has been constructed.	carboxylated graphene	95-116	ret proto-oncogene	Homo sapiens	74-77
33324391-1	2020	The drug resistance of first-line crizotinib therapy for ROS proto-oncogene 1, receptor tyrosine kinase (ROS1) fusion non-small cell lung cancer (NSCLC) is inevitable.	Crizotinib	34-44	ret proto-oncogene	Homo sapiens	79-103
33161982-1	2020	A signal "off-on" electrochemiluminescence resonance energy transfer (ECL-RET) sensor based on carboxylated graphene-like carbon nitride (C-g-C3N4) as donor and CuO nanoneedles as acceptor has been constructed.	cyanogen	122-136	ret proto-oncogene	Homo sapiens	74-77
33161982-1	2020	A signal "off-on" electrochemiluminescence resonance energy transfer (ECL-RET) sensor based on carboxylated graphene-like carbon nitride (C-g-C3N4) as donor and CuO nanoneedles as acceptor has been constructed.	c-g-c3n4	138-146	ret proto-oncogene	Homo sapiens	74-77
32945329-5	2020	ECL resonance energy transfer (ECL-RET) occurred between ZnGa2O4/g-C3N4 and gold nanoparticle/graphene nanocomposites, resulting in an apparent decrease of the ECL signal.	znga2o4	57-64	ret proto-oncogene	Homo sapiens	35-38
33245718-9	2020	Mubritinib was originally identified as a receptor tyrosine kinase (RTK) inhibitor selective for HER2/ErbB2.	TAK-165	0-10	ret proto-oncogene	Homo sapiens	42-66
33245718-9	2020	Mubritinib was originally identified as a receptor tyrosine kinase (RTK) inhibitor selective for HER2/ErbB2.	TAK-165	0-10	ret proto-oncogene	Homo sapiens	68-71
32823007-0	2020	Pyrrolo[2,3-d]pyrimidine derivatives as inhibitors of RET: Design, synthesis and biological evaluation.	Pyrrolo(2,3-d)pyrimidine	0-24	ret proto-oncogene	Homo sapiens	54-57
32945329-5	2020	ECL resonance energy transfer (ECL-RET) occurred between ZnGa2O4/g-C3N4 and gold nanoparticle/graphene nanocomposites, resulting in an apparent decrease of the ECL signal.	Graphite	94-102	ret proto-oncogene	Homo sapiens	35-38
32228166-2	2020	Previous studies evaluated whether single nucleotide polymorphisms (SNPs) within RET (a pivotal proto-oncogene for this disease) are associated with the risk for developing sMTC, but the results are inconclusive.	smtc	173-177	ret proto-oncogene	Homo sapiens	81-84
33173309-5	2020	Conclusion: Our findings expanded the spectrum of RET arrangement types and provided the basis for this hypothesis: acquired RET rearrangement and EGFR exon20 p.T790M loss potentially serve an additional resistance mechanism to osimertinib in EGFR-mutated non-small-cell lung cancer (NSCLC).	osimertinib	228-239	ret proto-oncogene	Homo sapiens	50-53
33173309-5	2020	Conclusion: Our findings expanded the spectrum of RET arrangement types and provided the basis for this hypothesis: acquired RET rearrangement and EGFR exon20 p.T790M loss potentially serve an additional resistance mechanism to osimertinib in EGFR-mutated non-small-cell lung cancer (NSCLC).	osimertinib	228-239	ret proto-oncogene	Homo sapiens	125-128
32228166-3	2020	METHODS: In this work we evaluated the association of RET-SNPs c.74-126G>T (rs2565206), p.Gly691Ser (rs1799939, G>A), p.Leu769= (rs1800861, G>T), p.Ser836= (rs1800862, C>T), and p.Ser904= (rs1800863, C>G) (listed in the order of their chromosomal location) with sMTC.	smtc	262-266	ret proto-oncogene	Homo sapiens	54-57
33154983-0	2020	Systemic and CNS Activity of Selective RET Inhibition With Selpercatinib (LOXO-292) in a Patient With RET-Mutant Medullary Thyroid Cancer With Extensive CNS Metastases.	Selpercatinib	59-72	ret proto-oncogene	Homo sapiens	39-42
33565438-6	2020	Ret-HE mean value in anemic patients was (25.84 +- 4.23 pg) and had good correlation (P <0.001) between Ret-HE, serum iron, ferritin, transferrin, and transferin saturation in dialysis patients.	Iron	118-122	ret proto-oncogene	Homo sapiens	0-3
33154983-0	2020	Systemic and CNS Activity of Selective RET Inhibition With Selpercatinib (LOXO-292) in a Patient With RET-Mutant Medullary Thyroid Cancer With Extensive CNS Metastases.	Selpercatinib	59-72	ret proto-oncogene	Homo sapiens	102-105
33084974-2	2021	Variants are frequently located in the RET extracellular cysteine-rich region domain, mainly affecting cysteines which are replaced by an alternative amino acid, resulting in a mispaired cysteine and the generation of RET dimers.	Cysteine	57-65	ret proto-oncogene	Homo sapiens	218-221
33084974-2	2021	Variants are frequently located in the RET extracellular cysteine-rich region domain, mainly affecting cysteines which are replaced by an alternative amino acid, resulting in a mispaired cysteine and the generation of RET dimers.	Cysteine	103-112	ret proto-oncogene	Homo sapiens	39-42
33084974-0	2021	A novel germline variant in RET gene resulting in an additional cysteine in a family with familial medullary thyroid carcinoma.	Cysteine	64-72	ret proto-oncogene	Homo sapiens	28-31
33084974-2	2021	Variants are frequently located in the RET extracellular cysteine-rich region domain, mainly affecting cysteines which are replaced by an alternative amino acid, resulting in a mispaired cysteine and the generation of RET dimers.	Cysteine	103-112	ret proto-oncogene	Homo sapiens	218-221
33084974-2	2021	Variants are frequently located in the RET extracellular cysteine-rich region domain, mainly affecting cysteines which are replaced by an alternative amino acid, resulting in a mispaired cysteine and the generation of RET dimers.	Cysteine	57-65	ret proto-oncogene	Homo sapiens	39-42
33084974-2	2021	Variants are frequently located in the RET extracellular cysteine-rich region domain, mainly affecting cysteines which are replaced by an alternative amino acid, resulting in a mispaired cysteine and the generation of RET dimers.	Cysteine	103-111	ret proto-oncogene	Homo sapiens	39-42
33084974-2	2021	Variants are frequently located in the RET extracellular cysteine-rich region domain, mainly affecting cysteines which are replaced by an alternative amino acid, resulting in a mispaired cysteine and the generation of RET dimers.	Cysteine	103-111	ret proto-oncogene	Homo sapiens	218-221
33084974-3	2021	We describe a novel c.1765A > T variant of RET proto-oncogene in a family with medullary thyroid carcinoma (MTC) that predicts the creation of an additional cysteine p.(Ser589Cys) in the cysteine-rich domain.	Cysteine	157-165	ret proto-oncogene	Homo sapiens	43-46
33084974-3	2021	We describe a novel c.1765A > T variant of RET proto-oncogene in a family with medullary thyroid carcinoma (MTC) that predicts the creation of an additional cysteine p.(Ser589Cys) in the cysteine-rich domain.	Cysteine	187-195	ret proto-oncogene	Homo sapiens	43-46
33066449-3	2020	The clinical use of the RTK inhibitor imatinib has significantly improved the management of GIST patients; however, imatinib resistance remains a challenge.	Imatinib Mesylate	38-46	ret proto-oncogene	Homo sapiens	24-27
32800552-3	2020	Vandetanib is a multiple tyrosine kinase targeting vascular endothelial growth factor receptor-2 (VEGFR2), EGFR, and the rearranged during transfection (RET) proto-oncogene.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	153-156
32955244-2	2020	In addition, the detection was made depending on the self-generated hydrogen peroxide (H2O2) etching triangular silver nanoparticles (T-Ag NPs) to make ECL recovery response of the originally quenched due to ECL-RET between Ru(II) complex (donor) and T-Ag NPs (receptor).	Hydrogen Peroxide	68-85	ret proto-oncogene	Homo sapiens	212-215
32955244-2	2020	In addition, the detection was made depending on the self-generated hydrogen peroxide (H2O2) etching triangular silver nanoparticles (T-Ag NPs) to make ECL recovery response of the originally quenched due to ECL-RET between Ru(II) complex (donor) and T-Ag NPs (receptor).	Hydrogen Peroxide	87-91	ret proto-oncogene	Homo sapiens	212-215
32955244-2	2020	In addition, the detection was made depending on the self-generated hydrogen peroxide (H2O2) etching triangular silver nanoparticles (T-Ag NPs) to make ECL recovery response of the originally quenched due to ECL-RET between Ru(II) complex (donor) and T-Ag NPs (receptor).	ru(ii)	224-230	ret proto-oncogene	Homo sapiens	212-215
32987493-1	2020	BACKGROUND: Anlotinib is a newly developed small molecule multiple receptor tyrosine kinase (RTK) inhibitor that was approved for the treatment of patients with lung cancer in China.	anlotinib	12-21	ret proto-oncogene	Homo sapiens	67-91
32987493-1	2020	BACKGROUND: Anlotinib is a newly developed small molecule multiple receptor tyrosine kinase (RTK) inhibitor that was approved for the treatment of patients with lung cancer in China.	anlotinib	12-21	ret proto-oncogene	Homo sapiens	93-96
32512399-4	2020	With distinctive core-shell morphology, the as-synthesized CoFe-NC/NC shows superior OER performance with low overpotential (270 mV) than IrO2 (340 mV) at 10 mA cm-2 and nearly close ORR activity with respect to Pt/C.	cofe	59-63	ret proto-oncogene	Homo sapiens	212-216
32512399-5	2020	When fabricated as zinc-air battery application, CoFe-NC/NC shows 58 mW cm-2 higher peak power density than that of air-cathodes made of Pt/C and IrO2.	cofe	49-53	ret proto-oncogene	Homo sapiens	137-141
32816064-5	2020	Intracellular tyrosine phosphorylation in RET and recruitment of adaptor proteins to phosphotyrosines are essential for various biological functions.	Tyrosine	14-22	ret proto-oncogene	Homo sapiens	42-45
32980111-0	2020	A self-enhanced ECL-RET immunosensor for the detection of CA19-9 antigen based on Ru(bpy)2(phen-NH2)2+ - Amine-rich nitrogen-doped carbon nanodots as probe and graphene oxide grafted hyperbranched aromatic polyamide as platform.	ru(bpy)2(phen-nh2)2+ - amine	82-110	ret proto-oncogene	Homo sapiens	20-23
32980111-0	2020	A self-enhanced ECL-RET immunosensor for the detection of CA19-9 antigen based on Ru(bpy)2(phen-NH2)2+ - Amine-rich nitrogen-doped carbon nanodots as probe and graphene oxide grafted hyperbranched aromatic polyamide as platform.	Nitrogen	116-124	ret proto-oncogene	Homo sapiens	20-23
32980111-0	2020	A self-enhanced ECL-RET immunosensor for the detection of CA19-9 antigen based on Ru(bpy)2(phen-NH2)2+ - Amine-rich nitrogen-doped carbon nanodots as probe and graphene oxide grafted hyperbranched aromatic polyamide as platform.	Carbon	131-137	ret proto-oncogene	Homo sapiens	20-23
32980111-0	2020	A self-enhanced ECL-RET immunosensor for the detection of CA19-9 antigen based on Ru(bpy)2(phen-NH2)2+ - Amine-rich nitrogen-doped carbon nanodots as probe and graphene oxide grafted hyperbranched aromatic polyamide as platform.	graphene oxide	160-174	ret proto-oncogene	Homo sapiens	20-23
32980111-0	2020	A self-enhanced ECL-RET immunosensor for the detection of CA19-9 antigen based on Ru(bpy)2(phen-NH2)2+ - Amine-rich nitrogen-doped carbon nanodots as probe and graphene oxide grafted hyperbranched aromatic polyamide as platform.	aromatic polyamide	197-215	ret proto-oncogene	Homo sapiens	20-23
32980111-2	2020	In the present study, a novel self-enhanced ECL-RET of Ru(bpy)2(phen-NH2)2+ as an efficient luminophore to the MoS2 nanosheets as effective quencher was designed for CA19-9 antigen analysis.	ru(bpy)2(phen-nh2)2+	55-75	ret proto-oncogene	Homo sapiens	48-51
32556722-2	2020	RET-dependent signaling elicited by GFLs has an important role in the development, maintenance and survival of dopamine and sensory neurons.	Dopamine	111-119	ret proto-oncogene	Homo sapiens	0-3
32816064-5	2020	Intracellular tyrosine phosphorylation in RET and recruitment of adaptor proteins to phosphotyrosines are essential for various biological functions.	Phosphotyrosine	85-101	ret proto-oncogene	Homo sapiens	42-45
32870383-0	2020	GDNF/RET signaling in dopamine neurons in vivo.	Dopamine	22-30	ret proto-oncogene	Homo sapiens	5-8
32835580-0	2020	Enhanced antitumor effect of alectinib in combination with cyclin-dependent kinase 4/6 inhibitor against RET-fusion-positive non-small cell lung cancer cells.	alectinib	29-38	ret proto-oncogene	Homo sapiens	105-108
32870383-1	2020	The glial cell line-derived neurotrophic factor (GDNF) and its canonical receptor Ret can signal both in tandem and separately to exert many vital functions in the midbrain dopamine system.	Dopamine	173-181	ret proto-oncogene	Homo sapiens	82-85
32870383-2	2020	It is known that Ret has effects on maintenance, physiology, protection and regeneration in the midbrain dopamine system, with the physiological functions of GDNF still somewhat unclear.	Dopamine	105-113	ret proto-oncogene	Homo sapiens	17-20
32870383-4	2020	In this review, we discuss the current knowledge of GDNF/Ret signaling in the dopamine system in vivo as well as crosstalk with pathology-associated proteins and their signaling in mammals.	Dopamine	78-86	ret proto-oncogene	Homo sapiens	57-60
33097651-2	2020	Multikinase inhibitors such as cabozantinib, lenvatinib and vandetanib have demonstrated activity in RET-dependent malignancies, and selective RET inhibitors (Selpercatinib and Pralsetinib) are in clinical trials.	vandetanib	60-70	ret proto-oncogene	Homo sapiens	101-104
33097651-2	2020	Multikinase inhibitors such as cabozantinib, lenvatinib and vandetanib have demonstrated activity in RET-dependent malignancies, and selective RET inhibitors (Selpercatinib and Pralsetinib) are in clinical trials.	Selpercatinib	159-172	ret proto-oncogene	Homo sapiens	143-146
32948239-0	2020	Total colonic aganglionosis and cleft palate in a newborn with Janus-cysteine 618 mutation of RET proto-oncogene: a case report.	janus-cysteine	63-77	ret proto-oncogene	Homo sapiens	94-97
32948239-6	2020	We identified a paternal heterozygous germline mutation c.1852 T > C, which results in the substitution of cysteine by arginine in the RET-receptor tyrosine kinase (p.C618R mutation).	Cysteine	107-115	ret proto-oncogene	Homo sapiens	135-163
32835580-2	2020	Although small molecule agents with RET kinase inhibitory activity such as alectinib, vandetanib, and cabozantinib have been clinically evaluated in RET-fusion-positive NSCLC, an effective monotherapy regimen has not been established.	alectinib	75-84	ret proto-oncogene	Homo sapiens	36-39
32835580-2	2020	Although small molecule agents with RET kinase inhibitory activity such as alectinib, vandetanib, and cabozantinib have been clinically evaluated in RET-fusion-positive NSCLC, an effective monotherapy regimen has not been established.	cabozantinib	102-114	ret proto-oncogene	Homo sapiens	36-39
32835580-2	2020	Although small molecule agents with RET kinase inhibitory activity such as alectinib, vandetanib, and cabozantinib have been clinically evaluated in RET-fusion-positive NSCLC, an effective monotherapy regimen has not been established.	cabozantinib	102-114	ret proto-oncogene	Homo sapiens	149-152
32835580-3	2020	We explored agents to use in combination with alectinib to enhance the antitumor effect of alectinib against RET-fusion cells.	alectinib	46-55	ret proto-oncogene	Homo sapiens	109-112
32835580-3	2020	We explored agents to use in combination with alectinib to enhance the antitumor effect of alectinib against RET-fusion cells.	alectinib	91-100	ret proto-oncogene	Homo sapiens	109-112
32835580-13	2020	Combination therapy with alectinib plus the CDK4/6 inhibitor enhanced the antitumor effect against RET-fusion-positive cells in vitro and in vivo.	alectinib	25-34	ret proto-oncogene	Homo sapiens	99-102
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
32882995-5	2020	Alectinib is known as an ALK inhibitor but also targets LTK, CHEK2, FLT3, PHKG2, and RET.	alectinib	0-9	ret proto-oncogene	Homo sapiens	85-88
32882995-6	2020	Sorafenib is a tyrosine kinase inhibitor that targets RAF kinase, KIT, VEGFR, PDGFR1beta, FLT3, and RET.	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	100-103
32143967-0	2020	Association Between RET Fusions and Efficacy of Pemetrexed-based Chemotherapy for Patients With Advanced NSCLC in China: A Multicenter Retrospective Study.	Pemetrexed	48-58	ret proto-oncogene	Homo sapiens	20-23
32143967-2	2020	We compared the efficacy of pemetrexed-based chemotherapy with other chemotherapy regimens in patients with NSCLC with different RET fusion subtypes.	Pemetrexed	28-38	ret proto-oncogene	Homo sapiens	129-132
32143967-15	2020	The overall survival of the patients with RET-rearranged NSCLC who had received pemetrexed-based chemotherapy versus no pemetrexed-based chemotherapy was 35.2 versus 22.6 months (P = .052).	Pemetrexed	80-90	ret proto-oncogene	Homo sapiens	42-45
32143967-17	2020	CONCLUSIONS: Pemetrexed-based treatment should be considered first when selecting the chemotherapy regimen for patients with NSCLC and RET rearrangements.	Pemetrexed	13-23	ret proto-oncogene	Homo sapiens	135-138
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
32817132-1	2020	BACKGROUND: Lenvatinib inhibits tyrosine kinases, including vascular endothelial growth factor (VEGF) receptor, fibroblast growth factor receptor, platelet-derived growth factor receptor alpha, RET proto-oncogene and KIT proto-oncogene, receptor tyrosine kinase.	lenvatinib	12-22	ret proto-oncogene	Homo sapiens	194-197
32846060-0	2020	Efficacy of Selpercatinib in RET Fusion-Positive Non-Small-Cell Lung Cancer.	Selpercatinib	12-25	ret proto-oncogene	Homo sapiens	29-32
32846060-6	2020	RESULTS: In the first 105 consecutively enrolled patients with RET fusion-positive NSCLC who had previously received at least platinum-based chemotherapy, the percentage with an objective response was 64% (95% confidence interval [CI], 54 to 73).	Platinum	126-134	ret proto-oncogene	Homo sapiens	63-66
32846060-12	2020	CONCLUSIONS: Selpercatinib had durable efficacy, including intracranial activity, with mainly low-grade toxic effects in patients with RET fusion-positive NSCLC who had previously received platinum-based chemotherapy and those who were previously untreated.	Selpercatinib	13-26	ret proto-oncogene	Homo sapiens	135-138
32846061-6	2020	RESULTS: In the first 55 consecutively enrolled patients with RET-mutant medullary thyroid cancer who had previously received vandetanib, cabozantinib, or both, the percentage who had a response was 69% (95% confidence interval [CI], 55 to 81), and 1-year progression-free survival was 82% (95% CI, 69 to 90).	vandetanib	126-136	ret proto-oncogene	Homo sapiens	62-65
32846061-6	2020	RESULTS: In the first 55 consecutively enrolled patients with RET-mutant medullary thyroid cancer who had previously received vandetanib, cabozantinib, or both, the percentage who had a response was 69% (95% confidence interval [CI], 55 to 81), and 1-year progression-free survival was 82% (95% CI, 69 to 90).	cabozantinib	138-150	ret proto-oncogene	Homo sapiens	62-65
32307878-6	2020	When considering both sensitivity and specificity, RET% appeared as the best marker of the hematological module for implying testosterone ester misuse.	testosterone ester	125-143	ret proto-oncogene	Homo sapiens	51-54
32307878-9	2020	The present results demonstrate that unexpected fluctuations in RET% can be indicative of testosterone doping if samples are collected 3-10 days after injection.	Testosterone	90-102	ret proto-oncogene	Homo sapiens	64-67
32392154-1	2020	Herein, an effective electrochemiluminescence resonance energy transfer (ECL-RET) immunosensing strategy was proposed using silver/ZnIn2S4/reduced graphene oxide composites (Ag/ZnIn2S4/RGO) as the ECL donor and gold decorated silicon dioxide nanoparticles (Au@SiO2 NPs) as the ECL acceptor.	Silver	124-130	ret proto-oncogene	Homo sapiens	77-80
32392154-1	2020	Herein, an effective electrochemiluminescence resonance energy transfer (ECL-RET) immunosensing strategy was proposed using silver/ZnIn2S4/reduced graphene oxide composites (Ag/ZnIn2S4/RGO) as the ECL donor and gold decorated silicon dioxide nanoparticles (Au@SiO2 NPs) as the ECL acceptor.	znin2s4	131-138	ret proto-oncogene	Homo sapiens	77-80
32392154-1	2020	Herein, an effective electrochemiluminescence resonance energy transfer (ECL-RET) immunosensing strategy was proposed using silver/ZnIn2S4/reduced graphene oxide composites (Ag/ZnIn2S4/RGO) as the ECL donor and gold decorated silicon dioxide nanoparticles (Au@SiO2 NPs) as the ECL acceptor.	graphene oxide	147-161	ret proto-oncogene	Homo sapiens	77-80
32392154-1	2020	Herein, an effective electrochemiluminescence resonance energy transfer (ECL-RET) immunosensing strategy was proposed using silver/ZnIn2S4/reduced graphene oxide composites (Ag/ZnIn2S4/RGO) as the ECL donor and gold decorated silicon dioxide nanoparticles (Au@SiO2 NPs) as the ECL acceptor.	Silicon Dioxide	226-241	ret proto-oncogene	Homo sapiens	77-80
32392154-1	2020	Herein, an effective electrochemiluminescence resonance energy transfer (ECL-RET) immunosensing strategy was proposed using silver/ZnIn2S4/reduced graphene oxide composites (Ag/ZnIn2S4/RGO) as the ECL donor and gold decorated silicon dioxide nanoparticles (Au@SiO2 NPs) as the ECL acceptor.	Gold	257-259	ret proto-oncogene	Homo sapiens	77-80
32392154-1	2020	Herein, an effective electrochemiluminescence resonance energy transfer (ECL-RET) immunosensing strategy was proposed using silver/ZnIn2S4/reduced graphene oxide composites (Ag/ZnIn2S4/RGO) as the ECL donor and gold decorated silicon dioxide nanoparticles (Au@SiO2 NPs) as the ECL acceptor.	Silicon Dioxide	260-264	ret proto-oncogene	Homo sapiens	77-80
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
32457362-7	2020	Regorafenib treatment inhibits known receptor tyrosine kinase targets RET and PDGFRbeta and intracellular signalling through the RAS/MAPK, PI3K/Akt/mTOR and Fos/Jun pathways.	regorafenib	0-11	ret proto-oncogene	Homo sapiens	70-73
32671719-1	2020	Cabozantinib (Cabometyx ) is a potent multikinase inhibitor targeting the vascular endothelial growth factor (VEGF) receptor 2, the mesenchymal-epithelial transition factor (MET) receptor, and the "anexelekto" (AXL) receptor tyrosine kinase.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	216-240
32671719-1	2020	Cabozantinib (Cabometyx ) is a potent multikinase inhibitor targeting the vascular endothelial growth factor (VEGF) receptor 2, the mesenchymal-epithelial transition factor (MET) receptor, and the "anexelekto" (AXL) receptor tyrosine kinase.	cabozantinib	14-23	ret proto-oncogene	Homo sapiens	216-240
32817132-1	2020	BACKGROUND: Lenvatinib inhibits tyrosine kinases, including vascular endothelial growth factor (VEGF) receptor, fibroblast growth factor receptor, platelet-derived growth factor receptor alpha, RET proto-oncogene and KIT proto-oncogene, receptor tyrosine kinase.	lenvatinib	12-22	ret proto-oncogene	Homo sapiens	237-261
32718536-0	2020	Identification of a Novel KIF5B-RET, ABHD17C-RET Double-Fusion Variant in Lung Adenocarcinoma and Response to Cabozantinib.	cabozantinib	110-122	ret proto-oncogene	Homo sapiens	32-35
32462295-7	2020	The calculated PPA rates were 53.6% (45/84) for ALK, 53.9% (14/26) for BRAF, 56.5% (13/23) for ERBB2, 67.8% (428/631) for EGFR, 64.2% (122/190) for KRAS, 58.6% (17/29) for MET, 54.6% (12/22) for RET, and 53.3% (8/15) for ROS1.	ppa	15-18	ret proto-oncogene	Homo sapiens	195-198
32329651-1	2020	BACKGROUND: Larotrectinib and entrectinib are FDA-approved therapies for patients with non-small cell lung cancer (NSCLC) with neurotrophic receptor tyrosine kinase gene fusion (TRK fusion-positive) whose cancer has metastasized and progressed.	larotrectinib	12-25	ret proto-oncogene	Homo sapiens	140-164
32329651-1	2020	BACKGROUND: Larotrectinib and entrectinib are FDA-approved therapies for patients with non-small cell lung cancer (NSCLC) with neurotrophic receptor tyrosine kinase gene fusion (TRK fusion-positive) whose cancer has metastasized and progressed.	entrectinib	30-41	ret proto-oncogene	Homo sapiens	140-164
32718536-0	2020	Identification of a Novel KIF5B-RET, ABHD17C-RET Double-Fusion Variant in Lung Adenocarcinoma and Response to Cabozantinib.	cabozantinib	110-122	ret proto-oncogene	Homo sapiens	45-48
32698171-3	2020	As an alternative, lanthanide doped upconverting phosphors (UCP) have emerged as a new class of materials for use in optical imaging and RET sensing; they exhibit high photo- and chemical stability and utilise near infrared excitation.	Lanthanoid Series Elements	19-29	ret proto-oncogene	Homo sapiens	137-140
32463152-14	2020	In this phase II single arm study, we evaluated the clinical activity of the small molecule MET/RET/VEGR2 inhibitor cabozantinib in patients with metastatic HR+ breast cancer with bone metastases.	cabozantinib	116-128	ret proto-oncogene	Homo sapiens	96-99
32702947-0	2021	Vandetanib in a child affected by neurofibromatosis type 1 and medullary thyroid carcinoma with both NF1 and homozygous RET proto-oncogen germ-line mutations.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	120-123
32702947-4	2021	Herein, we report the use and outcome of vandetanib in a pediatric MTC case in which NF1 gene and RET proto-oncogen mutation were identified together.	vandetanib	41-51	ret proto-oncogene	Homo sapiens	98-101
32645282-1	2020	BACKGROUND: Cabozantinib is a multikinase inhibitor of MET, VEGFR, AXL, and RET, which also has an effect on the tumour immune microenvironment by decreasing regulatory T cells and myeloid-derived suppressor cells.	cabozantinib	12-24	ret proto-oncogene	Homo sapiens	76-79
32724339-2	2020	Anlotinib (AL3818) is a novel oral receptor tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor 2 and 3, fibroblast growth factor 1-4, platelet-derived growth factor receptor alpha and beta, c-Kit and Ret.	anlotinib	0-9	ret proto-oncogene	Homo sapiens	229-232
32724339-2	2020	Anlotinib (AL3818) is a novel oral receptor tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor 2 and 3, fibroblast growth factor 1-4, platelet-derived growth factor receptor alpha and beta, c-Kit and Ret.	anlotinib	11-17	ret proto-oncogene	Homo sapiens	229-232
32709979-3	2021	We defined iron-limited erythropoiesis by a RET-He <5th percentile lower reference interval (<28 pg).	Iron	11-15	ret proto-oncogene	Homo sapiens	44-47
32493697-1	2020	The FDA has greenlighted selpercatinib, the first targeted therapy for RET-altered non-small cell lung cancer (NSCLC) and certain types of thyroid cancer.	Selpercatinib	25-38	ret proto-oncogene	Homo sapiens	71-74
32665044-4	2021	This study evaluated associations between maltreatment, intimate partner violence, and the RET intervention with changes in children"s diurnal cortisol regulation across the 1 year following the intervention, and the extent to which improvements in maternal elaborative reminiscing differed between intervention groups and mediated change in children"s physiological functioning.	Hydrocortisone	143-151	ret proto-oncogene	Homo sapiens	91-94
32665044-7	2021	Mothers" elaboration immediately after the intervention served as a mediator of RET"s effects on improvements in children"s diurnal cortisol regulation (steeper diurnal slopes) from baseline to 1 year following intervention.	Hydrocortisone	132-140	ret proto-oncogene	Homo sapiens	80-83
32660121-1	2020	The oral multi-target kinase inhibitor regorafenib, which targets the oncogenic receptor tyrosine kinase (RTK), is an effective therapeutic for patients with advanced gastrointestinal stromal tumors or metastatic colorectal cancer.	regorafenib	39-50	ret proto-oncogene	Homo sapiens	80-104
32660121-1	2020	The oral multi-target kinase inhibitor regorafenib, which targets the oncogenic receptor tyrosine kinase (RTK), is an effective therapeutic for patients with advanced gastrointestinal stromal tumors or metastatic colorectal cancer.	regorafenib	39-50	ret proto-oncogene	Homo sapiens	106-109
32557397-1	2020	Selpercatinib (RETEVMO ) is a receptor tyrosine kinase RET (rearranged during transfection) inhibitor being developed by Loxo Oncology for the treatment of cancers harbouring RET alterations.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	15-18
32557397-1	2020	Selpercatinib (RETEVMO ) is a receptor tyrosine kinase RET (rearranged during transfection) inhibitor being developed by Loxo Oncology for the treatment of cancers harbouring RET alterations.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	55-58
32593453-0	2020	Emergence of High Level of MET Amplification as Off-Target Resistance to Selpercatinib Treatment in KIF5B-RET NSCLC.	Selpercatinib	73-86	ret proto-oncogene	Homo sapiens	106-109
32593454-0	2020	Reply to "Emergence of High Level of MET Amplification During Treatment With Selpercatinib in KIF5B-RET NSCLC".	Selpercatinib	77-90	ret proto-oncogene	Homo sapiens	100-103
32660930-0	2021	Response to the Selective RET Inhibitor Selpercatinib (LOXO-292) in a Patient With RET Fusion-positive Atypical Lung Carcinoid.	Selpercatinib	40-53	ret proto-oncogene	Homo sapiens	26-29
32319659-9	2020	Interestingly, activation of TrkA by its cognate ligand NGF resulted in RET phosphorylation at Y905, Y1015, and Y1062, and this was inhibited in a dose-dependent manner by the TRK inhibitor (CEP-701).	y905	95-99	ret proto-oncogene	Homo sapiens	72-75
32319659-9	2020	Interestingly, activation of TrkA by its cognate ligand NGF resulted in RET phosphorylation at Y905, Y1015, and Y1062, and this was inhibited in a dose-dependent manner by the TRK inhibitor (CEP-701).	y1015	101-106	ret proto-oncogene	Homo sapiens	72-75
32319659-9	2020	Interestingly, activation of TrkA by its cognate ligand NGF resulted in RET phosphorylation at Y905, Y1015, and Y1062, and this was inhibited in a dose-dependent manner by the TRK inhibitor (CEP-701).	y1062	112-117	ret proto-oncogene	Homo sapiens	72-75
32694997-1	2020	The receptor tyrosine kinase inhibitor lapatinib, indicated to treat patients with HER2-positive breast cancer in combination with capecitabine, can cause severe hepatotoxicity.	Lapatinib	39-48	ret proto-oncogene	Homo sapiens	4-28
32694997-1	2020	The receptor tyrosine kinase inhibitor lapatinib, indicated to treat patients with HER2-positive breast cancer in combination with capecitabine, can cause severe hepatotoxicity.	Capecitabine	131-143	ret proto-oncogene	Homo sapiens	4-28
32660930-0	2021	Response to the Selective RET Inhibitor Selpercatinib (LOXO-292) in a Patient With RET Fusion-positive Atypical Lung Carcinoid.	Selpercatinib	40-53	ret proto-oncogene	Homo sapiens	83-86
32532875-6	2020	Once a primary cell culture became available, the RET inhibitor cabozantinib was tested but showed no appreciable efficacy in vitro, affirming with the western blot negative for RET protein expression that RET germline mutation could be only incidental.	cabozantinib	64-76	ret proto-oncogene	Homo sapiens	50-53
31911548-4	2020	Nineteen percent (5/27) of patients treated with first-line osimertinib had off-target genetic resistance (2 MET amplification, 1 KRAS mutation, 1 RET fusion, and 1 BRAF fusion) whereas 4% (1/27) had an acquired EGFR mutation (EGFR G724S).	osimertinib	60-71	ret proto-oncogene	Homo sapiens	147-150
32502444-2	2020	Lenvatinib is a novel multi-targeted inhibitor of VEGFR, FGFR, RET, c-Kit, and other kinases.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	63-66
31954111-5	2020	Western blot analysis showed that combination therapy inhibited phosphorylation of epidermal growth factor receptor (EGFR) (p&lt;0.01 in all cell lines) and Met receptor tyrosine kinase (MET) (p&lt;0.01 in all cell lines).	methionylmethionine	157-160	ret proto-oncogene	Homo sapiens	161-185
32460744-8	2020	Our experimental studies using cultured cells with focus on the expression and activity levels of intracellular signal transduction molecules such as c-SRC, c-RET, and oncogenic RET showed risks for malignant transformation and/or progression arose from arsenic and barium.	Arsenic	254-261	ret proto-oncogene	Homo sapiens	159-162
32100934-0	2020	Efficacy of Cabozantinib and Nivolumab in Treating Hepatocellular Carcinoma with RET Amplification, High Tumor Mutational Burden, and PD-L1 Expression.	cabozantinib	12-24	ret proto-oncogene	Homo sapiens	81-84
32100934-6	2020	To the best of our knowledge, this is the first clinical case report in the literature to describe the benefit of cabozantinib and nivolumab treatment in a patient with HCC and RET amplification, high TMB, and positive PD-L1 expression.	cabozantinib	114-126	ret proto-oncogene	Homo sapiens	177-180
32100934-8	2020	KEY POINTS: A patient with metastatic hepatocellular carcinoma (HCC) harboring RET amplification, high tumor mutational burden, and positive programmed death-ligand 1 expression responded well to the combination of cabozantinib and nivolumab therapy with progression-free survival of longer than 25 months.	cabozantinib	215-227	ret proto-oncogene	Homo sapiens	79-82
32207565-1	2020	BACKGROUND: Regorafenib is a small molecule multikinase inhibitor that inhibits multiple kinases including BRAF, KIT, PDGFRB, RAF, RET, and VEGFR1-3.	regorafenib	12-23	ret proto-oncogene	Homo sapiens	131-134
32460744-8	2020	Our experimental studies using cultured cells with focus on the expression and activity levels of intracellular signal transduction molecules such as c-SRC, c-RET, and oncogenic RET showed risks for malignant transformation and/or progression arose from arsenic and barium.	Barium	266-272	ret proto-oncogene	Homo sapiens	159-162
32298114-0	2020	Bioisosteric Discovery of NPA101.3, a Second-Generation RET/VEGFR2 Inhibitor Optimized for Single-Agent Polypharmacology.	npa101	26-32	ret proto-oncogene	Homo sapiens	56-59
32587778-10	2020	Upregulation of CD105 was abrogated by anlotinib, which targets multiple receptor tyrosine kinases including VEGFR2/3, FGFR1-4, PDGFRalpha/beta, C-Kit, and RET.	anlotinib	39-48	ret proto-oncogene	Homo sapiens	156-159
32298114-7	2020	Oral administration of NPA101.3 (10 mg/kg/day) completely prevented formation of tumors induced by RET/C634Y-transformed cells, while it weakened, but did not abrogate, formation of tumors induced by a control oncogene (HRAS/G12V).	npa101.	23-30	ret proto-oncogene	Homo sapiens	99-102
32266457-1	2020	PURPOSE: Anlotinib is a novel oral multi-targeted receptor tyrosine kinase inhibitor, which selectively inhibits VEGFR2/3, FGFR1-4, PDGFR alpha/beta, c-kit, and Ret.	anlotinib	9-18	ret proto-oncogene	Homo sapiens	161-164
32380538-4	2020	Receptor tyrosine kinase (RTK) pathway mutations were associated with primary resistance to ivosidenib.	ivosidenib	92-102	ret proto-oncogene	Homo sapiens	0-24
32380538-4	2020	Receptor tyrosine kinase (RTK) pathway mutations were associated with primary resistance to ivosidenib.	ivosidenib	92-102	ret proto-oncogene	Homo sapiens	26-29
32083304-1	2020	OBJECTIVE: Since the first discovery of rearranged during transfection (RET) fusion in lung adenocarcinoma in 2011, two tyrosine kinase inhibitors, namely vandetanib and cabozantinib, are currently available.	vandetanib	155-165	ret proto-oncogene	Homo sapiens	72-75
32083304-1	2020	OBJECTIVE: Since the first discovery of rearranged during transfection (RET) fusion in lung adenocarcinoma in 2011, two tyrosine kinase inhibitors, namely vandetanib and cabozantinib, are currently available.	cabozantinib	170-182	ret proto-oncogene	Homo sapiens	72-75
31900481-3	2020	Cabozantinib (CABO) is an inhibitor of c-MET, vascular endothelial growth factor receptor 2, AXL, and RET and approved for advanced kidney cancer, liver carcinoma after previous sorafenib, and medullary thyroid carcinoma.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	102-105
31900481-3	2020	Cabozantinib (CABO) is an inhibitor of c-MET, vascular endothelial growth factor receptor 2, AXL, and RET and approved for advanced kidney cancer, liver carcinoma after previous sorafenib, and medullary thyroid carcinoma.	cabozantinib	14-18	ret proto-oncogene	Homo sapiens	102-105
31711124-1	2020	RET (REarranged during Transfection), which encodes a receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor, plays a role as driver oncogene in a variety of human cancers.	Tyrosine	63-71	ret proto-oncogene	Homo sapiens	0-3
31897454-6	2020	ECL resonance energy transfer (ECL-RET) occurred inside the CdS-Ru nanoparticles and strong ECL emissions were obtained from CdS-Ru nanoparticles at both positive potential in the presence of tri-n-propylamine and at negative potential in the presence of peroxydisulfate.	tripropylamine	192-209	ret proto-oncogene	Homo sapiens	35-38
31897454-6	2020	ECL resonance energy transfer (ECL-RET) occurred inside the CdS-Ru nanoparticles and strong ECL emissions were obtained from CdS-Ru nanoparticles at both positive potential in the presence of tri-n-propylamine and at negative potential in the presence of peroxydisulfate.	potassium persulfate	255-270	ret proto-oncogene	Homo sapiens	35-38
32212604-3	2020	In the presence of the model target isocarbophos (ICP), the conjugation of two split-aptamers initiated the ECL-Resonance Energy Transfer (ECL-RET) between the Au nanorods and the Ru(bpy)32+ centers.	Gold	160-162	ret proto-oncogene	Homo sapiens	143-146
31711124-2	2020	Fusion of RET with several partner genes has been detected in papillary thyroid, lung, colorectal, pancreatic, and breast cancers, and tyrosine kinase inhibitors (TKIs) for RET (particularly RET-specific inhibitors) show promising therapeutic effects against such cancers.	Tyrosine	135-143	ret proto-oncogene	Homo sapiens	10-13
31711124-2	2020	Fusion of RET with several partner genes has been detected in papillary thyroid, lung, colorectal, pancreatic, and breast cancers, and tyrosine kinase inhibitors (TKIs) for RET (particularly RET-specific inhibitors) show promising therapeutic effects against such cancers.	Tyrosine	135-143	ret proto-oncogene	Homo sapiens	173-176
31711124-2	2020	Fusion of RET with several partner genes has been detected in papillary thyroid, lung, colorectal, pancreatic, and breast cancers, and tyrosine kinase inhibitors (TKIs) for RET (particularly RET-specific inhibitors) show promising therapeutic effects against such cancers.	Tyrosine	135-143	ret proto-oncogene	Homo sapiens	191-214
31711124-3	2020	Oncogenic mutations within the extracellular cysteine-rich and intracellular kinase domains of RET drive medullary thyroid carcinogenesis; the same mutations are also observed in a small subset of diverse cancers such as lung, colorectal, and breast cancers.	Cysteine	45-53	ret proto-oncogene	Homo sapiens	95-98
32083997-5	2020	Multikinase inhibitors with RET inhibitor activity, such as cabozantinib and vandetanib, have been explored in the clinic for tumors with activating RET gene alterations with modest clinical efficacy.	cabozantinib	60-72	ret proto-oncogene	Homo sapiens	28-31
32923911-0	2020	Activity of the Highly Specific RET Inhibitor Selpercatinib (LOXO-292) in Pediatric Patients With Tumors Harboring RET Gene Alterations.	Selpercatinib	46-59	ret proto-oncogene	Homo sapiens	32-35
32923911-0	2020	Activity of the Highly Specific RET Inhibitor Selpercatinib (LOXO-292) in Pediatric Patients With Tumors Harboring RET Gene Alterations.	Selpercatinib	46-59	ret proto-oncogene	Homo sapiens	115-118
32219805-0	2020	Effect of Lenvatinib on a Patient with Medullary Thyroid Carcinoma Liver Metastasis Caused by Multiple Endocrine Neoplasia Type 2A.	lenvatinib	10-20	ret proto-oncogene	Homo sapiens	94-130
32219805-1	2020	A 61-year-old female was diagnosed with multiple endocrine neoplasia type 2A (MEN2A), caused by a heterozygous point mutation in the RET gene (TGC to TAC at codon 634) resulting in the substitution of cytosine with leucine (C634Y).	Cytosine	201-209	ret proto-oncogene	Homo sapiens	40-76
32219805-1	2020	A 61-year-old female was diagnosed with multiple endocrine neoplasia type 2A (MEN2A), caused by a heterozygous point mutation in the RET gene (TGC to TAC at codon 634) resulting in the substitution of cytosine with leucine (C634Y).	Cytosine	201-209	ret proto-oncogene	Homo sapiens	78-83
32219805-1	2020	A 61-year-old female was diagnosed with multiple endocrine neoplasia type 2A (MEN2A), caused by a heterozygous point mutation in the RET gene (TGC to TAC at codon 634) resulting in the substitution of cytosine with leucine (C634Y).	Cytosine	201-209	ret proto-oncogene	Homo sapiens	133-136
32219805-1	2020	A 61-year-old female was diagnosed with multiple endocrine neoplasia type 2A (MEN2A), caused by a heterozygous point mutation in the RET gene (TGC to TAC at codon 634) resulting in the substitution of cytosine with leucine (C634Y).	Leucine	215-222	ret proto-oncogene	Homo sapiens	40-76
32219805-1	2020	A 61-year-old female was diagnosed with multiple endocrine neoplasia type 2A (MEN2A), caused by a heterozygous point mutation in the RET gene (TGC to TAC at codon 634) resulting in the substitution of cytosine with leucine (C634Y).	Leucine	215-222	ret proto-oncogene	Homo sapiens	78-83
32219805-1	2020	A 61-year-old female was diagnosed with multiple endocrine neoplasia type 2A (MEN2A), caused by a heterozygous point mutation in the RET gene (TGC to TAC at codon 634) resulting in the substitution of cytosine with leucine (C634Y).	Leucine	215-222	ret proto-oncogene	Homo sapiens	133-136
32219805-9	2020	At this point, the patient was doing well, suggesting that lenvatinib was effective in treating the MTC liver metastasis and may be one of the treatment for advanced MTC caused by C634Y mutation in the RET gene.	lenvatinib	59-69	ret proto-oncogene	Homo sapiens	202-205
32083997-5	2020	Multikinase inhibitors with RET inhibitor activity, such as cabozantinib and vandetanib, have been explored in the clinic for tumors with activating RET gene alterations with modest clinical efficacy.	cabozantinib	60-72	ret proto-oncogene	Homo sapiens	149-152
32083997-5	2020	Multikinase inhibitors with RET inhibitor activity, such as cabozantinib and vandetanib, have been explored in the clinic for tumors with activating RET gene alterations with modest clinical efficacy.	vandetanib	77-87	ret proto-oncogene	Homo sapiens	28-31
32083997-5	2020	Multikinase inhibitors with RET inhibitor activity, such as cabozantinib and vandetanib, have been explored in the clinic for tumors with activating RET gene alterations with modest clinical efficacy.	vandetanib	77-87	ret proto-oncogene	Homo sapiens	149-152
32083997-8	2020	In contrast, the recent discovery and clinical validation of highly potent selective RET inhibitors (pralsetinib, selpercatinib) demonstrating improved efficacy and a more favorable toxicity profile are poised to alter the landscape of RET-dependent cancers.	CRY1 protein, Arabidopsis	101-112	ret proto-oncogene	Homo sapiens	85-88
32083997-8	2020	In contrast, the recent discovery and clinical validation of highly potent selective RET inhibitors (pralsetinib, selpercatinib) demonstrating improved efficacy and a more favorable toxicity profile are poised to alter the landscape of RET-dependent cancers.	CRY1 protein, Arabidopsis	101-112	ret proto-oncogene	Homo sapiens	236-239
32083997-8	2020	In contrast, the recent discovery and clinical validation of highly potent selective RET inhibitors (pralsetinib, selpercatinib) demonstrating improved efficacy and a more favorable toxicity profile are poised to alter the landscape of RET-dependent cancers.	Selpercatinib	114-127	ret proto-oncogene	Homo sapiens	85-88
32083997-8	2020	In contrast, the recent discovery and clinical validation of highly potent selective RET inhibitors (pralsetinib, selpercatinib) demonstrating improved efficacy and a more favorable toxicity profile are poised to alter the landscape of RET-dependent cancers.	Selpercatinib	114-127	ret proto-oncogene	Homo sapiens	236-239
31988000-1	2020	INTRODUCTION: Novel RET-specific tyrosine kinase inhibitors (TKIs) such as selpercatinib (LOXO-292) have shown unprecedented efficacy in tumors positive for RET fusions or mutations, notably RET fusion-positive non-small lung cancer (NSCLC) and RET-mutated medullary thyroid cancer (MTC).	Selpercatinib	75-88	ret proto-oncogene	Homo sapiens	157-160
31851071-0	2020	Reticulocyte Hemoglobin Content (Ret He): A Simple Tool for Evaluation of Iron Status in Childhood Cancer.	Iron	74-78	ret proto-oncogene	Homo sapiens	0-3
31851071-11	2020	A trial of oral iron in patients with low Ret He may be useful to correct the associated anemia.	Iron	16-20	ret proto-oncogene	Homo sapiens	42-45
31988000-1	2020	INTRODUCTION: Novel RET-specific tyrosine kinase inhibitors (TKIs) such as selpercatinib (LOXO-292) have shown unprecedented efficacy in tumors positive for RET fusions or mutations, notably RET fusion-positive non-small lung cancer (NSCLC) and RET-mutated medullary thyroid cancer (MTC).	Selpercatinib	75-88	ret proto-oncogene	Homo sapiens	157-160
31988000-1	2020	INTRODUCTION: Novel RET-specific tyrosine kinase inhibitors (TKIs) such as selpercatinib (LOXO-292) have shown unprecedented efficacy in tumors positive for RET fusions or mutations, notably RET fusion-positive non-small lung cancer (NSCLC) and RET-mutated medullary thyroid cancer (MTC).	Tyrosine	33-41	ret proto-oncogene	Homo sapiens	20-23
31988000-1	2020	INTRODUCTION: Novel RET-specific tyrosine kinase inhibitors (TKIs) such as selpercatinib (LOXO-292) have shown unprecedented efficacy in tumors positive for RET fusions or mutations, notably RET fusion-positive non-small lung cancer (NSCLC) and RET-mutated medullary thyroid cancer (MTC).	Tyrosine	33-41	ret proto-oncogene	Homo sapiens	157-160
31988000-1	2020	INTRODUCTION: Novel RET-specific tyrosine kinase inhibitors (TKIs) such as selpercatinib (LOXO-292) have shown unprecedented efficacy in tumors positive for RET fusions or mutations, notably RET fusion-positive non-small lung cancer (NSCLC) and RET-mutated medullary thyroid cancer (MTC).	Selpercatinib	75-88	ret proto-oncogene	Homo sapiens	157-160
31988000-1	2020	INTRODUCTION: Novel RET-specific tyrosine kinase inhibitors (TKIs) such as selpercatinib (LOXO-292) have shown unprecedented efficacy in tumors positive for RET fusions or mutations, notably RET fusion-positive non-small lung cancer (NSCLC) and RET-mutated medullary thyroid cancer (MTC).	Tyrosine	33-41	ret proto-oncogene	Homo sapiens	157-160
31988000-1	2020	INTRODUCTION: Novel RET-specific tyrosine kinase inhibitors (TKIs) such as selpercatinib (LOXO-292) have shown unprecedented efficacy in tumors positive for RET fusions or mutations, notably RET fusion-positive non-small lung cancer (NSCLC) and RET-mutated medullary thyroid cancer (MTC).	Tyrosine	33-41	ret proto-oncogene	Homo sapiens	157-160
31988000-1	2020	INTRODUCTION: Novel RET-specific tyrosine kinase inhibitors (TKIs) such as selpercatinib (LOXO-292) have shown unprecedented efficacy in tumors positive for RET fusions or mutations, notably RET fusion-positive non-small lung cancer (NSCLC) and RET-mutated medullary thyroid cancer (MTC).	Selpercatinib	75-88	ret proto-oncogene	Homo sapiens	20-23
31988000-6	2020	RESULTS: Following a dramatic initial response to selpercatinib in a patient with KIF5B-RET NSCLC, analysis of circulating tumor DNA (CtDNA) demonstrated emergence of RET G810R, S and C mutations in the RET solvent front prior to the emergence of clinical resistance.	Selpercatinib	50-63	ret proto-oncogene	Homo sapiens	88-91
31988000-8	2020	Acquired mutations in RET G810 were identified in progressing tissue from a second patient with CCDC6-RET fusion-positive NSCLC and in plasma from additional RET fusion-positive NSCLC and RET-mutant MTC patients progressing on an ongoing phase 1/2 trial of selpercatinib.	Selpercatinib	257-270	ret proto-oncogene	Homo sapiens	22-25
31988000-9	2020	Preclinical studies demonstrated the presence of RET G810R mutations in a CCDC6-RET PDX model of acquired resistance to selpercatinib.	Selpercatinib	120-133	ret proto-oncogene	Homo sapiens	49-52
31988000-9	2020	Preclinical studies demonstrated the presence of RET G810R mutations in a CCDC6-RET PDX model of acquired resistance to selpercatinib.	Selpercatinib	120-133	ret proto-oncogene	Homo sapiens	80-83
31988000-10	2020	Structural modeling predicted that these mutations sterically hinder binding of selpercatinib, and in vitro assays confirmed loss of activity for both anti-RET MKIs and selective RET TKIs.	Selpercatinib	80-93	ret proto-oncogene	Homo sapiens	156-159
31988000-10	2020	Structural modeling predicted that these mutations sterically hinder binding of selpercatinib, and in vitro assays confirmed loss of activity for both anti-RET MKIs and selective RET TKIs.	Selpercatinib	80-93	ret proto-oncogene	Homo sapiens	179-182
31988000-11	2020	CONCLUSION: RET G810 solvent front mutations represent the first described recurrent mechanism of resistance to selective RET inhibition with selpercatinib.	Selpercatinib	142-155	ret proto-oncogene	Homo sapiens	12-15
31988000-11	2020	CONCLUSION: RET G810 solvent front mutations represent the first described recurrent mechanism of resistance to selective RET inhibition with selpercatinib.	Selpercatinib	142-155	ret proto-oncogene	Homo sapiens	122-125
32025680-0	2020	Colchicine selective interaction with oncogene RET G-quadruplex revealed by NMR.	Colchicine	0-10	ret proto-oncogene	Homo sapiens	47-50
32052681-3	2021	Regorafenib is an FDA approved oral multi-kinase inhibitor that blocks the activity of multiple protein kinases including those involved in the regulation of tumor angiogenesis [VEGFR1-3, TIE2], tumor microenvironment [PDGFR-beta, FGFR] and oncogenesis (KIT, RET, RAF-1, BRAF).	regorafenib	0-11	ret proto-oncogene	Homo sapiens	259-262
32067675-1	2020	An illustration based on the development of selpercatinib, a RET inhibitor.	Selpercatinib	44-57	ret proto-oncogene	Homo sapiens	61-64
32203581-6	2020	Melanized neurons displayed intense tyrosine hydroxylase and RET proto-oncogene expression in nigral neurons in the patient where CERE120 was directly delivered to the nigra.	cere120	130-137	ret proto-oncogene	Homo sapiens	61-64
32083257-2	2020	A quenching effect of BPNs on luminol ECL was achieved based on ECL resonance energy transfer (ECL-RET) with excited state luminol as the energy donor and BPNs as the energy acceptor.	Brompheniramine	22-26	ret proto-oncogene	Homo sapiens	99-102
32083257-2	2020	A quenching effect of BPNs on luminol ECL was achieved based on ECL resonance energy transfer (ECL-RET) with excited state luminol as the energy donor and BPNs as the energy acceptor.	Luminol	30-37	ret proto-oncogene	Homo sapiens	99-102
32083257-2	2020	A quenching effect of BPNs on luminol ECL was achieved based on ECL resonance energy transfer (ECL-RET) with excited state luminol as the energy donor and BPNs as the energy acceptor.	Luminol	123-130	ret proto-oncogene	Homo sapiens	99-102
32083257-2	2020	A quenching effect of BPNs on luminol ECL was achieved based on ECL resonance energy transfer (ECL-RET) with excited state luminol as the energy donor and BPNs as the energy acceptor.	Brompheniramine	155-159	ret proto-oncogene	Homo sapiens	99-102
32062451-1	2020	The RET proto-oncogene encodes receptor tyrosine kinase, expressed primarily in tissues of neural crest origin.	Tyrosine	40-48	ret proto-oncogene	Homo sapiens	4-7
32025680-3	2020	Here, mainly by NMR, we report that colchicine selectively binds to oncogene RET G4-DNA.	Colchicine	36-46	ret proto-oncogene	Homo sapiens	77-80
32064171-1	2020	REarranged during Transition (RET) is a tyrosine kinase associated with the development of several malignancies.	Tyrosine	40-48	ret proto-oncogene	Homo sapiens	30-33
32095692-6	2020	A nicotinamide analogue of ponatinib, HSN748, retains activity against FLT3, ABL1, RET, and PDGFRalpha/beta but loses activity against c-Src and P38alpha.	Niacinamide	2-14	ret proto-oncogene	Homo sapiens	83-86
32095692-6	2020	A nicotinamide analogue of ponatinib, HSN748, retains activity against FLT3, ABL1, RET, and PDGFRalpha/beta but loses activity against c-Src and P38alpha.	ponatinib	27-36	ret proto-oncogene	Homo sapiens	83-86
31829554-5	2020	Using the receptor tyrosine kinase (RTK) discoidin domain receptor 1 (DDR1) as a proof-of-concept target in a droplet-scale competition binding assay, we screened a 67,100-member solid-phase DEL of drug-like small molecules for competitive ligands of DDR1 and identified several known RTK inhibitor pharmacophores, including azaindole- and quinazolinone-containing monomers.	4-azaindole	325-334	ret proto-oncogene	Homo sapiens	10-34
31829554-5	2020	Using the receptor tyrosine kinase (RTK) discoidin domain receptor 1 (DDR1) as a proof-of-concept target in a droplet-scale competition binding assay, we screened a 67,100-member solid-phase DEL of drug-like small molecules for competitive ligands of DDR1 and identified several known RTK inhibitor pharmacophores, including azaindole- and quinazolinone-containing monomers.	4-azaindole	325-334	ret proto-oncogene	Homo sapiens	36-39
31829554-5	2020	Using the receptor tyrosine kinase (RTK) discoidin domain receptor 1 (DDR1) as a proof-of-concept target in a droplet-scale competition binding assay, we screened a 67,100-member solid-phase DEL of drug-like small molecules for competitive ligands of DDR1 and identified several known RTK inhibitor pharmacophores, including azaindole- and quinazolinone-containing monomers.	Quinazolinones	340-353	ret proto-oncogene	Homo sapiens	10-34
31829554-5	2020	Using the receptor tyrosine kinase (RTK) discoidin domain receptor 1 (DDR1) as a proof-of-concept target in a droplet-scale competition binding assay, we screened a 67,100-member solid-phase DEL of drug-like small molecules for competitive ligands of DDR1 and identified several known RTK inhibitor pharmacophores, including azaindole- and quinazolinone-containing monomers.	Quinazolinones	340-353	ret proto-oncogene	Homo sapiens	36-39
31645646-3	2020	RET is expressed as two main isoforms with unique C-terminal sequences that differ in protein interactions and subcellular trafficking in response to RET activation, and which also have distinct oncogenic potentials.	Carbon	50-51	ret proto-oncogene	Homo sapiens	0-3
31645646-7	2020	Our data show that the GRB2 adapter associates with RET51 through interactions with its C-terminal sequences, facilitating recruitment of active ARF6 and GGA3 interaction, and that depletion of GGA3 or ARF6 reduced RET51 recycling.	Carbon	88-89	ret proto-oncogene	Homo sapiens	52-57
32064171-5	2020	We have previously reported that a conserved cysteine in the MXXCW motif of RET is crucial to the disulfide-bonded dimerization-linked activation of RET kinases.	Cysteine	45-53	ret proto-oncogene	Homo sapiens	76-79
32064171-5	2020	We have previously reported that a conserved cysteine in the MXXCW motif of RET is crucial to the disulfide-bonded dimerization-linked activation of RET kinases.	Cysteine	45-53	ret proto-oncogene	Homo sapiens	149-152
32064171-5	2020	We have previously reported that a conserved cysteine in the MXXCW motif of RET is crucial to the disulfide-bonded dimerization-linked activation of RET kinases.	Disulfides	98-107	ret proto-oncogene	Homo sapiens	76-79
32064171-5	2020	We have previously reported that a conserved cysteine in the MXXCW motif of RET is crucial to the disulfide-bonded dimerization-linked activation of RET kinases.	Disulfides	98-107	ret proto-oncogene	Homo sapiens	149-152
32064171-6	2020	Reagents which bind to this cysteine may inhibit the activity of RET kinases through disulfide-bond mediated dimerization.	Cysteine	28-36	ret proto-oncogene	Homo sapiens	65-68
32064171-6	2020	Reagents which bind to this cysteine may inhibit the activity of RET kinases through disulfide-bond mediated dimerization.	Disulfides	85-94	ret proto-oncogene	Homo sapiens	65-68
32064171-11	2020	The great potency of these cysteine targeted peptides could indicate promising approaches for novel molecular-targeted therapies for RET-associated cancers.	Cysteine	27-35	ret proto-oncogene	Homo sapiens	133-136
31746350-0	2020	Salinomycin and its derivatives as potent RET transcriptional inhibitors for the treatment of medullary thyroid carcinoma.	salinomycin	0-11	ret proto-oncogene	Homo sapiens	42-45
32034713-2	2020	A receptor tyrosine kinase (RTK) is a tyrosine kinase located at the cellular membrane and is activated by binding of a ligand via its extracellular domain.	Tyrosine	11-19	ret proto-oncogene	Homo sapiens	28-31
31655384-5	2020	To establish a new ECL-RET system, Pd@Au core-shell nanoflower was prepared as a suitable ECL acceptor which could immobilize the detection-antibody (Ab2).	Palladium	35-37	ret proto-oncogene	Homo sapiens	23-26
31655384-5	2020	To establish a new ECL-RET system, Pd@Au core-shell nanoflower was prepared as a suitable ECL acceptor which could immobilize the detection-antibody (Ab2).	Gold	38-40	ret proto-oncogene	Homo sapiens	23-26
31608707-12	2020	Regorafenib is a multikinase inhibitor targeting BRAF, VEGFR-1/2/3, KIT, TIE-2, PDGFR-beta, fibroblast growth factor receptor 1 (FGFR-1), RET, RAF-1, and p38 MAP kinase.	regorafenib	0-11	ret proto-oncogene	Homo sapiens	138-141
31892559-5	2020	RESULTS: Taxotere inhibited tumor growth of NSCLC cells harboring drug resistance, and reduced the expression of phosphorylated MET proto-oncogene, receptor tyrosine kinase (MET).	Docetaxel	9-17	ret proto-oncogene	Homo sapiens	148-172
31746350-2	2020	The present study reports the first preclinical characterization of salinomycin and selected analogs as potent RET transcriptional inhibitors.	salinomycin	68-79	ret proto-oncogene	Homo sapiens	111-114
31746350-3	2020	Reverse transcription-PCR and immunoblotting revealed that salinomycin profoundly decreased RET expression in the TT human MTC cell line by inhibiting RET transcription.	salinomycin	59-70	ret proto-oncogene	Homo sapiens	92-95
31746350-3	2020	Reverse transcription-PCR and immunoblotting revealed that salinomycin profoundly decreased RET expression in the TT human MTC cell line by inhibiting RET transcription.	salinomycin	59-70	ret proto-oncogene	Homo sapiens	151-154
31746350-4	2020	Moreover, salinomycin resulted in remarkable anti-proliferative activity against MTC that is driven by RET (gain of function mutation) by selectively inhibiting the intracellular PI3K/Akt/mTOR signaling pathway.	salinomycin	10-21	ret proto-oncogene	Homo sapiens	103-106
31746350-7	2020	Some of the salinomycin derivatives showed the ability to reduce RET expression where others fail to alter RET expression.	salinomycin	12-23	ret proto-oncogene	Homo sapiens	65-68
31746350-8	2020	These results suggest that the RET-suppressing effect of salinomycin may be largely attributed to disruption of the Wnt pathway, presumably through interference with the ternary LRP6-Frizzled-Wnt complex.	salinomycin	57-68	ret proto-oncogene	Homo sapiens	31-34
32950976-3	2020	Reticulocyte haemoglobin (Ret-He) depends on available iron in blood, indirectly regulated by hepcidin.	Iron	55-59	ret proto-oncogene	Homo sapiens	0-3
31698333-0	2020	Alectinib activity in chemotherapy-refractory metastatic RET-rearranged non-small cell lung carcinomas: A case series.	alectinib	0-9	ret proto-oncogene	Homo sapiens	57-60
31698333-1	2020	OBJECTIVES: to report outcomes of four cases of chemo-refractory RET-rearranged non-small cell lung carcinomas (NSCLCs) treated with alectinib in a single center.	alectinib	133-142	ret proto-oncogene	Homo sapiens	65-68
31698333-2	2020	MATERIALS AND METHODS: we retrospectively assessed and reported the activity and tolerability of alectinib 600 mg twice daily in advanced and chemo-refractory RET-rearranged NSCLC patients treated in a Brazilian institution.	alectinib	97-106	ret proto-oncogene	Homo sapiens	159-162
31698333-11	2020	CONCLUSION: Although this is a small single center evaluation, alectinib was well tolerated and demonstrated clinical activity against advanced RET-rearranged NSCLCs, suggesting its potential role in this specific subset of malignancies.	alectinib	63-72	ret proto-oncogene	Homo sapiens	144-147
31559679-1	2019	The imine condensation reaction of 5,5"-(benzo[c][1,2,5]thiadiazole-4,7-diyl)diisophthalaldehyde with cyclohexanediamine resulted in a shape-persistent multifunctional tubular organic cage (MTC1).	Imines	4-9	ret proto-oncogene	Homo sapiens	190-194
31477837-7	2020	Significantly, we identify FGFR, RET, and MERTK as the first RTKs that can directly interact with and phosphorylate YAP/TAZ at multiple tyrosine residues independent of upstream Hippo signaling, thereby activating their functions in tumorigenesis.	Tyrosine	136-144	ret proto-oncogene	Homo sapiens	33-36
31825671-11	2020	Ret-He and Hypo-He can be used to assess iron supply for erythropoiesis in patients with IBD, to evaluate long-term (Hypo-He) and short-term (Ret-He) periods.	Iron	41-45	ret proto-oncogene	Homo sapiens	0-3
31655646-4	2019	Surprisingly, a stable and strong ECL signal was obtained based on the RET, which was used for signal-off detection of FA in the presence of coreactant K2S2O8.	Potassium	152-158	ret proto-oncogene	Homo sapiens	71-74
31559679-1	2019	The imine condensation reaction of 5,5"-(benzo[c][1,2,5]thiadiazole-4,7-diyl)diisophthalaldehyde with cyclohexanediamine resulted in a shape-persistent multifunctional tubular organic cage (MTC1).	benzo-1,2,3-thiadiazole	35-96	ret proto-oncogene	Homo sapiens	190-194
31559679-1	2019	The imine condensation reaction of 5,5"-(benzo[c][1,2,5]thiadiazole-4,7-diyl)diisophthalaldehyde with cyclohexanediamine resulted in a shape-persistent multifunctional tubular organic cage (MTC1).	1,2-cyclohexanediamine	102-120	ret proto-oncogene	Homo sapiens	190-194
31559679-3	2019	The subsequent reduction of MTC1 and palladium acetate with NaBH4 afforded cage-supported highly dispersed ultrafine palladium nanoparticles with a narrow particle size distribution of 1.9 +- 0.4 nm, denoted as Pd@MTC1-1/5.	palladium(II) acetate	37-54	ret proto-oncogene	Homo sapiens	214-218
31559679-3	2019	The subsequent reduction of MTC1 and palladium acetate with NaBH4 afforded cage-supported highly dispersed ultrafine palladium nanoparticles with a narrow particle size distribution of 1.9 +- 0.4 nm, denoted as Pd@MTC1-1/5.	Sodium	60-65	ret proto-oncogene	Homo sapiens	214-218
31559679-3	2019	The subsequent reduction of MTC1 and palladium acetate with NaBH4 afforded cage-supported highly dispersed ultrafine palladium nanoparticles with a narrow particle size distribution of 1.9 +- 0.4 nm, denoted as Pd@MTC1-1/5.	Palladium	37-46	ret proto-oncogene	Homo sapiens	214-218
31559679-3	2019	The subsequent reduction of MTC1 and palladium acetate with NaBH4 afforded cage-supported highly dispersed ultrafine palladium nanoparticles with a narrow particle size distribution of 1.9 +- 0.4 nm, denoted as Pd@MTC1-1/5.	Palladium	211-213	ret proto-oncogene	Homo sapiens	28-32
31559679-4	2019	Such ultrafine palladium nanoparticles in Pd@MTC1-1/5, in cooperation with photocatalytically active MTC1, enable efficient cascade reactions including visible light-induced aerobic hydroxylation of 4-nitrophenylboronic acid to 4-nitrophenol and the following hydrogenation reduction with NaBH4.	Palladium	15-24	ret proto-oncogene	Homo sapiens	45-49
31559679-4	2019	Such ultrafine palladium nanoparticles in Pd@MTC1-1/5, in cooperation with photocatalytically active MTC1, enable efficient cascade reactions including visible light-induced aerobic hydroxylation of 4-nitrophenylboronic acid to 4-nitrophenol and the following hydrogenation reduction with NaBH4.	Palladium	15-24	ret proto-oncogene	Homo sapiens	101-105
31559679-4	2019	Such ultrafine palladium nanoparticles in Pd@MTC1-1/5, in cooperation with photocatalytically active MTC1, enable efficient cascade reactions including visible light-induced aerobic hydroxylation of 4-nitrophenylboronic acid to 4-nitrophenol and the following hydrogenation reduction with NaBH4.	Palladium	42-44	ret proto-oncogene	Homo sapiens	45-49
31559679-4	2019	Such ultrafine palladium nanoparticles in Pd@MTC1-1/5, in cooperation with photocatalytically active MTC1, enable efficient cascade reactions including visible light-induced aerobic hydroxylation of 4-nitrophenylboronic acid to 4-nitrophenol and the following hydrogenation reduction with NaBH4.	Palladium	42-44	ret proto-oncogene	Homo sapiens	101-105
31559679-4	2019	Such ultrafine palladium nanoparticles in Pd@MTC1-1/5, in cooperation with photocatalytically active MTC1, enable efficient cascade reactions including visible light-induced aerobic hydroxylation of 4-nitrophenylboronic acid to 4-nitrophenol and the following hydrogenation reduction with NaBH4.	3-nitrobenzeneboronic acid	199-224	ret proto-oncogene	Homo sapiens	45-49
31559679-4	2019	Such ultrafine palladium nanoparticles in Pd@MTC1-1/5, in cooperation with photocatalytically active MTC1, enable efficient cascade reactions including visible light-induced aerobic hydroxylation of 4-nitrophenylboronic acid to 4-nitrophenol and the following hydrogenation reduction with NaBH4.	3-nitrobenzeneboronic acid	199-224	ret proto-oncogene	Homo sapiens	101-105
31559679-4	2019	Such ultrafine palladium nanoparticles in Pd@MTC1-1/5, in cooperation with photocatalytically active MTC1, enable efficient cascade reactions including visible light-induced aerobic hydroxylation of 4-nitrophenylboronic acid to 4-nitrophenol and the following hydrogenation reduction with NaBH4.	4-nitrophenol	228-241	ret proto-oncogene	Homo sapiens	45-49
31559679-4	2019	Such ultrafine palladium nanoparticles in Pd@MTC1-1/5, in cooperation with photocatalytically active MTC1, enable efficient cascade reactions including visible light-induced aerobic hydroxylation of 4-nitrophenylboronic acid to 4-nitrophenol and the following hydrogenation reduction with NaBH4.	4-nitrophenol	228-241	ret proto-oncogene	Homo sapiens	101-105
31559679-4	2019	Such ultrafine palladium nanoparticles in Pd@MTC1-1/5, in cooperation with photocatalytically active MTC1, enable efficient cascade reactions including visible light-induced aerobic hydroxylation of 4-nitrophenylboronic acid to 4-nitrophenol and the following hydrogenation reduction with NaBH4.	Sodium	289-294	ret proto-oncogene	Homo sapiens	45-49
31559679-4	2019	Such ultrafine palladium nanoparticles in Pd@MTC1-1/5, in cooperation with photocatalytically active MTC1, enable efficient cascade reactions including visible light-induced aerobic hydroxylation of 4-nitrophenylboronic acid to 4-nitrophenol and the following hydrogenation reduction with NaBH4.	Sodium	289-294	ret proto-oncogene	Homo sapiens	101-105
31478160-0	2019	Synchronous bilateral pheochromocytomas and bilobar medullary thyroid carcinoma revealed by 18F-FDOPA PET/CT in a MEN-2A asymptomatic patient.	fluorodopa F 18	92-101	ret proto-oncogene	Homo sapiens	114-120
31768065-3	2019	In this study, we uncovered activating mutations in CSF1R and rearrangements in RET and ALK that conferred dramatic responses to selective inhibition of RET (selpercatinib) and crizotinib, respectively, in patients with histiocytosis.	Crizotinib	177-187	ret proto-oncogene	Homo sapiens	80-83
31768065-3	2019	In this study, we uncovered activating mutations in CSF1R and rearrangements in RET and ALK that conferred dramatic responses to selective inhibition of RET (selpercatinib) and crizotinib, respectively, in patients with histiocytosis.	Selpercatinib	158-171	ret proto-oncogene	Homo sapiens	80-83
31715421-6	2019	RET fusions or rearrangements are somatic juxtapositions of 5" sequences from other genes with 3" RET sequences encoding tyrosine kinase.	Tyrosine	121-129	ret proto-oncogene	Homo sapiens	0-3
31715421-6	2019	RET fusions or rearrangements are somatic juxtapositions of 5" sequences from other genes with 3" RET sequences encoding tyrosine kinase.	Tyrosine	121-129	ret proto-oncogene	Homo sapiens	98-101
31715421-9	2019	Tyrosine kinase inhibitors are drugs that target kinases such as RET in RET-driven (RET-mutation or RET-fusion-positive) disease.	Tyrosine	0-8	ret proto-oncogene	Homo sapiens	65-68
31715421-9	2019	Tyrosine kinase inhibitors are drugs that target kinases such as RET in RET-driven (RET-mutation or RET-fusion-positive) disease.	Tyrosine	0-8	ret proto-oncogene	Homo sapiens	72-75
31715421-9	2019	Tyrosine kinase inhibitors are drugs that target kinases such as RET in RET-driven (RET-mutation or RET-fusion-positive) disease.	Tyrosine	0-8	ret proto-oncogene	Homo sapiens	72-75
31715421-9	2019	Tyrosine kinase inhibitors are drugs that target kinases such as RET in RET-driven (RET-mutation or RET-fusion-positive) disease.	Tyrosine	0-8	ret proto-oncogene	Homo sapiens	72-75
31715421-12	2019	Selective RET inhibitor drugs LOXO-292 (selpercatinib) and BLU-667 (pralsetinib) are also undergoing phase I/II and I clinical trials, respectively, with preliminary results demonstrating partial response and low incidence of serious adverse events.	Selpercatinib	40-53	ret proto-oncogene	Homo sapiens	10-13
31715421-12	2019	Selective RET inhibitor drugs LOXO-292 (selpercatinib) and BLU-667 (pralsetinib) are also undergoing phase I/II and I clinical trials, respectively, with preliminary results demonstrating partial response and low incidence of serious adverse events.	CRY1 protein, Arabidopsis	59-66	ret proto-oncogene	Homo sapiens	10-13
31715421-12	2019	Selective RET inhibitor drugs LOXO-292 (selpercatinib) and BLU-667 (pralsetinib) are also undergoing phase I/II and I clinical trials, respectively, with preliminary results demonstrating partial response and low incidence of serious adverse events.	CRY1 protein, Arabidopsis	68-79	ret proto-oncogene	Homo sapiens	10-13
31715421-13	2019	RET fusions provide a viable therapeutic target for oncologic treatment, and further study is warranted into the prevalence and pathogenesis of RET fusions as well as development of current and new tyrosine kinase inhibitors.	Tyrosine	198-206	ret proto-oncogene	Homo sapiens	0-3
31710864-0	2019	A phase 2 study of lenvatinib in patients with RET fusion-positive lung adenocarcinoma.	lenvatinib	19-29	ret proto-oncogene	Homo sapiens	47-50
31710864-4	2019	Lenvatinib is a multityrosine kinase inhibitor of vascular endothelial growth factor receptors 1-3, fibroblast growth factor receptors 1-4, RET, and other targets.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	140-143
31710864-5	2019	This study evaluated the safety and efficacy of lenvatinib in patients with RET fusion-positive lung adenocarcinoma.	lenvatinib	48-58	ret proto-oncogene	Homo sapiens	76-79
31710864-6	2019	MATERIALS AND METHODS: In this phase 2, multicenter, open-label study (NCT01877083), patients with RET-positive lung adenocarcinoma received oral lenvatinib 24 mg/day.	lenvatinib	146-156	ret proto-oncogene	Homo sapiens	99-102
31710864-15	2019	CONCLUSIONS: Lenvatinib demonstrated activity in patients with RET fusion-positive lung adenocarcinomas; although the response rate was relatively low, the median PFS supports the activity of lenvatinib in these patients.	lenvatinib	13-23	ret proto-oncogene	Homo sapiens	63-66
31768065-3	2019	In this study, we uncovered activating mutations in CSF1R and rearrangements in RET and ALK that conferred dramatic responses to selective inhibition of RET (selpercatinib) and crizotinib, respectively, in patients with histiocytosis.	Selpercatinib	158-171	ret proto-oncogene	Homo sapiens	153-156
31754623-0	2019	Plasma receptor tyrosine kinase RET in pulmonary arterial hypertension diagnosis and differentiation.	Tyrosine	16-24	ret proto-oncogene	Homo sapiens	32-35
31772157-5	2019	MRM retrieval + ketamine (RET + KET) effectively reduced the reinforcing effects of alcohol and long-term drinking levels, compared to ketamine or retrieval alone.	Ketamine	16-24	ret proto-oncogene	Homo sapiens	26-29
31772157-5	2019	MRM retrieval + ketamine (RET + KET) effectively reduced the reinforcing effects of alcohol and long-term drinking levels, compared to ketamine or retrieval alone.	Ethanol	84-91	ret proto-oncogene	Homo sapiens	26-29
31754623-5	2019	Results: Plasma proto-oncogene tyrosine-protein kinase receptor Ret (RET) was decreased (p&lt;0.04) in PAH compared with all disease groups and controls.	Tyrosine	31-39	ret proto-oncogene	Homo sapiens	64-67
31754623-5	2019	Results: Plasma proto-oncogene tyrosine-protein kinase receptor Ret (RET) was decreased (p&lt;0.04) in PAH compared with all disease groups and controls.	Tyrosine	31-39	ret proto-oncogene	Homo sapiens	69-72
31639374-1	2019	Crizotinib is an oral small-molecule tyrosine kinase inhibitor targeting anaplastic lymphoma kinase (ALK), ROS proto-oncogene 1, receptor tyrosine kinase (ROS1) and MET proto-oncogene, receptor tyrosine kinase (MET).	Crizotinib	0-10	ret proto-oncogene	Homo sapiens	129-153
31639374-1	2019	Crizotinib is an oral small-molecule tyrosine kinase inhibitor targeting anaplastic lymphoma kinase (ALK), ROS proto-oncogene 1, receptor tyrosine kinase (ROS1) and MET proto-oncogene, receptor tyrosine kinase (MET).	Crizotinib	0-10	ret proto-oncogene	Homo sapiens	185-209
31576385-1	2019	In this study, a wavelength-resolved electrochemiluminescence resonance energy transfer (ECL-RET) ratiometric immunosensor from Au nanoparticle functionalized graphite-like carbon nitride nanosheets (Au-g-C3N4) to Au nanoclusters (Au NCs) has been constructed for the first time.	Gold	128-130	ret proto-oncogene	Homo sapiens	93-96
31576385-1	2019	In this study, a wavelength-resolved electrochemiluminescence resonance energy transfer (ECL-RET) ratiometric immunosensor from Au nanoparticle functionalized graphite-like carbon nitride nanosheets (Au-g-C3N4) to Au nanoclusters (Au NCs) has been constructed for the first time.	Graphite	159-167	ret proto-oncogene	Homo sapiens	93-96
31576385-1	2019	In this study, a wavelength-resolved electrochemiluminescence resonance energy transfer (ECL-RET) ratiometric immunosensor from Au nanoparticle functionalized graphite-like carbon nitride nanosheets (Au-g-C3N4) to Au nanoclusters (Au NCs) has been constructed for the first time.	cyanogen	173-187	ret proto-oncogene	Homo sapiens	93-96
31576385-1	2019	In this study, a wavelength-resolved electrochemiluminescence resonance energy transfer (ECL-RET) ratiometric immunosensor from Au nanoparticle functionalized graphite-like carbon nitride nanosheets (Au-g-C3N4) to Au nanoclusters (Au NCs) has been constructed for the first time.	Gold	200-202	ret proto-oncogene	Homo sapiens	93-96
31576385-1	2019	In this study, a wavelength-resolved electrochemiluminescence resonance energy transfer (ECL-RET) ratiometric immunosensor from Au nanoparticle functionalized graphite-like carbon nitride nanosheets (Au-g-C3N4) to Au nanoclusters (Au NCs) has been constructed for the first time.	c3n4	205-209	ret proto-oncogene	Homo sapiens	93-96
31576385-1	2019	In this study, a wavelength-resolved electrochemiluminescence resonance energy transfer (ECL-RET) ratiometric immunosensor from Au nanoparticle functionalized graphite-like carbon nitride nanosheets (Au-g-C3N4) to Au nanoclusters (Au NCs) has been constructed for the first time.	Gold	200-202	ret proto-oncogene	Homo sapiens	93-96
31662016-3	2021	Reticulocyte hemoglobin content (RET-He), a measure of iron deficiency, has not been well evaluated prior to discharge in premature infants.Objectives: Our objectives were to evaluate RET-He and its correlation with serum ferritin (SF), an index of iron stores, at 35-36 weeks postmenstrual age (PMA) in <=32 weeks gestational age (GA) infants.Methods: We performed a prospective nested study involving 24-32 weeks GA infants who were receiving 2 mg/kg/day oral elemental iron with full enteral feedings at 35-36 weeks PMA.	Iron	55-59	ret proto-oncogene	Homo sapiens	33-36
31536726-9	2019	AKT inhibitor (AKTi) resistant HCC1806 showed decreased proliferation associated with downregulated dynamics of FRET-ERK when treated with KIs targeting protein receptor tyrosine kinase (RTK).	hcc1806	31-38	ret proto-oncogene	Homo sapiens	161-185
31536726-9	2019	AKT inhibitor (AKTi) resistant HCC1806 showed decreased proliferation associated with downregulated dynamics of FRET-ERK when treated with KIs targeting protein receptor tyrosine kinase (RTK).	hcc1806	31-38	ret proto-oncogene	Homo sapiens	187-190
31374369-12	2019	Timely lorlatinib administration or combined therapy with an ALK inhibitor and other receptor tyrosine-kinase inhibitors might constitute a potent strategy.	lorlatinib	7-17	ret proto-oncogene	Homo sapiens	85-109
31513960-4	2019	For the ECL analysis, s-PdNFs could effectively quench the ECL intensity of peroxydisulfate/oxygen (S2O82-/O2) system via ECL resonance energy transfer (ECL-RET).	Peroxydisulfate	76-91	ret proto-oncogene	Homo sapiens	157-160
31513960-4	2019	For the ECL analysis, s-PdNFs could effectively quench the ECL intensity of peroxydisulfate/oxygen (S2O82-/O2) system via ECL resonance energy transfer (ECL-RET).	Oxygen	92-98	ret proto-oncogene	Homo sapiens	157-160
31513960-4	2019	For the ECL analysis, s-PdNFs could effectively quench the ECL intensity of peroxydisulfate/oxygen (S2O82-/O2) system via ECL resonance energy transfer (ECL-RET).	s2o82-	100-106	ret proto-oncogene	Homo sapiens	157-160
31513960-4	2019	For the ECL analysis, s-PdNFs could effectively quench the ECL intensity of peroxydisulfate/oxygen (S2O82-/O2) system via ECL resonance energy transfer (ECL-RET).	Oxygen	107-109	ret proto-oncogene	Homo sapiens	157-160
31717697-0	2019	Oxygen Tension Regulates Lysosomal Activation and Receptor Tyrosine Kinase Degradation.	Oxygen	0-6	ret proto-oncogene	Homo sapiens	50-74
31717697-6	2019	Our results link oxygen tension and lysosomal activity, provide a molecular explanation of the malignant phenotype associated with hypoxic tumors, and suggest activation of lysosomes may provide therapeutic benefit in RTK-targeted cancer therapy.	Oxygen	17-23	ret proto-oncogene	Homo sapiens	218-221
31662016-9	2021	RET-He increases with an increase in iron stores, suggesting that additional iron supplementation prior to discharge to very premature infants with borderline low RET-He may help prevent iron deficiency during early infancy.	Iron	37-41	ret proto-oncogene	Homo sapiens	0-3
31662016-9	2021	RET-He increases with an increase in iron stores, suggesting that additional iron supplementation prior to discharge to very premature infants with borderline low RET-He may help prevent iron deficiency during early infancy.	Iron	77-81	ret proto-oncogene	Homo sapiens	0-3
31662016-9	2021	RET-He increases with an increase in iron stores, suggesting that additional iron supplementation prior to discharge to very premature infants with borderline low RET-He may help prevent iron deficiency during early infancy.	Iron	77-81	ret proto-oncogene	Homo sapiens	163-166
31514493-1	2019	A dual-wavelength ratiometric electrochemiluminescence resonance energy transfer (ECL-RET) aptasensor based on the carbon nitride nanosheet (g-C3N4 NS) and metal-organic frameworks (Ru@MOF) as energy donor-receptor pairs is firstly designed for detection of Amyloid-beta protein (Abeta).	cyanogen	115-129	ret proto-oncogene	Homo sapiens	86-89
31636608-4	2019	The BON1 cell line was used as a pNEN model and the well-known Receptor Tyrosine Kinase inhibitor Sunitinib was used in order to better investigate the different features of each method.	sunitinib	98-107	ret proto-oncogene	Homo sapiens	63-87
31649719-8	2019	In addition, we explored the effects of read-through reagents on RET nonsense mutations and showed that G418 significantly increased the full-length RET protein expression of p.Y263X in a dose-dependent manner, together with a mild recovery of p-ERK and p-STAT3.	antibiotic G 418	104-108	ret proto-oncogene	Homo sapiens	65-68
31649719-8	2019	In addition, we explored the effects of read-through reagents on RET nonsense mutations and showed that G418 significantly increased the full-length RET protein expression of p.Y263X in a dose-dependent manner, together with a mild recovery of p-ERK and p-STAT3.	antibiotic G 418	104-108	ret proto-oncogene	Homo sapiens	149-152
30360984-3	2019	Given that beta-hydroxy-beta-methyl-butyrate (HMB) supplementation during RET improves lean body mass in younger humans, and that we have shown that HMB acutely stimulates muscle protein synthesis (MPS) and inhibits breakdown; we hypothesized that chronic supplementation of HMB free acid (HMB-FA) would enhance MPS and muscle mass/function in response to RET in older people.	beta-hydroxyisovaleric acid	46-49	ret proto-oncogene	Homo sapiens	74-77
31351417-1	2019	Herein, a highly efficient dual-quenching biosensor based on electrochemiluminescence resonance energy transfer (ECL-RET) is designed utilizing Ru-In2S3 as ECL acceptor and alpha-MoO3-Au as ECL donor.	ru-in2s3	144-152	ret proto-oncogene	Homo sapiens	117-120
31351417-1	2019	Herein, a highly efficient dual-quenching biosensor based on electrochemiluminescence resonance energy transfer (ECL-RET) is designed utilizing Ru-In2S3 as ECL acceptor and alpha-MoO3-Au as ECL donor.	alpha-moo3-au	173-186	ret proto-oncogene	Homo sapiens	117-120
31351417-7	2019	Importantly, a novel ECL-RET pair of Ru-In2S3 (donor)/alpha-MoO3-Au (acceptor) is firstly developed, which opened an efficient way for highly sensitive detection of antibody in disease clinical and diagnosis analysis.	ru-in2s3	37-45	ret proto-oncogene	Homo sapiens	25-28
31351417-7	2019	Importantly, a novel ECL-RET pair of Ru-In2S3 (donor)/alpha-MoO3-Au (acceptor) is firstly developed, which opened an efficient way for highly sensitive detection of antibody in disease clinical and diagnosis analysis.	alpha-moo3-au	54-67	ret proto-oncogene	Homo sapiens	25-28
30360984-3	2019	Given that beta-hydroxy-beta-methyl-butyrate (HMB) supplementation during RET improves lean body mass in younger humans, and that we have shown that HMB acutely stimulates muscle protein synthesis (MPS) and inhibits breakdown; we hypothesized that chronic supplementation of HMB free acid (HMB-FA) would enhance MPS and muscle mass/function in response to RET in older people.	beta-hydroxyisovaleric acid	149-152	ret proto-oncogene	Homo sapiens	356-359
30360984-8	2019	RET induced strength increases (1-RM) in the exercised leg of both groups (398 +- 22N to 499 +- 30N HMB-FA vs. 396 +- 29N to 510 +- 43N PLA (both P &lt; 0.05)).	hmb-fa	100-106	ret proto-oncogene	Homo sapiens	0-3
31364476-11	2019	An in vitro assay revealed that the phosphorylation level of RET tyrosine 905 was relatively higher in the RET S409Y mutant than in wild-type (WT) RET.	Tyrosine	65-73	ret proto-oncogene	Homo sapiens	61-64
31409511-5	2019	Next generation sequencing (NGS) of paired tumor and peripheral blood revealed a germline pathogenic RET mutation, indicating the hereditary nature of MTC in this patient.	mtc	151-154	ret proto-oncogene	Homo sapiens	101-104
31364476-11	2019	An in vitro assay revealed that the phosphorylation level of RET tyrosine 905 was relatively higher in the RET S409Y mutant than in wild-type (WT) RET.	Tyrosine	65-73	ret proto-oncogene	Homo sapiens	107-110
31364476-11	2019	An in vitro assay revealed that the phosphorylation level of RET tyrosine 905 was relatively higher in the RET S409Y mutant than in wild-type (WT) RET.	Tyrosine	65-73	ret proto-oncogene	Homo sapiens	107-110
31416302-3	2019	The newly synthesized S-doped Lu2O3, which shows a 3 times better ECL performance than Lu2O3, was chosen as the donor in this ECL-RET system.	lu2o3	30-35	ret proto-oncogene	Homo sapiens	130-133
31576143-2	2019	The initial treatment strategy for RET rearranged NSCLC has been multi-target tyrosine kinase inhibition.	Tyrosine	78-86	ret proto-oncogene	Homo sapiens	35-38
31278686-4	2019	RESULTS: All MTCs and PHEOs were positive for RET9 and RET51.	pheos	22-27	ret proto-oncogene	Homo sapiens	55-60
31226468-0	2019	Identification of nicotinamide aminonaphthyridine compounds as potent RET kinase inhibitors and antitumor activities against RET rearranged lung adenocarcinoma.	nicotinamide aminonaphthyridine compounds	18-59	ret proto-oncogene	Homo sapiens	70-73
31226468-0	2019	Identification of nicotinamide aminonaphthyridine compounds as potent RET kinase inhibitors and antitumor activities against RET rearranged lung adenocarcinoma.	nicotinamide aminonaphthyridine compounds	18-59	ret proto-oncogene	Homo sapiens	125-128
31226468-5	2019	Our group previously reported that the benzamide aminonaphthyridine HSN356, a multikinase inhibitor, also inhibited RET.	benzamide aminonaphthyridine	39-67	ret proto-oncogene	Homo sapiens	116-119
31226468-5	2019	Our group previously reported that the benzamide aminonaphthyridine HSN356, a multikinase inhibitor, also inhibited RET.	hsn356	68-74	ret proto-oncogene	Homo sapiens	116-119
31226468-9	2019	Under similar conditions, BLU667 and vandetanib (two drugs being evaluated against RET-driven cancers in the clinic) inhibited the growth of LC-2/ad with IC50 values of ~10 and 328 nM respectively.	vandetanib	37-47	ret proto-oncogene	Homo sapiens	83-86
31278686-15	2019	RET9 was more highly expressed than RET51 in PHEOs.	pheos	45-50	ret proto-oncogene	Homo sapiens	36-41
31431614-2	2019	In this study, we delineate that KRAS-mutant lung cancer cells resistant to pemetrexed (MTA) and anti-MEK drug trametinib acquire an exquisite dependency on endoplasmic reticulum (ER) stress signaling, rendering resistant cancer cells selectively susceptible to blockage of HSP90, the receptor tyrosine kinase AXL, the eukaryotic translation initiation factor 4E (eIF4E), and the unfolded protein response (UPR).	Pemetrexed	76-86	ret proto-oncogene	Homo sapiens	285-309
31350450-1	2019	OBJECTIVE: The reticulocyte index reticulocyte hemoglobin equivalent (Ret-He) was evaluated as a marker of iron status.	Iron	107-111	ret proto-oncogene	Homo sapiens	70-73
31350450-7	2019	CONCLUSION: Ret-He values showed a slow uptrend with enteral iron supplementation following an initial decrease, suggesting that neonates are able to improve their iron sufficiency status with supplementation.	Iron	61-65	ret proto-oncogene	Homo sapiens	12-15
31350450-7	2019	CONCLUSION: Ret-He values showed a slow uptrend with enteral iron supplementation following an initial decrease, suggesting that neonates are able to improve their iron sufficiency status with supplementation.	Iron	164-168	ret proto-oncogene	Homo sapiens	12-15
31431614-2	2019	In this study, we delineate that KRAS-mutant lung cancer cells resistant to pemetrexed (MTA) and anti-MEK drug trametinib acquire an exquisite dependency on endoplasmic reticulum (ER) stress signaling, rendering resistant cancer cells selectively susceptible to blockage of HSP90, the receptor tyrosine kinase AXL, the eukaryotic translation initiation factor 4E (eIF4E), and the unfolded protein response (UPR).	trametinib	111-121	ret proto-oncogene	Homo sapiens	285-309
31534554-0	2019	ATF4 destabilizes RET through nonclassical GRP78 inhibition to enhance chemosensitivity to bortezomib in human osteosarcoma.	Bortezomib	91-101	ret proto-oncogene	Homo sapiens	18-21
31100409-4	2019	Activated RTK recruits Shc, via its phosphotyrosine binding (PTB) domain (ShcPTB), precipitating the release of Erk to engage in a signalling response.	Phosphotyrosine	36-51	ret proto-oncogene	Homo sapiens	10-13
31178471-0	2019	Aberrant Transcriptional Regulation of Super-enhancers by RET Finger Protein-histone Deacetylase 1 Complex in Glioblastoma: Chemoresistance to Temozolomide.	Temozolomide	143-155	ret proto-oncogene	Homo sapiens	58-61
31534554-11	2019	We found that ATF4 downregulation was tightly linked to the aberrant expression of RET, primarily due to RET stabilization in OS/BTZ cells.	Bortezomib	129-132	ret proto-oncogene	Homo sapiens	83-86
31534554-11	2019	We found that ATF4 downregulation was tightly linked to the aberrant expression of RET, primarily due to RET stabilization in OS/BTZ cells.	Bortezomib	129-132	ret proto-oncogene	Homo sapiens	105-108
31534554-12	2019	Loss of RET upregulated ATF4 and potentiated the apoptotic response to BTZ.	Bortezomib	71-74	ret proto-oncogene	Homo sapiens	8-11
31534554-13	2019	ATF4 recognized the TK domain of RET by recruiting its transactivated E3 ligase Cbl-c to accelerate RET proteasomal turnover, which in turn prevented BTZ resistance.	Bortezomib	150-153	ret proto-oncogene	Homo sapiens	33-36
31534554-13	2019	ATF4 recognized the TK domain of RET by recruiting its transactivated E3 ligase Cbl-c to accelerate RET proteasomal turnover, which in turn prevented BTZ resistance.	Bortezomib	150-153	ret proto-oncogene	Homo sapiens	100-103
31274634-5	2019	In case of several endocrine diseases coexistence as in MEN 2A, F-DOPA should be carefully analyzed.	fluorodopa F 18	64-70	ret proto-oncogene	Homo sapiens	56-62
31395059-1	2019	BACKGROUND: This study aimed to investigate the prognostic value of volumetric parameters on 18F- fluoro-2-deoxy-D-glucose (18F-FDG) positron emission tomography/computed tomography (PET/CT) in gastric-cancer patients, according to the expression status of c-MET (MET proto-oncogene, receptor tyrosine kinase), which was previously unclear.	Fluorodeoxyglucose F18	124-131	ret proto-oncogene	Homo sapiens	284-308
31360064-0	2019	Successful long-term treatment of non-small cell lung cancer positive for RET rearrangement with pemetrexed.	Pemetrexed	97-107	ret proto-oncogene	Homo sapiens	74-77
31461086-2	2019	Erdafitinib also binds to RET, colony-stimulating factor 1 receptor (CSF-1R), platelet-derived growth factor receptor alpha and beta (PDGFR-alpha and PDGFR-beta), Fms-related tyrosine kinase 4 (FLT4), KIT and vascular endothelial growth factor receptor 2 (VEGFR-2), exhibiting additional antitumor mechanisms resulting in cell kill.	erdafitinib	0-11	ret proto-oncogene	Homo sapiens	26-29
31392261-0	2019	Cryo-EM structure of the activated RET signaling complex reveals the importance of its cysteine-rich domain.	Cysteine	87-95	ret proto-oncogene	Homo sapiens	35-38
31392261-5	2019	Two key interaction points required for RET extracellular domain binding were observed: (i) the calcium-binding site in RET that contacts GFRalpha2 domain 3 and (ii) the RET cysteine-rich domain interaction with NRTN.	Calcium	96-103	ret proto-oncogene	Homo sapiens	40-43
31392261-5	2019	Two key interaction points required for RET extracellular domain binding were observed: (i) the calcium-binding site in RET that contacts GFRalpha2 domain 3 and (ii) the RET cysteine-rich domain interaction with NRTN.	Calcium	96-103	ret proto-oncogene	Homo sapiens	120-123
31392261-5	2019	Two key interaction points required for RET extracellular domain binding were observed: (i) the calcium-binding site in RET that contacts GFRalpha2 domain 3 and (ii) the RET cysteine-rich domain interaction with NRTN.	Calcium	96-103	ret proto-oncogene	Homo sapiens	120-123
31392261-5	2019	Two key interaction points required for RET extracellular domain binding were observed: (i) the calcium-binding site in RET that contacts GFRalpha2 domain 3 and (ii) the RET cysteine-rich domain interaction with NRTN.	Cysteine	174-182	ret proto-oncogene	Homo sapiens	40-43
31392261-5	2019	Two key interaction points required for RET extracellular domain binding were observed: (i) the calcium-binding site in RET that contacts GFRalpha2 domain 3 and (ii) the RET cysteine-rich domain interaction with NRTN.	Cysteine	174-182	ret proto-oncogene	Homo sapiens	120-123
31392261-5	2019	Two key interaction points required for RET extracellular domain binding were observed: (i) the calcium-binding site in RET that contacts GFRalpha2 domain 3 and (ii) the RET cysteine-rich domain interaction with NRTN.	Cysteine	174-182	ret proto-oncogene	Homo sapiens	120-123
31392261-6	2019	The structure highlights the importance of the RET cysteine-rich domain and allows proposition of a model to explain how complex formation leads to RET receptor dimerization and its activation.	Cysteine	51-59	ret proto-oncogene	Homo sapiens	47-50
31392261-6	2019	The structure highlights the importance of the RET cysteine-rich domain and allows proposition of a model to explain how complex formation leads to RET receptor dimerization and its activation.	Cysteine	51-59	ret proto-oncogene	Homo sapiens	148-151
31241892-2	2019	The ECL detection procedure was performed on a recyclable MnO2/AuNC-modified glassy carbon electrode interface by taking advantage of the ECL-RET between the AuNC probe and MnO2 nanomaterials (NMs) to quench the ECL intensity.	aunc	63-67	ret proto-oncogene	Homo sapiens	142-145
31241892-2	2019	The ECL detection procedure was performed on a recyclable MnO2/AuNC-modified glassy carbon electrode interface by taking advantage of the ECL-RET between the AuNC probe and MnO2 nanomaterials (NMs) to quench the ECL intensity.	aunc	158-162	ret proto-oncogene	Homo sapiens	142-145
30940655-8	2019	By targeting the RET-Src axis, regorafenib potently inhibited JAK1/2-STAT1 and MAPK signaling and subsequently attenuated the IFNgamma-induced PD-L1 and IDO1 expression without affecting MHC-I expression much.	regorafenib	31-42	ret proto-oncogene	Homo sapiens	17-20
30940655-9	2019	Moreover, RET and Src co-high expression was an independent unfavorable prognosis factor in melanoma patients with or without ICB through inhibiting the antitumor immune response.	indole-2-carboxylic acid	126-129	ret proto-oncogene	Homo sapiens	10-13
30940655-10	2019	CONCLUSIONS: Our data unveiled a new mechanism of alleviating IFNgamma-induced PD-L1 and IDO1 expression and provided a rationale to explore a novel combination of ICB with regorafenib clinically, especially in melanoma with RET/Src axis activation.	indole-2-carboxylic acid	164-167	ret proto-oncogene	Homo sapiens	225-228
31360064-3	2019	We here report a case of NSCLC positive for the CCDC6-RET fusion gene that benefited from treatment with pemetrexed over a period of 30 months, suggesting that thymidylate synthase-targeted drugs such as pemetrexed may show efficacy for NSCLC harboring RET fusions.	Pemetrexed	105-115	ret proto-oncogene	Homo sapiens	54-57
31360064-3	2019	We here report a case of NSCLC positive for the CCDC6-RET fusion gene that benefited from treatment with pemetrexed over a period of 30 months, suggesting that thymidylate synthase-targeted drugs such as pemetrexed may show efficacy for NSCLC harboring RET fusions.	Pemetrexed	105-115	ret proto-oncogene	Homo sapiens	253-256
31360064-3	2019	We here report a case of NSCLC positive for the CCDC6-RET fusion gene that benefited from treatment with pemetrexed over a period of 30 months, suggesting that thymidylate synthase-targeted drugs such as pemetrexed may show efficacy for NSCLC harboring RET fusions.	Pemetrexed	204-214	ret proto-oncogene	Homo sapiens	54-57
31360064-3	2019	We here report a case of NSCLC positive for the CCDC6-RET fusion gene that benefited from treatment with pemetrexed over a period of 30 months, suggesting that thymidylate synthase-targeted drugs such as pemetrexed may show efficacy for NSCLC harboring RET fusions.	Pemetrexed	204-214	ret proto-oncogene	Homo sapiens	253-256
31118272-9	2019	Comparisons of RET-nintedanib, RET(G810A), and RET-vandetanib crystal structures suggested that the solvent-front Ala-810 makes hydrophobic contacts with a methyl group and aniline in nintedanib and blocks water access to two oxygen atoms of vandetanib, resulting in an energetic penalty for burying polar groups.	nintedanib	19-29	ret proto-oncogene	Homo sapiens	15-18
31118272-0	2019	Structural basis of resistance of mutant RET protein-tyrosine kinase to its inhibitors nintedanib and vandetanib.	nintedanib	87-97	ret proto-oncogene	Homo sapiens	41-44
31118272-0	2019	Structural basis of resistance of mutant RET protein-tyrosine kinase to its inhibitors nintedanib and vandetanib.	vandetanib	102-112	ret proto-oncogene	Homo sapiens	41-44
31118272-10	2019	Of note, even though the p.L881V mutation did not affect sensitivity to nintedanib, RET(L881V) was resistant to nintedanib analogs lacking a phenyl group.	nintedanib	112-122	ret proto-oncogene	Homo sapiens	84-87
31118272-4	2019	Nintedanib is a RET TKI that inhibits the vandetanib-resistant RET(G810A) mutant.	nintedanib	0-10	ret proto-oncogene	Homo sapiens	16-19
31118272-4	2019	Nintedanib is a RET TKI that inhibits the vandetanib-resistant RET(G810A) mutant.	nintedanib	0-10	ret proto-oncogene	Homo sapiens	63-66
31118272-4	2019	Nintedanib is a RET TKI that inhibits the vandetanib-resistant RET(G810A) mutant.	vandetanib	42-52	ret proto-oncogene	Homo sapiens	16-19
31118272-4	2019	Nintedanib is a RET TKI that inhibits the vandetanib-resistant RET(G810A) mutant.	vandetanib	42-52	ret proto-oncogene	Homo sapiens	63-66
31118272-11	2019	These results provide structural insights into resistance of RET mutants against the TKIs nintedanib and vandetanib.	nintedanib	90-100	ret proto-oncogene	Homo sapiens	61-64
31118272-5	2019	Here, we determined the X-ray co-crystal structure of RET kinase domain-nintedanib complex to 1.87 A resolution and a RET(G810A) kinase domain crystal structure to 1.99 A resolution.	nintedanib	72-82	ret proto-oncogene	Homo sapiens	54-57
31118272-6	2019	We also identified a vandetanib-resistant RET(L881V) mutation previously found in familial medullary thyroid carcinoma.	vandetanib	21-31	ret proto-oncogene	Homo sapiens	42-45
31118272-7	2019	Drug-sensitivity profiling of RET(L881V) revealed that it remains sensitive to nintedanib.	nintedanib	79-89	ret proto-oncogene	Homo sapiens	30-33
31118272-8	2019	The RET-nintedanib co-crystal structure disclosed that Leu-730 in RET engages in hydrophobic interactions with the piperazine, anilino, and phenyl groups of nintedanib, providing a structural basis for explaining that the p.L730V mutation identified in nine independently isolated cell lines resistant to nintedanib.	nintedanib	8-18	ret proto-oncogene	Homo sapiens	4-7
31118272-8	2019	The RET-nintedanib co-crystal structure disclosed that Leu-730 in RET engages in hydrophobic interactions with the piperazine, anilino, and phenyl groups of nintedanib, providing a structural basis for explaining that the p.L730V mutation identified in nine independently isolated cell lines resistant to nintedanib.	nintedanib	8-18	ret proto-oncogene	Homo sapiens	66-69
31118272-8	2019	The RET-nintedanib co-crystal structure disclosed that Leu-730 in RET engages in hydrophobic interactions with the piperazine, anilino, and phenyl groups of nintedanib, providing a structural basis for explaining that the p.L730V mutation identified in nine independently isolated cell lines resistant to nintedanib.	Leucine	55-58	ret proto-oncogene	Homo sapiens	4-7
31118272-8	2019	The RET-nintedanib co-crystal structure disclosed that Leu-730 in RET engages in hydrophobic interactions with the piperazine, anilino, and phenyl groups of nintedanib, providing a structural basis for explaining that the p.L730V mutation identified in nine independently isolated cell lines resistant to nintedanib.	Leucine	55-58	ret proto-oncogene	Homo sapiens	66-69
31118272-8	2019	The RET-nintedanib co-crystal structure disclosed that Leu-730 in RET engages in hydrophobic interactions with the piperazine, anilino, and phenyl groups of nintedanib, providing a structural basis for explaining that the p.L730V mutation identified in nine independently isolated cell lines resistant to nintedanib.	Piperazine	115-125	ret proto-oncogene	Homo sapiens	4-7
31118272-8	2019	The RET-nintedanib co-crystal structure disclosed that Leu-730 in RET engages in hydrophobic interactions with the piperazine, anilino, and phenyl groups of nintedanib, providing a structural basis for explaining that the p.L730V mutation identified in nine independently isolated cell lines resistant to nintedanib.	Piperazine	115-125	ret proto-oncogene	Homo sapiens	66-69
31118272-8	2019	The RET-nintedanib co-crystal structure disclosed that Leu-730 in RET engages in hydrophobic interactions with the piperazine, anilino, and phenyl groups of nintedanib, providing a structural basis for explaining that the p.L730V mutation identified in nine independently isolated cell lines resistant to nintedanib.	nintedanib	157-167	ret proto-oncogene	Homo sapiens	4-7
31118272-8	2019	The RET-nintedanib co-crystal structure disclosed that Leu-730 in RET engages in hydrophobic interactions with the piperazine, anilino, and phenyl groups of nintedanib, providing a structural basis for explaining that the p.L730V mutation identified in nine independently isolated cell lines resistant to nintedanib.	nintedanib	157-167	ret proto-oncogene	Homo sapiens	66-69
31118272-8	2019	The RET-nintedanib co-crystal structure disclosed that Leu-730 in RET engages in hydrophobic interactions with the piperazine, anilino, and phenyl groups of nintedanib, providing a structural basis for explaining that the p.L730V mutation identified in nine independently isolated cell lines resistant to nintedanib.	nintedanib	157-167	ret proto-oncogene	Homo sapiens	4-7
31118272-8	2019	The RET-nintedanib co-crystal structure disclosed that Leu-730 in RET engages in hydrophobic interactions with the piperazine, anilino, and phenyl groups of nintedanib, providing a structural basis for explaining that the p.L730V mutation identified in nine independently isolated cell lines resistant to nintedanib.	nintedanib	157-167	ret proto-oncogene	Homo sapiens	66-69
31118272-9	2019	Comparisons of RET-nintedanib, RET(G810A), and RET-vandetanib crystal structures suggested that the solvent-front Ala-810 makes hydrophobic contacts with a methyl group and aniline in nintedanib and blocks water access to two oxygen atoms of vandetanib, resulting in an energetic penalty for burying polar groups.	ala-810	114-121	ret proto-oncogene	Homo sapiens	15-18
31118272-9	2019	Comparisons of RET-nintedanib, RET(G810A), and RET-vandetanib crystal structures suggested that the solvent-front Ala-810 makes hydrophobic contacts with a methyl group and aniline in nintedanib and blocks water access to two oxygen atoms of vandetanib, resulting in an energetic penalty for burying polar groups.	ala-810	114-121	ret proto-oncogene	Homo sapiens	31-34
31118272-9	2019	Comparisons of RET-nintedanib, RET(G810A), and RET-vandetanib crystal structures suggested that the solvent-front Ala-810 makes hydrophobic contacts with a methyl group and aniline in nintedanib and blocks water access to two oxygen atoms of vandetanib, resulting in an energetic penalty for burying polar groups.	ala-810	114-121	ret proto-oncogene	Homo sapiens	31-34
31372039-8	2019	Interestingly, RET fusion occurred only after osimertinib treatment, and contributed to drug resistance in 50% (6 of 12) of patients treated with osimertinib, indicating that fusions had different prevalence when functioning as resistance mechanisms to EGFR TKIs.	osimertinib	46-57	ret proto-oncogene	Homo sapiens	15-18
31372039-8	2019	Interestingly, RET fusion occurred only after osimertinib treatment, and contributed to drug resistance in 50% (6 of 12) of patients treated with osimertinib, indicating that fusions had different prevalence when functioning as resistance mechanisms to EGFR TKIs.	osimertinib	146-157	ret proto-oncogene	Homo sapiens	15-18
31118272-11	2019	These results provide structural insights into resistance of RET mutants against the TKIs nintedanib and vandetanib.	vandetanib	105-115	ret proto-oncogene	Homo sapiens	61-64
31058838-13	2019	Selective RET inhibitors, including LOXO-292 and BLU-667, are progressing in clinical trials.	Selpercatinib	36-44	ret proto-oncogene	Homo sapiens	10-13
30472213-7	2019	Loss of the iodine avidity only occurred in cases of RET/PTC hybrids (7/9 tumors), but not in RET/PTC-negative PTCs (0/41 tumors with available uptake information; p = 0.029).	Iodine	12-18	ret proto-oncogene	Homo sapiens	53-56
30472213-10	2019	The presence of RET rearrangements was associated with a significantly elevated risk to develop iodine refractory disease and lymph node metastases.	Iodine	96-102	ret proto-oncogene	Homo sapiens	16-19
30877105-6	2019	Transcriptomic analysis revealed that exposure to BETi potently downregulated a network of genes involved in receptor tyrosine kinase (RTK) signaling in SMARCA4/A2-deficient cells, including the oncogenic RTK HER3.	beti	50-54	ret proto-oncogene	Homo sapiens	109-133
30877105-6	2019	Transcriptomic analysis revealed that exposure to BETi potently downregulated a network of genes involved in receptor tyrosine kinase (RTK) signaling in SMARCA4/A2-deficient cells, including the oncogenic RTK HER3.	beti	50-54	ret proto-oncogene	Homo sapiens	135-138
30877105-6	2019	Transcriptomic analysis revealed that exposure to BETi potently downregulated a network of genes involved in receptor tyrosine kinase (RTK) signaling in SMARCA4/A2-deficient cells, including the oncogenic RTK HER3.	beti	50-54	ret proto-oncogene	Homo sapiens	205-208
31218225-0	2019	Copper (II) Ions Activate Ligand-Independent Receptor Tyrosine Kinase (RTK) Signaling Pathway.	cupric ion	0-11	ret proto-oncogene	Homo sapiens	45-69
31218225-0	2019	Copper (II) Ions Activate Ligand-Independent Receptor Tyrosine Kinase (RTK) Signaling Pathway.	cupric ion	0-11	ret proto-oncogene	Homo sapiens	71-74
31218225-4	2019	Herein, we reported the effect of copper (II) ions on the ligand-independent RTK cellular signaling pathway.	cupric ion	34-45	ret proto-oncogene	Homo sapiens	77-80
31218225-6	2019	Consequently, copper (II) ions initiate two RTK-mediated downstream signal transductions, including AKT and ERK.	cupric ion	14-25	ret proto-oncogene	Homo sapiens	44-47
31218225-8	2019	Our study proposes a novel role of copper in RTK-mediated signaling for growth factor-independent cancer cell proliferation and migration, implying that targeting both the copper (II) and growth factor in tumor microenvironments may be necessary for cancer treatment.	Copper	35-41	ret proto-oncogene	Homo sapiens	45-48
31218225-8	2019	Our study proposes a novel role of copper in RTK-mediated signaling for growth factor-independent cancer cell proliferation and migration, implying that targeting both the copper (II) and growth factor in tumor microenvironments may be necessary for cancer treatment.	Copper	172-178	ret proto-oncogene	Homo sapiens	45-48
30952243-1	2019	In this work, an innovative aptasensor based on electrochemiluminescence resonance energy transfer (ECL-RET) from CdTe quantum dots (QDs) to a cyanine dye (Cy5) fluorophore for the determination of Ochratoxin A (OTA) was fabricated.	cadmium telluride	114-118	ret proto-oncogene	Homo sapiens	104-107
30952243-1	2019	In this work, an innovative aptasensor based on electrochemiluminescence resonance energy transfer (ECL-RET) from CdTe quantum dots (QDs) to a cyanine dye (Cy5) fluorophore for the determination of Ochratoxin A (OTA) was fabricated.	thionine	143-150	ret proto-oncogene	Homo sapiens	104-107
30952243-1	2019	In this work, an innovative aptasensor based on electrochemiluminescence resonance energy transfer (ECL-RET) from CdTe quantum dots (QDs) to a cyanine dye (Cy5) fluorophore for the determination of Ochratoxin A (OTA) was fabricated.	cyanine dye 5	156-159	ret proto-oncogene	Homo sapiens	104-107
30952243-1	2019	In this work, an innovative aptasensor based on electrochemiluminescence resonance energy transfer (ECL-RET) from CdTe quantum dots (QDs) to a cyanine dye (Cy5) fluorophore for the determination of Ochratoxin A (OTA) was fabricated.	ochratoxin A	198-210	ret proto-oncogene	Homo sapiens	104-107
30952243-3	2019	After the immobilization with the capture DNA (cDNA) and the sequential hybridization with the probe DNA-modified Cy5 (pDNA, the aptamer of OTA), the ECL signal enhanced obviously through the ECL-RET.	cyanine dye 5	114-117	ret proto-oncogene	Homo sapiens	196-199
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
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
30929576-3	2019	RET has been targeted by tyrosine kinase inhibitors (TKIs), such as cabozantinib and vandetanib.	cabozantinib	68-80	ret proto-oncogene	Homo sapiens	0-3
30929576-3	2019	RET has been targeted by tyrosine kinase inhibitors (TKIs), such as cabozantinib and vandetanib.	vandetanib	85-95	ret proto-oncogene	Homo sapiens	0-3
30131091-10	2019	Moreover, an adenocarcinoma patient harboring concurrent RET fusion and EGFR L858R responded to combinatorial treatment of cabozantinib and osimertinib, with a progression-free survival of 5 months.	cabozantinib	123-135	ret proto-oncogene	Homo sapiens	57-60
30131091-10	2019	Moreover, an adenocarcinoma patient harboring concurrent RET fusion and EGFR L858R responded to combinatorial treatment of cabozantinib and osimertinib, with a progression-free survival of 5 months.	osimertinib	140-151	ret proto-oncogene	Homo sapiens	57-60
31058838-13	2019	Selective RET inhibitors, including LOXO-292 and BLU-667, are progressing in clinical trials.	CRY1 protein, Arabidopsis	49-56	ret proto-oncogene	Homo sapiens	10-13
30975543-15	2019	The RET inhibitor, Sorafenib, is proposed as a potential treatment for resistant ACRO.	Sorafenib	19-28	ret proto-oncogene	Homo sapiens	4-7
32914006-0	2019	Use of Cabozantinib in a Patient With EGFR-Mutated Non-Small-Cell Lung Cancer Harboring Acquired CCDC6-RET Fusion.	cabozantinib	7-19	ret proto-oncogene	Homo sapiens	103-106
30718102-1	2019	BACKGROUND: Cabozantinib inhibits tyrosine kinases including MET, AXL, VEGFR2, RET, KIT, and ROS1 and has demonstrated antitumor activity in multiple tumor types.	cabozantinib	12-24	ret proto-oncogene	Homo sapiens	79-82
31104454-7	2019	After 14 days of intervention, mean Ret-He level in group 1 changed from 24.43+-1.64 to 28.21+-1.72 pg/ L (P=0.000).	Helium	40-42	ret proto-oncogene	Homo sapiens	36-39
30968565-11	2019	CONCLUSION: In cost constraints settings, a simple investigation like Ret He alone or with serum ferritin can help us to diagnose and differentiate between the different types of anemia accompanying rheumatological disorders without doing other serum iron studies and expensive tests like transferrin receptor protein which are not readily available.	Iron	251-255	ret proto-oncogene	Homo sapiens	70-73
31104454-8	2019	Mean Ret-He level in group 2 changed from 24.31+-1.42 to 27.03+-2.14 pg/L (P=0.000).	Helium	9-11	ret proto-oncogene	Homo sapiens	5-8
31104454-9	2019	Statistical analysis showed a significant increase in Ret-He levels in both groups; Ret-He levels were significantly higher in the experimental group than in the control group (P&lt;0.05).	Helium	58-60	ret proto-oncogene	Homo sapiens	54-57
31104454-9	2019	Statistical analysis showed a significant increase in Ret-He levels in both groups; Ret-He levels were significantly higher in the experimental group than in the control group (P&lt;0.05).	Helium	88-90	ret proto-oncogene	Homo sapiens	84-87
31104454-10	2019	CONCLUSION: Children with IDA receiving iron preparations with L. reuteri DSM 17938 for 14 days show higher Ret-He levels than those receiving iron preparations alone.	Iron	40-44	ret proto-oncogene	Homo sapiens	108-111
31104454-10	2019	CONCLUSION: Children with IDA receiving iron preparations with L. reuteri DSM 17938 for 14 days show higher Ret-He levels than those receiving iron preparations alone.	Helium	112-114	ret proto-oncogene	Homo sapiens	108-111
30962732-11	2019	The limitations in terms of activity and tolerability of the various multikinase inhibitors prompted the investigation of new highly selective RET inhibitors, such as RXDX-105, BLU-667, and LOXO-292.	agerafenib	167-175	ret proto-oncogene	Homo sapiens	143-146
30684857-2	2019	In this paper, a novel and efficient ECL-RET in 2D/2D heterostructured g-C3N4/MnO2 was developed using g-C3N4 nanosheets (g-C3N4 NSs) as energy donor and MnO2 nanosheets (MnO2 NSs) as energy acceptor.	manganese dioxide	78-82	ret proto-oncogene	Homo sapiens	41-44
30684857-2	2019	In this paper, a novel and efficient ECL-RET in 2D/2D heterostructured g-C3N4/MnO2 was developed using g-C3N4 nanosheets (g-C3N4 NSs) as energy donor and MnO2 nanosheets (MnO2 NSs) as energy acceptor.	manganese dioxide	154-158	ret proto-oncogene	Homo sapiens	41-44
30684857-5	2019	In the absence of GSH, MnO2 significantly quenched the ECL intensity of g-C3N4 owing to ECL-RET in this 2D/2D g-C3N4/MnO2 heterostructure (ECL signal "off").	manganese dioxide	23-27	ret proto-oncogene	Homo sapiens	92-95
30684857-7	2019	Under the optimal conditions, the designed ECL-RET signal "off-on" sensor realized the sensitive detection of GSH ranged from 0.2-100 muM with the detection limit of 0.05 muM.	Glutathione	110-113	ret proto-oncogene	Homo sapiens	47-50
30684857-8	2019	Furthermore, the as-prepared ECL-RET sensor exhibits good performance in the determination of GSH in human serum samples.	Glutathione	94-97	ret proto-oncogene	Homo sapiens	33-36
30857134-3	2019	In this paper, we report tC-modified fluorescent probes that contain RET-related sequence C4GC4GC4GC4A.	Technetium	25-27	ret proto-oncogene	Homo sapiens	69-72
30487236-0	2019	A Phase I/Ib Trial of the VEGFR-Sparing Multikinase RET Inhibitor RXDX-105.	agerafenib	66-74	ret proto-oncogene	Homo sapiens	52-55
30487236-2	2019	The safety and antitumor activity of the multikinase RET inhibitor RXDX-105 were explored in a phase I/Ib trial.	agerafenib	67-75	ret proto-oncogene	Homo sapiens	53-56
30528315-1	2019	INTRODUCTION: Cabozantinib, an orally bioavailable tyrosine kinase inhibitor with activity against MET, vascular endothelial growth factor receptor 2, AXL, ROS1, and RET was assessed in patients with non-small-cell lung carcinoma (NSCLC) as part of a phase II randomized discontinuation trial with cohorts from 9 tumor types.	cabozantinib	14-26	ret proto-oncogene	Homo sapiens	166-169
30587441-1	2019	INTRODUCTION: Cabozantinib is a receptor tyrosine kinases inhibitor that targets MET (c-MET), VEGF receptor 2 (VEGFR2), RET, AXL, KIT, FLT-3, and TIE-2 and previously showed promising single agent activity in recurrent ovarian cancer.	cabozantinib	14-26	ret proto-oncogene	Homo sapiens	120-123
30853893-0	2019	Artemin and an Artemin-Derived Peptide, Artefin, Induce Neuronal Survival, and Differentiation Through Ret and NCAM.	artefin	40-47	ret proto-oncogene	Homo sapiens	103-106
30853893-4	2019	We designed a small peptide, artefin, that could interact with GFRalpha3 and demonstrated that this peptide agonist induces RET phosphorylation and mimics the biological functions of ARTN - neuroprotection and neurite outgrowth.	artefin	29-36	ret proto-oncogene	Homo sapiens	124-127
30853893-6	2019	We showed that biological effects of ARTN and artefin can be inhibited by abrogation of both NCAM and RET, suggesting a more complex signaling mechanism that previously thought.	artefin	46-53	ret proto-oncogene	Homo sapiens	102-105
30863099-3	2019	Apatinib, a tyrosine kinase inhibitor that selectively inhibits the vascular endothelial growth factor receptor and mildly inhibits c-Kit, PDGFR-beta, RET, and c-SRC, has been reported to show efficacy among some patients with malignant supratentorial gliomas.	apatinib	0-8	ret proto-oncogene	Homo sapiens	151-154
30277655-0	2019	First-in-Human Studies for a Selective RET Tyrosine Kinase Inhibitor, GSK3179106, to Investigate the Safety, Tolerability, and Pharmacokinetics in Healthy Volunteers.	GSK3179106	70-80	ret proto-oncogene	Homo sapiens	39-42
30277655-2	2019	GSK3179106 is a RET kinase inhibitor that was administered in double-blind, randomized, placebo-controlled single-dose and repeat-dose studies in healthy subjects to investigate its pharmacokinetics and safety/tolerability.	GSK3179106	0-10	ret proto-oncogene	Homo sapiens	16-19
30685073-1	2019	Lenvatinib is a multikinase inhibitor of vascular endothelial growth factor (VEGF) receptors 1-3, fibroblast growth factor receptors 1-4, RET, KIT, and platelet-derived growth factor receptor-alpha.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	138-141
31496915-0	2019	The Importance of RET-He in the Diagnosis of Iron Deficiency and Iron Deficiency Anemia and the Evaluation of Response to Oral Iron Therapy.	Iron	45-49	ret proto-oncogene	Homo sapiens	18-21
31496915-7	2019	On the 5th day of treatment, the ID and IDA group showed no significant differences in terms of Hb while the RET-He level demonstrated a significant increase.	Helium	113-115	ret proto-oncogene	Homo sapiens	109-112
31496915-8	2019	The increase in the RET-He level observed in the IDA group on the 5th day was significantly higher compared to the increase observed in the ID group.	Helium	24-26	ret proto-oncogene	Homo sapiens	20-23
30705592-4	2019	Due to ponatinib"s unique multi-targeted characteristics, further studies have demonstrated its ability to target other important tyrosine kinases (FGFR, PDGFR, SRC, RET, KIT, and FLT1) in other human malignancies.	ponatinib	7-16	ret proto-oncogene	Homo sapiens	166-169
30343157-2	2019	In this protocol, the glucose functionalized carboxylic g-C3N4 nanosheets (g-C3N4-COOH@Glu) and MnO2 nanoparticles covered carboxylic multi-wall carbon nanotubes (BSA@MnO2-MWCNTs-COOH@Glu) were synthesized and acted as ECL-RET electron donor and acceptor, respectively.	Glucose	22-29	ret proto-oncogene	Homo sapiens	223-226
30547579-3	2019	Au-CNN shows a high and steady ECL signal centered at 455 nm, which is well-matched with the adsorption of GPRu-Au; thereby, a highly efficient electrochemiluminescent resonance energy transfer (ECL-RET) sensing platform is designed.	Gold	0-2	ret proto-oncogene	Homo sapiens	199-202
30547579-3	2019	Au-CNN shows a high and steady ECL signal centered at 455 nm, which is well-matched with the adsorption of GPRu-Au; thereby, a highly efficient electrochemiluminescent resonance energy transfer (ECL-RET) sensing platform is designed.	gpru-au	107-114	ret proto-oncogene	Homo sapiens	199-202
29967251-2	2019	We hypothesized that inhibition of protein N-linked glycosylation, an endoplasmic reticulum co- and posttranslational modification crucial for RTK maturation and activation, could provide a new therapeutic approach for glioma radiosensitization.Experimental Design: We investigated the effects of a small-molecule inhibitor of the oligosaccharyltransferase (NGI-1) on EGFR family receptors, MET, PDGFR, and FGFR1.	Nitrogen	43-44	ret proto-oncogene	Homo sapiens	143-146
29967251-11	2019	CONCLUSIONS: This study suggests that oligosaccharyltransferase inhibition with NGI-1 is a novel approach to radiosensitize malignant gliomas with enhanced RTK signaling.See related commentary by Wahl and Lawrence, p. 455.	NGI-1	80-85	ret proto-oncogene	Homo sapiens	156-159
30404949-7	2019	These data highlight microexon skipping as a mechanism to spatially restrict signaling and provide a mechanistic link between RTK-initiated phosphoinositide microdomains and Arf6 during signal transduction and cancer cell migration.	Phosphatidylinositols	140-156	ret proto-oncogene	Homo sapiens	126-129
30837349-2	2019	METHODS: Three patients( 2F, 1M; age 28,46 and 50 years) with MEN 2A syndrome who underwent 68Ga-DOTATATE PET/CT scan were prospectively evaluated.	Dotatate	97-105	ret proto-oncogene	Homo sapiens	62-68
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	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	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	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.	Iodides	186-192	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.	Nickel	204-207	ret proto-oncogene	Homo sapiens	108-111
31485557-0	2019	Response to Selective RET Inhibition With LOXO-292 in a Patient With RET Fusion-Positive Lung Cancer With Leptomeningeal Metastases.	Selpercatinib	42-50	ret proto-oncogene	Homo sapiens	22-25
31485557-0	2019	Response to Selective RET Inhibition With LOXO-292 in a Patient With RET Fusion-Positive Lung Cancer With Leptomeningeal Metastases.	Selpercatinib	42-50	ret proto-oncogene	Homo sapiens	69-72
30653139-0	2019	RET fusion in advanced non-small-cell lung cancer and response to cabozantinib: A case report.	cabozantinib	66-78	ret proto-oncogene	Homo sapiens	0-3
30653139-5	2019	In this report, we present a RET-positive case that benefited from cabozantinib treatment.	cabozantinib	67-79	ret proto-oncogene	Homo sapiens	29-32
31092758-1	2019	Lenvatinib is an oral multikinase inhibitor that targets VEGF receptors 1-3, FGF receptors 1-4, PDGF receptor alpha, RET, and KIT.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	117-120
30297385-4	2019	Vandetanib (V), a multitargeted tyrosine kinase inhibitor approved for the treatment of MTC, is thought to inhibit RET in MTC.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	115-118
30297385-5	2019	Supported by preclinical studies demonstrating that bortezomib (B) administration lowered RET mRNA and protein levels, we conducted a phase I study in advanced solid tumors of vandetanib in combination with bortezomib.	Bortezomib	52-62	ret proto-oncogene	Homo sapiens	90-93
30257958-4	2018	The selective RET inhibitors BLU-667 and cabozantinib resensitized CCDC6-RET-expressing cells to EGFR inhibition.	cabozantinib	41-53	ret proto-oncogene	Homo sapiens	14-17
30257958-4	2018	The selective RET inhibitors BLU-667 and cabozantinib resensitized CCDC6-RET-expressing cells to EGFR inhibition.	cabozantinib	41-53	ret proto-oncogene	Homo sapiens	73-76
30257958-5	2018	Finally, we treated 2 patients with EGFR-mutant NSCLC and RET-mediated resistance with osimertinib and BLU-667.	osimertinib	87-98	ret proto-oncogene	Homo sapiens	58-61
30446652-7	2018	Subsequent treatment with the RET inhibitor cabozantinib led to a rapid clinical and radiographic response.	cabozantinib	44-56	ret proto-oncogene	Homo sapiens	30-33
30121423-4	2018	The electrochemical impedance spectroscopy (EIS) results showed that the impedance value (Ret) increased with the concentration of H2O2 in the range of 0-60 mumol/L with the correlation of 0.990 which acted as an oxidative stress model inducer.	Hydrogen Peroxide	131-135	ret proto-oncogene	Homo sapiens	90-93
30121423-7	2018	A significant correlation was observed between reactive oxygen species (ROS) values and Ret values following the concentrations of Ph, thus demonstrating the good biological relevance of cell-based electrochemical method.	Reactive Oxygen Species	47-70	ret proto-oncogene	Homo sapiens	88-91
30121423-7	2018	A significant correlation was observed between reactive oxygen species (ROS) values and Ret values following the concentrations of Ph, thus demonstrating the good biological relevance of cell-based electrochemical method.	Reactive Oxygen Species	72-75	ret proto-oncogene	Homo sapiens	88-91
30385724-3	2018	Sitravatinib is a spectrum-selective tyrosine kinase inhibitor targeting TAM (TYRO3, AXL, MerTK) and split tyrosine-kinase domain-containing receptors (VEGFR and PDGFR families and KIT) plus RET and MET, targets that contribute to the immunosuppressive tumor microenvironment.	sitravatinib	0-12	ret proto-oncogene	Homo sapiens	191-194
30220234-2	2018	Lenvatinib, an orally active inhibitor of multiple receptor tyrosine kinases (VEGFR 1-3, FGFR 1-4, PDGFRa, RET and KIT), showed preclinical and clinical activity in the treatment of solid tumors, including HCC.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	107-110
30140071-8	2018	Ret-He was significantly lower among iron-deficient infants, at 4 months mean difference (95% CI) -4.2 pg/L (-6.1 to -2.4) and at 12 months mean difference (95% CI) -3.4 pg/L (-5.0 to -1.8).	Iron	37-41	ret proto-oncogene	Homo sapiens	0-3
30140071-9	2018	CONCLUSIONS: This longitudinal study presents Ret-He reference intervals based on non-anemic and non-iron-deficient infants and constitutes a step towards standardizing Ret-He as a pre-anemia biomarker of iron deficiency in children.	Iron	101-105	ret proto-oncogene	Homo sapiens	46-49
30226445-2	2018	Infrequently, children with PTC may present with or develop disease not amenable to surgery or radioactive iodine (RAI), and systemic therapy may be an option.	radioactive iodine	95-113	ret proto-oncogene	Homo sapiens	28-31
30226445-2	2018	Infrequently, children with PTC may present with or develop disease not amenable to surgery or radioactive iodine (RAI), and systemic therapy may be an option.	Insulin, Short-Acting	115-118	ret proto-oncogene	Homo sapiens	28-31
30226445-4	2018	The effect of lenvatinib in children with PTC has not been reported.	lenvatinib	14-24	ret proto-oncogene	Homo sapiens	42-45
30226445-5	2018	PATIENT FINDINGS: Three children with metastatic PTC not amenable or refractory to RAI who responded to lenvatinib are reported.	lenvatinib	104-114	ret proto-oncogene	Homo sapiens	49-52
30226445-7	2018	The first patient is a 14-year-old female who was initially treated with sorafenib for extensive PTC not amenable to upfront surgery or RAI.	Sorafenib	73-82	ret proto-oncogene	Homo sapiens	97-100
30226445-17	2018	SUMMARY: Three pediatric patients are reported with metastatic PTC not amenable or refractory to RAI who achieved a response on lenvatinib.	lenvatinib	128-138	ret proto-oncogene	Homo sapiens	63-66
30226445-18	2018	CONCLUSION: Lenvatinib therapy is well tolerated and demonstrated clinical activity in children with advanced PTC.	lenvatinib	12-22	ret proto-oncogene	Homo sapiens	110-113
30226445-19	2018	Lenvatinib should be considered in children with PTC that is refractory or not amenable to conventional management.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	49-52
30040982-3	2018	Both GFRA1 and RET are membrane proteins which are N-glycosylated but no O-linked sialylation site on GFRA1 or RET has been reported.	Nitrogen	51-52	ret proto-oncogene	Homo sapiens	15-18
30101528-4	2018	Traditional chemotherapy is marginally effective against this form, and erlotinib and gefitinib were introduced as first-line treatments based on the observation that the epidermal growth factor receptor (EGFR), a receptor tyrosine kinase (RTK), is mutated in several cases and, thus, represents a druggable target.	Erlotinib Hydrochloride	72-81	ret proto-oncogene	Homo sapiens	214-238
30101528-4	2018	Traditional chemotherapy is marginally effective against this form, and erlotinib and gefitinib were introduced as first-line treatments based on the observation that the epidermal growth factor receptor (EGFR), a receptor tyrosine kinase (RTK), is mutated in several cases and, thus, represents a druggable target.	Erlotinib Hydrochloride	72-81	ret proto-oncogene	Homo sapiens	240-243
30101528-4	2018	Traditional chemotherapy is marginally effective against this form, and erlotinib and gefitinib were introduced as first-line treatments based on the observation that the epidermal growth factor receptor (EGFR), a receptor tyrosine kinase (RTK), is mutated in several cases and, thus, represents a druggable target.	Gefitinib	86-95	ret proto-oncogene	Homo sapiens	214-238
30101528-4	2018	Traditional chemotherapy is marginally effective against this form, and erlotinib and gefitinib were introduced as first-line treatments based on the observation that the epidermal growth factor receptor (EGFR), a receptor tyrosine kinase (RTK), is mutated in several cases and, thus, represents a druggable target.	Gefitinib	86-95	ret proto-oncogene	Homo sapiens	240-243
30295264-6	2018	All of 43 patients showed decreased G6PD activity,while the level of their indirect serum bilirubin(IBIL)was positively correlated with reticulocyte percentage(Ret%,r=0.5881,P=0.013) and mean corpuscular volume(MCV,r=0.6854,P=0.0024).	Bilirubin	90-99	ret proto-oncogene	Homo sapiens	160-163
30295264-6	2018	All of 43 patients showed decreased G6PD activity,while the level of their indirect serum bilirubin(IBIL)was positively correlated with reticulocyte percentage(Ret%,r=0.5881,P=0.013) and mean corpuscular volume(MCV,r=0.6854,P=0.0024).	ibil	100-104	ret proto-oncogene	Homo sapiens	160-163
30148617-6	2018	Like midostaurin, the metabolites potently inhibit mutant forms of FLT3 and KIT and several additional kinases that either are directly involved in the deregulated signaling pathways or have been implicated as playing a role in AML via stromal support, such as IGF1R, LYN, PDPK1, RET, SYK, TRKA, and VEGFR2.	midostaurin	5-16	ret proto-oncogene	Homo sapiens	280-283
30148952-2	2018	Interestingly, we reveal that they can be readily quenched ("turn off") via a facile surface coating with bioinspired polydopamine (PDA) polymerized from dopamine (DA), resulting from PDA-triggered TRL resonance energy transfer (TRL-RET).	polydopamine	118-130	ret proto-oncogene	Homo sapiens	233-236
30148952-2	2018	Interestingly, we reveal that they can be readily quenched ("turn off") via a facile surface coating with bioinspired polydopamine (PDA) polymerized from dopamine (DA), resulting from PDA-triggered TRL resonance energy transfer (TRL-RET).	polydopamine	132-135	ret proto-oncogene	Homo sapiens	233-236
30148952-2	2018	Interestingly, we reveal that they can be readily quenched ("turn off") via a facile surface coating with bioinspired polydopamine (PDA) polymerized from dopamine (DA), resulting from PDA-triggered TRL resonance energy transfer (TRL-RET).	Dopamine	122-130	ret proto-oncogene	Homo sapiens	233-236
30148952-2	2018	Interestingly, we reveal that they can be readily quenched ("turn off") via a facile surface coating with bioinspired polydopamine (PDA) polymerized from dopamine (DA), resulting from PDA-triggered TRL resonance energy transfer (TRL-RET).	Dopamine	133-135	ret proto-oncogene	Homo sapiens	233-236
30148952-2	2018	Interestingly, we reveal that they can be readily quenched ("turn off") via a facile surface coating with bioinspired polydopamine (PDA) polymerized from dopamine (DA), resulting from PDA-triggered TRL resonance energy transfer (TRL-RET).	polydopamine	184-187	ret proto-oncogene	Homo sapiens	233-236
30148952-3	2018	By integrated with the thiol-induced inhibition of PDA formation, an ingenious inorganic-organic hybrid tongue-mimic sensor array is thus unveiled for noninvasive pattern recognition of thiols in biofluids in a TRL-RET-reversed "turn on" format toward healthcare monitoring.	Sulfhydryl Compounds	23-28	ret proto-oncogene	Homo sapiens	215-218
30148952-3	2018	By integrated with the thiol-induced inhibition of PDA formation, an ingenious inorganic-organic hybrid tongue-mimic sensor array is thus unveiled for noninvasive pattern recognition of thiols in biofluids in a TRL-RET-reversed "turn on" format toward healthcare monitoring.	Sulfhydryl Compounds	186-192	ret proto-oncogene	Homo sapiens	215-218
30073833-1	2018	This paper describes an electrochemiluminescence resonance energy transfer (ECL-RET) system using Ru(bpy)32+-doped silica nanoparticles (RuSi NPs) as the ECL donor and hollow Au nanocages as the ECL acceptor.	ru(bpy)32+	98-108	ret proto-oncogene	Homo sapiens	80-83
30073833-1	2018	This paper describes an electrochemiluminescence resonance energy transfer (ECL-RET) system using Ru(bpy)32+-doped silica nanoparticles (RuSi NPs) as the ECL donor and hollow Au nanocages as the ECL acceptor.	Silicon Dioxide	115-121	ret proto-oncogene	Homo sapiens	80-83
30073833-1	2018	This paper describes an electrochemiluminescence resonance energy transfer (ECL-RET) system using Ru(bpy)32+-doped silica nanoparticles (RuSi NPs) as the ECL donor and hollow Au nanocages as the ECL acceptor.	Gold	175-177	ret proto-oncogene	Homo sapiens	80-83
29908090-3	2018	EXPERIMENTAL APPROACH: We identified and analysed mutations in the RET kinase domain that conferred resistance to the TKIs cabozantinib, lenvatinib, vandetanib and nintedanib using RET kinase-dependent BaF3/KIF5B-RET (BaF3/KR) cells.	cabozantinib	123-135	ret proto-oncogene	Homo sapiens	181-184
29908090-3	2018	EXPERIMENTAL APPROACH: We identified and analysed mutations in the RET kinase domain that conferred resistance to the TKIs cabozantinib, lenvatinib, vandetanib and nintedanib using RET kinase-dependent BaF3/KIF5B-RET (BaF3/KR) cells.	lenvatinib	137-147	ret proto-oncogene	Homo sapiens	181-184
29908090-3	2018	EXPERIMENTAL APPROACH: We identified and analysed mutations in the RET kinase domain that conferred resistance to the TKIs cabozantinib, lenvatinib, vandetanib and nintedanib using RET kinase-dependent BaF3/KIF5B-RET (BaF3/KR) cells.	vandetanib	149-159	ret proto-oncogene	Homo sapiens	181-184
29908090-3	2018	EXPERIMENTAL APPROACH: We identified and analysed mutations in the RET kinase domain that conferred resistance to the TKIs cabozantinib, lenvatinib, vandetanib and nintedanib using RET kinase-dependent BaF3/KIF5B-RET (BaF3/KR) cells.	nintedanib	164-174	ret proto-oncogene	Homo sapiens	181-184
30135308-4	2018	Using human MTC cells that are either sensitive or resistant to vandetanib, we demonstrate that palbociclib (CDK4/6 inhibitor) is not cytotoxic to MTC cells but that they are highly sensitive to dinaciclib (CDK1/2/5/9 inhibitor) accompanied by reduced CDK9 and RET protein and mRNA levels.	palbociclib	96-107	ret proto-oncogene	Homo sapiens	261-264
30135308-9	2018	Finally, combined inhibition of dinaciclib with a RET kinase inhibitor was synergistic.	dinaciclib	32-42	ret proto-oncogene	Homo sapiens	50-53
29860229-1	2018	LOXO-292, a selective and potent RET inhibitor, led to tumor shrinkage in RET fusion-positive and RET-mutant cancers alike, according to phase I data reported at the 2018 American Society of Clinical Oncology Annual Meeting.	Selpercatinib	0-8	ret proto-oncogene	Homo sapiens	33-36
30913403-3	2019	(2019) show that Ret and Fat4, which are expressed on the surface of the UB and surrounding stromal cells, respectively, interact directly to restrict branching during UB outgrowth.	BM	73-75	ret proto-oncogene	Homo sapiens	17-20
29268569-6	2018	On d 14, the apparent total tract digestibility (ATTD) of dry matter (DM), ether extract (EE), and gross energy in RET03 treatment was higher (p&amp;lt;0.05) than those in RET treatment, while the ATTD of N was increased (p&amp;lt;0.05) by RET03 treatment.	Ether	75-80	ret proto-oncogene	Homo sapiens	115-118
29268569-6	2018	On d 14, the apparent total tract digestibility (ATTD) of dry matter (DM), ether extract (EE), and gross energy in RET03 treatment was higher (p&amp;lt;0.05) than those in RET treatment, while the ATTD of N was increased (p&amp;lt;0.05) by RET03 treatment.	Adenosine Monophosphate	145-148	ret proto-oncogene	Homo sapiens	115-118
29268569-7	2018	On d 28, broilers fed RET03 diet had higher (p&amp;lt;0.05) ATTD of DM than those fed RET and RET015 diets, while the ATTD of EE in BDT and RET03 treatments was increased (p&amp;lt;0.05) compared with RET and RET015 treatments.	Adenosine Monophosphate	47-50	ret proto-oncogene	Homo sapiens	22-25
30935646-1	2019	Cabozantinib is a multitargeted tyrosine kinase inhibitor, with activity against vascular endothelial growth factor receptor, as well as MET, RET, and AXL.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	142-145
29912274-8	2018	A second patient with KIF5B-RET fusion-positive lung cancer, acquired resistance to alectinib and symptomatic brain metastases experienced a dramatic response in the brain, and her symptoms resolved.	alectinib	84-93	ret proto-oncogene	Homo sapiens	28-31
29860229-1	2018	LOXO-292, a selective and potent RET inhibitor, led to tumor shrinkage in RET fusion-positive and RET-mutant cancers alike, according to phase I data reported at the 2018 American Society of Clinical Oncology Annual Meeting.	Selpercatinib	0-8	ret proto-oncogene	Homo sapiens	74-77
29860229-1	2018	LOXO-292, a selective and potent RET inhibitor, led to tumor shrinkage in RET fusion-positive and RET-mutant cancers alike, according to phase I data reported at the 2018 American Society of Clinical Oncology Annual Meeting.	Selpercatinib	0-8	ret proto-oncogene	Homo sapiens	74-77
30032842-1	2018	OBJECTIVES: Anlotinib is a novel multi-target tyrosine Kinase inhibitor that inhibits VEGFR2/3, FGFR1-4, PDGFD alpha/beta, c-Kit and Ret.	anlotinib	12-21	ret proto-oncogene	Homo sapiens	133-136
29759226-1	2018	Luminol-nitrogen doped graphene quantum dot (luminol-NGQDs) nanocomposite was synthesized and a novel electrochemiluminescence resonance energy transfer (ECL-RET) process occurred between luminol as the donor and NGQDs as the acceptor in the composite.	Luminol	0-7	ret proto-oncogene	Homo sapiens	158-161
30210625-11	2018	In colon cancer PDCs with NCOA4-RET fusion, vandetanib potently inhibited AKT and ERK phosphorylation.	vandetanib	44-54	ret proto-oncogene	Homo sapiens	32-35
30210625-12	2018	This study shows that vandetanib might be one of useful treatment strategies for CRC patient with NCOA4-RET fusion.	vandetanib	22-32	ret proto-oncogene	Homo sapiens	104-107
30210625-7	2018	We tested whether the PDCs from RET fusion colon cancer were sensitive to carbozantinib, sorafenib, vandetanib, and PD0331992.	cabozantinib	74-87	ret proto-oncogene	Homo sapiens	32-35
30210625-7	2018	We tested whether the PDCs from RET fusion colon cancer were sensitive to carbozantinib, sorafenib, vandetanib, and PD0331992.	Sorafenib	89-98	ret proto-oncogene	Homo sapiens	32-35
30210625-7	2018	We tested whether the PDCs from RET fusion colon cancer were sensitive to carbozantinib, sorafenib, vandetanib, and PD0331992.	vandetanib	100-110	ret proto-oncogene	Homo sapiens	32-35
30210625-7	2018	We tested whether the PDCs from RET fusion colon cancer were sensitive to carbozantinib, sorafenib, vandetanib, and PD0331992.	pd0331992	116-125	ret proto-oncogene	Homo sapiens	32-35
29759226-1	2018	Luminol-nitrogen doped graphene quantum dot (luminol-NGQDs) nanocomposite was synthesized and a novel electrochemiluminescence resonance energy transfer (ECL-RET) process occurred between luminol as the donor and NGQDs as the acceptor in the composite.	Nitrogen	8-16	ret proto-oncogene	Homo sapiens	158-161
29759226-1	2018	Luminol-nitrogen doped graphene quantum dot (luminol-NGQDs) nanocomposite was synthesized and a novel electrochemiluminescence resonance energy transfer (ECL-RET) process occurred between luminol as the donor and NGQDs as the acceptor in the composite.	Graphite	23-31	ret proto-oncogene	Homo sapiens	158-161
29759226-1	2018	Luminol-nitrogen doped graphene quantum dot (luminol-NGQDs) nanocomposite was synthesized and a novel electrochemiluminescence resonance energy transfer (ECL-RET) process occurred between luminol as the donor and NGQDs as the acceptor in the composite.	Luminol	45-52	ret proto-oncogene	Homo sapiens	158-161
29759226-1	2018	Luminol-nitrogen doped graphene quantum dot (luminol-NGQDs) nanocomposite was synthesized and a novel electrochemiluminescence resonance energy transfer (ECL-RET) process occurred between luminol as the donor and NGQDs as the acceptor in the composite.	Luminol	188-195	ret proto-oncogene	Homo sapiens	158-161
29759226-2	2018	This ECL-RET effect helped luminol-NGQDs composite produced an anodic ECL signal without coreactants.	Luminol	27-34	ret proto-oncogene	Homo sapiens	9-12
30093982-4	2018	In the clinical setting, the benefit of the most developed RET inhibitors, i.e., cabozantinb, vandetanib and lenvatinb, in terms of response and median progressionfree survival has been demonstrated.	cabozantinb	81-92	ret proto-oncogene	Homo sapiens	59-62
29916688-3	2018	Furthermore, the ECL resonance energy transfer (ECL-RET) could occur between UiO-67/Ru(bpy)32+ (ECL donor) and Au@SiO2 nanoparticles (ECL acceptor), resulting in a conspicuously decreased ECL response.	Gold	111-113	ret proto-oncogene	Homo sapiens	52-55
29916688-3	2018	Furthermore, the ECL resonance energy transfer (ECL-RET) could occur between UiO-67/Ru(bpy)32+ (ECL donor) and Au@SiO2 nanoparticles (ECL acceptor), resulting in a conspicuously decreased ECL response.	Silicon Dioxide	114-118	ret proto-oncogene	Homo sapiens	52-55
29916688-4	2018	The ECL spectrum of UiO-67/Ru(bpy)32+ which exhibited strong ECL intensity has suitable spectral overlap with the absorption spectrum of Au@SiO2, which further proved the occurrence of the ECL-RET action.	Gold	137-139	ret proto-oncogene	Homo sapiens	193-196
29916688-4	2018	The ECL spectrum of UiO-67/Ru(bpy)32+ which exhibited strong ECL intensity has suitable spectral overlap with the absorption spectrum of Au@SiO2, which further proved the occurrence of the ECL-RET action.	Silicon Dioxide	140-144	ret proto-oncogene	Homo sapiens	193-196
29916688-7	2018	Meanwhile, this work provides an important reference for the application of metal-organic frameworks in the ECL and ECL-RET study and also exhibits potential capability in the detection of other hormones.	Metals	76-81	ret proto-oncogene	Homo sapiens	120-123
30093982-4	2018	In the clinical setting, the benefit of the most developed RET inhibitors, i.e., cabozantinb, vandetanib and lenvatinb, in terms of response and median progressionfree survival has been demonstrated.	vandetanib	94-104	ret proto-oncogene	Homo sapiens	59-62
30093982-4	2018	In the clinical setting, the benefit of the most developed RET inhibitors, i.e., cabozantinb, vandetanib and lenvatinb, in terms of response and median progressionfree survival has been demonstrated.	lenvatinb	109-118	ret proto-oncogene	Homo sapiens	59-62
29697413-2	2018	Our present data show that BGJ398, a selective fibroblast growth factor receptor (FGFR) inhibitor, sensitizes imatinib (IM)-resistant GIST cells with receptor tyrosine kinase (RTK) switch (loss of c-KIT/gain of pFGFR2a) to the low doses of topoisomerase II inhibitors - doxorubicin (Dox) and etoposide (Eto).	infigratinib	27-33	ret proto-oncogene	Homo sapiens	150-174
30038711-0	2018	RET fusions observed in lung and colorectal cancers are sensitive to ponatinib.	ponatinib	69-78	ret proto-oncogene	Homo sapiens	0-3
30038711-4	2018	Identifying ponatinib as the most potent RET inhibitor tested, we used ponatinib to gauge therapeutic responsiveness in RET fusion-positive patient-derived xenograft (PDX) models.	ponatinib	12-21	ret proto-oncogene	Homo sapiens	41-44
30038711-6	2018	By comparing ponatinib activity in RET fusion-positive and RET fusion-negative PDX models alongside a standard of care chemotherapeutic agent, we show that RET fusions in colorectal tumors are therapeutically responsive to RET inhibition.	ponatinib	13-22	ret proto-oncogene	Homo sapiens	35-38
29697413-2	2018	Our present data show that BGJ398, a selective fibroblast growth factor receptor (FGFR) inhibitor, sensitizes imatinib (IM)-resistant GIST cells with receptor tyrosine kinase (RTK) switch (loss of c-KIT/gain of pFGFR2a) to the low doses of topoisomerase II inhibitors - doxorubicin (Dox) and etoposide (Eto).	infigratinib	27-33	ret proto-oncogene	Homo sapiens	176-179
29697413-2	2018	Our present data show that BGJ398, a selective fibroblast growth factor receptor (FGFR) inhibitor, sensitizes imatinib (IM)-resistant GIST cells with receptor tyrosine kinase (RTK) switch (loss of c-KIT/gain of pFGFR2a) to the low doses of topoisomerase II inhibitors - doxorubicin (Dox) and etoposide (Eto).	Imatinib Mesylate	110-118	ret proto-oncogene	Homo sapiens	150-174
29697413-2	2018	Our present data show that BGJ398, a selective fibroblast growth factor receptor (FGFR) inhibitor, sensitizes imatinib (IM)-resistant GIST cells with receptor tyrosine kinase (RTK) switch (loss of c-KIT/gain of pFGFR2a) to the low doses of topoisomerase II inhibitors - doxorubicin (Dox) and etoposide (Eto).	Imatinib Mesylate	110-118	ret proto-oncogene	Homo sapiens	176-179
29695833-4	2018	Using a novel doxycycline-inducible transgenic mouse model with the MMTV promoter controlling Ret expression, we show that overexpression of wild-type Ret in the mammary epithelium produces mammary tumors, displaying a morphology that recapitulates characteristics of human luminal breast tumors.	Doxycycline	14-25	ret proto-oncogene	Homo sapiens	94-97
29695833-4	2018	Using a novel doxycycline-inducible transgenic mouse model with the MMTV promoter controlling Ret expression, we show that overexpression of wild-type Ret in the mammary epithelium produces mammary tumors, displaying a morphology that recapitulates characteristics of human luminal breast tumors.	Doxycycline	14-25	ret proto-oncogene	Homo sapiens	151-154
29695833-6	2018	Moreover, tumors rapidly regress after doxycycline withdrawal, indicating that Ret is the driving oncoprotein.	Doxycycline	39-50	ret proto-oncogene	Homo sapiens	79-82
29656442-2	2018	In the phase 3 Study of (E7080) Lenvatinib in Differentiated Cancer of the Thyroid (SELECT) trial, HTN was the most frequent adverse event of lenvatinib, an inhibitor of VEGFR1, VEGFR2, VEGFR3, fibroblast growth factor receptor 1 (FGFR1), FGFR2, FGFR3, FGFR4, platelet-derived growth factor receptor alpha (PDGFRalpha), ret proto-oncogene (RET), and stem cell factor receptor (KIT).	lenvatinib	142-152	ret proto-oncogene	Homo sapiens	320-323
29656442-2	2018	In the phase 3 Study of (E7080) Lenvatinib in Differentiated Cancer of the Thyroid (SELECT) trial, HTN was the most frequent adverse event of lenvatinib, an inhibitor of VEGFR1, VEGFR2, VEGFR3, fibroblast growth factor receptor 1 (FGFR1), FGFR2, FGFR3, FGFR4, platelet-derived growth factor receptor alpha (PDGFRalpha), ret proto-oncogene (RET), and stem cell factor receptor (KIT).	lenvatinib	142-152	ret proto-oncogene	Homo sapiens	340-343
29359239-3	2018	Regorafenib is a potent inhibitor of angiogenic (VEGFR 1-3, PDGFR-b) as well as oncogenic (c-KIT, RET, FGFR, Raf) kinases.	regorafenib	0-11	ret proto-oncogene	Homo sapiens	98-101
30034590-8	2018	GSK3179106 is a potent, selective, and gut-restricted pyridone hinge binder small molecule RET kinase inhibitor with a RET IC50 of 0.3 nM and is efficacious in vivo.	GSK3179106	0-10	ret proto-oncogene	Homo sapiens	91-94
30034590-8	2018	GSK3179106 is a potent, selective, and gut-restricted pyridone hinge binder small molecule RET kinase inhibitor with a RET IC50 of 0.3 nM and is efficacious in vivo.	GSK3179106	0-10	ret proto-oncogene	Homo sapiens	119-122
30034590-8	2018	GSK3179106 is a potent, selective, and gut-restricted pyridone hinge binder small molecule RET kinase inhibitor with a RET IC50 of 0.3 nM and is efficacious in vivo.	Pyridones	54-62	ret proto-oncogene	Homo sapiens	91-94
29755294-4	2018	Methods: Receptor tyrosine kinase (RTK) pathways in temozolomide (TMZ) treatment naive or TMZ resistant human GBM biopsies and GBM cells were investigated by proteome profiling and immunoblotting of a subset of proteins.	Temozolomide	52-64	ret proto-oncogene	Homo sapiens	9-33
29755294-4	2018	Methods: Receptor tyrosine kinase (RTK) pathways in temozolomide (TMZ) treatment naive or TMZ resistant human GBM biopsies and GBM cells were investigated by proteome profiling and immunoblotting of a subset of proteins.	Temozolomide	52-64	ret proto-oncogene	Homo sapiens	35-38
29755294-4	2018	Methods: Receptor tyrosine kinase (RTK) pathways in temozolomide (TMZ) treatment naive or TMZ resistant human GBM biopsies and GBM cells were investigated by proteome profiling and immunoblotting of a subset of proteins.	Temozolomide	66-69	ret proto-oncogene	Homo sapiens	9-33
29755294-4	2018	Methods: Receptor tyrosine kinase (RTK) pathways in temozolomide (TMZ) treatment naive or TMZ resistant human GBM biopsies and GBM cells were investigated by proteome profiling and immunoblotting of a subset of proteins.	Temozolomide	66-69	ret proto-oncogene	Homo sapiens	35-38
29755294-4	2018	Methods: Receptor tyrosine kinase (RTK) pathways in temozolomide (TMZ) treatment naive or TMZ resistant human GBM biopsies and GBM cells were investigated by proteome profiling and immunoblotting of a subset of proteins.	Temozolomide	90-93	ret proto-oncogene	Homo sapiens	9-33
29755294-4	2018	Methods: Receptor tyrosine kinase (RTK) pathways in temozolomide (TMZ) treatment naive or TMZ resistant human GBM biopsies and GBM cells were investigated by proteome profiling and immunoblotting of a subset of proteins.	Temozolomide	90-93	ret proto-oncogene	Homo sapiens	35-38
29755294-5	2018	Resistance to drugs and RTK pathway inhibitors was assessed by MTT assays.	monooxyethylene trimethylolpropane tristearate	63-66	ret proto-oncogene	Homo sapiens	24-27
29755294-7	2018	Results: We analyzed activation of RTK pathways by proteome profiling of tumor samples of patients which were diagnosed a secondary GBM and underwent surgery and patients which underwent a second surgery after TMZ treatment due to recurrence of the tumor.	Temozolomide	210-213	ret proto-oncogene	Homo sapiens	35-38
29512753-11	2018	Additionally, a Cell Counting Kit-8 assay demonstrated that specific inhibitors of NOS3 and BDNF/neurotrophic receptor tyrosine kinase, type 2 signaling reduced the IC50 of MCF-7/MDR cells in response to various anticancer drugs, including adriamycin, cisplatin and 5-fluorouracil.	Doxorubicin	240-250	ret proto-oncogene	Homo sapiens	110-134
29436591-2	2018	Sorafenib (SOR), a multikinase inhibitor of Raf/mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (ERK) signaling and the receptor tyrosine kinase, is recognized as the standard therapeutic strategy for patients with advanced HCC.	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	150-174
29517103-1	2018	Lenvatinib is an oral, multitargeted tyrosine kinase inhibitor (TKI) of VEGFR1-VEGFR3, FGFR1-FGFR4, PDGFRalpha, RET and v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog (KIT) signaling networks involved in tumor angiogenesis.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	112-115
28013235-8	2018	Furthermore, our KDR gene fusion network analysis revealed six of the seven kinases with the highest DoF scores (ALK, BRAF, MET, NTRK1, NTRK3 and RET) were all observed in thyroid carcinoma.	dof	101-104	ret proto-oncogene	Homo sapiens	146-149
28836866-7	2018	Importantly, variant allele frequency (VAF) of some mutated genes (RET, SF3B1, ASXL1) decreased after 9 months of treatment in Aza-responder patients.	Azathioprine	127-130	ret proto-oncogene	Homo sapiens	67-70
29717360-9	2018	Graphical abstract An Au/Cu alloy flower-like nanocomposite (Au/Cu NFs) is firstly synthesized as an acceptor to constitute an electrochemiluminescence-resonance energy transfer (ECL-RET) system for sensitive measurement of Sudan I, while Au nanoparticles (Au NPs) functionalized graphitic carbon nitride (g-C3N4) acted as a donor.	Gold	22-24	ret proto-oncogene	Homo sapiens	183-186
29717360-9	2018	Graphical abstract An Au/Cu alloy flower-like nanocomposite (Au/Cu NFs) is firstly synthesized as an acceptor to constitute an electrochemiluminescence-resonance energy transfer (ECL-RET) system for sensitive measurement of Sudan I, while Au nanoparticles (Au NPs) functionalized graphitic carbon nitride (g-C3N4) acted as a donor.	Copper	25-27	ret proto-oncogene	Homo sapiens	183-186
29717360-9	2018	Graphical abstract An Au/Cu alloy flower-like nanocomposite (Au/Cu NFs) is firstly synthesized as an acceptor to constitute an electrochemiluminescence-resonance energy transfer (ECL-RET) system for sensitive measurement of Sudan I, while Au nanoparticles (Au NPs) functionalized graphitic carbon nitride (g-C3N4) acted as a donor.	Gold	61-63	ret proto-oncogene	Homo sapiens	183-186
29717360-9	2018	Graphical abstract An Au/Cu alloy flower-like nanocomposite (Au/Cu NFs) is firstly synthesized as an acceptor to constitute an electrochemiluminescence-resonance energy transfer (ECL-RET) system for sensitive measurement of Sudan I, while Au nanoparticles (Au NPs) functionalized graphitic carbon nitride (g-C3N4) acted as a donor.	graphitic carbon nitride	280-304	ret proto-oncogene	Homo sapiens	183-186
29717360-9	2018	Graphical abstract An Au/Cu alloy flower-like nanocomposite (Au/Cu NFs) is firstly synthesized as an acceptor to constitute an electrochemiluminescence-resonance energy transfer (ECL-RET) system for sensitive measurement of Sudan I, while Au nanoparticles (Au NPs) functionalized graphitic carbon nitride (g-C3N4) acted as a donor.	g-c3n4	306-312	ret proto-oncogene	Homo sapiens	183-186
29512753-11	2018	Additionally, a Cell Counting Kit-8 assay demonstrated that specific inhibitors of NOS3 and BDNF/neurotrophic receptor tyrosine kinase, type 2 signaling reduced the IC50 of MCF-7/MDR cells in response to various anticancer drugs, including adriamycin, cisplatin and 5-fluorouracil.	Cisplatin	252-261	ret proto-oncogene	Homo sapiens	110-134
29512753-11	2018	Additionally, a Cell Counting Kit-8 assay demonstrated that specific inhibitors of NOS3 and BDNF/neurotrophic receptor tyrosine kinase, type 2 signaling reduced the IC50 of MCF-7/MDR cells in response to various anticancer drugs, including adriamycin, cisplatin and 5-fluorouracil.	Fluorouracil	266-280	ret proto-oncogene	Homo sapiens	110-134
29662626-4	2018	In this project, we showed that disruption of the EGFR/ErbB2-dependent signalling by lapatinib and CP-724714, two inhibitors of the receptor tyrosine kinase (RTK), dramatically reduced the amplitude of the SOCE in breast cancer cells.	Lapatinib	85-94	ret proto-oncogene	Homo sapiens	132-156
29440177-4	2018	Ponatinib was tested for efficacy in two patient-derived xenograft (PDX) models and one cell-line xenograft model of SCCOHT.Results: The receptor tyrosine kinase (RTK) family was enriched in siRNA screen hits, with FGFRs and PDGFRs being overlapping hits between drug and siRNA screens.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	137-161
29440177-4	2018	Ponatinib was tested for efficacy in two patient-derived xenograft (PDX) models and one cell-line xenograft model of SCCOHT.Results: The receptor tyrosine kinase (RTK) family was enriched in siRNA screen hits, with FGFRs and PDGFRs being overlapping hits between drug and siRNA screens.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	163-166
29440177-6	2018	We further identified ponatinib as the most effective clinically approved RTK inhibitor.	ponatinib	22-31	ret proto-oncogene	Homo sapiens	74-77
29436676-7	2018	Our results demonstrated greater expression of p-RET and CXCR4 in cisplatin-resistant neuroblastomas (NBs).	Cisplatin	66-75	ret proto-oncogene	Homo sapiens	49-52
29436676-8	2018	Vandetanib significantly inhibited SH-SY5Y-R cell proliferation, colony formation, and invasion, while downregulating p-RET and CXCR4 expression.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	120-123
29662626-4	2018	In this project, we showed that disruption of the EGFR/ErbB2-dependent signalling by lapatinib and CP-724714, two inhibitors of the receptor tyrosine kinase (RTK), dramatically reduced the amplitude of the SOCE in breast cancer cells.	Lapatinib	85-94	ret proto-oncogene	Homo sapiens	158-161
29717218-0	2018	Ganetespib targets multiple levels of the receptor tyrosine kinase signaling cascade and preferentially inhibits ErbB2-overexpressing breast cancer cells.	STA 9090	0-10	ret proto-oncogene	Homo sapiens	42-66
29665843-13	2018	Notably, the effects induced by the RET G533C variant were abolished by vandetanib.	vandetanib	72-82	ret proto-oncogene	Homo sapiens	36-39
29571998-2	2018	Patients whose tumors possess RET fusion are associated with clinical benefit from the treatment with multi-kinase inhibitors such as cabozantinib and vandetanib.	cabozantinib	134-146	ret proto-oncogene	Homo sapiens	30-33
29571998-2	2018	Patients whose tumors possess RET fusion are associated with clinical benefit from the treatment with multi-kinase inhibitors such as cabozantinib and vandetanib.	vandetanib	151-161	ret proto-oncogene	Homo sapiens	30-33
29433850-1	2018	BACKGROUND: In a phase 2 trial, lenvatinib, an inhibitor of VEGF receptors 1-3, FGF receptors 1-4, PDGF receptor alpha, RET, and KIT, showed activity in hepatocellular carcinoma.	lenvatinib	32-42	ret proto-oncogene	Homo sapiens	120-123
29662626-4	2018	In this project, we showed that disruption of the EGFR/ErbB2-dependent signalling by lapatinib and CP-724714, two inhibitors of the receptor tyrosine kinase (RTK), dramatically reduced the amplitude of the SOCE in breast cancer cells.	2-methoxy-N-(3-(4-((3-methyl-4-((6-methyl-3-pyridinyl)oxy)phenyl)amino)-6-quinazolinyl)-2-propenyl)acetamide	99-108	ret proto-oncogene	Homo sapiens	132-156
29662626-4	2018	In this project, we showed that disruption of the EGFR/ErbB2-dependent signalling by lapatinib and CP-724714, two inhibitors of the receptor tyrosine kinase (RTK), dramatically reduced the amplitude of the SOCE in breast cancer cells.	2-methoxy-N-(3-(4-((3-methyl-4-((6-methyl-3-pyridinyl)oxy)phenyl)amino)-6-quinazolinyl)-2-propenyl)acetamide	99-108	ret proto-oncogene	Homo sapiens	158-161
29563833-4	2018	This agent is a novel oral diphenylurea-based multikinase inhibitor that is active against several angiogenic receptor tyrosine kinases (RTKs; VEGFR-1, VEGFR-2, VEGFR-3, TIE-2), oncogenic RTKs (c-KIT, RET), stromal RTKs (PDGFR-B, FGFR-1), and intracellular signaling kinases (c-RAF/RAF-1, BRAF, BRAFV600E).	Carbanilides	27-39	ret proto-oncogene	Homo sapiens	201-204
29553126-3	2018	We evaluated the potential importance of 1,25(OH)2D3 in the diagnosis and treatment of papillary thyroid cancer (PTC).	25(oh)2d3	43-52	ret proto-oncogene	Homo sapiens	113-116
29553126-7	2018	The effect of 1,25(OH)2D3 on the proliferation and apoptosis of PTC cell lines were studied by Cell Counting Kit (CCK)-8 assay and Annexin V/propidium iodide staining, respectively.	Calcitriol	14-25	ret proto-oncogene	Homo sapiens	64-67
29553126-10	2018	RESULTS The preoperative serum level of 1,25(OH)2D3 in PTC was obviously lower than that in nodular goiter (NG) (P&lt;0.05).	25(oh)2d3	42-51	ret proto-oncogene	Homo sapiens	55-58
29553126-12	2018	1,25(OH)2D3 inhibited the proliferation and induced the apoptosis of PTC cells, and increased CAMP expression significantly, whereas CAMP knockdown demonstrated opposite effects.	Calcitriol	0-11	ret proto-oncogene	Homo sapiens	69-72
29553126-14	2018	It may also become 1,25(OH)2D3 may a potential target for drug action to treat PTC through CAMP.	Calcitriol	19-30	ret proto-oncogene	Homo sapiens	79-82
29514104-2	2018	We applied comprehensive phosphoproteomics to unravel differential regulators of receptor tyrosine kinase (RTK)-initiated signaling networks upon activation by Pdgf-betabeta, Fgf-2, or Igf-1 and identified more than 40,000 phosphorylation sites, including many phosphotyrosine sites without additional enrichment.	Phosphotyrosine	261-276	ret proto-oncogene	Homo sapiens	81-105
29514104-2	2018	We applied comprehensive phosphoproteomics to unravel differential regulators of receptor tyrosine kinase (RTK)-initiated signaling networks upon activation by Pdgf-betabeta, Fgf-2, or Igf-1 and identified more than 40,000 phosphorylation sites, including many phosphotyrosine sites without additional enrichment.	Phosphotyrosine	261-276	ret proto-oncogene	Homo sapiens	107-110
28938186-4	2018	In this protocol, mesoporous carbon nanospheres were adopted to immobilize ECL reactant Ru(bpy)32+ and antibody via nafion to acquire the RET donor nanocomposites (MOCs/nafion/Ru(bpy)32+/antibody), which were tightly interconnected with epoxy group functionalized Fe3O4 nanoparticles.	Methane	18-35	ret proto-oncogene	Homo sapiens	138-141
29434222-0	2018	A secondary RET mutation in the activation loop conferring resistance to vandetanib.	vandetanib	73-83	ret proto-oncogene	Homo sapiens	12-15
28858679-2	2018	In this work, a novel tris(bipyridine) ruthenium(II) derivative (Ru(bpy)2(mcbpy)2+-PEI-ABEI) with high ECL efficiency due to the binary intramolecular ECL self-catalyzed property including intramolecular co-reaction and intramolecular ECL-RET, was prepared for the construction of immunosensor.	tris(bipyridine) ruthenium(ii)	22-52	ret proto-oncogene	Homo sapiens	239-242
28858679-2	2018	In this work, a novel tris(bipyridine) ruthenium(II) derivative (Ru(bpy)2(mcbpy)2+-PEI-ABEI) with high ECL efficiency due to the binary intramolecular ECL self-catalyzed property including intramolecular co-reaction and intramolecular ECL-RET, was prepared for the construction of immunosensor.	(bpy)2(	67-74	ret proto-oncogene	Homo sapiens	239-242
28858679-4	2018	Meanwhile, ABEI, as an effective energy transfer donor, could further increase the ECL intensity of Ru(bpy)2(mcbpy)2+ (as energy transfer receptor) by intramolecular ECL-RET.	ru(bpy)2(mcbpy)2+	100-117	ret proto-oncogene	Homo sapiens	170-173
29515414-1	2018	Lenvatinib is an oral tyrosine kinase inhibitor of vascular endothelial growth factor receptors 1, 2, and 3, fibroblast growth factor receptors 1 through 4, as well as platelet-derived growth factor receptor alpha, RET, and KIT.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	215-218
29434222-1	2018	Resistance to vandetanib, a type I RET kinase inhibitor, developed in a patient with metastatic lung adenocarcinoma harboring a CCDC6-RET fusion that initially exhibited a response to treatment.	vandetanib	14-24	ret proto-oncogene	Homo sapiens	35-38
29434222-1	2018	Resistance to vandetanib, a type I RET kinase inhibitor, developed in a patient with metastatic lung adenocarcinoma harboring a CCDC6-RET fusion that initially exhibited a response to treatment.	vandetanib	14-24	ret proto-oncogene	Homo sapiens	134-137
29434222-3	2018	The S904F mutation confers resistance to vandetanib by increasing the ATP affinity and autophosphorylation activity of RET kinase.	vandetanib	41-51	ret proto-oncogene	Homo sapiens	119-122
29434222-3	2018	The S904F mutation confers resistance to vandetanib by increasing the ATP affinity and autophosphorylation activity of RET kinase.	Adenosine Triphosphate	70-73	ret proto-oncogene	Homo sapiens	119-122
29018141-0	2018	Vitamin D regulation of GDNF/Ret signaling in dopaminergic neurons.	Vitamin D	0-9	ret proto-oncogene	Homo sapiens	29-32
29142004-7	2018	Clinical investigators and the pharmaceutical industry are focusing on the development of the next generation of MTTs, which have minimal toxicity and greater specificity for mutated RET.	Monooxyethylene trimethylolpropane tristearate	113-117	ret proto-oncogene	Homo sapiens	183-186
29018141-5	2018	The absence of vitamin D ligand in gestation reduces C-Ret expression, but not GDNF and GFRalpha1, in embryo forebrains.	Vitamin D	15-24	ret proto-oncogene	Homo sapiens	53-58
29018141-7	2018	In the presence of vitamin D, C-Ret mRNA and protein expression were increased.	Vitamin D	19-28	ret proto-oncogene	Homo sapiens	30-35
29018141-8	2018	The chromatin immunoprecipitation results suggested that C-Ret is directly regulated by vitamin D via VDR.	Vitamin D	88-97	ret proto-oncogene	Homo sapiens	57-62
29556564-6	2018	Interestingly, ShcD-RET association reduced the viability and migration of SK-N-AS cells.	sk-n-as	75-82	ret proto-oncogene	Homo sapiens	20-23
29018141-12	2018	These data extend our knowledge of the diverse and important roles played by vitamin D in dopamine physiology.-Pertile, R. A. N., Cui, X., Hammond, L., Eyles, D. W. Vitamin D regulation of GDNF/Ret signaling in dopaminergic neurons.	Vitamin D	165-174	ret proto-oncogene	Homo sapiens	194-197
29284153-7	2018	Several drugs targeting RET have been approved by the FDA for the treatment of cancer: (i) cabozantinib and vandetanib for medullary thyroid carcinomas and (ii) lenvatinib and sorafenib for differentiated thyroid cancers.	cabozantinib	91-103	ret proto-oncogene	Homo sapiens	24-27
29284153-7	2018	Several drugs targeting RET have been approved by the FDA for the treatment of cancer: (i) cabozantinib and vandetanib for medullary thyroid carcinomas and (ii) lenvatinib and sorafenib for differentiated thyroid cancers.	vandetanib	108-118	ret proto-oncogene	Homo sapiens	24-27
29284153-7	2018	Several drugs targeting RET have been approved by the FDA for the treatment of cancer: (i) cabozantinib and vandetanib for medullary thyroid carcinomas and (ii) lenvatinib and sorafenib for differentiated thyroid cancers.	lenvatinib	161-171	ret proto-oncogene	Homo sapiens	24-27
29284153-7	2018	Several drugs targeting RET have been approved by the FDA for the treatment of cancer: (i) cabozantinib and vandetanib for medullary thyroid carcinomas and (ii) lenvatinib and sorafenib for differentiated thyroid cancers.	Sorafenib	176-185	ret proto-oncogene	Homo sapiens	24-27
29284153-10	2018	Previous X-ray studies indicated that vandetanib binds within the ATP-binding pocket and forms a hydrogen bond with A807 within the RET hinge and it makes hydrophobic contact with L881 of the catalytic spine which occurs in the floor of the adenine-binding pocket.	vandetanib	38-48	ret proto-oncogene	Homo sapiens	132-135
29284153-10	2018	Previous X-ray studies indicated that vandetanib binds within the ATP-binding pocket and forms a hydrogen bond with A807 within the RET hinge and it makes hydrophobic contact with L881 of the catalytic spine which occurs in the floor of the adenine-binding pocket.	a807	116-120	ret proto-oncogene	Homo sapiens	132-135
29441947-5	2018	Brefelamide pretreatment inhibited GDNF-induced cell proliferation and expression of rearranged during transfection (RET).	brefelamide	0-11	ret proto-oncogene	Homo sapiens	85-115
29662541-1	2018	Cabozantinib is an oral multitargeted tyrosine kinase inhibitor (TKI) that potently inhibits MET and AXL, both associated with poor prognosis in renal cell carcinoma (RCC), next to vascular endothelial growth factor receptor 2, KIT, FLT3 and RET.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	242-245
28937965-1	2018	Artemin (ARTN) is a member of glial cell line-derived neurotrophic factor (GDNF) family of ligands, and its signaling is mediated via a multi-component receptor complex including the glycosylphosphatidylinositol-anchored GDNF family receptors a (GFRa1, GFRa3) and RET receptor tyrosine kinase.	Glycosylphosphatidylinositols	183-211	ret proto-oncogene	Homo sapiens	264-267
29441947-5	2018	Brefelamide pretreatment inhibited GDNF-induced cell proliferation and expression of rearranged during transfection (RET).	brefelamide	0-11	ret proto-oncogene	Homo sapiens	117-120
30032643-1	2018	Lenvatinib is a small-molecule tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor (VEGFR1-3), fibroblast growth factor receptor (FGFR1-4), platelet-derived growth factor receptor alpha (PDGFRalpha), stem cell factor receptor (KIT), and rearranged during transfection (RET).	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	269-299
30032643-1	2018	Lenvatinib is a small-molecule tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor (VEGFR1-3), fibroblast growth factor receptor (FGFR1-4), platelet-derived growth factor receptor alpha (PDGFRalpha), stem cell factor receptor (KIT), and rearranged during transfection (RET).	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	301-304
30957057-0	2018	Acquired ALK and RET Gene Fusions as Mechanisms of Resistance to Osimertinib in EGFR-Mutant Lung Cancers.	osimertinib	65-76	ret proto-oncogene	Homo sapiens	17-20
29128428-3	2018	In large retrospective studies, RET rearrangements correlate with adenocarcinoma histologic subtype, never-smoking status, younger age, more advanced disease stage, potentially higher chemosensitivity (in particular, to pemetrexed-based regimens), and coexistence of other genomic alterations.	Pemetrexed	220-230	ret proto-oncogene	Homo sapiens	32-35
30069768-0	2018	Lenvantinib: A Tyrosine Kinase Inhibitor of VEGFR 1-3, FGFR 1-4, PDGFRalpha, KIT and RET.	lenvantinib	0-11	ret proto-oncogene	Homo sapiens	85-88
29468981-1	2018	BACKGROUND AND OBJECTIVE: Lenvatinib is an oral, multitargeted Tyrosine Kinase Inhibitor (TKI) of Vascular Endothelial Growth Factor Receptors (VEGFR1-VEGFR3), fibroblast growth factor receptors (FGFR1-FGFR4), Platelet-Derived Growth Factor Receptor (PDGFR)alpha, rearranged during transfection (RET), and v-kit (KIT) signaling networks implicated in tumor angiogenesis.	lenvatinib	26-36	ret proto-oncogene	Homo sapiens	264-294
29468981-1	2018	BACKGROUND AND OBJECTIVE: Lenvatinib is an oral, multitargeted Tyrosine Kinase Inhibitor (TKI) of Vascular Endothelial Growth Factor Receptors (VEGFR1-VEGFR3), fibroblast growth factor receptors (FGFR1-FGFR4), Platelet-Derived Growth Factor Receptor (PDGFR)alpha, rearranged during transfection (RET), and v-kit (KIT) signaling networks implicated in tumor angiogenesis.	lenvatinib	26-36	ret proto-oncogene	Homo sapiens	296-299
30069768-1	2018	Lenvatinib is an oral receptor tyrosine kinase inhibitor (TKI) with activity against vascular endothelial growth factor (VEGF) receptors 1-3, fibroblast growth factor receptors (FGFR) 1-4, platelet-derived growth factor receptor-alpha (PDGFRalpha), and RET and KIT proto-oncogenes.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	253-256
30069758-1	2018	Regorafenib (BAY 73-4506, Stivarga ) is an oral diphenylurea multi-kinase inhibitor that targets angiogenic (VEGFR1-3, TIE2), stromal (PDGFR-beta, FGFR), and oncogenic receptor tyrosine kinases (KIT, RET, and RAF).	regorafenib	0-11	ret proto-oncogene	Homo sapiens	200-203
28236116-1	2017	Lenvatinib is a multikinase inhibitor that targets vascular endothelial growth factor (VEGF) receptors 1-3, fibroblast growth factor receptors 1-4, platelet-derived growth factor receptor-alpha, and RET and KIT proto-oncogenes.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	199-202
30069758-1	2018	Regorafenib (BAY 73-4506, Stivarga ) is an oral diphenylurea multi-kinase inhibitor that targets angiogenic (VEGFR1-3, TIE2), stromal (PDGFR-beta, FGFR), and oncogenic receptor tyrosine kinases (KIT, RET, and RAF).	regorafenib	13-24	ret proto-oncogene	Homo sapiens	200-203
30069760-0	2018	Cabozantinib: Multi-kinase Inhibitor of MET, AXL, RET, and VEGFR2.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	50-53
30069760-1	2018	Cabozantinib is a receptor tyrosine kinase inhibitor (TKI) with activity against a broad range of targets, including MET, RET, AXL, VEGFR2, FLT3, and c-KIT.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	122-125
29253861-8	2017	Receptor Tyrosine Kinase translocated to the cell membrane in BPDF but not in LPDF or CPDF incubated endothelial cells.	bpdf	62-66	ret proto-oncogene	Homo sapiens	0-24
29159332-5	2017	This approach uncovered that cells on 2D hydrogels and spheroids encapsulated in 3D hydrogels were less responsive to receptor tyrosine kinase (RTK)-targeting drugs sorafenib and lapatinib, but not cytotoxic drugs, compared to single cells in hydrogels and cells on plastic.	Sorafenib	165-174	ret proto-oncogene	Homo sapiens	118-142
29159332-5	2017	This approach uncovered that cells on 2D hydrogels and spheroids encapsulated in 3D hydrogels were less responsive to receptor tyrosine kinase (RTK)-targeting drugs sorafenib and lapatinib, but not cytotoxic drugs, compared to single cells in hydrogels and cells on plastic.	Sorafenib	165-174	ret proto-oncogene	Homo sapiens	144-147
29159332-5	2017	This approach uncovered that cells on 2D hydrogels and spheroids encapsulated in 3D hydrogels were less responsive to receptor tyrosine kinase (RTK)-targeting drugs sorafenib and lapatinib, but not cytotoxic drugs, compared to single cells in hydrogels and cells on plastic.	Lapatinib	179-188	ret proto-oncogene	Homo sapiens	144-147
28946813-8	2017	RESULTS: Twenty-six single VUS in RET without any well-defined risk profiles were found in 33 patients.	3-[(3~{a}~{S},4~{S},6~{a}~{R})-4-carboxy-2,3,4,5,6,6~{a}-hexahydro-1~{H}-pyrrolo[2,3-c]pyrrol-3~{a}-yl]propyl-$l^{3}-oxidanyl-bis(oxidanyl)boranuide	27-30	ret proto-oncogene	Homo sapiens	34-37
28762645-3	2017	OBJECTIVE: Evaluate the effectiveness and tolerability of a double-conjugate retinoid cream (AlphaRet Overnight Cream; AHA-Ret) in improving visible signs of photoaging vs 1.0% retinol or 0.025% tretinoin.	Retinoids	77-85	ret proto-oncogene	Homo sapiens	98-101
28762645-15	2017	AHA-Ret induced less Erythema vs retinol and was more tolerable vs retinol and tretinoin.	Vitamin A	33-40	ret proto-oncogene	Homo sapiens	4-7
28762645-15	2017	AHA-Ret induced less Erythema vs retinol and was more tolerable vs retinol and tretinoin.	Vitamin A	67-74	ret proto-oncogene	Homo sapiens	4-7
28762645-15	2017	AHA-Ret induced less Erythema vs retinol and was more tolerable vs retinol and tretinoin.	Tretinoin	79-88	ret proto-oncogene	Homo sapiens	4-7
28946813-11	2017	A study of the entire cohort showed that patients carrying pathogenic variants or VUS in RET together with PHEO were diagnosed earlier than the others.	3-[(3~{a}~{S},4~{S},6~{a}~{R})-4-carboxy-2,3,4,5,6,6~{a}-hexahydro-1~{H}-pyrrolo[2,3-c]pyrrol-3~{a}-yl]propyl-$l^{3}-oxidanyl-bis(oxidanyl)boranuide	82-85	ret proto-oncogene	Homo sapiens	89-92
29045520-8	2017	In an exploratory assessment of OS, progression-free survival, and objective response rate, cabozantinib appeared to have a larger treatment effect in patients with RET M918T mutation-positive tumors compared with patients not harboring this mutation.	cabozantinib	92-104	ret proto-oncogene	Homo sapiens	165-168
29312610-0	2017	Inhibitor repurposing reveals ALK, LTK, FGFR, RET and TRK kinases as the targets of AZD1480.	AZD 1480	84-91	ret proto-oncogene	Homo sapiens	46-49
29312610-5	2017	We demonstrate that AZD1480 inhibits ALK, LTK, FGFR1-3, RET and TRKA-C kinases and uncover a physical basis of this specificity.	AZD 1480	20-27	ret proto-oncogene	Homo sapiens	56-59
29045520-9	2017	For patients with RET M918T-positive disease, median OS was 44.3 months for cabozantinib versus 18.9 months for placebo [HR, 0.60; 95% CI, 0.38-0.94; P = 0.03 (not adjusted for multiple subgroup analyses)], with corresponding values of 20.2 versus 21.5 months (HR, 1.12; 95% CI, 0.70-1.82; P = 0.63) in the RET M918T-negative subgroup.	cabozantinib	76-88	ret proto-oncogene	Homo sapiens	18-21
29045520-9	2017	For patients with RET M918T-positive disease, median OS was 44.3 months for cabozantinib versus 18.9 months for placebo [HR, 0.60; 95% CI, 0.38-0.94; P = 0.03 (not adjusted for multiple subgroup analyses)], with corresponding values of 20.2 versus 21.5 months (HR, 1.12; 95% CI, 0.70-1.82; P = 0.63) in the RET M918T-negative subgroup.	cabozantinib	76-88	ret proto-oncogene	Homo sapiens	307-310
29045520-14	2017	Exploratory analyses suggest that patients with RET M918T-positive tumors may experience a greater treatment benefit with cabozantinib.	cabozantinib	122-134	ret proto-oncogene	Homo sapiens	48-51
29262623-0	2017	Small molecule inhibitor regorafenib inhibits RET signaling in neuroblastoma cells and effectively suppresses tumor growth in vivo.	regorafenib	25-36	ret proto-oncogene	Homo sapiens	46-49
29059635-1	2017	BACKGROUND: Cabozantinib is an inhibitor of tyrosine kinases, including MET, vascular endothelial growth factor receptor, AXL and RET.	cabozantinib	12-24	ret proto-oncogene	Homo sapiens	130-133
28952196-5	2017	Direct DNA analyses of isolated MTC paraffin-embedded specimens revealed two RET proto-oncogene missense point mutations in exon 11 (i.e., C630R and C634W).	Paraffin	36-44	ret proto-oncogene	Homo sapiens	77-80
31093354-2	2017	Lenvatinib, an MKI targeting vascular endothelial growth factor receptor, fibroblast growth factor receptor, platelet-derived growth factor receptor, c-Kit, and RET, has shown efficacy in stabilizing previously progressive disease, with emerging evidence of a possible benefit in terms of overall survival.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	161-164
29262623-4	2017	Herein we report that RET is required for NB cell proliferation and that the small molecule inhibitor regorafenib (BAY 73-4506) blocks glial cell derived neurotrophic factor (GDNF)-induced RET signaling in NB cells and inhibits NB growth both in vitro and in vivo.	regorafenib	102-113	ret proto-oncogene	Homo sapiens	189-192
29262623-4	2017	Herein we report that RET is required for NB cell proliferation and that the small molecule inhibitor regorafenib (BAY 73-4506) blocks glial cell derived neurotrophic factor (GDNF)-induced RET signaling in NB cells and inhibits NB growth both in vitro and in vivo.	regorafenib	115-126	ret proto-oncogene	Homo sapiens	189-192
29262623-8	2017	In summary, our study suggests that RET is a potential therapeutic target in NB, and that using a novel RET inhibitor, like regorafenib, should be investigated as a therapeutic treatment option for children with NB.	regorafenib	124-135	ret proto-oncogene	Homo sapiens	104-107
28949508-2	2017	The high ECL efficiency of Ru-PEI-ABEI was originated from the dual intramolecular self-catalysis including intramolecular coreaction between polyethylenimine (PEI) and Ru(bpy)2(mcbpy)2+, and intramolecular ECL resonance energy transfer (ECL-RET) from N-(aminobutyl)-N-(ethylisoluminol) (ABEI) to Ru(bpy)2(mcbpy)2+, which would generate a strong initial ECL signal.	ru-pei	27-33	ret proto-oncogene	Homo sapiens	242-245
28949508-2	2017	The high ECL efficiency of Ru-PEI-ABEI was originated from the dual intramolecular self-catalysis including intramolecular coreaction between polyethylenimine (PEI) and Ru(bpy)2(mcbpy)2+, and intramolecular ECL resonance energy transfer (ECL-RET) from N-(aminobutyl)-N-(ethylisoluminol) (ABEI) to Ru(bpy)2(mcbpy)2+, which would generate a strong initial ECL signal.	N-(4-Aminobutyl)-N-ethylisoluminol	34-38	ret proto-oncogene	Homo sapiens	242-245
28688972-8	2017	The notion of merging RTK (receptor tyrosine kinase) inhibition with suppression of invasion and possible inhibition of EMT has contributed to the credibility of combretastatins as anti-cancer agents.	combretastatin	162-177	ret proto-oncogene	Homo sapiens	22-25
28949508-2	2017	The high ECL efficiency of Ru-PEI-ABEI was originated from the dual intramolecular self-catalysis including intramolecular coreaction between polyethylenimine (PEI) and Ru(bpy)2(mcbpy)2+, and intramolecular ECL resonance energy transfer (ECL-RET) from N-(aminobutyl)-N-(ethylisoluminol) (ABEI) to Ru(bpy)2(mcbpy)2+, which would generate a strong initial ECL signal.	Polyethyleneimine	142-158	ret proto-oncogene	Homo sapiens	242-245
28949508-2	2017	The high ECL efficiency of Ru-PEI-ABEI was originated from the dual intramolecular self-catalysis including intramolecular coreaction between polyethylenimine (PEI) and Ru(bpy)2(mcbpy)2+, and intramolecular ECL resonance energy transfer (ECL-RET) from N-(aminobutyl)-N-(ethylisoluminol) (ABEI) to Ru(bpy)2(mcbpy)2+, which would generate a strong initial ECL signal.	Polyethyleneimine	30-33	ret proto-oncogene	Homo sapiens	242-245
29066909-4	2017	Apatinib is a novel oral small-molecule tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2) and may also be effective on Ret, c-KIT, and c-src.	apatinib	0-8	ret proto-oncogene	Homo sapiens	189-192
31556266-1	2017	Aim: To evaluate reticulocyte hemoglobin (RET-Hb) vis-a-vis immature reticulocyte fraction (IRF) as an earliest indicator of response to iron therapy in iron deficiency anemia (IDA), by assessing change in RET-He and IRF at 48 hours after initiation of intravenous iron therapy.	Iron	137-141	ret proto-oncogene	Homo sapiens	42-45
31556266-1	2017	Aim: To evaluate reticulocyte hemoglobin (RET-Hb) vis-a-vis immature reticulocyte fraction (IRF) as an earliest indicator of response to iron therapy in iron deficiency anemia (IDA), by assessing change in RET-He and IRF at 48 hours after initiation of intravenous iron therapy.	Iron	153-157	ret proto-oncogene	Homo sapiens	42-45
31556266-10	2017	RET-He and IRF increased significantly at 48 hours after initiation of intravenous iron therapy (post therapy) as compared to baseline (pre therapy) in both the two groups as well when all patients were considered together.	Iron	83-87	ret proto-oncogene	Homo sapiens	0-3
31556266-13	2017	Conclusion: RET-Hb, a real time indicator of iron supply (hemoglobinization) to the developing RBC"s, is the earliest marker of response to iron therapy as compared to IRF (representative of reticulocyte count).	Iron	45-49	ret proto-oncogene	Homo sapiens	12-15
31556266-13	2017	Conclusion: RET-Hb, a real time indicator of iron supply (hemoglobinization) to the developing RBC"s, is the earliest marker of response to iron therapy as compared to IRF (representative of reticulocyte count).	Iron	140-144	ret proto-oncogene	Homo sapiens	12-15
28688972-8	2017	The notion of merging RTK (receptor tyrosine kinase) inhibition with suppression of invasion and possible inhibition of EMT has contributed to the credibility of combretastatins as anti-cancer agents.	combretastatin	162-177	ret proto-oncogene	Homo sapiens	27-51
28877471-7	2017	However, combining the RET inhibitor sorafenib with drugs that target EGFR, microtubules, or FGFR led to strong efficacy in both Drosophila and human cell line KIF5B-RET models.	Sorafenib	37-46	ret proto-oncogene	Homo sapiens	166-169
28768491-2	2017	These GISTs generally respond well to therapy with the RTK inhibitor imatinib mesylate (IM), although initial response is genotype-dependent.	Imatinib Mesylate	69-86	ret proto-oncogene	Homo sapiens	55-58
28639308-4	2017	Herein we present the development and the preliminary evaluation of a new sub-micromolar wt RET/V804M RET inhibitor, N-(2-fluoro-5-trifluoromethylphenyl)-N"-{4"-[(2""-benzamido)pyridin-4""-ylamino]phenyl}urea (69), endowed with a 4-anilinopyridine structure, starting from our previously identified 4-anilinopyrimidine hit compound.	N-(2-fluoro-5-trifluoromethylphenyl)-N'-(4'-((2'-benzamido)pyridin-4'-ylamino)phenyl)urea	117-208	ret proto-oncogene	Homo sapiens	92-95
28639308-4	2017	Herein we present the development and the preliminary evaluation of a new sub-micromolar wt RET/V804M RET inhibitor, N-(2-fluoro-5-trifluoromethylphenyl)-N"-{4"-[(2""-benzamido)pyridin-4""-ylamino]phenyl}urea (69), endowed with a 4-anilinopyridine structure, starting from our previously identified 4-anilinopyrimidine hit compound.	N-(2-fluoro-5-trifluoromethylphenyl)-N'-(4'-((2'-benzamido)pyridin-4'-ylamino)phenyl)urea	117-208	ret proto-oncogene	Homo sapiens	102-105
28639308-4	2017	Herein we present the development and the preliminary evaluation of a new sub-micromolar wt RET/V804M RET inhibitor, N-(2-fluoro-5-trifluoromethylphenyl)-N"-{4"-[(2""-benzamido)pyridin-4""-ylamino]phenyl}urea (69), endowed with a 4-anilinopyridine structure, starting from our previously identified 4-anilinopyrimidine hit compound.	N-Phenylpyridin-4-amine	230-247	ret proto-oncogene	Homo sapiens	92-95
28639308-4	2017	Herein we present the development and the preliminary evaluation of a new sub-micromolar wt RET/V804M RET inhibitor, N-(2-fluoro-5-trifluoromethylphenyl)-N"-{4"-[(2""-benzamido)pyridin-4""-ylamino]phenyl}urea (69), endowed with a 4-anilinopyridine structure, starting from our previously identified 4-anilinopyrimidine hit compound.	N-Phenylpyridin-4-amine	230-247	ret proto-oncogene	Homo sapiens	102-105
28639308-4	2017	Herein we present the development and the preliminary evaluation of a new sub-micromolar wt RET/V804M RET inhibitor, N-(2-fluoro-5-trifluoromethylphenyl)-N"-{4"-[(2""-benzamido)pyridin-4""-ylamino]phenyl}urea (69), endowed with a 4-anilinopyridine structure, starting from our previously identified 4-anilinopyrimidine hit compound.	N-phenylpyrimidin-4-amine	299-318	ret proto-oncogene	Homo sapiens	92-95
28639308-4	2017	Herein we present the development and the preliminary evaluation of a new sub-micromolar wt RET/V804M RET inhibitor, N-(2-fluoro-5-trifluoromethylphenyl)-N"-{4"-[(2""-benzamido)pyridin-4""-ylamino]phenyl}urea (69), endowed with a 4-anilinopyridine structure, starting from our previously identified 4-anilinopyrimidine hit compound.	N-phenylpyrimidin-4-amine	299-318	ret proto-oncogene	Homo sapiens	102-105
28347966-2	2017	The results revealed that SiQDs can not only greatly enhance luminol ECL, but also act as energy acceptor to construct a novel ECL resonance energy transfer (ECL-RET) system with luminol.	Luminol	61-68	ret proto-oncogene	Homo sapiens	162-165
28347966-2	2017	The results revealed that SiQDs can not only greatly enhance luminol ECL, but also act as energy acceptor to construct a novel ECL resonance energy transfer (ECL-RET) system with luminol.	Luminol	179-186	ret proto-oncogene	Homo sapiens	162-165
28703624-3	2017	Cabozantinib is oral, small-molecule tyrosine kinase inhibitor that primarily targets MET, VEGFR2, AXL and RET, with additional effect on KIT and FLT3.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	107-110
28868184-11	2017	RET overactivation in MEN2B lead to a large increase in intrinsic nerve fibres in the myenteric and submucosal ganglia, with a relative increase in NOS-IR nerve fibres in the circular muscle and VIP and SP in the submucosal ganglia and mucosa.	TFF2 protein, human	203-205	ret proto-oncogene	Homo sapiens	0-3
28868184-11	2017	RET overactivation in MEN2B lead to a large increase in intrinsic nerve fibres in the myenteric and submucosal ganglia, with a relative increase in NOS-IR nerve fibres in the circular muscle and VIP and SP in the submucosal ganglia and mucosa.	TFF2 protein, human	203-205	ret proto-oncogene	Homo sapiens	22-27
28768491-2	2017	These GISTs generally respond well to therapy with the RTK inhibitor imatinib mesylate (IM), although initial response is genotype-dependent.	Imatinib Mesylate	88-90	ret proto-oncogene	Homo sapiens	55-58
28915580-6	2017	In line with these clinical evidences computer simulations, biophysical techniques and in vitro experiments demonstrated that the receptor tyrosine kinase KIT carrying the Delta574-580 mutation displays constitutive phosphorylation, which can be switched-off upon Imatinib treatment.	Imatinib Mesylate	264-272	ret proto-oncogene	Homo sapiens	130-154
26986978-2	2017	Vandetanib, a small molecule receptor tyrosine kinase inhibitor of VEGFR-2, VEGFR-3, RET, and EGFR, demonstrated synergy with radiation and chemotherapy in preclinical models.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	85-88
28860428-3	2017	Genomic profiling of each cancer were analyzed and newdrug applications of label expansion are in preparation based on the results of several registration studies including investigator-initiated trial of vandetanib for RET fusion gene positive non-small cell lung cancer.	vandetanib	205-215	ret proto-oncogene	Homo sapiens	220-223
28500237-2	2017	Ponatinib is a multi-kinase inhibitor with low-nanomolar potency against the RET kinase domain.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	77-80
28500237-3	2017	Here, we demonstrate that ponatinib exhibits potent antiproliferative activity in RET fusion-positive LC-2/ad lung adenocarcinoma cells and inhibits phosphorylation of the RET fusion protein and signaling through ERK1/2 and AKT.	ponatinib	26-35	ret proto-oncogene	Homo sapiens	82-85
28500237-3	2017	Here, we demonstrate that ponatinib exhibits potent antiproliferative activity in RET fusion-positive LC-2/ad lung adenocarcinoma cells and inhibits phosphorylation of the RET fusion protein and signaling through ERK1/2 and AKT.	ponatinib	26-35	ret proto-oncogene	Homo sapiens	172-175
28743001-4	2017	We show that CRL3GCL promotes PGC fate by mediating degradation of Torso, a receptor tyrosine kinase (RTK) and major determinant of somatic cell fate.	crl3gcl	13-20	ret proto-oncogene	Homo sapiens	76-100
28743001-4	2017	We show that CRL3GCL promotes PGC fate by mediating degradation of Torso, a receptor tyrosine kinase (RTK) and major determinant of somatic cell fate.	crl3gcl	13-20	ret proto-oncogene	Homo sapiens	102-105
28082048-13	2017	Four patients with tumors harboring CCDC6-RET and KIF5B-RET fusions showed pronounced and durable responses to platinum-based chemotherapy that lasted for 8 to 15 months.	Platinum	111-119	ret proto-oncogene	Homo sapiens	42-45
28433712-0	2017	Common PHOX2B poly-alanine contractions impair RET gene transcription, predisposing to Hirschsprung disease.	polyalanine	14-26	ret proto-oncogene	Homo sapiens	47-50
28082048-13	2017	Four patients with tumors harboring CCDC6-RET and KIF5B-RET fusions showed pronounced and durable responses to platinum-based chemotherapy that lasted for 8 to 15 months.	Platinum	111-119	ret proto-oncogene	Homo sapiens	56-59
28011461-0	2017	Antitumor Activity of RXDX-105 in Multiple Cancer Types with RET Rearrangements or Mutations.	agerafenib	22-30	ret proto-oncogene	Homo sapiens	61-64
28299633-2	2017	The recent development of automated systems for hematology analysis has made it possible to measure reticulocyte hemoglobin equivalent (RET-He), which is thought to reflect iron content in reticulocytes, in the same sample used for complete blood count tests.	Iron	173-177	ret proto-oncogene	Homo sapiens	136-139
28299633-12	2017	RET-He changed in parallel with changes in Hb during iron administration for 21 IDA patients.	Iron	53-57	ret proto-oncogene	Homo sapiens	0-3
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
28693255-4	2017	Lack of oxygen activates hypoxia-inducible factor (HIF) protein, which is followed by the upregulation of growth factors, including vascular endothelial growth factor and activation of the RTK signaling pathway.	Oxygen	8-14	ret proto-oncogene	Homo sapiens	189-192
28342760-15	2017	Correction of this mutation in iPSC using CRISPR/Cas9 editing, as well as the RET G731del mutation that causes Hirschsprung disease with total colonic aganglionosis, restored ENCC function.	g731del	82-89	ret proto-oncogene	Homo sapiens	78-81
28629549-0	2017	Intracranial and Systemic Response to Alectinib in a Patient with RET-KIF5B Oncogenic Fusion.	alectinib	38-47	ret proto-oncogene	Homo sapiens	66-69
28011461-3	2017	RXDX-105 is a small molecule kinase inhibitor that potently inhibits RET.	agerafenib	0-8	ret proto-oncogene	Homo sapiens	69-72
28011461-4	2017	The purpose of the preclinical and clinical studies was to evaluate the potential of RXDX-105 as an effective therapy for cancers driven by RET alterations.Experimental design: The RET-inhibitory activity of RXDX-105 was assessed by biochemical and cellular assays, followed by in vivo tumor growth inhibition studies in cell line- and patient-derived xenograft models.	agerafenib	208-216	ret proto-oncogene	Homo sapiens	181-184
28011461-8	2017	Additionally, a patient with advanced RET-rearranged lung cancer had a rapid and sustained response to RXDX-105 in both intracranial and extracranial disease.Conclusions: These data support the inclusion of patients bearing RET alterations in ongoing and future molecularly enriched clinical trials to explore RXDX-105 efficacy across a variety of tumor types.	agerafenib	103-111	ret proto-oncogene	Homo sapiens	38-41
28011461-8	2017	Additionally, a patient with advanced RET-rearranged lung cancer had a rapid and sustained response to RXDX-105 in both intracranial and extracranial disease.Conclusions: These data support the inclusion of patients bearing RET alterations in ongoing and future molecularly enriched clinical trials to explore RXDX-105 efficacy across a variety of tumor types.	agerafenib	103-111	ret proto-oncogene	Homo sapiens	224-227
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
28615362-4	2017	We report that potent inhibitors, such as AD80 or ponatinib, that stably bind in the DFG-out conformation of RET may overcome these limitations and selectively kill RET-rearranged tumors.	AD80	42-46	ret proto-oncogene	Homo sapiens	109-112
28615362-4	2017	We report that potent inhibitors, such as AD80 or ponatinib, that stably bind in the DFG-out conformation of RET may overcome these limitations and selectively kill RET-rearranged tumors.	AD80	42-46	ret proto-oncogene	Homo sapiens	165-168
28615362-4	2017	We report that potent inhibitors, such as AD80 or ponatinib, that stably bind in the DFG-out conformation of RET may overcome these limitations and selectively kill RET-rearranged tumors.	ponatinib	50-59	ret proto-oncogene	Homo sapiens	109-112
28615362-4	2017	We report that potent inhibitors, such as AD80 or ponatinib, that stably bind in the DFG-out conformation of RET may overcome these limitations and selectively kill RET-rearranged tumors.	ponatinib	50-59	ret proto-oncogene	Homo sapiens	165-168
28615362-4	2017	We report that potent inhibitors, such as AD80 or ponatinib, that stably bind in the DFG-out conformation of RET may overcome these limitations and selectively kill RET-rearranged tumors.	1,3-Diphenylguanidine	85-88	ret proto-oncogene	Homo sapiens	109-112
28615362-4	2017	We report that potent inhibitors, such as AD80 or ponatinib, that stably bind in the DFG-out conformation of RET may overcome these limitations and selectively kill RET-rearranged tumors.	1,3-Diphenylguanidine	85-88	ret proto-oncogene	Homo sapiens	165-168
28635216-9	2017	It was also found that RET/PTC rearrangement was associated with an abnormal increase in TSH level of one month after surgery (P= 0.037).	Thyrotropin	89-92	ret proto-oncogene	Homo sapiens	23-26
28635216-9	2017	It was also found that RET/PTC rearrangement was associated with an abnormal increase in TSH level of one month after surgery (P= 0.037).	Thyrotropin	89-92	ret proto-oncogene	Homo sapiens	27-30
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
29088743-0	2017	In vitro and in vivo anti-tumor activity of alectinib in tumor cells with NCOA4-RET.	alectinib	44-53	ret proto-oncogene	Homo sapiens	80-83
28404842-4	2017	In the presence of doxycycline, HD10.6 cells mature to exhibit neuronal morphology and express sensory neuron-associated markers such as neurotrophin receptors TrkA, TrkB, TrkC, and RET and the sensory neurofilament peripherin.	Doxycycline	19-30	ret proto-oncogene	Homo sapiens	182-185
28336808-2	2017	Using the chemical scaffold of the JAK2 inhibitor TG101348, we developed and characterized single agents which potently and simultaneously inhibit BRD4 and a specific set of oncogenic tyrosine kinases including JAK2, FLT3, RET, and ROS1.	Fedratinib	50-58	ret proto-oncogene	Homo sapiens	223-226
29088743-3	2017	Recent clinical trials for RET fusion-positive NSCLC using vandetanib or cabozantinib demonstrated positive clinical response and considerable differential activities for RET inhibitors among fusion partners.	vandetanib	59-69	ret proto-oncogene	Homo sapiens	27-30
29088743-3	2017	Recent clinical trials for RET fusion-positive NSCLC using vandetanib or cabozantinib demonstrated positive clinical response and considerable differential activities for RET inhibitors among fusion partners.	vandetanib	59-69	ret proto-oncogene	Homo sapiens	171-174
29088743-3	2017	Recent clinical trials for RET fusion-positive NSCLC using vandetanib or cabozantinib demonstrated positive clinical response and considerable differential activities for RET inhibitors among fusion partners.	cabozantinib	73-85	ret proto-oncogene	Homo sapiens	27-30
29088743-3	2017	Recent clinical trials for RET fusion-positive NSCLC using vandetanib or cabozantinib demonstrated positive clinical response and considerable differential activities for RET inhibitors among fusion partners.	cabozantinib	73-85	ret proto-oncogene	Homo sapiens	171-174
29088743-4	2017	Alectinib, an approved ALK inhibitor, is reported to inhibit KIF5B-RET and CCDC6-RET.	alectinib	0-9	ret proto-oncogene	Homo sapiens	67-70
29088743-4	2017	Alectinib, an approved ALK inhibitor, is reported to inhibit KIF5B-RET and CCDC6-RET.	alectinib	0-9	ret proto-oncogene	Homo sapiens	81-84
29088743-5	2017	However, the activity of alectinib with respect to RET with other fusion partners is unknown.	alectinib	25-34	ret proto-oncogene	Homo sapiens	51-54
29088743-6	2017	In the present study, we investigated the effects of alectinib on NCOA4-RET fusion-positive tumor cells in vitro and in vivo.	alectinib	53-62	ret proto-oncogene	Homo sapiens	72-75
29088743-7	2017	Alectinib inhibited the viability of NCOA4-RET-positive EHMES-10 cells, as well as CCDC6-RET-positive LC-2/ad and TPC-1 cells.	alectinib	0-9	ret proto-oncogene	Homo sapiens	43-46
29088743-11	2017	These results suggest that alectinib may be a promising RET inhibitor against tumors positive for not only KIF5B-RET and CCDC6-RET, but also NCOA4-RET.	alectinib	27-36	ret proto-oncogene	Homo sapiens	56-59
29088743-11	2017	These results suggest that alectinib may be a promising RET inhibitor against tumors positive for not only KIF5B-RET and CCDC6-RET, but also NCOA4-RET.	alectinib	27-36	ret proto-oncogene	Homo sapiens	113-116
29088743-11	2017	These results suggest that alectinib may be a promising RET inhibitor against tumors positive for not only KIF5B-RET and CCDC6-RET, but also NCOA4-RET.	alectinib	27-36	ret proto-oncogene	Homo sapiens	113-116
29088743-11	2017	These results suggest that alectinib may be a promising RET inhibitor against tumors positive for not only KIF5B-RET and CCDC6-RET, but also NCOA4-RET.	alectinib	27-36	ret proto-oncogene	Homo sapiens	113-116
28464908-2	2017	Foretinib is an inhibitor of c-Met, VEGF receptor 2 (VEGFR-2), platelet-derived growth factor receptor beta (PDGFRB), AXL, Fms-like tyrosine kinase 3 (FLT3), angiopoiten receptor (TIE-2), RET and RON kinases.	GSK 1363089	0-9	ret proto-oncogene	Homo sapiens	188-191
28375615-4	2017	We demonstrate that the MET receptor tyrosine kinase (MET) is specifically expressed in a subset of 5-HT neurons within the caudal part of the dorsal raphe nuclei (DRC) that is encompassed by the classic B6 serotonin cell group.	Serotonin	207-216	ret proto-oncogene	Homo sapiens	28-52
28477875-1	2017	Cabozantinib is an oral multiple tyrosine kinase receptor inhibitor (ITK): VEGFR2, c-MET and RET.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	93-96
28477875-3	2017	Cabozantinib improve progression-free survival (PFS) in progressive metastatic medullary thyroid cancer (MTC): 4 months in the placebo group and 11.2 months in the cabozantinib group (P&lt;0.001) in all patient subgroups including those with or without prior ITK and RET mutation status.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	267-270
28469506-6	2017	The most frequent RET mutations in patients with MEN2A occurred at codon 634 on exon 11: p.Cys634Tyr, p.Cys634Trp, and p.Cys634Arg.	cys634trp	104-113	ret proto-oncogene	Homo sapiens	18-21
28650002-2	2017	Cabozantinib is a novel multikinase inhibitor with activity against vascular endothelial growth factor receptor (VEGFR), proto-oncogene tyrosine-protein kinase receptor Ret and other kinases that recently joined this impressive list of approved agents.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	121-172
28506408-5	2017	In MEN2A, Codon 634 in exon 11 (Cys634Arg), corresponding to a cysteine in the extracellular cysteine-rich domain, is the most commonly altered codon.	Cysteine	63-71	ret proto-oncogene	Homo sapiens	3-8
28506408-5	2017	In MEN2A, Codon 634 in exon 11 (Cys634Arg), corresponding to a cysteine in the extracellular cysteine-rich domain, is the most commonly altered codon.	Cysteine	93-101	ret proto-oncogene	Homo sapiens	3-8
28460442-7	2017	Treatment with EGF robustly induced phosphorylation of RET at Tyr-905 in A+AD cells with wild type EGFR.	Tyrosine	62-65	ret proto-oncogene	Homo sapiens	55-58
28390257-2	2017	Under oxidative conditions, vitamin A radical cation (RET+) can be formed.	Vitamin A	28-37	ret proto-oncogene	Homo sapiens	54-57
28390257-5	2017	Here, we employed nanosecond laser flash photolysis (LFP) to generate RET+ (lambdamax=580nm in methanol) and examine its reactivity toward a wide range of biological molecules including amino acids, vitamins, carotenoids, naturally-occurring phenols, neurotransmitters such as catecholamines, wide range of phenol derivatives and some selected electron-donors.	Methanol	95-103	ret proto-oncogene	Homo sapiens	70-73
28390257-5	2017	Here, we employed nanosecond laser flash photolysis (LFP) to generate RET+ (lambdamax=580nm in methanol) and examine its reactivity toward a wide range of biological molecules including amino acids, vitamins, carotenoids, naturally-occurring phenols, neurotransmitters such as catecholamines, wide range of phenol derivatives and some selected electron-donors.	Carotenoids	209-220	ret proto-oncogene	Homo sapiens	70-73
28390257-9	2017	Vitamin E and carotenoids are the most efficient quenchers for the RET+ (diffusion-controlled reactions).	Vitamin E	0-9	ret proto-oncogene	Homo sapiens	67-70
28390257-9	2017	Vitamin E and carotenoids are the most efficient quenchers for the RET+ (diffusion-controlled reactions).	Carotenoids	14-25	ret proto-oncogene	Homo sapiens	67-70
28390257-10	2017	Importantly, our results clearly indicate that the reactivity of RET+ is as strong as that of the powerful trichloromethylperoxyl radical (CCl3O2).	trichloromethylperoxyl radical	107-137	ret proto-oncogene	Homo sapiens	65-68
28390257-10	2017	Importantly, our results clearly indicate that the reactivity of RET+ is as strong as that of the powerful trichloromethylperoxyl radical (CCl3O2).	Methyldioxy, trichloro-	139-145	ret proto-oncogene	Homo sapiens	65-68
28469506-6	2017	The most frequent RET mutations in patients with MEN2A occurred at codon 634 on exon 11: p.Cys634Tyr, p.Cys634Trp, and p.Cys634Arg.	cys634trp	104-113	ret proto-oncogene	Homo sapiens	49-54
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
27842445-1	2017	Cabozantinib inhibits a variety of cellular receptors including VEGFR1-3, MET, AXL, RET, FLT3 and KIT.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	84-87
27683183-6	2017	Two cases with lung (KIF5B-RET) and medullary thyroid carcinoma (RET M918T) that responded to a vandetanib (multikinase RET inhibitor)-containing regimen are shown.Conclusions:RET aberrations were seen in 1.8% of diverse cancers, with most cases harboring actionable, albeit distinct, coexisting alterations.	vandetanib	96-106	ret proto-oncogene	Homo sapiens	27-30
27683183-6	2017	Two cases with lung (KIF5B-RET) and medullary thyroid carcinoma (RET M918T) that responded to a vandetanib (multikinase RET inhibitor)-containing regimen are shown.Conclusions:RET aberrations were seen in 1.8% of diverse cancers, with most cases harboring actionable, albeit distinct, coexisting alterations.	vandetanib	96-106	ret proto-oncogene	Homo sapiens	65-68
27683183-6	2017	Two cases with lung (KIF5B-RET) and medullary thyroid carcinoma (RET M918T) that responded to a vandetanib (multikinase RET inhibitor)-containing regimen are shown.Conclusions:RET aberrations were seen in 1.8% of diverse cancers, with most cases harboring actionable, albeit distinct, coexisting alterations.	vandetanib	96-106	ret proto-oncogene	Homo sapiens	65-68
27683183-6	2017	Two cases with lung (KIF5B-RET) and medullary thyroid carcinoma (RET M918T) that responded to a vandetanib (multikinase RET inhibitor)-containing regimen are shown.Conclusions:RET aberrations were seen in 1.8% of diverse cancers, with most cases harboring actionable, albeit distinct, coexisting alterations.	vandetanib	96-106	ret proto-oncogene	Homo sapiens	65-68
27704266-1	2017	BACKGROUND: Lenvatinib is an oral inhibitor of vascular endothelial growth factor receptor 1-3, fibroblast growth factor receptor 1-4, platelet-derived growth factor receptor alpha, RET, and KIT.	lenvatinib	12-22	ret proto-oncogene	Homo sapiens	182-185
29120119-2	2017	Immunohistochemistry was performed on formalin-fixed, paraffin-embeddedtissue by the RET, p27 and cyclin D1 antibodies.	Formaldehyde	38-46	ret proto-oncogene	Homo sapiens	85-88
28259610-2	2017	Vandetanib is a novel tyrosine kinase inhibitor of VEGFR2, RET, and EGFR, all of which are in involved in the pathogenesis of pancreatic cancer.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	59-62
28068878-0	2017	Long-Term Control of Hypercortisolism by Vandetanib in a Case of Medullary Thyroid Carcinoma with a Somatic RET Mutation.	vandetanib	41-51	ret proto-oncogene	Homo sapiens	108-111
28068878-5	2017	Vandetanib, an oral multi-TKI that targets RET in particular, was initiated, and a rapid reversal of the hypercortisolism was observed without any change in tumor size.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	43-46
28553188-0	2017	Incidental Detection of Synchronous Medullary Thyroid Carcinoma with Bilateral Adrenal Pheochromocytoma on Iodine-123 Metaiodobenzylguanidine Scintigraphy, Leading to Diagnosis of Multiple Endocrine Neoplasia 2A.	3-Iodobenzylguanidine	118-141	ret proto-oncogene	Homo sapiens	180-211
28350084-13	2017	In conclusion, patients with TP53 mutations, RET mutations and sorafenib-targeted gene mutations were demonstrated to be associated with poor HCC prognosis, which suggests that both TP53 and RET may serve as biomarkers of prognostic evaluation and targeted therapy in HCC.	Sorafenib	63-72	ret proto-oncogene	Homo sapiens	191-194
29120119-2	2017	Immunohistochemistry was performed on formalin-fixed, paraffin-embeddedtissue by the RET, p27 and cyclin D1 antibodies.	Paraffin	54-62	ret proto-oncogene	Homo sapiens	85-88
27704398-6	2017	Genetic testing revealed the presence of a heterozygous variant of unknown significance (VUS) in the cysteine-rich region of exon 10 in the RET gene (c.1846G&gt;C, p.E616Q), in both affected siblings and their unaffected mother.	Cysteine	101-109	ret proto-oncogene	Homo sapiens	140-143
28069693-3	2017	Here, we demonstrate that treatment with non-cytotoxic levels of environmental chemicals (benzene and diethylnitrosamine) or chemotherapeutic agents (etoposide and doxorubicin) generates significant DNA breakage within RET at levels similar to those generated by fragile site-inducing laboratory chemicals.	Benzene	90-97	ret proto-oncogene	Homo sapiens	219-222
28069693-3	2017	Here, we demonstrate that treatment with non-cytotoxic levels of environmental chemicals (benzene and diethylnitrosamine) or chemotherapeutic agents (etoposide and doxorubicin) generates significant DNA breakage within RET at levels similar to those generated by fragile site-inducing laboratory chemicals.	Diethylnitrosamine	102-120	ret proto-oncogene	Homo sapiens	219-222
28069693-3	2017	Here, we demonstrate that treatment with non-cytotoxic levels of environmental chemicals (benzene and diethylnitrosamine) or chemotherapeutic agents (etoposide and doxorubicin) generates significant DNA breakage within RET at levels similar to those generated by fragile site-inducing laboratory chemicals.	Etoposide	150-159	ret proto-oncogene	Homo sapiens	219-222
28069693-3	2017	Here, we demonstrate that treatment with non-cytotoxic levels of environmental chemicals (benzene and diethylnitrosamine) or chemotherapeutic agents (etoposide and doxorubicin) generates significant DNA breakage within RET at levels similar to those generated by fragile site-inducing laboratory chemicals.	Doxorubicin	164-175	ret proto-oncogene	Homo sapiens	219-222
28073897-0	2017	Identification of ALK, ROS1, and RET Fusions by a Multiplexed mRNA-Based Assay in Formalin-Fixed, Paraffin-Embedded Samples from Advanced Non-Small-Cell Lung Cancer Patients.	Formaldehyde	82-90	ret proto-oncogene	Homo sapiens	33-36
28073897-0	2017	Identification of ALK, ROS1, and RET Fusions by a Multiplexed mRNA-Based Assay in Formalin-Fixed, Paraffin-Embedded Samples from Advanced Non-Small-Cell Lung Cancer Patients.	Paraffin	98-106	ret proto-oncogene	Homo sapiens	33-36
27704398-8	2017	Variants in the cysteine-rich region of the RET gene, outside of the key cysteine residues, may contribute to the development of MEN2 in a less aggressive manner, with a lower penetrance of MTC.	Cysteine	16-24	ret proto-oncogene	Homo sapiens	44-47
27704398-8	2017	Variants in the cysteine-rich region of the RET gene, outside of the key cysteine residues, may contribute to the development of MEN2 in a less aggressive manner, with a lower penetrance of MTC.	Cysteine	73-81	ret proto-oncogene	Homo sapiens	44-47
28193239-9	2017	In particular, buformin suppressed stem cell populations and self-renewal in vitro, which was associated with inhibited receptor tyrosine kinase (RTK) and mTOR signaling.	Buformin	15-23	ret proto-oncogene	Homo sapiens	120-144
27511638-1	2017	An inorganic NaMgSO4 F fluoride material was prepared by the wet chemical method and studied for its photoluminescence (PL) and resonant-non-resonant energy transfer (RET and NORET) capabilities between Ce3+    Tb3+ , Ce3+    Eu3+ and Ce3+    Dy3+ rare earth ions.	namgso4 f fluoride	13-31	ret proto-oncogene	Homo sapiens	167-170
27511638-4	2017	The purpose of the present study is to understand the RET and NORET effects of Tb3+ , Eu3+ and Dy3+ co-doping in a NaMgSO4 F:Ce3+ luminescent material, which could be used as a green-emitting material for lamp phosphors.	namgso4	115-122	ret proto-oncogene	Homo sapiens	54-57
28209747-7	2017	Two of these MTC patients with novel alterations in RET experienced clinical benefit from vandetanib treatment.	vandetanib	90-100	ret proto-oncogene	Homo sapiens	52-55
28181547-2	2017	It is well known that RET mutations affecting the cysteine-rich region of the protein (MEN2A-like mutations) are correlated with different phenotypes than those in the kinase domain (MEN2B-like mutations).	Cysteine	50-58	ret proto-oncogene	Homo sapiens	22-25
28193239-9	2017	In particular, buformin suppressed stem cell populations and self-renewal in vitro, which was associated with inhibited receptor tyrosine kinase (RTK) and mTOR signaling.	Buformin	15-23	ret proto-oncogene	Homo sapiens	146-149
28193239-12	2017	We further demonstrated that buformin-mediated in vivo inhibition of MEC stemness is associated with suppressed activation of mTOR, RTK, ER, and beta-catenin signaling pathways.	Buformin	29-37	ret proto-oncogene	Homo sapiens	132-135
28450652-1	2017	AIM: to evaluate the correlation and the concordance between reticulocyte hemoglobin equivalent (RET-He) and reticulocyte hemoglobin content (CHr) as well as to obtain the cut-off value of RET-He as the target of iron supplementation in chronic kidney disease (CKD) patients undergoing hemodialysis.	Iron	213-217	ret proto-oncogene	Homo sapiens	189-192
27933682-1	2017	The intermolecular electrochemiluminescence resonance energy transfer (ECL-RET) between luminol and Ru(bpy)32+ was studied extensively to achieve the sensitive bioanalysis owing to the perfect spectral overlap of the donor and acceptor, but it still suffers from the challenging issue of low energy-transfer efficiency.	Luminol	88-95	ret proto-oncogene	Homo sapiens	75-78
27933682-1	2017	The intermolecular electrochemiluminescence resonance energy transfer (ECL-RET) between luminol and Ru(bpy)32+ was studied extensively to achieve the sensitive bioanalysis owing to the perfect spectral overlap of the donor and acceptor, but it still suffers from the challenging issue of low energy-transfer efficiency.	ru(bpy)32+	100-110	ret proto-oncogene	Homo sapiens	75-78
27933682-2	2017	The intramolecular ECL-RET towards the novel ECL compound containing the donor of luminol and the acceptor of Ru(bpy)2 (mcpbpy)2+ (Lum-Ru) was designed and investigated.	Luminol	82-89	ret proto-oncogene	Homo sapiens	23-26
28145866-4	2017	Treatment with inhibitors targeting the RTK/MAPK pathway increased reactive oxygen species (ROS) in cells with intact KEAP1, and loss of KEAP1 abrogated this increase.	Reactive Oxygen Species	67-90	ret proto-oncogene	Homo sapiens	40-43
28145866-4	2017	Treatment with inhibitors targeting the RTK/MAPK pathway increased reactive oxygen species (ROS) in cells with intact KEAP1, and loss of KEAP1 abrogated this increase.	Reactive Oxygen Species	92-95	ret proto-oncogene	Homo sapiens	40-43
27933682-3	2017	With the high-efficient ECL-RET in one molecule, the highly intense ECL signal of Lum-Ru was obtained owing to the short path of energy transmission and less energy loss between luminol and Ru(bpy)2 (mcpbpy)2+ .	Luminol	178-185	ret proto-oncogene	Homo sapiens	28-31
27966990-0	2017	Site-Specific N-Glycosylation of Endothelial Cell Receptor Tyrosine Kinase VEGFR-2.	Nitrogen	14-15	ret proto-oncogene	Homo sapiens	50-74
27966990-3	2017	N-glycosylation plays a central role in RTK ligand binding, trafficking, and stability.	Nitrogen	0-1	ret proto-oncogene	Homo sapiens	40-43
27803005-0	2017	Vandetanib in pretreated patients with advanced non-small cell lung cancer-harboring RET rearrangement: a phase II clinical trial.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	85-88
27803005-15	2017	Conclusion: Vandetanib is moderately active in pretreated patients with advanced NSCLC-harboring RET rearrangements.	vandetanib	12-22	ret proto-oncogene	Homo sapiens	97-100
28145234-0	2017	Two recent phase 2 trials of vandetanib in RET-rearranged NSCLC.	vandetanib	29-39	ret proto-oncogene	Homo sapiens	43-46
27814560-0	2017	Identification of a novel 5-amino-3-(5-cyclopropylisoxazol-3-yl)-1-isopropyl-1H-pyrazole-4-carboxamide as a specific RET kinase inhibitor.	5-amino-3-(5-cyclopropylisoxazol-3-yl)-1-isopropyl-1h-pyrazole-4-carboxamide	26-102	ret proto-oncogene	Homo sapiens	117-120
27814560-4	2017	In a recent effort we identified a novel and specific RET inhibitor of 5-aminopyrazole-4-carboxamide scaffold, which was designed to enhance the metabolic stability of the pyrazolopyrimidine scaffold.	3-Amino-1H-pyrazole-4-carboxamide	71-100	ret proto-oncogene	Homo sapiens	54-57
27814560-4	2017	In a recent effort we identified a novel and specific RET inhibitor of 5-aminopyrazole-4-carboxamide scaffold, which was designed to enhance the metabolic stability of the pyrazolopyrimidine scaffold.	1H-pyrazolo[4,3-d]pyrimidine	172-190	ret proto-oncogene	Homo sapiens	54-57
27922668-3	2017	We developed in vitro a resistance model to pan-VEGFR inhibition and explored the simultaneous inhibition of VEGFR and MET in neuroblastoma models in vitro and in vivo using cabozantinib, an inhibitor of the tyrosine kinases including VEGFR2, MET, AXL and RET.	cabozantinib	174-186	ret proto-oncogene	Homo sapiens	256-259
29237911-4	2017	SETTINGS AND DESIGN: This study was conducted to determine whether RET dysfunction involves an induced mutation into SK-N-MC cells.	sk-n-mc	117-124	ret proto-oncogene	Homo sapiens	67-70
29237911-6	2017	SK-N-MC cells with different RET plasmids treated/untreated by GDNF, AKT and ERK1/2 phosphorylation detected by specific antibodies.	sk-n-mc	0-7	ret proto-oncogene	Homo sapiens	29-32
29237911-8	2017	CONCLUSION: RET dysfunction involves an induced mutation into SK-N-MC cells.	sk-n-mc	62-69	ret proto-oncogene	Homo sapiens	12-15
28955006-0	2017	Phase I/II study of alectinib in lung cancer with RET fusion gene: study protocol.	alectinib	20-29	ret proto-oncogene	Homo sapiens	50-53
28955006-2	2017	Alectinib is an approved anaplastic lymphoma kinase (ALK) inhibitor that may also be effective for RET fusion-positive NSCLC.	alectinib	0-9	ret proto-oncogene	Homo sapiens	99-102
28955006-8	2017	CONCLUSION: This is the first study to investigate the safety and preliminary efficacy of alectinib in RET fusion-positive NSCLC patients.	alectinib	90-99	ret proto-oncogene	Homo sapiens	103-106
28955006-9	2017	If successful, alectinib treatment may lead to substantial and important changes in the management of NSCLC with RET fusion genes.	alectinib	15-24	ret proto-oncogene	Homo sapiens	113-116
28092043-2	2017	Their ability to distinguish binding to over thousands of potential phosphotyrosine (pTyr) ligands within the cell is critical for the fidelity of receptor tyrosine kinase (RTK) signaling.	Phosphotyrosine	68-83	ret proto-oncogene	Homo sapiens	147-171
27825616-0	2017	Vandetanib in patients with previously treated RET-rearranged advanced non-small-cell lung cancer (LURET): an open-label, multicentre phase 2 trial.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	47-50
27825616-2	2017	Vandetanib is a multitargeted tyrosine kinase inhibitor exhibiting RET kinase activity.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	67-70
27825616-3	2017	We aimed to assess the efficacy and safety of vandetanib in patients with advanced RET-rearranged NSCLC.	vandetanib	46-56	ret proto-oncogene	Homo sapiens	83-86
27825616-13	2017	INTERPRETATION: Vandetanib showed clinical antitumour activity and a manageable safety profile in patients with advanced RET-rearranged NSCLC.	vandetanib	16-26	ret proto-oncogene	Homo sapiens	6-9
28092043-2	2017	Their ability to distinguish binding to over thousands of potential phosphotyrosine (pTyr) ligands within the cell is critical for the fidelity of receptor tyrosine kinase (RTK) signaling.	Phosphotyrosine	68-83	ret proto-oncogene	Homo sapiens	173-176
28092043-2	2017	Their ability to distinguish binding to over thousands of potential phosphotyrosine (pTyr) ligands within the cell is critical for the fidelity of receptor tyrosine kinase (RTK) signaling.	Phosphotyrosine	85-89	ret proto-oncogene	Homo sapiens	147-171
28092043-2	2017	Their ability to distinguish binding to over thousands of potential phosphotyrosine (pTyr) ligands within the cell is critical for the fidelity of receptor tyrosine kinase (RTK) signaling.	Phosphotyrosine	85-89	ret proto-oncogene	Homo sapiens	173-176
27807062-0	2016	In vitro transforming potential, intracellular signaling properties and sensitivity to a kinase inhibitor (sorafenib) of RET proto-oncogene variants Glu511Lys, Ser649Leu and Arg886Trp.	Sorafenib	107-116	ret proto-oncogene	Homo sapiens	121-124
27873490-8	2017	Reversible EGFR-TKI (gefitinib) resensitized cancer cells to RET inhibitors, even in the presence of EGF.	Gefitinib	21-30	ret proto-oncogene	Homo sapiens	61-64
27525386-8	2016	Cabozantinib appeared to prolong PFS versus the placebo in the RET mutation-positive subgroup (hazard ratio [HR], 0.23; 95% confidence interval [CI], 0.14-0.38; P &lt; .0001), the RET mutation-unknown subgroup (HR, 0.30; 95% CI, 0.16-0.57; P = .0001), and the RAS mutation-positive subgroup (HR, 0.15; 95% CI, 0.02-1.10; P = .0317).	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	180-183
27525386-9	2016	The RET M918T subgroup achieved the greatest observed PFS benefit from cabozantinib versus the placebo (HR, 0.15; 95% CI, 0.08-0.28; P &lt; .0001).	cabozantinib	71-83	ret proto-oncogene	Homo sapiens	4-7
27525386-13	2016	CONCLUSIONS: These data suggest that cabozantinib provides the greatest clinical benefit to patients with MTC who have RET M918T or RAS mutations.	cabozantinib	37-49	ret proto-oncogene	Homo sapiens	119-122
28704831-2	2017	Due to the short life span of reticulocytes, Ret-He reflects current iron availability for erythropoiesis more accurately than other common erythrocyte indices.	Iron	69-73	ret proto-oncogene	Homo sapiens	45-48
28042325-3	2017	In normal physiological conditions, the fluorescence and ROS generation ability of Ce6 are quenched by GNPs via RET; but in cancerous cells, the fluorescence and the ROS generation of Ce6 could be recovered by cleavage of Au-S bond through high level of intracellular GSH for real-time imaging and in demand PDT.	ros	57-60	ret proto-oncogene	Homo sapiens	112-115
28042325-3	2017	In normal physiological conditions, the fluorescence and ROS generation ability of Ce6 are quenched by GNPs via RET; but in cancerous cells, the fluorescence and the ROS generation of Ce6 could be recovered by cleavage of Au-S bond through high level of intracellular GSH for real-time imaging and in demand PDT.	ce6	83-86	ret proto-oncogene	Homo sapiens	112-115
28042325-3	2017	In normal physiological conditions, the fluorescence and ROS generation ability of Ce6 are quenched by GNPs via RET; but in cancerous cells, the fluorescence and the ROS generation of Ce6 could be recovered by cleavage of Au-S bond through high level of intracellular GSH for real-time imaging and in demand PDT.	ce6	184-187	ret proto-oncogene	Homo sapiens	112-115
27525386-0	2016	Correlative analyses of RET and RAS mutations in a phase 3 trial of cabozantinib in patients with progressive, metastatic medullary thyroid cancer.	cabozantinib	68-80	ret proto-oncogene	Homo sapiens	24-27
27525386-8	2016	Cabozantinib appeared to prolong PFS versus the placebo in the RET mutation-positive subgroup (hazard ratio [HR], 0.23; 95% confidence interval [CI], 0.14-0.38; P &lt; .0001), the RET mutation-unknown subgroup (HR, 0.30; 95% CI, 0.16-0.57; P = .0001), and the RAS mutation-positive subgroup (HR, 0.15; 95% CI, 0.02-1.10; P = .0317).	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	63-66
27817859-6	2016	Lenvatinib (Lenvima ) is a tyrosine kinase inhibitor (TKI) targeting the VEGFR1-3, FGFR 1-4, PDGFR-alpha, RET and c-kit.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	106-109
27539727-4	2016	Because activating RET mutations occur in over 90 % of hereditary and 40 % of sporadic MTC, clinical trials of several RET-targeting multikinase inhibitors (MKIs) have resulted in FDA approval of vandetanib and cabozantinib for the treatment of MTC.	vandetanib	196-206	ret proto-oncogene	Homo sapiens	19-22
27539727-4	2016	Because activating RET mutations occur in over 90 % of hereditary and 40 % of sporadic MTC, clinical trials of several RET-targeting multikinase inhibitors (MKIs) have resulted in FDA approval of vandetanib and cabozantinib for the treatment of MTC.	vandetanib	196-206	ret proto-oncogene	Homo sapiens	119-122
27539727-4	2016	Because activating RET mutations occur in over 90 % of hereditary and 40 % of sporadic MTC, clinical trials of several RET-targeting multikinase inhibitors (MKIs) have resulted in FDA approval of vandetanib and cabozantinib for the treatment of MTC.	cabozantinib	211-223	ret proto-oncogene	Homo sapiens	19-22
27539727-4	2016	Because activating RET mutations occur in over 90 % of hereditary and 40 % of sporadic MTC, clinical trials of several RET-targeting multikinase inhibitors (MKIs) have resulted in FDA approval of vandetanib and cabozantinib for the treatment of MTC.	cabozantinib	211-223	ret proto-oncogene	Homo sapiens	119-122
27825636-0	2016	Cabozantinib in patients with advanced RET-rearranged non-small-cell lung cancer: an open-label, single-centre, phase 2, single-arm trial.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	39-42
27825636-2	2016	Cabozantinib is a multikinase inhibitor with activity against RET that produced a 10% overall response in unselected patients with lung cancers.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	62-65
27825636-3	2016	To assess the activity of cabozantinib in patients with RET-rearranged lung cancers, we did a prospective phase 2 trial in this molecular subgroup.	cabozantinib	26-38	ret proto-oncogene	Homo sapiens	56-59
27825636-16	2016	INTERPRETATION: The reported activity of cabozantinib in patients with RET-rearranged lung cancers defines RET rearrangements as actionable drivers in patients with lung cancers.	cabozantinib	41-53	ret proto-oncogene	Homo sapiens	6-9
27825636-16	2016	INTERPRETATION: The reported activity of cabozantinib in patients with RET-rearranged lung cancers defines RET rearrangements as actionable drivers in patients with lung cancers.	cabozantinib	41-53	ret proto-oncogene	Homo sapiens	71-74
27825638-2	2016	Cabozantinib, a small molecule tyrosine kinase inhibitor, targets MET, VEGFR, RET, ROS1, and AXL, which are implicated in lung cancer tumorigenesis.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	78-81
27802516-0	2016	Administration of Menadione, Vitamin K3, Ameliorates Off-Target Effects on Corneal Epithelial Wound Healing Due to Receptor Tyrosine Kinase Inhibition.	Vitamin K 3	18-27	ret proto-oncogene	Homo sapiens	115-139
27802516-0	2016	Administration of Menadione, Vitamin K3, Ameliorates Off-Target Effects on Corneal Epithelial Wound Healing Due to Receptor Tyrosine Kinase Inhibition.	Vitamin K 3	29-39	ret proto-oncogene	Homo sapiens	115-139
27794403-18	2016	RET-rearranged patients may benefit more from pemetrexed-based regimen.	Pemetrexed	46-56	ret proto-oncogene	Homo sapiens	0-3
27805332-10	2016	RET-He was the only significant predictor of bone marrow iron stores (at P &lt; 0.05).	Iron	57-61	ret proto-oncogene	Homo sapiens	0-3
27805332-13	2016	CONCLUSIONS: RET-He correlated significantly with serum ferritin and is also a better predictor of bone marrow iron stores than the latter.	Iron	111-115	ret proto-oncogene	Homo sapiens	13-16
27805332-1	2016	AIM: To evaluate reticulocyte hemoglobin (RET-He) vis-a-vis serum ferritin as a marker of bone marrow iron store in iron deficiency anemia (IDA).	Iron	102-106	ret proto-oncogene	Homo sapiens	42-45
27544060-0	2016	Clinical Activity of Alectinib in Advanced RET-Rearranged Non-Small Cell Lung Cancer.	alectinib	21-30	ret proto-oncogene	Homo sapiens	43-46
27544060-2	2016	Alectinib is an anaplastic lymphoma kinase tyrosine kinase inhibitor (TKI) that also has anti-RET activity in vitro.	alectinib	0-9	ret proto-oncogene	Homo sapiens	94-97
27544060-3	2016	The clinical activity of alectinib in patients with RET-rearranged NSCLC has not yet been reported.	alectinib	25-34	ret proto-oncogene	Homo sapiens	52-55
27544060-4	2016	METHODS: We have described four patients with advanced RET-rearranged NSCLC who were treated with alectinib (600 mg twice daily [n = 3] or 900 mg twice daily [n = 1]) as part of single-patient compassionate use protocols or off-label use of the commercially available drug.	alectinib	98-107	ret proto-oncogene	Homo sapiens	55-58
27544060-10	2016	A fourth patient who was RET TKI-naive had primary progression while receiving alectinib.	alectinib	79-88	ret proto-oncogene	Homo sapiens	25-28
27544060-11	2016	CONCLUSIONS: Alectinib demonstrated preliminary antitumor activity in patients with advanced RET-rearranged NSCLC, most of whom had received prior RET inhibitors.	alectinib	13-22	ret proto-oncogene	Homo sapiens	93-96
27544060-11	2016	CONCLUSIONS: Alectinib demonstrated preliminary antitumor activity in patients with advanced RET-rearranged NSCLC, most of whom had received prior RET inhibitors.	alectinib	13-22	ret proto-oncogene	Homo sapiens	147-150
27544060-12	2016	Larger prospective studies with longer follow-up are needed to assess the efficacy of alectinib in RET-rearranged NSCLC and other RET-driven malignancies.	alectinib	86-95	ret proto-oncogene	Homo sapiens	99-102
27760157-7	2016	The tyrosine kinase activity was measured with a human receptor tyrosine kinase (RTK) detection kit using a horseradish peroxidase (HRP)-conjugated phosphotyrosine (pY20) antibody as the substrate.	py20	165-169	ret proto-oncogene	Homo sapiens	81-84
27802347-0	2016	RET/PTC Rearrangements Are Associated with Elevated Postoperative TSH Levels and Multifocal Lesions in Papillary Thyroid Cancer without Concomitant Thyroid Benign Disease.	Thyrotropin	66-69	ret proto-oncogene	Homo sapiens	0-3
27802347-0	2016	RET/PTC Rearrangements Are Associated with Elevated Postoperative TSH Levels and Multifocal Lesions in Papillary Thyroid Cancer without Concomitant Thyroid Benign Disease.	Thyrotropin	66-69	ret proto-oncogene	Homo sapiens	4-7
27802347-10	2016	RET/PTC rearrangement was also correlated with higher TSH levels at one month post-surgery (P = 0.037).	Thyrotropin	54-57	ret proto-oncogene	Homo sapiens	0-3
27802347-10	2016	RET/PTC rearrangement was also correlated with higher TSH levels at one month post-surgery (P = 0.037).	Thyrotropin	54-57	ret proto-oncogene	Homo sapiens	4-7
27716285-1	2016	BACKGROUND: Anlotinib is a novel multi-target tyrosine kinase inhibitor that is designed to primarily inhibit VEGFR2/3, FGFR1-4, PDGFR alpha/beta, c-Kit, and Ret.	anlotinib	12-21	ret proto-oncogene	Homo sapiens	158-161
27299777-5	2016	Their performance was corroborated with two innovative proofs-of-concept that centered on the luminol transduction chemistry: a first time reported ECL assay based on the enzymatic reaction between an indoxyl substrate and the enzyme alkaline phosphatase, and the electrochemiluminescence resonance energy transfer (ECL-RET) process triggered by the electro-oxidized luminol to the acceptor fluorescein.	Luminol	94-101	ret proto-oncogene	Homo sapiens	320-323
27717313-3	2016	Gene analysis in this patient disclosed a heterozygous p.S811F mutation was in Ret gene exon 14, resulting in a substitution of phenylalanine for serine.	Phenylalanine	128-141	ret proto-oncogene	Homo sapiens	79-82
27717313-3	2016	Gene analysis in this patient disclosed a heterozygous p.S811F mutation was in Ret gene exon 14, resulting in a substitution of phenylalanine for serine.	Serine	146-152	ret proto-oncogene	Homo sapiens	79-82
27717313-4	2016	The large side chain of phenylalanine obstructed the opening of the hydrophobic pocket of the Ret molecule causing interference with its interaction with adenosine triphosphate and consequent marked reduction in its enzyme activity.	Adenosine Triphosphate	154-176	ret proto-oncogene	Homo sapiens	94-97
27299777-5	2016	Their performance was corroborated with two innovative proofs-of-concept that centered on the luminol transduction chemistry: a first time reported ECL assay based on the enzymatic reaction between an indoxyl substrate and the enzyme alkaline phosphatase, and the electrochemiluminescence resonance energy transfer (ECL-RET) process triggered by the electro-oxidized luminol to the acceptor fluorescein.	indoxyl	201-208	ret proto-oncogene	Homo sapiens	320-323
27299777-8	2016	Graphical abstract Schematic representation of the ECL-RET: from luminol-H2O2 system to fluorescein, the micro-spectrometer for the light collection and the 3D representation of the ECL-RET reaction.	Luminol	65-72	ret proto-oncogene	Homo sapiens	55-58
27299777-8	2016	Graphical abstract Schematic representation of the ECL-RET: from luminol-H2O2 system to fluorescein, the micro-spectrometer for the light collection and the 3D representation of the ECL-RET reaction.	Hydrogen Peroxide	73-77	ret proto-oncogene	Homo sapiens	55-58
27299777-8	2016	Graphical abstract Schematic representation of the ECL-RET: from luminol-H2O2 system to fluorescein, the micro-spectrometer for the light collection and the 3D representation of the ECL-RET reaction.	Fluorescein	88-99	ret proto-oncogene	Homo sapiens	55-58
27339111-2	2016	Lenvatinib inhibits VEGFR1-3, FGFR1-4, PDGFRbeta, RET and KIT proto-oncogenes.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	50-53
27294358-4	2016	Also observed in this study, however, was increased N-sulphation detected by antibody 10E4 indicating that not only 6-O sulphation but also N-sulphation may contribute to increased RTK cell signalling in mammary tumours.	Nitrogen	52-53	ret proto-oncogene	Homo sapiens	181-184
27633255-0	2016	miR-449 overexpression inhibits papillary thyroid carcinoma cell growth by targeting RET kinase-beta-catenin signaling pathway.	mir-449	0-7	ret proto-oncogene	Homo sapiens	85-88
27574129-0	2016	Iodine regulates G2/M progression induced by CCL21/CCR7 interaction in primary cultures of papillary thyroid cancer cells with RET/PTC expression.	Iodine	0-6	ret proto-oncogene	Homo sapiens	127-130
27496134-5	2016	By culturing KIF5B-RET-dependent BaF3 (B/KR) cells with increasing concentrations of cabozantinib or vandetanib, we identified cabozantinib-resistant RETV804L mutation and vandetanib-resistant-RETG810A mutation.	vandetanib	101-111	ret proto-oncogene	Homo sapiens	19-22
27496134-5	2016	By culturing KIF5B-RET-dependent BaF3 (B/KR) cells with increasing concentrations of cabozantinib or vandetanib, we identified cabozantinib-resistant RETV804L mutation and vandetanib-resistant-RETG810A mutation.	cabozantinib	127-139	ret proto-oncogene	Homo sapiens	19-22
27496134-5	2016	By culturing KIF5B-RET-dependent BaF3 (B/KR) cells with increasing concentrations of cabozantinib or vandetanib, we identified cabozantinib-resistant RETV804L mutation and vandetanib-resistant-RETG810A mutation.	vandetanib	172-182	ret proto-oncogene	Homo sapiens	19-22
27496134-5	2016	By culturing KIF5B-RET-dependent BaF3 (B/KR) cells with increasing concentrations of cabozantinib or vandetanib, we identified cabozantinib-resistant RETV804L mutation and vandetanib-resistant-RETG810A mutation.	cabozantinib	85-97	ret proto-oncogene	Homo sapiens	19-22
27574129-2	2016	During rearranged during transfection (RET)/papillary thyroid carcinoma (PTC) 3 activation, excess iodine can act as a protective agent in thyroid follicular cells.	Iodine	99-105	ret proto-oncogene	Homo sapiens	39-42
27574129-11	2016	These results suggest that CCL21/CCR7 interaction contributes to G2/M progression of RET/PTC-expressing cells via the ERK pathway in association with 10-5 M NaI.	Sodium Iodide	157-160	ret proto-oncogene	Homo sapiens	85-88
27273837-8	2016	Somehow, this RET R114H mutation proved to have a role in the etiology of both CIPO and HSCR and could contribute to a more diffuse imbalance of gut dysmotility.	cipo	79-83	ret proto-oncogene	Homo sapiens	14-17
27494860-0	2016	Apatinib inhibits cellular invasion and migration by fusion kinase KIF5B-RET via suppressing RET/Src signaling pathway.	apatinib	0-8	ret proto-oncogene	Homo sapiens	73-76
27494860-0	2016	Apatinib inhibits cellular invasion and migration by fusion kinase KIF5B-RET via suppressing RET/Src signaling pathway.	apatinib	0-8	ret proto-oncogene	Homo sapiens	93-96
27494860-3	2016	We also investigate the anti-tumor activity of Apatinib, a potent inhibitor of VEGFR-2, PDGFR-beta, c-Src and RET, in RET-rearranged lung adenocarcinoma, together with the mechanisms underlying.	apatinib	47-55	ret proto-oncogene	Homo sapiens	110-113
27494860-5	2016	Apatinib exerted its anti-cancer effect not only via cytotoxicity, but also via inhibition of migration and invasion by suppressing RET/Src signaling pathway, supporting a potential role for Apatinib in the treatment of KIF5B-RET driven tumors.	apatinib	0-8	ret proto-oncogene	Homo sapiens	132-135
27494860-5	2016	Apatinib exerted its anti-cancer effect not only via cytotoxicity, but also via inhibition of migration and invasion by suppressing RET/Src signaling pathway, supporting a potential role for Apatinib in the treatment of KIF5B-RET driven tumors.	apatinib	0-8	ret proto-oncogene	Homo sapiens	226-229
27481946-1	2016	Downstream of receptor tyrosine kinase and G protein-coupled receptor (GPCR) stimulation, the phosphatidylinositol 3,4,5-trisphosphate (PIP3)-dependent Rac exchange factor (PREX) family of guanine nucleotide exchange factors (GEFs) activates Rho GTPases, leading to important roles for PREX proteins in numerous cellular processes and diseases, including cancer.	phosphatidylinositol 3,4,5-triphosphate	94-134	ret proto-oncogene	Homo sapiens	14-38
27481946-1	2016	Downstream of receptor tyrosine kinase and G protein-coupled receptor (GPCR) stimulation, the phosphatidylinositol 3,4,5-trisphosphate (PIP3)-dependent Rac exchange factor (PREX) family of guanine nucleotide exchange factors (GEFs) activates Rho GTPases, leading to important roles for PREX proteins in numerous cellular processes and diseases, including cancer.	PIP3	136-140	ret proto-oncogene	Homo sapiens	14-38
27618325-8	2016	Currently, Food and Drug Administration-approved molecularly targeted therapies for metastatic RAI-refractory thyroid cancer, including sorafenib, lenvatinib, vandetanib, and cabozantinib, target the vascular endothelial growth factor receptor and RET kinases.	Sorafenib	136-145	ret proto-oncogene	Homo sapiens	248-251
27618325-8	2016	Currently, Food and Drug Administration-approved molecularly targeted therapies for metastatic RAI-refractory thyroid cancer, including sorafenib, lenvatinib, vandetanib, and cabozantinib, target the vascular endothelial growth factor receptor and RET kinases.	cabozantinib	175-187	ret proto-oncogene	Homo sapiens	248-251
27031188-2	2016	It was based on the ECL resonance energy transfer (ECL-RET) of CdTe/CdS coresmall/shellthick quantum dots (QDs) to gold nanorods (AuNRs).	cadmium telluride	63-67	ret proto-oncogene	Homo sapiens	55-58
27171212-2	2016	The diamagnetic complex shows a highly intense AIE induced by NEt3H(+), which disappears after picric acid recognition and subsequently RET will quench the emission intensity.	net3h	62-67	ret proto-oncogene	Homo sapiens	136-139
27171212-2	2016	The diamagnetic complex shows a highly intense AIE induced by NEt3H(+), which disappears after picric acid recognition and subsequently RET will quench the emission intensity.	picric acid	95-106	ret proto-oncogene	Homo sapiens	136-139
27031188-2	2016	It was based on the ECL resonance energy transfer (ECL-RET) of CdTe/CdS coresmall/shellthick quantum dots (QDs) to gold nanorods (AuNRs).	Cadmium	68-71	ret proto-oncogene	Homo sapiens	55-58
27131066-0	2016	An orally available tyrosine kinase ALK and RET dual inhibitor bearing the tetracyclic benzo[b]carbazolone core.	carbazolone	95-106	ret proto-oncogene	Homo sapiens	44-47
27351133-0	2016	Targeting of RET oncogene by naphthalene diimide-mediated gene promoter G-quadruplex stabilization exerts anti-tumor activity in oncogene-addicted human medullary thyroid cancer.	naphthalenediimide	29-48	ret proto-oncogene	Homo sapiens	13-16
27351133-4	2016	Here, we report that exposure of MTC cells to a tri-substituted naphthalene diimide (NDI) resulted in a significant antiproliferative activity paralleled by inhibition of RET expression.	tri-substituted naphthalene diimide	48-83	ret proto-oncogene	Homo sapiens	171-174
27351133-4	2016	Here, we report that exposure of MTC cells to a tri-substituted naphthalene diimide (NDI) resulted in a significant antiproliferative activity paralleled by inhibition of RET expression.	naphthalenediimide	85-88	ret proto-oncogene	Homo sapiens	171-174
27460868-4	2016	Besides, due to the ECL resonance energy transfer (ECL-RET) strategy between the large amount of Au nanorods (Au NRs) on the ternary composite surface and the CdS:Eu QDs, the ECL intensity of QDs was further quenched.	Gold	97-99	ret proto-oncogene	Homo sapiens	55-58
27259358-8	2016	Finally, RTK-enriched cell lines from both series exhibited enhanced sensitivity to the small molecule EGFR inhibitor erlotinib, indicating that their phosphosignature may provide a predictive biomarker for response to this targeted therapy.	Erlotinib Hydrochloride	118-127	ret proto-oncogene	Homo sapiens	9-12
27226544-7	2016	RET(DeltaE345), in contrast, displays higher baseline autophosphorylation, specifically on the catalytic tyrosine, Tyr(905), and also on one of the most important signaling residues, Tyr(1062) These data provide the first evidence for a physiologic role of these isoforms in RET pathway function.	Tyrosine	105-113	ret proto-oncogene	Homo sapiens	0-3
27226544-7	2016	RET(DeltaE345), in contrast, displays higher baseline autophosphorylation, specifically on the catalytic tyrosine, Tyr(905), and also on one of the most important signaling residues, Tyr(1062) These data provide the first evidence for a physiologic role of these isoforms in RET pathway function.	Tyrosine	115-118	ret proto-oncogene	Homo sapiens	0-3
27226544-7	2016	RET(DeltaE345), in contrast, displays higher baseline autophosphorylation, specifically on the catalytic tyrosine, Tyr(905), and also on one of the most important signaling residues, Tyr(1062) These data provide the first evidence for a physiologic role of these isoforms in RET pathway function.	Tyrosine	183-186	ret proto-oncogene	Homo sapiens	0-3
27398740-3	2016	Lenvatinib is an oral potent multi kinase inhibitor [MKI] of different growth factor receptors including VEGFR1/Flt-1, VEGFR2/KDR, VEGFR3, FGFR1,2,3,4, PDGFR-beta as well as RET and KIT signaling networks.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	174-177
27460868-4	2016	Besides, due to the ECL resonance energy transfer (ECL-RET) strategy between the large amount of Au nanorods (Au NRs) on the ternary composite surface and the CdS:Eu QDs, the ECL intensity of QDs was further quenched.	Gold	110-112	ret proto-oncogene	Homo sapiens	55-58
27460868-4	2016	Besides, due to the ECL resonance energy transfer (ECL-RET) strategy between the large amount of Au nanorods (Au NRs) on the ternary composite surface and the CdS:Eu QDs, the ECL intensity of QDs was further quenched.	Cadmium	159-162	ret proto-oncogene	Homo sapiens	55-58
27387652-0	2016	Linifanib (ABT-869) Potentiates the Efficacy of Chemotherapeutic Agents through the Suppression of Receptor Tyrosine Kinase-Mediated AKT/mTOR Signaling Pathways in Gastric Cancer.	N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N1-(2-fluoro-5-methylphenyl)urea	0-9	ret proto-oncogene	Homo sapiens	99-123
27090738-7	2016	The inhibition of RET signaling significantly increased the sensitivity of HNSCC cells to the EGFR inhibitor erlotinib in both in vitro and in vivo models.	Erlotinib Hydrochloride	109-118	ret proto-oncogene	Homo sapiens	18-21
27387652-0	2016	Linifanib (ABT-869) Potentiates the Efficacy of Chemotherapeutic Agents through the Suppression of Receptor Tyrosine Kinase-Mediated AKT/mTOR Signaling Pathways in Gastric Cancer.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	11-14	ret proto-oncogene	Homo sapiens	99-123
27387652-2	2016	Here, we demonstrate that linifanib (ABT-869), a novel multi-targeted receptor tyrosine kinase inhibitor, markedly augments cytotoxicity of chemotherapies in human gastric cancer.	N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N1-(2-fluoro-5-methylphenyl)urea	26-35	ret proto-oncogene	Homo sapiens	70-94
27387652-2	2016	Here, we demonstrate that linifanib (ABT-869), a novel multi-targeted receptor tyrosine kinase inhibitor, markedly augments cytotoxicity of chemotherapies in human gastric cancer.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	37-40	ret proto-oncogene	Homo sapiens	70-94
27056998-0	2016	Clinical outcomes with pemetrexed-based systemic therapies in RET-rearranged lung cancers.	Pemetrexed	23-33	ret proto-oncogene	Homo sapiens	62-65
27056998-2	2016	While previous series have shown durable clinical benefit with pemetrexed-based therapies in ALK- and ROS1-rearranged lung cancers, the benefits of pemetrexed-based treatments in patients with RET-rearranged lung cancers relative to other genomic subsets have not previously been explored.	Pemetrexed	148-158	ret proto-oncogene	Homo sapiens	193-196
27056998-9	2016	CONCLUSION: Durable benefits with pemetrexed-based therapies in RET-rearranged lung cancers are comparable with ALK- and ROS1-rearranged lung cancers.	Pemetrexed	34-44	ret proto-oncogene	Homo sapiens	64-67
27056998-10	2016	When selecting therapies for patients with RET-rearranged lung cancers, pemetrexed-containing regimens should be considered.	Pemetrexed	72-82	ret proto-oncogene	Homo sapiens	43-46
25366691-0	2016	Effect of the RET Inhibitor Vandetanib in a Patient With RET Fusion-Positive Metastatic Non-Small-Cell Lung Cancer.	vandetanib	28-38	ret proto-oncogene	Homo sapiens	14-17
27150058-6	2016	These results demonstrated that KIAA1217-RET fusion represents a novel oncogenic driver gene, the products of which are sensitive to vandetanib treatment, and suggested that the KIAA1217-RET-fusion gene is a promising target for lung cancer treatment.	vandetanib	133-143	ret proto-oncogene	Homo sapiens	41-44
27150058-6	2016	These results demonstrated that KIAA1217-RET fusion represents a novel oncogenic driver gene, the products of which are sensitive to vandetanib treatment, and suggested that the KIAA1217-RET-fusion gene is a promising target for lung cancer treatment.	vandetanib	133-143	ret proto-oncogene	Homo sapiens	187-190
27429741-4	2016	Vandetanib and cabozantinib, both multi-kinase inhibitors with RET activity, are approved for use in medullary thyroid carcinoma, but additional pharmacological activities, most notably inhibition of vascular endothelial growth factor - VEGFR2 (KDR), lead to dose-limiting toxicity.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	63-66
27429741-4	2016	Vandetanib and cabozantinib, both multi-kinase inhibitors with RET activity, are approved for use in medullary thyroid carcinoma, but additional pharmacological activities, most notably inhibition of vascular endothelial growth factor - VEGFR2 (KDR), lead to dose-limiting toxicity.	cabozantinib	15-27	ret proto-oncogene	Homo sapiens	63-66
27429741-6	2016	In an earlier publication [Newton et al, 2016; 1] we reported the discovery of a series of 2-substituted phenol quinazolines as potent and selective RET kinase inhibitors.	2-substituted phenol quinazolines	91-124	ret proto-oncogene	Homo sapiens	149-152
25366691-0	2016	Effect of the RET Inhibitor Vandetanib in a Patient With RET Fusion-Positive Metastatic Non-Small-Cell Lung Cancer.	vandetanib	28-38	ret proto-oncogene	Homo sapiens	57-60
27034161-3	2016	More recently, RET over-expression has emerged as a new player in ER-positive (ER+) BC, and as a potential target to enhance sensitivity and avoid resistance to tamoxifen therapy.Therefore, targeting the RET pathway may lead to new therapies in ER+ BC.	Tamoxifen	161-170	ret proto-oncogene	Homo sapiens	15-18
27101322-4	2016	When gold nanoparticles/graphene oxide (AuNPs/GO) nanocomposites were modified on the aptamer through the S-Au bond to form a sandwich-like structure, the ECL resonance energy transfer (ECL-RET) could occur between Ru(bpy)3(2+) and AuNPs/GO nanocomposites, resulting in an apparent decrease of ECL signal.	graphene oxide	24-38	ret proto-oncogene	Homo sapiens	190-193
27101322-4	2016	When gold nanoparticles/graphene oxide (AuNPs/GO) nanocomposites were modified on the aptamer through the S-Au bond to form a sandwich-like structure, the ECL resonance energy transfer (ECL-RET) could occur between Ru(bpy)3(2+) and AuNPs/GO nanocomposites, resulting in an apparent decrease of ECL signal.	aunps	40-45	ret proto-oncogene	Homo sapiens	190-193
27101322-4	2016	When gold nanoparticles/graphene oxide (AuNPs/GO) nanocomposites were modified on the aptamer through the S-Au bond to form a sandwich-like structure, the ECL resonance energy transfer (ECL-RET) could occur between Ru(bpy)3(2+) and AuNPs/GO nanocomposites, resulting in an apparent decrease of ECL signal.	Gold	40-42	ret proto-oncogene	Homo sapiens	190-193
27101322-4	2016	When gold nanoparticles/graphene oxide (AuNPs/GO) nanocomposites were modified on the aptamer through the S-Au bond to form a sandwich-like structure, the ECL resonance energy transfer (ECL-RET) could occur between Ru(bpy)3(2+) and AuNPs/GO nanocomposites, resulting in an apparent decrease of ECL signal.	ru(bpy)3	215-223	ret proto-oncogene	Homo sapiens	190-193
27101322-4	2016	When gold nanoparticles/graphene oxide (AuNPs/GO) nanocomposites were modified on the aptamer through the S-Au bond to form a sandwich-like structure, the ECL resonance energy transfer (ECL-RET) could occur between Ru(bpy)3(2+) and AuNPs/GO nanocomposites, resulting in an apparent decrease of ECL signal.	aunps	232-237	ret proto-oncogene	Homo sapiens	190-193
27034161-3	2016	More recently, RET over-expression has emerged as a new player in ER-positive (ER+) BC, and as a potential target to enhance sensitivity and avoid resistance to tamoxifen therapy.Therefore, targeting the RET pathway may lead to new therapies in ER+ BC.	Tamoxifen	161-170	ret proto-oncogene	Homo sapiens	204-207
26780347-6	2016	Moreover, we have reported that three kinds of oxidative stress, ultraviolet light-induced stress, osmotic stress and arsenic-induced stress, modulate kinase activity of RET-PTC1 without an extracellular domain as well as c-RET by conformational change of RET protein (dimerization) via disulfide bond formation.	Arsenic	118-125	ret proto-oncogene	Homo sapiens	170-173
26419617-1	2016	Regorafenib, an oral small-molecule multi kinase inhibitor, is able to block Vascular Endothelial Growth Factor Receptors (VEGFR-1, 2, and 3), Platelet-Derived Growth Factor Receptors (PDGF), Fibroblast Growth Factor (FGF) receptor 1, Raf, TIE-2, and the kinases KIT, RET, and BRAF.	regorafenib	0-11	ret proto-oncogene	Homo sapiens	268-271
26667237-3	2016	Reticulocyte hemoglobin equivalent (Ret-He) may be useful for assessing iron status.	Iron	72-76	ret proto-oncogene	Homo sapiens	0-3
26667237-8	2016	CONCLUSIONS: Ret-He is a more relevant marker of iron status than ferritin and TSAT.	Iron	49-53	ret proto-oncogene	Homo sapiens	13-16
26865419-4	2016	A novel oral multikinase inhibitor regorafenib inhibits receptor tyrosine kinases expressed on stromal cells (vascular endothelial growth factor receptor 1-3, TIE2, PDGFR-beta, and fibroblast growth factors) and tumor cells (c-KIT, RET, and BRAF).	regorafenib	35-46	ret proto-oncogene	Homo sapiens	232-235
26945007-8	2016	In vivo, immunostaining of CCH and MTC using an anti-RET antibody demonstrated increased RET expression.	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	27-30	ret proto-oncogene	Homo sapiens	53-56
26945007-8	2016	In vivo, immunostaining of CCH and MTC using an anti-RET antibody demonstrated increased RET expression.	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	27-30	ret proto-oncogene	Homo sapiens	89-92
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
26874741-0	2016	The discovery of 2-substituted phenol quinazolines as potent RET kinase inhibitors with improved KDR selectivity.	2-substituted phenol quinazolines	17-50	ret proto-oncogene	Homo sapiens	61-64
26874741-4	2016	Herein we report our efforts towards identifying a potent and selective RET inhibitor using vandetanib 1 as the starting point for structure-based drug design.	vandetanib 1	92-104	ret proto-oncogene	Homo sapiens	72-75
26780347-6	2016	Moreover, we have reported that three kinds of oxidative stress, ultraviolet light-induced stress, osmotic stress and arsenic-induced stress, modulate kinase activity of RET-PTC1 without an extracellular domain as well as c-RET by conformational change of RET protein (dimerization) via disulfide bond formation.	Arsenic	118-125	ret proto-oncogene	Homo sapiens	224-227
26780347-6	2016	Moreover, we have reported that three kinds of oxidative stress, ultraviolet light-induced stress, osmotic stress and arsenic-induced stress, modulate kinase activity of RET-PTC1 without an extracellular domain as well as c-RET by conformational change of RET protein (dimerization) via disulfide bond formation.	Arsenic	118-125	ret proto-oncogene	Homo sapiens	224-227
26780347-6	2016	Moreover, we have reported that three kinds of oxidative stress, ultraviolet light-induced stress, osmotic stress and arsenic-induced stress, modulate kinase activity of RET-PTC1 without an extracellular domain as well as c-RET by conformational change of RET protein (dimerization) via disulfide bond formation.	Disulfides	287-296	ret proto-oncogene	Homo sapiens	170-173
26780347-7	2016	The oxidative stresses also modulate kinase activity of RET-PTC1 with cysteine 365 (C365) replaced by alanine with promotion of dimer formation, but not with cysteine 376 (C376) replaced by alanine.	Cysteine	70-78	ret proto-oncogene	Homo sapiens	56-59
26874741-5	2016	Phenolic anilinoquinazolines exemplified by 6 showed improved affinities towards RET but, unsurprisingly, suffered from high metabolic clearance.	anilinoquinazoline	9-28	ret proto-oncogene	Homo sapiens	81-84
26780347-7	2016	The oxidative stresses also modulate kinase activity of RET-PTC1 with cysteine 365 (C365) replaced by alanine with promotion of dimer formation, but not with cysteine 376 (C376) replaced by alanine.	Alanine	102-109	ret proto-oncogene	Homo sapiens	56-59
26780347-7	2016	The oxidative stresses also modulate kinase activity of RET-PTC1 with cysteine 365 (C365) replaced by alanine with promotion of dimer formation, but not with cysteine 376 (C376) replaced by alanine.	Alanine	190-197	ret proto-oncogene	Homo sapiens	56-59
26780347-8	2016	Since C376 of Ret-PTC-1 or its equivalent is most highly conserved and crucial for activity in PTKs, the cysteine could be one of major targets for oxidative stresses.	Cysteine	105-113	ret proto-oncogene	Homo sapiens	14-17
26715573-1	2016	BACKGROUND: Vandetanib is a multitargeted tyrosine kinase inhibitor that affects vascular endothelial growth factor receptor (VEGF), epidermal growth factor (EGF), and rearranged during transfection (RET) mediated receptors which are important for growth and invasion of biliary and pancreatic cancers.	vandetanib	12-22	ret proto-oncogene	Homo sapiens	200-203
26950000-0	2016	Defects in the calcium-binding region drastically affect the cadherin-like domains of RET tyrosine kinase.	Calcium	15-22	ret proto-oncogene	Homo sapiens	86-89
26950000-3	2016	In this article, the functionally significant mutations in the RET CLD1-4 calcium-binding site which lead to HSCR, and depletion of calcium ions in the RET CLD1-4 calcium binding site, were investigated by molecular dynamics simulations--to understand the mechanistic action of the mutations or loss of calcium ions in altering the protein kinase structure, dynamics, and stability.	Calcium	132-139	ret proto-oncogene	Homo sapiens	152-155
26973202-2	2016	Emerging clinical studies have demonstrated that patients with RET-rearranged NSCLC may also benefit from existing RET TKIs, including cabozantinib and vandetanib.	cabozantinib	135-147	ret proto-oncogene	Homo sapiens	63-66
26973202-2	2016	Emerging clinical studies have demonstrated that patients with RET-rearranged NSCLC may also benefit from existing RET TKIs, including cabozantinib and vandetanib.	cabozantinib	135-147	ret proto-oncogene	Homo sapiens	115-118
26973202-2	2016	Emerging clinical studies have demonstrated that patients with RET-rearranged NSCLC may also benefit from existing RET TKIs, including cabozantinib and vandetanib.	vandetanib	152-162	ret proto-oncogene	Homo sapiens	63-66
26950000-3	2016	In this article, the functionally significant mutations in the RET CLD1-4 calcium-binding site which lead to HSCR, and depletion of calcium ions in the RET CLD1-4 calcium binding site, were investigated by molecular dynamics simulations--to understand the mechanistic action of the mutations or loss of calcium ions in altering the protein kinase structure, dynamics, and stability.	Calcium	132-139	ret proto-oncogene	Homo sapiens	152-155
26950000-3	2016	In this article, the functionally significant mutations in the RET CLD1-4 calcium-binding site which lead to HSCR, and depletion of calcium ions in the RET CLD1-4 calcium binding site, were investigated by molecular dynamics simulations--to understand the mechanistic action of the mutations or loss of calcium ions in altering the protein kinase structure, dynamics, and stability.	Calcium	74-81	ret proto-oncogene	Homo sapiens	63-66
26950000-7	2016	Overall, the findings may provide useful structural insights into the molecular mechanism underlying RET calcium-binding site mutations and assist in development of novel drugs targeting the extracellular ligand contact site of wildtype RET.	Calcium	105-112	ret proto-oncogene	Homo sapiens	101-104
26950000-7	2016	Overall, the findings may provide useful structural insights into the molecular mechanism underlying RET calcium-binding site mutations and assist in development of novel drugs targeting the extracellular ligand contact site of wildtype RET.	Calcium	105-112	ret proto-oncogene	Homo sapiens	237-240
26950000-3	2016	In this article, the functionally significant mutations in the RET CLD1-4 calcium-binding site which lead to HSCR, and depletion of calcium ions in the RET CLD1-4 calcium binding site, were investigated by molecular dynamics simulations--to understand the mechanistic action of the mutations or loss of calcium ions in altering the protein kinase structure, dynamics, and stability.	Calcium	132-139	ret proto-oncogene	Homo sapiens	152-155
26853088-0	2016	Synthesis of a [(18)F]-labeled ceritinib analogue for positron emission tomography of anaplastic lymphoma kinase, a receptor tyrosine kinase, in lung cancer.	ceritinib	31-40	ret proto-oncogene	Homo sapiens	116-140
27042004-3	2016	Sorafenib targets C-RAF, B-RAF, VEGF receptor-1, -2, -3, PDGF receptor-beta, RET, c-kit, and Flt-3.	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	77-80
26833126-2	2016	Targeting HER2(+) tumors with trastuzumab or the receptor tyrosine kinase (RTK) inhibitor lapatinib significantly improves survival, yet tumor resistance and progression of metastatic disease still develop over time.	Lapatinib	90-99	ret proto-oncogene	Homo sapiens	49-73
26833126-2	2016	Targeting HER2(+) tumors with trastuzumab or the receptor tyrosine kinase (RTK) inhibitor lapatinib significantly improves survival, yet tumor resistance and progression of metastatic disease still develop over time.	Lapatinib	90-99	ret proto-oncogene	Homo sapiens	75-78
29899907-3	2016	Herein, by employing Thioflavin T (ThT) as a signal transducer, we integrated multiple components based on RET (a type of proto-oncogene) into a logic gate combinatorial library, including basic logic gates (NOR, INHIBIT, IMPLICATION), a single three-input NOR gate, and combinatorial gates (INHIBIT-OR, NOT-AND-NOR).	thioflavin T	21-33	ret proto-oncogene	Homo sapiens	107-110
29899907-3	2016	Herein, by employing Thioflavin T (ThT) as a signal transducer, we integrated multiple components based on RET (a type of proto-oncogene) into a logic gate combinatorial library, including basic logic gates (NOR, INHIBIT, IMPLICATION), a single three-input NOR gate, and combinatorial gates (INHIBIT-OR, NOT-AND-NOR).	thioflavin T	35-38	ret proto-oncogene	Homo sapiens	107-110
26471688-5	2016	The use of a single RET-PA (i.e. retrorsine) for construction of calibration was based on high similarities with no significant differences demonstrated by the calibration curves constructed by peak areas of extract ion chromatograms of fragment ion at m/z 120.0813 or 138.0919 versus concentrations of five representative RET-PAs.	retrorsine	33-43	ret proto-oncogene	Homo sapiens	20-23
26898613-0	2016	Sorafenib treatment for patients with RET fusion-positive non-small cell lung cancer.	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	38-41
26765577-7	2016	RESULTS: Exome sequencing revealed a 6-nucleotide/2-amino acid in-frame deletion in exon 7 of RET (c.1512_1517delGGAGGG, p.505_506del).	6-nucleotide	37-49	ret proto-oncogene	Homo sapiens	94-97
26898613-2	2016	Sorafenib, a multi-kinase inhibitor, has potent anti-RET activity.	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	53-56
26765577-7	2016	RESULTS: Exome sequencing revealed a 6-nucleotide/2-amino acid in-frame deletion in exon 7 of RET (c.1512_1517delGGAGGG, p.505_506del).	2-amino acid	50-62	ret proto-oncogene	Homo sapiens	94-97
26898613-3	2016	We conducted a study to evaluate the efficacy of sorafenib in a small number of patients with RET fusion-positive NSCLC.	Sorafenib	49-58	ret proto-oncogene	Homo sapiens	94-97
26765577-8	2016	In vitro expression showed that phosphorylation of the crucial tyrosine 905 was much stronger in the p.505_506del RET mutant compared with WT RET, indicating ligand-independent autophosphorylation.	Tyrosine	63-71	ret proto-oncogene	Homo sapiens	114-117
26832794-8	2016	The effect of the TKI vandetanib on proliferation and tumor growth response of MCF-7 cells was dependent upon expression of TFAP2C, and dual KD of RET and EGFR eliminated the effects of vandetanib.	vandetanib	186-196	ret proto-oncogene	Homo sapiens	147-150
26765577-8	2016	In vitro expression showed that phosphorylation of the crucial tyrosine 905 was much stronger in the p.505_506del RET mutant compared with WT RET, indicating ligand-independent autophosphorylation.	Tyrosine	63-71	ret proto-oncogene	Homo sapiens	142-145
26832794-11	2016	Response to vandetanib was mediated through the TFAP2C target genes EGFR and RET.	vandetanib	12-22	ret proto-oncogene	Homo sapiens	77-80
27014456-1	2016	In a patient with multiple endocrine neoplasia type 2A (MEN2A), an inverted physiological ratio between urinary normetanephrines and metanephrines is an early marker of recurrence in epinephrine-secreting pheochromocytoma, and 131I MIBG treatment appears to be a useful therapeutic option in order to avoid multiple invasive surgical procedures in pheochromocytomatosis.	Normetanephrine	112-128	ret proto-oncogene	Homo sapiens	18-54
27014456-1	2016	In a patient with multiple endocrine neoplasia type 2A (MEN2A), an inverted physiological ratio between urinary normetanephrines and metanephrines is an early marker of recurrence in epinephrine-secreting pheochromocytoma, and 131I MIBG treatment appears to be a useful therapeutic option in order to avoid multiple invasive surgical procedures in pheochromocytomatosis.	Normetanephrine	112-128	ret proto-oncogene	Homo sapiens	56-61
27014456-1	2016	In a patient with multiple endocrine neoplasia type 2A (MEN2A), an inverted physiological ratio between urinary normetanephrines and metanephrines is an early marker of recurrence in epinephrine-secreting pheochromocytoma, and 131I MIBG treatment appears to be a useful therapeutic option in order to avoid multiple invasive surgical procedures in pheochromocytomatosis.	3-Iodobenzylguanidine	227-236	ret proto-oncogene	Homo sapiens	18-54
27014456-1	2016	In a patient with multiple endocrine neoplasia type 2A (MEN2A), an inverted physiological ratio between urinary normetanephrines and metanephrines is an early marker of recurrence in epinephrine-secreting pheochromocytoma, and 131I MIBG treatment appears to be a useful therapeutic option in order to avoid multiple invasive surgical procedures in pheochromocytomatosis.	3-Iodobenzylguanidine	227-236	ret proto-oncogene	Homo sapiens	56-61
26861698-9	2016	GICs showed diverse drug sensitivity, but inhibitions of RTK and RAF/MEK or PI3K by combinations such as EGFR inhibitor and MEK inhibitor, sorafenib and U0126, erlotinib and BKM120, and EGFR inhibitor and sorafenib showed synergy in different subtypes of GICs.	Sorafenib	139-148	ret proto-oncogene	Homo sapiens	57-60
26861698-9	2016	GICs showed diverse drug sensitivity, but inhibitions of RTK and RAF/MEK or PI3K by combinations such as EGFR inhibitor and MEK inhibitor, sorafenib and U0126, erlotinib and BKM120, and EGFR inhibitor and sorafenib showed synergy in different subtypes of GICs.	U 0126	153-158	ret proto-oncogene	Homo sapiens	57-60
26454118-6	2016	Besides, we investigated the cytotoxicity and receptor tyrosine kinase (RET) expression in cells exposed to BP-3.	oxybenzone	108-112	ret proto-oncogene	Homo sapiens	46-70
26572832-1	2016	OBJECTIVE: Controversy surrounds the importance of the different amino acids substituting for cysteine in REarranged during Transfection (RET) codon 634 for multiple endocrine neoplasia 2A (MEN 2A).	Cysteine	94-102	ret proto-oncogene	Homo sapiens	106-136
26572832-1	2016	OBJECTIVE: Controversy surrounds the importance of the different amino acids substituting for cysteine in REarranged during Transfection (RET) codon 634 for multiple endocrine neoplasia 2A (MEN 2A).	Cysteine	94-102	ret proto-oncogene	Homo sapiens	138-141
26572832-1	2016	OBJECTIVE: Controversy surrounds the importance of the different amino acids substituting for cysteine in REarranged during Transfection (RET) codon 634 for multiple endocrine neoplasia 2A (MEN 2A).	Cysteine	94-102	ret proto-oncogene	Homo sapiens	157-188
26572832-1	2016	OBJECTIVE: Controversy surrounds the importance of the different amino acids substituting for cysteine in REarranged during Transfection (RET) codon 634 for multiple endocrine neoplasia 2A (MEN 2A).	Cysteine	94-102	ret proto-oncogene	Homo sapiens	190-196
26572832-10	2016	CONCLUSIONS: In codon 634, arginine substitutions for cysteine may cause slightly higher penetrance rates of MEN 2A which, overall, are too small to treat carriers differently.	Arginine	27-35	ret proto-oncogene	Homo sapiens	109-115
26572832-10	2016	CONCLUSIONS: In codon 634, arginine substitutions for cysteine may cause slightly higher penetrance rates of MEN 2A which, overall, are too small to treat carriers differently.	Cysteine	54-62	ret proto-oncogene	Homo sapiens	109-115
26454118-6	2016	Besides, we investigated the cytotoxicity and receptor tyrosine kinase (RET) expression in cells exposed to BP-3.	oxybenzone	108-112	ret proto-oncogene	Homo sapiens	72-75
26867945-1	2016	Lenvatinib (Lenvima ) is an oral, multi-targeted tyrosine kinase inhibitor (TKI) of vascular endothelial growth factor (VEGF) receptors 1, 2 and 3, fibroblast growth factor receptors 1, 2, 3 and 4, platelet-derived growth factor receptor alpha, and RET and KIT signalling networks, which are implicated in tumour growth and maintenance.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	249-252
26867945-1	2016	Lenvatinib (Lenvima ) is an oral, multi-targeted tyrosine kinase inhibitor (TKI) of vascular endothelial growth factor (VEGF) receptors 1, 2 and 3, fibroblast growth factor receptors 1, 2, 3 and 4, platelet-derived growth factor receptor alpha, and RET and KIT signalling networks, which are implicated in tumour growth and maintenance.	lenvatinib	12-19	ret proto-oncogene	Homo sapiens	249-252
26786320-1	2016	BACKGROUND: Sorafenib is an orally active multikinase tyrosine kinase inhibitor (TKI) that targets B-type Raf kinase (BRAF), vascular endothelial growth factor receptors (VEGFR) 1 and 2, and rearranged during transfection (RET), inducing anti-angiogenic and pro-apoptotic actions in a wide range of solid tumors.	Sorafenib	12-21	ret proto-oncogene	Homo sapiens	191-221
26786320-1	2016	BACKGROUND: Sorafenib is an orally active multikinase tyrosine kinase inhibitor (TKI) that targets B-type Raf kinase (BRAF), vascular endothelial growth factor receptors (VEGFR) 1 and 2, and rearranged during transfection (RET), inducing anti-angiogenic and pro-apoptotic actions in a wide range of solid tumors.	Sorafenib	12-21	ret proto-oncogene	Homo sapiens	223-226
26843961-12	2016	The macroscopic black aspect can mislead to the diagnosis of a metastasis deriving from a malignant melanoma.RET mutation are seen in catecholamine and non-catecholamine producing tumors of the same cellular origin.	Catecholamines	134-147	ret proto-oncogene	Homo sapiens	109-112
26652860-0	2016	A Pyrazolo[3,4-d]pyrimidin-4-amine Derivative Containing an Isoxazole Moiety Is a Selective and Potent Inhibitor of RET Gatekeeper Mutants.	8-aza-7-deazaadenine	2-34	ret proto-oncogene	Homo sapiens	116-119
26652860-0	2016	A Pyrazolo[3,4-d]pyrimidin-4-amine Derivative Containing an Isoxazole Moiety Is a Selective and Potent Inhibitor of RET Gatekeeper Mutants.	Isoxazoles	60-69	ret proto-oncogene	Homo sapiens	116-119
26652860-2	2016	The gatekeeper mutants (V804L or V804M) of RET are resistant to currently approved RET inhibitors such as cabozantinib and vandetanib.	cabozantinib	106-118	ret proto-oncogene	Homo sapiens	43-46
26652860-2	2016	The gatekeeper mutants (V804L or V804M) of RET are resistant to currently approved RET inhibitors such as cabozantinib and vandetanib.	cabozantinib	106-118	ret proto-oncogene	Homo sapiens	83-86
26652860-2	2016	The gatekeeper mutants (V804L or V804M) of RET are resistant to currently approved RET inhibitors such as cabozantinib and vandetanib.	vandetanib	123-133	ret proto-oncogene	Homo sapiens	43-46
26652860-2	2016	The gatekeeper mutants (V804L or V804M) of RET are resistant to currently approved RET inhibitors such as cabozantinib and vandetanib.	vandetanib	123-133	ret proto-oncogene	Homo sapiens	83-86
26728598-5	2016	In this report, we show that the Src homology phosphotyrosyl phosphatase 2 (SHP2) is a master regulator of RTK expression and signaling in BTBC.	btbc	139-143	ret proto-oncogene	Homo sapiens	107-110
26678514-6	2016	Lenvatinib targets vascular endothelial growth factor receptors 1-3 (VEGFR1-3), fibroblast growth factor receptors 1-4 (FGFR-1-4), RET, c-kit, and platelet-derived growth factor receptor alpha (PDGFRalpha).	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	131-134
25863490-2	2016	Several lines of evidence suggest that RET function could be influenced by cyclic AMP (cAMP)-dependent protein kinase A (PKA) activity.	Cyclic AMP	75-85	ret proto-oncogene	Homo sapiens	39-42
25863490-2	2016	Several lines of evidence suggest that RET function could be influenced by cyclic AMP (cAMP)-dependent protein kinase A (PKA) activity.	Cyclic AMP	87-91	ret proto-oncogene	Homo sapiens	39-42
26724763-1	2016	Herein, a novel electrochemiluminescence resonance energy transfer (ECL-RET) biosensor using graphene quantum dots (GQDs) as donor and graphene oxide (GO) as acceptor for monitoring the activity of protein kinase was presented for the first time.	Graphite	93-101	ret proto-oncogene	Homo sapiens	72-75
26724763-1	2016	Herein, a novel electrochemiluminescence resonance energy transfer (ECL-RET) biosensor using graphene quantum dots (GQDs) as donor and graphene oxide (GO) as acceptor for monitoring the activity of protein kinase was presented for the first time.	graphene oxide	135-149	ret proto-oncogene	Homo sapiens	72-75
27900224-2	2016	We present the case of a patient with MEN IIb, after bilateral adrenalectomies, on maintenance steroid replacement, who underwent a neuroma resection and developed severe hypotension.	Steroids	95-102	ret proto-oncogene	Homo sapiens	38-45
26843961-12	2016	The macroscopic black aspect can mislead to the diagnosis of a metastasis deriving from a malignant melanoma.RET mutation are seen in catecholamine and non-catecholamine producing tumors of the same cellular origin.	Catecholamines	156-169	ret proto-oncogene	Homo sapiens	109-112
26651387-3	2016	AREAS COVERED: Regorafenib, an oral multitargeted inhibitor with activity against multiple kinases including KIT, RET, RAF1, BRAF, angiogenesis (VEGFR, TIE-2) and those involved in tumor microenvironment (PDGFR and FGFR) was introduced after the successful Phase III GRID (GIST - Regorafenib In progressive Disease) clinical trial.	regorafenib	15-26	ret proto-oncogene	Homo sapiens	114-117
26536165-1	2016	Cabozantinib (XL-184) is a potent inhibitor of MET, VEGFR 2/KDR, RET and other receptor tyrosine kinases, such as KIT, AXL and FLT3.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	65-68
26536165-1	2016	Cabozantinib (XL-184) is a potent inhibitor of MET, VEGFR 2/KDR, RET and other receptor tyrosine kinases, such as KIT, AXL and FLT3.	cabozantinib	14-20	ret proto-oncogene	Homo sapiens	65-68
26536165-7	2016	Expert Commentary: Cabozantinib constitutes an effective treatment option with acceptable toxicity in MTC patients showing either germinal or sporadic tumor RET M918T mutation as the drug prolonged OS in these subjects.	cabozantinib	19-31	ret proto-oncogene	Homo sapiens	157-160
27141568-1	2016	INTRODUCTION: Reticulocyte hemoglobin equivalent (RET-He) is a new parameter for evaluating iron status.	Iron	92-96	ret proto-oncogene	Homo sapiens	50-53
27207748-7	2016	One case with a RET M918T mutation developed acquired resistance to progressively dose-escalated vandetanib.	vandetanib	97-107	ret proto-oncogene	Homo sapiens	16-19
27141568-2	2016	This study aims to assess diagnostic value and investigate RET-He as early predictor of response to intravenous iron supplementation.	Iron	112-116	ret proto-oncogene	Homo sapiens	59-62
27141568-10	2016	CONCLUSION: RET-He is a useful marker of iron deficiency and early predictor of response to intravenous iron supplementation in regular hemodialysis patients.	Iron	41-45	ret proto-oncogene	Homo sapiens	12-15
26675484-2	2015	These mutations can be targeted by RTK inhibitors (TKIs) such as erlotinib.	Erlotinib Hydrochloride	65-74	ret proto-oncogene	Homo sapiens	35-38
26555190-2	2015	While Ret signaling clearly impacts on the development, maintenance and regeneration of the mesostriatal DA system, the physiological functions of GDNF for the DA system are still unclear.	Dopamine	105-107	ret proto-oncogene	Homo sapiens	6-9
26555190-5	2015	Here, we review the current knowledge of GDNF and Ret signaling and function in the midbrain DA system, and their crosstalk with proteins and signaling pathways associated with PD.	Dopamine	93-95	ret proto-oncogene	Homo sapiens	50-53
26698662-1	2015	In insects, brain-derived Prothoracicotropic hormone (PTTH) activates the receptor tyrosine kinase (RTK) Torso to initiate metamorphosis through the release of ecdysone.	Ecdysone	160-168	ret proto-oncogene	Homo sapiens	74-98
26698662-1	2015	In insects, brain-derived Prothoracicotropic hormone (PTTH) activates the receptor tyrosine kinase (RTK) Torso to initiate metamorphosis through the release of ecdysone.	Ecdysone	160-168	ret proto-oncogene	Homo sapiens	100-103
26677336-6	2015	Nintedanib (formally known as BIBF 1120) is a triple angiokinase inhibitor of VEGF, fibroblast growth factor, platelet-derived growth factor signaling with lesser activity against RET, Flt-3, and Src.	nintedanib	0-10	ret proto-oncogene	Homo sapiens	180-183
26677336-6	2015	Nintedanib (formally known as BIBF 1120) is a triple angiokinase inhibitor of VEGF, fibroblast growth factor, platelet-derived growth factor signaling with lesser activity against RET, Flt-3, and Src.	nintedanib	30-39	ret proto-oncogene	Homo sapiens	180-183
26240273-3	2015	The fully human anti-RET antibody (Y078) was conjugated to the DM1 and DM4 derivatives of the potent cytotoxic agent maytansine using thioether and disulfide linkers, respectively.	Maytansine	71-74	ret proto-oncogene	Homo sapiens	21-24
26240273-3	2015	The fully human anti-RET antibody (Y078) was conjugated to the DM1 and DM4 derivatives of the potent cytotoxic agent maytansine using thioether and disulfide linkers, respectively.	Maytansine	117-127	ret proto-oncogene	Homo sapiens	21-24
26240273-3	2015	The fully human anti-RET antibody (Y078) was conjugated to the DM1 and DM4 derivatives of the potent cytotoxic agent maytansine using thioether and disulfide linkers, respectively.	Sulfides	134-143	ret proto-oncogene	Homo sapiens	21-24
26377589-0	2015	Cabozantinib for the treatment of non-small cell lung cancer with KIF5B-RET fusion.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	72-75
25971960-0	2015	Receptor Tyrosine Kinase Expression Predicts Response to Sunitinib in Breast Cancer.	Sunitinib	57-66	ret proto-oncogene	Homo sapiens	0-24
26377589-3	2015	Several related clinical trials for non-small cell lung cancer (NSCLC) with KIF5B-RET rearrangements using existing RET inhibitors, such as cabozantinib, lenvatinib, vandetanib, sunitinib, ponatinib, and AUY922, have been swiftly initiated by the discovery of the KIF5B-RET fusion gene.	cabozantinib	140-152	ret proto-oncogene	Homo sapiens	82-85
26377589-3	2015	Several related clinical trials for non-small cell lung cancer (NSCLC) with KIF5B-RET rearrangements using existing RET inhibitors, such as cabozantinib, lenvatinib, vandetanib, sunitinib, ponatinib, and AUY922, have been swiftly initiated by the discovery of the KIF5B-RET fusion gene.	ponatinib	189-198	ret proto-oncogene	Homo sapiens	82-85
26377589-3	2015	Several related clinical trials for non-small cell lung cancer (NSCLC) with KIF5B-RET rearrangements using existing RET inhibitors, such as cabozantinib, lenvatinib, vandetanib, sunitinib, ponatinib, and AUY922, have been swiftly initiated by the discovery of the KIF5B-RET fusion gene.	5-(2,4-dihydroxy-5-isopropylphenyl)-4-(4-morpholin-4-ylmethylphenyl)isoxazole-3-carboxylic acid ethylamide	204-210	ret proto-oncogene	Homo sapiens	82-85
26377589-4	2015	Anti-RET activity and the status of clinical development of cabozantinib for KIF5B-RET fusion-positive NSCLC are discussed.	cabozantinib	60-72	ret proto-oncogene	Homo sapiens	83-86
26498137-0	2015	Curcumin-induced downregulation of Axl receptor tyrosine kinase inhibits cell proliferation and circumvents chemoresistance in non-small lung cancer cells.	Curcumin	0-8	ret proto-oncogene	Homo sapiens	39-63
26498137-10	2015	Taken together, our data imply that Axl RTK is a novel target of curcumin through which it exerts anti-proliferative effect in both parental and chemoresistant NSCLC cells.	Curcumin	65-73	ret proto-oncogene	Homo sapiens	40-43
26798849-3	2015	Lenvatinib (E-7080), an orally active inhibitor of multiple receptor tyrosine kinases including vascular endothelial growth factor receptors (VEGFR) 1, 2 and 3, proto-oncogene tyrosine-protein kinase receptor Ret and mast/stem cell growth factor receptor Kit, yielded highly promising early clinical data, even when given after progression on first-line therapy.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	209-212
26498137-2	2015	In the present study, we demonstrated the effect of curcumin, a phytochemical of the plant Curcuma longa, on expression and activation of Axl receptor tyrosine kinase (RTK) which plays an important role in cell survival, proliferation and anti-apoptosis.	Curcumin	52-60	ret proto-oncogene	Homo sapiens	142-166
26498137-2	2015	In the present study, we demonstrated the effect of curcumin, a phytochemical of the plant Curcuma longa, on expression and activation of Axl receptor tyrosine kinase (RTK) which plays an important role in cell survival, proliferation and anti-apoptosis.	Curcumin	52-60	ret proto-oncogene	Homo sapiens	168-171
26798590-0	2015	Alectinib in RET-rearranged non-small cell lung cancer-Another progress in precision medicine?	alectinib	0-9	ret proto-oncogene	Homo sapiens	13-16
26798590-3	2015	Alectinib, a second generation ALK inhibitor, was shown to block growth of cells with RET fusions.	alectinib	0-9	ret proto-oncogene	Homo sapiens	86-89
26798590-4	2015	Thus alectinib should be further evaluated within clinical trials in patients with RET fusion-positive adenocarcinomas of the lung.	alectinib	5-14	ret proto-oncogene	Homo sapiens	83-86
26408683-1	2015	BACKGROUND: The cellular N-methyl-N"-nitroso-guanidine human osteosarcoma transforming gene (c-MET) protein is the receptor tyrosine kinase for hepatocyte growth factor.	n-methyl-n"-nitroso-guanidine	25-54	ret proto-oncogene	Homo sapiens	115-139
26622180-3	2015	Nintedanib is a small-molecule tyrosine kinase inhibitor that targets receptors for vascular endothelial growth factor, platelet-derived growth factor, and fibroblast growth factor as well as RET (rearranged during transfection) and Flt3.	nintedanib	0-10	ret proto-oncogene	Homo sapiens	192-195
26622180-3	2015	Nintedanib is a small-molecule tyrosine kinase inhibitor that targets receptors for vascular endothelial growth factor, platelet-derived growth factor, and fibroblast growth factor as well as RET (rearranged during transfection) and Flt3.	nintedanib	0-10	ret proto-oncogene	Homo sapiens	197-227
26693082-9	2015	Treatment with vandetanib, a RET inhibitor was initiated; his metastatic disease has been stable, without symptoms or recurrent cutaneous metastasis, for 2 years following the discovery of his metastatic nose tumor.	vandetanib	15-25	ret proto-oncogene	Homo sapiens	29-32
26473815-6	2015	In this paper we report on three tC-modified fluorescent probes that contain RET related sequences as a proton recognizing aptamer.	Technetium	33-35	ret proto-oncogene	Homo sapiens	77-80
26237499-3	2015	Sorafenib is a small molecule that blocks the activation of C-RAF, B-RAF, c-KIT, FLT-3, RET, VEGFR-2, VEGFR-3 and PDGFR approved for advanced renal cell and hepatocellular carcinoma (b, c).	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	88-91
26208525-2	2015	Activity of dovitinib (TKI258), a potent inhibitor of FGFR, VEGFR, and PDGFR, in RET-rearranged LADC has not been reported.	4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one	12-21	ret proto-oncogene	Homo sapiens	81-84
25402977-2	2015	This study evaluated the efficacy and safety of dovitinib, an RTK inhibitor with in vitro inhibitory activity against FGFR, in patients with relapsed or refractory MM with or without t(4;14) translocation.	4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one	48-57	ret proto-oncogene	Homo sapiens	62-65
26264277-5	2015	Furthermore, the SphK1 inhibitor safingol synergistically sensitized EGCG-induced proapoptotic cell death and tumor suppression in multiple myeloma cells by promoting the prevention of RTK phosphorylation and activation of death-associated protein kinase 1 (DAPK1).	safingol	33-41	ret proto-oncogene	Homo sapiens	185-188
26264277-5	2015	Furthermore, the SphK1 inhibitor safingol synergistically sensitized EGCG-induced proapoptotic cell death and tumor suppression in multiple myeloma cells by promoting the prevention of RTK phosphorylation and activation of death-associated protein kinase 1 (DAPK1).	epigallocatechin gallate	69-73	ret proto-oncogene	Homo sapiens	185-188
26294741-12	2015	In addition, using kinome-wide inhibition profiling analysis, we first identified potential new target kinases of AZD4547, including MAP4K3, MAP4K5, IRR, RET, and FLT3.	AZD4547	114-121	ret proto-oncogene	Homo sapiens	154-157
26208525-9	2015	Taken together, these findings suggest that dovitinib can be a potential therapeutic option for RET-rearranged LADC, in which acquired resistance to dovitinib can be overcome by targeting Src.	4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one	149-158	ret proto-oncogene	Homo sapiens	96-99
26208525-2	2015	Activity of dovitinib (TKI258), a potent inhibitor of FGFR, VEGFR, and PDGFR, in RET-rearranged LADC has not been reported.	4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one	23-29	ret proto-oncogene	Homo sapiens	81-84
26208525-3	2015	The aims of the study are to explore antitumor effects and mechanisms of acquired resistance of dovitinib in RET-rearranged LADC.	4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one	96-105	ret proto-oncogene	Homo sapiens	109-112
26208525-4	2015	Using structural modeling and in vitro analysis, we demonstrated that dovitinib induced cell-cycle arrest at G0-G1 phase and apoptosis by selective inhibition of RET kinase activity and ERK1/2 signaling in RET-rearranged LC-2/ad cells.	4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one	70-79	ret proto-oncogene	Homo sapiens	162-165
26208525-4	2015	Using structural modeling and in vitro analysis, we demonstrated that dovitinib induced cell-cycle arrest at G0-G1 phase and apoptosis by selective inhibition of RET kinase activity and ERK1/2 signaling in RET-rearranged LC-2/ad cells.	4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one	70-79	ret proto-oncogene	Homo sapiens	206-209
26208525-9	2015	Taken together, these findings suggest that dovitinib can be a potential therapeutic option for RET-rearranged LADC, in which acquired resistance to dovitinib can be overcome by targeting Src.	4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one	44-53	ret proto-oncogene	Homo sapiens	96-99
26258321-11	2015	Compared with RAS or PAX8/PPARG-positive TCs, BRAFV600E or RET/PTC-positive TCs were more often associated with stage III/IV disease (40% vs 15%, P &lt; 0.001) and recurrence (10% vs 0.7%, P &lt; 0.001; mean follow-up 33 +- 21 mo).	Technetium	76-79	ret proto-oncogene	Homo sapiens	59-62
26327919-1	2015	Regorafenib (Stivarga, BAY 73-4506; Bayer Pharma AG, Berlin, Germany) is an oral multikinase inhibitor that targets the angiogenic tumor microenvironment and oncogenic kinases including vascular endothelial growth factor receptor 2 (VEGFR2), VEGFR1, VEGFR3, fibroblast growth factor receptor 1 (FGFR1), RAF, KIT, RET and BRAF.	regorafenib	0-11	ret proto-oncogene	Homo sapiens	313-316
26026391-1	2015	BACKGROUND &amp; AIMS: Receptor tyrosine kinase (RTK) inhibitors have advanced colon cancer treatment.	Adenosine Monophosphate	12-15	ret proto-oncogene	Homo sapiens	23-47
26026391-1	2015	BACKGROUND &amp; AIMS: Receptor tyrosine kinase (RTK) inhibitors have advanced colon cancer treatment.	Adenosine Monophosphate	12-15	ret proto-oncogene	Homo sapiens	49-52
26026391-7	2015	Some mice were given the RTK inhibitor imatinib after injection of cancer cells; tumor growth was measured based on bioluminescence.	Imatinib Mesylate	39-47	ret proto-oncogene	Homo sapiens	25-28
26187428-6	2015	Furthermore analysis of the clinical database revealed one additional NCOA4-RET rearrangement co-existing with activated EGFR mutation in an EGFR-mutated NSCLC patient who had progressed on afatinib.	Afatinib	190-198	ret proto-oncogene	Homo sapiens	76-79
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
26307103-0	2015	Selective repression of RET proto-oncogene in medullary thyroid carcinoma by a natural alkaloid berberine.	Alkaloids	87-95	ret proto-oncogene	Homo sapiens	24-27
26307103-0	2015	Selective repression of RET proto-oncogene in medullary thyroid carcinoma by a natural alkaloid berberine.	Berberine	96-105	ret proto-oncogene	Homo sapiens	24-27
26327919-1	2015	Regorafenib (Stivarga, BAY 73-4506; Bayer Pharma AG, Berlin, Germany) is an oral multikinase inhibitor that targets the angiogenic tumor microenvironment and oncogenic kinases including vascular endothelial growth factor receptor 2 (VEGFR2), VEGFR1, VEGFR3, fibroblast growth factor receptor 1 (FGFR1), RAF, KIT, RET and BRAF.	regorafenib	13-21	ret proto-oncogene	Homo sapiens	313-316
26307103-3	2015	In this study we have demonstrated a therapeutic strategy for MTC by suppressing the transcription of RET proto-oncogene though the stabilization of G-quadruplex structure formed on the promoter region of this gene using a natural product berberine.	Berberine	239-248	ret proto-oncogene	Homo sapiens	102-105
26307103-4	2015	METHODS: Medullary thyroid carcinoma (MTC) TT cell line has been used to evaluate the effects of berberine on RET expression and its downstream signaling pathways.	Berberine	97-106	ret proto-oncogene	Homo sapiens	110-113
26405692-2	2015	The G-quadruplex (G4) sequences regulating the c-MYC, KRAS, VEGF, BCL-2, HIF-1alpha, and RET oncogenes, as examples, are targets for oxidation at loop and 5"-core guanines (G) as showcased in this study by CO3 - oxidation of the VEGF G4.	Guanine	163-171	ret proto-oncogene	Homo sapiens	89-92
26405692-2	2015	The G-quadruplex (G4) sequences regulating the c-MYC, KRAS, VEGF, BCL-2, HIF-1alpha, and RET oncogenes, as examples, are targets for oxidation at loop and 5"-core guanines (G) as showcased in this study by CO3 - oxidation of the VEGF G4.	co3	206-209	ret proto-oncogene	Homo sapiens	89-92
26230144-1	2015	Pt(II) dbbpy bisacetylide (dbbpy = 4,4"-di(tert-butyl)-2,2"-bipyridine) complex (Pt-1) with two different Bodipy ligands was prepared with the goal to attain broad-band visible light absorbing, efficient funneling of the photoexcitation energy (via resonance energy transfer, RET) to the energy acceptor and high triplet formation quantum yields.	pt(ii) dbbpy bisacetylide	0-25	ret proto-oncogene	Homo sapiens	276-279
26307103-5	2015	The specificity of berberine was demonstrated by using the papillary thyroid carcinoma TPC1 cell line, which lacks the G-quadruplex forming sequence on the RET promoter region due to chromosomal rearrangement.	Berberine	19-28	ret proto-oncogene	Homo sapiens	156-159
26307103-6	2015	RESULTS: Berberine suppressed the RET expression by more than 90 % in MTC TT cells at a concentration of 2.5 mug/ml with minimal effect on the TPC1 cells.	Berberine	9-18	ret proto-oncogene	Homo sapiens	34-37
26307103-8	2015	The down-regulation of RET with berberine further inhibited the cell proliferation through cell cycle arrest and activation of apoptosis in TT cells, which was confirmed by a 2-fold increase in the caspase-3 activity and the down-regulation of cell-cycle regulatory proteins.	Berberine	32-41	ret proto-oncogene	Homo sapiens	23-26
26307103-9	2015	CONCLUSION: Our data strongly suggest that the G-quadruplex forming region and the stabilization of this structure play a critical role in mediating the repressive effect of berberine on RET transcription.	Berberine	174-183	ret proto-oncogene	Homo sapiens	187-190
25435367-2	2015	For therapy of advanced MTC, the Food and Drug Administration recently approved vandetanib and cabozantinib, the tyrosine kinase inhibitors targeting RET, vascular endothelial growth factor receptor, epidermal growth factor receptor and/or c-MET.	vandetanib	80-90	ret proto-oncogene	Homo sapiens	150-153
25435367-2	2015	For therapy of advanced MTC, the Food and Drug Administration recently approved vandetanib and cabozantinib, the tyrosine kinase inhibitors targeting RET, vascular endothelial growth factor receptor, epidermal growth factor receptor and/or c-MET.	cabozantinib	95-107	ret proto-oncogene	Homo sapiens	150-153
25794958-5	2015	Owing to the reduction of coreactant H2O2 resulting from G-quadruplex-hemin DNAzyme catalytic reaction and the ECL energy transfer (ECL-RET) between AuNPs and GQDs, the ECL intensity of GQDs was significantly decreased.	Hydrogen Peroxide	37-41	ret proto-oncogene	Homo sapiens	136-139
26230144-1	2015	Pt(II) dbbpy bisacetylide (dbbpy = 4,4"-di(tert-butyl)-2,2"-bipyridine) complex (Pt-1) with two different Bodipy ligands was prepared with the goal to attain broad-band visible light absorbing, efficient funneling of the photoexcitation energy (via resonance energy transfer, RET) to the energy acceptor and high triplet formation quantum yields.	dbbpy	7-12	ret proto-oncogene	Homo sapiens	276-279
26230144-1	2015	Pt(II) dbbpy bisacetylide (dbbpy = 4,4"-di(tert-butyl)-2,2"-bipyridine) complex (Pt-1) with two different Bodipy ligands was prepared with the goal to attain broad-band visible light absorbing, efficient funneling of the photoexcitation energy (via resonance energy transfer, RET) to the energy acceptor and high triplet formation quantum yields.	4,4"-di(tert-butyl)-2,2"-bipyridine)	35-71	ret proto-oncogene	Homo sapiens	276-279
26339399-1	2015	The present study investigated the effect of valproic acid (VPA) on the inhibition of RET signaling and induction of apoptosis in human thyroid carcinoma cells.	Valproic Acid	45-58	ret proto-oncogene	Homo sapiens	86-89
26268359-4	2015	We tested KIF5B-RET translocation in Formalin Fixed Paraffin Embedded using fluorescence in situ hybridization.	Formaldehyde	37-45	ret proto-oncogene	Homo sapiens	16-19
26268359-4	2015	We tested KIF5B-RET translocation in Formalin Fixed Paraffin Embedded using fluorescence in situ hybridization.	Paraffin	52-60	ret proto-oncogene	Homo sapiens	16-19
26033033-0	2015	C-Cell Neoplasia in Asymptomatic Carriers of RET Mutation in Extracellular Cysteine-Rich and Intracellular Tyrosine Kinase Domain.	Cysteine	75-83	ret proto-oncogene	Homo sapiens	45-48
26153718-1	2015	In this paper, a novel electrochemiluminescence resonance energy transfer (ECL-RET) system from O2/S2O8(2-) to a kind of amino-terminated perylene derivative (PTC-NH2) was demonstrated for the first time, which was then applied to construct a ratiometric aptasensor for lead ion (Pb(2+)) detection.	Oxygen	96-98	ret proto-oncogene	Homo sapiens	79-82
26153718-1	2015	In this paper, a novel electrochemiluminescence resonance energy transfer (ECL-RET) system from O2/S2O8(2-) to a kind of amino-terminated perylene derivative (PTC-NH2) was demonstrated for the first time, which was then applied to construct a ratiometric aptasensor for lead ion (Pb(2+)) detection.	s2o8	99-103	ret proto-oncogene	Homo sapiens	79-82
26153718-1	2015	In this paper, a novel electrochemiluminescence resonance energy transfer (ECL-RET) system from O2/S2O8(2-) to a kind of amino-terminated perylene derivative (PTC-NH2) was demonstrated for the first time, which was then applied to construct a ratiometric aptasensor for lead ion (Pb(2+)) detection.	Perylene	138-146	ret proto-oncogene	Homo sapiens	79-82
26153718-1	2015	In this paper, a novel electrochemiluminescence resonance energy transfer (ECL-RET) system from O2/S2O8(2-) to a kind of amino-terminated perylene derivative (PTC-NH2) was demonstrated for the first time, which was then applied to construct a ratiometric aptasensor for lead ion (Pb(2+)) detection.	Peptichemio	159-162	ret proto-oncogene	Homo sapiens	79-82
26153718-1	2015	In this paper, a novel electrochemiluminescence resonance energy transfer (ECL-RET) system from O2/S2O8(2-) to a kind of amino-terminated perylene derivative (PTC-NH2) was demonstrated for the first time, which was then applied to construct a ratiometric aptasensor for lead ion (Pb(2+)) detection.	Amido radical	163-166	ret proto-oncogene	Homo sapiens	79-82
26015560-6	2015	These major metabolites each possess in vitro inhibition potencies &lt;=1/10th of parent cabozantinib against the targeted kinases MET, RET, and VEGFR2/KDR.	cabozantinib	89-101	ret proto-oncogene	Homo sapiens	136-139
25736215-4	2015	In RET G691S polymorphism, the overall distribution of variant alleles (GA + AA) in cases was 62.9% as against 44.5% in controls (P &lt; 0.05) whereas frequency of RET L769L variant alleles (TG + GG) in cases was 70% versus 88% in controls (P &lt; 0.05).	Arsenic	85-87	ret proto-oncogene	Homo sapiens	3-6
25736215-5	2015	In RET S904S, frequency of variant alleles (CG + GG) in cases was 56% versus 44% in controls (P &lt; 0.05).	cysteinylglycine	44-46	ret proto-oncogene	Homo sapiens	3-6
26170630-1	2015	Vandetanib is a once-daily orally available tyrosine kinase inhibitor that works by blocking RET (REarranged during Transfection), vascular endothelial growth factor receptor (VEGFR-2, VEGFR-3), and epidermal growth factor receptor and to a lesser extent VEGFR-1, which are important targets in thyroid cancer (TC).	vandetanib	0-10	ret proto-oncogene	Homo sapiens	93-96
26170630-1	2015	Vandetanib is a once-daily orally available tyrosine kinase inhibitor that works by blocking RET (REarranged during Transfection), vascular endothelial growth factor receptor (VEGFR-2, VEGFR-3), and epidermal growth factor receptor and to a lesser extent VEGFR-1, which are important targets in thyroid cancer (TC).	vandetanib	0-10	ret proto-oncogene	Homo sapiens	98-128
26339399-1	2015	The present study investigated the effect of valproic acid (VPA) on the inhibition of RET signaling and induction of apoptosis in human thyroid carcinoma cells.	Valproic Acid	60-63	ret proto-oncogene	Homo sapiens	86-89
26043760-5	2015	The results suggest (1) the dimensionality in which RET occurs is dependent on the RuDCBPY concentration ranging from one-dimensional at very low concentrations up to three-dimensional at high concentration, (2) the occupancy of RuDCBPY within UiO-67-DCBPY is not uniform throughout the crystallites such that RuDCBPY densely populates the outer layers of the MOF at low concentrations, and (3) the average separation distance between RuDCBPY centers is ~21 A.	rudcbpy	83-90	ret proto-oncogene	Homo sapiens	52-55
26044359-0	2015	Characterization of interactions and pharmacophore development for DFG-out inhibitors to RET tyrosine kinase.	1,3-Diphenylguanidine	67-70	ret proto-oncogene	Homo sapiens	89-92
26043760-5	2015	The results suggest (1) the dimensionality in which RET occurs is dependent on the RuDCBPY concentration ranging from one-dimensional at very low concentrations up to three-dimensional at high concentration, (2) the occupancy of RuDCBPY within UiO-67-DCBPY is not uniform throughout the crystallites such that RuDCBPY densely populates the outer layers of the MOF at low concentrations, and (3) the average separation distance between RuDCBPY centers is ~21 A.	rudcbpy	229-236	ret proto-oncogene	Homo sapiens	52-55
26043760-5	2015	The results suggest (1) the dimensionality in which RET occurs is dependent on the RuDCBPY concentration ranging from one-dimensional at very low concentrations up to three-dimensional at high concentration, (2) the occupancy of RuDCBPY within UiO-67-DCBPY is not uniform throughout the crystallites such that RuDCBPY densely populates the outer layers of the MOF at low concentrations, and (3) the average separation distance between RuDCBPY centers is ~21 A.	uio-67-dcbpy	244-256	ret proto-oncogene	Homo sapiens	52-55
26043760-5	2015	The results suggest (1) the dimensionality in which RET occurs is dependent on the RuDCBPY concentration ranging from one-dimensional at very low concentrations up to three-dimensional at high concentration, (2) the occupancy of RuDCBPY within UiO-67-DCBPY is not uniform throughout the crystallites such that RuDCBPY densely populates the outer layers of the MOF at low concentrations, and (3) the average separation distance between RuDCBPY centers is ~21 A.	rudcbpy	229-236	ret proto-oncogene	Homo sapiens	52-55
26043760-5	2015	The results suggest (1) the dimensionality in which RET occurs is dependent on the RuDCBPY concentration ranging from one-dimensional at very low concentrations up to three-dimensional at high concentration, (2) the occupancy of RuDCBPY within UiO-67-DCBPY is not uniform throughout the crystallites such that RuDCBPY densely populates the outer layers of the MOF at low concentrations, and (3) the average separation distance between RuDCBPY centers is ~21 A.	rudcbpy	229-236	ret proto-oncogene	Homo sapiens	52-55
25982012-12	2015	The addition of everolimus may have both overcome the AKT2 amplification to produce a response in addition to its direct effects on the RET gene.	Everolimus	16-26	ret proto-oncogene	Homo sapiens	136-139
25982012-0	2015	Systemic and CNS activity of the RET inhibitor vandetanib combined with the mTOR inhibitor everolimus in KIF5B-RET re-arranged non-small cell lung cancer with brain metastases.	vandetanib	47-57	ret proto-oncogene	Homo sapiens	33-36
25982012-0	2015	Systemic and CNS activity of the RET inhibitor vandetanib combined with the mTOR inhibitor everolimus in KIF5B-RET re-arranged non-small cell lung cancer with brain metastases.	vandetanib	47-57	ret proto-oncogene	Homo sapiens	111-114
25982012-0	2015	Systemic and CNS activity of the RET inhibitor vandetanib combined with the mTOR inhibitor everolimus in KIF5B-RET re-arranged non-small cell lung cancer with brain metastases.	Everolimus	91-101	ret proto-oncogene	Homo sapiens	111-114
25982012-2	2015	The RET tyrosine kinase inhibitor, vandetanib, suppresses fusion-induced, anchorage-independent growth activity.	vandetanib	35-45	ret proto-oncogene	Homo sapiens	4-7
26044359-2	2015	Abt-348, Birb-796, Motesanib and Sorafenib are DFG-out multi-kinase inhibitors that have been reported to inhibit RET activity with good IC50 values.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	0-3	ret proto-oncogene	Homo sapiens	114-117
26044359-2	2015	Abt-348, Birb-796, Motesanib and Sorafenib are DFG-out multi-kinase inhibitors that have been reported to inhibit RET activity with good IC50 values.	birb	9-13	ret proto-oncogene	Homo sapiens	114-117
26044359-2	2015	Abt-348, Birb-796, Motesanib and Sorafenib are DFG-out multi-kinase inhibitors that have been reported to inhibit RET activity with good IC50 values.	motesanib diphosphate	19-28	ret proto-oncogene	Homo sapiens	114-117
26044359-2	2015	Abt-348, Birb-796, Motesanib and Sorafenib are DFG-out multi-kinase inhibitors that have been reported to inhibit RET activity with good IC50 values.	Sorafenib	33-42	ret proto-oncogene	Homo sapiens	114-117
26044359-2	2015	Abt-348, Birb-796, Motesanib and Sorafenib are DFG-out multi-kinase inhibitors that have been reported to inhibit RET activity with good IC50 values.	1,3-Diphenylguanidine	47-50	ret proto-oncogene	Homo sapiens	114-117
26044359-3	2015	Although the DFG-out conformation has attracted great interest in the design of type II inhibitors, the structural requirements for binding to the RET DFG-out conformation remains unclear.	1,3-Diphenylguanidine	151-154	ret proto-oncogene	Homo sapiens	147-150
26044359-4	2015	Herein, the DFG-out conformation of RET was determined by homology modelling, the four inhibitors were docked, and the binding modes investigated by molecular dynamics simulation.	1,3-Diphenylguanidine	12-15	ret proto-oncogene	Homo sapiens	36-39
26044359-9	2015	The results reported herein will be useful in future rational design of novel DFG-out RET inhibitors.	1,3-Diphenylguanidine	78-81	ret proto-oncogene	Homo sapiens	86-89
26065416-4	2015	Constitutive activation of RET in a SK-N-MC cell line model reduces cell sensitivity to chemotherapy.	sk-n-mc	36-43	ret proto-oncogene	Homo sapiens	27-30
25694125-5	2015	Gain-of-function mutations in the REarranged during transfection (RET) proto-oncogene have been identified in 98 % of hMTC and 50 % of sMTC.	hmtc	118-122	ret proto-oncogene	Homo sapiens	34-64
25694125-5	2015	Gain-of-function mutations in the REarranged during transfection (RET) proto-oncogene have been identified in 98 % of hMTC and 50 % of sMTC.	hmtc	118-122	ret proto-oncogene	Homo sapiens	66-69
25694125-5	2015	Gain-of-function mutations in the REarranged during transfection (RET) proto-oncogene have been identified in 98 % of hMTC and 50 % of sMTC.	smtc	135-139	ret proto-oncogene	Homo sapiens	34-64
25694125-5	2015	Gain-of-function mutations in the REarranged during transfection (RET) proto-oncogene have been identified in 98 % of hMTC and 50 % of sMTC.	smtc	135-139	ret proto-oncogene	Homo sapiens	66-69
25694125-11	2015	In the present study, six different mutations were identified in exon10 of RET in 14 patients with sMTC and FMTC that were restricted to codons 611, 618, and 620, but not in codon 609.	smtc	99-103	ret proto-oncogene	Homo sapiens	75-78
25768669-7	2015	Sorafenib blocked RET, AKT, and ERK1/2 phosphorylation, whereas cabozantinib blocked RET and AKT phosphorylation.	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	18-21
26046350-3	2015	These three compounds shared a 3-trifluoromethyl-4-methylpiperazinephenyl pharmacophore that stabilizes the "DFG-out" inactive conformation of RET activation loop.	3-trifluoromethyl-4-methylpiperazinephenyl	31-73	ret proto-oncogene	Homo sapiens	143-146
26046350-3	2015	These three compounds shared a 3-trifluoromethyl-4-methylpiperazinephenyl pharmacophore that stabilizes the "DFG-out" inactive conformation of RET activation loop.	1,3-Diphenylguanidine	109-112	ret proto-oncogene	Homo sapiens	143-146
25625428-2	2015	Several related clinical trials for non-small-cell lung cancer (NSCLC) with KIF5B-RET rearrangements using existing RET inhibitors, such as lenvatinib, vandetanib, sunitinib, ponatinib, cabozantinib, and AUY922, have been swiftly initiated by the discovery of the KIF5B-RET fusion gene.	lenvatinib	140-150	ret proto-oncogene	Homo sapiens	82-85
25625428-2	2015	Several related clinical trials for non-small-cell lung cancer (NSCLC) with KIF5B-RET rearrangements using existing RET inhibitors, such as lenvatinib, vandetanib, sunitinib, ponatinib, cabozantinib, and AUY922, have been swiftly initiated by the discovery of the KIF5B-RET fusion gene.	cabozantinib	186-198	ret proto-oncogene	Homo sapiens	82-85
25625428-2	2015	Several related clinical trials for non-small-cell lung cancer (NSCLC) with KIF5B-RET rearrangements using existing RET inhibitors, such as lenvatinib, vandetanib, sunitinib, ponatinib, cabozantinib, and AUY922, have been swiftly initiated by the discovery of the KIF5B-RET fusion gene.	5-(2,4-dihydroxy-5-isopropylphenyl)-4-(4-morpholin-4-ylmethylphenyl)isoxazole-3-carboxylic acid ethylamide	204-210	ret proto-oncogene	Homo sapiens	82-85
25944708-4	2015	In this work, photoswitchable RET kinase inhibitors based on azo-functionalized pyrazolopyrimidines were developed, enabling photonic control of RET activity.	anthrone	61-64	ret proto-oncogene	Homo sapiens	30-33
25944708-4	2015	In this work, photoswitchable RET kinase inhibitors based on azo-functionalized pyrazolopyrimidines were developed, enabling photonic control of RET activity.	anthrone	61-64	ret proto-oncogene	Homo sapiens	145-148
25944708-4	2015	In this work, photoswitchable RET kinase inhibitors based on azo-functionalized pyrazolopyrimidines were developed, enabling photonic control of RET activity.	pyrazolopyrimidines	80-99	ret proto-oncogene	Homo sapiens	30-33
25944708-4	2015	In this work, photoswitchable RET kinase inhibitors based on azo-functionalized pyrazolopyrimidines were developed, enabling photonic control of RET activity.	pyrazolopyrimidines	80-99	ret proto-oncogene	Homo sapiens	145-148
25768669-7	2015	Sorafenib blocked RET, AKT, and ERK1/2 phosphorylation, whereas cabozantinib blocked RET and AKT phosphorylation.	cabozantinib	64-76	ret proto-oncogene	Homo sapiens	85-88
25768669-11	2015	CONCLUSIONS: Sorafenib and cabozantinib had marked effects on cell proliferation, cell cycle arrest, and signal transduction pathways in PTC cells harboring RET/PTC1 rearrangement.	Sorafenib	13-22	ret proto-oncogene	Homo sapiens	157-160
25768669-11	2015	CONCLUSIONS: Sorafenib and cabozantinib had marked effects on cell proliferation, cell cycle arrest, and signal transduction pathways in PTC cells harboring RET/PTC1 rearrangement.	cabozantinib	27-39	ret proto-oncogene	Homo sapiens	157-160
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
25826078-0	2015	Mer receptor tyrosine kinase is frequently overexpressed in human non-small cell lung cancer, confirming resistance to erlotinib.	Erlotinib Hydrochloride	119-128	ret proto-oncogene	Homo sapiens	4-28
25898937-5	2015	According to the current state of knowledge CCH without a germline mutation in the RET protooncogene, designated as non-MEN2-associated CCH, seems to be unrelated to the development of sporadic MTC.	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	136-139	ret proto-oncogene	Homo sapiens	83-86
25816194-5	2015	Graphene is also embedded with a trace amount of manganese impurities originating from a prior graphite oxidation process, which facilitates the thiol-functionalized graphene to function as a hybrid electrocatalyst for oxygen reduction reactions in alkaline medium with an onset potential lower than for Pt/C.	Graphite	0-8	ret proto-oncogene	Homo sapiens	304-308
25816194-5	2015	Graphene is also embedded with a trace amount of manganese impurities originating from a prior graphite oxidation process, which facilitates the thiol-functionalized graphene to function as a hybrid electrocatalyst for oxygen reduction reactions in alkaline medium with an onset potential lower than for Pt/C.	Sulfhydryl Compounds	145-150	ret proto-oncogene	Homo sapiens	304-308
25816194-5	2015	Graphene is also embedded with a trace amount of manganese impurities originating from a prior graphite oxidation process, which facilitates the thiol-functionalized graphene to function as a hybrid electrocatalyst for oxygen reduction reactions in alkaline medium with an onset potential lower than for Pt/C.	Graphite	166-174	ret proto-oncogene	Homo sapiens	304-308
25831049-0	2015	Anti-tumour effects of antibodies targeting the extracellular cysteine-rich region of the receptor tyrosine kinase EphB4.	Cysteine	62-70	ret proto-oncogene	Homo sapiens	90-114
25714734-2	2015	MATERIALS AND METHODS: RET and REG were labeled directly with (99m)Tc and their binding efficiency to tumor cells was measured in human nonsmall cell lung cancer H1299 cells.	Technetium	67-69	ret proto-oncogene	Homo sapiens	23-26
25887790-6	2015	Analyses of individual cells treated with the multi-tyrosine kinase inhibitor vandetanib reveal that, while the ribosomal genes and many other so-called house-keeping genes reduce their relative expression diversity during the drug treatment, the genes that are directly targeted by vandetanib, the EGFR and RET genes, remain constant.	vandetanib	78-88	ret proto-oncogene	Homo sapiens	308-311
25887790-6	2015	Analyses of individual cells treated with the multi-tyrosine kinase inhibitor vandetanib reveal that, while the ribosomal genes and many other so-called house-keeping genes reduce their relative expression diversity during the drug treatment, the genes that are directly targeted by vandetanib, the EGFR and RET genes, remain constant.	vandetanib	283-293	ret proto-oncogene	Homo sapiens	308-311
25795101-1	2015	Lenvatinib (Lenvima ) is a multitargeted receptor kinase inhibitor that inhibits the kinase activities of vascular endothelial-derived growth factor receptors 1, 2 and 3, fibroblast growth factor receptors 1, 2, 3 and 4, platelet-derived growth factor receptor alpha, RET and KIT.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	268-271
25795101-1	2015	Lenvatinib (Lenvima ) is a multitargeted receptor kinase inhibitor that inhibits the kinase activities of vascular endothelial-derived growth factor receptors 1, 2 and 3, fibroblast growth factor receptors 1, 2, 3 and 4, platelet-derived growth factor receptor alpha, RET and KIT.	lenvatinib	12-19	ret proto-oncogene	Homo sapiens	268-271
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.	cediranib	83-92	ret proto-oncogene	Homo sapiens	27-30
25881079-0	2015	A retrospective analysis of RET translocation, gene copy number gain and expression in NSCLC patients treated with vandetanib in four randomized Phase III studies.	vandetanib	115-125	ret proto-oncogene	Homo sapiens	28-31
25881079-4	2015	Seven tumor samples were positive for RET rearrangements (vandetanib, n = 3; comparator, n = 4).	vandetanib	58-68	ret proto-oncogene	Homo sapiens	38-41
25881079-8	2015	The objective response rate was similar in the vandetanib and comparator arms for patients positive for RET copy number gains or RET protein expression.	vandetanib	47-57	ret proto-oncogene	Homo sapiens	104-107
24662821-3	2015	The polypurine/polypyrimidine tract in the proximal promoter region of the human RET gene (-51 to -33 relative to transcription start site) is essential for basal transcriptional activity of this gene.	polypurine	4-14	ret proto-oncogene	Homo sapiens	81-84
24662821-3	2015	The polypurine/polypyrimidine tract in the proximal promoter region of the human RET gene (-51 to -33 relative to transcription start site) is essential for basal transcriptional activity of this gene.	polypyrimidine	15-29	ret proto-oncogene	Homo sapiens	81-84
24662821-6	2015	In this study, NSC194598, a derivative of indeno[1,2,3-de]quinazoline, was found to be a novel G-quadruplex interactive agent that interfered with transcriptional activation of mutated RET gene in human medullary thyroid carcinoma TT cells.	Indeno[1,2,3-de]quinazoline	42-69	ret proto-oncogene	Homo sapiens	185-188
25799134-4	2015	This was investigated in pediatric low grade astrocytoma and ependymoma cell lines treated with receptor tyrosine kinase (RTK) inhibitors e.g. sorafenib, dasatinib, canertinib and crizotinib.	Sorafenib	143-152	ret proto-oncogene	Homo sapiens	122-125
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.	cediranib	83-92	ret proto-oncogene	Homo sapiens	68-71
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
25605317-1	2015	INTRODUCTION: Sorafenib (Nexavar) is an oral multi-kinase inhibitor targeting B-type Raf kinase (BRAF) (both wild type and BRAF(V600E)), VEGFR1, VEGFR2, VEGFR3, PDGFRbeta and RET (also RET/PTC) influencing both differentiated thyroid cancer (DTC) cell proliferation and angiogenesis.	Sorafenib	14-23	ret proto-oncogene	Homo sapiens	175-178
25605317-1	2015	INTRODUCTION: Sorafenib (Nexavar) is an oral multi-kinase inhibitor targeting B-type Raf kinase (BRAF) (both wild type and BRAF(V600E)), VEGFR1, VEGFR2, VEGFR3, PDGFRbeta and RET (also RET/PTC) influencing both differentiated thyroid cancer (DTC) cell proliferation and angiogenesis.	Sorafenib	14-23	ret proto-oncogene	Homo sapiens	185-188
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
25605317-1	2015	INTRODUCTION: Sorafenib (Nexavar) is an oral multi-kinase inhibitor targeting B-type Raf kinase (BRAF) (both wild type and BRAF(V600E)), VEGFR1, VEGFR2, VEGFR3, PDGFRbeta and RET (also RET/PTC) influencing both differentiated thyroid cancer (DTC) cell proliferation and angiogenesis.	Sorafenib	25-32	ret proto-oncogene	Homo sapiens	175-178
25816031-9	2015	For trunk displacement, only TFG obtained a reduction statistical significance from PRE to the POST test (P = 0.002), supporting this result in the RET test.	2,2,2-Trifluoro-1-{5-[(3-Phenyl-5,6-Dihydroimidazo[1,2-A]pyrazin-7(8h)-Yl)carbonyl]thiophen-2-Yl}ethane-1,1-Diol	29-32	ret proto-oncogene	Homo sapiens	148-151
25605317-1	2015	INTRODUCTION: Sorafenib (Nexavar) is an oral multi-kinase inhibitor targeting B-type Raf kinase (BRAF) (both wild type and BRAF(V600E)), VEGFR1, VEGFR2, VEGFR3, PDGFRbeta and RET (also RET/PTC) influencing both differentiated thyroid cancer (DTC) cell proliferation and angiogenesis.	Sorafenib	25-32	ret proto-oncogene	Homo sapiens	185-188
25720956-5	2015	We find that vandetanib can directly inhibit RET activity, which influences the Rho-JNK pathway.	vandetanib	13-23	ret proto-oncogene	Homo sapiens	45-48
25374061-0	2015	Overexpression of miR-218 inhibits hepatocellular carcinoma cell growth through RET.	mir-218	18-25	ret proto-oncogene	Homo sapiens	80-83
25576915-0	2015	Multiple receptor tyrosine kinase activation attenuates therapeutic efficacy of the fibroblast growth factor receptor 2 inhibitor AZD4547 in FGFR2 amplified gastric cancer.	AZD4547	130-137	ret proto-oncogene	Homo sapiens	9-33
25576915-3	2015	In this study, we demonstrated that several receptor tyrosine kinase (RTK), including EGFR, HER3 and MET, activations contributed to AZD4547 (a selective FGFR2 inhibitor) hyposensitivity in FGFR2 amplified GC cells.	AZD4547	133-140	ret proto-oncogene	Homo sapiens	44-68
25576915-3	2015	In this study, we demonstrated that several receptor tyrosine kinase (RTK), including EGFR, HER3 and MET, activations contributed to AZD4547 (a selective FGFR2 inhibitor) hyposensitivity in FGFR2 amplified GC cells.	AZD4547	133-140	ret proto-oncogene	Homo sapiens	70-73
25767701-2	2015	A patient, operated for a medullary thyroid carcinoma (MTC) with a positive RET mutation, showed several peritoneal nodes on a computed tomography (CT), with increased Thyrocalcitonine.	thyrocalcitonine	168-184	ret proto-oncogene	Homo sapiens	76-79
25638620-12	2015	RET and MEN association was noted in 5 kindreds (14.3%) related to RET variations at Cysteine sites.	Cysteine	85-93	ret proto-oncogene	Homo sapiens	0-3
25427282-1	2015	IMPORTANCE: Cabozantinib S-malate is a vascular endothelial growth factor receptor 2, c-MET, and RET multitargeted tyrosine kinase inhibitor that has antiangiogenic and antitumorigenic properties with potential efficacy for the treatment of several cancers.	cabozantinib	12-33	ret proto-oncogene	Homo sapiens	97-100
25504634-2	2015	We report here the pharmacologic characterization of the triazolopyridazine derivative SAR125844, a potent and highly selective inhibitor of the MET receptor tyrosine kinase (RTK), for intravenous administration.	tetraazaisoindole	57-75	ret proto-oncogene	Homo sapiens	149-173
25504634-2	2015	We report here the pharmacologic characterization of the triazolopyridazine derivative SAR125844, a potent and highly selective inhibitor of the MET receptor tyrosine kinase (RTK), for intravenous administration.	tetraazaisoindole	57-75	ret proto-oncogene	Homo sapiens	175-178
25504634-2	2015	We report here the pharmacologic characterization of the triazolopyridazine derivative SAR125844, a potent and highly selective inhibitor of the MET receptor tyrosine kinase (RTK), for intravenous administration.	SAR125844	87-96	ret proto-oncogene	Homo sapiens	149-173
25504634-2	2015	We report here the pharmacologic characterization of the triazolopyridazine derivative SAR125844, a potent and highly selective inhibitor of the MET receptor tyrosine kinase (RTK), for intravenous administration.	SAR125844	87-96	ret proto-oncogene	Homo sapiens	175-178
25638620-12	2015	RET and MEN association was noted in 5 kindreds (14.3%) related to RET variations at Cysteine sites.	Cysteine	85-93	ret proto-oncogene	Homo sapiens	67-70
25301453-4	2015	The effect of ZLJ33 on pancreatic cancer was mainly mediated by inactivation of p-PDGFRbeta, p-c-Raf, and p-RET.	zlj33	14-19	ret proto-oncogene	Homo sapiens	108-111
25522765-2	2015	However, elevated expression of hepatocyte growth factor (HGF), a ligand of the MET receptor tyrosine kinase, causes erlotinib resistance.	Erlotinib Hydrochloride	117-126	ret proto-oncogene	Homo sapiens	84-108
26457501-0	2015	Catecholamine crisis as a first manifestation of familial bilateral pheochromocytoma caused by RET proto-oncogene mutation in codon C 634R.	Catecholamines	0-13	ret proto-oncogene	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
26098203-3	2015	Despite the successful clinical use of imatinib mesylate, a selective receptor tyrosine kinase (RTK) inhibitor that targets KIT, PDGFRA and BCR-ABL, we still do not have treatment for the long-term control of advanced GIST.	Imatinib Mesylate	39-56	ret proto-oncogene	Homo sapiens	70-94
26098203-3	2015	Despite the successful clinical use of imatinib mesylate, a selective receptor tyrosine kinase (RTK) inhibitor that targets KIT, PDGFRA and BCR-ABL, we still do not have treatment for the long-term control of advanced GIST.	Imatinib Mesylate	39-56	ret proto-oncogene	Homo sapiens	96-99
26457501-3	2015	The authors present a case study of three family members with bilateral pheochromocytoma in the course of MEN 2A, a catecholamine crisis being the first manifestation of the syndrome in one of them.	Catecholamines	116-129	ret proto-oncogene	Homo sapiens	106-112
26075440-1	2015	Lenvatinib mesylate (E7080; 4-[3-chloro-4-(N"-cyclopropylureido) phenoxy] 7-methoxyquinoline-6-carboxamide mesylate) is an oral molecule that inhibits multiple tyrosine kinase receptors such as VEGF-R-1-3, FGF-R-1-4, RET, c-KIT and PDGF-R-beta.	lenvatinib	0-19	ret proto-oncogene	Homo sapiens	217-220
25103625-0	2014	Selective activity over a constitutively active RET-variant of the oral multikinase inhibitor dovitinib: results of the CNIO-BR002 phase I-trial.	4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one	94-103	ret proto-oncogene	Homo sapiens	48-51
26075440-1	2015	Lenvatinib mesylate (E7080; 4-[3-chloro-4-(N"-cyclopropylureido) phenoxy] 7-methoxyquinoline-6-carboxamide mesylate) is an oral molecule that inhibits multiple tyrosine kinase receptors such as VEGF-R-1-3, FGF-R-1-4, RET, c-KIT and PDGF-R-beta.	lenvatinib	28-115	ret proto-oncogene	Homo sapiens	217-220
25319894-1	2015	Receptor tyrosine kinase (RTK) signaling exists in equilibrium between RTK tyrosyl phosphorylation and RTK tyrosyl dephosphorylation.	cyclo(tyrosyl-tyrosyl)	75-82	ret proto-oncogene	Homo sapiens	0-24
25319894-1	2015	Receptor tyrosine kinase (RTK) signaling exists in equilibrium between RTK tyrosyl phosphorylation and RTK tyrosyl dephosphorylation.	cyclo(tyrosyl-tyrosyl)	75-82	ret proto-oncogene	Homo sapiens	26-29
25319894-1	2015	Receptor tyrosine kinase (RTK) signaling exists in equilibrium between RTK tyrosyl phosphorylation and RTK tyrosyl dephosphorylation.	cyclo(tyrosyl-tyrosyl)	75-82	ret proto-oncogene	Homo sapiens	71-74
25319894-1	2015	Receptor tyrosine kinase (RTK) signaling exists in equilibrium between RTK tyrosyl phosphorylation and RTK tyrosyl dephosphorylation.	cyclo(tyrosyl-tyrosyl)	75-82	ret proto-oncogene	Homo sapiens	71-74
25319894-1	2015	Receptor tyrosine kinase (RTK) signaling exists in equilibrium between RTK tyrosyl phosphorylation and RTK tyrosyl dephosphorylation.	cyclo(tyrosyl-tyrosyl)	107-114	ret proto-oncogene	Homo sapiens	0-24
25319894-1	2015	Receptor tyrosine kinase (RTK) signaling exists in equilibrium between RTK tyrosyl phosphorylation and RTK tyrosyl dephosphorylation.	cyclo(tyrosyl-tyrosyl)	107-114	ret proto-oncogene	Homo sapiens	26-29
26484847-1	2015	INTRODUCTION: Lenvatinib is an oral multitargeted tyrosine kinase inhibitor of VEGFR1,2,3,4, FGFR1,2,3,4, PDGFR-alpha as well as RET and KIT signaling network.	lenvatinib	14-24	ret proto-oncogene	Homo sapiens	129-132
27014708-10	2015	For the treatment of advanced MTC cases, the broad spectrum receptor tyrosine kinase inhibitors vandetanib and cabozantinib, which also inhibit RET, are used although they are not always effective.	vandetanib	96-106	ret proto-oncogene	Homo sapiens	144-147
27014708-10	2015	For the treatment of advanced MTC cases, the broad spectrum receptor tyrosine kinase inhibitors vandetanib and cabozantinib, which also inhibit RET, are used although they are not always effective.	cabozantinib	111-123	ret proto-oncogene	Homo sapiens	144-147
25319894-2	2015	Despite a detailed understanding of RTK tyrosyl phosphorylation, much less is known about RTK tyrosyl dephosphorylation.	cyclo(tyrosyl-tyrosyl)	40-47	ret proto-oncogene	Homo sapiens	36-39
25319894-2	2015	Despite a detailed understanding of RTK tyrosyl phosphorylation, much less is known about RTK tyrosyl dephosphorylation.	cyclo(tyrosyl-tyrosyl)	94-101	ret proto-oncogene	Homo sapiens	90-93
26152149-1	2015	Cabozantinib is an oral once-daily multitarget tyrosine kinase inhibitor of MET, VEGFR2, RET, acting against KIT, AXL, FLT3 and Tie-2.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	89-92
26152149-3	2015	In a Phase III clinical study, cabozantinib improved PFS (11.2 months versus 4.0 months in the placebo group) of patients with MTC (independently of age, bone metastases, RET status and prior treatment).	cabozantinib	31-43	ret proto-oncogene	Homo sapiens	171-174
26152149-5	2015	Cabozantinib has been also evaluated in metastatic DTC patients, because they have activation on tyrosine kinases, including MET, VEGFR2 and RET, suggesting the possible use of cabozantinib in metastatic DTC.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	141-144
25528764-0	2014	The role of AXL and the in vitro activity of the receptor tyrosine kinase inhibitor BGB324 in Ewing sarcoma.	bemcentinib	84-90	ret proto-oncogene	Homo sapiens	49-73
25349307-0	2014	Alectinib shows potent antitumor activity against RET-rearranged non-small cell lung cancer.	alectinib	0-9	ret proto-oncogene	Homo sapiens	50-53
25349307-4	2014	We newly verified that alectinib inhibited RET kinase activity and the growth of RET fusion-positive cells by suppressing RET phosphorylation.	alectinib	23-32	ret proto-oncogene	Homo sapiens	43-46
25349307-4	2014	We newly verified that alectinib inhibited RET kinase activity and the growth of RET fusion-positive cells by suppressing RET phosphorylation.	alectinib	23-32	ret proto-oncogene	Homo sapiens	81-84
25349307-4	2014	We newly verified that alectinib inhibited RET kinase activity and the growth of RET fusion-positive cells by suppressing RET phosphorylation.	alectinib	23-32	ret proto-oncogene	Homo sapiens	81-84
25349307-7	2014	In addition, alectinib showed kinase inhibitory activity against RET gatekeeper mutations (RET V804L and V804M) and blocked cell growth driven by the KIF5B-RET V804L and V804M.	alectinib	13-22	ret proto-oncogene	Homo sapiens	65-68
25349307-7	2014	In addition, alectinib showed kinase inhibitory activity against RET gatekeeper mutations (RET V804L and V804M) and blocked cell growth driven by the KIF5B-RET V804L and V804M.	alectinib	13-22	ret proto-oncogene	Homo sapiens	91-94
25349307-7	2014	In addition, alectinib showed kinase inhibitory activity against RET gatekeeper mutations (RET V804L and V804M) and blocked cell growth driven by the KIF5B-RET V804L and V804M.	alectinib	13-22	ret proto-oncogene	Homo sapiens	91-94
25349307-8	2014	Our results suggest that alectinib is effective against RET fusion-positive tumors.	alectinib	25-34	ret proto-oncogene	Homo sapiens	56-59
25349307-9	2014	Thus, alectinib might be a therapeutic option for patients with RET fusion-positive NSCLC.	alectinib	6-15	ret proto-oncogene	Homo sapiens	64-67
25361206-1	2014	In this work, electrogenerated chemiluminescence resonance energy transfer (ECL-RET) between luminol as a donor and CdSe@ZnS quantum dots (QDs) as an acceptor was reported in neutral conditions.	Luminol	93-100	ret proto-oncogene	Homo sapiens	80-83
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
25409876-10	2014	Interestingly, SPP86 and PF573228 inhibited RET/PTC1 and GDNF- RET induced activation of Akt and MAPK signaling to a similar degree.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	25-33	ret proto-oncogene	Homo sapiens	63-66
25409876-0	2014	Selective inhibition of RET mediated cell proliferation in vitro by the kinase inhibitor SPP86.	SPP-86	89-94	ret proto-oncogene	Homo sapiens	24-27
25409876-8	2014	In TPC1 cells, the inhibition of RET phosphorylation required co-exposure to SPP86 and the focal adhesion kinase (FAK) inhibitor PF573228.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	129-137	ret proto-oncogene	Homo sapiens	33-36
25409876-9	2014	In MCF7 cells, SPP86 inhibited RET- induced phosphatidylinositide 3-kinases (PI3K)/Akt and MAPK signaling and estrogen receptoralpha (ERalpha) phosphorylation, and inhibited proliferation to a similar degree as tamoxifen.	Tamoxifen	211-220	ret proto-oncogene	Homo sapiens	31-34
25409876-10	2014	Interestingly, SPP86 and PF573228 inhibited RET/PTC1 and GDNF- RET induced activation of Akt and MAPK signaling to a similar degree.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	25-33	ret proto-oncogene	Homo sapiens	44-47
25361206-1	2014	In this work, electrogenerated chemiluminescence resonance energy transfer (ECL-RET) between luminol as a donor and CdSe@ZnS quantum dots (QDs) as an acceptor was reported in neutral conditions.	cdse	116-120	ret proto-oncogene	Homo sapiens	80-83
25361206-4	2014	Another stronger anodic ECL peak observed at more positive potential (1.10 V) could be assigned to the ECL-RET between the excited state of luminol and the QDs.	Luminol	140-147	ret proto-oncogene	Homo sapiens	107-110
25232968-5	2014	A RET DFG-out homology model was established and utilized to predict Type-II inhibitor binding modes.	1,3-Diphenylguanidine	6-9	ret proto-oncogene	Homo sapiens	2-5
24643705-2	2014	The gene responsible for MEN2A is the RET proto-oncogene and about 95 % of MEN2A patients have germline mutations in five specific cysteine codons (609, 611, 618, 620 and 634).	Cysteine	131-139	ret proto-oncogene	Homo sapiens	25-30
24643705-2	2014	The gene responsible for MEN2A is the RET proto-oncogene and about 95 % of MEN2A patients have germline mutations in five specific cysteine codons (609, 611, 618, 620 and 634).	Cysteine	131-139	ret proto-oncogene	Homo sapiens	38-41
24643705-2	2014	The gene responsible for MEN2A is the RET proto-oncogene and about 95 % of MEN2A patients have germline mutations in five specific cysteine codons (609, 611, 618, 620 and 634).	Cysteine	131-139	ret proto-oncogene	Homo sapiens	75-80
25436805-0	2014	RET-rearranged lung adenocarcinomas with lymphangitic spread, psammoma bodies, and clinical responses to cabozantinib.	cabozantinib	105-117	ret proto-oncogene	Homo sapiens	0-3
25436805-10	2014	Three of the patients were treated with the RET inhibitor cabozantinib.	cabozantinib	58-70	ret proto-oncogene	Homo sapiens	44-47
25084146-0	2014	Novel metal complexes of naphthalimide-cyclam conjugates as potential multi-target receptor tyrosine kinase (RTK) inhibitors: synthesis and biological evaluation.	Metals	6-11	ret proto-oncogene	Homo sapiens	83-107
25314669-1	2014	Asparagine-linked glycosylation is an endoplasmic reticulum co- and post-translational modification that enables the transit and function of receptor tyrosine kinase (RTK) glycoproteins.	Asparagine	0-10	ret proto-oncogene	Homo sapiens	141-165
25314669-1	2014	Asparagine-linked glycosylation is an endoplasmic reticulum co- and post-translational modification that enables the transit and function of receptor tyrosine kinase (RTK) glycoproteins.	Asparagine	0-10	ret proto-oncogene	Homo sapiens	167-170
25084146-0	2014	Novel metal complexes of naphthalimide-cyclam conjugates as potential multi-target receptor tyrosine kinase (RTK) inhibitors: synthesis and biological evaluation.	Metals	6-11	ret proto-oncogene	Homo sapiens	109-112
25084146-0	2014	Novel metal complexes of naphthalimide-cyclam conjugates as potential multi-target receptor tyrosine kinase (RTK) inhibitors: synthesis and biological evaluation.	naphthalimide-cyclam	25-45	ret proto-oncogene	Homo sapiens	83-107
25084146-0	2014	Novel metal complexes of naphthalimide-cyclam conjugates as potential multi-target receptor tyrosine kinase (RTK) inhibitors: synthesis and biological evaluation.	naphthalimide-cyclam	25-45	ret proto-oncogene	Homo sapiens	109-112
25197551-1	2014	BACKGROUND: Lenvatinib is an oral inhibitor of multiple receptor tyrosine kinases (RTKs) targeting vascular endothelial growth factor receptor (VEGFR1-3), fibroblast growth factor receptor (FGFR1-4), platelet growth factor receptor alpha (PDGFR alpha), RET and KIT.	lenvatinib	12-22	ret proto-oncogene	Homo sapiens	253-256
25102375-1	2014	BACKGROUND: Cabozantinib targets tyrosine kinases including MET, vascular endothelial growth factor (VEGF) receptor 2, and rearranged during transfection (RET).	cabozantinib	12-24	ret proto-oncogene	Homo sapiens	123-153
25102375-1	2014	BACKGROUND: Cabozantinib targets tyrosine kinases including MET, vascular endothelial growth factor (VEGF) receptor 2, and rearranged during transfection (RET).	cabozantinib	12-24	ret proto-oncogene	Homo sapiens	155-158
25242331-6	2014	The RET(ECD) cysteine-rich domain (CRD) contacts both ligand components and makes homotypic membrane-proximal interactions occluding three different antibody epitopes.	Cysteine	13-21	ret proto-oncogene	Homo sapiens	4-7
25117183-1	2014	BACKGROUND AND OBJECTIVE: Vandetanib is a selective inhibitor of vascular endothelial growth factor receptor (VEGFR), epidermal growth factor receptor (EGFR) and rearranged during transfection (RET) signalling, indicated for the treatment of medullary thyroid cancer.	vandetanib	26-36	ret proto-oncogene	Homo sapiens	194-197
24931161-1	2014	CLM29 (a pyrazolo[3,4-d]pyrimidine, that inhibits RET, epidermal growth factor receptor, vascular endothelial growth factor receptor, and has an anti-angiogenic activity) has anti-neoplastic activity in papillary dedifferentiated thyroid cancer.	clm29	0-5	ret proto-oncogene	Homo sapiens	50-53
25296193-2	2014	Vandetanib, a RET tyrosine-kinase inhibitor, significantly increased progression free survival and is the first treatment approved in France for unresectable, locally advanced or metastatic MTC that is symptomatic or progressive.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	14-17
25122427-9	2014	Stable cells became sensitized to the RET tyrosine kinase inhibitors, vandetanib and ponatinib.	vandetanib	70-80	ret proto-oncogene	Homo sapiens	38-41
25122427-9	2014	Stable cells became sensitized to the RET tyrosine kinase inhibitors, vandetanib and ponatinib.	ponatinib	85-94	ret proto-oncogene	Homo sapiens	38-41
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.	Sorafenib	78-87	ret proto-oncogene	Homo sapiens	47-50
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.	motesanib diphosphate	89-98	ret proto-oncogene	Homo sapiens	47-50
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
24931161-1	2014	CLM29 (a pyrazolo[3,4-d]pyrimidine, that inhibits RET, epidermal growth factor receptor, vascular endothelial growth factor receptor, and has an anti-angiogenic activity) has anti-neoplastic activity in papillary dedifferentiated thyroid cancer.	pyrazolo(3,4-d)pyrimidine	9-34	ret proto-oncogene	Homo sapiens	50-53
24781685-0	2014	The value of Ret-Hb and sTfR in the diagnosis of iron depletion in healthy, young children.	Iron	49-53	ret proto-oncogene	Homo sapiens	13-16
24951334-4	2014	Integrated molecular docking and SAR studies resulted in the discovery of a novel class of pyridone MET inhibitors with high potency (IC50 of 0.005 muM) and efficient selectivity (&gt;5000 fold) to VEGFR-2, c-Kit and RET kinases.	Pyridones	91-99	ret proto-oncogene	Homo sapiens	217-220
25056653-1	2014	Cabozantinib (Cometriq( )) is an orally administered small molecule inhibitor of multiple tyrosine kinase receptors, including those involved in the pathogenesis of medullary thyroid cancer (MTC) [i.e. rearranged during transfection (RET), MET and vascular endothelial growth factor receptor (VEGFR)-2].	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	202-232
25056653-1	2014	Cabozantinib (Cometriq( )) is an orally administered small molecule inhibitor of multiple tyrosine kinase receptors, including those involved in the pathogenesis of medullary thyroid cancer (MTC) [i.e. rearranged during transfection (RET), MET and vascular endothelial growth factor receptor (VEGFR)-2].	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	234-237
25056653-1	2014	Cabozantinib (Cometriq( )) is an orally administered small molecule inhibitor of multiple tyrosine kinase receptors, including those involved in the pathogenesis of medullary thyroid cancer (MTC) [i.e. rearranged during transfection (RET), MET and vascular endothelial growth factor receptor (VEGFR)-2].	cabozantinib	14-22	ret proto-oncogene	Homo sapiens	202-232
25056653-1	2014	Cabozantinib (Cometriq( )) is an orally administered small molecule inhibitor of multiple tyrosine kinase receptors, including those involved in the pathogenesis of medullary thyroid cancer (MTC) [i.e. rearranged during transfection (RET), MET and vascular endothelial growth factor receptor (VEGFR)-2].	cabozantinib	14-22	ret proto-oncogene	Homo sapiens	234-237
24608042-2	2014	Previously, we have found the density of TAMs correlated with lymph node metastasis in papillary thyroid carcinoma (PTC).	tams	41-45	ret proto-oncogene	Homo sapiens	116-119
24608042-10	2014	These findings indicated that TAMs may facilitate PTC cell metastasis through CXCL8 and its paracrine interaction with CXCR1/2.	tams	30-34	ret proto-oncogene	Homo sapiens	50-53
24781685-1	2014	OBJECTIVES: Reticulocyte hemoglobin (Ret-Hb) content and soluble transferrin receptor (sTfR) are described as promising biomarkers in the analysis of iron status.	Iron	150-154	ret proto-oncogene	Homo sapiens	12-15
24781685-3	2014	We hypothesized that young children to iron depletion, using the WHO cutoff of ferritin &lt;12 mug/l, would have lower Ret-Hb and higher sTfR concentrations compared to children with a ferritin &gt;=level 12 mug/l.	Iron	39-43	ret proto-oncogene	Homo sapiens	119-122
24781685-6	2014	RESULTS: We showed that concentrations of Ret-Hb and sTfR are similar in children with and without iron depletion.	Iron	99-103	ret proto-oncogene	Homo sapiens	42-45
24781685-9	2014	CONCLUSIONS: Our results showed that the discriminative value of Ret-Hb and sTfR for the detection of iron depletion is limited.	Iron	102-106	ret proto-oncogene	Homo sapiens	65-68
25187680-0	2014	Molecular docking of 1H-pyrazole derivatives to receptor tyrosine kinase and protein kinase for screening potential inhibitors.	pyrazole	21-32	ret proto-oncogene	Homo sapiens	48-72
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.	Platinum	39-47	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	ret proto-oncogene	Homo sapiens	148-151
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
25085632-12	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	ret proto-oncogene	Homo sapiens	196-199
24827972-5	2014	We introduce a nanosensor based on upconversion resonance energy transfer (UC-RET) between an upconverting nanoparticle (UCNP) and a fluorogenic pH-dependent dye pHrodo  Red that was covalently bound to the aminosilane surface of the nanoparticles.	pHrodo red	162-173	ret proto-oncogene	Homo sapiens	78-81
25012508-1	2014	BACKGROUND: Nintedanib is a potent, oral angiokinase inhibitor that targets VEGF, PDGF and FGF signalling, as well as RET and Flt3.	nintedanib	12-22	ret proto-oncogene	Homo sapiens	118-121
24924416-3	2014	We assessed whether vandetanib, an inhibitor of VEGF, epidermal growth factor receptor and RET signalling, improved uNTx response when added to fulvestrant (F) in breast cancer patients with bone metastases.	vandetanib	20-30	ret proto-oncogene	Homo sapiens	91-94
24779031-1	2014	The epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase (RTK), which catalyzes protein phosphorylation reactions by transferring the gamma-phosphoryl group from an ATP molecule to the hydroxyl group of tyrosine residues in protein substrates.	Adenosine Triphosphate	182-185	ret proto-oncogene	Homo sapiens	49-73
24779031-1	2014	The epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase (RTK), which catalyzes protein phosphorylation reactions by transferring the gamma-phosphoryl group from an ATP molecule to the hydroxyl group of tyrosine residues in protein substrates.	Adenosine Triphosphate	182-185	ret proto-oncogene	Homo sapiens	75-78
24779031-1	2014	The epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase (RTK), which catalyzes protein phosphorylation reactions by transferring the gamma-phosphoryl group from an ATP molecule to the hydroxyl group of tyrosine residues in protein substrates.	Tyrosine	58-66	ret proto-oncogene	Homo sapiens	75-78
24827972-5	2014	We introduce a nanosensor based on upconversion resonance energy transfer (UC-RET) between an upconverting nanoparticle (UCNP) and a fluorogenic pH-dependent dye pHrodo  Red that was covalently bound to the aminosilane surface of the nanoparticles.	2-cyanoethyldimethyl(diethyl)aminosilane	207-218	ret proto-oncogene	Homo sapiens	78-81
24955023-6	2014	Small molecule tyrosine kinase inhibitors targeting BRAF-mediated events, vascular endothelial growth factor receptors, RET/PTC rearrangements, and other molecular targets, show promising results to improve treatment of radioiodine resistant, recurrent, and aggressive PTC.	Iodine-131	220-231	ret proto-oncogene	Homo sapiens	120-123
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
24375110-0	2014	VEGFR, RET, and RAF/MEK/ERK pathway take part in the inhibition of osteosarcoma MG63 cells with sorafenib treatment.	Sorafenib	96-105	ret proto-oncogene	Homo sapiens	7-10
24709487-1	2014	BACKGROUND: Vandetanib is an oral tyrosine kinase inhibitor of VEGFR-2/3, EGFR and RET, which has demonstrated clinical activity as a single agent and in combination with taxanes.	vandetanib	12-22	ret proto-oncogene	Homo sapiens	83-86
24707967-1	2014	This work describes a new electrochemiluminescence resonance energy transfer (ECL-RET) system with graphene oxide(GO)-Au/RuSi@Ru(bpy)3(2+)/chitosan (CS) composites as the ECL donor and Au@Ag2S nanoparticles (NPs) as ECL the acceptor for the first time.	graphene oxide	99-113	ret proto-oncogene	Homo sapiens	82-85
24707967-1	2014	This work describes a new electrochemiluminescence resonance energy transfer (ECL-RET) system with graphene oxide(GO)-Au/RuSi@Ru(bpy)3(2+)/chitosan (CS) composites as the ECL donor and Au@Ag2S nanoparticles (NPs) as ECL the acceptor for the first time.	Cesium	149-151	ret proto-oncogene	Homo sapiens	82-85
24375110-6	2014	The present study confirmed that sorafenib could inhibit the proliferation of OS MG63 cells and caused a series of biomolecule effects, including the change of VEGFR2 and ERK gene expression, and the phosphorylation alteration of VEGFR2, RET, and MEK1 proteins.	Sorafenib	33-42	ret proto-oncogene	Homo sapiens	238-241
24375110-5	2014	In the present study, we performed assays of cell proliferation, RT-PCR, and western blot to investigate the effect of sorafenib on OS MG63 cells and to elucidate the molecular actions of sorafenib against RTKs VEGFR2 and RET, as well as MEK/ERK signaling pathway.	Sorafenib	188-197	ret proto-oncogene	Homo sapiens	222-225
24375110-7	2014	VEGFR2, RET, and MEK/ERK signaling pathway are involved in the pharmacological mechanism of sorafenib.	Sorafenib	92-101	ret proto-oncogene	Homo sapiens	8-11
24722163-0	2014	Experience with erlotinib in lung adenocarcinoma harboring a coexisting KIF5B-RET fusion gene and EGFR mutation: report of a rare case.	Erlotinib Hydrochloride	16-25	ret proto-oncogene	Homo sapiens	78-81
24483157-0	2014	The HIV protease inhibitor nelfinavir down-regulates RET signaling and induces apoptosis in medullary thyroid cancer cells.	Nelfinavir	27-37	ret proto-oncogene	Homo sapiens	53-56
24713656-7	2014	Furthermore, an ATP-competitive EPHA2 RTK inhibitor, ALW-II-41-27, reduced the number of viable NSCLC cells in a time-dependent and dose-dependent manner in vitro and induced tumor regression in human NSCLC xenografts in vivo.	Adenosine Triphosphate	16-19	ret proto-oncogene	Homo sapiens	38-41
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
24526731-10	2014	CONCLUSIONS: Vandetanib potentiated the antigrowth effects of tamoxifen in breast cancer, which was mediated through RET activation.	vandetanib	13-23	ret proto-oncogene	Homo sapiens	117-120
24526731-10	2014	CONCLUSIONS: Vandetanib potentiated the antigrowth effects of tamoxifen in breast cancer, which was mediated through RET activation.	Tamoxifen	62-71	ret proto-oncogene	Homo sapiens	117-120
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
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
24045439-9	2014	Inhibition of RET either by gene knockdown or by treatment with sunitinib or vandetanib reduced RET-dependent growth of luminal breast cancer cells.	vandetanib	77-87	ret proto-oncogene	Homo sapiens	14-17
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.	vandetanib	77-87	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.	Tamoxifen	42-51	ret proto-oncogene	Homo sapiens	137-140
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
24045439-12	2014	Whereas targeting the ER pathway altered cell proliferation, as measured by Ki-67 and S-phase, anti-RET primarily increased apoptosis, as demonstrated by cleaved caspase 3 and increased TUNEL (terminal deoxyneucleotidyl transferase dUTP nick end labeling) expression in xenografts.	deoxyuridine triphosphate	232-236	ret proto-oncogene	Homo sapiens	100-103
24437351-0	2014	The involvement of reactive oxygen species derived from NADPH oxidase-1 activation on the constitutive tyrosine auto-phosphorylation of RET proteins.	Reactive Oxygen Species	19-42	ret proto-oncogene	Homo sapiens	136-139
24449676-6	2014	CONCLUSIONS: The majority of mutations in this disorder affect cysteine residues in the cysteine-rich region of the extracellular domain of the RET protein, disrupting normal cysteine pairing.	Cysteine	63-71	ret proto-oncogene	Homo sapiens	144-147
24449676-6	2014	CONCLUSIONS: The majority of mutations in this disorder affect cysteine residues in the cysteine-rich region of the extracellular domain of the RET protein, disrupting normal cysteine pairing.	Cysteine	88-96	ret proto-oncogene	Homo sapiens	144-147
24449676-6	2014	CONCLUSIONS: The majority of mutations in this disorder affect cysteine residues in the cysteine-rich region of the extracellular domain of the RET protein, disrupting normal cysteine pairing.	Cysteine	88-96	ret proto-oncogene	Homo sapiens	144-147
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	Hydrogen Peroxide	0-4	ret proto-oncogene	Homo sapiens	64-67
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	Hydrogen Peroxide	0-4	ret proto-oncogene	Homo sapiens	68-73
24437351-0	2014	The involvement of reactive oxygen species derived from NADPH oxidase-1 activation on the constitutive tyrosine auto-phosphorylation of RET proteins.	Tyrosine	103-111	ret proto-oncogene	Homo sapiens	136-139
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	Hydrogen Peroxide	0-4	ret proto-oncogene	Homo sapiens	78-81
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	Hydrogen Peroxide	0-4	ret proto-oncogene	Homo sapiens	82-87
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	Tyrosine	31-39	ret proto-oncogene	Homo sapiens	64-67
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	Tyrosine	31-39	ret proto-oncogene	Homo sapiens	68-73
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	Tyrosine	31-39	ret proto-oncogene	Homo sapiens	78-81
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	Tyrosine	31-39	ret proto-oncogene	Homo sapiens	82-87
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	diphenyliodonium	167-183	ret proto-oncogene	Homo sapiens	64-67
24437351-2	2014	In this study, we analyzed the participation of ROS in the RET tyrosine auto-phosphorylation.	Reactive Oxygen Species	48-51	ret proto-oncogene	Homo sapiens	59-62
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	diphenyliodonium	167-183	ret proto-oncogene	Homo sapiens	68-73
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	diphenyliodonium	167-183	ret proto-oncogene	Homo sapiens	78-81
24437351-2	2014	In this study, we analyzed the participation of ROS in the RET tyrosine auto-phosphorylation.	Tyrosine	63-71	ret proto-oncogene	Homo sapiens	59-62
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	diphenyliodonium	167-183	ret proto-oncogene	Homo sapiens	82-87
24744988-12	2014	Similarly, several marketed tyrosine kinase inhibitors (TKIs) in the US (sorafenib, sunitinib, vandetanib, cabozantinib, regorafenib) are potent RET inhibitors in vitro.	Sorafenib	73-82	ret proto-oncogene	Homo sapiens	145-148
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	diphenyliodonium	185-188	ret proto-oncogene	Homo sapiens	64-67
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	diphenyliodonium	185-188	ret proto-oncogene	Homo sapiens	68-73
24437351-4	2014	H2O2 enhanced the constitutive tyrosine auto-phosphorylation of RET-MEN2A and RET-MEN2B proteins, and this increase was attenuated by treatment with the NOX inhibitor diphenyliodonium (DPI) or catalase.	diphenyliodonium	185-188	ret proto-oncogene	Homo sapiens	78-81
24437351-6	2014	Elevated ROS derived from NOX1 activation and downregulation of SOD in NIH3T3RET-MEN2A and NIH3T3RET-MEN 2B cells may be involved in RET constitutive tyrosine auto-phosphorylation, and scavengers of ROS such as catalase and blocking NOX1 are useful for targeting RET tyrosine kinase activation in cancer.	Reactive Oxygen Species	9-12	ret proto-oncogene	Homo sapiens	81-86
24437351-6	2014	Elevated ROS derived from NOX1 activation and downregulation of SOD in NIH3T3RET-MEN2A and NIH3T3RET-MEN 2B cells may be involved in RET constitutive tyrosine auto-phosphorylation, and scavengers of ROS such as catalase and blocking NOX1 are useful for targeting RET tyrosine kinase activation in cancer.	Reactive Oxygen Species	9-12	ret proto-oncogene	Homo sapiens	77-80
24437351-6	2014	Elevated ROS derived from NOX1 activation and downregulation of SOD in NIH3T3RET-MEN2A and NIH3T3RET-MEN 2B cells may be involved in RET constitutive tyrosine auto-phosphorylation, and scavengers of ROS such as catalase and blocking NOX1 are useful for targeting RET tyrosine kinase activation in cancer.	Reactive Oxygen Species	9-12	ret proto-oncogene	Homo sapiens	97-100
24437351-6	2014	Elevated ROS derived from NOX1 activation and downregulation of SOD in NIH3T3RET-MEN2A and NIH3T3RET-MEN 2B cells may be involved in RET constitutive tyrosine auto-phosphorylation, and scavengers of ROS such as catalase and blocking NOX1 are useful for targeting RET tyrosine kinase activation in cancer.	Tyrosine	150-158	ret proto-oncogene	Homo sapiens	81-86
24437351-6	2014	Elevated ROS derived from NOX1 activation and downregulation of SOD in NIH3T3RET-MEN2A and NIH3T3RET-MEN 2B cells may be involved in RET constitutive tyrosine auto-phosphorylation, and scavengers of ROS such as catalase and blocking NOX1 are useful for targeting RET tyrosine kinase activation in cancer.	Tyrosine	150-158	ret proto-oncogene	Homo sapiens	77-80
24437351-6	2014	Elevated ROS derived from NOX1 activation and downregulation of SOD in NIH3T3RET-MEN2A and NIH3T3RET-MEN 2B cells may be involved in RET constitutive tyrosine auto-phosphorylation, and scavengers of ROS such as catalase and blocking NOX1 are useful for targeting RET tyrosine kinase activation in cancer.	Reactive Oxygen Species	199-202	ret proto-oncogene	Homo sapiens	81-86
24437351-6	2014	Elevated ROS derived from NOX1 activation and downregulation of SOD in NIH3T3RET-MEN2A and NIH3T3RET-MEN 2B cells may be involved in RET constitutive tyrosine auto-phosphorylation, and scavengers of ROS such as catalase and blocking NOX1 are useful for targeting RET tyrosine kinase activation in cancer.	Reactive Oxygen Species	199-202	ret proto-oncogene	Homo sapiens	77-80
24744988-0	2014	Will the Requirement by the US FDA to Simultaneously Co-Develop Companion Diagnostics (CDx) Delay the Approval of Receptor Tyrosine Kinase Inhibitors for RTK-Rearranged (ROS1-, RET-, AXL-, PDGFR-alpha-, NTRK1-) Non-Small Cell Lung Cancer Globally?	Cefadroxil	87-90	ret proto-oncogene	Homo sapiens	177-180
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
24744988-12	2014	Similarly, several marketed tyrosine kinase inhibitors (TKIs) in the US (sorafenib, sunitinib, vandetanib, cabozantinib, regorafenib) are potent RET inhibitors in vitro.	vandetanib	95-105	ret proto-oncogene	Homo sapiens	145-148
24744988-12	2014	Similarly, several marketed tyrosine kinase inhibitors (TKIs) in the US (sorafenib, sunitinib, vandetanib, cabozantinib, regorafenib) are potent RET inhibitors in vitro.	cabozantinib	107-119	ret proto-oncogene	Homo sapiens	145-148
24744988-12	2014	Similarly, several marketed tyrosine kinase inhibitors (TKIs) in the US (sorafenib, sunitinib, vandetanib, cabozantinib, regorafenib) are potent RET inhibitors in vitro.	regorafenib	121-132	ret proto-oncogene	Homo sapiens	145-148
24744988-13	2014	It does not make sense for any one pharmaceutical company to shoulder the full cost of developing a particular CDx for RET-rearranged NSCLC where, once approved, it may be used by other pharmaceutical companies to gain addition labeling approval for their own RET inhibitors.	Cefadroxil	111-114	ret proto-oncogene	Homo sapiens	119-122
24744988-13	2014	It does not make sense for any one pharmaceutical company to shoulder the full cost of developing a particular CDx for RET-rearranged NSCLC where, once approved, it may be used by other pharmaceutical companies to gain addition labeling approval for their own RET inhibitors.	Cefadroxil	111-114	ret proto-oncogene	Homo sapiens	260-263
24563328-3	2014	The expression analysis of selected genes involved in tamoxifen/estrogen and receptor tyrosine kinase signaling pathways can help to further decipher mechanisms of recurrence in ER+ tumors and contribute to the development of prognostic and possibly predictive biomarkers.	Tamoxifen	54-63	ret proto-oncogene	Homo sapiens	77-101
24425877-10	2014	There were only two major ubiquitination sites in Ret51, Lys(1060) and Lys(1107), and the combined mutation of these lysines almost completely eliminated both the ubiquitination and degradation of Ret51.	Lysine	57-60	ret proto-oncogene	Homo sapiens	50-55
24022366-9	2014	We discuss how RET signaling balances activating and inhibitory signals emanating from its docking tyrosines and its interaction with upstream and downstream regulators to precisely modulate different aspects of Wolffian duct patterning and branching morphogenesis.	Tyrosine	99-108	ret proto-oncogene	Homo sapiens	15-18
24425877-10	2014	There were only two major ubiquitination sites in Ret51, Lys(1060) and Lys(1107), and the combined mutation of these lysines almost completely eliminated both the ubiquitination and degradation of Ret51.	Lysine	57-60	ret proto-oncogene	Homo sapiens	197-202
24425877-10	2014	There were only two major ubiquitination sites in Ret51, Lys(1060) and Lys(1107), and the combined mutation of these lysines almost completely eliminated both the ubiquitination and degradation of Ret51.	Lysine	71-74	ret proto-oncogene	Homo sapiens	197-202
24425877-10	2014	There were only two major ubiquitination sites in Ret51, Lys(1060) and Lys(1107), and the combined mutation of these lysines almost completely eliminated both the ubiquitination and degradation of Ret51.	Lysine	117-124	ret proto-oncogene	Homo sapiens	50-55
24425877-10	2014	There were only two major ubiquitination sites in Ret51, Lys(1060) and Lys(1107), and the combined mutation of these lysines almost completely eliminated both the ubiquitination and degradation of Ret51.	Lysine	117-124	ret proto-oncogene	Homo sapiens	197-202
24560924-4	2014	Structural analysis of oncogenic M918T and wild-type RET kinase domains reveal a cis-inhibitory mechanism involving tethering contacts between the glycine-rich loop, activation loop, and alphaC-helix.	Glycine	147-154	ret proto-oncogene	Homo sapiens	53-56
24327398-1	2014	BACKGROUND: In their previous analysis of papillary thyroid carcinomas (PTCs) from an Ukrainian-American cohort that was exposed to iodine-131 ((131) I) from the Chernobyl accident, the authors identified RET/PTC rearrangements and other driver mutations in 60% of tumors.	Iodine	132-138	ret proto-oncogene	Homo sapiens	205-208
24327398-1	2014	BACKGROUND: In their previous analysis of papillary thyroid carcinomas (PTCs) from an Ukrainian-American cohort that was exposed to iodine-131 ((131) I) from the Chernobyl accident, the authors identified RET/PTC rearrangements and other driver mutations in 60% of tumors.	Iodine	132-138	ret proto-oncogene	Homo sapiens	72-75
24900886-4	2014	Kinase selectivity profiling revealed that 14c was a multitargeted inhibitor, and it also exhibited good potency against VEGFR-1, PDGFR-beta, and RET.	Carbon-14	43-46	ret proto-oncogene	Homo sapiens	146-149
24399074-2	2014	The aim of the present study was to investigate whether vandetanib (a RET inhibitor) inhibits proliferation, migration and invasion of NB cells in vitro.	vandetanib	56-66	ret proto-oncogene	Homo sapiens	70-73
24336963-5	2014	We mapped the deleterious mutants, modelled mutant proteins and deciphered the impact of mutations on drug binding mechanisms in the RET crystal structure of PDB ID: with the potential inhibitor vandetanib by docking analysis.	vandetanib	195-205	ret proto-oncogene	Homo sapiens	133-136
24559322-1	2014	Regorafenib is an oral multikinase inhibitor that blocks the activity of protein kinases involved in the regulation of tumor angiogenesis (VEGFR1, 2, 3; angiopoietin-1 receptor), oncogenesis (stem cell growth factor receptor; RET; BRAF including BRAFV600E), and tumor microenvironment (PDGFR-beta and FGFR).	regorafenib	0-11	ret proto-oncogene	Homo sapiens	226-229
24342537-6	2014	RESULTS: aPS/PT were found in 41.3% and 46.7% of SLE patients by the aPS/PT(ih) and the aPS/PT(c), respectively.	Adenosine Phosphosulfate	9-12	ret proto-oncogene	Homo sapiens	92-97
24342537-6	2014	RESULTS: aPS/PT were found in 41.3% and 46.7% of SLE patients by the aPS/PT(ih) and the aPS/PT(c), respectively.	Platinum	13-15	ret proto-oncogene	Homo sapiens	92-97
24190702-1	2014	PURPOSE: Lenvatinib is an oral multi-targeted tyrosine kinase inhibitor of VEGFR1-3, FGFR1-4, PDGFRbeta, RET, and KIT.	lenvatinib	9-19	ret proto-oncogene	Homo sapiens	105-108
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
24276455-6	2014	RESULTS: Sunitinib and cisplatin synergistically inhibited the growth of MZ-CRC-1 cells harboring the RET M918T activating mutation.	Cisplatin	23-32	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.	Cisplatin	25-34	ret proto-oncogene	Homo sapiens	142-145
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
23885719-0	2014	Effects of silencing the RET/PTC1 oncogene in papillary thyroid carcinoma by siRNA-squalene nanoparticles with and without fusogenic companion GALA-cholesterol.	Squalene	83-91	ret proto-oncogene	Homo sapiens	25-28
24256343-7	2014	RESULTS: Vandetanib displays antiproliferative and antiangiogenic activities and inhibits RET autophosphorylation.	vandetanib	9-19	ret proto-oncogene	Homo sapiens	90-93
24756792-1	2014	Regorafenib (BAY 73-4506, Stivarga ) is an oral diphenylurea multikinase inhibitor that targets angiogenic (VEGFR1-3, TIE2), stromal (PDGFR-beta, FGFR), and oncogenic receptor tyrosine kinases (KIT, RET, and RAF).	regorafenib	0-11	ret proto-oncogene	Homo sapiens	199-202
24756792-1	2014	Regorafenib (BAY 73-4506, Stivarga ) is an oral diphenylurea multikinase inhibitor that targets angiogenic (VEGFR1-3, TIE2), stromal (PDGFR-beta, FGFR), and oncogenic receptor tyrosine kinases (KIT, RET, and RAF).	regorafenib	13-24	ret proto-oncogene	Homo sapiens	199-202
24756794-0	2014	Cabozantinib: a MET, RET, and VEGFR2 tyrosine kinase inhibitor.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	21-24
24756794-1	2014	Cabozantinib is a receptor tyrosine kinase inhibitor with activity against MET, VEGFR2, FLT3, c-KIT, and RET.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	105-108
24299515-4	2014	Vandetanib, initially developed to target other receptors, demonstrated anti-rearranged during transfection (anti-RET) kinase activity.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	114-117
24272205-6	2014	CDKN2A, IDH2, MET, and RET mutations were observed only in EGC.	(-)-Epigallocatechin	59-62	ret proto-oncogene	Homo sapiens	23-26
25295214-2	2014	Lenvatinib mesilate (lenvatinib) is a potent inhibitor of VEGF receptors (VEGFR1-3) and other prooncogenic and prooncogenic receptor tyrosine kinases, including fibroblast growth factor receptors (FGFR1-4), platelet derived growth factor receptor alpha (PDGFRalpha), KIT, and RET.	LENVATINIB MESYLATE	0-19	ret proto-oncogene	Homo sapiens	276-279
25295214-2	2014	Lenvatinib mesilate (lenvatinib) is a potent inhibitor of VEGF receptors (VEGFR1-3) and other prooncogenic and prooncogenic receptor tyrosine kinases, including fibroblast growth factor receptors (FGFR1-4), platelet derived growth factor receptor alpha (PDGFRalpha), KIT, and RET.	lenvatinib	21-31	ret proto-oncogene	Homo sapiens	276-279
25295214-7	2014	Lenvatinib also inhibited the phosphorylation of RET with the activated mutation C634W in TT cells.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	49-52
25295214-8	2014	These data demonstrate that lenvatinib provides antitumor activity mainly via angiogenesis inhibition but also inhibits FGFR and RET signaling pathway in preclinical human thyroid cancer models.	lenvatinib	28-38	ret proto-oncogene	Homo sapiens	129-132
23872421-9	2013	Collectively, these findings demonstrated the hitherto unrecognized and novel role of specific GFRalpha2 and RET isoforms in mediating NRTN activation of STAT3 and the transcription independent mechanism whereby the mitochondria localized P-Ser-STAT3 mediated NRTN induced neurite outgrowth.	Serine	241-244	ret proto-oncogene	Homo sapiens	109-112
24386391-5	2013	The phosphomimic at this site confers a level of kinase activation and NFkappaB nuclear localization exceeding the iconic mutant S177E/S181E, demonstrating that RTK-mediated Tyr phosphorylation of IKKbeta has the potential to directly regulate NFkappaB transcriptional activation.	Tyrosine	174-177	ret proto-oncogene	Homo sapiens	161-164
24391906-6	2013	We propose a model in which retinoid signaling in the stroma activates expression of Ecm1, which in turn down-regulates Ret expression in the ureteric bud cleft, where bifurcation normally occurs and normal branching progresses.	Retinoids	28-36	ret proto-oncogene	Homo sapiens	120-123
23705946-0	2013	In vitro and in vivo activity of cabozantinib (XL184), an inhibitor of RET, MET, and VEGFR2, in a model of medullary thyroid cancer.	cabozantinib	33-45	ret proto-oncogene	Homo sapiens	71-74
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
24005613-3	2013	Vandetanib is an oral once daily administered inhibitor of VEGFR-, EGFR- and RET-signaling with activity in combination with chemotherapy in some solid tumours.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	77-80
23705946-3	2013	Cabozantinib is a potent inhibitor of MET, RET, and vascular endothelial factor receptor 2 (VEGFR2), as well as other tyrosine kinases that have been implicated in tumor development and progression.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	43-46
24061856-4	2013	We now demonstrate that such intracellular cAMP regulation is mediated by a novel noncanonical signaling pathway resulting from OPRM1 being converted to a receptor tyrosine kinase (RTK)-like entity.	Cyclic AMP	43-47	ret proto-oncogene	Homo sapiens	155-179
24061856-4	2013	We now demonstrate that such intracellular cAMP regulation is mediated by a novel noncanonical signaling pathway resulting from OPRM1 being converted to a receptor tyrosine kinase (RTK)-like entity.	Cyclic AMP	43-47	ret proto-oncogene	Homo sapiens	181-184
24061856-9	2013	Hence, the phosphorylation of OPRM1 at Tyr(336) by Src serves as the trigger for the conversion of a classic Gi/Go-coupled receptor into an RTK-like entity, resulting in a noncanonical pathway even after the original Gi/Go signals are blunted.	Tyrosine	39-42	ret proto-oncogene	Homo sapiens	140-143
23705946-0	2013	In vitro and in vivo activity of cabozantinib (XL184), an inhibitor of RET, MET, and VEGFR2, in a model of medullary thyroid cancer.	cabozantinib	47-52	ret proto-oncogene	Homo sapiens	71-74
23705946-4	2013	The object of this study was to determine the in vitro biochemical and cellular inhibitory profile of cabozantinib against RET, and in vivo antitumor efficacy using a xenograft model of MTC.	cabozantinib	102-114	ret proto-oncogene	Homo sapiens	123-126
23705946-5	2013	METHODS: Cabozantinib was evaluated in biochemical and cell-based assays that determined the potency of the compound against wild type and activating mutant forms of RET.	cabozantinib	9-21	ret proto-oncogene	Homo sapiens	166-169
24131278-4	2013	For the detection of C533G mutation of the RET gene, biotinylated oligonucleotide probes were used.	Oligonucleotides	66-81	ret proto-oncogene	Homo sapiens	43-46
23705946-7	2013	RESULTS: In biochemical assays, cabozantinib inhibited multiple forms of oncogenic RET kinase activity, including M918T and Y791F mutants.	cabozantinib	32-44	ret proto-oncogene	Homo sapiens	83-86
23705946-10	2013	Moreover, immunohistochemical analyses of tumors revealed that cabozantinib reduced levels of phosphorylated MET and RET, and decreased tumor cellularity, proliferation, and vascularization.	cabozantinib	63-75	ret proto-oncogene	Homo sapiens	117-120
23705946-11	2013	CONCLUSIONS: Cabozantinib is a potent inhibitor of RET and prevalent mutationally activated forms of RET known to be associated with MTC, and effectively inhibits the growth of a MTC tumor cell model in vitro and in vivo.	cabozantinib	13-25	ret proto-oncogene	Homo sapiens	51-54
23705946-11	2013	CONCLUSIONS: Cabozantinib is a potent inhibitor of RET and prevalent mutationally activated forms of RET known to be associated with MTC, and effectively inhibits the growth of a MTC tumor cell model in vitro and in vivo.	cabozantinib	13-25	ret proto-oncogene	Homo sapiens	101-104
23991695-6	2013	Clinical trials are underway to investigate the therapeutic effects of RET tyrosine kinase inhibitors, such as vandetanib (ZD6474) and cabozantinib (XL184), in patients with RET fusion-positive non-small-cell lung cancer.	vandetanib	111-121	ret proto-oncogene	Homo sapiens	71-74
24235841-4	2013	The paraganglioma responded to sorafenib, a novel multi-tyrosine kinase inhibitor that targets angiogenesis, the Raf-kinase pathway, the platelet-derived growth factor Ret, and c-Kit.	Sorafenib	31-40	ret proto-oncogene	Homo sapiens	168-171
23991695-6	2013	Clinical trials are underway to investigate the therapeutic effects of RET tyrosine kinase inhibitors, such as vandetanib (ZD6474) and cabozantinib (XL184), in patients with RET fusion-positive non-small-cell lung cancer.	vandetanib	111-121	ret proto-oncogene	Homo sapiens	174-177
23991695-6	2013	Clinical trials are underway to investigate the therapeutic effects of RET tyrosine kinase inhibitors, such as vandetanib (ZD6474) and cabozantinib (XL184), in patients with RET fusion-positive non-small-cell lung cancer.	vandetanib	123-129	ret proto-oncogene	Homo sapiens	71-74
23991695-6	2013	Clinical trials are underway to investigate the therapeutic effects of RET tyrosine kinase inhibitors, such as vandetanib (ZD6474) and cabozantinib (XL184), in patients with RET fusion-positive non-small-cell lung cancer.	vandetanib	123-129	ret proto-oncogene	Homo sapiens	174-177
23991695-6	2013	Clinical trials are underway to investigate the therapeutic effects of RET tyrosine kinase inhibitors, such as vandetanib (ZD6474) and cabozantinib (XL184), in patients with RET fusion-positive non-small-cell lung cancer.	cabozantinib	135-147	ret proto-oncogene	Homo sapiens	174-177
23856028-2	2013	For MTC therapy, the Food and Drug Administration recently approved vandetanib and cabozantinib, multi-kinase inhibitors targeting RET and other tyrosine kinase receptors of vascular endothelial growth factor, epidermal growth factor, or hepatocyte growth factor.	vandetanib	68-78	ret proto-oncogene	Homo sapiens	131-134
24002501-1	2013	PURPOSE: Cabozantinib, a tyrosine kinase inhibitor (TKI) of hepatocyte growth factor receptor (MET), vascular endothelial growth factor receptor 2, and rearranged during transfection (RET), demonstrated clinical activity in patients with medullary thyroid cancer (MTC) in phase I.	cabozantinib	9-21	ret proto-oncogene	Homo sapiens	152-182
24002501-7	2013	Prolonged PFS with cabozantinib was observed across all subgroups including by age, prior TKI treatment, and RET mutation status (hereditary or sporadic).	cabozantinib	19-31	ret proto-oncogene	Homo sapiens	109-112
23856031-0	2013	Antitumor activities of the targeted multi-tyrosine kinase inhibitor lenvatinib (E7080) against RET gene fusion-driven tumor models.	lenvatinib	69-79	ret proto-oncogene	Homo sapiens	96-99
23856031-0	2013	Antitumor activities of the targeted multi-tyrosine kinase inhibitor lenvatinib (E7080) against RET gene fusion-driven tumor models.	lenvatinib	81-86	ret proto-oncogene	Homo sapiens	96-99
23856031-3	2013	Here we evaluated lenvatinib in RET gene fusion-driven preclinical models.	lenvatinib	18-28	ret proto-oncogene	Homo sapiens	32-35
23856031-4	2013	In cellular assays, lenvatinib inhibited auto-phosphorylation of KIF5B-RET, CCDC6-RET, and NcoA4-RET.	lenvatinib	20-30	ret proto-oncogene	Homo sapiens	71-74
23856031-4	2013	In cellular assays, lenvatinib inhibited auto-phosphorylation of KIF5B-RET, CCDC6-RET, and NcoA4-RET.	lenvatinib	20-30	ret proto-oncogene	Homo sapiens	82-85
23856031-4	2013	In cellular assays, lenvatinib inhibited auto-phosphorylation of KIF5B-RET, CCDC6-RET, and NcoA4-RET.	lenvatinib	20-30	ret proto-oncogene	Homo sapiens	82-85
23856031-5	2013	Lenvatinib suppressed the growth of CCDC6-RET human thyroid and lung cancer cell lines, and as well, suppressed anchorage-independent growth and tumorigenicity of RET gene fusion-transformed NIH3T3 cells.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	42-45
23856031-5	2013	Lenvatinib suppressed the growth of CCDC6-RET human thyroid and lung cancer cell lines, and as well, suppressed anchorage-independent growth and tumorigenicity of RET gene fusion-transformed NIH3T3 cells.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	163-166
23856031-6	2013	These results demonstrate that lenvatinib can exert antitumor activity against RET gene fusion-driven tumor models by inhibiting oncogenic RET gene fusion signaling.	lenvatinib	31-41	ret proto-oncogene	Homo sapiens	79-82
23856031-6	2013	These results demonstrate that lenvatinib can exert antitumor activity against RET gene fusion-driven tumor models by inhibiting oncogenic RET gene fusion signaling.	lenvatinib	31-41	ret proto-oncogene	Homo sapiens	139-142
23856028-2	2013	For MTC therapy, the Food and Drug Administration recently approved vandetanib and cabozantinib, multi-kinase inhibitors targeting RET and other tyrosine kinase receptors of vascular endothelial growth factor, epidermal growth factor, or hepatocyte growth factor.	cabozantinib	83-95	ret proto-oncogene	Homo sapiens	131-134
23584948-3	2013	Vandetanib (Caprelsa( ), AstraZeneca) is a once-daily oral tyrosine kinase inhibitor that selectively inhibits signalling mediated by growth-factor receptor tyrosine kinase RET (constitutively activated in roughly 60 % of all MTCs), vascular endothelial growth-factor receptors 2 and 3, and epidermal growth-factor receptors.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	173-176
23584948-3	2013	Vandetanib (Caprelsa( ), AstraZeneca) is a once-daily oral tyrosine kinase inhibitor that selectively inhibits signalling mediated by growth-factor receptor tyrosine kinase RET (constitutively activated in roughly 60 % of all MTCs), vascular endothelial growth-factor receptors 2 and 3, and epidermal growth-factor receptors.	vandetanib	12-20	ret proto-oncogene	Homo sapiens	173-176
23584948-3	2013	Vandetanib (Caprelsa( ), AstraZeneca) is a once-daily oral tyrosine kinase inhibitor that selectively inhibits signalling mediated by growth-factor receptor tyrosine kinase RET (constitutively activated in roughly 60 % of all MTCs), vascular endothelial growth-factor receptors 2 and 3, and epidermal growth-factor receptors.	astrazeneca	25-36	ret proto-oncogene	Homo sapiens	173-176
24040417-4	2013	The purpose of this study was to investigate these initial events through the detection of aphidicolin (APH)-induced DNA breakage within the RET oncogene, in which 144 APH-induced DNA breakpoints were mapped on the nucleotide level in human thyroid cells within intron 11 of RET, the breakpoint cluster region found in patients.	Aphidicolin	91-102	ret proto-oncogene	Homo sapiens	141-144
23921591-5	2013	TGF-beta-mediated GDNF signaling slightly elevated the phosphorylation state of Ret, the canonical coreceptor for the GPI-linked (glycosyl-phosphatidylinositol) GFRa1.	gpi-linked (glycosyl-phosphatidylinositol	118-159	ret proto-oncogene	Homo sapiens	80-83
24040417-4	2013	The purpose of this study was to investigate these initial events through the detection of aphidicolin (APH)-induced DNA breakage within the RET oncogene, in which 144 APH-induced DNA breakpoints were mapped on the nucleotide level in human thyroid cells within intron 11 of RET, the breakpoint cluster region found in patients.	Aphidicolin	91-102	ret proto-oncogene	Homo sapiens	275-278
24040417-4	2013	The purpose of this study was to investigate these initial events through the detection of aphidicolin (APH)-induced DNA breakage within the RET oncogene, in which 144 APH-induced DNA breakpoints were mapped on the nucleotide level in human thyroid cells within intron 11 of RET, the breakpoint cluster region found in patients.	Aphidicolin	104-107	ret proto-oncogene	Homo sapiens	141-144
24040417-4	2013	The purpose of this study was to investigate these initial events through the detection of aphidicolin (APH)-induced DNA breakage within the RET oncogene, in which 144 APH-induced DNA breakpoints were mapped on the nucleotide level in human thyroid cells within intron 11 of RET, the breakpoint cluster region found in patients.	Aphidicolin	104-107	ret proto-oncogene	Homo sapiens	275-278
24040417-6	2013	Co-treatment of thyroid cells with APH and the topoisomerase catalytic inhibitors, betulinic acid and merbarone, significantly decreased APH-induced fragile site breakage within RET intron 11 and within the common fragile site FRA3B.	betulinic acid	83-97	ret proto-oncogene	Homo sapiens	178-181
24040417-6	2013	Co-treatment of thyroid cells with APH and the topoisomerase catalytic inhibitors, betulinic acid and merbarone, significantly decreased APH-induced fragile site breakage within RET intron 11 and within the common fragile site FRA3B.	merbarone	102-111	ret proto-oncogene	Homo sapiens	178-181
23766359-2	2013	Vandetanib, a VEGF and EGF receptor inhibitor, blocks RET tyrosine kinase activity and is active in adults with hereditary MTC.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	54-57
23828865-4	2013	Treatment of the RET mutant cell lines TT, TPC-1, and MZ-CRC-1 with AST487, a RET kinase inhibitor, suppressed growth and showed profound and sustained inhibition of mTOR signaling, which was recapitulated by siRNA-mediated RET knockdown.	AST 487	68-74	ret proto-oncogene	Homo sapiens	17-20
23828865-4	2013	Treatment of the RET mutant cell lines TT, TPC-1, and MZ-CRC-1 with AST487, a RET kinase inhibitor, suppressed growth and showed profound and sustained inhibition of mTOR signaling, which was recapitulated by siRNA-mediated RET knockdown.	AST 487	68-74	ret proto-oncogene	Homo sapiens	78-81
23828865-4	2013	Treatment of the RET mutant cell lines TT, TPC-1, and MZ-CRC-1 with AST487, a RET kinase inhibitor, suppressed growth and showed profound and sustained inhibition of mTOR signaling, which was recapitulated by siRNA-mediated RET knockdown.	AST 487	68-74	ret proto-oncogene	Homo sapiens	78-81
23766359-12	2013	CONCLUSION: Using an innovative trial design and selecting patients based on target gene expression, we conclude that vandetanib 100 mg/m(2)/d is a well-tolerated and highly active new treatment for children and adolescents with MEN2B and locally advanced or metastatic MTC.	vandetanib	118-128	ret proto-oncogene	Homo sapiens	229-234
24169328-15	2013	CONCLUSIONS: The mutations of RET proto-oncognene of PHEO in MEN2A are frequently located at codon 634.	proto-oncognene	34-49	ret proto-oncogene	Homo sapiens	30-33
24169328-15	2013	CONCLUSIONS: The mutations of RET proto-oncognene of PHEO in MEN2A are frequently located at codon 634.	proto-oncognene	34-49	ret proto-oncogene	Homo sapiens	61-66
23738733-8	2013	The Alphascreen phosphotyrosine assay kit was used to investigate PDGFbeta receptor tyrosine kinase inhibition by suramin.	Suramin	114-121	ret proto-oncogene	Homo sapiens	75-99
23822199-7	2013	RESULTS: Vandetanib displays antiproliferative and antiangiogenic activities and inhibits RET auto-phosphorylation.	vandetanib	9-19	ret proto-oncogene	Homo sapiens	90-93
23578175-10	2013	Moreover, treatment with RET-inhibitors, including vandetanib, reduced cell viability, which was accompanied by the downregulation of the AKT and ERK1/2 signaling pathways.	vandetanib	51-61	ret proto-oncogene	Homo sapiens	25-28
23560814-1	2013	Ret transgenic mouse model of skin malignant melanoma is characterized by the overexpression of the human ret transgene in melanin-containing cells.	Melanins	123-130	ret proto-oncogene	Homo sapiens	106-109
23650283-8	2013	Both these effects were selectively reverted by the RET kinase inhibitor, NVP-BBT594.	BBT594	78-84	ret proto-oncogene	Homo sapiens	52-55
23533264-0	2013	Response to Cabozantinib in patients with RET fusion-positive lung adenocarcinomas.	cabozantinib	12-24	ret proto-oncogene	Homo sapiens	42-45
23533264-5	2013	We report preliminary data for the first three patients treated with the RET inhibitor cabozantinib on a prospective phase II trial for patients with RET fusion-positive NSCLCs (NCT01639508).	cabozantinib	87-99	ret proto-oncogene	Homo sapiens	73-76
23533264-5	2013	We report preliminary data for the first three patients treated with the RET inhibitor cabozantinib on a prospective phase II trial for patients with RET fusion-positive NSCLCs (NCT01639508).	cabozantinib	87-99	ret proto-oncogene	Homo sapiens	150-153
23690991-0	2013	miR-219-5p inhibits receptor tyrosine kinase pathway by targeting EGFR in glioblastoma.	mir-219-5p	0-10	ret proto-oncogene	Homo sapiens	20-44
23487538-2	2013	Vandetanib, a tyrosine kinase inhibitor (TKI) targeting vascular endothelial growth factor receptor 2, epidermal growth factor receptor, and RET, has been approved by the FDA for the treatment of locally advanced or metastatic MTC.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	141-144
23436219-0	2013	RET/PTC and PAX8/PPARgamma chromosomal rearrangements in post-Chernobyl thyroid cancer and their association with iodine-131 radiation dose and other characteristics.	Iodine	114-120	ret proto-oncogene	Homo sapiens	0-3
23436219-11	2013	These data support the relationship between chromosomal rearrangements, but not point mutations, and (131) I exposure and point to a possible role of iodine deficiency in generation of RET/PTC rearrangements in these patients.	Iodine	150-156	ret proto-oncogene	Homo sapiens	185-188
23329180-1	2013	Mutations in REarranged during Transfection (RET) receptor tyrosine, followed by the oncogenic activation of RET kinase is responsible for the development of medullary thyroid carcinoma (MTC) that responds poorly to conventional chemotherapy.	Tyrosine	59-67	ret proto-oncogene	Homo sapiens	13-43
23329180-1	2013	Mutations in REarranged during Transfection (RET) receptor tyrosine, followed by the oncogenic activation of RET kinase is responsible for the development of medullary thyroid carcinoma (MTC) that responds poorly to conventional chemotherapy.	Tyrosine	59-67	ret proto-oncogene	Homo sapiens	45-48
23329180-5	2013	A search for the upstream signaling revealed that theaflavin-induced disruption of lipid raft caused interference in anchorage of RET in lipid raft that in turn stalled phosphorylation of Ras and PI3Kinase.	theaflavin	50-60	ret proto-oncogene	Homo sapiens	130-133
23329180-7	2013	These findings not only unveil a hitherto unexplained mechanism underlying theaflavin-induced MTC death, but also validate RET as a promising and potential target for MTC therapy.	theaflavin	75-85	ret proto-oncogene	Homo sapiens	123-126
23526464-0	2013	Ponatinib (AP24534) is a novel potent inhibitor of oncogenic RET mutants associated with thyroid cancer.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	61-64
23526464-0	2013	Ponatinib (AP24534) is a novel potent inhibitor of oncogenic RET mutants associated with thyroid cancer.	ponatinib	11-18	ret proto-oncogene	Homo sapiens	61-64
23526464-3	2013	OBJECTIVE: We tested whether ponatinib inhibited RET kinase and oncogenic activity.	ponatinib	29-38	ret proto-oncogene	Homo sapiens	49-52
23526464-4	2013	METHODS: Ponatinib activity was studied by an in vitro RET immunocomplex kinase assay and immunoblotting.	ponatinib	9-18	ret proto-oncogene	Homo sapiens	55-58
23526464-7	2013	RESULTS: Ponatinib inhibited immunopurified RET kinase at the IC50 of 25.8 nM (95% confidence interval [CI] = 23.15-28.77 nM).	ponatinib	9-18	ret proto-oncogene	Homo sapiens	44-47
23526464-9	2013	Ponatinib blunted phosphorylation of point-mutant and rearranged RET-derived oncoproteins and inhibited proliferation of RET-transformed fibroblasts and RET mutant thyroid carcinoma cells.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	65-68
23526464-9	2013	Ponatinib blunted phosphorylation of point-mutant and rearranged RET-derived oncoproteins and inhibited proliferation of RET-transformed fibroblasts and RET mutant thyroid carcinoma cells.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	121-124
23526464-9	2013	Ponatinib blunted phosphorylation of point-mutant and rearranged RET-derived oncoproteins and inhibited proliferation of RET-transformed fibroblasts and RET mutant thyroid carcinoma cells.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	121-124
23526464-11	2013	Ponatinib-treated TT cell tumors displayed a reduction in the mitotic index, RET phosphorylation, and signaling.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	77-80
23526464-12	2013	CONCLUSIONS: Ponatinib is a potent inhibitor of RET kinase and has promising preclinical activity in models of RET-driven medullary thyroid carcinoma.	ponatinib	13-22	ret proto-oncogene	Homo sapiens	48-51
23526464-12	2013	CONCLUSIONS: Ponatinib is a potent inhibitor of RET kinase and has promising preclinical activity in models of RET-driven medullary thyroid carcinoma.	ponatinib	13-22	ret proto-oncogene	Homo sapiens	111-114
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
23584301-0	2013	A patient with lung adenocarcinoma and RET fusion treated with vandetanib.	vandetanib	63-73	ret proto-oncogene	Homo sapiens	39-42
23533265-5	2013	Cancer cells driven by ALK amplification and oncogenic rearrangements of ROS1 and RET kinase genes were also sensitive to ganetespib exposure.	STA 9090	122-132	ret proto-oncogene	Homo sapiens	82-85
23610528-2	2013	Regorafenib is an oral small-molecule multi kinase inhibitor, binding to several intracellular kinases, with powerful inhibitory activity against vascular endothelial growth factor receptors (VEGFR-1,VEGFR-2, and VEGFR-3), platelet-derived growth factor receptor, fibroblast growth factor receptor 1, Raf, TIE-2, and the kinases KIT, RET, and BRAF.	regorafenib	0-11	ret proto-oncogene	Homo sapiens	334-337
23547958-16	2013	CONCLUSIONS: Sporadic PHPT, MEN1- and MEN2A-related PHPT are three distinct entities as is reflected preoperatively by differences in gender, age at diagnosis and calcium and PTH levels.	Calcium	163-170	ret proto-oncogene	Homo sapiens	38-43
23229684-0	2013	(18)F-DOPA PET/CT revealed synchronous neuroendocrine tumors in two sisters with MEN2A syndrome.	fluorodopa F 18	4-10	ret proto-oncogene	Homo sapiens	81-86
23231950-1	2013	Vandetanib (ZD6474, Caprelsa, AstraZeneca), an oral small-molecule tyrosine kinase inhibitor (TKI) that targets the rearranged during transfection receptor (RET), VEGF receptor (VEGFR2-3), and EGF receptor (EGFR), is the first systemic therapy approved by the U.S. Food and Drug Administration (FDA) for the treatment of symptomatic or progressive advanced medullary thyroid cancer (MTC).	vandetanib	0-10	ret proto-oncogene	Homo sapiens	157-160
23544171-12	2013	Importantly, phospho-RTK arrays revealed novel targets for cediranib and sunitinib therapy.	cediranib	59-68	ret proto-oncogene	Homo sapiens	21-24
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
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.	motesanib diphosphate	0-9	ret proto-oncogene	Homo sapiens	182-185
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.	Sorafenib	11-20	ret proto-oncogene	Homo sapiens	182-185
23274758-1	2013	The effectiveness of vandetanib, an agent that targets RET, VEGFR and EGFR signaling, against EGFR-mutant lung cancer cells with PTEN loss was investigated.	vandetanib	21-31	ret proto-oncogene	Homo sapiens	55-58
23660265-7	2013	Gene analysis confirmed heterozygous mis-sense mutation at codon 918 in exon 16 of RET proto-oncogene in which thymine was replaced by cytosine (ATG ACG).	Thymine	111-118	ret proto-oncogene	Homo sapiens	83-86
23660265-7	2013	Gene analysis confirmed heterozygous mis-sense mutation at codon 918 in exon 16 of RET proto-oncogene in which thymine was replaced by cytosine (ATG ACG).	Cytosine	135-143	ret proto-oncogene	Homo sapiens	83-86
23660265-7	2013	Gene analysis confirmed heterozygous mis-sense mutation at codon 918 in exon 16 of RET proto-oncogene in which thymine was replaced by cytosine (ATG ACG).	acceleratory factor from growth hormone	149-152	ret proto-oncogene	Homo sapiens	83-86
23552883-0	2013	Downregulation of miRNA-31 induces taxane resistance in ovarian cancer cells through increase of receptor tyrosine kinase MET.	mirna-31	18-26	ret proto-oncogene	Homo sapiens	97-121
23552883-0	2013	Downregulation of miRNA-31 induces taxane resistance in ovarian cancer cells through increase of receptor tyrosine kinase MET.	taxane	35-41	ret proto-oncogene	Homo sapiens	97-121
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.	vandetanib	22-32	ret proto-oncogene	Homo sapiens	182-185
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
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.	lenvatinib	45-55	ret proto-oncogene	Homo sapiens	182-185
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.	Imatinib Mesylate	57-65	ret proto-oncogene	Homo sapiens	182-185
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.	cabozantinib	70-82	ret proto-oncogene	Homo sapiens	182-185
23554805-4	2013	A missense mutation of TGG (Trp) to TGC (Cys) at codon 634 (the classic MEN2A mutation) in exon 11 of the RET gene was detected in 3 family members, including the proband.	Tryptophan	28-31	ret proto-oncogene	Homo sapiens	72-77
23554805-4	2013	A missense mutation of TGG (Trp) to TGC (Cys) at codon 634 (the classic MEN2A mutation) in exon 11 of the RET gene was detected in 3 family members, including the proband.	Tryptophan	28-31	ret proto-oncogene	Homo sapiens	106-109
23554805-4	2013	A missense mutation of TGG (Trp) to TGC (Cys) at codon 634 (the classic MEN2A mutation) in exon 11 of the RET gene was detected in 3 family members, including the proband.	Cysteine	41-44	ret proto-oncogene	Homo sapiens	72-77
23554805-4	2013	A missense mutation of TGG (Trp) to TGC (Cys) at codon 634 (the classic MEN2A mutation) in exon 11 of the RET gene was detected in 3 family members, including the proband.	Cysteine	41-44	ret proto-oncogene	Homo sapiens	106-109
23063249-3	2013	The aim of this study was to investigate whether the Ret-He level as calculated by the Sysmex XE-5000 automated blood analyser is a useful parameter for the diagnosis of IDA in a geriatric hospitalized population.	Helium	57-59	ret proto-oncogene	Homo sapiens	53-56
24501868-6	2013	RESULTS: After HT along with the increase of Hb from 89, 7+/-10,0 to 119+/-13,3, there was significant decrease in Ret % from 2,4+/-1,1 to 1,4+/-0,5 7-10 day after HT There was also a reduction of Thr from 391,5+/-131,5 to 250, 7+/-57,2 and blood lactate in mmol/l from 2,5+/-1,1 to 1,5+/-0,7.	Threonine	197-200	ret proto-oncogene	Homo sapiens	115-118
24501868-6	2013	RESULTS: After HT along with the increase of Hb from 89, 7+/-10,0 to 119+/-13,3, there was significant decrease in Ret % from 2,4+/-1,1 to 1,4+/-0,5 7-10 day after HT There was also a reduction of Thr from 391,5+/-131,5 to 250, 7+/-57,2 and blood lactate in mmol/l from 2,5+/-1,1 to 1,5+/-0,7.	Lactic Acid	247-254	ret proto-oncogene	Homo sapiens	115-118
23202050-3	2013	Vandetanib selectively targets RET, vascular endothelial growth factor receptor-2, and epidermal growth factor receptor dependent signaling.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	31-34
23873422-4	2013	RESULTS: Molecular-genetic examination of VHL, RET, SDHB, SDHC and SDHD genes revealed inherited predisposition for PHEO in three of 15 patients (20%): RET mutations typical for MEN 2a in two patients and VHL mutation in one patient.	pheo	116-120	ret proto-oncogene	Homo sapiens	152-155
23158190-0	2012	Novel withanolides target medullary thyroid cancer through inhibition of both RET phosphorylation and the mammalian target of rapamycin pathway.	Withanolides	6-18	ret proto-oncogene	Homo sapiens	78-81
23802154-6	2013	Results suggest that occupational exposure to low doses of airborne Pb is able to influence lines of the hematopoietic system in exposed workers, with special reference to %RET.	Lead	68-70	ret proto-oncogene	Homo sapiens	173-176
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
23319867-3	2013	Cabozantinib is an orally bioavailable tyrosine kinase inhibitor which blocks MET, VEGRF2 and RET, and has shown considerable activity in medullary thyroid cancer in a Phase III trial, including in heavily pretreated patients.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	94-97
23154560-4	2012	LC-2/ad showed distinctive sensitivity to the RET inhibitor, vandetanib, among 39 non-small lung cancer cell lines.	vandetanib	61-71	ret proto-oncogene	Homo sapiens	46-49
23158190-7	2012	Unique from other targeted therapies, withanolides suppressed RET and Akt phosphorylation and protein expression (in a concentration- and time-dependent manner) as well as mTOR activity and translational activity of 4E-BP1 and protein synthesis mediated by p70S6kinase activation at IC(50) concentrations.	Withanolides	38-50	ret proto-oncogene	Homo sapiens	62-65
23158190-3	2012	We hypothesize that these withanolides uniquely inhibit RET phosphorylation and the mammalian target of rapamycin (mTOR) pathway in MTC cells as a mechanism of antiproliferation and apoptosis.	Withanolides	26-38	ret proto-oncogene	Homo sapiens	56-59
23355942-4	2012	The aim of this study was to establish short-term effects of iron supplementation on the hemoglobin content of reticulocytes (Ret-He) and red blood cells (RBC-He) in case of suspected iron deficient erythropoiesis (IDE) in the third trimester of pregnancy.	Iron	61-65	ret proto-oncogene	Homo sapiens	126-129
23355942-6	2012	After iron supplementation, reticulocyte counts increased from 0.061+-0.015x10(12)/L to 0.079+-0.026x10(12)/L and Ret-He increased from 23.6+-2.8 pg to 28.3+-2.6 pg (P=&lt;0.001).	Iron	6-10	ret proto-oncogene	Homo sapiens	114-117
23104465-3	2012	Cabozantinib is an oral multitargeted TKI with activity against multiple receptors including RET, vascular endothelial growth factor receptor type 2 (VEGFR2), and MET that has been evaluated in MTC in the preclinical and clinical arenas.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	93-96
23170308-4	2012	In addition, vandetanib is an inhibitor of the RET (rearranged during transfection) gene, a proto-oncogene often mutated in familial MTC.	vandetanib	13-23	ret proto-oncogene	Homo sapiens	47-50
23170308-4	2012	In addition, vandetanib is an inhibitor of the RET (rearranged during transfection) gene, a proto-oncogene often mutated in familial MTC.	vandetanib	13-23	ret proto-oncogene	Homo sapiens	52-82
22898678-2	2012	We aimed to assess efficacy and safety of vandetanib, a tyrosine kinase inhibitor of RET, VEGFR and EGFR signalling, in this setting.	vandetanib	42-52	ret proto-oncogene	Homo sapiens	85-88
22941289-0	2012	The important roles of RET, VEGFR2 and the RAF/MEK/ERK pathway in cancer treatment with sorafenib.	Sorafenib	88-97	ret proto-oncogene	Homo sapiens	23-26
22941289-1	2012	AIM: To elucidate the roles of receptor tyrosine kinases RET and VEGFR2 and the RAF/MEK/ERK signaling cascade in cancer treatment with sorafenib.	Sorafenib	135-144	ret proto-oncogene	Homo sapiens	57-60
22941289-7	2012	RESULTS: Sorafenib potently suppressed the activities of cRAF, VEGFR2, and RET with IC(50) values of 20.9, 4 and 0.4 nmol/L, respectively.	Sorafenib	9-18	ret proto-oncogene	Homo sapiens	75-78
22941289-8	2012	Sorafenib inhibited cRAF, VEGFR2, and RET via non-ATP-competitive, ATP-competitive and mixed-type modes, respectively.	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	38-41
22941289-12	2012	CONCLUSION: This study provides novel evidence that protein kinases RET and VEGFR2 play crucial roles in cancer treatment with sorafenib.	Sorafenib	127-136	ret proto-oncogene	Homo sapiens	68-71
22803838-9	2012	CONCLUSIONS: Our study has shown a significant association between RET/PTC rearrangements and FHCCs with a solid growth pattern, thus raising the possibility of using tyrosine kinase inhibitors for the treatment of patients with FHCCs, which are often refractory to radioiodine treatment.	Iodine-131	266-277	ret proto-oncogene	Homo sapiens	67-70
22803838-9	2012	CONCLUSIONS: Our study has shown a significant association between RET/PTC rearrangements and FHCCs with a solid growth pattern, thus raising the possibility of using tyrosine kinase inhibitors for the treatment of patients with FHCCs, which are often refractory to radioiodine treatment.	Iodine-131	266-277	ret proto-oncogene	Homo sapiens	71-74
22513837-5	2012	One patient was treated with Sorafenib, a specific inhibitor of the RET TK function, and demonstrated cytological and clinical remissions.	Sorafenib	29-38	ret proto-oncogene	Homo sapiens	68-71
22982678-8	2012	Finally, we found that a rare human single nucleotide polymorphism causing a R186H substitution in the PTB domain abolishes tyrosine phosphorylation of Dok-4 by Ret.	Tyrosine	124-132	ret proto-oncogene	Homo sapiens	161-164
22844123-0	2012	Prostaglandin E2 induces oncostatin M expression in human chronic wound macrophages through Axl receptor tyrosine kinase pathway.	Dinoprostone	0-16	ret proto-oncogene	Homo sapiens	96-120
22844123-8	2012	In human m, PGE2 phosphorylated Axl, a receptor tyrosine kinase (RTK).	Dinoprostone	12-16	ret proto-oncogene	Homo sapiens	39-63
22844123-8	2012	In human m, PGE2 phosphorylated Axl, a receptor tyrosine kinase (RTK).	Dinoprostone	12-16	ret proto-oncogene	Homo sapiens	65-68
22844123-9	2012	Axl phosphorylation was also induced by a cAMP analogue demonstrating interplay between the cAMP and RTK pathways.	Cyclic AMP	42-46	ret proto-oncogene	Homo sapiens	101-104
22627809-4	2012	LPA-induced migration was partially blocked by either Gbetagamma or RTK inhibitor and completely blocked by both inhibitors.	lysophosphatidic acid	0-3	ret proto-oncogene	Homo sapiens	68-71
22936184-8	2012	CONCLUSIONS: This preliminary study indicates that the expression patterns of ERbeta1 and ERbeta2 differ between malignant PTC lesions and benign NTG tissue, and their expression might be involved in the female predominance of PTC during the reproductive years.	Nitroglycerin	146-149	ret proto-oncogene	Homo sapiens	123-126
22484209-3	2012	The aim of this study was to investigate the effect of vandetanib, an oral tyrosine kinase inhibitor of EGFR, VEGFR 2 and RET kinases, on the functionality of P-gp after a 24h-treatment at therapeutic concentration (2muM), and its ability to increase the cytotoxicity of chemotherapeutic agents in multidrug resistance cancer cells.	vandetanib	55-65	ret proto-oncogene	Homo sapiens	122-125
22667325-3	2012	Molecules such as vandetanib that inhibit VEGFR and EGFR have also been reported to inhibit other receptors, including RET and additional kinases, and may be beneficial in treating patients with solid tumors.	vandetanib	18-28	ret proto-oncogene	Homo sapiens	119-122
22584256-1	2012	We demonstrate efficient excitonic sensitization of crystalline Si nanomembranes via combined effects of radiative (RET) and nonradiative (NRET) energy transfer from a proximal monolayer of colloidal semiconductor nanocrystals.	Silicon	64-66	ret proto-oncogene	Homo sapiens	116-119
22811067-3	2012	A tyrosine phosphorylation-mimic mutant (Y80E-Grb7-SH2) is largely dimerization deficient and binds a tyrosine-phosphorylated peptide representative of the receptor tyrosine kinase (RTK) erbB2 with differing thermodynamic characteristics than the wild-type SH2 domain.	Tyrosine	2-10	ret proto-oncogene	Homo sapiens	156-180
22811067-3	2012	A tyrosine phosphorylation-mimic mutant (Y80E-Grb7-SH2) is largely dimerization deficient and binds a tyrosine-phosphorylated peptide representative of the receptor tyrosine kinase (RTK) erbB2 with differing thermodynamic characteristics than the wild-type SH2 domain.	Tyrosine	2-10	ret proto-oncogene	Homo sapiens	182-185
22811067-3	2012	A tyrosine phosphorylation-mimic mutant (Y80E-Grb7-SH2) is largely dimerization deficient and binds a tyrosine-phosphorylated peptide representative of the receptor tyrosine kinase (RTK) erbB2 with differing thermodynamic characteristics than the wild-type SH2 domain.	Tyrosine	102-110	ret proto-oncogene	Homo sapiens	156-180
22811067-3	2012	A tyrosine phosphorylation-mimic mutant (Y80E-Grb7-SH2) is largely dimerization deficient and binds a tyrosine-phosphorylated peptide representative of the receptor tyrosine kinase (RTK) erbB2 with differing thermodynamic characteristics than the wild-type SH2 domain.	Tyrosine	102-110	ret proto-oncogene	Homo sapiens	182-185
22715896-1	2012	Vandetanib, an orally active, small-molecule, multitargeted tyrosine kinase inhibitor, demonstrates potent inhibitory activity against vascular endothelial growth factor receptor (VEGFR)-2 and -3, epidermal growth factor receptor (EGFR) and the rearranged during transfection (RET) tyrosine kinase receptor.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	277-280
22715896-5	2012	Although the correlation between RET mutation status and clinical outcome could not be clearly evaluated in this trial, it is notable that, among patients with sporadic disease, vandetanib not only demonstrated a PFS benefit in the subgroup confirmed as having a RET mutation, but also in the subgroup for whom the RET mutation status was unknown.	vandetanib	178-188	ret proto-oncogene	Homo sapiens	33-36
22715896-5	2012	Although the correlation between RET mutation status and clinical outcome could not be clearly evaluated in this trial, it is notable that, among patients with sporadic disease, vandetanib not only demonstrated a PFS benefit in the subgroup confirmed as having a RET mutation, but also in the subgroup for whom the RET mutation status was unknown.	vandetanib	178-188	ret proto-oncogene	Homo sapiens	263-266
22715896-5	2012	Although the correlation between RET mutation status and clinical outcome could not be clearly evaluated in this trial, it is notable that, among patients with sporadic disease, vandetanib not only demonstrated a PFS benefit in the subgroup confirmed as having a RET mutation, but also in the subgroup for whom the RET mutation status was unknown.	vandetanib	178-188	ret proto-oncogene	Homo sapiens	263-266
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
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
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
22442268-1	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
22442268-3	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
22577890-1	2012	INTRODUCTION: Regorafenib (BAY 73-4506) is a novel, orally active, diphenylurea multikinase inhibitor of VEGFR1-3, c-KIT, TIE-2, PDGFR-beta, FGFR-1, RET, RAF-1, BRAF and p38 MAP kinase.	regorafenib	14-25	ret proto-oncogene	Homo sapiens	149-152
22577890-1	2012	INTRODUCTION: Regorafenib (BAY 73-4506) is a novel, orally active, diphenylurea multikinase inhibitor of VEGFR1-3, c-KIT, TIE-2, PDGFR-beta, FGFR-1, RET, RAF-1, BRAF and p38 MAP kinase.	regorafenib	27-38	ret proto-oncogene	Homo sapiens	149-152
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
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
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.	Docetaxel	223-232	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.	Docetaxel	223-232	ret proto-oncogene	Homo sapiens	262-265
22494075-4	2012	When Ru(bpy)(3)(2+) labeled antibodies were selectively captured by the corresponding antigens on the CdS nanorod spot array, ECL-RET from the CdS nanorod (donor) by cathodic emission in the presence of K(2)S(2)O(8) to Ru(bpy)(3)(2+) (acceptor) occurred.	ru(bpy)(3)(2+)	5-19	ret proto-oncogene	Homo sapiens	130-133
22559926-0	2012	Preparation of 3-substituted-1-isopropyl-1H-pyrazolo[3,4-d]pyrimidin-4-amines as RET kinase inhibitors.	3-substituted-1-isopropyl-1h-pyrazolo[3,4-d]pyrimidin-4-amines	15-77	ret proto-oncogene	Homo sapiens	81-84
22559926-1	2012	A series of 3-substituted-1-isopropyl-1H-pyrazolo[3,4-d]pyrimidin-4-amines have been designed, synthesized, and evaluated as RET protein kinase inhibitors.	3-substituted-1-isopropyl-1h-pyrazolo[3,4-d]pyrimidin-4-amines	12-74	ret proto-oncogene	Homo sapiens	125-128
22323563-7	2012	The predominant rearrangement type was RET/PTC3, which is characteristic of human thyroid cancer arising early after Chernobyl-related radioactive iodine exposure.	Iodine	147-153	ret proto-oncogene	Homo sapiens	39-42
22494075-4	2012	When Ru(bpy)(3)(2+) labeled antibodies were selectively captured by the corresponding antigens on the CdS nanorod spot array, ECL-RET from the CdS nanorod (donor) by cathodic emission in the presence of K(2)S(2)O(8) to Ru(bpy)(3)(2+) (acceptor) occurred.	Cadmium	102-105	ret proto-oncogene	Homo sapiens	130-133
22494075-4	2012	When Ru(bpy)(3)(2+) labeled antibodies were selectively captured by the corresponding antigens on the CdS nanorod spot array, ECL-RET from the CdS nanorod (donor) by cathodic emission in the presence of K(2)S(2)O(8) to Ru(bpy)(3)(2+) (acceptor) occurred.	Cadmium	143-146	ret proto-oncogene	Homo sapiens	130-133
22494075-4	2012	When Ru(bpy)(3)(2+) labeled antibodies were selectively captured by the corresponding antigens on the CdS nanorod spot array, ECL-RET from the CdS nanorod (donor) by cathodic emission in the presence of K(2)S(2)O(8) to Ru(bpy)(3)(2+) (acceptor) occurred.	ru(bpy)(	5-13	ret proto-oncogene	Homo sapiens	130-133
22504184-5	2012	Here we report point mutations at three residues within the kinase domain of FLT3-ITD that confer substantial in vitro resistance to AC220 (quizartinib), an active investigational inhibitor of FLT3, KIT, PDGFRA, PDGFRB and RET; evolution of AC220-resistant substitutions at two of these amino acid positions was observed in eight of eight FLT3-ITD-positive AML patients with acquired resistance to AC220.	quizartinib	140-151	ret proto-oncogene	Homo sapiens	223-226
22421192-1	2012	PURPOSE: Regorafenib is a novel oral multikinase inhibitor of angiogenic (VEGFR1-3, TIE2), stromal (PDGFR-beta, FGFR), and oncogenic kinases (KIT, RET, and RAF).	regorafenib	9-20	ret proto-oncogene	Homo sapiens	147-150
22343387-5	2012	SUMMARY: Recently, vandetanib (ZD6474), an inhibitor of vascular endothelial growth factor receptor (VEGFR) 2 and VEGFR 3, RET, and epidermal growth factor receptor (EGFR), was approved for the treatment of adults with symptomatic or progressive MTC.	vandetanib	19-29	ret proto-oncogene	Homo sapiens	123-126
22343387-5	2012	SUMMARY: Recently, vandetanib (ZD6474), an inhibitor of vascular endothelial growth factor receptor (VEGFR) 2 and VEGFR 3, RET, and epidermal growth factor receptor (EGFR), was approved for the treatment of adults with symptomatic or progressive MTC.	vandetanib	31-37	ret proto-oncogene	Homo sapiens	123-126
22452486-7	2012	EF(RET) was positively correlated with EFs of coemitted particulate matter (EF(PM)) and phenanthrene (EF(PHE)) for crop residue and coal, but not for wood.	phenanthrene	88-100	ret proto-oncogene	Homo sapiens	3-6
22452486-7	2012	EF(RET) was positively correlated with EFs of coemitted particulate matter (EF(PM)) and phenanthrene (EF(PHE)) for crop residue and coal, but not for wood.	Phenylalanine	105-108	ret proto-oncogene	Homo sapiens	3-6
22080168-2	2012	Linifanib is a novel, orally active multi-targeted receptor tyrosine kinase (RTK) inhibitor that exhibits potent antitumor and antiangiogenic activities against a broad spectrum of experimental tumors and malignancies in patients.	N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N1-(2-fluoro-5-methylphenyl)urea	0-9	ret proto-oncogene	Homo sapiens	51-75
22080168-2	2012	Linifanib is a novel, orally active multi-targeted receptor tyrosine kinase (RTK) inhibitor that exhibits potent antitumor and antiangiogenic activities against a broad spectrum of experimental tumors and malignancies in patients.	N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N1-(2-fluoro-5-methylphenyl)urea	0-9	ret proto-oncogene	Homo sapiens	77-80
23960782-0	2012	The immunopharmacologic potential of Semaxanib and new generation directed therapeutic drugs: Receptor tyrosine kinase regulation with anti-tumorigenensis/angiogenesis properties.	Semaxinib	37-46	ret proto-oncogene	Homo sapiens	94-118
23113396-3	2012	The mutations that change a cysteine with another aminoacid (mainly in exons 10 and 11) give a risk of familial medullary thyroid carcinoma (FTMC) and MEN 2A.	Cysteine	28-36	ret proto-oncogene	Homo sapiens	151-157
23113396-6	2012	We present our results in screening for RET protooncogene mutations associated with TMC in patients with HD.	trimethylchlorosilane	84-87	ret proto-oncogene	Homo sapiens	40-43
22286373-3	2012	Some clinical trials have been conducted showing the ability of targeted therapies able to inhibit RET(sorafenib, imatinib, vandetanib) in stabilizing the course of the disease.	Sorafenib	103-112	ret proto-oncogene	Homo sapiens	99-102
22286373-3	2012	Some clinical trials have been conducted showing the ability of targeted therapies able to inhibit RET(sorafenib, imatinib, vandetanib) in stabilizing the course of the disease.	Imatinib Mesylate	114-122	ret proto-oncogene	Homo sapiens	99-102
22286373-3	2012	Some clinical trials have been conducted showing the ability of targeted therapies able to inhibit RET(sorafenib, imatinib, vandetanib) in stabilizing the course of the disease.	vandetanib	124-134	ret proto-oncogene	Homo sapiens	99-102
22364402-1	2012	The purpose of this study was to investigate whether a long-acting methylphenidate formulation (MPH-ret) is as effective as two doses of immediate-release methylphenidate (MPH-IR) in reducing attention-deficit/hyperactivity disorder (ADHD) symptoms including inattention, impulsivity, and hyperactivity during the course of the day.	Methylphenidate	67-82	ret proto-oncogene	Homo sapiens	100-103
22370318-1	2012	PURPOSE: Vandetanib is a once-daily oral inhibitor of vascular endothelial growth factor receptor, epidermal growth factor receptor (EGFR), and RET signaling.	vandetanib	9-19	ret proto-oncogene	Homo sapiens	144-147
22740998-3	2012	Our results showed that dasatinib exhibits prominent cytostatic activity both in vitro and in vivo against thyroid cancer cell lines with RET/PTC rearrangement (BHP2-7) and KRAS mutation (Cal62).	Dasatinib	24-33	ret proto-oncogene	Homo sapiens	138-141
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
22197381-4	2012	Structural analysis showed that retinoids bind BSA via hydrophilic and hydrophobic interactions with overall binding constants of K(Ret)(-BSA) = 5.3 (+-0.8) x 10(6) M(-1) and K(Retac-BSA) = 2.3 (+-0.4) x 10(6) M(-1).	Retinoids	32-41	ret proto-oncogene	Homo sapiens	132-135
22352786-2	2012	Despite their broad interest, fundamental questions about their reaction mechanism remain to be answered, especially for those GTs that transfer the sugar with net retention of the configuration at the anomeric carbon (retaining glycosyltransferases, ret-GTs).	Sugars	149-154	ret proto-oncogene	Homo sapiens	164-167
22352786-2	2012	Despite their broad interest, fundamental questions about their reaction mechanism remain to be answered, especially for those GTs that transfer the sugar with net retention of the configuration at the anomeric carbon (retaining glycosyltransferases, ret-GTs).	Carbon	211-217	ret proto-oncogene	Homo sapiens	164-167
22242557-5	2012	Interestingly, danusertib also inhibits several receptor tyrosine kinases such as Abl, Ret, FGFR-1 and TrkA.	danusertib	15-25	ret proto-oncogene	Homo sapiens	87-90
22304922-5	2012	Ret also mediates GPI-anchored GFRalpha1 signaling in response to GDNF, a diffusible chemoattractant in the limb, indicating that Ret is a multifunctional coreceptor for guidance molecules.	Glycosylphosphatidylinositols	18-21	ret proto-oncogene	Homo sapiens	0-3
22304922-5	2012	Ret also mediates GPI-anchored GFRalpha1 signaling in response to GDNF, a diffusible chemoattractant in the limb, indicating that Ret is a multifunctional coreceptor for guidance molecules.	Glycosylphosphatidylinositols	18-21	ret proto-oncogene	Homo sapiens	130-133
22336242-1	2012	BACKGROUND AND OBJECTIVE: Vandetanib is a once-daily oral multi-target inhibitor of vascular endothelial growth factor receptor, epidermal growth factor receptor, and rearranged during transfection (RET) tyrosine kinases.	vandetanib	26-36	ret proto-oncogene	Homo sapiens	167-197
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
22336242-1	2012	BACKGROUND AND OBJECTIVE: Vandetanib is a once-daily oral multi-target inhibitor of vascular endothelial growth factor receptor, epidermal growth factor receptor, and rearranged during transfection (RET) tyrosine kinases.	vandetanib	26-36	ret proto-oncogene	Homo sapiens	199-202
22204741-0	2012	N4-Aryl-6-substitutedphenylmethyl-7H-pyrrolo[2,3-d]pyrimidine-2,4-diamines as receptor tyrosine kinase inhibitors.	n4-aryl-6-substitutedphenylmethyl-7h-pyrrolo[2,3-d]pyrimidine-2,4-diamines	0-74	ret proto-oncogene	Homo sapiens	78-102
22221201-0	2012	VX-322: a novel dual receptor tyrosine kinase inhibitor for the treatment of acute myelogenous leukemia.	N3-(4-(4-morpholinocyclohexyl)phenyl)-1-(pyridin-2-yl)-1H-1,2,4-triazole-3,5-diamine	0-6	ret proto-oncogene	Homo sapiens	21-45
22128160-5	2012	Furthermore, pharmacological and mutagenesis assays revealed that protein kinase C (PKC) and high K(+) depolarization increase RET surface levels through phosphorylation of the Thr(675) residue in the Box1 motif.	Threonine	177-180	ret proto-oncogene	Homo sapiens	127-130
22128160-6	2012	Finally, we found that the phosphorylation status of the Thr(675) residue influences RET mediated response to GDNF stimulation.	Threonine	57-60	ret proto-oncogene	Homo sapiens	85-88
22109971-9	2012	Cells treated with everolimus demonstrated activation of Akt and Ret via TORC2 complex-dependent and TORC2 complex-independent mechanisms respectively.	Everolimus	19-29	ret proto-oncogene	Homo sapiens	65-68
22204741-1	2012	Six novel N(4)-substitutedphenyl-6-substitutedphenylmethyl-7H-pyrrolo[2,3-d]pyrimidine-2,4-diamines were synthesized as multiple receptor tyrosine kinase (RTK) inhibitors and antitumor agents.	n(4)-substitutedphenyl-6-substitutedphenylmethyl-7h-pyrrolo[2,3-d]pyrimidine-2,4-diamines	10-99	ret proto-oncogene	Homo sapiens	129-153
22204741-1	2012	Six novel N(4)-substitutedphenyl-6-substitutedphenylmethyl-7H-pyrrolo[2,3-d]pyrimidine-2,4-diamines were synthesized as multiple receptor tyrosine kinase (RTK) inhibitors and antitumor agents.	n(4)-substitutedphenyl-6-substitutedphenylmethyl-7h-pyrrolo[2,3-d]pyrimidine-2,4-diamines	10-99	ret proto-oncogene	Homo sapiens	155-158
22204741-5	2012	The results indicate that the RTK inhibitory profile could be modulated with slight variations to the N(4)-aryl-6-substitutedphenylmethyl-7H-pyrrolo[2,3-d]pyrimidine-2,4-diamino scaffold.	n(4)-aryl-6-substitutedphenylmethyl-7h-pyrrolo[2,3-d]pyrimidine-2,4-diamino	102-177	ret proto-oncogene	Homo sapiens	30-33
21638122-10	2012	RESULTS: SIM010603 inhibited stem cell factor receptor (Kit), vascular endothelial growth factor receptor-2 (VEGFR-2), platelet-derived growth factor receptor-beta (PDGFR-beta), glial cell line-derived neurotrophic factor receptor (Rearranged during Transfection; RET), and Fms-like tyrosine kinase-3 (FLT3) with IC(50) values between 5.0 and 68.1 nmol/l.	N-(2-(diethylamino)ethyl)-2-methyl-7-(1,2-dihydro-5-fluoro-2-oxo-3H-indol-3-ylidene)-4,5,6,7-tetrahydro-1H-indole-3-carboxamide	9-18	ret proto-oncogene	Homo sapiens	264-267
24451769-3	2012	Vandetanib, an orally bioavailable inhibitor of the RET kinase that is constitutively activated in MTC, has now been approved by the U.S. Food and Drug Administration (FDA) for use in progressive and symptomatic metastatic MTC; it has been shown to delay time to progression relative to placebo in a randomized phase III trial.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	52-55
22025146-2	2012	Vandetanib, a once-daily oral inhibitor of RET kinase, vascular endothelial growth factor receptor, and epidermal growth factor receptor signaling, has previously shown antitumor activity in a phase II study of patients with advanced hereditary MTC.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	43-46
23193472-3	2012	In addition to the usual iron parameters, the iron status of erythrocytes can be determined by measuring reticulocyte hemoglobin (RET-He).	Iron	46-50	ret proto-oncogene	Homo sapiens	130-133
22500115-4	2012	Vandetanib is an oral TKI that targets VEGF receptors 2 and 3, RET, and at higher concentrations, the epidermal growth factor (EGF) receptor.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	63-66
22783588-1	2012	BACKGROUND: The effect of combined administration of the multi-targeted receptor tyrosine kinase (RTK) inhibitor (Sorafenib) and chemotherapy (Pemetrexed) is still unknown.	Sorafenib	114-123	ret proto-oncogene	Homo sapiens	72-96
22783588-1	2012	BACKGROUND: The effect of combined administration of the multi-targeted receptor tyrosine kinase (RTK) inhibitor (Sorafenib) and chemotherapy (Pemetrexed) is still unknown.	Sorafenib	114-123	ret proto-oncogene	Homo sapiens	98-101
22214462-2	2012	Sorafenib (Nexavar), a novel bi-aryl urea BAY 43-9006, is an orally administered multikinase inhibitor with activity against RAS/RAF kinases multikinase inhibitor with activity against RAF kinases and several receptor tyrosine kinases, including vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), FLT3, Ret, and c-Kit.	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	354-357
22214462-2	2012	Sorafenib (Nexavar), a novel bi-aryl urea BAY 43-9006, is an orally administered multikinase inhibitor with activity against RAS/RAF kinases multikinase inhibitor with activity against RAF kinases and several receptor tyrosine kinases, including vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), FLT3, Ret, and c-Kit.	Sorafenib	11-18	ret proto-oncogene	Homo sapiens	354-357
22928011-1	2012	XB130, a novel adaptor protein, mediates RET/PTC chromosome rearrangement-related thyroid cancer cell proliferation and survival through phosphatidyl-inositol-3-kinase (PI3K)/Akt pathway.	Phosphatidylinositols	137-158	ret proto-oncogene	Homo sapiens	41-44
23056499-0	2012	AZD1480 blocks growth and tumorigenesis of RET- activated thyroid cancer cell lines.	AZD 1480	0-7	ret proto-oncogene	Homo sapiens	43-46
23056499-3	2012	Here, we tested the efficacy of a JAK1/2- inhibitor, AZD1480, in the in vitro and in vivo growth of thyroid cancer cell lines expressing oncogenic RET.	AZD 1480	53-60	ret proto-oncogene	Homo sapiens	147-150
23056499-9	2012	In conclusion, AZD1480 effectively blocks proliferation and tumor growth of activated RET- thyroid cancer cell lines, likely through direct RET inhibition in cancer cells as well as by modulation of the microenvironment (e.g. via JAK/phospho-STAT3 inhibition in endothelial cells).	AZD 1480	15-22	ret proto-oncogene	Homo sapiens	86-89
22928011-1	2012	XB130, a novel adaptor protein, mediates RET/PTC chromosome rearrangement-related thyroid cancer cell proliferation and survival through phosphatidyl-inositol-3-kinase (PI3K)/Akt pathway.	Phosphatidylinositols	137-158	ret proto-oncogene	Homo sapiens	45-48
23056499-9	2012	In conclusion, AZD1480 effectively blocks proliferation and tumor growth of activated RET- thyroid cancer cell lines, likely through direct RET inhibition in cancer cells as well as by modulation of the microenvironment (e.g. via JAK/phospho-STAT3 inhibition in endothelial cells).	AZD 1480	15-22	ret proto-oncogene	Homo sapiens	140-143
23056499-10	2012	Thus, AZD1480 should be considered as a therapeutic agent for the treatment of RET- activated thyroid cancers.	AZD 1480	6-13	ret proto-oncogene	Homo sapiens	79-82
21978374-0	2011	Down-regulation of estrogen receptor-alpha and rearranged during transfection tyrosine kinase is associated with withaferin a-induced apoptosis in MCF-7 breast cancer cells.	withaferin A	113-125	ret proto-oncogene	Homo sapiens	47-77
21926191-3	2011	Cabozantinib (XL184) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and FLT3.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	239-242
21926191-3	2011	Cabozantinib (XL184) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and FLT3.	cabozantinib	14-19	ret proto-oncogene	Homo sapiens	239-242
21831957-7	2011	In addition, RAF265 had significant RET inhibitory activity (IC50 = 25-50 nmol/L for RET(C634W)).	RAF265	13-19	ret proto-oncogene	Homo sapiens	36-39
21831957-7	2011	In addition, RAF265 had significant RET inhibitory activity (IC50 = 25-50 nmol/L for RET(C634W)).	RAF265	13-19	ret proto-oncogene	Homo sapiens	85-88
22973453-9	2012	Many novel interactions were also observed with phosphopeptides corresponding to ErbB receptor tyrosines not previously reported to be phosphorylated by mass spectrometry, suggesting the existence of many biologically relevant RTK sites that may be phosphorylated but below the detection threshold of standard mass spectrometry procedures.	Tyrosine	95-104	ret proto-oncogene	Homo sapiens	227-230
22355350-0	2012	RET PLCgamma phosphotyrosine binding domain regulates Ca2+ signaling and neocortical neuronal migration.	Phosphotyrosine	13-28	ret proto-oncogene	Homo sapiens	0-3
22355350-3	2012	Here we report that the RET receptor induces calcium (Ca(2+)) signaling and regulates neocortical neuronal progenitor migration through the Phospholipase-C gamma (PLCgamma) binding domain Tyr1015.	Calcium	45-52	ret proto-oncogene	Homo sapiens	24-27
21253810-1	2011	The most important mutation associated with Multiple Endocrine Neoplasia type 2B (MEN 2B) is the change of thymine to cytosine in codon 918 of exon 16 in the RET oncogene (ATG   ACG).	Thymine	107-114	ret proto-oncogene	Homo sapiens	44-80
21253810-1	2011	The most important mutation associated with Multiple Endocrine Neoplasia type 2B (MEN 2B) is the change of thymine to cytosine in codon 918 of exon 16 in the RET oncogene (ATG   ACG).	Thymine	107-114	ret proto-oncogene	Homo sapiens	82-88
21253810-1	2011	The most important mutation associated with Multiple Endocrine Neoplasia type 2B (MEN 2B) is the change of thymine to cytosine in codon 918 of exon 16 in the RET oncogene (ATG   ACG).	Thymine	107-114	ret proto-oncogene	Homo sapiens	158-161
21253810-1	2011	The most important mutation associated with Multiple Endocrine Neoplasia type 2B (MEN 2B) is the change of thymine to cytosine in codon 918 of exon 16 in the RET oncogene (ATG   ACG).	Cytosine	118-126	ret proto-oncogene	Homo sapiens	44-80
21253810-1	2011	The most important mutation associated with Multiple Endocrine Neoplasia type 2B (MEN 2B) is the change of thymine to cytosine in codon 918 of exon 16 in the RET oncogene (ATG   ACG).	Cytosine	118-126	ret proto-oncogene	Homo sapiens	82-88
21253810-1	2011	The most important mutation associated with Multiple Endocrine Neoplasia type 2B (MEN 2B) is the change of thymine to cytosine in codon 918 of exon 16 in the RET oncogene (ATG   ACG).	Cytosine	118-126	ret proto-oncogene	Homo sapiens	158-161
22146228-1	2011	XL-184 (cabozantinib) is a novel, small-molecule, multitargeted receptor tyrosine kinase inhibitor with particular activity against hepatocyte growth factor receptor (tyrosine-protein kinase Met), vascular endothelial growth factor receptor 2 (VEGFR-2) and proto-oncogene tyrosine-protein kinase receptor Ret.	cabozantinib	0-6	ret proto-oncogene	Homo sapiens	257-308
22146228-1	2011	XL-184 (cabozantinib) is a novel, small-molecule, multitargeted receptor tyrosine kinase inhibitor with particular activity against hepatocyte growth factor receptor (tyrosine-protein kinase Met), vascular endothelial growth factor receptor 2 (VEGFR-2) and proto-oncogene tyrosine-protein kinase receptor Ret.	cabozantinib	8-20	ret proto-oncogene	Homo sapiens	257-308
21951623-8	2011	CASE PRESENTATION: In this case report, we present a 59-year-old Caucasian female with refractory adenoid cystic carcinoma of the maxilla metastatic to the lung that responded to sorafenib, a novel multi-tyrosine kinase inhibitor, which targets angiogenesis, Raf kinase pathway, platelet-derived growth factor Ret, and c-Kit.	Sorafenib	179-188	ret proto-oncogene	Homo sapiens	310-313
21737465-0	2011	Steroid hormone modulation of RET through two estrogen responsive enhancers in breast cancer.	Steroids	0-15	ret proto-oncogene	Homo sapiens	30-33
21737465-1	2011	RET, a gene causatively mutated in Hirschsprung disease and cancer, has recently been implicated in breast cancer estrogen (E2) independence and tamoxifen resistance.	Tamoxifen	145-154	ret proto-oncogene	Homo sapiens	0-3
21737465-2	2011	RET displays both E2 and retinoic acid (RA)-dependent transcriptional modulation in E2-responsive breast cancers.	Tretinoin	25-38	ret proto-oncogene	Homo sapiens	0-3
21737465-2	2011	RET displays both E2 and retinoic acid (RA)-dependent transcriptional modulation in E2-responsive breast cancers.	Tretinoin	40-42	ret proto-oncogene	Homo sapiens	0-3
21737465-3	2011	However, the regulatory elements through which the steroid hormone transcriptional regulation of RET is mediated are poorly defined.	Steroids	51-66	ret proto-oncogene	Homo sapiens	97-100
21741956-5	2011	Cell treatment with the anti-tumor Ret kinase inhibitor RPI-1 inhibited tyrosine phosphorylation of procaspase-8, likely inducing its local activation, followed by downregulation of both Ret and Fap-1, and translocation of CD95 into lipid rafts.	Tyrosine	72-80	ret proto-oncogene	Homo sapiens	35-38
21857110-0	2011	Synergistic growth inhibition of cancer cells harboring the RET/PTC1 oncogene by staurosporine and rotenone involves enhanced cell death.	Staurosporine	81-94	ret proto-oncogene	Homo sapiens	60-63
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
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
21725210-8	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
21807000-0	2011	Orthovanadate-induced cell death in RET/PTC1-harboring cancer cells involves the activation of caspases and altered signaling through PI3K/Akt/mTOR.	Vanadates	0-13	ret proto-oncogene	Homo sapiens	36-39
21807000-5	2011	Here, the aim was to characterize the effects of orthovanadate in thyroid cancer cells harboring RET/PTC1.	Vanadates	49-62	ret proto-oncogene	Homo sapiens	97-100
21807000-10	2011	In contrast, treatment with inhibitory concentrations of orthovanadate results in increased phosphorylation of tyrosine 451 of RET/PTC1 and activation of the mTOR/S6R branch of the PI3K/Akt signaling pathway.	Vanadates	57-70	ret proto-oncogene	Homo sapiens	127-130
21807000-10	2011	In contrast, treatment with inhibitory concentrations of orthovanadate results in increased phosphorylation of tyrosine 451 of RET/PTC1 and activation of the mTOR/S6R branch of the PI3K/Akt signaling pathway.	Tyrosine	111-119	ret proto-oncogene	Homo sapiens	127-130
21857110-0	2011	Synergistic growth inhibition of cancer cells harboring the RET/PTC1 oncogene by staurosporine and rotenone involves enhanced cell death.	Rotenone	99-107	ret proto-oncogene	Homo sapiens	60-63
21614375-1	2011	In this paper, an electrochemiluminescence resonance energy transfer (ECL-RET) system from CdS quantum dot to Ru(bpy)(3)(2+) was developed for the first time.	Cadmium	91-94	ret proto-oncogene	Homo sapiens	74-77
21715537-1	2011	PURPOSE: The purpose of the study was to assess the endocrine effects of vandetanib, a multikinase inhibitor targeting RET, vascular endothelial growth factor receptor, and epidermal growth factor receptor, in 39 patients with progressive thyroid cancer included in two randomized placebo-controlled trials using vandetanib 300 mg/d.	vandetanib	73-83	ret proto-oncogene	Homo sapiens	119-122
21515317-5	2011	An application of the Ad-multi-shRNA vector carrying four same shRNA-sequences against the RET finger protein, an oncogene known to desensitize cells to oxidative stress and cisplatin, resulted in an enhanced cytotoxic effect of cisplatin, demonstrating the advantages of the Ad-multi-shRNA vector for silencing target genes.	Cisplatin	174-183	ret proto-oncogene	Homo sapiens	91-94
21515317-5	2011	An application of the Ad-multi-shRNA vector carrying four same shRNA-sequences against the RET finger protein, an oncogene known to desensitize cells to oxidative stress and cisplatin, resulted in an enhanced cytotoxic effect of cisplatin, demonstrating the advantages of the Ad-multi-shRNA vector for silencing target genes.	Cisplatin	229-238	ret proto-oncogene	Homo sapiens	91-94
21819606-7	2011	Hereditary medullary thyroid cancers (MTC) have been shown to be highly responsive to a multitargeted tyrosine kinase inhibitor vandetanib, which exerts specific activity towards mutated RET receptor.	vandetanib	128-138	ret proto-oncogene	Homo sapiens	187-190
21614375-1	2011	In this paper, an electrochemiluminescence resonance energy transfer (ECL-RET) system from CdS quantum dot to Ru(bpy)(3)(2+) was developed for the first time.	2,2'-Dipyridyl	113-116	ret proto-oncogene	Homo sapiens	74-77
21770481-1	2011	Vandetanib is an orally active antagonist of vascular endothelial growth factor (VEGF) receptor-2 (VEGFR-2), epidermal growth factor receptor (EGFR or HER1 or ErbB1) and RET kinase, and is now available in the US for the treatment of metastatic medullary thyroid cancer (MTC).	vandetanib	0-10	ret proto-oncogene	Homo sapiens	170-173
21212155-1	2011	BACKGROUND: Sorafenib is a small-molecule multitargeted kinase inhibitor that blocks the activation of C-RAF, B-RAF, c-KIT, FLT-3, RET, vascular endothelial growth factor receptor 2 (VEGFR-2), VEGFR-3 and platelet-derived growth factor receptor beta.	Sorafenib	12-21	ret proto-oncogene	Homo sapiens	131-134
21551259-0	2011	In vitro transforming potential, intracellular signaling properties, and sensitivity to a kinase inhibitor (sorafenib) of RET proto-oncogene variants Glu511Lys, Ser649Leu, and Arg886Trp.	Sorafenib	108-117	ret proto-oncogene	Homo sapiens	122-125
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
21551259-9	2011	The three RET variants analyzed here were sensitive to treatment with sorafenib.	Sorafenib	70-79	ret proto-oncogene	Homo sapiens	10-13
21454698-4	2011	The identification of focal adhesion kinase (FAK) as a direct substrate for RET kinase revealed (i) a RET-FAK transactivation mechanism consisting of direct phosphorylation of FAK Tyr-576/577 by RET and a reciprocal phosphorylation of RET by FAK, which crucially is able to rescue the kinase-impaired RET K758M mutant and (ii) that FAK binds RET via its FERM domain.	Tyrosine	180-183	ret proto-oncogene	Homo sapiens	76-79
21606412-1	2011	PURPOSE: XL184 (cabozantinib) is a potent inhibitor of MET, vascular endothelial growth factor receptor 2 (VEGFR2), and RET, with robust antiangiogenic, antitumor, and anti-invasive effects in preclinical models.	cabozantinib	9-14	ret proto-oncogene	Homo sapiens	120-123
21606412-1	2011	PURPOSE: XL184 (cabozantinib) is a potent inhibitor of MET, vascular endothelial growth factor receptor 2 (VEGFR2), and RET, with robust antiangiogenic, antitumor, and anti-invasive effects in preclinical models.	cabozantinib	16-28	ret proto-oncogene	Homo sapiens	120-123
21606412-13	2011	Cabozantinib may provide clinical benefit by simultaneously targeting multiple pathways of importance in MTC, including MET, VEGFR2, and RET.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	137-140
21470995-7	2011	RESULTS: XL184 and vandetanib most effectively inhibited cell proliferation, RET autophosphorylation in combination with a reduction of RET expression, and ERK phosphorylation in MTC-TT and MZ-CRC-1, respectively.	vandetanib	19-29	ret proto-oncogene	Homo sapiens	77-80
21470995-7	2011	RESULTS: XL184 and vandetanib most effectively inhibited cell proliferation, RET autophosphorylation in combination with a reduction of RET expression, and ERK phosphorylation in MTC-TT and MZ-CRC-1, respectively.	vandetanib	19-29	ret proto-oncogene	Homo sapiens	136-139
21470995-8	2011	TPC-1 cells showed a decrease in RET autophosphorylation after treatment with XL184, but no effect was observed on ERK activation.	cabozantinib	78-83	ret proto-oncogene	Homo sapiens	33-36
21470995-9	2011	CONCLUSION: There is indeed specificity for different RET mutations, with XL184 being the most potent inhibitor in MEN2A and PTC and vandetanib the most effective in MEN2B in vitro.	vandetanib	133-143	ret proto-oncogene	Homo sapiens	54-57
21470995-9	2011	CONCLUSION: There is indeed specificity for different RET mutations, with XL184 being the most potent inhibitor in MEN2A and PTC and vandetanib the most effective in MEN2B in vitro.	vandetanib	133-143	ret proto-oncogene	Homo sapiens	166-171
21815478-2	2011	The reticulocyte hemoglobin equivalent (RET-He) is an indirect measure of the functional iron available for the erythropoiesis over the previous 2-3 days.	Iron	89-93	ret proto-oncogene	Homo sapiens	40-43
21815478-5	2011	Two of 14 patients in the absence of post-PABD iron replacement developed marked anemia with low RET-He levels after PABD, suggesting that this anemia was due to iron deficiency.	Helium	101-103	ret proto-oncogene	Homo sapiens	97-100
21815478-6	2011	Of 26 patients receiving post-PABD iron replacement, 8 who had already showed low RET-He levels at PABD developed statistically significant reduction in hemoglobin levels after PABD despite adequate iron replacement, indicating that the 8 patients had iron deficiency prior to PABD.	Iron	35-39	ret proto-oncogene	Homo sapiens	82-85
21815478-6	2011	Of 26 patients receiving post-PABD iron replacement, 8 who had already showed low RET-He levels at PABD developed statistically significant reduction in hemoglobin levels after PABD despite adequate iron replacement, indicating that the 8 patients had iron deficiency prior to PABD.	Helium	86-88	ret proto-oncogene	Homo sapiens	82-85
21170960-4	2011	Furthermore, regorafenib inhibits additional angiogenic kinases (VEGFR1/3, platelet-derived growth factor receptor-beta and fibroblast growth factor receptor 1) and the mutant oncogenic kinases KIT, RET and B-RAF.	regorafenib	13-24	ret proto-oncogene	Homo sapiens	199-202
21454698-6	2011	Finally, our data indicate that FAK inhibitors could be used as potential therapeutic agents for patients with multiple endocrine neoplasia type 2 tumors because both, treatment with the FAK kinase inhibitor NVP-TAE226 and FAK down-regulation by siRNA reduced RET phosphorylation and signaling as well as the proliferation and survival of tumor and transfected cell lines expressing oncogenic RET.	TAE226	212-218	ret proto-oncogene	Homo sapiens	260-263
21454698-6	2011	Finally, our data indicate that FAK inhibitors could be used as potential therapeutic agents for patients with multiple endocrine neoplasia type 2 tumors because both, treatment with the FAK kinase inhibitor NVP-TAE226 and FAK down-regulation by siRNA reduced RET phosphorylation and signaling as well as the proliferation and survival of tumor and transfected cell lines expressing oncogenic RET.	TAE226	212-218	ret proto-oncogene	Homo sapiens	393-396
21454698-4	2011	The identification of focal adhesion kinase (FAK) as a direct substrate for RET kinase revealed (i) a RET-FAK transactivation mechanism consisting of direct phosphorylation of FAK Tyr-576/577 by RET and a reciprocal phosphorylation of RET by FAK, which crucially is able to rescue the kinase-impaired RET K758M mutant and (ii) that FAK binds RET via its FERM domain.	Tyrosine	180-183	ret proto-oncogene	Homo sapiens	102-105
21454698-4	2011	The identification of focal adhesion kinase (FAK) as a direct substrate for RET kinase revealed (i) a RET-FAK transactivation mechanism consisting of direct phosphorylation of FAK Tyr-576/577 by RET and a reciprocal phosphorylation of RET by FAK, which crucially is able to rescue the kinase-impaired RET K758M mutant and (ii) that FAK binds RET via its FERM domain.	Tyrosine	180-183	ret proto-oncogene	Homo sapiens	102-105
21454698-4	2011	The identification of focal adhesion kinase (FAK) as a direct substrate for RET kinase revealed (i) a RET-FAK transactivation mechanism consisting of direct phosphorylation of FAK Tyr-576/577 by RET and a reciprocal phosphorylation of RET by FAK, which crucially is able to rescue the kinase-impaired RET K758M mutant and (ii) that FAK binds RET via its FERM domain.	Tyrosine	180-183	ret proto-oncogene	Homo sapiens	102-105
21454698-4	2011	The identification of focal adhesion kinase (FAK) as a direct substrate for RET kinase revealed (i) a RET-FAK transactivation mechanism consisting of direct phosphorylation of FAK Tyr-576/577 by RET and a reciprocal phosphorylation of RET by FAK, which crucially is able to rescue the kinase-impaired RET K758M mutant and (ii) that FAK binds RET via its FERM domain.	Tyrosine	180-183	ret proto-oncogene	Homo sapiens	102-105
21454698-4	2011	The identification of focal adhesion kinase (FAK) as a direct substrate for RET kinase revealed (i) a RET-FAK transactivation mechanism consisting of direct phosphorylation of FAK Tyr-576/577 by RET and a reciprocal phosphorylation of RET by FAK, which crucially is able to rescue the kinase-impaired RET K758M mutant and (ii) that FAK binds RET via its FERM domain.	Tyrosine	180-183	ret proto-oncogene	Homo sapiens	102-105
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
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
21518456-10	2011	SRE and TRE reporter assays demonstrated that co-expression of Spry1 with E1A(13S) abolishes the inhibitory function of Spry1 in RTK signalling, which is consequently accompanied with a decrease of E1A13S-induced gene expression.	5-chloro-3-tert-butyl-2'-chloro-4'-nitrosalicylanilide	78-81	ret proto-oncogene	Homo sapiens	129-132
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
21350000-1	2011	PURPOSE: We investigated whether vandetanib, an inhibitor of the tyrosine kinase activities of vascular endothelial growth factor receptor-2 (VEGFR-2), epidermal growth factor receptor (EGFR), and rearranged during transfection (RET), could augment the antitumor activity of radiation with or without cisplatin in preclinical in vitro and in vivo models of human head and neck squamous cell carcinoma (HNSCC).	vandetanib	33-43	ret proto-oncogene	Homo sapiens	229-232
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
21289252-13	2011	CONCLUSIONS: Inhibiting the Ras/Raf/MAPK kinase/ERK and RET kinase pathways with sorafenib and tipifarnib is well tolerated and active against thyroid cancer.	Sorafenib	81-90	ret proto-oncogene	Homo sapiens	56-59
21289252-13	2011	CONCLUSIONS: Inhibiting the Ras/Raf/MAPK kinase/ERK and RET kinase pathways with sorafenib and tipifarnib is well tolerated and active against thyroid cancer.	tipifarnib	95-105	ret proto-oncogene	Homo sapiens	56-59
21773063-0	2011	Models for the prediction of receptor tyrosine kinase inhibitory activity of substituted 3-aminoindazole analogues.	1H-Indazol-3-amine	89-104	ret proto-oncogene	Homo sapiens	29-53
22466090-1	2011	The approval of receptor tyrosine kinase (RTK) targeted agent sorafenib as the first effective drug for the systemic treatment of advanced hepatocellular carcinoma (HCC) represents a milestone in the treatment of this disease.	Sorafenib	62-71	ret proto-oncogene	Homo sapiens	16-40
20952403-0	2011	Chromatin and DNA methylation dynamics during retinoic acid-induced RET gene transcriptional activation in neuroblastoma cells.	Tretinoin	46-59	ret proto-oncogene	Homo sapiens	68-71
20952403-1	2011	Although it is well known that RET gene is strongly activated by retinoic acid (RA) in neuroblastoma cells, the mechanisms underlying such activation are still poorly understood.	Tretinoin	65-78	ret proto-oncogene	Homo sapiens	31-34
20952403-1	2011	Although it is well known that RET gene is strongly activated by retinoic acid (RA) in neuroblastoma cells, the mechanisms underlying such activation are still poorly understood.	Tretinoin	80-82	ret proto-oncogene	Homo sapiens	31-34
21206969-6	2011	Data from the current study showed that 2 muM quercetin, a low concentration that represents less than 10% of its IC50 growth-inhibitory concentration as calculated from the average of eight distinct cancer cell lines, decreased the activity of 16 kinases by more than 80%, including ABL1, Aurora-A, -B, -C, CLK1, FLT3, JAK3, MET, NEK4, NEK9, PAK3, PIM1, RET, FGF-R2, PDGF-Ralpha and -Rss.	Quercetin	46-55	ret proto-oncogene	Homo sapiens	355-358
22466090-1	2011	The approval of receptor tyrosine kinase (RTK) targeted agent sorafenib as the first effective drug for the systemic treatment of advanced hepatocellular carcinoma (HCC) represents a milestone in the treatment of this disease.	Sorafenib	62-71	ret proto-oncogene	Homo sapiens	42-45
20977903-1	2011	BACKGROUND &amp; AIMS: Two noncoding variations in RET-the T allele of the single nucleotide polymorphism (SNP) rs2435357 (Enh1:C&gt;T) and the A allele of the SNP rs2506004 (Enh2:C&gt;A)-are associated with Hirschsprung"s disease.	Adenosine Monophosphate	12-15	ret proto-oncogene	Homo sapiens	51-54
21233183-2	2011	We therefore hypothesized that metabolic imaging could allow noninvasive detection of response to the RET inhibitor vandetanib in vivo.	vandetanib	116-126	ret proto-oncogene	Homo sapiens	102-105
21142131-1	2011	The neutral molecule temperature dependence of the rate coefficient for the electron transfer reaction from H(2)O to N(2)(+) is determined using a coaxial molecular beam radio frequency ring electrode ion trap (CoMB-RET) method.	Water	108-113	ret proto-oncogene	Homo sapiens	216-219
21142131-1	2011	The neutral molecule temperature dependence of the rate coefficient for the electron transfer reaction from H(2)O to N(2)(+) is determined using a coaxial molecular beam radio frequency ring electrode ion trap (CoMB-RET) method.	Nitrogen	117-118	ret proto-oncogene	Homo sapiens	216-219
22016822-10	2011	All together these results suggest that RET kinase activation is crucial for beta-catenin stabilization (pY654), localization and its signaling pathway activation but not for beta-catenin/RET physical interactions, in human papillary thyroid carcinomas.	py654	105-110	ret proto-oncogene	Homo sapiens	40-43
22016822-5	2011	Here, we investigated the effects of the ZD6474, a small molecule RET-inhibitor, on RET/beta-catenin interaction.	vandetanib	41-47	ret proto-oncogene	Homo sapiens	66-69
22016822-11	2011	In conclusion, ZD6474, by inhibiting RET kinase, down-modulates beta-catenin pathway leading its recruitment to the membrane by E-cadherin.	vandetanib	15-21	ret proto-oncogene	Homo sapiens	37-40
22016822-5	2011	Here, we investigated the effects of the ZD6474, a small molecule RET-inhibitor, on RET/beta-catenin interaction.	vandetanib	41-47	ret proto-oncogene	Homo sapiens	84-87
20497437-2	2011	These mutations cause changes in either the cysteine-rich extracellular domain or, less commonly, the non-cysteine intracellular domains of the RET protein.	Cysteine	106-114	ret proto-oncogene	Homo sapiens	144-147
22016822-6	2011	We confirmed the ZD6474 mediated-inhibition of recombinant RET kinase and of growth of cells expressing RET/PTC.	vandetanib	17-23	ret proto-oncogene	Homo sapiens	59-62
22016822-6	2011	We confirmed the ZD6474 mediated-inhibition of recombinant RET kinase and of growth of cells expressing RET/PTC.	vandetanib	17-23	ret proto-oncogene	Homo sapiens	104-107
22016822-9	2011	Surprisingly, RET and beta-catenin co-immunoprecipitated in both ZD6474-treated and untreated TPC1 cells, suggesting that RET/beta-catenin interaction might not be affected by RET kinase inactivation.	vandetanib	65-71	ret proto-oncogene	Homo sapiens	14-17
20497437-7	2011	This review summarizes the genotypic and phenotypic characteristics of RET codon 804 mutation, a prototype for the less well-defined non-cysteine RET mutations associated with MEN 2.	Cysteine	137-145	ret proto-oncogene	Homo sapiens	71-74
21070478-7	2011	BRAF(V600E) mutation was absent but RET/PTC1 rearrangement was found in only two (6.7%) cases of WDT-UMP.	wdt-ump	97-104	ret proto-oncogene	Homo sapiens	36-39
20497437-3	2011	The genotype-phenotype correlations of classical cysteine RET mutations have been the subject of several comprehensive reviews.	Cysteine	49-57	ret proto-oncogene	Homo sapiens	58-61
21921646-1	2011	OBJECTIVES: Vandetanib is an oral inhibitor of vascular endothelial growth factor receptor, epidermal growth factor receptor and RET (REarranged during Transfection) signaling.	vandetanib	12-22	ret proto-oncogene	Homo sapiens	129-132
21836817-1	2011	Vandetanib (ZD6474) is an orally bioavailable small molecule tyrosine kinase inhibitor of multiple growth factor receptors, including RET (Rearrange during transfection), vascular endothelial growth factor receptor-2 (VEGFR-2) and epidermal growth factor receptor (EGFR).	vandetanib	0-10	ret proto-oncogene	Homo sapiens	134-137
21836817-1	2011	Vandetanib (ZD6474) is an orally bioavailable small molecule tyrosine kinase inhibitor of multiple growth factor receptors, including RET (Rearrange during transfection), vascular endothelial growth factor receptor-2 (VEGFR-2) and epidermal growth factor receptor (EGFR).	vandetanib	0-10	ret proto-oncogene	Homo sapiens	139-168
21836817-1	2011	Vandetanib (ZD6474) is an orally bioavailable small molecule tyrosine kinase inhibitor of multiple growth factor receptors, including RET (Rearrange during transfection), vascular endothelial growth factor receptor-2 (VEGFR-2) and epidermal growth factor receptor (EGFR).	vandetanib	12-18	ret proto-oncogene	Homo sapiens	134-137
21836817-1	2011	Vandetanib (ZD6474) is an orally bioavailable small molecule tyrosine kinase inhibitor of multiple growth factor receptors, including RET (Rearrange during transfection), vascular endothelial growth factor receptor-2 (VEGFR-2) and epidermal growth factor receptor (EGFR).	vandetanib	12-18	ret proto-oncogene	Homo sapiens	139-168
20960036-0	2011	High glucose promotes cell proliferation and enhances GDNF and RET expression in pancreatic cancer cells.	Glucose	5-12	ret proto-oncogene	Homo sapiens	63-66
21110809-2	2011	RET protein comprises an extracellular portion with four cadherine-like domains and a cysteine- rich region important for intermolecular interactions; a hydrophobic transmembrane domain; an intracellular part comprising the juxtamembrane domain with regulatory function and the catalytic domain that phosphorylates the tyrosine residues of substrates.	Cysteine	86-94	ret proto-oncogene	Homo sapiens	0-3
21110809-2	2011	RET protein comprises an extracellular portion with four cadherine-like domains and a cysteine- rich region important for intermolecular interactions; a hydrophobic transmembrane domain; an intracellular part comprising the juxtamembrane domain with regulatory function and the catalytic domain that phosphorylates the tyrosine residues of substrates.	Tyrosine	319-327	ret proto-oncogene	Homo sapiens	0-3
20960036-5	2011	Glucose concentrations could alter the expression of GDNF and RET in a concentration-dependent manner, correspondingly with the alterations of cell proliferation.	Glucose	0-7	ret proto-oncogene	Homo sapiens	62-65
20960036-6	2011	Up-regulation of GDNF and RET ligand-receptor interaction might participate in the glucose-induced cancer progression.	Glucose	83-90	ret proto-oncogene	Homo sapiens	26-29
21921646-1	2011	OBJECTIVES: Vandetanib is an oral inhibitor of vascular endothelial growth factor receptor, epidermal growth factor receptor and RET (REarranged during Transfection) signaling.	vandetanib	12-22	ret proto-oncogene	Homo sapiens	134-164
22174910-4	2011	Considering the role of RAS and RAF as downstream signals of both the EGFR and VEGFR pathways, we treated resistant cells with sorafenib, an inhibitor of C-RAF, B-RAF, c-KIT, FLT-3, RET, VEGFR-2, VEGFR-3, and PDGFR-beta.	Sorafenib	127-136	ret proto-oncogene	Homo sapiens	182-185
21542403-13	2010	On genetic testing, an RET point mutation at the high-risk 634 cysteine allele was identified in 11 cases.	Cysteine	63-71	ret proto-oncogene	Homo sapiens	23-26
22440657-3	2011	OBJECTIVE: To evaluate the ability of Reticulocyte Hemoglobin Equivalent (RET-He) to predict iron deficiency, taking as a reference standard to the increase of hemoglobin in response to iron intake.	Iron	93-97	ret proto-oncogene	Homo sapiens	74-77
22440657-10	2011	CONCLUSIONS: According to these results it could consider to Ret-He and the Ret-He/IST combination of clinical utility for the identification of the iron deficit in patients in chronic haemodialysis.	Iron	149-153	ret proto-oncogene	Homo sapiens	61-64
22440657-10	2011	CONCLUSIONS: According to these results it could consider to Ret-He and the Ret-He/IST combination of clinical utility for the identification of the iron deficit in patients in chronic haemodialysis.	Iron	149-153	ret proto-oncogene	Homo sapiens	76-79
20672370-1	2010	BACKGROUND: Sorafenib is an inhibitor of multiple kinases (e.g., VEGF receptors, PDGFR, FLT3, RET, BRAF, KIT) and is approved by FDA for treatment of two adult cancers.	Sorafenib	12-21	ret proto-oncogene	Homo sapiens	94-97
21386776-1	2010	Forty percent to 50% of acetylcholine receptor antibody-seronegative patients with myasthenia gravis have muscle-specific receptor tyrosine kinase antibodies.	Acetylcholine	24-37	ret proto-oncogene	Homo sapiens	122-146
20943719-0	2011	The tyrosine kinase inhibitor ZD6474 blocks proliferation of RET mutant medullary thyroid carcinoma cells.	vandetanib	30-36	ret proto-oncogene	Homo sapiens	61-64
20943719-2	2011	ZD6474 (vandetanib) is an ATP-competitive inhibitor of RET, epidermal growth factor receptor (EGFR), and vascular endothelial growth factor receptors kinases.	vandetanib	0-6	ret proto-oncogene	Homo sapiens	55-58
20943719-2	2011	ZD6474 (vandetanib) is an ATP-competitive inhibitor of RET, epidermal growth factor receptor (EGFR), and vascular endothelial growth factor receptors kinases.	vandetanib	8-18	ret proto-oncogene	Homo sapiens	55-58
20943719-2	2011	ZD6474 (vandetanib) is an ATP-competitive inhibitor of RET, epidermal growth factor receptor (EGFR), and vascular endothelial growth factor receptors kinases.	Adenosine Triphosphate	26-29	ret proto-oncogene	Homo sapiens	55-58
20943719-6	2011	Adoptive expression of the ZD6474-resistant V804M RET mutant rescued proliferation of TT cells under ZD6474 treatment, showing that RET is a key ZD6474 target in these MTC cells.	vandetanib	27-33	ret proto-oncogene	Homo sapiens	50-53
20943719-6	2011	Adoptive expression of the ZD6474-resistant V804M RET mutant rescued proliferation of TT cells under ZD6474 treatment, showing that RET is a key ZD6474 target in these MTC cells.	vandetanib	27-33	ret proto-oncogene	Homo sapiens	132-135
20943719-6	2011	Adoptive expression of the ZD6474-resistant V804M RET mutant rescued proliferation of TT cells under ZD6474 treatment, showing that RET is a key ZD6474 target in these MTC cells.	vandetanib	101-107	ret proto-oncogene	Homo sapiens	50-53
20943719-6	2011	Adoptive expression of the ZD6474-resistant V804M RET mutant rescued proliferation of TT cells under ZD6474 treatment, showing that RET is a key ZD6474 target in these MTC cells.	vandetanib	101-107	ret proto-oncogene	Homo sapiens	132-135
20943719-6	2011	Adoptive expression of the ZD6474-resistant V804M RET mutant rescued proliferation of TT cells under ZD6474 treatment, showing that RET is a key ZD6474 target in these MTC cells.	vandetanib	101-107	ret proto-oncogene	Homo sapiens	50-53
20943719-6	2011	Adoptive expression of the ZD6474-resistant V804M RET mutant rescued proliferation of TT cells under ZD6474 treatment, showing that RET is a key ZD6474 target in these MTC cells.	vandetanib	101-107	ret proto-oncogene	Homo sapiens	132-135
20943719-8	2011	This suggests that simultaneous inhibition of RET and EGFR by ZD6474 may overcome the risk of MTC cells to escape from RET blockade through compensatory over-activation of EGFR.	vandetanib	62-68	ret proto-oncogene	Homo sapiens	46-49
20943719-8	2011	This suggests that simultaneous inhibition of RET and EGFR by ZD6474 may overcome the risk of MTC cells to escape from RET blockade through compensatory over-activation of EGFR.	vandetanib	62-68	ret proto-oncogene	Homo sapiens	119-122
20796177-1	2010	We examined the effect of concanamycin A and bafilomycin A1, inhibitors of the vacuolar proton-ATPase, on maturation and expression of Ret, a tyrosine kinase receptor for glial cell line-derived neurotrophic factor.	concanamycin A	26-40	ret proto-oncogene	Homo sapiens	135-138
20796177-1	2010	We examined the effect of concanamycin A and bafilomycin A1, inhibitors of the vacuolar proton-ATPase, on maturation and expression of Ret, a tyrosine kinase receptor for glial cell line-derived neurotrophic factor.	bafilomycin	45-56	ret proto-oncogene	Homo sapiens	135-138
20796177-2	2010	Ret appeared as 150- and 170-kDa bands on sodium dodecyl sulfate-polyacrylamide gel electrophoresis gels and both forms were sensitive to peptide-N-glycosidase F. Western and immunocytochemical analyses revealed that the 150-kDa immature form of Ret accumulated in the Golgi apparatus upon treatment with vacuolar proton-ATPase inhibitors, whereas, the 170-kDa mature form of Ret was dramatically decreased.	Sodium Dodecyl Sulfate	42-64	ret proto-oncogene	Homo sapiens	0-3
20796177-2	2010	Ret appeared as 150- and 170-kDa bands on sodium dodecyl sulfate-polyacrylamide gel electrophoresis gels and both forms were sensitive to peptide-N-glycosidase F. Western and immunocytochemical analyses revealed that the 150-kDa immature form of Ret accumulated in the Golgi apparatus upon treatment with vacuolar proton-ATPase inhibitors, whereas, the 170-kDa mature form of Ret was dramatically decreased.	polyacrylamide	65-79	ret proto-oncogene	Homo sapiens	0-3
20955590-0	2010	Dasatinib reduces FAK phosphorylation increasing the effects of RPI-1 inhibition in a RET/PTC1-expressing cell line.	Dasatinib	0-9	ret proto-oncogene	Homo sapiens	86-89
20973951-4	2010	Under experimental conditions Grb7 is tyrosine phosphorylated by the Tie2/Tie-2/Tek angiogenic receptor tyrosine kinase (RTK).	Tyrosine	38-46	ret proto-oncogene	Homo sapiens	95-119
20973951-4	2010	Under experimental conditions Grb7 is tyrosine phosphorylated by the Tie2/Tie-2/Tek angiogenic receptor tyrosine kinase (RTK).	Tyrosine	38-46	ret proto-oncogene	Homo sapiens	121-124
20802287-6	2010	The results indicated that malondialdehyde (MDA) significantly decreased (p &lt; 0.05) in both groups immediately after RET; however, there was no significant acute alteration in glutathione (GSH) level in both groups (p &gt; 0.05).	Malondialdehyde	27-42	ret proto-oncogene	Homo sapiens	120-123
20682772-2	2010	In the receptor tyrosine kinase RET, a receptor for GDNF (glial cell line-derived neurotrophic factor), the functions of the majority of tyrosine residues that become phosphorylated are still unknown.	Tyrosine	16-24	ret proto-oncogene	Homo sapiens	32-35
20682772-3	2010	Here we have identified the protein-tyrosine phosphatase SHP2 as a novel direct interactor of RET and the first effector known to bind to phosphorylated Tyr(687) in the juxtamembrane region of the receptor.	Tyrosine	153-156	ret proto-oncogene	Homo sapiens	94-97
20682772-4	2010	We show that SHP2 is recruited to RET upon ligand binding in a cooperative fashion, such that both interaction with Tyr(687) and association with components of the Tyr(1062) signaling complex are required for stable recruitment of SHP2 to the receptor.	Tyrosine	116-119	ret proto-oncogene	Homo sapiens	34-37
20682772-4	2010	We show that SHP2 is recruited to RET upon ligand binding in a cooperative fashion, such that both interaction with Tyr(687) and association with components of the Tyr(1062) signaling complex are required for stable recruitment of SHP2 to the receptor.	Tyrosine	164-167	ret proto-oncogene	Homo sapiens	34-37
20682772-6	2010	Furthermore, we find that activation of protein kinase A (PKA) by forskolin reduces the recruitment of SHP2 to RET and negatively affects ligand-mediated neurite outgrowth.	Colforsin	66-75	ret proto-oncogene	Homo sapiens	111-114
20682772-7	2010	In agreement with this, mutation of Ser(696), a known PKA phosphorylation site in RET, enhances SHP2 binding to the receptor and eliminates the effect of forskolin on ligand-induced outgrowth.	Serine	36-39	ret proto-oncogene	Homo sapiens	82-85
20682772-8	2010	Together, these findings establish SHP2 as a novel positive regulator of the neurotrophic activities of RET and reveal Tyr(687) as a critical platform for integration of RET and PKA signals.	Tyrosine	119-122	ret proto-oncogene	Homo sapiens	170-173
20576526-9	2010	Earlier studies showing LPA-induced Erk1/2 activation being fully dependent on RTK transactivation have all been performed in cell lines and transfected cells.	lysophosphatidic acid	24-27	ret proto-oncogene	Homo sapiens	79-82
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
20521125-4	2010	The presence of the polymorphic change L769L in the RET gene predisposes to the development of sMTC and also lowers the age of onset of MTC in carriers of the homozygous polymorphic variant L769L.	smtc	95-99	ret proto-oncogene	Homo sapiens	52-55
20802287-7	2010	After 6 weeks of training, pre-RET values of MDA significantly decreased and pre-RET values of GSH significantly increased in both hypertrophy- and strength-intensity groups (p &lt; 0.05).	Glutathione	95-98	ret proto-oncogene	Homo sapiens	81-84
20802287-9	2010	This study indicated that hypertrophy- and strength-intensity whole-body RET performed regularly for 6 weeks, decreased MDA concentration and increased GSH level in healthy young men.	Glutathione	152-155	ret proto-oncogene	Homo sapiens	73-76
19850519-10	2010	The carriers of the A1470T polymorphism in the MTC1 gene seem to exhibit a worse lactate transport capability into the less active muscle cells for oxidation.	Lactic Acid	81-88	ret proto-oncogene	Homo sapiens	47-51
20531297-0	2010	Targeting the receptor tyrosine kinase RET sensitizes breast cancer cells to tamoxifen treatment and reveals a role for RET in endocrine resistance.	Tamoxifen	77-86	ret proto-oncogene	Homo sapiens	39-42
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	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	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.	Iodides	128-134	ret proto-oncogene	Homo sapiens	192-195
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
20629553-6	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
20629553-7	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
20629553-10	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.	Sodium	101-107	ret proto-oncogene	Homo sapiens	23-26
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	ret proto-oncogene	Homo sapiens	282-285
20531297-5	2010	In tamoxifen response experiments, RET downregulation resulted in 6.2-fold increase in sensitivity of MCF7 cells to antiproliferative effects of tamoxifen, whereas GDNF stimulation had a protective effect against the drug.	Tamoxifen	3-12	ret proto-oncogene	Homo sapiens	35-38
20531297-5	2010	In tamoxifen response experiments, RET downregulation resulted in 6.2-fold increase in sensitivity of MCF7 cells to antiproliferative effects of tamoxifen, whereas GDNF stimulation had a protective effect against the drug.	Tamoxifen	145-154	ret proto-oncogene	Homo sapiens	35-38
20531297-6	2010	In tamoxifen-resistant (TAM(R)-1) MCF7 cells, targeting RET restored tamoxifen sensitivity.	Tamoxifen	3-12	ret proto-oncogene	Homo sapiens	56-59
20531297-6	2010	In tamoxifen-resistant (TAM(R)-1) MCF7 cells, targeting RET restored tamoxifen sensitivity.	Tamoxifen	69-78	ret proto-oncogene	Homo sapiens	56-59
20531297-7	2010	Finally, examination of two independent tissue microarrays of primary human breast cancers revealed that expression of RET protein was significantly associated with ERalpha-positive tumors and that in primary tumors from patients who subsequently developed invasive recurrence after adjuvant tamoxifen treatment, there was a twofold increase in the number of RET-positive tumors.	Tamoxifen	292-301	ret proto-oncogene	Homo sapiens	119-122
20531297-7	2010	Finally, examination of two independent tissue microarrays of primary human breast cancers revealed that expression of RET protein was significantly associated with ERalpha-positive tumors and that in primary tumors from patients who subsequently developed invasive recurrence after adjuvant tamoxifen treatment, there was a twofold increase in the number of RET-positive tumors.	Tamoxifen	292-301	ret proto-oncogene	Homo sapiens	359-362
20531297-8	2010	Together these findings identify RET as a potentially important therapeutic target in ERalpha-positive breast cancers and in particular in tamoxifen-resistant tumors.	Tamoxifen	139-148	ret proto-oncogene	Homo sapiens	33-36
20444924-4	2010	OBJECTIVE: Our aim was to investigate whether RET protein half-life depends on HSP90 and to dissect the molecular pathway responsible for the degradation of RET upon HSP90 inhibition by 17-AAG.	tanespimycin	186-192	ret proto-oncogene	Homo sapiens	46-49
20701442-4	2010	Additional studies in non-small-cell lung cancer have suggested that the k-ras mutation may be a negative predictor of response to the EGF receptor tyrosine kinase inhibitors erlotinib and gefitinib.	Gefitinib	189-198	ret proto-oncogene	Homo sapiens	139-163
20661087-1	2010	INTRODUCTION: Vandetanib is a once-daily oral agent that selectively inhibits vascular endothelial growth factor receptor, epidermal growth factor receptor, and RET (REarranged during Transfection) signaling.	vandetanib	14-24	ret proto-oncogene	Homo sapiens	161-164
20661087-1	2010	INTRODUCTION: Vandetanib is a once-daily oral agent that selectively inhibits vascular endothelial growth factor receptor, epidermal growth factor receptor, and RET (REarranged during Transfection) signaling.	vandetanib	14-24	ret proto-oncogene	Homo sapiens	166-196
20442138-4	2010	The substitution of the tyrosine 905 of RET51, a key residue phosphorylated by both GDNF and NGF, disrupts the RET51/FKBP52 complex.	Tyrosine	24-32	ret proto-oncogene	Homo sapiens	40-45
20442138-4	2010	The substitution of the tyrosine 905 of RET51, a key residue phosphorylated by both GDNF and NGF, disrupts the RET51/FKBP52 complex.	Tyrosine	24-32	ret proto-oncogene	Homo sapiens	111-116
20442138-6	2010	To clarify if RET51/FKBP52 complex should exert its function in DA neurons, we used an indirect approach by screening the genes encoding for RET51 and FKBP52 in a group of 30 Parkinson"s disease patients.	Dopamine	64-66	ret proto-oncogene	Homo sapiens	14-19
20409618-0	2010	Inhibitors of the RET tyrosine kinase based on a 2-(alkylsulfanyl)-4-(3-thienyl)nicotinonitrile scaffold.	2-(alkylsulfanyl)-4-(3-thienyl)nicotinonitrile	49-95	ret proto-oncogene	Homo sapiens	18-21
20409618-1	2010	In an approach to optimize 2-(4-fluorobenzylsulfanyl)-4-(2-thienyl)-5,6,7,8-tetrahydroquinoline-3-carbonitrile (1a), a weak inhibitor of the cancer-related tyrosine kinase RET originating from a screening campaign, analogues with 3-thienyl substitution were prepared.	CHEMBL1172697	27-110	ret proto-oncogene	Homo sapiens	172-175
20409618-2	2010	Among the novel derivatives, 2-amino-6-{[2-(4-chlorophenyl)-2-oxoethyl]sulfanyl}-4-(3-thienyl)pyridine-3,5-dicarbonitrile (13 g) was identified as a submicromolar RET inhibitor, displaying 3- and 100-fold selectivity versus ALK and ABL kinases, respectively.	CHEMBL1172147	29-121	ret proto-oncogene	Homo sapiens	163-166
20701442-4	2010	Additional studies in non-small-cell lung cancer have suggested that the k-ras mutation may be a negative predictor of response to the EGF receptor tyrosine kinase inhibitors erlotinib and gefitinib.	Erlotinib Hydrochloride	175-184	ret proto-oncogene	Homo sapiens	139-163
20516206-7	2010	The comparison of the prevalence of RET germline mutations in the present study with those published by other European studies showed a higher prevalence of Val804Met and Ser891Ala mutations and a lower prevalence of Leu790Phe and Tyr791Phe (P&lt;0.0001).	leu790phe	217-226	ret proto-oncogene	Homo sapiens	36-39
20689759-0	2010	Ron receptor tyrosine kinase activation confers resistance to tamoxifen in breast cancer cell lines.	Tamoxifen	62-71	ret proto-oncogene	Homo sapiens	4-28
20689759-9	2010	In summary, these results illustrate a novel connection between the Ron receptor tyrosine kinase and an important mechanism of tamoxifen resistance in breast cancer.	Tamoxifen	127-136	ret proto-oncogene	Homo sapiens	72-96
20444924-4	2010	OBJECTIVE: Our aim was to investigate whether RET protein half-life depends on HSP90 and to dissect the molecular pathway responsible for the degradation of RET upon HSP90 inhibition by 17-AAG.	tanespimycin	186-192	ret proto-oncogene	Homo sapiens	157-160
20444924-6	2010	RESULTS: 17-AAG induced a 26S proteasome-dependent degradation of wild-type RET and MEN2-associated RET mutants.	tanespimycin	9-15	ret proto-oncogene	Homo sapiens	76-79
20444924-6	2010	RESULTS: 17-AAG induced a 26S proteasome-dependent degradation of wild-type RET and MEN2-associated RET mutants.	tanespimycin	9-15	ret proto-oncogene	Homo sapiens	100-103
20444924-9	2010	17-AAG blocked RET downstream effectors and RET-dependent transcriptional activation of gene promoters.	tanespimycin	0-6	ret proto-oncogene	Homo sapiens	15-18
20444924-9	2010	17-AAG blocked RET downstream effectors and RET-dependent transcriptional activation of gene promoters.	tanespimycin	0-6	ret proto-oncogene	Homo sapiens	44-47
20530713-2	2010	Oncomine data indicate that expression of components of the ARTN signaling pathway (ARTN, GFRA3, and RET) is increased in neoplastic compared with normal lung tissues; increased expression of ARTN in NSCLC also predicted metastasis to lymph nodes and a higher grade in certain NSCLC subtypes.	oncomine	0-8	ret proto-oncogene	Homo sapiens	101-104
20444924-11	2010	CONCLUSION: RET and MEN2-associated RET mutants rely on HSP90 for protein stability, and HSP90 blockade by 17-AAG promotes RET degradation.	tanespimycin	107-113	ret proto-oncogene	Homo sapiens	36-39
20444924-11	2010	CONCLUSION: RET and MEN2-associated RET mutants rely on HSP90 for protein stability, and HSP90 blockade by 17-AAG promotes RET degradation.	tanespimycin	107-113	ret proto-oncogene	Homo sapiens	36-39
20570559-1	2010	BACKGROUND: Vandetanib is a once-daily oral inhibitor of vascular endothelial growth factor receptor (VEGFR), epidermal growth factor receptor (EGFR), and rearranged during transfection (RET) tyrosine kinases.	vandetanib	12-22	ret proto-oncogene	Homo sapiens	155-185
20570559-1	2010	BACKGROUND: Vandetanib is a once-daily oral inhibitor of vascular endothelial growth factor receptor (VEGFR), epidermal growth factor receptor (EGFR), and rearranged during transfection (RET) tyrosine kinases.	vandetanib	12-22	ret proto-oncogene	Homo sapiens	187-190
20470206-15	2010	CONCLUSIONS: Taken together, our findings demonstrate that sulindac treatment reverses beta-catenin activity in 8505-C and KTC-1 cell lines with the BRAF(V600E), but not in TPC-1 cells with the RET/PTC mutation.	Sulindac	59-67	ret proto-oncogene	Homo sapiens	194-197
20473317-4	2010	We identify two unpaired cysteines that predispose human RET to maturation impediments in the endoplasmic reticulum and establish a quantitative cell-based RET maturation assay that offers a biochemical correlate of HSCR disease severity.	Cysteine	25-34	ret proto-oncogene	Homo sapiens	57-60
20470206-15	2010	CONCLUSIONS: Taken together, our findings demonstrate that sulindac treatment reverses beta-catenin activity in 8505-C and KTC-1 cell lines with the BRAF(V600E), but not in TPC-1 cells with the RET/PTC mutation.	Sulindac	59-67	ret proto-oncogene	Homo sapiens	198-201
20424115-0	2010	Role of H2O2 in RET/PTC1 chromosomal rearrangement produced by ionizing radiation in human thyroid cells.	Hydrogen Peroxide	8-12	ret proto-oncogene	Homo sapiens	16-19
20456957-0	2010	Serotonin derivatives as a new class of non-ATP-competitive receptor tyrosine kinase inhibitors.	Serotonin	0-9	ret proto-oncogene	Homo sapiens	60-84
20424115-8	2010	Pretreatment of cells with catalase, a scavenger of H(2)O(2), significantly decreased RET/PTC1 rearrangement formation.	Water	52-57	ret proto-oncogene	Homo sapiens	86-89
20456957-0	2010	Serotonin derivatives as a new class of non-ATP-competitive receptor tyrosine kinase inhibitors.	Adenosine Triphosphate	44-47	ret proto-oncogene	Homo sapiens	60-84
20456957-3	2010	The majority of the known small molecules RTK inhibitors are ATP-competitive and they are multiple targeted inhibitors.	Adenosine Triphosphate	61-64	ret proto-oncogene	Homo sapiens	42-45
20424115-9	2010	Finally, RET/PTC chromosomal rearrangement was detected in HTori-3.1 cells after exposure of cells to H(2)O(2) (25 micromol/L), at a dose that did not affect the cell viability.	Hydrogen Peroxide	102-110	ret proto-oncogene	Homo sapiens	9-12
20456957-4	2010	We describe here serotonin derivatives as a new class of multiple targeted RTK inhibitors.	Serotonin	17-26	ret proto-oncogene	Homo sapiens	75-78
20456957-5	2010	In contrast to most other RTK inhibitors they act via a non-ATP-competitive (allosteric) mechanism.	Adenosine Triphosphate	60-63	ret proto-oncogene	Homo sapiens	26-29
20235151-3	2010	Arsenic further activated RET-MEN2A kinase, which was already 3- to 10-fold augmented by genetic mutation compared with c-RET kinase activity, with promotion of disulfide bond-mediated dimerization of RET-MEN2A protein (superactivation).	Disulfides	161-170	ret proto-oncogene	Homo sapiens	205-210
20235151-0	2010	A redox-linked novel pathway for arsenic-mediated RET tyrosine kinase activation.	Arsenic	33-40	ret proto-oncogene	Homo sapiens	50-53
20225331-0	2010	A novel therapeutic combination for neuroblastoma: the vascular endothelial growth factor receptor/epidermal growth factor receptor/rearranged during transfection inhibitor vandetanib with 13-cis-retinoic acid.	vandetanib	173-183	ret proto-oncogene	Homo sapiens	132-162
20225331-2	2010	Vandetanib (ZD6474, Zactima) is an inhibitor of the vascular endothelial growth factor receptor, epidermal growth factor receptor, and rearranged during transfection (RET) tyrosine kinases, which have each been implicated in neuroblastoma pathogenesis.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	135-165
20225331-2	2010	Vandetanib (ZD6474, Zactima) is an inhibitor of the vascular endothelial growth factor receptor, epidermal growth factor receptor, and rearranged during transfection (RET) tyrosine kinases, which have each been implicated in neuroblastoma pathogenesis.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	167-170
20225331-2	2010	Vandetanib (ZD6474, Zactima) is an inhibitor of the vascular endothelial growth factor receptor, epidermal growth factor receptor, and rearranged during transfection (RET) tyrosine kinases, which have each been implicated in neuroblastoma pathogenesis.	vandetanib	12-18	ret proto-oncogene	Homo sapiens	135-165
20225331-2	2010	Vandetanib (ZD6474, Zactima) is an inhibitor of the vascular endothelial growth factor receptor, epidermal growth factor receptor, and rearranged during transfection (RET) tyrosine kinases, which have each been implicated in neuroblastoma pathogenesis.	vandetanib	12-18	ret proto-oncogene	Homo sapiens	167-170
20225331-4	2010	METHODS: The authors evaluated the effects of vandetanib with and without CRA on RET phosphorylation and on the proliferation and survival of human neuroblastoma cell lines in vitro.	vandetanib	46-56	ret proto-oncogene	Homo sapiens	81-84
20225331-6	2010	RESULTS: Vandetanib treatment inhibited RET phosphorylation and resulted in induction of apoptosis in the majority of neuroblastoma cell lines in vitro, whereas CRA treatment induced morphologic differentiation and cell-cycle arrest.	vandetanib	9-19	ret proto-oncogene	Homo sapiens	40-43
20235151-1	2010	We examined the biochemical effects of arsenic on the activities of RET proto-oncogene (c-RET protein tyrosine kinases) and RET oncogene (RET-MEN2A and RET-PTC1 protein tyrosine kinases) products.	Arsenic	39-46	ret proto-oncogene	Homo sapiens	68-71
20235151-2	2010	Arsenic activated c-RET kinase with promotion of disulfide bond-mediated dimerization of c-RET protein.	Arsenic	0-7	ret proto-oncogene	Homo sapiens	20-23
20235151-4	2010	Arsenic also increased extracellular domain-deleted RET-PTC1 kinase activity with promotion of disulfide bond-mediated dimerization of RET-PTC1 protein.	Arsenic	0-7	ret proto-oncogene	Homo sapiens	52-55
20235151-2	2010	Arsenic activated c-RET kinase with promotion of disulfide bond-mediated dimerization of c-RET protein.	Arsenic	0-7	ret proto-oncogene	Homo sapiens	91-94
20235151-2	2010	Arsenic activated c-RET kinase with promotion of disulfide bond-mediated dimerization of c-RET protein.	Disulfides	49-58	ret proto-oncogene	Homo sapiens	91-94
20235151-4	2010	Arsenic also increased extracellular domain-deleted RET-PTC1 kinase activity with promotion of disulfide bond-mediated dimerization of RET-PTC1 protein.	Arsenic	0-7	ret proto-oncogene	Homo sapiens	135-138
20235151-3	2010	Arsenic further activated RET-MEN2A kinase, which was already 3- to 10-fold augmented by genetic mutation compared with c-RET kinase activity, with promotion of disulfide bond-mediated dimerization of RET-MEN2A protein (superactivation).	Arsenic	0-7	ret proto-oncogene	Homo sapiens	26-29
20235151-4	2010	Arsenic also increased extracellular domain-deleted RET-PTC1 kinase activity with promotion of disulfide bond-mediated dimerization of RET-PTC1 protein.	Disulfides	95-104	ret proto-oncogene	Homo sapiens	135-138
20235151-3	2010	Arsenic further activated RET-MEN2A kinase, which was already 3- to 10-fold augmented by genetic mutation compared with c-RET kinase activity, with promotion of disulfide bond-mediated dimerization of RET-MEN2A protein (superactivation).	Arsenic	0-7	ret proto-oncogene	Homo sapiens	30-35
20235151-3	2010	Arsenic further activated RET-MEN2A kinase, which was already 3- to 10-fold augmented by genetic mutation compared with c-RET kinase activity, with promotion of disulfide bond-mediated dimerization of RET-MEN2A protein (superactivation).	Arsenic	0-7	ret proto-oncogene	Homo sapiens	205-210
20235151-5	2010	Arsenic increased RET-PTC1 kinase activity with cysteine 365 (C365) replaced by alanine with promotion of dimer formation but not with cysteine 376 (C376) replaced by alanine.	Arsenic	0-7	ret proto-oncogene	Homo sapiens	18-21
20235151-5	2010	Arsenic increased RET-PTC1 kinase activity with cysteine 365 (C365) replaced by alanine with promotion of dimer formation but not with cysteine 376 (C376) replaced by alanine.	Cysteine	48-56	ret proto-oncogene	Homo sapiens	18-21
20235151-5	2010	Arsenic increased RET-PTC1 kinase activity with cysteine 365 (C365) replaced by alanine with promotion of dimer formation but not with cysteine 376 (C376) replaced by alanine.	Alanine	80-87	ret proto-oncogene	Homo sapiens	18-21
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Arsenic	25-32	ret proto-oncogene	Homo sapiens	56-59
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Arsenic	25-32	ret proto-oncogene	Homo sapiens	117-120
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Arsenic	25-32	ret proto-oncogene	Homo sapiens	117-120
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Arsenic	25-32	ret proto-oncogene	Homo sapiens	117-120
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Cysteine	161-169	ret proto-oncogene	Homo sapiens	56-59
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Cysteine	161-169	ret proto-oncogene	Homo sapiens	117-120
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Cysteine	161-169	ret proto-oncogene	Homo sapiens	117-120
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Cysteine	161-169	ret proto-oncogene	Homo sapiens	117-120
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Cysteine	229-237	ret proto-oncogene	Homo sapiens	56-59
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Cysteine	229-237	ret proto-oncogene	Homo sapiens	117-120
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Cysteine	229-237	ret proto-oncogene	Homo sapiens	117-120
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Cysteine	229-237	ret proto-oncogene	Homo sapiens	117-120
20235151-7	2010	Moreover, arsenic enhanced the activity of immunoprecipitated RET protein with increase in thiol-dependent dimer formation.	Arsenic	10-17	ret proto-oncogene	Homo sapiens	62-65
20235151-7	2010	Moreover, arsenic enhanced the activity of immunoprecipitated RET protein with increase in thiol-dependent dimer formation.	Sulfhydryl Compounds	91-96	ret proto-oncogene	Homo sapiens	62-65
20235151-8	2010	As arsenic (14.2 microM) was detected in the cells cultured with arsenic (100 microM), direct association between arsenic and RET in the cells might modulate dimer formation.	Arsenic	3-10	ret proto-oncogene	Homo sapiens	126-129
20235151-8	2010	As arsenic (14.2 microM) was detected in the cells cultured with arsenic (100 microM), direct association between arsenic and RET in the cells might modulate dimer formation.	Arsenic	65-72	ret proto-oncogene	Homo sapiens	126-129
20235151-8	2010	As arsenic (14.2 microM) was detected in the cells cultured with arsenic (100 microM), direct association between arsenic and RET in the cells might modulate dimer formation.	Arsenic	65-72	ret proto-oncogene	Homo sapiens	126-129
20235151-9	2010	Thus, we demonstrated a novel redox-linked mechanism of activation of arsenic-mediated RET proto-oncogene and oncogene products.	Arsenic	70-77	ret proto-oncogene	Homo sapiens	87-90
21432543-9	2010	The ADH1B*2 and ALDH2*2 haplotype was estimated to have a significantly higher influence on MN-RET frequency than the ADH1B*2 and ALDH2*1 haplotype (P = 0.00035), and the frequency of alcohol consumption played a significant role in MN-RET frequency on the background of the ADH1B*2 and ALDH2*1 haplotype (P = 0.012).	Alcohols	184-191	ret proto-oncogene	Homo sapiens	95-98
20368568-2	2010	Sorafenib, a multikinase inhibitor targeting Ret and VEGFR, showed antitumor activity in preclinical studies of MTC.	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	45-48
20210798-9	2010	The binding affinity of the DOK-6 phosphotyrosine-binding (PTB) domain to RET was much lower than that of the DOK-1, DOK-4, and SHC PTB domains to RET.	Phosphotyrosine	34-49	ret proto-oncogene	Homo sapiens	74-77
20704575-5	2010	Combined treatments with CPT-11 or SN-38 significantly increased caspase 3/7 activity compared with RET siRNA, CPT-11 or SN-38 treatment alone.	Irinotecan	25-31	ret proto-oncogene	Homo sapiens	100-103
20026268-0	2010	A negative regulatory role for Y1111 on the Tie-2 RTK.	2,2-Bis(4-hydroxy-3,5-dimethylphenyl)propane	31-36	ret proto-oncogene	Homo sapiens	50-53
20704575-5	2010	Combined treatments with CPT-11 or SN-38 significantly increased caspase 3/7 activity compared with RET siRNA, CPT-11 or SN-38 treatment alone.	Irinotecan	35-40	ret proto-oncogene	Homo sapiens	100-103
20704575-7	2010	These findings that RET siRNA enhanced sensitivity for CPT-11 will provide a novel strategy for the treatment of MTC with RET mutation.	Irinotecan	55-61	ret proto-oncogene	Homo sapiens	20-23
20704575-7	2010	These findings that RET siRNA enhanced sensitivity for CPT-11 will provide a novel strategy for the treatment of MTC with RET mutation.	Irinotecan	55-61	ret proto-oncogene	Homo sapiens	122-125
19624802-13	2010	Iron supplements given to the patients with low TSAT or ferritin, RET-He responded within 2 weeks, and this seemed to be a potential advantage of using RET-He in the estimation of iron status.	Iron	180-184	ret proto-oncogene	Homo sapiens	152-155
19624802-14	2010	RET-He is a new parameter, equivalent value to CHr, and is easily measurable on the widely spread and popular blood cell counter and is a sensitive and specific marker of iron status in dialysis patients.	Iron	171-175	ret proto-oncogene	Homo sapiens	0-3
19624802-2	2010	The cellular iron status of the patients can be determined from the recently available measurement of reticulocyte hemoglobin equivalent (RET-He).	Iron	13-17	ret proto-oncogene	Homo sapiens	138-141
20119574-3	2010	The majority of germline mutations in FMTC have been found in exons 10 and 11 of the RET proto-oncogene, specifically within the cysteine codons 609, 611, 618, 620, and 634.	Cysteine	129-137	ret proto-oncogene	Homo sapiens	85-88
19624802-3	2010	RET-He is measured on the basis of automated fluorescent flow cytometry which in the reticulocyte channel, using a polymethine dye, also measures the mean value of the forward light scatter intensity of mature red blood cells and reticulocytes.	VPM chloride	115-126	ret proto-oncogene	Homo sapiens	0-3
19624802-6	2010	Secondly, we investigated the changes in RET-He during iron supplementation for iron-deficient patients to determine whether this marker is a prospective and reliable indicator of iron sufficiency.	Iron	55-59	ret proto-oncogene	Homo sapiens	41-44
19624802-13	2010	Iron supplements given to the patients with low TSAT or ferritin, RET-He responded within 2 weeks, and this seemed to be a potential advantage of using RET-He in the estimation of iron status.	Iron	0-4	ret proto-oncogene	Homo sapiens	66-69
19624802-13	2010	Iron supplements given to the patients with low TSAT or ferritin, RET-He responded within 2 weeks, and this seemed to be a potential advantage of using RET-He in the estimation of iron status.	Iron	0-4	ret proto-oncogene	Homo sapiens	152-155
20117004-0	2010	Synthesis, structure-activity relationship and crystallographic studies of 3-substituted indolin-2-one RET inhibitors.	3-substituted indolin-2-one	75-102	ret proto-oncogene	Homo sapiens	103-106
20117004-1	2010	The synthesis, structure-activity relationships (SAR) and structural data of a series of indolin-2-one inhibitors of RET tyrosine kinase are described.	indolin-2-one	89-102	ret proto-oncogene	Homo sapiens	117-120
20117004-2	2010	These compounds were designed to explore the available space around the indolinone scaffold within RET active site.	Oxindoles	72-82	ret proto-oncogene	Homo sapiens	99-102
20117004-7	2010	These data provide important information for the development of indolinone inhibitors for the treatment of RET-driven cancers.	Oxindoles	64-74	ret proto-oncogene	Homo sapiens	107-110
20065189-3	2010	This open-label, phase II study assessed the efficacy of vandetanib, a selective oral inhibitor of RET, vascular endothelial growth factor receptor, and epidermal growth factor receptor signaling, in patients with advanced hereditary MTC.	vandetanib	57-67	ret proto-oncogene	Homo sapiens	99-102
20119574-5	2010	We report a RET mutation in exon10, codon 618 that causes substitution of a cysteine by a serine in the cysteine-rich domain of the RET receptor in a three-generation FMTC family composed of 30 members with 11 carriers.	Cysteine	76-84	ret proto-oncogene	Homo sapiens	12-15
20119574-5	2010	We report a RET mutation in exon10, codon 618 that causes substitution of a cysteine by a serine in the cysteine-rich domain of the RET receptor in a three-generation FMTC family composed of 30 members with 11 carriers.	Cysteine	76-84	ret proto-oncogene	Homo sapiens	132-135
20119574-5	2010	We report a RET mutation in exon10, codon 618 that causes substitution of a cysteine by a serine in the cysteine-rich domain of the RET receptor in a three-generation FMTC family composed of 30 members with 11 carriers.	Serine	90-96	ret proto-oncogene	Homo sapiens	12-15
20119574-5	2010	We report a RET mutation in exon10, codon 618 that causes substitution of a cysteine by a serine in the cysteine-rich domain of the RET receptor in a three-generation FMTC family composed of 30 members with 11 carriers.	Serine	90-96	ret proto-oncogene	Homo sapiens	132-135
20119574-5	2010	We report a RET mutation in exon10, codon 618 that causes substitution of a cysteine by a serine in the cysteine-rich domain of the RET receptor in a three-generation FMTC family composed of 30 members with 11 carriers.	Cysteine	104-112	ret proto-oncogene	Homo sapiens	12-15
20119574-5	2010	We report a RET mutation in exon10, codon 618 that causes substitution of a cysteine by a serine in the cysteine-rich domain of the RET receptor in a three-generation FMTC family composed of 30 members with 11 carriers.	Cysteine	104-112	ret proto-oncogene	Homo sapiens	132-135
20119574-7	2010	The FMTC with cysteine RET mutations found in the Korean population is consistent with the clinical pattern reported worldwide; to date there have been no ethnic differences identified for FMTC.	Cysteine	14-22	ret proto-oncogene	Homo sapiens	23-26
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.	Imatinib Mesylate	45-62	ret proto-oncogene	Homo sapiens	4-28
20152359-2	2010	Specifically, HSCR-MEN2 cosegregation mostly relates to the cysteine-rich area at the RET-620 (the "Janus gene").	Cysteine	60-68	ret proto-oncogene	Homo sapiens	86-89
20545254-5	2010	The authors report three different cases in which doxazosin was used: as preoperative preparation of a patient with pheochromocytoma, as preparation for therapy in I-131-MIBG of a patient with a malignant pheochromocytoma, and as a pre-cesarean preparation in a pregnant woman with multiple endocrine neoplasia type 2A (MEN-2A).	Doxazosin	50-59	ret proto-oncogene	Homo sapiens	282-318
20545254-5	2010	The authors report three different cases in which doxazosin was used: as preoperative preparation of a patient with pheochromocytoma, as preparation for therapy in I-131-MIBG of a patient with a malignant pheochromocytoma, and as a pre-cesarean preparation in a pregnant woman with multiple endocrine neoplasia type 2A (MEN-2A).	Doxazosin	50-59	ret proto-oncogene	Homo sapiens	320-326
20606413-9	2010	CONCLUSION: Fluctuations in Ret-He and DF-HYPO XE have to be taken into account when these parameters are used for the assessment of iron-deficient states.	Iron	133-137	ret proto-oncogene	Homo sapiens	28-31
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.	Imatinib Mesylate	45-62	ret proto-oncogene	Homo sapiens	30-33
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
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.	Imatinib Mesylate	45-53	ret proto-oncogene	Homo sapiens	4-28
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.	Imatinib Mesylate	45-53	ret proto-oncogene	Homo sapiens	30-33
19879134-0	2009	Imidazo[1,2-a]pyrazine diaryl ureas: inhibitors of the receptor tyrosine kinase EphB4.	imidazo(1,2-a)pyrazine	0-22	ret proto-oncogene	Homo sapiens	55-79
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
20696054-6	2010	Genes whose protein products are targeted by the RET inhibitors sunitinib and sorafenib correlated with being amplified and or highly expressed.	Sorafenib	78-87	ret proto-oncogene	Homo sapiens	49-52
20415234-2	2010	Cellular iron status can be determined by the recently available method of measuring the reticulocyte hemoglobin equivalent (RET-He).	Iron	9-13	ret proto-oncogene	Homo sapiens	125-128
19879134-0	2009	Imidazo[1,2-a]pyrazine diaryl ureas: inhibitors of the receptor tyrosine kinase EphB4.	diaryl ureas	23-35	ret proto-oncogene	Homo sapiens	55-79
19344417-8	2009	Serum hepcidin, Ret-H(e) and Delta-H(e) (Ret-H(e) minus RBC-H(e)) are promising biomarkers to select those individuals who will benefit from iron supplements in malaria endemic regions, while the sTfR/log ferritin ratio should be used with caution to assess iron status during malaria.	Iron	141-145	ret proto-oncogene	Homo sapiens	16-19
19900702-10	2009	We also showed the downregulation of phosphorylation on RET phosphotyrosine residue 905 in BeWo cells with phosphorylation specific antibodies and immunocytochemistry.	Phosphotyrosine	60-75	ret proto-oncogene	Homo sapiens	56-59
19808973-3	2009	EXEL-2880 (XL880, GSK1363089) is a small-molecule kinase inhibitor that targets members of the HGF and VEGF receptor tyrosine kinase families, with additional inhibitory activity toward KIT, Flt-3, platelet-derived growth factor receptor beta, and Tie-2.	GSK 1363089	18-28	ret proto-oncogene	Homo sapiens	108-132
19687425-1	2009	BACKGROUND: Photosensitivity has been reported in patients who were treated with vandetanib (ZD6474), an inhibitor of epidermal growth factor receptor, vascular endothelial growth factor receptor, and the RET (rearranged during transfection) kinases.	vandetanib	81-91	ret proto-oncogene	Homo sapiens	205-208
19687425-1	2009	BACKGROUND: Photosensitivity has been reported in patients who were treated with vandetanib (ZD6474), an inhibitor of epidermal growth factor receptor, vascular endothelial growth factor receptor, and the RET (rearranged during transfection) kinases.	vandetanib	81-91	ret proto-oncogene	Homo sapiens	210-240
19687425-1	2009	BACKGROUND: Photosensitivity has been reported in patients who were treated with vandetanib (ZD6474), an inhibitor of epidermal growth factor receptor, vascular endothelial growth factor receptor, and the RET (rearranged during transfection) kinases.	vandetanib	93-99	ret proto-oncogene	Homo sapiens	205-208
19687425-1	2009	BACKGROUND: Photosensitivity has been reported in patients who were treated with vandetanib (ZD6474), an inhibitor of epidermal growth factor receptor, vascular endothelial growth factor receptor, and the RET (rearranged during transfection) kinases.	vandetanib	93-99	ret proto-oncogene	Homo sapiens	210-240
19320641-3	2009	NB-39-nu neuroblastoma cells show high expression and elevated tyrosine phosphorylation of RET, although short interfering RNA against RET (RET siRNA) did not significantly inhibit cell proliferation or suppression of basal levels of phosphorylation of extracellular regulated kinase (ERK)1/2 or protein kinase B (AKT).	Tyrosine	63-71	ret proto-oncogene	Homo sapiens	91-94
19934279-0	2009	SGX523 is an exquisitely selective, ATP-competitive inhibitor of the MET receptor tyrosine kinase with antitumor activity in vivo.	6-(6-(1-methyl-1H-pyrazol-4-yl)-(1,2,4)triazolo(4,3-b)pyridazin-3-ylsulfanyl)quinoline	0-6	ret proto-oncogene	Homo sapiens	73-97
19934279-0	2009	SGX523 is an exquisitely selective, ATP-competitive inhibitor of the MET receptor tyrosine kinase with antitumor activity in vivo.	Adenosine Triphosphate	36-39	ret proto-oncogene	Homo sapiens	73-97
19834598-13	2009	Notably, Gli1 did not induce N-MYC expression in neuroblastoma cells, but strongly induced RET, a known mediator of RA effect.	Radium	116-118	ret proto-oncogene	Homo sapiens	91-94
19946413-1	2009	BACKGROUND: Vandetanib is a once-daily oral inhibitor of VEGFR, EGFR and RET signaling pathways.	vandetanib	12-22	ret proto-oncogene	Homo sapiens	73-76
19618960-3	2009	The high peroxidase activity of hemin complexed with intramolecular parallel G-quadruplex-forming sequences in gene promoters (such as c-Myc, VEGF, c-Kit21, HIF-1alpha, and RET) may imply a potential mechanism of hemin-mediated cellular injury.	Hemin	32-37	ret proto-oncogene	Homo sapiens	173-176
19649251-0	2009	GDNF selectively induces microglial activation and neuronal survival in CA1/CA3 hippocampal regions exposed to NMDA insult through Ret/ERK signalling.	N-Methylaspartate	111-115	ret proto-oncogene	Homo sapiens	131-134
19649251-9	2009	Interestingly, confocal images revealed that upon NMDA exposure, Ret activation occurred in microglial cells in the CA3 and CA1 following GDNF exposure.	N-Methylaspartate	50-54	ret proto-oncogene	Homo sapiens	65-68
19884740-2	2009	AIM: The aim of this study was to recognize the prevalence of RET/PTC expression in PTC from the endemically iodine-deficient region in Northern India and to correlate the expression with the clinicopathologic prognostic factors.	Iodine	109-115	ret proto-oncogene	Homo sapiens	62-65
19884740-2	2009	AIM: The aim of this study was to recognize the prevalence of RET/PTC expression in PTC from the endemically iodine-deficient region in Northern India and to correlate the expression with the clinicopathologic prognostic factors.	Iodine	109-115	ret proto-oncogene	Homo sapiens	66-69
19884740-2	2009	AIM: The aim of this study was to recognize the prevalence of RET/PTC expression in PTC from the endemically iodine-deficient region in Northern India and to correlate the expression with the clinicopathologic prognostic factors.	Iodine	109-115	ret proto-oncogene	Homo sapiens	84-87
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
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
19344417-8	2009	Serum hepcidin, Ret-H(e) and Delta-H(e) (Ret-H(e) minus RBC-H(e)) are promising biomarkers to select those individuals who will benefit from iron supplements in malaria endemic regions, while the sTfR/log ferritin ratio should be used with caution to assess iron status during malaria.	Iron	141-145	ret proto-oncogene	Homo sapiens	41-44
19344417-8	2009	Serum hepcidin, Ret-H(e) and Delta-H(e) (Ret-H(e) minus RBC-H(e)) are promising biomarkers to select those individuals who will benefit from iron supplements in malaria endemic regions, while the sTfR/log ferritin ratio should be used with caution to assess iron status during malaria.	Iron	258-262	ret proto-oncogene	Homo sapiens	41-44
18987170-10	2009	RET proto-oncogen mutations were documented in 22 (8%) patients (medullary thyroid cancer:18, CCH:4).	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	94-97	ret proto-oncogene	Homo sapiens	0-3
19445625-8	2009	DNA analysis demonstrated a mutation in codon 804 of the RET proto-oncogene resulting in a Valine to Methionine (V804M) substitution.	Valine	91-97	ret proto-oncogene	Homo sapiens	57-60
19445625-8	2009	DNA analysis demonstrated a mutation in codon 804 of the RET proto-oncogene resulting in a Valine to Methionine (V804M) substitution.	Methionine	101-111	ret proto-oncogene	Homo sapiens	57-60
19447868-1	2009	PURPOSE: Vandetanib [vascular endothelial growth factor (VEGF) receptor/epidermal growth factor receptor/RET inhibitor] has shown improvements in progression-free survival (PFS) in advanced non-small cell lung cancer in three randomized phase II studies: vandetanib versus gefitinib (study 3), docetaxel +/- vandetanib (study 6), and carboplatin-paclitaxel and/or vandetanib (study 7).	vandetanib	9-19	ret proto-oncogene	Homo sapiens	105-108
19223551-4	2009	In addition, RET/PTC physically interacts with beta-catenin and increases its phosphotyrosine content.	Phosphotyrosine	78-93	ret proto-oncogene	Homo sapiens	13-16
19223551-6	2009	Moreover, through the ERK pathway, RET/PTC stimulates cyclic AMP-responsive element binding protein (CREB) phosphorylation and promotes the formation of a beta-catenin-CREB-CREB-binding protein/p300 transcriptional complex.	Cyclic AMP	54-64	ret proto-oncogene	Homo sapiens	35-38
19002384-1	2009	BACKGROUND: Vandetanib (ZACTIMA) is a once-daily oral inhibitor of vascular endothelial growth factor, epidermal growth factor and RET receptor tyrosine kinases.	vandetanib	12-22	ret proto-oncogene	Homo sapiens	131-134
24410643-1	2009	Sorafenib is an oral multikinase inhibitor targeting Raf, VEGF receptor, PDGF receptor, c-kit, Flt-3 and rearranged during transfection (RET).	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	105-135
19029224-0	2009	Identification of tyrosine 806 as a molecular determinant of RET kinase sensitivity to ZD6474.	Tyrosine	18-26	ret proto-oncogene	Homo sapiens	61-64
19029224-0	2009	Identification of tyrosine 806 as a molecular determinant of RET kinase sensitivity to ZD6474.	vandetanib	87-93	ret proto-oncogene	Homo sapiens	61-64
19029224-1	2009	ZD6474 (vandetanib, Zactima, Astra Zeneca) is an anilinoquinazoline used to target the receptor tyrosine kinase RET in familial and sporadic thyroid carcinoma (IC(50): 100 nM).	vandetanib	0-6	ret proto-oncogene	Homo sapiens	112-115
19029224-1	2009	ZD6474 (vandetanib, Zactima, Astra Zeneca) is an anilinoquinazoline used to target the receptor tyrosine kinase RET in familial and sporadic thyroid carcinoma (IC(50): 100 nM).	vandetanib	8-18	ret proto-oncogene	Homo sapiens	112-115
19029224-1	2009	ZD6474 (vandetanib, Zactima, Astra Zeneca) is an anilinoquinazoline used to target the receptor tyrosine kinase RET in familial and sporadic thyroid carcinoma (IC(50): 100 nM).	anilinoquinazoline	49-67	ret proto-oncogene	Homo sapiens	112-115
19029224-2	2009	The aim of this study was to identify molecular determinants of RET sensitivity to ZD6474.	vandetanib	83-89	ret proto-oncogene	Homo sapiens	64-67
19029224-3	2009	Here, we show that mutation of RET tyrosine 806 to cysteine (Y806C) induced RET kinase resistance to ZD6474 (IC(50): 933 nM).	vandetanib	101-107	ret proto-oncogene	Homo sapiens	31-34
19029224-3	2009	Here, we show that mutation of RET tyrosine 806 to cysteine (Y806C) induced RET kinase resistance to ZD6474 (IC(50): 933 nM).	vandetanib	101-107	ret proto-oncogene	Homo sapiens	76-79
19029224-8	2009	We conclude that Y806 is a molecular determinant of RET sensitivity to ZD6474.	y806	17-21	ret proto-oncogene	Homo sapiens	52-55
19029224-8	2009	We conclude that Y806 is a molecular determinant of RET sensitivity to ZD6474.	vandetanib	71-77	ret proto-oncogene	Homo sapiens	52-55
24410643-1	2009	Sorafenib is an oral multikinase inhibitor targeting Raf, VEGF receptor, PDGF receptor, c-kit, Flt-3 and rearranged during transfection (RET).	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	137-140
21475823-5	2009	dHPLC techniques were employed to screen the RET coding region in 23 patients presenting with INDB and 30 patients with a combined HSCR+INDB phenotype.	indb	94-98	ret proto-oncogene	Homo sapiens	45-48
21475823-5	2009	dHPLC techniques were employed to screen the RET coding region in 23 patients presenting with INDB and 30 patients with a combined HSCR+INDB phenotype.	dhplc	0-5	ret proto-oncogene	Homo sapiens	45-48
21475823-5	2009	dHPLC techniques were employed to screen the RET coding region in 23 patients presenting with INDB and 30 patients with a combined HSCR+INDB phenotype.	indb	136-140	ret proto-oncogene	Homo sapiens	45-48
21475823-9	2009	Our results suggest an involvement of RET in the pathogenesis of intestinal INDB, although by different molecular mechanisms than those leading to HSCR.	indb	76-80	ret proto-oncogene	Homo sapiens	38-41
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
19060924-4	2009	RET/PTC induced robust tyrosine phosphorylation of XB130, which promoted its subsequent association with the p85alpha subunit of phosphatidylinositol 3-kinase (PI 3-kinase).	Tyrosine	23-31	ret proto-oncogene	Homo sapiens	0-3
19060924-4	2009	RET/PTC induced robust tyrosine phosphorylation of XB130, which promoted its subsequent association with the p85alpha subunit of phosphatidylinositol 3-kinase (PI 3-kinase).	Tyrosine	23-31	ret proto-oncogene	Homo sapiens	4-7
19060924-5	2009	We identified tyrosine 54 of XB130 as the major target of RET/PTC-mediated phosphorylation and a critical binding site for the SH2 domains of p85alpha.	Tyrosine	14-22	ret proto-oncogene	Homo sapiens	58-61
19060924-5	2009	We identified tyrosine 54 of XB130 as the major target of RET/PTC-mediated phosphorylation and a critical binding site for the SH2 domains of p85alpha.	Tyrosine	14-22	ret proto-oncogene	Homo sapiens	62-65
19211364-5	2009	Vandetanib, an inhibitor of RET and VEGFR tyrosine-kinases, is promising in medullary thyroid cancers.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	28-31
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
19095577-6	2009	In addition to the germline heterozygous APC Ex 2-3 duplication mutation, a somatic homozygous silent p. Thr1493Thr gene variant was found in the neoplastic cells along with RET/PTC rearrangement.	thr1493thr	105-115	ret proto-oncogene	Homo sapiens	174-177
19095577-6	2009	In addition to the germline heterozygous APC Ex 2-3 duplication mutation, a somatic homozygous silent p. Thr1493Thr gene variant was found in the neoplastic cells along with RET/PTC rearrangement.	thr1493thr	105-115	ret proto-oncogene	Homo sapiens	178-181
18845906-6	2009	A novel heterozygous mutation of a 3-bp (GAC) deletion at codon 631 (D631del) of exon 11, resulting in the deletion of an aspartic acid at the locus, was identified in four MEN2A patients and one phenotypically normal family member.	Aspartic Acid	122-135	ret proto-oncogene	Homo sapiens	173-178
19169490-8	2008	In the present case, prompt sequential dosage of calcium, diagnosis of PHT, and genetic analysis would have resulted in pancreatitis prevention and early MEN2A management.	Calcium	49-56	ret proto-oncogene	Homo sapiens	154-159
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.	vandetanib	89-99	ret proto-oncogene	Homo sapiens	68-71
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.	Sorafenib	101-110	ret proto-oncogene	Homo sapiens	68-71
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
18752792-13	2008	In conclusion, this case report of MEN 2A linked to a 634 RET mutation was peculiar by its revelation mode (1) hyperparathyroidism moreover linked to an adenoma and (2) associated with diabetes, mechanisms of which are probably multifactorial (familial type 2 diabetes, hypercalcemia, catecholamines excess).	Catecholamines	285-299	ret proto-oncogene	Homo sapiens	35-41
18752792-13	2008	In conclusion, this case report of MEN 2A linked to a 634 RET mutation was peculiar by its revelation mode (1) hyperparathyroidism moreover linked to an adenoma and (2) associated with diabetes, mechanisms of which are probably multifactorial (familial type 2 diabetes, hypercalcemia, catecholamines excess).	Catecholamines	285-299	ret proto-oncogene	Homo sapiens	58-61
18845535-9	2008	Furthermore, we have shown by mutagenesis and enzyme-linked immunosorbent assays of RET phosphorylation that RET probably interacts with GFR alpha 1 residues Arg-190, Lys-194, Arg-197, Gln-198, Lys-202, Arg-257, Arg-259, Glu-323, and Asp-324 upon both domains 2 and 3.	Arginine	158-161	ret proto-oncogene	Homo sapiens	84-87
18845535-9	2008	Furthermore, we have shown by mutagenesis and enzyme-linked immunosorbent assays of RET phosphorylation that RET probably interacts with GFR alpha 1 residues Arg-190, Lys-194, Arg-197, Gln-198, Lys-202, Arg-257, Arg-259, Glu-323, and Asp-324 upon both domains 2 and 3.	Arginine	158-161	ret proto-oncogene	Homo sapiens	109-112
18845535-9	2008	Furthermore, we have shown by mutagenesis and enzyme-linked immunosorbent assays of RET phosphorylation that RET probably interacts with GFR alpha 1 residues Arg-190, Lys-194, Arg-197, Gln-198, Lys-202, Arg-257, Arg-259, Glu-323, and Asp-324 upon both domains 2 and 3.	Lysine	167-170	ret proto-oncogene	Homo sapiens	109-112
18845535-9	2008	Furthermore, we have shown by mutagenesis and enzyme-linked immunosorbent assays of RET phosphorylation that RET probably interacts with GFR alpha 1 residues Arg-190, Lys-194, Arg-197, Gln-198, Lys-202, Arg-257, Arg-259, Glu-323, and Asp-324 upon both domains 2 and 3.	Arginine	176-179	ret proto-oncogene	Homo sapiens	84-87
18845535-9	2008	Furthermore, we have shown by mutagenesis and enzyme-linked immunosorbent assays of RET phosphorylation that RET probably interacts with GFR alpha 1 residues Arg-190, Lys-194, Arg-197, Gln-198, Lys-202, Arg-257, Arg-259, Glu-323, and Asp-324 upon both domains 2 and 3.	Arginine	176-179	ret proto-oncogene	Homo sapiens	109-112
18845535-9	2008	Furthermore, we have shown by mutagenesis and enzyme-linked immunosorbent assays of RET phosphorylation that RET probably interacts with GFR alpha 1 residues Arg-190, Lys-194, Arg-197, Gln-198, Lys-202, Arg-257, Arg-259, Glu-323, and Asp-324 upon both domains 2 and 3.	Glutamine	185-188	ret proto-oncogene	Homo sapiens	84-87
18845535-9	2008	Furthermore, we have shown by mutagenesis and enzyme-linked immunosorbent assays of RET phosphorylation that RET probably interacts with GFR alpha 1 residues Arg-190, Lys-194, Arg-197, Gln-198, Lys-202, Arg-257, Arg-259, Glu-323, and Asp-324 upon both domains 2 and 3.	Glutamine	185-188	ret proto-oncogene	Homo sapiens	109-112
18845535-9	2008	Furthermore, we have shown by mutagenesis and enzyme-linked immunosorbent assays of RET phosphorylation that RET probably interacts with GFR alpha 1 residues Arg-190, Lys-194, Arg-197, Gln-198, Lys-202, Arg-257, Arg-259, Glu-323, and Asp-324 upon both domains 2 and 3.	Lysine	194-197	ret proto-oncogene	Homo sapiens	109-112
18845535-9	2008	Furthermore, we have shown by mutagenesis and enzyme-linked immunosorbent assays of RET phosphorylation that RET probably interacts with GFR alpha 1 residues Arg-190, Lys-194, Arg-197, Gln-198, Lys-202, Arg-257, Arg-259, Glu-323, and Asp-324 upon both domains 2 and 3.	Arginine	176-179	ret proto-oncogene	Homo sapiens	84-87
18845535-9	2008	Furthermore, we have shown by mutagenesis and enzyme-linked immunosorbent assays of RET phosphorylation that RET probably interacts with GFR alpha 1 residues Arg-190, Lys-194, Arg-197, Gln-198, Lys-202, Arg-257, Arg-259, Glu-323, and Asp-324 upon both domains 2 and 3.	Arginine	176-179	ret proto-oncogene	Homo sapiens	109-112
18845535-9	2008	Furthermore, we have shown by mutagenesis and enzyme-linked immunosorbent assays of RET phosphorylation that RET probably interacts with GFR alpha 1 residues Arg-190, Lys-194, Arg-197, Gln-198, Lys-202, Arg-257, Arg-259, Glu-323, and Asp-324 upon both domains 2 and 3.	Arginine	176-179	ret proto-oncogene	Homo sapiens	84-87
18845535-9	2008	Furthermore, we have shown by mutagenesis and enzyme-linked immunosorbent assays of RET phosphorylation that RET probably interacts with GFR alpha 1 residues Arg-190, Lys-194, Arg-197, Gln-198, Lys-202, Arg-257, Arg-259, Glu-323, and Asp-324 upon both domains 2 and 3.	Arginine	176-179	ret proto-oncogene	Homo sapiens	109-112
18845535-9	2008	Furthermore, we have shown by mutagenesis and enzyme-linked immunosorbent assays of RET phosphorylation that RET probably interacts with GFR alpha 1 residues Arg-190, Lys-194, Arg-197, Gln-198, Lys-202, Arg-257, Arg-259, Glu-323, and Asp-324 upon both domains 2 and 3.	Glutamic Acid	221-224	ret proto-oncogene	Homo sapiens	109-112
18845535-9	2008	Furthermore, we have shown by mutagenesis and enzyme-linked immunosorbent assays of RET phosphorylation that RET probably interacts with GFR alpha 1 residues Arg-190, Lys-194, Arg-197, Gln-198, Lys-202, Arg-257, Arg-259, Glu-323, and Asp-324 upon both domains 2 and 3.	Aspartic Acid	234-237	ret proto-oncogene	Homo sapiens	109-112
18845535-11	2008	This may explain how GDNF.GFR alpha 1 can mediate cell adhesion and how heparin might inhibit GDNF signaling through RET.	Heparin	72-79	ret proto-oncogene	Homo sapiens	117-120
18794325-0	2008	Age-related neoplastic risk profiles and penetrance estimations in multiple endocrine neoplasia type 2A caused by germ line RET Cys634Trp (TGC&gt;TGG) mutation.	cys634trp	128-137	ret proto-oncogene	Homo sapiens	124-127
18976163-13	2008	In addition, at least in females with CCH RET germline mutation, screening is recommended even if the family history is negative for MTC.	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	38-41	ret proto-oncogene	Homo sapiens	42-45
18521934-6	2008	On the other hand, methiothepin, an inverse agonist of 5-HT GPCRs activated endogenous ApTrkl to the same extent as 5-HT, suggesting a transactivation mechanism due to a novel coupling of GPCRs to receptor tyrosine kinase (RTK) activation that is also activated through inverse agonist binding.	Methiothepin	19-31	ret proto-oncogene	Homo sapiens	197-221
18762555-9	2008	Inhibition of the PI3K pathway also significantly increased iodide uptake ( approximately 3.5-fold) in BHP 2-7 papillary thyroid cancer cells (Ret/PTC1 positive), engineered to constitutively express NIS.	Iodides	60-66	ret proto-oncogene	Homo sapiens	143-146
18799615-3	2008	Only in Ret/PTC1-positive TPC-1 cells did cAMP markedly inhibit the Raf/ERK cascade, leading to mTOR pathway inhibition, repression of cyclin D1 and p21 and p27 accumulation.	Cyclic AMP	42-46	ret proto-oncogene	Homo sapiens	8-11
18521934-6	2008	On the other hand, methiothepin, an inverse agonist of 5-HT GPCRs activated endogenous ApTrkl to the same extent as 5-HT, suggesting a transactivation mechanism due to a novel coupling of GPCRs to receptor tyrosine kinase (RTK) activation that is also activated through inverse agonist binding.	Methiothepin	19-31	ret proto-oncogene	Homo sapiens	223-226
18284634-10	2008	CONCLUSIONS: RET genotypes including two intronic RET variants were associated with the risk of developing sMTC and to more aggressive behaviour.	smtc	107-111	ret proto-oncogene	Homo sapiens	13-16
18284634-10	2008	CONCLUSIONS: RET genotypes including two intronic RET variants were associated with the risk of developing sMTC and to more aggressive behaviour.	smtc	107-111	ret proto-oncogene	Homo sapiens	50-53
18331611-9	2008	CONCLUSIONS: Our data demonstrate that the RET G691S variant could modulate the age of onset of sMTC as demonstrated previously for familial tumours.	smtc	96-100	ret proto-oncogene	Homo sapiens	43-46
18631007-0	2008	A new germline point mutation in Ret exon 8 (cys515ser) in a family with medullary thyroid carcinoma.	cys515ser	45-54	ret proto-oncogene	Homo sapiens	33-36
19044764-9	2008	Calculated k(RET) and k(Lambda) values at 298.15 K are consistent with a substantial contribution from k(dep) for OH(X)+Ar but not for OH(X)+He.	Argon	120-122	ret proto-oncogene	Homo sapiens	13-16
18682802-3	2008	Tyrosine phosphorylation events mediated by aberrant activation of Receptor Tyrosine Kinase (RTK) pathways have been proven to be involved in the development of several diseases including cancer.	Tyrosine	0-8	ret proto-oncogene	Homo sapiens	67-91
18682802-3	2008	Tyrosine phosphorylation events mediated by aberrant activation of Receptor Tyrosine Kinase (RTK) pathways have been proven to be involved in the development of several diseases including cancer.	Tyrosine	0-8	ret proto-oncogene	Homo sapiens	93-96
18682802-4	2008	To understand the systems biology of RTK activation, we have developed a phosphor-proteome focused on tyrosine phosphorylation events under insulin and EGF signaling pathways using the PhosphoScan technique coupled with high-throughput mass spectrometry analysis.	Tyrosine	102-110	ret proto-oncogene	Homo sapiens	37-40
18248647-5	2008	RESULTS: We found that the cysteine insertion, due to the Y606C mutation, results in increased receptor dimerization, which is accompanied by an increased tyrosine phosphorylation of the Y905 residue in the RET/Y606C, demonstrating that the Y606C mutation is associated with constitutive receptor activation.	Cysteine	27-35	ret proto-oncogene	Homo sapiens	207-210
18248647-5	2008	RESULTS: We found that the cysteine insertion, due to the Y606C mutation, results in increased receptor dimerization, which is accompanied by an increased tyrosine phosphorylation of the Y905 residue in the RET/Y606C, demonstrating that the Y606C mutation is associated with constitutive receptor activation.	Tyrosine	155-163	ret proto-oncogene	Homo sapiens	207-210
18394855-0	2008	Gas1 reduces Ret tyrosine 1062 phosphorylation and alters GDNF-mediated intracellular signaling.	Tyrosine	17-25	ret proto-oncogene	Homo sapiens	13-16
18394855-1	2008	The present results show that the expression of Growth Arrest Specific1 (Gas1) in SH-SY5Y neuroblastoma cells significantly inhibits the increased phosphorylation of tyrosine 1062 of the Ret receptor tyrosine kinase induced by glial-cell-line-derived neurotrophic factor (GDNF).	Tyrosine	166-174	ret proto-oncogene	Homo sapiens	187-190
18631007-1	2008	BACKGROUND: A novel Cys-Ser Ret germline point mutation in a 58-year-old woman with bilateral medullary thyroid carcinoma (MTC) prompted us to perform genetic analysis of the family and evaluate the biological consequences of such a mutation.	Cys-Ser	20-27	ret proto-oncogene	Homo sapiens	28-31
18715070-1	2008	Valence and dipole-bound negative ions of the nitroethane (NE) molecule and its clusters are studied using photoelectron spectroscopy (PES), Rydberg electron transfer (RET) techniques, and ab initio methods.	nitroethane	46-57	ret proto-oncogene	Homo sapiens	168-171
18715070-5	2008	RET experiments show that Rydberg electrons can be attached to NE both as dipole-bound and valence bound anion states.	dipole	74-80	ret proto-oncogene	Homo sapiens	0-3
18715070-7	2008	Using previous models for relating the maximum in the RET dependence of the Rydberg effective principle number n(max)(*), the dipole-bound electron affinity is predicted to be approximately 25 meV.	dipole	126-132	ret proto-oncogene	Homo sapiens	54-57
18676765-9	2008	Because RET/PTC rearrangements are unique to thyroid carcinomas, our findings support the clinical evaluation of sorafenib for patients with PTC and the identification of patients most likely to respond to sorafenib treatment.	Sorafenib	113-122	ret proto-oncogene	Homo sapiens	8-11
18676765-9	2008	Because RET/PTC rearrangements are unique to thyroid carcinomas, our findings support the clinical evaluation of sorafenib for patients with PTC and the identification of patients most likely to respond to sorafenib treatment.	Sorafenib	206-215	ret proto-oncogene	Homo sapiens	8-11
18362203-8	2008	Furthermore, LPA stimulated C/EBPbeta phosphorylation and activity through a novel mechanism integrating GPCR signals and a permissive activity from a receptor tyrosine kinase (RTK).	lysophosphatidic acid	13-16	ret proto-oncogene	Homo sapiens	151-175
18362203-8	2008	Furthermore, LPA stimulated C/EBPbeta phosphorylation and activity through a novel mechanism integrating GPCR signals and a permissive activity from a receptor tyrosine kinase (RTK).	lysophosphatidic acid	13-16	ret proto-oncogene	Homo sapiens	177-180
18651802-6	2008	Synergistic inhibitory effects were observed when PD0325901 was combined with phosphatidylinositol 3-kinase (PI3K) or NF-kappaB pathway inhibitors in most cells, including the RET/PTC1-harboring cells.	mirdametinib	50-59	ret proto-oncogene	Homo sapiens	176-179
18751369-0	2008	RET activation inhibits doxorubicin-induced apoptosis in SK-N-MC cells.	Doxorubicin	24-35	ret proto-oncogene	Homo sapiens	0-3
18751369-0	2008	RET activation inhibits doxorubicin-induced apoptosis in SK-N-MC cells.	sk-n-mc	57-64	ret proto-oncogene	Homo sapiens	0-3
18751369-2	2008	MATERIALS AND METHODS: Each RET isoform was separately expressed in SK-N-MC cells (neural crest-derived tumor) and the impact of RET activation on doxorubicin-induced apoptosis was examined.	sk-n-mc	68-75	ret proto-oncogene	Homo sapiens	28-31
18751369-3	2008	RESULTS: The activation of RET9 and RET51 in the SK-N-MC cells significantly reduced the doxorubicin-induced apoptosis by 50%, compared to untreated cells.	sk-n-mc	49-56	ret proto-oncogene	Homo sapiens	36-41
18751369-3	2008	RESULTS: The activation of RET9 and RET51 in the SK-N-MC cells significantly reduced the doxorubicin-induced apoptosis by 50%, compared to untreated cells.	Doxorubicin	89-100	ret proto-oncogene	Homo sapiens	36-41
18751369-5	2008	In the presence of a MAP (mitogen-activated protein) kinase inhibitor or a RET kinase inhibitor, the RET-activated/drug-treated cells displayed nearly 75% and 100% of the doxorubicin-induced apoptosis of the drug-treated cells without RET activation, respectively.	Doxorubicin	171-182	ret proto-oncogene	Homo sapiens	75-78
18751369-5	2008	In the presence of a MAP (mitogen-activated protein) kinase inhibitor or a RET kinase inhibitor, the RET-activated/drug-treated cells displayed nearly 75% and 100% of the doxorubicin-induced apoptosis of the drug-treated cells without RET activation, respectively.	Doxorubicin	171-182	ret proto-oncogene	Homo sapiens	101-104
18751369-5	2008	In the presence of a MAP (mitogen-activated protein) kinase inhibitor or a RET kinase inhibitor, the RET-activated/drug-treated cells displayed nearly 75% and 100% of the doxorubicin-induced apoptosis of the drug-treated cells without RET activation, respectively.	Doxorubicin	171-182	ret proto-oncogene	Homo sapiens	101-104
18751369-6	2008	CONCLUSION: In SK-N-MC cells, downstream activation of MAP kinase, by both RET9 and RET51, appears to mediate the majority of RET-dependent resistance to chemotherapeutically induced apoptosis.	sk-n-mc	15-22	ret proto-oncogene	Homo sapiens	84-89
18751369-6	2008	CONCLUSION: In SK-N-MC cells, downstream activation of MAP kinase, by both RET9 and RET51, appears to mediate the majority of RET-dependent resistance to chemotherapeutically induced apoptosis.	sk-n-mc	15-22	ret proto-oncogene	Homo sapiens	75-78
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
18364248-0	2008	Novel dual targeting strategy with vandetanib induces tumor cell apoptosis and inhibits angiogenesis in malignant pleural mesothelioma cells expressing RET oncogenic rearrangement.	vandetanib	35-45	ret proto-oncogene	Homo sapiens	152-155
18364248-2	2008	In the present study, we investigated the therapeutic efficacy of vandetanib (ZD6474), an inhibitor of VEGFR-2, EGFR and RET tyrosine kinases, in an orthotopic model of MPM.	vandetanib	66-76	ret proto-oncogene	Homo sapiens	121-124
18364248-2	2008	In the present study, we investigated the therapeutic efficacy of vandetanib (ZD6474), an inhibitor of VEGFR-2, EGFR and RET tyrosine kinases, in an orthotopic model of MPM.	vandetanib	78-84	ret proto-oncogene	Homo sapiens	121-124
18364248-7	2008	Our results suggest that using vandetanib to target RET-dependent tumor cell proliferation and survival and VEGFR-2-dependent tumor angiogenesis may be promising against MPM expressing RET oncogenic rearrangement and VEGF.	vandetanib	31-41	ret proto-oncogene	Homo sapiens	52-55
18364248-7	2008	Our results suggest that using vandetanib to target RET-dependent tumor cell proliferation and survival and VEGFR-2-dependent tumor angiogenesis may be promising against MPM expressing RET oncogenic rearrangement and VEGF.	vandetanib	31-41	ret proto-oncogene	Homo sapiens	185-188
18299806-5	2008	For the cross talk of integrin with RTK, ROS may suppress paxillin-associated protein tyrosine phosphatase (PTP-PEST) relieving its negative regulatory effects.	Reactive Oxygen Species	41-44	ret proto-oncogene	Homo sapiens	36-39
18418222-7	2008	Activation of the RET kinase pathway was evaluated using immunohistochemistry (IHC) and western blot analysis of total phosphorylated tyrosine and downstream signalling targets of the RET pathway.	Tyrosine	134-142	ret proto-oncogene	Homo sapiens	18-21
18322301-4	2008	PATIENTS: Fifteen individuals from five kindreds were identified as carriers of a RET protooncogene mutation in exon 11 codon 649 (TCG(Ser)--&gt;TTG(Leu)).	TMG-chitotriomycin	131-134	ret proto-oncogene	Homo sapiens	82-85
18189271-4	2008	We show here that RET migration in neuroepitheliomal and non-neuronal cells is elicited by the activation of specific signaling pathways initiated by the competitive recruitment of the FRS2 adaptor molecule to tyrosine 1062 (Y1062) in RET.	Tyrosine	210-218	ret proto-oncogene	Homo sapiens	18-21
18322301-4	2008	PATIENTS: Fifteen individuals from five kindreds were identified as carriers of a RET protooncogene mutation in exon 11 codon 649 (TCG(Ser)--&gt;TTG(Leu)).	Serine	135-138	ret proto-oncogene	Homo sapiens	82-85
18322301-4	2008	PATIENTS: Fifteen individuals from five kindreds were identified as carriers of a RET protooncogene mutation in exon 11 codon 649 (TCG(Ser)--&gt;TTG(Leu)).	Hydrotopotecan	145-148	ret proto-oncogene	Homo sapiens	82-85
18322301-4	2008	PATIENTS: Fifteen individuals from five kindreds were identified as carriers of a RET protooncogene mutation in exon 11 codon 649 (TCG(Ser)--&gt;TTG(Leu)).	Leucine	149-152	ret proto-oncogene	Homo sapiens	82-85
18365214-9	2008	MTC is mostly associated with variations in the 5 cysteine RET radicals and codon-risk management protocols are of considerable value but not infallible.	Cysteine	50-58	ret proto-oncogene	Homo sapiens	59-62
18498667-11	2008	In addition, the activation of PLD by pervanadate triggered phosphorylation of tyrosine 705 residue on STAT-3, and its phosphorylation was dramatically higher in TPC-1 cells (from papillary carcinoma) that have an endogenous RET/PTC1 than in ARO cells (from anaplastic carcinoma) without alteration of total STAT-3 expression.	pervanadate	38-49	ret proto-oncogene	Homo sapiens	225-228
18273880-4	2008	Ser691 is a predicted phosphorylation site and our analysis of transfected cells showed that the Gly691Ser Ret mutant can efficiently interact and associate with a 75-80-kD tyrosine phosphorylated cellular protein, an event not seen with wild-type Ret.	Tyrosine	173-181	ret proto-oncogene	Homo sapiens	107-110
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
18355321-3	2008	Ret can propagate biochemical signaling from within concentrates in cholesterol-rich membrane microdomains or lipid rafts, or outside such regions, but the mechanisms for, and consequences of, Ret translocation between these membrane compartments remain largely unclear.	Cholesterol	68-79	ret proto-oncogene	Homo sapiens	0-3
18355321-8	2008	We have identified a previously unknown mechanism in which phosphotyrosine-binding domain-containing adaptors, by means of relocating Ret receptor complexes to lipid rafts, segregate diverse signaling and cellular functions mediated by Ret.	Phosphotyrosine	59-74	ret proto-oncogene	Homo sapiens	134-137
18355321-8	2008	We have identified a previously unknown mechanism in which phosphotyrosine-binding domain-containing adaptors, by means of relocating Ret receptor complexes to lipid rafts, segregate diverse signaling and cellular functions mediated by Ret.	Phosphotyrosine	59-74	ret proto-oncogene	Homo sapiens	236-239
18273880-4	2008	Ser691 is a predicted phosphorylation site and our analysis of transfected cells showed that the Gly691Ser Ret mutant can efficiently interact and associate with a 75-80-kD tyrosine phosphorylated cellular protein, an event not seen with wild-type Ret.	Tyrosine	173-181	ret proto-oncogene	Homo sapiens	248-251
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
18027835-4	2008	The reticulocyte hemoglobin content (CHr or Ret-He) provides an indirect measure of the functional iron available for new red blood cell production over the previous 3-4 days.	Iron	99-103	ret proto-oncogene	Homo sapiens	44-47
18445656-0	2008	Medullary thyroid cancer: targeting the RET kinase pathway with sorafenib/tipifarnib.	Sorafenib	64-73	ret proto-oncogene	Homo sapiens	40-43
18445656-0	2008	Medullary thyroid cancer: targeting the RET kinase pathway with sorafenib/tipifarnib.	tipifarnib	74-84	ret proto-oncogene	Homo sapiens	40-43
18445656-4	2008	We report here a rapid response to a sorafenib (RET and RAF kinase and vascular endothelial growth factor receptor inhibitor)--based regimen in a patient with sporadic MTC who had advanced, progressive disease and a novel RET kinase aberration at exon 11 shown in tumor tissue.	Sorafenib	37-46	ret proto-oncogene	Homo sapiens	48-51
18445656-4	2008	We report here a rapid response to a sorafenib (RET and RAF kinase and vascular endothelial growth factor receptor inhibitor)--based regimen in a patient with sporadic MTC who had advanced, progressive disease and a novel RET kinase aberration at exon 11 shown in tumor tissue.	Sorafenib	37-46	ret proto-oncogene	Homo sapiens	222-225
18299477-9	2008	CCH associated with V804M RET mutation is a precancerous condition and surgery is recommended.	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	0-3	ret proto-oncogene	Homo sapiens	26-29
18316596-6	2008	As a result of RET-mediated tyrosine phosphorylation, beta-catenin escapes cytosolic down-regulation by the adenomatous polyposis coli/Axin/glycogen synthase kinase-3 complex and accumulates in the nucleus, where it can stimulate beta-catenin-specific transcriptional programs in a RET-dependent fashion.	Tyrosine	28-36	ret proto-oncogene	Homo sapiens	15-18
18316596-6	2008	As a result of RET-mediated tyrosine phosphorylation, beta-catenin escapes cytosolic down-regulation by the adenomatous polyposis coli/Axin/glycogen synthase kinase-3 complex and accumulates in the nucleus, where it can stimulate beta-catenin-specific transcriptional programs in a RET-dependent fashion.	Tyrosine	28-36	ret proto-oncogene	Homo sapiens	282-285
18286198-2	2008	Retinoic acid (RA)-treatment of neuroblastoma (NB) cells implicates activation of Ret and TrkB RTKs as critical step to induce cell differentiation.	Tretinoin	15-17	ret proto-oncogene	Homo sapiens	0-3
18304343-11	2008	CONCLUSION: These data suggest that FTI may be applied as an effective inhibitor for RET/PTC3-oncogene induced pro-inflammatory mediators.	FTI	36-39	ret proto-oncogene	Homo sapiens	85-88
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
18096130-10	2008	In conclusion, firstly, all MEN2a women should be screened for a pheochromocytoma with a 24-h urinary metanephrine and normetanephrine evaluation before or early during pregnancy, even with normal blood pressure; secondly, pheochromocytoma diagnosed during pregnancy should be operated on during pregnancy because of the risks for both mother and baby; thirdly, after medical therapy, retroperitoneal laparoscopic adrenalectomy can be performed during the second trimester of pregnancy.	Metanephrine	102-114	ret proto-oncogene	Homo sapiens	28-33
18096130-10	2008	In conclusion, firstly, all MEN2a women should be screened for a pheochromocytoma with a 24-h urinary metanephrine and normetanephrine evaluation before or early during pregnancy, even with normal blood pressure; secondly, pheochromocytoma diagnosed during pregnancy should be operated on during pregnancy because of the risks for both mother and baby; thirdly, after medical therapy, retroperitoneal laparoscopic adrenalectomy can be performed during the second trimester of pregnancy.	Normetanephrine	119-134	ret proto-oncogene	Homo sapiens	28-33
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 malate sutent	8-31	ret proto-oncogene	Homo sapiens	148-151
17599050-4	2007	At least three different tyrosine residues (Tyr905, Tyr1062, Tyr1096) of the RET(MEN 2B) precursor are phosphorylated before the oncogenic receptor reaches the cell surface.	Tyrosine	25-33	ret proto-oncogene	Homo sapiens	77-80
18245671-5	2008	ZD6474 inhibited the phosphorylation of RET in neuroblastoma cells and had a direct effect on tumor cell viability in seven neuroblastoma cell lines.	vandetanib	0-6	ret proto-oncogene	Homo sapiens	40-43
18079153-2	2008	In this study, we have used chitosan-coated poly(isobutylcyanoacrylate) nanoparticles to deliver siRNA with a complementary sequence to the fusion oncogene ret/PTC1.	Chitosan	28-36	ret proto-oncogene	Homo sapiens	156-159
18079153-2	2008	In this study, we have used chitosan-coated poly(isobutylcyanoacrylate) nanoparticles to deliver siRNA with a complementary sequence to the fusion oncogene ret/PTC1.	Enbucrilate	44-71	ret proto-oncogene	Homo sapiens	156-159
17599050-4	2007	At least three different tyrosine residues (Tyr905, Tyr1062, Tyr1096) of the RET(MEN 2B) precursor are phosphorylated before the oncogenic receptor reaches the cell surface.	Tyrosine	25-33	ret proto-oncogene	Homo sapiens	81-87
18022416-9	2007	Application of the developed method to the quantitation of total RET esters-type PAs in Senecio scandens from different regions of China is also reported.	Esters	69-75	ret proto-oncogene	Homo sapiens	65-68
17761947-6	2007	The results show that LKB1 inhibits rearranged in transformation (RET)/papillary thyroid carcinoma (PTC)-dependent activation of signal transducer and activator of transcription 3 (STAT3), which is mediated by phosphorylation of STAT3 tyrosine 705 by RET/PTC.	Tyrosine	235-243	ret proto-oncogene	Homo sapiens	66-69
18022416-9	2007	Application of the developed method to the quantitation of total RET esters-type PAs in Senecio scandens from different regions of China is also reported.	Pyrrolizidine Alkaloids	81-84	ret proto-oncogene	Homo sapiens	65-68
17895320-7	2007	The distribution of RET mutations in cysteine and noncysteine encoding codons was significantly different in the two groups of patients, with the prevalence of RET mutations in noncysteine codons being higher in MTC that presented as apparently sporadic (P < 0.0001).	Cysteine	37-45	ret proto-oncogene	Homo sapiens	20-23
17895320-7	2007	The distribution of RET mutations in cysteine and noncysteine encoding codons was significantly different in the two groups of patients, with the prevalence of RET mutations in noncysteine codons being higher in MTC that presented as apparently sporadic (P < 0.0001).	noncysteine	50-61	ret proto-oncogene	Homo sapiens	20-23
17895320-7	2007	The distribution of RET mutations in cysteine and noncysteine encoding codons was significantly different in the two groups of patients, with the prevalence of RET mutations in noncysteine codons being higher in MTC that presented as apparently sporadic (P < 0.0001).	noncysteine	177-188	ret proto-oncogene	Homo sapiens	160-163
17715395-5	2007	These interactions are dependent on the RTK kinase activity and autophosphorylation of specific tyrosine residues in the carboxyl terminus.	Tyrosine	96-104	ret proto-oncogene	Homo sapiens	40-43
17761947-6	2007	The results show that LKB1 inhibits rearranged in transformation (RET)/papillary thyroid carcinoma (PTC)-dependent activation of signal transducer and activator of transcription 3 (STAT3), which is mediated by phosphorylation of STAT3 tyrosine 705 by RET/PTC.	Tyrosine	235-243	ret proto-oncogene	Homo sapiens	100-103
17962474-0	2007	Constitutive and AP20187-induced Ret activation in photoreceptors does not protect from light-induced damage.	AP20187	17-24	ret proto-oncogene	Homo sapiens	33-36
18032931-2	2007	In vitro studies with cellular models of human thyroid carcinoma cells demonstrated that the adoptive expression of oncogenic RET/PTC1, Ha-RASV12 or BRAFV600E enhances Skp2 and reduces p27 protein expression in a MAP kinase-dependent manner; that RAS/BRAF/MAP kinase-dependent control of p27 expression in thyroid cancer cells occurs by regulating the stability of Skp2 and p27 protein; and that antisense oligonucleotides to p27 suppress growth arrest induced by MEK inhibitors.	Oligonucleotides	406-422	ret proto-oncogene	Homo sapiens	126-129
18261274-1	2007	OBJECTIVE: To detect the mutations of RET proto-oncogene in two Chinese families with multiple endocrine neoplasia type 2A (MEN2A) and to study the clinical application of pentagastrin stimulation test in the diagnosis and follow-up of MEN2A.	Pentagastrin	172-184	ret proto-oncogene	Homo sapiens	124-129
18261274-1	2007	OBJECTIVE: To detect the mutations of RET proto-oncogene in two Chinese families with multiple endocrine neoplasia type 2A (MEN2A) and to study the clinical application of pentagastrin stimulation test in the diagnosis and follow-up of MEN2A.	Pentagastrin	172-184	ret proto-oncogene	Homo sapiens	236-241
18261274-1	2007	OBJECTIVE: To detect the mutations of RET proto-oncogene in two Chinese families with multiple endocrine neoplasia type 2A (MEN2A) and to study the clinical application of pentagastrin stimulation test in the diagnosis and follow-up of MEN2A.	Pentagastrin	172-184	ret proto-oncogene	Homo sapiens	38-41
17664273-6	2007	In contrast, inhibition of oncogenic B-RAF- or epidermal growth factor-induced ERK1/2 phosphorylation required micromolar concentrations of Sorafenib demonstrating the high specificity of this drug in targeting RET.	Sorafenib	140-149	ret proto-oncogene	Homo sapiens	211-214
17664273-0	2007	Sorafenib functions to potently suppress RET tyrosine kinase activity by direct enzymatic inhibition and promoting RET lysosomal degradation independent of proteasomal targeting.	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	41-44
17471236-6	2007	RET tyrosine residues 905 and 981 are important determinants for functional binding of the adaptor, as removal of both autophosphorylation sites displaces its recruitment.	Tyrosine	4-12	ret proto-oncogene	Homo sapiens	0-3
17664273-7	2007	Moreover, prolonged exposure to Sorafenib resulted in inhibition of cell proliferation and RET protein degradation.	Sorafenib	32-41	ret proto-oncogene	Homo sapiens	91-94
17664273-0	2007	Sorafenib functions to potently suppress RET tyrosine kinase activity by direct enzymatic inhibition and promoting RET lysosomal degradation independent of proteasomal targeting.	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	115-118
17664273-2	2007	In this study, the ability of Sorafenib (BAY 43-9006) to act as a RET inhibitor was investigated.	Sorafenib	30-39	ret proto-oncogene	Homo sapiens	66-69
17664273-8	2007	Using lysosomal and proteasomal inhibitors, we demonstrate that Sorafenib induces RET lysosomal degradation independent of proteasomal targeting.	Sorafenib	64-73	ret proto-oncogene	Homo sapiens	82-85
17664273-2	2007	In this study, the ability of Sorafenib (BAY 43-9006) to act as a RET inhibitor was investigated.	Sorafenib	41-52	ret proto-oncogene	Homo sapiens	66-69
17664273-9	2007	Furthermore, we provide a structural model of the Sorafenib.RET complex in which Sorafenib binds to and induces the DFG(out) conformation of the RET kinase domain.	Sorafenib	50-59	ret proto-oncogene	Homo sapiens	60-63
17664273-3	2007	Sorafenib inhibited the activity of purified recombinant kinase domain of wild type RET and RET(V804M) with IC(50) values of 5.9 and 7.9 nm, respectively.	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	84-87
17664273-3	2007	Sorafenib inhibited the activity of purified recombinant kinase domain of wild type RET and RET(V804M) with IC(50) values of 5.9 and 7.9 nm, respectively.	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	92-95
17664273-9	2007	Furthermore, we provide a structural model of the Sorafenib.RET complex in which Sorafenib binds to and induces the DFG(out) conformation of the RET kinase domain.	Sorafenib	50-59	ret proto-oncogene	Homo sapiens	145-148
17664273-5	2007	In cell-based assays, Sorafenib inhibited the kinase activity and signaling of wild type and oncogenic RET in MEN2 tumor and established cell lines at a concentration between 15 and 150 nm.	Sorafenib	22-31	ret proto-oncogene	Homo sapiens	103-106
17664273-9	2007	Furthermore, we provide a structural model of the Sorafenib.RET complex in which Sorafenib binds to and induces the DFG(out) conformation of the RET kinase domain.	Sorafenib	81-90	ret proto-oncogene	Homo sapiens	60-63
17664273-9	2007	Furthermore, we provide a structural model of the Sorafenib.RET complex in which Sorafenib binds to and induces the DFG(out) conformation of the RET kinase domain.	Sorafenib	81-90	ret proto-oncogene	Homo sapiens	145-148
17664273-9	2007	Furthermore, we provide a structural model of the Sorafenib.RET complex in which Sorafenib binds to and induces the DFG(out) conformation of the RET kinase domain.	1,3-Diphenylguanidine	116-119	ret proto-oncogene	Homo sapiens	60-63
17664273-9	2007	Furthermore, we provide a structural model of the Sorafenib.RET complex in which Sorafenib binds to and induces the DFG(out) conformation of the RET kinase domain.	1,3-Diphenylguanidine	116-119	ret proto-oncogene	Homo sapiens	145-148
17664273-11	2007	In addition, because inhibition of RET is not impaired by mutation of the Val(804) gatekeeper residue, MEN2 tumors may be less susceptible to acquired Sorafenib resistance.	Sorafenib	151-160	ret proto-oncogene	Homo sapiens	35-38
17638907-0	2007	The RET kinase inhibitor NVP-AST487 blocks growth and calcitonin gene expression through distinct mechanisms in medullary thyroid cancer cells.	AST 487	29-35	ret proto-oncogene	Homo sapiens	4-7
17672459-1	2007	A polypurine (guanine)/polypyrimidine (cytosine)-rich sequence within the proximal promoter region of the human RET oncogene has been shown to be essential for RET basal transcription.	polypurine	2-12	ret proto-oncogene	Homo sapiens	112-115
17672459-1	2007	A polypurine (guanine)/polypyrimidine (cytosine)-rich sequence within the proximal promoter region of the human RET oncogene has been shown to be essential for RET basal transcription.	polypurine	2-12	ret proto-oncogene	Homo sapiens	160-163
17672459-1	2007	A polypurine (guanine)/polypyrimidine (cytosine)-rich sequence within the proximal promoter region of the human RET oncogene has been shown to be essential for RET basal transcription.	Guanine	14-21	ret proto-oncogene	Homo sapiens	112-115
17672459-1	2007	A polypurine (guanine)/polypyrimidine (cytosine)-rich sequence within the proximal promoter region of the human RET oncogene has been shown to be essential for RET basal transcription.	Guanine	14-21	ret proto-oncogene	Homo sapiens	160-163
17672459-1	2007	A polypurine (guanine)/polypyrimidine (cytosine)-rich sequence within the proximal promoter region of the human RET oncogene has been shown to be essential for RET basal transcription.	polypyrimidine	23-37	ret proto-oncogene	Homo sapiens	112-115
17672459-1	2007	A polypurine (guanine)/polypyrimidine (cytosine)-rich sequence within the proximal promoter region of the human RET oncogene has been shown to be essential for RET basal transcription.	polypyrimidine	23-37	ret proto-oncogene	Homo sapiens	160-163
17709622-11	2007	RESULTS: Using Western blot analysis, we detected the dephosphorylation of ERK1/2 in PTC cells carrying the RET/PTC1 rearrangement or a BRAF mutation after treating the cells with 2 MEK1/2 inhibitors (PD98059 and U0126).	U 0126	213-218	ret proto-oncogene	Homo sapiens	108-111
17709622-12	2007	In addition, both PD98059 and U0126 completely inhibited the growth of the PTC cells carrying a BRAF mutation but partially inhibited the growth of the PTC cells carrying the RET/PTC1 rearrangement.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	18-25	ret proto-oncogene	Homo sapiens	175-178
17709622-12	2007	In addition, both PD98059 and U0126 completely inhibited the growth of the PTC cells carrying a BRAF mutation but partially inhibited the growth of the PTC cells carrying the RET/PTC1 rearrangement.	U 0126	30-35	ret proto-oncogene	Homo sapiens	175-178
17672459-1	2007	A polypurine (guanine)/polypyrimidine (cytosine)-rich sequence within the proximal promoter region of the human RET oncogene has been shown to be essential for RET basal transcription.	Cytosine	39-47	ret proto-oncogene	Homo sapiens	112-115
17672459-1	2007	A polypurine (guanine)/polypyrimidine (cytosine)-rich sequence within the proximal promoter region of the human RET oncogene has been shown to be essential for RET basal transcription.	Cytosine	39-47	ret proto-oncogene	Homo sapiens	160-163
17709622-11	2007	RESULTS: Using Western blot analysis, we detected the dephosphorylation of ERK1/2 in PTC cells carrying the RET/PTC1 rearrangement or a BRAF mutation after treating the cells with 2 MEK1/2 inhibitors (PD98059 and U0126).	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	201-208	ret proto-oncogene	Homo sapiens	108-111
17344192-7	2007	A further study using cyclohexamide (a protein synthesis inhibitor) suggests that both RTK and JNK/SAPK contributed to the protein synthesis-independent early phase in hypotonic stress-induced Na(+) transport, but not to the protein synthesis-dependent late phase.	4-[2-(3,5-dimethyl-2-oxocyclohexyl)-2-hydroxyethyl]piperidine-2,6-dione	22-35	ret proto-oncogene	Homo sapiens	87-90
17638907-2	2007	NVP-AST487, a N,N"-diphenyl urea with an IC(50) of 0.88 mumol/L on RET kinase, inhibited RET autophosphorylation and activation of downstream effectors, and potently inhibited the growth of human thyroid cancer cell lines with activating mutations of RET but not of lines without RET mutations.	n,n"-diphenyl urea	14-32	ret proto-oncogene	Homo sapiens	67-70
17556544-2	2007	Here, we show that GW2974 (HER2/EGF receptor tyrosine kinase inhibitor), but not trastuzumab, activates AMP-activated protein kinase (AMPK), initiating a metabolic stress response in human cardiomyocytes that protects against TNFalpha-induced cell death.	GW2974	19-25	ret proto-oncogene	Homo sapiens	36-60
17548251-1	2007	BACKGROUND: Signal regulatory protein alpha1 (Sirpalpha1) is a member of Sirps families containing four immunoreceptor tyrosine-based inhibitory motifs (ITIMs) domains in the cytoplasm of and an activated substrate of receptor tyrosine kinase (RTK), that negatively regulates the RTK-dependent cell proliferating signal transduction pathway.	Tyrosine	119-127	ret proto-oncogene	Homo sapiens	218-242
17639053-5	2007	RET genetic analyses were performed at the germline and tissue levels in MTC and CCH cases.	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	81-84	ret proto-oncogene	Homo sapiens	0-3
17490619-6	2007	We show that the VEGF-A isoform VEGF(165) induces RET-tyr(1062) phosphorylation in addition to VEGFR2 autophosphorylation, that VEGF(165) and GDNF have additive effects on RET-tyr(1062) phosphorylation, and that VEGFR2 and RET co-immunoprecipitate.	Tyrosine	54-57	ret proto-oncogene	Homo sapiens	50-53
17490619-8	2007	Similarly, in embryonic kidney explants VEGF(165) induces RET-tyr(1062) phosphorylation and upregulates GDNF.	Tyrosine	62-65	ret proto-oncogene	Homo sapiens	58-61
17548251-1	2007	BACKGROUND: Signal regulatory protein alpha1 (Sirpalpha1) is a member of Sirps families containing four immunoreceptor tyrosine-based inhibitory motifs (ITIMs) domains in the cytoplasm of and an activated substrate of receptor tyrosine kinase (RTK), that negatively regulates the RTK-dependent cell proliferating signal transduction pathway.	Tyrosine	119-127	ret proto-oncogene	Homo sapiens	244-247
17548251-1	2007	BACKGROUND: Signal regulatory protein alpha1 (Sirpalpha1) is a member of Sirps families containing four immunoreceptor tyrosine-based inhibitory motifs (ITIMs) domains in the cytoplasm of and an activated substrate of receptor tyrosine kinase (RTK), that negatively regulates the RTK-dependent cell proliferating signal transduction pathway.	Tyrosine	119-127	ret proto-oncogene	Homo sapiens	280-283
17431108-0	2007	The RET oncogene is a critical component of transcriptional programs associated with retinoic acid-induced differentiation in neuroblastoma.	Tretinoin	85-98	ret proto-oncogene	Homo sapiens	4-7
17499312-9	2007	Receptor tyrosine kinase assays revealed that IGF-1-stimulated IGF-1R tyrosine kinase activation was also abrogated by curcumin in a dose-dependent manner.	Curcumin	119-127	ret proto-oncogene	Homo sapiens	0-24
17453286-5	2007	(2) Among the high-risk RET mutations, those in codon 634 cause higher penetrance rates of the multiple endocrine neoplasia 2A phenotype (MTC, pheochromocytoma, and parathyroid hyperplasia/adenoma) than mutations in codons 609, 611, 618, and 620, irrespective of the amino acid substituting for cysteine (grade C).	Cysteine	295-303	ret proto-oncogene	Homo sapiens	24-27
17358032-10	2007	Specifically, mean %MN-RET in cord blood of ZDV-exposed infants was 1.67 +/- 0.34 compared with 0.16 +/- 0.06 in non-ZDV ART-exposed infants (P = 0.006) and 0.12 +/- 0.02 in control cord bloods (P &lt; 0.0001).	Zidovudine	44-47	ret proto-oncogene	Homo sapiens	23-26
17358032-11	2007	%MN-RET in ZDV-exposed newborns decreased over the first 6 months of life to levels comparable to cord blood controls.	Zidovudine	11-14	ret proto-oncogene	Homo sapiens	4-7
17343372-0	2007	Discovery of N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N"-(2-fluoro-5-methylphenyl)urea (ABT-869), a 3-aminoindazole-based orally active multitargeted receptor tyrosine kinase inhibitor.	N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N1-(2-fluoro-5-methylphenyl)urea	13-83	ret proto-oncogene	Homo sapiens	147-171
17343372-0	2007	Discovery of N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N"-(2-fluoro-5-methylphenyl)urea (ABT-869), a 3-aminoindazole-based orally active multitargeted receptor tyrosine kinase inhibitor.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	85-88	ret proto-oncogene	Homo sapiens	147-171
17343372-0	2007	Discovery of N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N"-(2-fluoro-5-methylphenyl)urea (ABT-869), a 3-aminoindazole-based orally active multitargeted receptor tyrosine kinase inhibitor.	1H-Indazol-3-amine	97-112	ret proto-oncogene	Homo sapiens	147-171
17343372-1	2007	In our continued efforts to search for potent and novel receptor tyrosine kinase (RTK) inhibitors as potential anticancer agents, we discovered, through a structure-based design, that 3-aminoindazole could serve as an efficient hinge-binding template for kinase inhibitors.	1H-Indazol-3-amine	184-199	ret proto-oncogene	Homo sapiens	56-80
17343372-1	2007	In our continued efforts to search for potent and novel receptor tyrosine kinase (RTK) inhibitors as potential anticancer agents, we discovered, through a structure-based design, that 3-aminoindazole could serve as an efficient hinge-binding template for kinase inhibitors.	1H-Indazol-3-amine	184-199	ret proto-oncogene	Homo sapiens	82-85
17343372-2	2007	By incorporating an N,N"-diaryl urea moiety at the C4-position of 3-aminodazole, a series of RTK inhibitors were generated, which potently inhibited the tyrosine kinase activity of the vascular endothelial growth factor receptor and the platelet-derived growth factor receptor families.	n,n"-diaryl urea	20-36	ret proto-oncogene	Homo sapiens	93-96
17343372-2	2007	By incorporating an N,N"-diaryl urea moiety at the C4-position of 3-aminodazole, a series of RTK inhibitors were generated, which potently inhibited the tyrosine kinase activity of the vascular endothelial growth factor receptor and the platelet-derived growth factor receptor families.	3-aminodazole	66-79	ret proto-oncogene	Homo sapiens	93-96
17358032-9	2007	Tenfold increases in %MN-RET were seen in women and infants who received ZDV-containing ART prenatally; no increases were detected in three women and infants who received prenatal ART without ZDV.	Zidovudine	73-76	ret proto-oncogene	Homo sapiens	25-28
17431108-6	2007	RET, a receptor tyrosine kinase involved with differentiation, was consistently up-regulated throughout the time course of RA treatment in the majority of neuroblastic tumor cell lines.	Tretinoin	123-125	ret proto-oncogene	Homo sapiens	0-3
17097365-9	2007	Our patient was a heterozygote carrier of GAG--&gt;GAC mutation (Glu 768 Asp) in exon 13, codon 768 of the RET proto-oncogene.	Glycosaminoglycans	42-45	ret proto-oncogene	Homo sapiens	107-110
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
17209045-1	2007	The precise role of STAT3 Ser(727) phosphorylation in RET-mediated cell transformation and oncogenesis is not well understood.	Serine	26-29	ret proto-oncogene	Homo sapiens	54-57
17209045-2	2007	In this study, we have shown that familial medullary thyroid carcinoma (FMTC) mutants RET(Y791F) and RET(S891A) induced, in addition to Tyr(705) phosphorylation, constitutive STAT3 Ser(727) phosphorylation.	Tyrosine	136-139	ret proto-oncogene	Homo sapiens	86-89
17209045-2	2007	In this study, we have shown that familial medullary thyroid carcinoma (FMTC) mutants RET(Y791F) and RET(S891A) induced, in addition to Tyr(705) phosphorylation, constitutive STAT3 Ser(727) phosphorylation.	Tyrosine	136-139	ret proto-oncogene	Homo sapiens	101-104
17209045-2	2007	In this study, we have shown that familial medullary thyroid carcinoma (FMTC) mutants RET(Y791F) and RET(S891A) induced, in addition to Tyr(705) phosphorylation, constitutive STAT3 Ser(727) phosphorylation.	Serine	181-184	ret proto-oncogene	Homo sapiens	86-89
17209045-2	2007	In this study, we have shown that familial medullary thyroid carcinoma (FMTC) mutants RET(Y791F) and RET(S891A) induced, in addition to Tyr(705) phosphorylation, constitutive STAT3 Ser(727) phosphorylation.	Serine	181-184	ret proto-oncogene	Homo sapiens	101-104
17209045-3	2007	Using inhibitors and dominant negative constructs, we have demonstrated that RET(Y791F) and RET(S891A) induce STAT3 Ser(727) phosphorylation via a canonical Ras/ERK1/2 pathway and that integration of the Ras/ERK1/2/ELK-1 and STAT3 pathways was required for up-regulation of the c-fos promoter by FMTC-RET.	Serine	116-119	ret proto-oncogene	Homo sapiens	77-80
17209045-3	2007	Using inhibitors and dominant negative constructs, we have demonstrated that RET(Y791F) and RET(S891A) induce STAT3 Ser(727) phosphorylation via a canonical Ras/ERK1/2 pathway and that integration of the Ras/ERK1/2/ELK-1 and STAT3 pathways was required for up-regulation of the c-fos promoter by FMTC-RET.	Serine	116-119	ret proto-oncogene	Homo sapiens	92-95
17209045-3	2007	Using inhibitors and dominant negative constructs, we have demonstrated that RET(Y791F) and RET(S891A) induce STAT3 Ser(727) phosphorylation via a canonical Ras/ERK1/2 pathway and that integration of the Ras/ERK1/2/ELK-1 and STAT3 pathways was required for up-regulation of the c-fos promoter by FMTC-RET.	Serine	116-119	ret proto-oncogene	Homo sapiens	92-95
17209045-10	2007	These data show that FMTC-RET mutants activate a Ras/ERK1/2/STAT3 Ser(727) pathway, which plays an important role in cell mitogenicity and transformation.	Serine	66-69	ret proto-oncogene	Homo sapiens	26-29
17279407-3	2007	Special attention should be paid to rare patients who carry mutations of one of the critical cysteine residues of these exons, known to predispose to MEN2A.	Cysteine	93-101	ret proto-oncogene	Homo sapiens	150-155
16843637-0	2006	RET oncoproteins induce tyrosine phosphorylation changes of proteins involved in RNA metabolism.	Tyrosine	24-32	ret proto-oncogene	Homo sapiens	0-3
17934909-1	2007	RET (REarranged during Transfection) is a transmembrane receptor tyrosine kinase that is activated by a complex consisting of a soluble glial cell line-derived neurotrophic factor (GDNF) family ligand (GFL) and a glycosyl phosphatidylinositol-anchored co-receptor, GDNF family receptors alpha (GFRalpha).	Phosphatidylinositols	222-242	ret proto-oncogene	Homo sapiens	0-3
17934909-1	2007	RET (REarranged during Transfection) is a transmembrane receptor tyrosine kinase that is activated by a complex consisting of a soluble glial cell line-derived neurotrophic factor (GDNF) family ligand (GFL) and a glycosyl phosphatidylinositol-anchored co-receptor, GDNF family receptors alpha (GFRalpha).	Phosphatidylinositols	222-242	ret proto-oncogene	Homo sapiens	5-35
17353176-11	2007	In comparison with CHr, the value of 30.5 pg for RET-He appeared to be the best cut-off point with a very good sensitivity and specificity to determine patients needing iron supplementation.	Iron	169-173	ret proto-oncogene	Homo sapiens	49-52
17353176-12	2007	Our study showed an excellent diagnostic efficiency of RET-He to evaluate patients needing iron support and demonstrated a strict correspondence between the classic CHr and the new Ret-He.	Iron	91-95	ret proto-oncogene	Homo sapiens	55-58
18314611-2	2007	One very effective tyrosine kinase inhibitor is imatinib mesylate inhibiting the KIT receptor tyrosine kinase in gastrointestinal stromal tumors (GISTs) which often carry activating mutations in the KIT gene.	Imatinib Mesylate	48-65	ret proto-oncogene	Homo sapiens	85-109
18314625-3	2007	In this context, gene-specific siRNA against IGF-signalling components as well as IGF1R selective receptor tyrosine kinase (RTK)-inhibitors (tyrphostins) may therefore offer new therapeutic options since both small interfering RNAs (siRNA) and small inhibitory molecules significantly reduce IGFIR signalling in HCC cell lines.	Tyrphostins	141-152	ret proto-oncogene	Homo sapiens	98-122
18314625-3	2007	In this context, gene-specific siRNA against IGF-signalling components as well as IGF1R selective receptor tyrosine kinase (RTK)-inhibitors (tyrphostins) may therefore offer new therapeutic options since both small interfering RNAs (siRNA) and small inhibitory molecules significantly reduce IGFIR signalling in HCC cell lines.	Tyrphostins	141-152	ret proto-oncogene	Homo sapiens	124-127
17270543-2	2007	Children of families with RET cysteine mutations (exons 10, 11, 13, and 16) may develop early metastatic tumours and require prophylactic thyroidectomy.	Cysteine	30-38	ret proto-oncogene	Homo sapiens	26-29
17217081-2	2007	All seven TRPCs (TRPC1 through TRPC7) can be activated through Gq/11 receptors or receptor tyrosine kinase (RTK) by mechanisms downstream of phospholipase C. The last decade saw a rapidly growing interest in understanding the role of TRPC channels in calcium entry pathways as well as in understanding the signal(s) responsible for TRPC activation.	Calcium	251-258	ret proto-oncogene	Homo sapiens	82-106
17217081-2	2007	All seven TRPCs (TRPC1 through TRPC7) can be activated through Gq/11 receptors or receptor tyrosine kinase (RTK) by mechanisms downstream of phospholipase C. The last decade saw a rapidly growing interest in understanding the role of TRPC channels in calcium entry pathways as well as in understanding the signal(s) responsible for TRPC activation.	Calcium	251-258	ret proto-oncogene	Homo sapiens	108-111
17178882-2	2006	Sorafenib (BAY 43-9006, Nexavar) is a multikinase inhibitor with activity against Raf kinase and several receptor tyrosine kinases, including vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor (PDGFR), FLT3, Ret, and c-Kit.	Sorafenib	0-9	ret proto-oncogene	Homo sapiens	253-256
17178882-2	2006	Sorafenib (BAY 43-9006, Nexavar) is a multikinase inhibitor with activity against Raf kinase and several receptor tyrosine kinases, including vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor (PDGFR), FLT3, Ret, and c-Kit.	Sorafenib	11-22	ret proto-oncogene	Homo sapiens	253-256
17178882-2	2006	Sorafenib (BAY 43-9006, Nexavar) is a multikinase inhibitor with activity against Raf kinase and several receptor tyrosine kinases, including vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor (PDGFR), FLT3, Ret, and c-Kit.	Sorafenib	24-31	ret proto-oncogene	Homo sapiens	253-256
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
17260470-0	2006	[RET gene cys 634 trp mutation in a multiple endocrine neoplasia type 2A kindred].	Cysteine	10-13	ret proto-oncogene	Homo sapiens	1-4
17260470-0	2006	[RET gene cys 634 trp mutation in a multiple endocrine neoplasia type 2A kindred].	Cysteine	10-13	ret proto-oncogene	Homo sapiens	36-72
17260470-0	2006	[RET gene cys 634 trp mutation in a multiple endocrine neoplasia type 2A kindred].	Tryptophan	18-21	ret proto-oncogene	Homo sapiens	1-4
17260470-0	2006	[RET gene cys 634 trp mutation in a multiple endocrine neoplasia type 2A kindred].	Tryptophan	18-21	ret proto-oncogene	Homo sapiens	36-72
17260470-6	2006	This missense point mutation arisen in heterozygosity and caused a substitution of Cys to Trp residue at codon 634 ( Cys 634 Trp) in RET protein.	Cysteine	83-86	ret proto-oncogene	Homo sapiens	133-136
17260470-6	2006	This missense point mutation arisen in heterozygosity and caused a substitution of Cys to Trp residue at codon 634 ( Cys 634 Trp) in RET protein.	Tryptophan	90-93	ret proto-oncogene	Homo sapiens	133-136
17260470-6	2006	This missense point mutation arisen in heterozygosity and caused a substitution of Cys to Trp residue at codon 634 ( Cys 634 Trp) in RET protein.	Cysteine	117-120	ret proto-oncogene	Homo sapiens	133-136
17260470-6	2006	This missense point mutation arisen in heterozygosity and caused a substitution of Cys to Trp residue at codon 634 ( Cys 634 Trp) in RET protein.	Tryptophan	125-128	ret proto-oncogene	Homo sapiens	133-136
17260470-7	2006	CONCLUSION: The genotype of the family is identified as Cys 634 Trp substitution of RET gene.	Cysteine	56-59	ret proto-oncogene	Homo sapiens	84-87
17260470-7	2006	CONCLUSION: The genotype of the family is identified as Cys 634 Trp substitution of RET gene.	Tryptophan	64-67	ret proto-oncogene	Homo sapiens	84-87
17108110-2	2006	The disease is caused primarily by a methionine to threonine substitution of residue 918 in the kinase domain of the RET receptor (2B-RET); however, the molecular mechanisms that lead to the disease phenotype are unclear.	Methionine	37-47	ret proto-oncogene	Homo sapiens	117-120
17108110-2	2006	The disease is caused primarily by a methionine to threonine substitution of residue 918 in the kinase domain of the RET receptor (2B-RET); however, the molecular mechanisms that lead to the disease phenotype are unclear.	Methionine	37-47	ret proto-oncogene	Homo sapiens	134-137
17108110-2	2006	The disease is caused primarily by a methionine to threonine substitution of residue 918 in the kinase domain of the RET receptor (2B-RET); however, the molecular mechanisms that lead to the disease phenotype are unclear.	Threonine	51-60	ret proto-oncogene	Homo sapiens	117-120
17108110-2	2006	The disease is caused primarily by a methionine to threonine substitution of residue 918 in the kinase domain of the RET receptor (2B-RET); however, the molecular mechanisms that lead to the disease phenotype are unclear.	Threonine	51-60	ret proto-oncogene	Homo sapiens	134-137
16928683-8	2006	We also present the structures of the RET tyrosine kinase domain bound to two inhibitors, the pyrazolopyrimidine PP1 and the clinically relevant 4-anilinoquinazoline ZD6474.	anilinoquinazoline	145-165	ret proto-oncogene	Homo sapiens	38-41
16928683-8	2006	We also present the structures of the RET tyrosine kinase domain bound to two inhibitors, the pyrazolopyrimidine PP1 and the clinically relevant 4-anilinoquinazoline ZD6474.	vandetanib	166-172	ret proto-oncogene	Homo sapiens	38-41
16934227-4	2006	We have shown that the RTK inhibitor GW282974A (an analogue of GW2016; lapatinib) is effective in chemosensitisation of drug resistant EGFR over-expressing cells giving rise to a synergistic effect when used in combination with either cisplatin or paclitaxel in chemosensitivity assays.	GW2974	37-46	ret proto-oncogene	Homo sapiens	23-26
16934227-4	2006	We have shown that the RTK inhibitor GW282974A (an analogue of GW2016; lapatinib) is effective in chemosensitisation of drug resistant EGFR over-expressing cells giving rise to a synergistic effect when used in combination with either cisplatin or paclitaxel in chemosensitivity assays.	N-(3-chloro-4-((3-fluorobenzyl)oxy)phenyl-6-(5-((methylsulfonyl)ethyl)aminomethyl)-2-furyl)-4-quinazolinamine	63-69	ret proto-oncogene	Homo sapiens	23-26
16934227-4	2006	We have shown that the RTK inhibitor GW282974A (an analogue of GW2016; lapatinib) is effective in chemosensitisation of drug resistant EGFR over-expressing cells giving rise to a synergistic effect when used in combination with either cisplatin or paclitaxel in chemosensitivity assays.	Lapatinib	71-80	ret proto-oncogene	Homo sapiens	23-26
16934227-4	2006	We have shown that the RTK inhibitor GW282974A (an analogue of GW2016; lapatinib) is effective in chemosensitisation of drug resistant EGFR over-expressing cells giving rise to a synergistic effect when used in combination with either cisplatin or paclitaxel in chemosensitivity assays.	Cisplatin	235-244	ret proto-oncogene	Homo sapiens	23-26
16934227-4	2006	We have shown that the RTK inhibitor GW282974A (an analogue of GW2016; lapatinib) is effective in chemosensitisation of drug resistant EGFR over-expressing cells giving rise to a synergistic effect when used in combination with either cisplatin or paclitaxel in chemosensitivity assays.	Paclitaxel	248-258	ret proto-oncogene	Homo sapiens	23-26
16999719-7	2006	Ret He is a reliable marker of cellular hemoglobin content and can be used to identify the presence of iron-deficient states.	Iron	103-107	ret proto-oncogene	Homo sapiens	0-3
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
16849418-3	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.	Semaxinib	122-128	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.	Semaxinib	122-128	ret proto-oncogene	Homo sapiens	162-165
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.	orantinib	134-140	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.	orantinib	134-140	ret proto-oncogene	Homo sapiens	162-165
16995874-1	2006	ZD6474 (Zactima, AstraZeneca, Macclesfield, UK) is an orally available, small-molecule inhibitor of vascular endothelial growth factor receptor-2 and epidermal growth factor receptor tyrosine kinases, with additional activity versus rearranged during transfection (RET).	vandetanib	0-6	ret proto-oncogene	Homo sapiens	265-268
16732321-1	2006	In patients with medullary thyroid carcinoma (MTC) and type 2A multiple endocrine neoplasia (MEN2A), mutations of cysteine residues in the extracellular juxtamembrane region of the RET receptor tyrosine kinase cause the formation of covalent receptor dimers linked by intermolecular disulfide bonds between unpaired cysteines, followed by oncogenic activation of the RET kinase.	Cysteine	114-122	ret proto-oncogene	Homo sapiens	93-98
16732321-1	2006	In patients with medullary thyroid carcinoma (MTC) and type 2A multiple endocrine neoplasia (MEN2A), mutations of cysteine residues in the extracellular juxtamembrane region of the RET receptor tyrosine kinase cause the formation of covalent receptor dimers linked by intermolecular disulfide bonds between unpaired cysteines, followed by oncogenic activation of the RET kinase.	Cysteine	114-122	ret proto-oncogene	Homo sapiens	181-184
16732321-1	2006	In patients with medullary thyroid carcinoma (MTC) and type 2A multiple endocrine neoplasia (MEN2A), mutations of cysteine residues in the extracellular juxtamembrane region of the RET receptor tyrosine kinase cause the formation of covalent receptor dimers linked by intermolecular disulfide bonds between unpaired cysteines, followed by oncogenic activation of the RET kinase.	Cysteine	114-122	ret proto-oncogene	Homo sapiens	367-370
16732321-1	2006	In patients with medullary thyroid carcinoma (MTC) and type 2A multiple endocrine neoplasia (MEN2A), mutations of cysteine residues in the extracellular juxtamembrane region of the RET receptor tyrosine kinase cause the formation of covalent receptor dimers linked by intermolecular disulfide bonds between unpaired cysteines, followed by oncogenic activation of the RET kinase.	Disulfides	283-292	ret proto-oncogene	Homo sapiens	93-98
16732321-1	2006	In patients with medullary thyroid carcinoma (MTC) and type 2A multiple endocrine neoplasia (MEN2A), mutations of cysteine residues in the extracellular juxtamembrane region of the RET receptor tyrosine kinase cause the formation of covalent receptor dimers linked by intermolecular disulfide bonds between unpaired cysteines, followed by oncogenic activation of the RET kinase.	Disulfides	283-292	ret proto-oncogene	Homo sapiens	181-184
16732321-1	2006	In patients with medullary thyroid carcinoma (MTC) and type 2A multiple endocrine neoplasia (MEN2A), mutations of cysteine residues in the extracellular juxtamembrane region of the RET receptor tyrosine kinase cause the formation of covalent receptor dimers linked by intermolecular disulfide bonds between unpaired cysteines, followed by oncogenic activation of the RET kinase.	Cysteine	316-325	ret proto-oncogene	Homo sapiens	93-98
16732321-1	2006	In patients with medullary thyroid carcinoma (MTC) and type 2A multiple endocrine neoplasia (MEN2A), mutations of cysteine residues in the extracellular juxtamembrane region of the RET receptor tyrosine kinase cause the formation of covalent receptor dimers linked by intermolecular disulfide bonds between unpaired cysteines, followed by oncogenic activation of the RET kinase.	Cysteine	316-325	ret proto-oncogene	Homo sapiens	181-184
16732321-4	2006	Mutagenesis studies indicated the involvement of the evolutionary conserved residues Ser-649 and Ser-653 in RET-TM oligomerization.	Serine	85-88	ret proto-oncogene	Homo sapiens	108-114
16732321-4	2006	Mutagenesis studies indicated the involvement of the evolutionary conserved residues Ser-649 and Ser-653 in RET-TM oligomerization.	Serine	97-100	ret proto-oncogene	Homo sapiens	108-114
16732321-7	2006	When introduced in the context of C634R - a cysteine replacement that is prevalent in MEN2A cases - the A639G/A641R mutations significantly reduced dimer formation and transforming activity in this otherwise highly oncogenic RET variant.	Cysteine	44-52	ret proto-oncogene	Homo sapiens	86-91
16732321-7	2006	When introduced in the context of C634R - a cysteine replacement that is prevalent in MEN2A cases - the A639G/A641R mutations significantly reduced dimer formation and transforming activity in this otherwise highly oncogenic RET variant.	Cysteine	44-52	ret proto-oncogene	Homo sapiens	225-228
16732321-8	2006	These data suggest that a strong propensity to self-association in the RET-TM underlies - and may be required for - dimer formation and oncogenic activation of juxtamembrane cysteine mutants of RET, and explains the close proximity to the plasma membrane of cysteine residues implicated in MEN2A and MTC syndromes.	Cysteine	174-182	ret proto-oncogene	Homo sapiens	71-74
16732321-8	2006	These data suggest that a strong propensity to self-association in the RET-TM underlies - and may be required for - dimer formation and oncogenic activation of juxtamembrane cysteine mutants of RET, and explains the close proximity to the plasma membrane of cysteine residues implicated in MEN2A and MTC syndromes.	Cysteine	174-182	ret proto-oncogene	Homo sapiens	290-295
16732321-8	2006	These data suggest that a strong propensity to self-association in the RET-TM underlies - and may be required for - dimer formation and oncogenic activation of juxtamembrane cysteine mutants of RET, and explains the close proximity to the plasma membrane of cysteine residues implicated in MEN2A and MTC syndromes.	Cysteine	258-266	ret proto-oncogene	Homo sapiens	71-74
16732321-8	2006	These data suggest that a strong propensity to self-association in the RET-TM underlies - and may be required for - dimer formation and oncogenic activation of juxtamembrane cysteine mutants of RET, and explains the close proximity to the plasma membrane of cysteine residues implicated in MEN2A and MTC syndromes.	Cysteine	258-266	ret proto-oncogene	Homo sapiens	194-197
16732321-8	2006	These data suggest that a strong propensity to self-association in the RET-TM underlies - and may be required for - dimer formation and oncogenic activation of juxtamembrane cysteine mutants of RET, and explains the close proximity to the plasma membrane of cysteine residues implicated in MEN2A and MTC syndromes.	Cysteine	258-266	ret proto-oncogene	Homo sapiens	290-295
17409986-1	2006	INTRODUCTION: ZD6474 (vandetanib) is an orally available inhibitor of vascular endothelial growth factor receptor, epidermal growth factor receptor, and RET receptor tyrosine kinase activity.	vandetanib	14-20	ret proto-oncogene	Homo sapiens	153-156
17409986-1	2006	INTRODUCTION: ZD6474 (vandetanib) is an orally available inhibitor of vascular endothelial growth factor receptor, epidermal growth factor receptor, and RET receptor tyrosine kinase activity.	vandetanib	22-32	ret proto-oncogene	Homo sapiens	153-156
16847065-0	2006	Engineering the recruitment of phosphotyrosine binding domain-containing adaptor proteins reveals distinct roles for RET receptor-mediated cell survival.	Phosphotyrosine	31-46	ret proto-oncogene	Homo sapiens	117-120
16847065-2	2006	The recruitment at the phosphorylated Tyr(1062) site in RET of a number of different phosphotyrosine binding (PTB) domain-containing adaptor proteins, including Shc and Frs2, plays a dominant role for the multiple different biological functions of the RET receptor during development, including stimulation of cell survival.	Tyrosine	38-41	ret proto-oncogene	Homo sapiens	56-59
16847065-2	2006	The recruitment at the phosphorylated Tyr(1062) site in RET of a number of different phosphotyrosine binding (PTB) domain-containing adaptor proteins, including Shc and Frs2, plays a dominant role for the multiple different biological functions of the RET receptor during development, including stimulation of cell survival.	Tyrosine	38-41	ret proto-oncogene	Homo sapiens	252-255
16847065-2	2006	The recruitment at the phosphorylated Tyr(1062) site in RET of a number of different phosphotyrosine binding (PTB) domain-containing adaptor proteins, including Shc and Frs2, plays a dominant role for the multiple different biological functions of the RET receptor during development, including stimulation of cell survival.	Phosphotyrosine	85-100	ret proto-oncogene	Homo sapiens	56-59
16847065-2	2006	The recruitment at the phosphorylated Tyr(1062) site in RET of a number of different phosphotyrosine binding (PTB) domain-containing adaptor proteins, including Shc and Frs2, plays a dominant role for the multiple different biological functions of the RET receptor during development, including stimulation of cell survival.	Phosphotyrosine	85-100	ret proto-oncogene	Homo sapiens	252-255
17136225-3	2006	Vandetanib is a novel multitargeted kinase inhibitor exhibiting potent activity against vascular endothelial growth factor receptor-2 (VEGFR-2; kinase insert domain-containing receptor [KDR]) and, to a lesser extent, epidermal growth factor receptor (EGFR) and RET kinase.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	261-264
17136225-6	2006	Furthermore, vandetanib exerts activity against oncogenic RET kinase, the overexpression of which is common in medullary and papillary thyroid carcinomas.	vandetanib	13-23	ret proto-oncogene	Homo sapiens	58-61
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
16849418-4	2006	DESIGN: SU11248, SU5416, and SU6668 were synthesized, and their inhibitory potencies were evaluated using an in vitro RET/PTC kinase assay.	orantinib	29-35	ret proto-oncogene	Homo sapiens	118-121
16849418-4	2006	DESIGN: SU11248, SU5416, and SU6668 were synthesized, and their inhibitory potencies were evaluated using an in vitro RET/PTC kinase assay.	orantinib	29-35	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.	Semaxinib	48-54	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.	orantinib	56-62	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	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.	Semaxinib	236-242	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.	orantinib	255-261	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	278-285	ret proto-oncogene	Homo sapiens	160-163
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
16849418-7	2006	Thus, SU11248 effectively inhibits the kinase activity of RET/PTC3.	Sunitinib	6-13	ret proto-oncogene	Homo sapiens	58-61
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.	y705	17-21	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.	y705	17-21	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	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	ret proto-oncogene	Homo sapiens	262-265
17032739-0	2006	Inhibition of RET tyrosine kinase by SU5416.	Semaxinib	37-43	ret proto-oncogene	Homo sapiens	14-17
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
17032739-4	2006	We found that SU5416 inhibits RET with similar potency, both in cell-free assays and in cells, thus causing proliferation arrest in oncogenic RET-transfected cells and in papillary thyroid carcinoma (PTC) cells expressing the RET/PTC1 oncogene, but not in RET-negative control cells.	Semaxinib	14-20	ret proto-oncogene	Homo sapiens	30-33
17032739-4	2006	We found that SU5416 inhibits RET with similar potency, both in cell-free assays and in cells, thus causing proliferation arrest in oncogenic RET-transfected cells and in papillary thyroid carcinoma (PTC) cells expressing the RET/PTC1 oncogene, but not in RET-negative control cells.	Semaxinib	14-20	ret proto-oncogene	Homo sapiens	142-145
17032739-4	2006	We found that SU5416 inhibits RET with similar potency, both in cell-free assays and in cells, thus causing proliferation arrest in oncogenic RET-transfected cells and in papillary thyroid carcinoma (PTC) cells expressing the RET/PTC1 oncogene, but not in RET-negative control cells.	Semaxinib	14-20	ret proto-oncogene	Homo sapiens	142-145
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.	Tyrosine	130-138	ret proto-oncogene	Homo sapiens	0-3
17032739-4	2006	We found that SU5416 inhibits RET with similar potency, both in cell-free assays and in cells, thus causing proliferation arrest in oncogenic RET-transfected cells and in papillary thyroid carcinoma (PTC) cells expressing the RET/PTC1 oncogene, but not in RET-negative control cells.	Semaxinib	14-20	ret proto-oncogene	Homo sapiens	142-145
17032739-5	2006	SU5416 inhibited RET-mediated signaling through the extracellular signal regulated kinase (ERK) and JNK pathways.	Semaxinib	0-6	ret proto-oncogene	Homo sapiens	17-20
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.	Tyrosine	130-138	ret proto-oncogene	Homo sapiens	4-7
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	ret proto-oncogene	Homo sapiens	148-151
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
16490247-3	2006	We expressed recombinant RET kinase domain (rRET) containing the active site, the ATP binding pocket, and the activation loop with regulatory activity, with the Baculovirus expression system.	Adenosine Triphosphate	82-85	ret proto-oncogene	Homo sapiens	25-28
16896007-8	2006	99mTc-DIDA/DISIDA percent retention at 1 hour (1-hour RET) correlated to baseline serum bilirubin (P = .008).	99mtc-dida	0-10	ret proto-oncogene	Homo sapiens	54-57
16896007-8	2006	99mTc-DIDA/DISIDA percent retention at 1 hour (1-hour RET) correlated to baseline serum bilirubin (P = .008).	disida	11-17	ret proto-oncogene	Homo sapiens	54-57
16896007-8	2006	99mTc-DIDA/DISIDA percent retention at 1 hour (1-hour RET) correlated to baseline serum bilirubin (P = .008).	Bilirubin	88-97	ret proto-oncogene	Homo sapiens	54-57
16896007-9	2006	Both 99mTc-DIDA/DISIDA and MIBI 1-hour RET correlated with SN-38 area under the curve (AUC; P &lt; .01).	Irinotecan	59-64	ret proto-oncogene	Homo sapiens	39-42
16896007-10	2006	On multiple regression analysis, SN-38 AUC = -215 + 18.68 x bilirubin + 4.27 x MIBI 1-hour RET (P = .009, R2 = 44.2%).	Irinotecan	33-38	ret proto-oncogene	Homo sapiens	91-94
16865277-8	2006	Our findings indicate that although gastric cancer does not seem to harbour mutations which render the cancer cells constitutively susceptible to gefitinib, the co-administration of ASA can strengthen RTK inhibitor activity in adenocarcinoma cells by EGFR activation.	Aspirin	182-185	ret proto-oncogene	Homo sapiens	201-204
16954442-2	2006	Single base pair missense mutations in the extracellular Cys-rich domain are responsible for most MEN2A and familial MTC (FMTC) cases.	Cysteine	57-60	ret proto-oncogene	Homo sapiens	98-103
16490247-4	2006	RET was purified by a two-step procedure consisting of an anion exchange chromatography followed by nickel affinity chromatography.	Nickel	100-106	ret proto-oncogene	Homo sapiens	0-3
17102091-8	2006	MEN 2A is primarily associated with substitutions at five extracellular cysteine residues, while 95% of MEN 2B is associated with a single methionine to threonine mutation in the kinase domain (M918T).	Cysteine	72-80	ret proto-oncogene	Homo sapiens	0-6
17102091-8	2006	MEN 2A is primarily associated with substitutions at five extracellular cysteine residues, while 95% of MEN 2B is associated with a single methionine to threonine mutation in the kinase domain (M918T).	Methionine	139-149	ret proto-oncogene	Homo sapiens	104-110
17102091-8	2006	MEN 2A is primarily associated with substitutions at five extracellular cysteine residues, while 95% of MEN 2B is associated with a single methionine to threonine mutation in the kinase domain (M918T).	Threonine	153-162	ret proto-oncogene	Homo sapiens	104-110
16829704-13	2006	RET gene analysis showed a codon 918 mutation in exon 16 resulting in an ATG (methionine) to ACG (threonine) substitution, but analysis of the patient"s parents showed the wild type.	Methionine	78-88	ret proto-oncogene	Homo sapiens	0-3
16829704-13	2006	RET gene analysis showed a codon 918 mutation in exon 16 resulting in an ATG (methionine) to ACG (threonine) substitution, but analysis of the patient"s parents showed the wild type.	acceleratory factor from growth hormone	93-96	ret proto-oncogene	Homo sapiens	0-3
16829704-13	2006	RET gene analysis showed a codon 918 mutation in exon 16 resulting in an ATG (methionine) to ACG (threonine) substitution, but analysis of the patient"s parents showed the wild type.	Threonine	98-107	ret proto-oncogene	Homo sapiens	0-3
16678414-1	2006	The 3-benzimidazol-2-yl-1H-indazole scaffold was developed as an alternate scaffold for our receptor tyrosine kinase (RTK) inhibitor program.	3-(1H-BENZIMIDAZOL-2-YL)-1H-INDAZOLE	4-35	ret proto-oncogene	Homo sapiens	92-116
16678414-1	2006	The 3-benzimidazol-2-yl-1H-indazole scaffold was developed as an alternate scaffold for our receptor tyrosine kinase (RTK) inhibitor program.	3-(1H-BENZIMIDAZOL-2-YL)-1H-INDAZOLE	4-35	ret proto-oncogene	Homo sapiens	118-121
16772843-2	2006	Screening for MEN 2B revealed a polymorphism of the RET proto-oncogene at codon 691 with a glycine to serine conversion.	Glycine	91-98	ret proto-oncogene	Homo sapiens	14-20
16772843-2	2006	Screening for MEN 2B revealed a polymorphism of the RET proto-oncogene at codon 691 with a glycine to serine conversion.	Glycine	91-98	ret proto-oncogene	Homo sapiens	52-55
16772843-2	2006	Screening for MEN 2B revealed a polymorphism of the RET proto-oncogene at codon 691 with a glycine to serine conversion.	Serine	102-108	ret proto-oncogene	Homo sapiens	14-20
16772843-2	2006	Screening for MEN 2B revealed a polymorphism of the RET proto-oncogene at codon 691 with a glycine to serine conversion.	Serine	102-108	ret proto-oncogene	Homo sapiens	52-55
17065770-3	2006	Almost all mutations in MEN 2A involve one of the cysteines in the extracellular domain of the RET receptor.	Cysteine	50-59	ret proto-oncogene	Homo sapiens	24-30
17065770-3	2006	Almost all mutations in MEN 2A involve one of the cysteines in the extracellular domain of the RET receptor.	Cysteine	50-59	ret proto-oncogene	Homo sapiens	95-98
17065770-7	2006	RESULTS: We identified a heterozygous germ line missense mutation at codon 634 of exon 11 in the RET gene that causes a cysteine to arginine amino acid substitution in the DNA of the proband; this mutation was not found in the DNA of the parents or relatives.	Cysteine	120-128	ret proto-oncogene	Homo sapiens	97-100
17065770-7	2006	RESULTS: We identified a heterozygous germ line missense mutation at codon 634 of exon 11 in the RET gene that causes a cysteine to arginine amino acid substitution in the DNA of the proband; this mutation was not found in the DNA of the parents or relatives.	arginine amino acid	132-151	ret proto-oncogene	Homo sapiens	97-100
16469774-6	2006	This is the first report demonstrating that the introduction of an intracellular cysteine can activate RET.	Cysteine	81-89	ret proto-oncogene	Homo sapiens	103-106
16849523-0	2006	An autocrine loop involving ret and glial cell-derived neurotrophic factor mediates retinoic acid-induced neuroblastoma cell differentiation.	Tretinoin	84-97	ret proto-oncogene	Homo sapiens	28-31
16849523-1	2006	In several neuroblastoma cell lines, retinoic acid (RA)-induced differentiation is coupled to increased expression of functional neurotrophic factor receptors, including Trk family receptors and the glial cell-derived neurotrophic factor receptor, Ret.	Tretinoin	37-50	ret proto-oncogene	Homo sapiens	248-251
16849523-1	2006	In several neuroblastoma cell lines, retinoic acid (RA)-induced differentiation is coupled to increased expression of functional neurotrophic factor receptors, including Trk family receptors and the glial cell-derived neurotrophic factor receptor, Ret.	Tretinoin	52-54	ret proto-oncogene	Homo sapiens	248-251
16849523-5	2006	Using a 2"-fluoro-RNA aptamer and a truncated Ret protein as specific inhibitors of Ret, we show that RA-induced differentiation is mediated by a positive autocrine loop that sustains Ret downstream signaling and depends on glial cell-derived neurotrophic factor expression and release.	Tretinoin	102-104	ret proto-oncogene	Homo sapiens	46-49
16849523-5	2006	Using a 2"-fluoro-RNA aptamer and a truncated Ret protein as specific inhibitors of Ret, we show that RA-induced differentiation is mediated by a positive autocrine loop that sustains Ret downstream signaling and depends on glial cell-derived neurotrophic factor expression and release.	Tretinoin	102-104	ret proto-oncogene	Homo sapiens	84-87
16849523-5	2006	Using a 2"-fluoro-RNA aptamer and a truncated Ret protein as specific inhibitors of Ret, we show that RA-induced differentiation is mediated by a positive autocrine loop that sustains Ret downstream signaling and depends on glial cell-derived neurotrophic factor expression and release.	Tretinoin	102-104	ret proto-oncogene	Homo sapiens	84-87
16849523-6	2006	This report shows that in SK-N-BE(2) cells, stimulation of Ret is a major upstream mechanism needed to mediate RA-induced differentiation.	Tretinoin	111-113	ret proto-oncogene	Homo sapiens	59-62
16712668-0	2006	Occurrence of the Cys611Tyr mutation and a novel Arg886Trp substitution in the RET proto-oncogene in multiple endocrine neoplasia type 2 families and sporadic medullary thyroid carcinoma cases originating from the central region of Portugal.	arg886trp	49-58	ret proto-oncogene	Homo sapiens	79-82
16712668-8	2006	We have also characterized a novel RET mutation, Arg886Trp, located in the tyrosine kinase domain, which was found in an AS-MTC case.	arg886trp	49-58	ret proto-oncogene	Homo sapiens	35-38
16712668-10	2006	These data, along with the finding of a novel RET mutation (Arg886Trp), have important implications towards facilitating and improving the molecular diagnosis of hereditary MTC on a regional basis.	arg886trp	60-69	ret proto-oncogene	Homo sapiens	46-49
16782438-0	2006	Cellular effects of imatinib on medullary thyroid cancer cells harboring multiple endocrine neoplasia Type 2A and 2B associated RET mutations.	Imatinib Mesylate	20-28	ret proto-oncogene	Homo sapiens	128-131
16782438-6	2006	RESULTS: Imatinib inhibited RET Y1062 phosphorylation in a dose-dependent manner after 1.5 hours of exposure.	Imatinib Mesylate	9-17	ret proto-oncogene	Homo sapiens	28-31
16782438-11	2006	CONCLUSIONS: Imatinib inhibits RET-mediated MTC cell growth affecting RET protein levels in vitro in a dose-dependent manner.	Imatinib Mesylate	13-21	ret proto-oncogene	Homo sapiens	31-34
16782438-11	2006	CONCLUSIONS: Imatinib inhibits RET-mediated MTC cell growth affecting RET protein levels in vitro in a dose-dependent manner.	Imatinib Mesylate	13-21	ret proto-oncogene	Homo sapiens	70-73
16782438-12	2006	The concentration of imatinib necessary to inhibit RET in vitro, however, makes it impossible to conclude that imatinib monotherapy will be a good option for systemic therapy of MTC.	Imatinib Mesylate	21-29	ret proto-oncogene	Homo sapiens	51-54
16707008-14	2006	CONCLUSION: These data suggest that a RET germline mutation is necessary for development of CCH, that allelic imbalance between mutant and wild-type RET may set off tumorigenesis, and that somatic VHL gene alterations may not play a major role in tumorigenesis of MEN2A-associated MTC.	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	92-95	ret proto-oncogene	Homo sapiens	38-41
16697720-1	2006	BACKGROUND &amp; AIMS: Gain-of-function mutations in the KIT receptor tyrosine kinase gene and rare mutations in the platelet-derived growth factor receptor alpha (PDGFRA) gene are important events in gastrointestinal stromal tumor (GIST) development.	Adenosine Monophosphate	12-15	ret proto-oncogene	Homo sapiens	61-85
31627617-3	2006	Familial forms of MTCG are caused by point mutations in the RET proto-oncogen (Rearranged during Transfection).	mtcg	18-22	ret proto-oncogene	Homo sapiens	60-63
16484222-4	2006	By using RET/PTC3 molecules mutated in specific tyrosine autophosphorylation sites, we characterized Tyr(981), a known binding site for c-Src, as a major determinant of RET/PTC3-induced Erk8 activation, although, surprisingly, the underlying mechanism did not strictly depend on the activity of Src.	Tyrosine	48-56	ret proto-oncogene	Homo sapiens	9-12
16484222-4	2006	By using RET/PTC3 molecules mutated in specific tyrosine autophosphorylation sites, we characterized Tyr(981), a known binding site for c-Src, as a major determinant of RET/PTC3-induced Erk8 activation, although, surprisingly, the underlying mechanism did not strictly depend on the activity of Src.	Tyrosine	101-104	ret proto-oncogene	Homo sapiens	9-12
16484222-4	2006	By using RET/PTC3 molecules mutated in specific tyrosine autophosphorylation sites, we characterized Tyr(981), a known binding site for c-Src, as a major determinant of RET/PTC3-induced Erk8 activation, although, surprisingly, the underlying mechanism did not strictly depend on the activity of Src.	Tyrosine	101-104	ret proto-oncogene	Homo sapiens	169-172
16484222-5	2006	In contrast, we present evidence that RET/PTC3 acts on Erk8 through Tyr(981)-mediated activation of c-Abl.	Tyrosine	68-71	ret proto-oncogene	Homo sapiens	38-41
16648571-0	2006	Preclinical activity of ABT-869, a multitargeted receptor tyrosine kinase inhibitor.	N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N1-(2-fluoro-5-methylphenyl)urea	24-31	ret proto-oncogene	Homo sapiens	49-73
16648571-1	2006	ABT-869 is a structurally novel, receptor tyrosine kinase (RTK) inhibitor that is a potent inhibitor of members of the vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) receptor families (e.g., KDR IC50 = 4 nmol/L) but has much less activity (IC50s &gt; 1 micromol/L) against unrelated RTKs, soluble tyrosine kinases, or serine/threonine kinases.	N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N1-(2-fluoro-5-methylphenyl)urea	0-7	ret proto-oncogene	Homo sapiens	33-57
16648571-1	2006	ABT-869 is a structurally novel, receptor tyrosine kinase (RTK) inhibitor that is a potent inhibitor of members of the vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) receptor families (e.g., KDR IC50 = 4 nmol/L) but has much less activity (IC50s &gt; 1 micromol/L) against unrelated RTKs, soluble tyrosine kinases, or serine/threonine kinases.	N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N1-(2-fluoro-5-methylphenyl)urea	0-7	ret proto-oncogene	Homo sapiens	59-62
16648571-2	2006	The inhibition profile of ABT-869 is evident in cellular assays of RTK phosphorylation (IC50 = 2, 4, and 7 nmol/L for PDGFR-beta, KDR, and CSF-1R, respectively) and VEGF-stimulated proliferation (IC50 = 0.2 nmol/L for human endothelial cells).	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	26-29	ret proto-oncogene	Homo sapiens	67-70
16525057-1	2006	The receptor tyrosine kinase (RTK) Ret is activated by the formation of a complex consisting of ligands such as glial cell line-derived neurotrophic factor (GDNF) and glycerophosphatidylinositol-anchored coreceptors termed GFRalphas.	glycerophosphatidylinositol	167-194	ret proto-oncogene	Homo sapiens	4-28
16525057-1	2006	The receptor tyrosine kinase (RTK) Ret is activated by the formation of a complex consisting of ligands such as glial cell line-derived neurotrophic factor (GDNF) and glycerophosphatidylinositol-anchored coreceptors termed GFRalphas.	glycerophosphatidylinositol	167-194	ret proto-oncogene	Homo sapiens	30-33
16525057-1	2006	The receptor tyrosine kinase (RTK) Ret is activated by the formation of a complex consisting of ligands such as glial cell line-derived neurotrophic factor (GDNF) and glycerophosphatidylinositol-anchored coreceptors termed GFRalphas.	glycerophosphatidylinositol	167-194	ret proto-oncogene	Homo sapiens	35-38
16222701-5	2006	Several additional lines of evidence supported the above conclusion: (i) furosemide inhibits phosphorylation of MAPK kinase (MEK) induced by receptor tyrosine kinase (RTK) ligands, such as PDGF, FGF, and EGF.	Furosemide	73-83	ret proto-oncogene	Homo sapiens	141-165
16222701-5	2006	Several additional lines of evidence supported the above conclusion: (i) furosemide inhibits phosphorylation of MAPK kinase (MEK) induced by receptor tyrosine kinase (RTK) ligands, such as PDGF, FGF, and EGF.	Furosemide	73-83	ret proto-oncogene	Homo sapiens	167-170
17080598-3	2006	Several key elements of BR response have been identified using both genetic and biochemical approaches, and molecular models that parallel Wingless (Wnt), transforming growth factor beta (TGF beta) and receptor tyrosine kinase (RTK) signalling in animals have been proposed.	Brassinosteroids	24-26	ret proto-oncogene	Homo sapiens	202-226
17080598-3	2006	Several key elements of BR response have been identified using both genetic and biochemical approaches, and molecular models that parallel Wingless (Wnt), transforming growth factor beta (TGF beta) and receptor tyrosine kinase (RTK) signalling in animals have been proposed.	Brassinosteroids	24-26	ret proto-oncogene	Homo sapiens	228-231
16534860-11	2006	The frequency of RET proto-oncogene mutation is quite different between IND and HD in Chinese population.	indole	72-75	ret proto-oncogene	Homo sapiens	17-20
16427628-2	2006	We showed that all RET-PTC-1 mutants in which the C in this motif (C376) was replaced with glycine, lysine, threonine or serine lost their activity in vitro.	Glycine	91-98	ret proto-oncogene	Homo sapiens	19-22
16427628-2	2006	We showed that all RET-PTC-1 mutants in which the C in this motif (C376) was replaced with glycine, lysine, threonine or serine lost their activity in vitro.	Lysine	100-106	ret proto-oncogene	Homo sapiens	19-22
16427628-2	2006	We showed that all RET-PTC-1 mutants in which the C in this motif (C376) was replaced with glycine, lysine, threonine or serine lost their activity in vitro.	Threonine	108-117	ret proto-oncogene	Homo sapiens	19-22
16427628-2	2006	We showed that all RET-PTC-1 mutants in which the C in this motif (C376) was replaced with glycine, lysine, threonine or serine lost their activity in vitro.	Serine	121-127	ret proto-oncogene	Homo sapiens	19-22
16254036-5	2006	To determine the key RAF isoform mediating RET/PTC-induced ERK phosphorylation, we stably transfected doxycycline-inducible RET/PTC3-expressing thyroid PCCL3 cells with small interfering RNA vectors to induce selective knockdown of BRAF or CRAF.	Doxycycline	102-113	ret proto-oncogene	Homo sapiens	47-50
16254036-7	2006	Selective knockdown of BRAF prevented RET/PTC-dependent down-regulation of the sodium iodide symporter, a gene that confers key biological effects of RET/PTC in PTCs.	Sodium Iodide	79-92	ret proto-oncogene	Homo sapiens	38-41
16254036-7	2006	Selective knockdown of BRAF prevented RET/PTC-dependent down-regulation of the sodium iodide symporter, a gene that confers key biological effects of RET/PTC in PTCs.	Sodium Iodide	79-92	ret proto-oncogene	Homo sapiens	42-45
16254036-7	2006	Selective knockdown of BRAF prevented RET/PTC-dependent down-regulation of the sodium iodide symporter, a gene that confers key biological effects of RET/PTC in PTCs.	Sodium Iodide	79-92	ret proto-oncogene	Homo sapiens	150-153
16254036-7	2006	Selective knockdown of BRAF prevented RET/PTC-dependent down-regulation of the sodium iodide symporter, a gene that confers key biological effects of RET/PTC in PTCs.	Sodium Iodide	79-92	ret proto-oncogene	Homo sapiens	154-157
16386942-9	2006	Combining the results from the three cross-sectional studies, a negative correlation between folate status and fMN-Trf-Ret was obtained (p&lt;0.05).	Folic Acid	93-99	ret proto-oncogene	Homo sapiens	119-122
16166596-0	2006	IGF-1 receptor tyrosine kinase inhibition by the cyclolignan PPP induces G2/M-phase accumulation and apoptosis in multiple myeloma cells.	cyclolignan	49-60	ret proto-oncogene	Homo sapiens	6-30
16166596-2	2006	Recently, members of the cyclolignan family have been shown to selectively inhibit the receptor tyrosine kinase (RTK) activity of the IGF-1R beta-chain.	cyclolignan	25-36	ret proto-oncogene	Homo sapiens	87-111
16166596-2	2006	Recently, members of the cyclolignan family have been shown to selectively inhibit the receptor tyrosine kinase (RTK) activity of the IGF-1R beta-chain.	cyclolignan	25-36	ret proto-oncogene	Homo sapiens	113-116
16166596-10	2006	Taken together, we suggest that interfering with the IGF-1 RTK by using the cyclolignan PPP offers a novel and selective therapeutic strategy for MM.	picropodophyllin	76-91	ret proto-oncogene	Homo sapiens	59-62
17175894-2	2006	Reticulocyte hemoglobin content (RET-He) is considered to be an actual indicator reflecting functional iron availability for erythropoiesis.	Iron	103-107	ret proto-oncogene	Homo sapiens	33-36
16401709-1	2006	The introduction of imatinib, an orally administered inhibitor of the KIT receptor tyrosine kinase, is prompting revision of the management algorithms that have traditionally guided the treatment of gastrointestinal stromal tumor (GIST).	Imatinib Mesylate	20-28	ret proto-oncogene	Homo sapiens	74-98
17064855-3	2006	Elucidation of the aberrant receptor tyrosine kinase (RTK) model of GIST pathogenesis through mutations in c-kit and platelet-derived growth factor alpha PDGFRalpha proto-oncogenes has been prerequisite to the use of imatinib mesylate (STI571, Gleevec; Novartis, Switzerland), a molecular inhibitor of several tyrosine kinases, in the treatment of GISTs.	Imatinib Mesylate	217-234	ret proto-oncogene	Homo sapiens	28-52
17064855-3	2006	Elucidation of the aberrant receptor tyrosine kinase (RTK) model of GIST pathogenesis through mutations in c-kit and platelet-derived growth factor alpha PDGFRalpha proto-oncogenes has been prerequisite to the use of imatinib mesylate (STI571, Gleevec; Novartis, Switzerland), a molecular inhibitor of several tyrosine kinases, in the treatment of GISTs.	Imatinib Mesylate	217-234	ret proto-oncogene	Homo sapiens	54-57
16487008-7	2006	Polymorphisms for the ret proto-oncogene coding region were identified in codon 769 of exon 13 (LeuCTT--> LeuCTG) at a frequency of 13% (3/24) and in codon 904 of exon 15 (SerTCC--> SerTCG) at a frequency of 16.6% (4/24).	sertcc	172-178	ret proto-oncogene	Homo sapiens	22-25
16487008-7	2006	Polymorphisms for the ret proto-oncogene coding region were identified in codon 769 of exon 13 (LeuCTT--> LeuCTG) at a frequency of 13% (3/24) and in codon 904 of exon 15 (SerTCC--> SerTCG) at a frequency of 16.6% (4/24).	sertcg	182-188	ret proto-oncogene	Homo sapiens	22-25
16715702-6	2006	Molecular-genetic study of RET-protooncogene and gene BRAF in 6 blood samples from PTC-bearers established RET-mutation (mother and daughter) in codon 891 (exon 15) G2673A (TCG-&gt;TCA).	TMG-chitotriomycin	173-176	ret proto-oncogene	Homo sapiens	107-110
16715702-6	2006	Molecular-genetic study of RET-protooncogene and gene BRAF in 6 blood samples from PTC-bearers established RET-mutation (mother and daughter) in codon 891 (exon 15) G2673A (TCG-&gt;TCA).	Trichloroacetic Acid	181-184	ret proto-oncogene	Homo sapiens	107-110
16343103-1	2005	OBJECTIVE: We have identified a large kindred with multiple endocrine neoplasia 2A (MEN 2A) due to a mutation at RET codon 609 that results in a cysteine to serine substitution, a mutation previously identified in only one case in the literature.	Cysteine	145-153	ret proto-oncogene	Homo sapiens	51-82
16343103-1	2005	OBJECTIVE: We have identified a large kindred with multiple endocrine neoplasia 2A (MEN 2A) due to a mutation at RET codon 609 that results in a cysteine to serine substitution, a mutation previously identified in only one case in the literature.	Cysteine	145-153	ret proto-oncogene	Homo sapiens	84-90
16343103-1	2005	OBJECTIVE: We have identified a large kindred with multiple endocrine neoplasia 2A (MEN 2A) due to a mutation at RET codon 609 that results in a cysteine to serine substitution, a mutation previously identified in only one case in the literature.	Cysteine	145-153	ret proto-oncogene	Homo sapiens	113-116
16343103-1	2005	OBJECTIVE: We have identified a large kindred with multiple endocrine neoplasia 2A (MEN 2A) due to a mutation at RET codon 609 that results in a cysteine to serine substitution, a mutation previously identified in only one case in the literature.	Serine	157-163	ret proto-oncogene	Homo sapiens	51-82
16343103-1	2005	OBJECTIVE: We have identified a large kindred with multiple endocrine neoplasia 2A (MEN 2A) due to a mutation at RET codon 609 that results in a cysteine to serine substitution, a mutation previously identified in only one case in the literature.	Serine	157-163	ret proto-oncogene	Homo sapiens	84-90
16343103-1	2005	OBJECTIVE: We have identified a large kindred with multiple endocrine neoplasia 2A (MEN 2A) due to a mutation at RET codon 609 that results in a cysteine to serine substitution, a mutation previously identified in only one case in the literature.	Serine	157-163	ret proto-oncogene	Homo sapiens	113-116
16412353-5	2005	The expression of Ret protein in the intestinal tissue was detected by using immunohistochemical SABC technique with mouse anti-Ret monoclonal antibody.	sabc	97-101	ret proto-oncogene	Homo sapiens	18-21
16123037-6	2005	We further demonstrated that specific temporal adjustment of ligand-induced AKT activation is dependent upon a lipid-based cholesterol-sensitive environment, and this control step is bypassed by MEN2A RET mutants.	Cholesterol	123-134	ret proto-oncogene	Homo sapiens	201-204
16756963-3	2006	In the present study, we investigated the efficacy and the cellular bases of antitumor activity of the indolinone Ret tyrosine kinase inhibitor RPI-1 against large established s.c. TT tumor xenograft, a human medullary thyroid carcinoma (MTC) harboring oncogenic MEN-2A-type RET mutation.	Oxindoles	103-113	ret proto-oncogene	Homo sapiens	114-117
15994200-0	2005	Regulation of protein kinase B tyrosine phosphorylation by thyroid-specific oncogenic RET/PTC kinases.	Tyrosine	31-39	ret proto-oncogene	Homo sapiens	86-89
16756963-6	2006	In treated tumors, Ret was tyrosine dephosphorylated.	Tyrosine	27-35	ret proto-oncogene	Homo sapiens	19-22
16868024-5	2006	In addition, we describe a novel interaction between palladin and Eps8, a receptor tyrosine kinase (RTK) substrate that participates in the activation of the Rac-specific guanine nucleotide-exchange function of Sos-1.	Guanine Nucleotides	171-189	ret proto-oncogene	Homo sapiens	74-98
16868024-5	2006	In addition, we describe a novel interaction between palladin and Eps8, a receptor tyrosine kinase (RTK) substrate that participates in the activation of the Rac-specific guanine nucleotide-exchange function of Sos-1.	Guanine Nucleotides	171-189	ret proto-oncogene	Homo sapiens	100-103
15994200-0	2005	Regulation of protein kinase B tyrosine phosphorylation by thyroid-specific oncogenic RET/PTC kinases.	Tyrosine	31-39	ret proto-oncogene	Homo sapiens	90-93
15994200-4	2005	RET/PTC-transfected cells showed tyrosine phosphorylation of endogenous and exogenous PKB, which was independent of phosphorylation of T308 and S473 regulated by the upstream kinases phosphoinositide-dependent kinase-1 and -2, respectively.	Tyrosine	33-41	ret proto-oncogene	Homo sapiens	0-3
15994200-4	2005	RET/PTC-transfected cells showed tyrosine phosphorylation of endogenous and exogenous PKB, which was independent of phosphorylation of T308 and S473 regulated by the upstream kinases phosphoinositide-dependent kinase-1 and -2, respectively.	Tyrosine	33-41	ret proto-oncogene	Homo sapiens	4-7
15994200-6	2005	RET/PTC-mediated tyrosine phosphorylation results in the activation of PKB kinase activity.	Tyrosine	17-25	ret proto-oncogene	Homo sapiens	0-3
15994200-6	2005	RET/PTC-mediated tyrosine phosphorylation results in the activation of PKB kinase activity.	Tyrosine	17-25	ret proto-oncogene	Homo sapiens	4-7
15994200-8	2005	In summary, these observations suggest that RET/PTC is able to phosphorylate the Y315 residue of PKB, an event that results in maximal activation of PKB for RET/PTC-induced thyroid tumorigenesis.	y315	81-85	ret proto-oncogene	Homo sapiens	44-47
15994200-8	2005	In summary, these observations suggest that RET/PTC is able to phosphorylate the Y315 residue of PKB, an event that results in maximal activation of PKB for RET/PTC-induced thyroid tumorigenesis.	y315	81-85	ret proto-oncogene	Homo sapiens	48-51
15994200-8	2005	In summary, these observations suggest that RET/PTC is able to phosphorylate the Y315 residue of PKB, an event that results in maximal activation of PKB for RET/PTC-induced thyroid tumorigenesis.	y315	81-85	ret proto-oncogene	Homo sapiens	157-160
15994200-8	2005	In summary, these observations suggest that RET/PTC is able to phosphorylate the Y315 residue of PKB, an event that results in maximal activation of PKB for RET/PTC-induced thyroid tumorigenesis.	y315	81-85	ret proto-oncogene	Homo sapiens	161-164
15940252-4	2005	This association is constitutive, but, in the presence of RET oncoproteins, both RAI and GAB 1 are tyrosine-phosphorylated, and the stoichiometry of this interaction remarkably increases.	Tyrosine	99-107	ret proto-oncogene	Homo sapiens	58-61
16091499-9	2005	We not only confirmed the previously described association with G691S and S904S (for heterozygotes: odds ratio, 1.85; range, 1.22-2.82; P = 0.004), but we found a novel protective effect associated with a specific haplotype (odds ratio, 0.39; range, 0.21-0.72; P = 0.005) revealing the existence of different genetic variants in the RET oncogene that either increase or decrease risk of sMTC.	smtc	387-391	ret proto-oncogene	Homo sapiens	333-336
16254257-0	2005	p-p70S6K (Thr 389) Expression in nodular sclerosing hodgkin"s disease as evidence for receptor tyrosine kinase signaling.	Threonine	10-13	ret proto-oncogene	Homo sapiens	86-110
16356097-1	2005	Primary hyperparathyroidism (PHP; serum calcium 2.75 mmol/L, PTH 226 pg/ml) had been the first clinical manifestation of MEN-2A in a female patient (aged 55 years) with a mutation (Y791F, TAT--&gt;TTT) in exon 13 of the RET proto-oncogene.	Calcium	40-47	ret proto-oncogene	Homo sapiens	121-127
16226999-0	2005	Iodine 123 metaiodobenzylguanidine radio-guided navigation surgery for recurrent medullary thyroid carcinoma in a girl with multiple endocrine neoplasia type 2B.	Iodine	0-6	ret proto-oncogene	Homo sapiens	124-160
16226999-0	2005	Iodine 123 metaiodobenzylguanidine radio-guided navigation surgery for recurrent medullary thyroid carcinoma in a girl with multiple endocrine neoplasia type 2B.	3-Iodobenzylguanidine	11-34	ret proto-oncogene	Homo sapiens	124-160
16226999-3	2005	The authors performed iodine 123 metaiodobenzylguanidine ((123)I-MIBG) radio-guided navigation surgery for recurrent MTC in a 14-year-old girl with MEN 2B.	Iodine	22-28	ret proto-oncogene	Homo sapiens	148-154
16226999-3	2005	The authors performed iodine 123 metaiodobenzylguanidine ((123)I-MIBG) radio-guided navigation surgery for recurrent MTC in a 14-year-old girl with MEN 2B.	3-Iodobenzylguanidine	33-56	ret proto-oncogene	Homo sapiens	148-154
16226999-3	2005	The authors performed iodine 123 metaiodobenzylguanidine ((123)I-MIBG) radio-guided navigation surgery for recurrent MTC in a 14-year-old girl with MEN 2B.	3-Iodobenzylguanidine	65-69	ret proto-oncogene	Homo sapiens	148-154
16226999-8	2005	Intraoperative (123)I-MIBG scanning is of substantial benefit for children with MEN 2B undergoing surgery for recurrent MTC.	Iodine	0-1	ret proto-oncogene	Homo sapiens	80-86
16226999-8	2005	Intraoperative (123)I-MIBG scanning is of substantial benefit for children with MEN 2B undergoing surgery for recurrent MTC.	3-Iodobenzylguanidine	22-26	ret proto-oncogene	Homo sapiens	80-86
16153436-6	2005	RESULTS: Immunoprecipitated, mutant RET from cells or the recombinant RET kinase domain was able to directly phosphorylate tyrosine residues on FAK.	Tyrosine	123-131	ret proto-oncogene	Homo sapiens	36-39
16201624-5	2005	Ratios of 1,7-dimethylphenanthrane (DMP) to 1,7-DMP plus 2,6-DMP [1,7/(1,7 + 2,6)-DMP], retene to retene plus chrysene [Ret/(Ret + Chy)], and fluoranthene to fluoranthene plus pyrene [FI/(FI + Py)] provide additional source discrimination throughoutthe core.	dmp	36-39	ret proto-oncogene	Homo sapiens	120-123
16201624-5	2005	Ratios of 1,7-dimethylphenanthrane (DMP) to 1,7-DMP plus 2,6-DMP [1,7/(1,7 + 2,6)-DMP], retene to retene plus chrysene [Ret/(Ret + Chy)], and fluoranthene to fluoranthene plus pyrene [FI/(FI + Py)] provide additional source discrimination throughoutthe core.	dmp	36-39	ret proto-oncogene	Homo sapiens	125-128
16201624-5	2005	Ratios of 1,7-dimethylphenanthrane (DMP) to 1,7-DMP plus 2,6-DMP [1,7/(1,7 + 2,6)-DMP], retene to retene plus chrysene [Ret/(Ret + Chy)], and fluoranthene to fluoranthene plus pyrene [FI/(FI + Py)] provide additional source discrimination throughoutthe core.	retene	98-104	ret proto-oncogene	Homo sapiens	120-123
16201624-5	2005	Ratios of 1,7-dimethylphenanthrane (DMP) to 1,7-DMP plus 2,6-DMP [1,7/(1,7 + 2,6)-DMP], retene to retene plus chrysene [Ret/(Ret + Chy)], and fluoranthene to fluoranthene plus pyrene [FI/(FI + Py)] provide additional source discrimination throughoutthe core.	retene	98-104	ret proto-oncogene	Homo sapiens	125-128
16015630-0	2005	RET gene rearrangements (RET/PTC1 and RET/PTC3) in papillary thyroid carcinomas from an iodine-rich country (Japan).	Iodine	88-94	ret proto-oncogene	Homo sapiens	0-3
16015630-0	2005	RET gene rearrangements (RET/PTC1 and RET/PTC3) in papillary thyroid carcinomas from an iodine-rich country (Japan).	Iodine	88-94	ret proto-oncogene	Homo sapiens	25-28
16015630-0	2005	RET gene rearrangements (RET/PTC1 and RET/PTC3) in papillary thyroid carcinomas from an iodine-rich country (Japan).	Iodine	88-94	ret proto-oncogene	Homo sapiens	25-28
16015630-1	2005	BACKGROUND: The frequency of RET rearrangements (RET/PTC) in papillary thyroid carcinomas varies significantly according to geographic area, with the greatest incidence reported in the Belarus region, which is iodine-deficient and was contaminated severely after the Chernobyl reactor accident, and with the lowest incidence in iodine-rich, nonirradiated Japan.	Iodine	210-216	ret proto-oncogene	Homo sapiens	29-32
16015630-1	2005	BACKGROUND: The frequency of RET rearrangements (RET/PTC) in papillary thyroid carcinomas varies significantly according to geographic area, with the greatest incidence reported in the Belarus region, which is iodine-deficient and was contaminated severely after the Chernobyl reactor accident, and with the lowest incidence in iodine-rich, nonirradiated Japan.	Iodine	210-216	ret proto-oncogene	Homo sapiens	49-52
16015630-1	2005	BACKGROUND: The frequency of RET rearrangements (RET/PTC) in papillary thyroid carcinomas varies significantly according to geographic area, with the greatest incidence reported in the Belarus region, which is iodine-deficient and was contaminated severely after the Chernobyl reactor accident, and with the lowest incidence in iodine-rich, nonirradiated Japan.	Iodine	328-334	ret proto-oncogene	Homo sapiens	29-32
16015630-1	2005	BACKGROUND: The frequency of RET rearrangements (RET/PTC) in papillary thyroid carcinomas varies significantly according to geographic area, with the greatest incidence reported in the Belarus region, which is iodine-deficient and was contaminated severely after the Chernobyl reactor accident, and with the lowest incidence in iodine-rich, nonirradiated Japan.	Iodine	328-334	ret proto-oncogene	Homo sapiens	49-52
16277170-12	2005	Mutation analysis of the ret proto-oncogene revealed a missense point mutation at position 634 in exon 11, which gives rise to the substitution of a cysteine codon with a tyrosine residue.	Cysteine	149-157	ret proto-oncogene	Homo sapiens	25-28
16277170-12	2005	Mutation analysis of the ret proto-oncogene revealed a missense point mutation at position 634 in exon 11, which gives rise to the substitution of a cysteine codon with a tyrosine residue.	Tyrosine	171-179	ret proto-oncogene	Homo sapiens	25-28
16153436-6	2005	RESULTS: Immunoprecipitated, mutant RET from cells or the recombinant RET kinase domain was able to directly phosphorylate tyrosine residues on FAK.	Tyrosine	123-131	ret proto-oncogene	Homo sapiens	70-73
16153436-10	2005	Furthermore, tyrosine residues in DOK1, the p85 subunit of phosphatidylinositol 3" kinase, JNK 1 and 2, P-38, and phospholipase-gamma were directly phosphorylated by RET.	Tyrosine	13-21	ret proto-oncogene	Homo sapiens	166-169
16153436-11	2005	CONCLUSIONS: RET directly phosphorylates tyrosine residues on FAK, ERK 1/2, DOK1, the p85 subunit of of phosphatidylinositol 3" kinase, JNK 1 and 2, P-38, and phospholipase-gamma.	Tyrosine	41-49	ret proto-oncogene	Homo sapiens	13-16
16158949-10	2005	We conclude that DHPLC is a fast, sensitive, cost-efficient and reliable method for the scanning of ret germline mutations.	dhplc	17-22	ret proto-oncogene	Homo sapiens	100-103
15922853-1	2005	Receptor tyrosine kinase (RTK) targeted agents such as trastuzumab, imatinib, bevacizumab, and gefitinib inhibitors have illustrated the utility of targeting this protein class for treatment of selected cancers.	Gefitinib	95-104	ret proto-oncogene	Homo sapiens	0-24
15922853-1	2005	Receptor tyrosine kinase (RTK) targeted agents such as trastuzumab, imatinib, bevacizumab, and gefitinib inhibitors have illustrated the utility of targeting this protein class for treatment of selected cancers.	Gefitinib	95-104	ret proto-oncogene	Homo sapiens	26-29
15922853-1	2005	Receptor tyrosine kinase (RTK) targeted agents such as trastuzumab, imatinib, bevacizumab, and gefitinib inhibitors have illustrated the utility of targeting this protein class for treatment of selected cancers.	Imatinib Mesylate	68-76	ret proto-oncogene	Homo sapiens	0-24
15922853-1	2005	Receptor tyrosine kinase (RTK) targeted agents such as trastuzumab, imatinib, bevacizumab, and gefitinib inhibitors have illustrated the utility of targeting this protein class for treatment of selected cancers.	Imatinib Mesylate	68-76	ret proto-oncogene	Homo sapiens	26-29
16029119-3	2005	Mutations in six exons (10, 11, 13, 14, 15, and 16) located in either cysteine-rich or tyrosine kinase domains cause one of three distinctive clinical subtypes: familial MTC, multiple endocrine neoplasia (MEN) type 2A (including variants with Hirschsprung"s disease and cutaneous lichen amyloidosis), and MEN 2B.	Cysteine	70-78	ret proto-oncogene	Homo sapiens	305-311
15866462-6	2005	About 3 days after 131I administration, the frequency of micronucleated-Tf-Ret (f(MN-Tf-Ret)) increases within 1 day to a maximum and declines in the following 2-5 days to its value before treatment.	Iodine-131	19-23	ret proto-oncogene	Homo sapiens	75-78
15866462-6	2005	About 3 days after 131I administration, the frequency of micronucleated-Tf-Ret (f(MN-Tf-Ret)) increases within 1 day to a maximum and declines in the following 2-5 days to its value before treatment.	Iodine-131	19-23	ret proto-oncogene	Homo sapiens	88-91
15677445-6	2005	A constitutive complex of Grb2 and Cbl could be recruited to both receptor isoforms via docking of Shc to phosphorylated Tyr-1062 in RET.	Tyrosine	121-124	ret proto-oncogene	Homo sapiens	133-136
15867345-5	2005	Recently, the low molecular weight tyrosine kinase inhibitor ZD6474 was found to block the enzymatic activity of RET-derived oncoproteins in cultured cell lines.	vandetanib	61-67	ret proto-oncogene	Homo sapiens	113-116
15867345-7	2005	Here we show that, when fed orally, ZD6474 suppressed RET-mediated phenotypes within the context of this in vivo model.	vandetanib	36-42	ret proto-oncogene	Homo sapiens	54-57
15867345-10	2005	Our results support the view that targeting chemical kinase inhibitors such as ZD6474 to tissues with oncogenic forms of RET is a useful treatment strategy for RET-dependent carcinomas.	vandetanib	79-85	ret proto-oncogene	Homo sapiens	121-124
15867345-10	2005	Our results support the view that targeting chemical kinase inhibitors such as ZD6474 to tissues with oncogenic forms of RET is a useful treatment strategy for RET-dependent carcinomas.	vandetanib	79-85	ret proto-oncogene	Homo sapiens	160-163
15677445-8	2005	In addition, phosphorylation of Tyr-1096, which is present in RET51 but absent in RET9, endowed the longer isoform with a second route to recruit the Grb2.Cbl complex.	Tyrosine	32-35	ret proto-oncogene	Homo sapiens	62-67
15769183-3	2005	Nuclease-resistant aptamers that recognize the human receptor tyrosine kinase RET were obtained using RET-expressing cells as targets in a modified SELEX procedure.	selex	148-153	ret proto-oncogene	Homo sapiens	78-81
15592804-3	2005	The second, a novel mutation in codon 641, changes alanine to serine in the transmembrane domain of the RET protein.	Alanine	51-58	ret proto-oncogene	Homo sapiens	104-107
15592804-3	2005	The second, a novel mutation in codon 641, changes alanine to serine in the transmembrane domain of the RET protein.	Serine	62-68	ret proto-oncogene	Homo sapiens	104-107
15709206-4	2005	Treatment with STI571 resulted in inhibition of RET phosphorylation, cell proliferation, tumor growth and invasiveness.	Imatinib Mesylate	15-21	ret proto-oncogene	Homo sapiens	48-51
15659598-9	2005	In dopaminergic neuron-like SHSY5Y cells, ibogaine treatment upregulated the GDNF pathway as indicated by increases in phosphorylation of the GDNF receptor, Ret, and the downstream kinase, ERK1 (extracellular signal-regulated kinase 1).	Ibogaine	42-50	ret proto-oncogene	Homo sapiens	157-160
15548547-8	2005	Moreover, we identified an HSCR patient with a Gly322Ser TTF-1 mutation that compromises activation of transcription from HSCR-associated RET promoter haplotypes.	gly322ser	47-56	ret proto-oncogene	Homo sapiens	138-141
15864435-7	2005	These EGF-mediated effects on the glycosyltransferase and MUC5AC mRNAs were blocked when cells were first exposed to AG1478, an EGF receptor tyrosine kinase inhibitor.	RTKI cpd	117-123	ret proto-oncogene	Homo sapiens	132-156
15693160-2	2004	We have identified three different anti-RET drugs: two pyrazolo-pyrimidines, PP1 and PP2 and an anilinoquinazoline, ZD6474 (AstraZeneca).	pyrazolo-pyrimidines	55-75	ret proto-oncogene	Homo sapiens	40-43
16232085-10	2005	Correlations of biochemical iron markers with RET-H(e) were as weak as with CHr in patients with ACD and acute phase response.	Iron	28-32	ret proto-oncogene	Homo sapiens	46-49
16232085-11	2005	In a diagnostic plot to identify iron status, RET-H(e) could replace CHr without any loss of sensitivity or specificity.	Iron	33-37	ret proto-oncogene	Homo sapiens	46-49
16232085-15	2005	RET-H(e) is as valuable as CHr for the diagnosis of iron-restricted erythropoiesis.	Iron	52-56	ret proto-oncogene	Homo sapiens	0-3
16232085-16	2005	The combination of RET-H(e) and the sTfR-F index in a diagnostic plot offers an attractive tool for the evaluation of iron status and identification of the progression of ID.	Iron	118-122	ret proto-oncogene	Homo sapiens	19-22
15693160-2	2004	We have identified three different anti-RET drugs: two pyrazolo-pyrimidines, PP1 and PP2 and an anilinoquinazoline, ZD6474 (AstraZeneca).	anilinoquinazoline	96-114	ret proto-oncogene	Homo sapiens	40-43
15531548-2	2004	We describe here a novel germline homozygous mutation in exon 15 of the RET gene that determines an amino acid substitution (Ala-&gt;Thr) at codon 883.	Alanine	125-128	ret proto-oncogene	Homo sapiens	72-75
15531548-2	2004	We describe here a novel germline homozygous mutation in exon 15 of the RET gene that determines an amino acid substitution (Ala-&gt;Thr) at codon 883.	Threonine	133-136	ret proto-oncogene	Homo sapiens	72-75
15693160-2	2004	We have identified three different anti-RET drugs: two pyrazolo-pyrimidines, PP1 and PP2 and an anilinoquinazoline, ZD6474 (AstraZeneca).	vandetanib	116-122	ret proto-oncogene	Homo sapiens	40-43
15693160-4	2004	Finally, mutation of RET V804 to methionine or leucine, found in MTC patients, induces resistance to the three drugs.	Methionine	33-43	ret proto-oncogene	Homo sapiens	21-24
15693160-4	2004	Finally, mutation of RET V804 to methionine or leucine, found in MTC patients, induces resistance to the three drugs.	Leucine	47-54	ret proto-oncogene	Homo sapiens	21-24
15351743-2	2004	We previously reported that tyrosine 1062 in RET receptor tyrosine kinase activated by glial cell line-derived neurotrophic factor (GDNF) represents a binding site for the Shc-Grb2-Gab1 complex, and that the p85 subunit of phosphatidylinositol 3-kinase (PI3K) and SHP2 tyrosine phosphatase is associated with Gab1 in GDNF-treated cells.	Tyrosine	28-36	ret proto-oncogene	Homo sapiens	45-48
15485908-1	2004	The receptor tyrosine kinases (RTKs) RET, MET, and RON all carry the Met(p+1loop)--&gt;Thr point mutation (i.e., 2B mutation), leading to the formation of tumors with high metastatic potential.	Threonine	87-90	ret proto-oncogene	Homo sapiens	37-40
15302866-2	2004	It has been shown that RET/PTC1 decreases expression of the sodium/iodide symporter (NIS), the molecule that mediates radioiodide therapy for thyroid cancer.	radioiodide	118-129	ret proto-oncogene	Homo sapiens	23-26
15302866-4	2004	Inhibition of hsp90 function with 17-allylamino-17-demothoxygeldanamycin (17-AAG) reduces RET/PTC1 protein levels.	17-allylamino-17-demothoxygeldanamycin	34-72	ret proto-oncogene	Homo sapiens	90-93
15302866-0	2004	Inhibition of heat shock protein 90, a novel RET/PTC1-associated protein, increases radioiodide accumulation in thyroid cells.	radioiodide	84-95	ret proto-oncogene	Homo sapiens	45-48
15302866-2	2004	It has been shown that RET/PTC1 decreases expression of the sodium/iodide symporter (NIS), the molecule that mediates radioiodide therapy for thyroid cancer.	Nickel	85-88	ret proto-oncogene	Homo sapiens	23-26
15379552-2	2004	In addition to RTK-specific tyrosine phosphorylation, these docking proteins also can be phosphorylated on serine/threonine residues affecting signal transduction.	Tyrosine	28-36	ret proto-oncogene	Homo sapiens	15-18
15258756-4	2004	The purpose of our study was to assess whether gamma (gamma) radiation using a Caesium 137 source can induce specific ret rearrangements in a human thyroid epithelial cell culture model.	Cesium-137	79-90	ret proto-oncogene	Homo sapiens	118-121
15379552-2	2004	In addition to RTK-specific tyrosine phosphorylation, these docking proteins also can be phosphorylated on serine/threonine residues affecting signal transduction.	Serine	107-113	ret proto-oncogene	Homo sapiens	15-18
15379552-2	2004	In addition to RTK-specific tyrosine phosphorylation, these docking proteins also can be phosphorylated on serine/threonine residues affecting signal transduction.	Threonine	114-123	ret proto-oncogene	Homo sapiens	15-18
15184865-0	2004	Disease associated mutations at valine 804 in the RET receptor tyrosine kinase confer resistance to selective kinase inhibitors.	Valine	32-38	ret proto-oncogene	Homo sapiens	50-53
15548358-1	2004	The platelet-derived growth factor receptor (PDGFR) is a receptor tyrosine kinase overexpressed in a subset of solid tumors and therefore is the target of drugs inhibiting this function such as imatinib mesylate (Gleevec).	Imatinib Mesylate	194-211	ret proto-oncogene	Homo sapiens	57-81
15548358-1	2004	The platelet-derived growth factor receptor (PDGFR) is a receptor tyrosine kinase overexpressed in a subset of solid tumors and therefore is the target of drugs inhibiting this function such as imatinib mesylate (Gleevec).	Imatinib Mesylate	213-220	ret proto-oncogene	Homo sapiens	57-81
15265706-6	2004	Different patterns were observed between cells naturally expressing RET and cells induced to expression of RET by treatment with sodium butyrate, an inhibitor of histone deacetylases.	Butyric Acid	129-144	ret proto-oncogene	Homo sapiens	68-71
15265706-6	2004	Different patterns were observed between cells naturally expressing RET and cells induced to expression of RET by treatment with sodium butyrate, an inhibitor of histone deacetylases.	Butyric Acid	129-144	ret proto-oncogene	Homo sapiens	107-110
15184865-1	2004	We have recently demonstrated that the pyrazolopyrimidines PP1 and PP2 and the 4-anilinoquinazoline ZD6474 display a strong inhibitory activity (IC(50)&lt; or =100 nM) towards constitutively active oncogenic RET kinases.	pyrazolopyrimidines	39-58	ret proto-oncogene	Homo sapiens	208-211
15184865-1	2004	We have recently demonstrated that the pyrazolopyrimidines PP1 and PP2 and the 4-anilinoquinazoline ZD6474 display a strong inhibitory activity (IC(50)&lt; or =100 nM) towards constitutively active oncogenic RET kinases.	anilinoquinazoline	79-99	ret proto-oncogene	Homo sapiens	208-211
15184865-1	2004	We have recently demonstrated that the pyrazolopyrimidines PP1 and PP2 and the 4-anilinoquinazoline ZD6474 display a strong inhibitory activity (IC(50)&lt; or =100 nM) towards constitutively active oncogenic RET kinases.	vandetanib	100-106	ret proto-oncogene	Homo sapiens	208-211
15184865-3	2004	In contrast, MEN2-associated swap of bulky hydrophobic leucine or methionine residues for valine 804 in the RET kinase domain causes resistance to the three compounds.	Leucine	55-62	ret proto-oncogene	Homo sapiens	108-111
15184865-4	2004	Substitution of valine 804 with the small amino- acid glycine renders the RET kinase even more susceptible to inhibition (ZD6474 IC(50): 20 nM) than the wild-type kinase.	Valine	16-22	ret proto-oncogene	Homo sapiens	74-77
15184865-4	2004	Substitution of valine 804 with the small amino- acid glycine renders the RET kinase even more susceptible to inhibition (ZD6474 IC(50): 20 nM) than the wild-type kinase.	Glycine	54-61	ret proto-oncogene	Homo sapiens	74-77
15184865-5	2004	Our data identify valine 804 of RET as a structural determinant mediating resistance to pyrazolopyrimidines and 4-anilinoquinazolines.	Valine	18-24	ret proto-oncogene	Homo sapiens	32-35
15184865-5	2004	Our data identify valine 804 of RET as a structural determinant mediating resistance to pyrazolopyrimidines and 4-anilinoquinazolines.	pyrazolopyrimidines	88-107	ret proto-oncogene	Homo sapiens	32-35
15184865-5	2004	Our data identify valine 804 of RET as a structural determinant mediating resistance to pyrazolopyrimidines and 4-anilinoquinazolines.	anilinoquinazoline	112-133	ret proto-oncogene	Homo sapiens	32-35
15286999-5	2004	One of these alleles, SosM98, which contains a single amino acid substitution in the RacGEF motif, functions as a dominant negative in vivo to downregulate RTK signaling.	sosm98	22-28	ret proto-oncogene	Homo sapiens	156-159
15271413-3	2004	All 60 MEN2A patients had RET mutations in a cysteine-rich domain.	Cysteine	45-53	ret proto-oncogene	Homo sapiens	7-12
15292360-3	2004	Genetic analysis of the RET protooncogene in this family revealed an exon 15 missense mutation at codon 891 that resulted in a serine to alanine amino acid substitution.	Serine	127-133	ret proto-oncogene	Homo sapiens	24-27
15292360-3	2004	Genetic analysis of the RET protooncogene in this family revealed an exon 15 missense mutation at codon 891 that resulted in a serine to alanine amino acid substitution.	alanine amino acid	137-155	ret proto-oncogene	Homo sapiens	24-27
15320968-0	2004	Frequency of RET proto-oncogene mutations in patients with normal and with moderately elevated pentagastrin-stimulated serum concentrations of calcitonin.	Pentagastrin	95-107	ret proto-oncogene	Homo sapiens	13-16
15271413-3	2004	All 60 MEN2A patients had RET mutations in a cysteine-rich domain.	Cysteine	45-53	ret proto-oncogene	Homo sapiens	26-29
15229154-0	2004	Potential utility of Ret-Y in the diagnosis of iron-restricted erythropoiesis.	Iron	47-51	ret proto-oncogene	Homo sapiens	21-24
15240641-3	2004	RET-activating mutations involve two important functional areas of the receptor: the cysteine-rich extracellular domain and the intracellular tyrosine kinase domain.	Cysteine	85-93	ret proto-oncogene	Homo sapiens	0-3
15031289-4	2004	Spry acts as a conserved inhibitor of RTK signaling, and tyrosine phosphorylation of Spry is indispensable for its inhibitory activity.	Tyrosine	57-65	ret proto-oncogene	Homo sapiens	38-41
15172989-1	2004	We show that treatment of a panel of thyroid carcinoma cell lines naturally harboring the RET/PTC1 oncogene, with the RET kinase inhibitors PP1 and ZD6474, results in reversible G(1) arrest.	vandetanib	148-154	ret proto-oncogene	Homo sapiens	90-93
15172989-1	2004	We show that treatment of a panel of thyroid carcinoma cell lines naturally harboring the RET/PTC1 oncogene, with the RET kinase inhibitors PP1 and ZD6474, results in reversible G(1) arrest.	vandetanib	148-154	ret proto-oncogene	Homo sapiens	118-121
15172989-5	2004	Reduction of p27Kip1 protein levels by antisense oligonucleotides abrogated the G(1) arrest induced by RET/PTC blockade.	Oligonucleotides	49-65	ret proto-oncogene	Homo sapiens	103-106
15172989-5	2004	Reduction of p27Kip1 protein levels by antisense oligonucleotides abrogated the G(1) arrest induced by RET/PTC blockade.	Oligonucleotides	49-65	ret proto-oncogene	Homo sapiens	107-110
15717656-3	2004	MEN 2B hallmarks (i.e. plasma thyrocalcitonin and urinary metanephrines) may be systematically investigated in neuroendocrine tumors of the prostate, and conversely prostate examination may be performed in the periodic screening of MEN 2B male patients.	Metanephrine	58-71	ret proto-oncogene	Homo sapiens	0-6
14766744-0	2004	Tyrosine 981, a novel ret autophosphorylation site, binds c-Src to mediate neuronal survival.	Tyrosine	0-8	ret proto-oncogene	Homo sapiens	22-25
15152080-2	2004	We hypothesized that acute resistance exercise (RE) and training (RET) would increase DHEA steroids, and the magnitude of the increase would be influenced by a steroid sulfatase (STS) gene variation.	dhea steroids	86-99	ret proto-oncogene	Homo sapiens	66-69
15152080-5	2004	RET reduced resting DHEAS (-122 ng/ml, P &lt; 0.01) and decreased DHEA response to RE (-50%, P &lt; 0.05).	Dehydroepiandrosterone	20-24	ret proto-oncogene	Homo sapiens	0-3
15129118-5	2004	METHODS: Immunohistochemical analysis for transforming growth factor-beta1 and glial cell line-derived neurotrophic factor and their receptors TbetaR II, GFRalpha-1, and Ret was performed on formalin-fixed, paraffin-embedded archival surgical specimens.	Formaldehyde	191-199	ret proto-oncogene	Homo sapiens	170-173
14963042-8	2004	The PH and PTB domains of Dok-4 were also required for tyrosine phosphorylation of Dok-4 by Fyn and Ret.	Tyrosine	55-63	ret proto-oncogene	Homo sapiens	100-103
14766744-5	2004	Here we show by multiple approaches that Ret tyrosine 981 constitutes the major binding site of the Src homology 2 domain of Src and therefore the primary residue responsible for Src activation upon Ret engagement.	Tyrosine	45-53	ret proto-oncogene	Homo sapiens	41-44
14766744-5	2004	Here we show by multiple approaches that Ret tyrosine 981 constitutes the major binding site of the Src homology 2 domain of Src and therefore the primary residue responsible for Src activation upon Ret engagement.	Tyrosine	45-53	ret proto-oncogene	Homo sapiens	199-202
14766744-6	2004	Other tyrosines such as 1015 and 1029 may contribute to the overall interaction between Ret and Src, as judged by overexpression experiments.	Tyrosine	6-15	ret proto-oncogene	Homo sapiens	88-91
14766744-7	2004	By generating a phosphospecific antibody, we demonstrate that tyrosine 981 is a novel autophosphorylation site in Ret.	Tyrosine	62-70	ret proto-oncogene	Homo sapiens	114-117
15157557-17	2004	Pentagastrin- or calcium-stimulated plasma CT testing is useful in identifying CCH or early MTC in carriers of RET mutations that are associated with late onset MTC.	Pentagastrin	0-12	ret proto-oncogene	Homo sapiens	111-114
15080300-7	2004	RET-Y is correlated closely with CHr and is useful for diagnosis and early monitoring after the administration of intravenous iron.	Iron	126-130	ret proto-oncogene	Homo sapiens	0-3
14715928-4	2004	These mutations constitutively activate RET due to aberrant disulfide homodimerization and diminish the level of RET at the plasma membrane.	Disulfides	60-69	ret proto-oncogene	Homo sapiens	40-43
14711813-1	2004	The catalytic and signaling activities of RET, a receptor-type tyrosine kinase, are regulated by the autophosphorylation of several tyrosine residues in the cytoplasmic region of RET.	Tyrosine	63-71	ret proto-oncogene	Homo sapiens	42-45
14711813-1	2004	The catalytic and signaling activities of RET, a receptor-type tyrosine kinase, are regulated by the autophosphorylation of several tyrosine residues in the cytoplasmic region of RET.	Tyrosine	63-71	ret proto-oncogene	Homo sapiens	179-182
14711813-2	2004	Some studies have revealed a few possible autophosphorylation sites of RET by [(32)P]phosphopeptide mapping or by using specific anti-phosphotyrosine antibodies.	Phosphorus-32	78-84	ret proto-oncogene	Homo sapiens	71-74
14711813-2	2004	Some studies have revealed a few possible autophosphorylation sites of RET by [(32)P]phosphopeptide mapping or by using specific anti-phosphotyrosine antibodies.	Phosphotyrosine	134-149	ret proto-oncogene	Homo sapiens	71-74
14711813-4	2004	Both the autophosphorylation and kinase activity of myelin basic protein as an external substrate of the recombinant RET protein were substantially elevated in the presence of ATP without stimulation by a glial cell line-derived neurotrophic factor, a natural ligand for RET.	Adenosine Triphosphate	176-179	ret proto-oncogene	Homo sapiens	117-120
14711813-5	2004	Mass spectrometric analysis revealed that RET Tyr(806), Tyr(809), Tyr(900), Tyr(905), Tyr(981), Tyr(1062), Tyr(1090), and Tyr(1096) were autophosphorylation sites.	Tyrosine	46-49	ret proto-oncogene	Homo sapiens	42-45
14711813-9	2004	These results provide convincing evidence for both previously suggested and new tyrosine autophosphorylation sites of RET as well as for novel functions of Tyr(806), Tyr(809), and Tyr(900) phosphorylation in both catalytic kinase activities and cell growth.	Tyrosine	80-88	ret proto-oncogene	Homo sapiens	118-121
15157557-17	2004	Pentagastrin- or calcium-stimulated plasma CT testing is useful in identifying CCH or early MTC in carriers of RET mutations that are associated with late onset MTC.	Calcium	17-24	ret proto-oncogene	Homo sapiens	111-114
14619940-3	2003	Genistein, a receptor tyrosine kinase (RTK) inhibitor, inhibited spontaneous AR.	Genistein	0-9	ret proto-oncogene	Homo sapiens	13-37
14607833-0	2004	Structural basis for the specific recognition of RET by the Dok1 phosphotyrosine binding domain.	Phosphotyrosine	65-80	ret proto-oncogene	Homo sapiens	49-52
15013219-4	2004	These signaling pathways are activated via binding of adaptor proteins to intracellular tyrosine residues of RET phosphorylated by its own kinase activity.	Tyrosine	88-96	ret proto-oncogene	Homo sapiens	109-112
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
15630203-7	2004	The decreased amount of TBARS in 5 microM Cry compared with control(0 microM) was the largest among 6 antioxidants (Cry, Car, Zea, Retinol(Ret), AsA, Toc) used in this experiment.	tbars	24-29	ret proto-oncogene	Homo sapiens	131-134
14619940-3	2003	Genistein, a receptor tyrosine kinase (RTK) inhibitor, inhibited spontaneous AR.	Genistein	0-9	ret proto-oncogene	Homo sapiens	39-42
14619940-4	2003	When the genistein was primed, hFF-induced AR was attenuated but the A23187-induced AR was not, suggesting that potentiation of AR by hFF attributed to the activation of RTK upstream the mobilization of Ca2+.	Genistein	9-18	ret proto-oncogene	Homo sapiens	170-173
12914961-4	2003	Interestingly, treating SH-SY5Y cells with retinoic acid greatly increases Ret protein levels and GDNF-induced Ret tyrosine phosphorylation, but does not affect the mitogenic action of GDNF and the activation of the Akt/p70S6K pathway.	Tretinoin	43-56	ret proto-oncogene	Homo sapiens	75-78
14602786-1	2003	Familial medullary thyroid carcinoma is related to germ-line mutations in the RET oncogene, mainly in cysteine codon 10 or 11, whereas noncysteine mutations in codons 13-15 are rare.	Cysteine	102-110	ret proto-oncogene	Homo sapiens	78-81
14602786-2	2003	We now report a new missense point mutation in exon 8 of the RET gene (1597G--&gt;T) corresponding to a Gly(533)Cys substitution in the cysteine-rich domain of RET protein in 76 patients from a 6-generation Brazilian family with 229 subjects, with ascendants from Spain.	Cysteine	136-144	ret proto-oncogene	Homo sapiens	61-64
14602786-2	2003	We now report a new missense point mutation in exon 8 of the RET gene (1597G--&gt;T) corresponding to a Gly(533)Cys substitution in the cysteine-rich domain of RET protein in 76 patients from a 6-generation Brazilian family with 229 subjects, with ascendants from Spain.	Cysteine	136-144	ret proto-oncogene	Homo sapiens	160-163
14559814-13	2003	The JM mutations also altered the c-MET RTK signaling, resulting in preferentially increased constitutive tyrosine phosphorylation of various cellular proteins, including the key focal adhesion protein paxillin on tyrosine residue Y31 (first CRKL-binding site), correlating with increased motility.	Tyrosine	106-114	ret proto-oncogene	Homo sapiens	40-43
14559814-13	2003	The JM mutations also altered the c-MET RTK signaling, resulting in preferentially increased constitutive tyrosine phosphorylation of various cellular proteins, including the key focal adhesion protein paxillin on tyrosine residue Y31 (first CRKL-binding site), correlating with increased motility.	Tyrosine	214-222	ret proto-oncogene	Homo sapiens	40-43
12914961-4	2003	Interestingly, treating SH-SY5Y cells with retinoic acid greatly increases Ret protein levels and GDNF-induced Ret tyrosine phosphorylation, but does not affect the mitogenic action of GDNF and the activation of the Akt/p70S6K pathway.	Tyrosine	115-123	ret proto-oncogene	Homo sapiens	111-114
12914961-4	2003	Interestingly, treating SH-SY5Y cells with retinoic acid greatly increases Ret protein levels and GDNF-induced Ret tyrosine phosphorylation, but does not affect the mitogenic action of GDNF and the activation of the Akt/p70S6K pathway.	Tretinoin	43-56	ret proto-oncogene	Homo sapiens	111-114
14666655-2	2003	We hypothesized that STI571 (Gleevec) would inhibit RET kinase and be a useful agent in the treatment of MTC.	Imatinib Mesylate	21-27	ret proto-oncogene	Homo sapiens	52-55
14666655-3	2003	MATERIALS AND METHODS: We determined the IC50 of STI571 for RET using an in vitro kinase assay and also examined the effects of STI571 on cellular proliferation and viability in TT cells, a human MTC cell line.	Imatinib Mesylate	49-55	ret proto-oncogene	Homo sapiens	60-63
14666655-7	2003	CONCLUSION: The concentrations of STI571 required to significantly inhibit RET and to inhibit TT cell proliferation are not clinically achievable.	Imatinib Mesylate	34-40	ret proto-oncogene	Homo sapiens	75-78
14870776-5	2003	The present report summarizes the cellular effects of the arylidene 2-indolinone Ret inhibitor RPI-1 (formerly Cpd1) on the human PTC cell line TPC-1 which spontaneously harbors the RET/PTC1 oncogene.	arylidene	58-67	ret proto-oncogene	Homo sapiens	81-84
14500395-4	2003	We show that the indolocarbazole derivatives, CEP-701 and CEP-751, inhibit RET in MTC cells.	Indolocarbazole	17-32	ret proto-oncogene	Homo sapiens	75-78
14870776-5	2003	The present report summarizes the cellular effects of the arylidene 2-indolinone Ret inhibitor RPI-1 (formerly Cpd1) on the human PTC cell line TPC-1 which spontaneously harbors the RET/PTC1 oncogene.	arylidene	58-67	ret proto-oncogene	Homo sapiens	182-185
14870776-5	2003	The present report summarizes the cellular effects of the arylidene 2-indolinone Ret inhibitor RPI-1 (formerly Cpd1) on the human PTC cell line TPC-1 which spontaneously harbors the RET/PTC1 oncogene.	2-oxindole	68-80	ret proto-oncogene	Homo sapiens	81-84
14870776-5	2003	The present report summarizes the cellular effects of the arylidene 2-indolinone Ret inhibitor RPI-1 (formerly Cpd1) on the human PTC cell line TPC-1 which spontaneously harbors the RET/PTC1 oncogene.	2-oxindole	68-80	ret proto-oncogene	Homo sapiens	182-185
12917021-0	2003	[SUCI02 inhibits HER-2/neu receptor tyrosine kinase phosphorylation and growth of HER-2/neu-overexpressing breast cancer cells].	N-(4-ethoyphenol)-2-hydroxy- acid amide	1-7	ret proto-oncogene	Homo sapiens	27-51
12630912-1	2003	Substitution of Cys-634 in the extracellular domain of the Ret tyrosine kinase receptor causes its dimerization and activation of its transforming potential.	Cysteine	16-19	ret proto-oncogene	Homo sapiens	59-62
12738763-6	2003	RET/PTC phosphorylates a specific tyrosine (Y9) residue located in the N-terminal region of PDK1.	Tyrosine	34-42	ret proto-oncogene	Homo sapiens	0-3
12738763-6	2003	RET/PTC phosphorylates a specific tyrosine (Y9) residue located in the N-terminal region of PDK1.	Tyrosine	34-42	ret proto-oncogene	Homo sapiens	4-7
12865274-0	2003	Rescue of human RET gene expression by sodium butyrate: a novel powerful tool for molecular studies in Hirschsprung disease.	Butyric Acid	39-54	ret proto-oncogene	Homo sapiens	16-19
12865274-5	2003	METHODS: The effect of sodium butyrate (NaB), a histone deacetylase inhibitor, on rescuing RET expression was tested by one round of reverse transcription- polymerase chain reaction from total RNA of treated lymphoblasts from both HSCR patients and control individuals.	Butyric Acid	23-38	ret proto-oncogene	Homo sapiens	91-94
12865274-5	2003	METHODS: The effect of sodium butyrate (NaB), a histone deacetylase inhibitor, on rescuing RET expression was tested by one round of reverse transcription- polymerase chain reaction from total RNA of treated lymphoblasts from both HSCR patients and control individuals.	nab	40-43	ret proto-oncogene	Homo sapiens	91-94
12865274-6	2003	RESULTS: Analysis of RET expression was possible by NaB treatment of RET negative cells, such as lymphoblasts.	nab	52-55	ret proto-oncogene	Homo sapiens	21-24
12865274-6	2003	RESULTS: Analysis of RET expression was possible by NaB treatment of RET negative cells, such as lymphoblasts.	nab	52-55	ret proto-oncogene	Homo sapiens	69-72
12943231-6	2003	In treated cells, Ret/Ptc1 tyrosine phosphorylation was abolished along with its binding to Shc and phospholipase C(gamma), thereby indicating abrogation of constitutive signaling mediated by the oncoprotein.	Tyrosine	27-35	ret proto-oncogene	Homo sapiens	18-21
12630912-2	2003	To gain further insight into the molecular basis leading to Ret activation we purified a mutant protein consisting of the entire ectodomain of the Ret carrying a Cys-634--&gt;Tyr substitution (EC-Ret(C634Y)).	Cysteine	162-165	ret proto-oncogene	Homo sapiens	147-150
12630912-2	2003	To gain further insight into the molecular basis leading to Ret activation we purified a mutant protein consisting of the entire ectodomain of the Ret carrying a Cys-634--&gt;Tyr substitution (EC-Ret(C634Y)).	Cysteine	162-165	ret proto-oncogene	Homo sapiens	147-150
12630912-2	2003	To gain further insight into the molecular basis leading to Ret activation we purified a mutant protein consisting of the entire ectodomain of the Ret carrying a Cys-634--&gt;Tyr substitution (EC-Ret(C634Y)).	Tyrosine	175-178	ret proto-oncogene	Homo sapiens	147-150
12630912-2	2003	To gain further insight into the molecular basis leading to Ret activation we purified a mutant protein consisting of the entire ectodomain of the Ret carrying a Cys-634--&gt;Tyr substitution (EC-Ret(C634Y)).	Tyrosine	175-178	ret proto-oncogene	Homo sapiens	147-150
12755958-2	2003	As is the case for other receptor tyrosine kinases, mutant RET recruits a variety of signalling molecules via phosphorylated tyrosine residues present in the kinase domain and carboxy-terminal tail.	Tyrosine	34-42	ret proto-oncogene	Homo sapiens	59-62
12738763-11	2003	In conclusion, RET/PTC-induced tyrosine phosphorylation of PDK1 may be one of the mechanisms by which it acts as an oncogenic tyrosine kinase in thyroid carcinogenesis.	Tyrosine	31-39	ret proto-oncogene	Homo sapiens	15-18
12738763-11	2003	In conclusion, RET/PTC-induced tyrosine phosphorylation of PDK1 may be one of the mechanisms by which it acts as an oncogenic tyrosine kinase in thyroid carcinogenesis.	Tyrosine	31-39	ret proto-oncogene	Homo sapiens	19-22
12755958-3	2003	As we previously reported, the signaling via phosphorylated tyrosine 1062 plays a crucial role in the transforming activities of both RET-MEN2A and RET-MEN2B mutant protein.	Tyrosine	60-68	ret proto-oncogene	Homo sapiens	134-137
12755958-3	2003	As we previously reported, the signaling via phosphorylated tyrosine 1062 plays a crucial role in the transforming activities of both RET-MEN2A and RET-MEN2B mutant protein.	Tyrosine	60-68	ret proto-oncogene	Homo sapiens	138-143
12755958-3	2003	As we previously reported, the signaling via phosphorylated tyrosine 1062 plays a crucial role in the transforming activities of both RET-MEN2A and RET-MEN2B mutant protein.	Tyrosine	60-68	ret proto-oncogene	Homo sapiens	148-151
12755958-3	2003	As we previously reported, the signaling via phosphorylated tyrosine 1062 plays a crucial role in the transforming activities of both RET-MEN2A and RET-MEN2B mutant protein.	Tyrosine	60-68	ret proto-oncogene	Homo sapiens	152-157
12755958-6	2003	In addition, RET is alternatively spliced to produce three isoforms and the splicing site is present just downstream of tyrosine 1062.	Tyrosine	120-128	ret proto-oncogene	Homo sapiens	13-16
12771945-3	2003	We have identified tyrosine 1062 in the RET carboxyl-terminal tail as the docking site for PKCalpha.	Tyrosine	19-27	ret proto-oncogene	Homo sapiens	40-43
12771945-6	2003	A threefold reduction of tyrosine phosphorylation levels of the constitutively active RET/MEN2A oncoprotein was observed upon coexpression with PKCalpha.	Tyrosine	25-33	ret proto-oncogene	Homo sapiens	86-89
12771945-6	2003	A threefold reduction of tyrosine phosphorylation levels of the constitutively active RET/MEN2A oncoprotein was observed upon coexpression with PKCalpha.	Tyrosine	25-33	ret proto-oncogene	Homo sapiens	90-95
12734540-2	2003	It has been reported that some families developed both MEN 2A/FMTC and HSCR, in which a mutation in a cysteine residue at codon 609, 618, or 620 in the RET gene was present.	Cysteine	102-110	ret proto-oncogene	Homo sapiens	55-61
12727845-2	2003	We show here that along with the inhibition of RET tyrosine phosphorylation, the pyrazolo-pyrimidine inhibitor PP1 induces RETMEN2A and RETMEN2B oncoprotein destruction.	Tyrosine	51-59	ret proto-oncogene	Homo sapiens	47-50
12727845-2	2003	We show here that along with the inhibition of RET tyrosine phosphorylation, the pyrazolo-pyrimidine inhibitor PP1 induces RETMEN2A and RETMEN2B oncoprotein destruction.	1H-pyrazolo[4,3-d]pyrimidine	81-100	ret proto-oncogene	Homo sapiens	47-50
12727845-9	2003	These observations lead us to favor two models for PP1-induced RET oncoprotein degradation: either PP1-mediated RET dephosphorylation per se targets the oncoproteins for destruction or alternatively, PP1 insertion in the RET ATP-binding pocket promotes a mechanism for fast stress-induced degradation.	Adenosine Triphosphate	225-228	ret proto-oncogene	Homo sapiens	63-66
12727845-9	2003	These observations lead us to favor two models for PP1-induced RET oncoprotein degradation: either PP1-mediated RET dephosphorylation per se targets the oncoproteins for destruction or alternatively, PP1 insertion in the RET ATP-binding pocket promotes a mechanism for fast stress-induced degradation.	Adenosine Triphosphate	225-228	ret proto-oncogene	Homo sapiens	112-115
12727845-9	2003	These observations lead us to favor two models for PP1-induced RET oncoprotein degradation: either PP1-mediated RET dephosphorylation per se targets the oncoproteins for destruction or alternatively, PP1 insertion in the RET ATP-binding pocket promotes a mechanism for fast stress-induced degradation.	Adenosine Triphosphate	225-228	ret proto-oncogene	Homo sapiens	112-115
12661006-0	2003	Fusion of FIG to the receptor tyrosine kinase ROS in a glioblastoma with an interstitial del(6)(q21q21).	ros	46-49	ret proto-oncogene	Homo sapiens	21-45
12661006-1	2003	The transmembrane proto-oncogene receptor tyrosine kinase (RTK) ROS is an orphan receptor that is aberrantly expressed in neoplasms of the central nervous system.	ros	64-67	ret proto-oncogene	Homo sapiens	33-57
12661006-1	2003	The transmembrane proto-oncogene receptor tyrosine kinase (RTK) ROS is an orphan receptor that is aberrantly expressed in neoplasms of the central nervous system.	ros	64-67	ret proto-oncogene	Homo sapiens	59-62
12734540-2	2003	It has been reported that some families developed both MEN 2A/FMTC and HSCR, in which a mutation in a cysteine residue at codon 609, 618, or 620 in the RET gene was present.	Cysteine	102-110	ret proto-oncogene	Homo sapiens	152-155
12734540-4	2003	A germline mutation in cysteine 611 of the RET gene was identified in this family, which introduced an amino-acid change from cysteine to serine.	Cysteine	23-31	ret proto-oncogene	Homo sapiens	43-46
12734540-4	2003	A germline mutation in cysteine 611 of the RET gene was identified in this family, which introduced an amino-acid change from cysteine to serine.	Cysteine	126-134	ret proto-oncogene	Homo sapiens	43-46
12734540-4	2003	A germline mutation in cysteine 611 of the RET gene was identified in this family, which introduced an amino-acid change from cysteine to serine.	Serine	138-144	ret proto-oncogene	Homo sapiens	43-46
12734540-5	2003	By biological and biochemical analyses of mutant RET proteins, we previously predicted the potentiality that amino-acid substitution for cysteine 611 as well as cysteines 609, 618, and 620 would promote the development of MEN 2A/FMTC and HSCR.	Cysteine	137-145	ret proto-oncogene	Homo sapiens	49-52
12734540-5	2003	By biological and biochemical analyses of mutant RET proteins, we previously predicted the potentiality that amino-acid substitution for cysteine 611 as well as cysteines 609, 618, and 620 would promote the development of MEN 2A/FMTC and HSCR.	Cysteine	137-145	ret proto-oncogene	Homo sapiens	222-228
12734540-5	2003	By biological and biochemical analyses of mutant RET proteins, we previously predicted the potentiality that amino-acid substitution for cysteine 611 as well as cysteines 609, 618, and 620 would promote the development of MEN 2A/FMTC and HSCR.	Cysteine	161-170	ret proto-oncogene	Homo sapiens	49-52
12734540-5	2003	By biological and biochemical analyses of mutant RET proteins, we previously predicted the potentiality that amino-acid substitution for cysteine 611 as well as cysteines 609, 618, and 620 would promote the development of MEN 2A/FMTC and HSCR.	Cysteine	161-170	ret proto-oncogene	Homo sapiens	222-228
12608895-3	2003	Expression of RET proto-oncogene was detected in 27.3% of FCDT by IHC and 25.5% by RT-PCR using a primer set at a regular break point.	fcdt	58-62	ret proto-oncogene	Homo sapiens	14-17
12679489-0	2003	Efficient inhibition of RET/papillary thyroid carcinoma oncogenic kinases by 4-amino-5-(4-chloro-phenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2).	AG 1879	77-141	ret proto-oncogene	Homo sapiens	24-27
12679489-2	2003	We have previously shown that pyrazolopyrimidine is a potent inhibitor of the RET kinase.	1H-pyrazolo[4,3-d]pyrimidine	30-48	ret proto-oncogene	Homo sapiens	78-81
12679489-3	2003	Here, we show that 4-amino-5-(4-chloro-phenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) (PP2), another pyrazolopyrimidine, blocks the enzymatic activity of the isolated RET kinase and RET/PTC1 oncoprotein at IC(50) in the nanomolar range.	AG 1879	19-84	ret proto-oncogene	Homo sapiens	166-169
12679489-3	2003	Here, we show that 4-amino-5-(4-chloro-phenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) (PP2), another pyrazolopyrimidine, blocks the enzymatic activity of the isolated RET kinase and RET/PTC1 oncoprotein at IC(50) in the nanomolar range.	AG 1879	19-84	ret proto-oncogene	Homo sapiens	181-184
12679489-3	2003	Here, we show that 4-amino-5-(4-chloro-phenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) (PP2), another pyrazolopyrimidine, blocks the enzymatic activity of the isolated RET kinase and RET/PTC1 oncoprotein at IC(50) in the nanomolar range.	1H-pyrazolo[4,3-d]pyrimidine	100-118	ret proto-oncogene	Homo sapiens	166-169
12679489-3	2003	Here, we show that 4-amino-5-(4-chloro-phenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) (PP2), another pyrazolopyrimidine, blocks the enzymatic activity of the isolated RET kinase and RET/PTC1 oncoprotein at IC(50) in the nanomolar range.	1H-pyrazolo[4,3-d]pyrimidine	100-118	ret proto-oncogene	Homo sapiens	181-184
12679489-7	2003	Thus, pyrazolopirimidines hold promise for the treatment of human cancers sustaining oncogenic activation of RET.	pyrazolopirimidines	6-25	ret proto-oncogene	Homo sapiens	109-112
12606135-4	2003	Both the proband and his father carry RET 634 germline mutation resulting in cysteine to arginine amino acid substitution.	Cysteine	77-85	ret proto-oncogene	Homo sapiens	38-41
12606135-4	2003	Both the proband and his father carry RET 634 germline mutation resulting in cysteine to arginine amino acid substitution.	arginine amino acid	89-108	ret proto-oncogene	Homo sapiens	38-41
12563086-14	2003	CONCLUSIONS: 1) ETT until 5 years of age in MEN-2A gene carriers results in significant reduction of MTC and MMTC in favor of CCH and improved disease-free long-term outcome.	mtc	101-104	ret proto-oncogene	Homo sapiens	44-50
12508108-5	2003	By contrast, mitogenic signaling by RTK targets, such as PI 3-kinase and MAP kinases, as well as RTK-mediated tyrosine phosphorylation do not appear to be affected by 480-Cbl expression.	Tyrosine	110-118	ret proto-oncogene	Homo sapiens	97-100
12563086-14	2003	CONCLUSIONS: 1) ETT until 5 years of age in MEN-2A gene carriers results in significant reduction of MTC and MMTC in favor of CCH and improved disease-free long-term outcome.	Adrenoglomerulotropin	109-113	ret proto-oncogene	Homo sapiens	44-50
12490842-7	2002	RESULTS: RET phosphorylation was inhibited at 24 hours of exposure to 5 to 20 micromol/L STI571 and 48 hours of exposure to genistein (200 micromol/L) and allyl-geldanamycin (6 micromol/L).	Imatinib Mesylate	89-95	ret proto-oncogene	Homo sapiens	9-12
12757658-3	2003	RESULTS: We found the same mutation Met(ATG)--&gt;Thr(ACG) at codon 918 in exon 16 of RET proto-oncogene in both the tumor (c)DNA and leukocyte DNA of the MEN-2B patient in the form of homozygous missense mutation, but there was no corresponding mutation in leukocytes DNA of his parents.	Threonine	50-53	ret proto-oncogene	Homo sapiens	86-89
12757658-3	2003	RESULTS: We found the same mutation Met(ATG)--&gt;Thr(ACG) at codon 918 in exon 16 of RET proto-oncogene in both the tumor (c)DNA and leukocyte DNA of the MEN-2B patient in the form of homozygous missense mutation, but there was no corresponding mutation in leukocytes DNA of his parents.	Threonine	50-53	ret proto-oncogene	Homo sapiens	155-161
12757658-3	2003	RESULTS: We found the same mutation Met(ATG)--&gt;Thr(ACG) at codon 918 in exon 16 of RET proto-oncogene in both the tumor (c)DNA and leukocyte DNA of the MEN-2B patient in the form of homozygous missense mutation, but there was no corresponding mutation in leukocytes DNA of his parents.	acceleratory factor from growth hormone	54-57	ret proto-oncogene	Homo sapiens	86-89
12757658-3	2003	RESULTS: We found the same mutation Met(ATG)--&gt;Thr(ACG) at codon 918 in exon 16 of RET proto-oncogene in both the tumor (c)DNA and leukocyte DNA of the MEN-2B patient in the form of homozygous missense mutation, but there was no corresponding mutation in leukocytes DNA of his parents.	acceleratory factor from growth hormone	54-57	ret proto-oncogene	Homo sapiens	155-161
12499271-0	2002	ZD6474, an orally available inhibitor of KDR tyrosine kinase activity, efficiently blocks oncogenic RET kinases.	vandetanib	0-6	ret proto-oncogene	Homo sapiens	100-103
12499271-3	2002	Here, we show that ZD6474, a low molecular weight tyrosine kinase inhibitor, blocks the enzymatic activity of RET-derived oncoproteins at a one-half maximal inhibitory concentration of 100 nM.	vandetanib	19-25	ret proto-oncogene	Homo sapiens	110-113
12499271-4	2002	ZD6474 blocked in vivo phosphorylation and signaling of the RET/PTC3 and RET/MEN2B oncoproteins and of an epidermal growth factor (EGF)-activated EGF-receptor/RET chimeric receptor.	vandetanib	0-6	ret proto-oncogene	Homo sapiens	60-63
12499271-4	2002	ZD6474 blocked in vivo phosphorylation and signaling of the RET/PTC3 and RET/MEN2B oncoproteins and of an epidermal growth factor (EGF)-activated EGF-receptor/RET chimeric receptor.	vandetanib	0-6	ret proto-oncogene	Homo sapiens	73-76
12499271-4	2002	ZD6474 blocked in vivo phosphorylation and signaling of the RET/PTC3 and RET/MEN2B oncoproteins and of an epidermal growth factor (EGF)-activated EGF-receptor/RET chimeric receptor.	vandetanib	0-6	ret proto-oncogene	Homo sapiens	77-82
12499271-4	2002	ZD6474 blocked in vivo phosphorylation and signaling of the RET/PTC3 and RET/MEN2B oncoproteins and of an epidermal growth factor (EGF)-activated EGF-receptor/RET chimeric receptor.	vandetanib	0-6	ret proto-oncogene	Homo sapiens	73-76
12499271-5	2002	RET/PTC3-transformed cells-treated ZD6474 lost proliferative autonomy and showed morphological reversion.	vandetanib	35-41	ret proto-oncogene	Homo sapiens	0-3
12490842-7	2002	RESULTS: RET phosphorylation was inhibited at 24 hours of exposure to 5 to 20 micromol/L STI571 and 48 hours of exposure to genistein (200 micromol/L) and allyl-geldanamycin (6 micromol/L).	allyl-geldanamycin	155-173	ret proto-oncogene	Homo sapiens	9-12
12490842-7	2002	RESULTS: RET phosphorylation was inhibited at 24 hours of exposure to 5 to 20 micromol/L STI571 and 48 hours of exposure to genistein (200 micromol/L) and allyl-geldanamycin (6 micromol/L).	Genistein	124-133	ret proto-oncogene	Homo sapiens	9-12
12188924-7	2002	Together, these findings for the first time demonstrate a role for NFATs in RTK and GPCR agonist-induced growth in VSMCs.	nfats	67-72	ret proto-oncogene	Homo sapiens	76-79
12490080-3	2002	So far, S836S of RET, is the only variant whose association with sMTC has been found in several European cohorts.	smtc	65-69	ret proto-oncogene	Homo sapiens	17-20
12205548-4	2002	Genetic analysis revealed a heterozygous RET protooncogene germline mutation in codon 791 (exon 13) (TAT(Tyr)--&gt;TTT(Phe)), followed by thyroidectomy and systematic central lymph node dissection.	Tyrosine	105-108	ret proto-oncogene	Homo sapiens	41-44
12395090-6	2002	Phosphorylation of extracellular regulated kinase was increased in the presence of heparin, although tyrosine phosphorylation of Ret receptor tyrosine kinase was not affected by heparin.	Tyrosine	101-109	ret proto-oncogene	Homo sapiens	129-132
12395090-6	2002	Phosphorylation of extracellular regulated kinase was increased in the presence of heparin, although tyrosine phosphorylation of Ret receptor tyrosine kinase was not affected by heparin.	Tyrosine	101-109	ret proto-oncogene	Homo sapiens	133-157
12406571-8	2002	Our data suggest that regulation of RET expression during development and in medullary thyroid carcinoma may be determined, at least in part, by this complex of Sp and Egr-1 proteins.	TFF2 protein, human	161-163	ret proto-oncogene	Homo sapiens	36-39
12205548-4	2002	Genetic analysis revealed a heterozygous RET protooncogene germline mutation in codon 791 (exon 13) (TAT(Tyr)--&gt;TTT(Phe)), followed by thyroidectomy and systematic central lymph node dissection.	Phenylalanine	119-122	ret proto-oncogene	Homo sapiens	41-44
12176011-5	2002	The RET docking tyrosine for Enigma is the last but one before the divergence between the two isoforms and we demonstrated that short-isoform-specific amino acid residues +2 to +4 to this tyrosine are required for the interaction of RET/PTC2 with Enigma.	Tyrosine	16-24	ret proto-oncogene	Homo sapiens	4-7
12091387-2	2002	To identify tyrosines in Ret that are autophosphorylation sites in neurons, we generated antibodies specific to phosphorylated Y905Ret, Y1015Ret, Y1062Ret, and Y1096Ret, all of which are autophosphorylated in cell lines.	Tyrosine	12-21	ret proto-oncogene	Homo sapiens	25-28
12091387-3	2002	All four of these tyrosines in Ret became phosphorylated rapidly upon activation by GFLs in sympathetic neurons.	Tyrosine	18-27	ret proto-oncogene	Homo sapiens	31-34
12091387-5	2002	Comparison of GFL activation of Ret9 and Ret51 revealed that phosphorylation of Tyr(905) and Tyr(1062) was greater and more sustained in Ret9 as compared with Ret51.	Tyrosine	80-83	ret proto-oncogene	Homo sapiens	41-46
12091387-5	2002	Comparison of GFL activation of Ret9 and Ret51 revealed that phosphorylation of Tyr(905) and Tyr(1062) was greater and more sustained in Ret9 as compared with Ret51.	Tyrosine	93-96	ret proto-oncogene	Homo sapiens	41-46
12091387-6	2002	In contrast, Tyr(1015) was more highly phosphorylated over time in Ret51 than in Ret9.	Tyrosine	13-16	ret proto-oncogene	Homo sapiens	67-72
12087092-7	2002	This suggested that the association of Nck to tyrosine 361 in Dok1 is necessary for the JNK and c-Jun activation by glial cell line-derived neurotrophic factor or RET-MEN2B.	Tyrosine	46-54	ret proto-oncogene	Homo sapiens	163-166
12087092-7	2002	This suggested that the association of Nck to tyrosine 361 in Dok1 is necessary for the JNK and c-Jun activation by glial cell line-derived neurotrophic factor or RET-MEN2B.	Tyrosine	46-54	ret proto-oncogene	Homo sapiens	167-172
12176011-5	2002	The RET docking tyrosine for Enigma is the last but one before the divergence between the two isoforms and we demonstrated that short-isoform-specific amino acid residues +2 to +4 to this tyrosine are required for the interaction of RET/PTC2 with Enigma.	Tyrosine	16-24	ret proto-oncogene	Homo sapiens	233-236
12176011-5	2002	The RET docking tyrosine for Enigma is the last but one before the divergence between the two isoforms and we demonstrated that short-isoform-specific amino acid residues +2 to +4 to this tyrosine are required for the interaction of RET/PTC2 with Enigma.	Tyrosine	188-196	ret proto-oncogene	Homo sapiens	4-7
12176011-5	2002	The RET docking tyrosine for Enigma is the last but one before the divergence between the two isoforms and we demonstrated that short-isoform-specific amino acid residues +2 to +4 to this tyrosine are required for the interaction of RET/PTC2 with Enigma.	Tyrosine	188-196	ret proto-oncogene	Homo sapiens	233-236
12168961-8	2002	The RET mutation in 21 patients was Cys--&gt;Tyr and in the remaining patient both in codon 634 in exon 11.	Cysteine	36-39	ret proto-oncogene	Homo sapiens	4-7
12168961-8	2002	The RET mutation in 21 patients was Cys--&gt;Tyr and in the remaining patient both in codon 634 in exon 11.	Tyrosine	45-48	ret proto-oncogene	Homo sapiens	4-7
12161537-4	2002	We here report on RET protein immunoreactivity in paraffin-embedded thyroid samples from 30 patients with papillary thyroid cancer who received radiation treatment during childhood for benign conditions at Michael Reese Hospital in Chicago, and in 34 patients identified from the tumor registry as having papillary thyroid cancer with no history of therapeutic radiation.	Paraffin	50-58	ret proto-oncogene	Homo sapiens	18-21
12123817-3	2002	Here we show that the histone deacetylase inhibitor sodium butyrate (NaB) increases RET transcription in cells displaying low levels of its mRNA, while it has no effect in cells expressing at high levels.	Butyric Acid	52-67	ret proto-oncogene	Homo sapiens	84-87
12091352-7	2002	In summary, SU11652, SU11654, and SU11655 are effective RTK inhibitors capable of disrupting the function of all forms of mutant Kit.	SU 11655	34-41	ret proto-oncogene	Homo sapiens	56-59
12091352-2	2002	To identify a receptor tyrosine kinase (RTK) inhibitor capable of blocking the function of mutant Kit, we evaluated 3 indolinones (SU11652, SU11654, and SU11655) that act as competitive inhibitors of adenosine triphosphate binding to several members of the split kinase family of RTKs, including VEGFR, FGFR, PDGFR, and Kit.	Oxindoles	118-129	ret proto-oncogene	Homo sapiens	40-43
12091352-2	2002	To identify a receptor tyrosine kinase (RTK) inhibitor capable of blocking the function of mutant Kit, we evaluated 3 indolinones (SU11652, SU11654, and SU11655) that act as competitive inhibitors of adenosine triphosphate binding to several members of the split kinase family of RTKs, including VEGFR, FGFR, PDGFR, and Kit.	SU 11652	131-138	ret proto-oncogene	Homo sapiens	40-43
12091352-2	2002	To identify a receptor tyrosine kinase (RTK) inhibitor capable of blocking the function of mutant Kit, we evaluated 3 indolinones (SU11652, SU11654, and SU11655) that act as competitive inhibitors of adenosine triphosphate binding to several members of the split kinase family of RTKs, including VEGFR, FGFR, PDGFR, and Kit.	toceranib phosphate	140-147	ret proto-oncogene	Homo sapiens	40-43
12091352-2	2002	To identify a receptor tyrosine kinase (RTK) inhibitor capable of blocking the function of mutant Kit, we evaluated 3 indolinones (SU11652, SU11654, and SU11655) that act as competitive inhibitors of adenosine triphosphate binding to several members of the split kinase family of RTKs, including VEGFR, FGFR, PDGFR, and Kit.	SU 11655	153-160	ret proto-oncogene	Homo sapiens	40-43
12091352-2	2002	To identify a receptor tyrosine kinase (RTK) inhibitor capable of blocking the function of mutant Kit, we evaluated 3 indolinones (SU11652, SU11654, and SU11655) that act as competitive inhibitors of adenosine triphosphate binding to several members of the split kinase family of RTKs, including VEGFR, FGFR, PDGFR, and Kit.	Adenosine Triphosphate	200-222	ret proto-oncogene	Homo sapiens	40-43
12091352-7	2002	In summary, SU11652, SU11654, and SU11655 are effective RTK inhibitors capable of disrupting the function of all forms of mutant Kit.	SU 11652	12-19	ret proto-oncogene	Homo sapiens	56-59
12091352-7	2002	In summary, SU11652, SU11654, and SU11655 are effective RTK inhibitors capable of disrupting the function of all forms of mutant Kit.	toceranib phosphate	21-28	ret proto-oncogene	Homo sapiens	56-59
12123817-3	2002	Here we show that the histone deacetylase inhibitor sodium butyrate (NaB) increases RET transcription in cells displaying low levels of its mRNA, while it has no effect in cells expressing at high levels.	nab	69-72	ret proto-oncogene	Homo sapiens	84-87
11886862-3	2002	Here we show that increased serine phosphorylation on RET receptor tyrosine kinase following cAMP elevation promotes lamellipodia formation of neuronal cells induced by glial cell line-derived neurotrophic factor (GDNF).	Serine	28-34	ret proto-oncogene	Homo sapiens	54-57
12056817-2	2002	We found a high level of IL-8 production in SK-N-MC human primitive neuroectodermal tumor cells transfected with the human RET gene (SK-N-MC (RET) cells) in response to glial cell line-derived neurotrophic factor (GDNF) stimulation.	sk-n-mc	44-51	ret proto-oncogene	Homo sapiens	123-126
12056817-2	2002	We found a high level of IL-8 production in SK-N-MC human primitive neuroectodermal tumor cells transfected with the human RET gene (SK-N-MC (RET) cells) in response to glial cell line-derived neurotrophic factor (GDNF) stimulation.	sk-n-mc	44-51	ret proto-oncogene	Homo sapiens	142-145
12056817-2	2002	We found a high level of IL-8 production in SK-N-MC human primitive neuroectodermal tumor cells transfected with the human RET gene (SK-N-MC (RET) cells) in response to glial cell line-derived neurotrophic factor (GDNF) stimulation.	sk-n-mc	133-140	ret proto-oncogene	Homo sapiens	123-126
12056817-2	2002	We found a high level of IL-8 production in SK-N-MC human primitive neuroectodermal tumor cells transfected with the human RET gene (SK-N-MC (RET) cells) in response to glial cell line-derived neurotrophic factor (GDNF) stimulation.	sk-n-mc	133-140	ret proto-oncogene	Homo sapiens	142-145
12056817-4	2002	To investigate which signaling pathways are responsible for IL-8 expression, we treated SK-N-MC (RET) cells with several kinase inhibitors before GDNF stimulation.	sk-n-mc	88-95	ret proto-oncogene	Homo sapiens	97-100
12056817-5	2002	The results showed that a MEK1 inhibitor, PD98059, a p38MAPK inhibitor, SB202190, and a protein kinase C (PKC) inhibitor, Calphostin C, markedly decreased the IL-8 secretion from SK-N-MC (RET) cells at 24 h after GDNF stimulation.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	42-49	ret proto-oncogene	Homo sapiens	188-191
12095936-5	2002	Mutations of extracellular cysteines are found in MEN2A patients, and a Met918Thr mutation is responsible for most MEN2B cases.	Cysteine	27-36	ret proto-oncogene	Homo sapiens	50-55
11925444-1	2002	Previously we have demonstrated that activation of p38 mitogen-activated protein kinase (MAPK) and induction of DNA synthesis in response to receptor tyrosine kinase (RTK) and G protein-coupled receptor (GPCR) agonists require NADH/NADPH-like oxidase activity in vascular smooth muscle cells (VSMC).	NAD	227-231	ret proto-oncogene	Homo sapiens	141-165
11925444-1	2002	Previously we have demonstrated that activation of p38 mitogen-activated protein kinase (MAPK) and induction of DNA synthesis in response to receptor tyrosine kinase (RTK) and G protein-coupled receptor (GPCR) agonists require NADH/NADPH-like oxidase activity in vascular smooth muscle cells (VSMC).	NAD	227-231	ret proto-oncogene	Homo sapiens	167-170
12037758-10	2002	According to the natural history of the disease, families with the genotype RET cys609gly should have a more benign disease than high-risk families (mutations at codon 634, 618).	cys609gly	80-89	ret proto-oncogene	Homo sapiens	76-79
12033991-2	2002	Missence mutations in the codon encoding cysteine 634 of the ret proto-oncogene have been found in 85% of the MEN 2A families.	Cysteine	41-49	ret proto-oncogene	Homo sapiens	61-64
12033991-2	2002	Missence mutations in the codon encoding cysteine 634 of the ret proto-oncogene have been found in 85% of the MEN 2A families.	Cysteine	41-49	ret proto-oncogene	Homo sapiens	110-116
11886862-3	2002	Here we show that increased serine phosphorylation on RET receptor tyrosine kinase following cAMP elevation promotes lamellipodia formation of neuronal cells induced by glial cell line-derived neurotrophic factor (GDNF).	Cyclic AMP	93-97	ret proto-oncogene	Homo sapiens	54-57
11886862-4	2002	We identified serine 696 in RET as a putative phosphorylation site by protein kinase A and found that mutation of this serine almost completely inhibited lamellipodia formation by GDNF without affecting activation of the PI3K/AKT signaling pathway.	Serine	14-20	ret proto-oncogene	Homo sapiens	28-31
11886862-4	2002	We identified serine 696 in RET as a putative phosphorylation site by protein kinase A and found that mutation of this serine almost completely inhibited lamellipodia formation by GDNF without affecting activation of the PI3K/AKT signaling pathway.	Serine	119-125	ret proto-oncogene	Homo sapiens	28-31
11886862-5	2002	Mutation of tyrosine 1062 in RET, whose phosphorylation is crucial for activation of PI3K, also inhibited lamellipodia formation by GDNF.	Tyrosine	12-20	ret proto-oncogene	Homo sapiens	29-32
11886862-6	2002	Inhibition of lamellipodia formation by mutation of either serine 696 or tyrosine 1062 was associated with decrease of the Rac1-guanine nucleotide exchange factor (GEF) activity, suggesting that this activity is regulated by two different signaling pathways via serine 696 and tyrosine 1062 in RET.	Serine	59-65	ret proto-oncogene	Homo sapiens	294-297
11886862-6	2002	Inhibition of lamellipodia formation by mutation of either serine 696 or tyrosine 1062 was associated with decrease of the Rac1-guanine nucleotide exchange factor (GEF) activity, suggesting that this activity is regulated by two different signaling pathways via serine 696 and tyrosine 1062 in RET.	Serine	262-268	ret proto-oncogene	Homo sapiens	294-297
11944888-1	2002	By use of a specifically sulfhydryl group-reactive chemical, 1,4-butanediyl-bismethanethiosulfonate (BMTS), we studied the localization of oxidative stress-responsive target cysteines for activation of a receptor-type protein tyrosine kinase, c-RET.	Cysteine	174-183	ret proto-oncogene	Homo sapiens	245-248
11944888-5	2002	These results suggest that cysteines in both the extracellular and the intracellular domains of RET can work as target sites of accessible BMTS and possibly other oxidative elements for structural modification and activation of RET kinase.	Cysteine	27-36	ret proto-oncogene	Homo sapiens	96-99
11944888-0	2002	Evidence of both extra- and intracellular cysteine targets of protein modification for activation of RET kinase.	Cysteine	42-50	ret proto-oncogene	Homo sapiens	101-104
11944888-1	2002	By use of a specifically sulfhydryl group-reactive chemical, 1,4-butanediyl-bismethanethiosulfonate (BMTS), we studied the localization of oxidative stress-responsive target cysteines for activation of a receptor-type protein tyrosine kinase, c-RET.	1,4-butanediylbismethanethiosulfonate	61-99	ret proto-oncogene	Homo sapiens	245-248
11944888-5	2002	These results suggest that cysteines in both the extracellular and the intracellular domains of RET can work as target sites of accessible BMTS and possibly other oxidative elements for structural modification and activation of RET kinase.	Cysteine	27-36	ret proto-oncogene	Homo sapiens	228-231
11935126-11	2002	CONCLUSIONS: This report of a newly-described kindred with the infrequent clinical association between MEN 2A and HSCR confirms the risk of the latter phenotype among carriers of RET exon 10 cysteine codon mutations.	Cysteine	191-199	ret proto-oncogene	Homo sapiens	103-109
11935126-11	2002	CONCLUSIONS: This report of a newly-described kindred with the infrequent clinical association between MEN 2A and HSCR confirms the risk of the latter phenotype among carriers of RET exon 10 cysteine codon mutations.	Cysteine	191-199	ret proto-oncogene	Homo sapiens	179-182
11839664-4	2002	In this work, we have developed a RET oligonucleotide microarray of 67 oligonucleotides to quickly detect RET mutations in MEN2 syndromes.	Oligonucleotides	71-87	ret proto-oncogene	Homo sapiens	34-37
11861385-2	2002	We found that the pyrazolo-pyrimidine PP1 inhibited RET-derived oncoproteins with a half maximal inhibitor concentration of 80 nM.	1H-pyrazolo[4,3-d]pyrimidine	18-37	ret proto-oncogene	Homo sapiens	52-55
11839664-4	2002	In this work, we have developed a RET oligonucleotide microarray of 67 oligonucleotides to quickly detect RET mutations in MEN2 syndromes.	Oligonucleotides	71-87	ret proto-oncogene	Homo sapiens	106-109
11839664-7	2002	More than 95% of MEN2B patients also had a predominant mutation type at codon 918 (Met--&gt;Thr).	Threonine	92-95	ret proto-oncogene	Homo sapiens	17-22
11754373-1	2002	BACKGROUND AND OBJECTIVES: We propose that a growth factor receptor tyrosine kinase (RTK) inhibitor, such as tyrphostin A47, could serve as an adjunct to estrogen replacement therapy (ERT) for postmenopausal breast cancer survivors.	tyrphostin 47	109-123	ret proto-oncogene	Homo sapiens	59-83
11900218-9	2002	All MEN 2B patients showed an ATG to ACG (Met918Thr) mutation.	acceleratory factor from growth hormone	37-40	ret proto-oncogene	Homo sapiens	4-10
11939755-4	2002	RESULTS: Sequencing analysis of the RET proto-oncogene revealed a Cys634Trp (TGC->TGG) mutation in all clinically affected family members and in an asymptomatic 5-year-old child who, after thyroidectomy, was found to have multicentric medullary thyroid carcinoma and C-cell hyperplasia.	cys634trp	66-75	ret proto-oncogene	Homo sapiens	36-39
11883863-3	2002	We report a family initially described as a familial MTC by pentagastrin stimulation test and clinical outcome, in which we found a 12 bp deletion within the catalytic domain of the protooncogene RET in the index case tumor alone.	Pentagastrin	60-72	ret proto-oncogene	Homo sapiens	196-199
11754373-1	2002	BACKGROUND AND OBJECTIVES: We propose that a growth factor receptor tyrosine kinase (RTK) inhibitor, such as tyrphostin A47, could serve as an adjunct to estrogen replacement therapy (ERT) for postmenopausal breast cancer survivors.	tyrphostin 47	109-123	ret proto-oncogene	Homo sapiens	85-88
11746981-4	2001	RET may thus not be excluded as a potential candidate for predisposition to some forms of NMTC.	nmtc	90-94	ret proto-oncogene	Homo sapiens	0-3
11564708-4	2001	Therefore, we investigated the impact of the tyrosine phosphatases SHP1 and SHP2 on the intrinsic tyrosine kinase activity and oncogenic potency of Ret with a 9-bp duplication in the cysteine-rich domain (codons 634-636), which was described in a patient with MEN type 2A recently.	Cysteine	183-191	ret proto-oncogene	Homo sapiens	148-151
11535584-5	2001	Using the neuroectodermic SK-N-MC cell line, we found that the Ret tyrosine kinase activity is essential for GDNF to induce phosphatidylinositol 3-kinase (PI3K)/Akt and ERK pathways as well as cell rescue.	sk-n-mc	26-33	ret proto-oncogene	Homo sapiens	63-66
11581189-7	2001	GDNF induced tyrosine phosphorylation of Ret.	Tyrosine	13-21	ret proto-oncogene	Homo sapiens	41-44
11581189-11	2001	Herbimycin A strongly inhibited the activation of Ret, FAK, c-Raf, and Erk-1 and -2; the phosphorylation of paxillin; and corneal epithelial cell migration.	herbimycin	0-12	ret proto-oncogene	Homo sapiens	50-53
11520496-2	2001	In this study, we examined the expression of the phosphorylation state of tyrosine residue 1062 (Tyr-1062) of Ret in the spinal cords of amyotrophic lateral sclerosis (ALS), using the phosphorylation state specific antibody at Tyr-1062 of Ret.	Tyrosine	74-82	ret proto-oncogene	Homo sapiens	110-113
11564857-0	2001	The sensitivity of activated Cys Ret mutants to glial cell line-derived neurotrophic factor is mandatory to rescue neuroectodermic cells from apoptosis.	Cysteine	29-32	ret proto-oncogene	Homo sapiens	33-36
11564857-2	2001	Instead, gain-of-function Cys mutations (e.g., Cys(609), Cys(620), and Cys(634)) of the same gene are responsible for thyroid carcinoma (MEN2A/familial medullary thyroid carcinoma) by causing a covalent Ret dimerization, leading to ligand-independent activation of its tyrosine kinase.	Cysteine	26-29	ret proto-oncogene	Homo sapiens	137-142
11564857-2	2001	Instead, gain-of-function Cys mutations (e.g., Cys(609), Cys(620), and Cys(634)) of the same gene are responsible for thyroid carcinoma (MEN2A/familial medullary thyroid carcinoma) by causing a covalent Ret dimerization, leading to ligand-independent activation of its tyrosine kinase.	Cysteine	26-29	ret proto-oncogene	Homo sapiens	203-206
11564857-2	2001	Instead, gain-of-function Cys mutations (e.g., Cys(609), Cys(620), and Cys(634)) of the same gene are responsible for thyroid carcinoma (MEN2A/familial medullary thyroid carcinoma) by causing a covalent Ret dimerization, leading to ligand-independent activation of its tyrosine kinase.	Cysteine	47-50	ret proto-oncogene	Homo sapiens	137-142
11564857-2	2001	Instead, gain-of-function Cys mutations (e.g., Cys(609), Cys(620), and Cys(634)) of the same gene are responsible for thyroid carcinoma (MEN2A/familial medullary thyroid carcinoma) by causing a covalent Ret dimerization, leading to ligand-independent activation of its tyrosine kinase.	Cysteine	47-50	ret proto-oncogene	Homo sapiens	137-142
11564857-2	2001	Instead, gain-of-function Cys mutations (e.g., Cys(609), Cys(620), and Cys(634)) of the same gene are responsible for thyroid carcinoma (MEN2A/familial medullary thyroid carcinoma) by causing a covalent Ret dimerization, leading to ligand-independent activation of its tyrosine kinase.	Cysteine	47-50	ret proto-oncogene	Homo sapiens	137-142
11564857-6	2001	Instead, we demonstrate that like the wild-type Ret, the Cys(634) Ret variant can trigger antiapoptotic pathways only in response to GDNF.	Cysteine	57-60	ret proto-oncogene	Homo sapiens	66-69
11564857-7	2001	In contrast, Cys(609) or Cys(620) mutations, which impair the terminal Ret glycosylation required for its insertion at the plasma membrane, abrogate GDNF-induced cell rescue.	Cysteine	13-16	ret proto-oncogene	Homo sapiens	71-74
11564857-7	2001	In contrast, Cys(609) or Cys(620) mutations, which impair the terminal Ret glycosylation required for its insertion at the plasma membrane, abrogate GDNF-induced cell rescue.	Cysteine	25-28	ret proto-oncogene	Homo sapiens	71-74
11445581-0	2001	Molecular modeling of the extracellular domain of the RET receptor tyrosine kinase reveals multiple cadherin-like domains and a calcium-binding site.	Calcium	128-135	ret proto-oncogene	Homo sapiens	54-57
11445581-0	2001	Molecular modeling of the extracellular domain of the RET receptor tyrosine kinase reveals multiple cadherin-like domains and a calcium-binding site.	Calcium	128-135	ret proto-oncogene	Homo sapiens	58-82
11520496-2	2001	In this study, we examined the expression of the phosphorylation state of tyrosine residue 1062 (Tyr-1062) of Ret in the spinal cords of amyotrophic lateral sclerosis (ALS), using the phosphorylation state specific antibody at Tyr-1062 of Ret.	Tyrosine	74-82	ret proto-oncogene	Homo sapiens	239-242
11520496-2	2001	In this study, we examined the expression of the phosphorylation state of tyrosine residue 1062 (Tyr-1062) of Ret in the spinal cords of amyotrophic lateral sclerosis (ALS), using the phosphorylation state specific antibody at Tyr-1062 of Ret.	Tyrosine	97-100	ret proto-oncogene	Homo sapiens	110-113
11520496-2	2001	In this study, we examined the expression of the phosphorylation state of tyrosine residue 1062 (Tyr-1062) of Ret in the spinal cords of amyotrophic lateral sclerosis (ALS), using the phosphorylation state specific antibody at Tyr-1062 of Ret.	Tyrosine	97-100	ret proto-oncogene	Homo sapiens	239-242
11520496-2	2001	In this study, we examined the expression of the phosphorylation state of tyrosine residue 1062 (Tyr-1062) of Ret in the spinal cords of amyotrophic lateral sclerosis (ALS), using the phosphorylation state specific antibody at Tyr-1062 of Ret.	Tyrosine	227-230	ret proto-oncogene	Homo sapiens	110-113
11520496-3	2001	The immunohistochemical study demonstrated that Tyr-1062 of Ret was phosphorylated to variable extents in the surviving motor neurons of all the ALS as well as controls studied.	Tyrosine	48-51	ret proto-oncogene	Homo sapiens	60-63
11520496-4	2001	This is the first report that the phosphorylation of Tyr-1062 occurred in neurons with nononcogenic type of Ret.	Tyrosine	53-56	ret proto-oncogene	Homo sapiens	108-111
11520496-5	2001	The Ret-signaling pathway by Tyr-1062 autophosphorylation is constitutively activated via the phosphatidylinositol 3-kinase and/or mitogen-activated protein kinase cascade for motoneuron survival even in the ALS motor neurons, supporting the view that GDNF is a candidate for therapeutic approach to ALS.	Tyrosine	29-32	ret proto-oncogene	Homo sapiens	4-7
11390647-3	2001	In this report we demonstrate that the docking protein FRS2 is tyrosine phosphorylated by ligand-stimulated and by constitutively activated oncogenic forms of RET.	Tyrosine	63-71	ret proto-oncogene	Homo sapiens	159-162
11418488-0	2001	Stable remission after administration of the receptor tyrosine kinase inhibitor SU5416 in a patient with refractory acute myeloid leukemia.	Semaxinib	80-86	ret proto-oncogene	Homo sapiens	45-69
11418488-1	2001	The small molecule receptor tyrosine kinase (RTK) inhibitor SU5416 targets the vascular endothelial growth factor receptor 2 and the stem cell factor receptor c-kit.	Semaxinib	60-66	ret proto-oncogene	Homo sapiens	19-43
11418488-1	2001	The small molecule receptor tyrosine kinase (RTK) inhibitor SU5416 targets the vascular endothelial growth factor receptor 2 and the stem cell factor receptor c-kit.	Semaxinib	60-66	ret proto-oncogene	Homo sapiens	45-48
11418488-6	2001	This is the first report of a stable remission achieved after administration of the RTK inhibitor SU5416 in a patient with AML relapse.	Semaxinib	98-104	ret proto-oncogene	Homo sapiens	84-87
11579677-5	2001	Thirty-five paraffin-embedded PTC samples from patients without a history of radiation exposure were studied.	Paraffin	12-20	ret proto-oncogene	Homo sapiens	30-33
11390647-4	2001	Complex formation between RET and FRS2 is mediated by binding of the phosphotyrosine-binding domain of FRS2 to pY1062, a residue in RET that also functions as a binding site for Shc.	Phosphotyrosine	69-84	ret proto-oncogene	Homo sapiens	26-29
11390647-4	2001	Complex formation between RET and FRS2 is mediated by binding of the phosphotyrosine-binding domain of FRS2 to pY1062, a residue in RET that also functions as a binding site for Shc.	Phosphotyrosine	69-84	ret proto-oncogene	Homo sapiens	132-135
11390647-6	2001	We demonstrate that oncogenic RET-PTC proteins are associated with FRS2 constitutively, leading to tyrosine phosphorylation of FRS2, MAP kinase stimulation, and cell proliferation.	Tyrosine	99-107	ret proto-oncogene	Homo sapiens	30-33
11491658-0	2001	Osmotic stress-mediated activation of RET kinases involves intracellular disulfide-bonded dimer formation.	Disulfides	73-82	ret proto-oncogene	Homo sapiens	38-41
11491658-2	2001	A few percentage of RET proteins normally formed disulfide-bonded dimers in the cell, and osmotic stress promoted formation of these dimers.	Disulfides	49-58	ret proto-oncogene	Homo sapiens	20-23
11491658-4	2001	Osmotic stress also promoted activation and disulfide-bonded dimerization of the extracellular domain-depleted mutant RET (RET-PTC-1), suggesting that the target amino acid(s) for dimerization is located intracellularly rather than in the cysteine-rich region of the extracellular domain.	Disulfides	44-53	ret proto-oncogene	Homo sapiens	118-121
11491658-4	2001	Osmotic stress also promoted activation and disulfide-bonded dimerization of the extracellular domain-depleted mutant RET (RET-PTC-1), suggesting that the target amino acid(s) for dimerization is located intracellularly rather than in the cysteine-rich region of the extracellular domain.	Disulfides	44-53	ret proto-oncogene	Homo sapiens	123-126
11491658-4	2001	Osmotic stress also promoted activation and disulfide-bonded dimerization of the extracellular domain-depleted mutant RET (RET-PTC-1), suggesting that the target amino acid(s) for dimerization is located intracellularly rather than in the cysteine-rich region of the extracellular domain.	Cysteine	239-247	ret proto-oncogene	Homo sapiens	118-121
11491658-4	2001	Osmotic stress also promoted activation and disulfide-bonded dimerization of the extracellular domain-depleted mutant RET (RET-PTC-1), suggesting that the target amino acid(s) for dimerization is located intracellularly rather than in the cysteine-rich region of the extracellular domain.	Cysteine	239-247	ret proto-oncogene	Homo sapiens	123-126
11491658-5	2001	In the mutant c-RET and RET-PTC-1 in which Cys987 of c-RET or Cys376 of RET-PTC-1 was replaced with Ala, the levels of intrinsic kinase activity were greatly reduced and barely increased in response to osmotic stress.	Alanine	100-103	ret proto-oncogene	Homo sapiens	16-19
11491658-5	2001	In the mutant c-RET and RET-PTC-1 in which Cys987 of c-RET or Cys376 of RET-PTC-1 was replaced with Ala, the levels of intrinsic kinase activity were greatly reduced and barely increased in response to osmotic stress.	Alanine	100-103	ret proto-oncogene	Homo sapiens	24-33
11491658-5	2001	In the mutant c-RET and RET-PTC-1 in which Cys987 of c-RET or Cys376 of RET-PTC-1 was replaced with Ala, the levels of intrinsic kinase activity were greatly reduced and barely increased in response to osmotic stress.	Alanine	100-103	ret proto-oncogene	Homo sapiens	24-27
11302967-8	2001	While HSCR and HSCR/IND showed over representation of a specific RET polymorphism in exon 2, IND exhibited a significantly lower frequency comparable with that of controls.	indole	20-23	ret proto-oncogene	Homo sapiens	65-68
11351254-3	2001	In sporadic MTCs the RET gene is mutated in codon 918, where a methionine is substituted to a threonine (M918T).	Methionine	63-73	ret proto-oncogene	Homo sapiens	21-24
11351254-3	2001	In sporadic MTCs the RET gene is mutated in codon 918, where a methionine is substituted to a threonine (M918T).	Threonine	94-103	ret proto-oncogene	Homo sapiens	21-24
11331212-3	2001	DESIGN: Here we present the only known family with a germline mutation of codon 611 TGC to TTC (exon 10) in the RET proto-oncogene leading to a replacement of cysteine by phenylalanine (Cys611Phe or C611F).	Cysteine	159-167	ret proto-oncogene	Homo sapiens	112-115
11331212-3	2001	DESIGN: Here we present the only known family with a germline mutation of codon 611 TGC to TTC (exon 10) in the RET proto-oncogene leading to a replacement of cysteine by phenylalanine (Cys611Phe or C611F).	Phenylalanine	171-184	ret proto-oncogene	Homo sapiens	112-115
11121408-7	2001	Interestingly, LAR expression significantly decreased the levels of disulfide-linked RET-MEN2A dimerization.	Disulfides	68-77	ret proto-oncogene	Homo sapiens	85-88
11316186-8	2001	A homozygous missense mutation (CGG-to-TGG) at RET codon 969 was identified in this patient, which resulted in an amino acid change from arginine to tryptophan.	Arginine	137-145	ret proto-oncogene	Homo sapiens	47-50
11316186-8	2001	A homozygous missense mutation (CGG-to-TGG) at RET codon 969 was identified in this patient, which resulted in an amino acid change from arginine to tryptophan.	Tryptophan	149-159	ret proto-oncogene	Homo sapiens	47-50
11121408-6	2001	Here we show that LAR reduces the constitutive tyrosine autophosphorylation and kinase activity of RET-MEN2A but not RET-MEN2B, accompanying a significant decrease of phosphorylation of phospholipase Cgamma, AKT, and ERK1/2.	Tyrosine	47-55	ret proto-oncogene	Homo sapiens	99-102
11360177-3	2001	Analyses by site directed-mutagenesis revealed that it binds to tyrosine 1062 in RET that is also known to be a binding site for the SHC adaptor protein.	Tyrosine	64-72	ret proto-oncogene	Homo sapiens	81-84
11360177-6	2001	These results suggest that tyrosine 1062 in RET provides a site for the interaction of multiple signaling molecules and that the balance of SHC and SNT/FRS2 binding may affect the nature of the intracellular signaling for cell proliferation, differentiation and survival induced by activated RET.	Tyrosine	27-35	ret proto-oncogene	Homo sapiens	44-47
11360177-6	2001	These results suggest that tyrosine 1062 in RET provides a site for the interaction of multiple signaling molecules and that the balance of SHC and SNT/FRS2 binding may affect the nature of the intracellular signaling for cell proliferation, differentiation and survival induced by activated RET.	Tyrosine	27-35	ret proto-oncogene	Homo sapiens	292-295
11386462-0	2001	A family of multiple endocrine neoplasia type 2A with the RET proto-oncogene mutation in codon 618 (Cys--&gt;Arg).	Cysteine	100-103	ret proto-oncogene	Homo sapiens	58-61
11386462-0	2001	A family of multiple endocrine neoplasia type 2A with the RET proto-oncogene mutation in codon 618 (Cys--&gt;Arg).	Arginine	109-112	ret proto-oncogene	Homo sapiens	58-61
11386462-3	2001	We report here three generations of one MEN-2 family with rare missense mutation at codon 618 (Cys--&gt;Arg) of the RET proto-oncogene.	Cysteine	95-98	ret proto-oncogene	Homo sapiens	116-119
11386462-3	2001	We report here three generations of one MEN-2 family with rare missense mutation at codon 618 (Cys--&gt;Arg) of the RET proto-oncogene.	Arginine	104-107	ret proto-oncogene	Homo sapiens	116-119
11121408-6	2001	Here we show that LAR reduces the constitutive tyrosine autophosphorylation and kinase activity of RET-MEN2A but not RET-MEN2B, accompanying a significant decrease of phosphorylation of phospholipase Cgamma, AKT, and ERK1/2.	Tyrosine	47-55	ret proto-oncogene	Homo sapiens	103-108
11121408-7	2001	Interestingly, LAR expression significantly decreased the levels of disulfide-linked RET-MEN2A dimerization.	Disulfides	68-77	ret proto-oncogene	Homo sapiens	89-94
11245446-0	2001	Increased in vivo phosphorylation of ret tyrosine 1062 is a potential pathogenetic mechanism of multiple endocrine neoplasia type 2B.	Tyrosine	41-49	ret proto-oncogene	Homo sapiens	37-40
11237712-0	2001	Activation of BMK1 via tyrosine 1062 in RET by GDNF and MEN2A mutation.	Tyrosine	23-31	ret proto-oncogene	Homo sapiens	40-43
11237712-0	2001	Activation of BMK1 via tyrosine 1062 in RET by GDNF and MEN2A mutation.	Tyrosine	23-31	ret proto-oncogene	Homo sapiens	56-61
11237712-5	2001	The level of BMK1 activation markedly decreased by replacement of tyrosine 1062 with phenylalanine (designated Y1062F) in RET, indicating the importance of downstream signaling via tyrosine 1062.	Tyrosine	66-74	ret proto-oncogene	Homo sapiens	122-125
11222636-1	2001	The glial cell line-derived neurotrophic factor (GDNF) family ligands (GFLs), consisting of GDNF, neurturin, persephin, and artemin, signal via a multicomponent complex composed of Ret tyrosine kinase and the glycosyl-phosphatidylinositol (GPI)-anchored coreceptors GFRalpha1-alpha4.	Glycosylphosphatidylinositols	209-238	ret proto-oncogene	Homo sapiens	181-184
11222636-1	2001	The glial cell line-derived neurotrophic factor (GDNF) family ligands (GFLs), consisting of GDNF, neurturin, persephin, and artemin, signal via a multicomponent complex composed of Ret tyrosine kinase and the glycosyl-phosphatidylinositol (GPI)-anchored coreceptors GFRalpha1-alpha4.	Glycosylphosphatidylinositols	240-243	ret proto-oncogene	Homo sapiens	181-184
11245446-2	2001	Although several familial medullary thyroid carcinoma and most MEN2A mutations involve substitutions of extracellular cysteine residues, in most MEN2B cases there is a methionine-to-threonine substitution at position 918 (M918T) of the Ret kinase domain.	Cysteine	118-126	ret proto-oncogene	Homo sapiens	63-68
11245446-7	2001	We show that the Ret-MEN2B mutation causes specific potentiated phosphorylation of tyrosine 1062 (Y1062) compared with Ret-MEN2A.	Tyrosine	83-91	ret proto-oncogene	Homo sapiens	17-20
11245446-7	2001	We show that the Ret-MEN2B mutation causes specific potentiated phosphorylation of tyrosine 1062 (Y1062) compared with Ret-MEN2A.	Tyrosine	83-91	ret proto-oncogene	Homo sapiens	21-26
11314023-12	2001	In the central ret mRNA region encoding the cysteine-rich, transmembrane, and main tyrosine kinase domains, no evidence of alternative splicing was detected.	Cysteine	44-52	ret proto-oncogene	Homo sapiens	15-18
11314023-13	2001	Two alternative splice events were detected in the ret mRNA encoding the C-terminal part of Ret protein harboring tyrosine residues important for Ret signaling, excluding exon 19, or retaining intron 19, respectively.	Tyrosine	114-122	ret proto-oncogene	Homo sapiens	51-54
11314023-13	2001	Two alternative splice events were detected in the ret mRNA encoding the C-terminal part of Ret protein harboring tyrosine residues important for Ret signaling, excluding exon 19, or retaining intron 19, respectively.	Tyrosine	114-122	ret proto-oncogene	Homo sapiens	92-95
11314023-13	2001	Two alternative splice events were detected in the ret mRNA encoding the C-terminal part of Ret protein harboring tyrosine residues important for Ret signaling, excluding exon 19, or retaining intron 19, respectively.	Tyrosine	114-122	ret proto-oncogene	Homo sapiens	146-149
11158032-12	2001	Furthermore, [(123)I]MIBG uptake was significantly higher in unilateral (P = 0.02), benign (P = 0.02), sporadic (P = 0.02), intraadrenal (P = 0.02), and capsular invasive (P = 0.03) PCCs than in bilateral, malignant, MEN2A/2B-related, extraadrenal, and noninvasive PCCs, respectively.	3-Iodobenzylguanidine	21-25	ret proto-oncogene	Homo sapiens	217-222
11338505-3	2001	The familial medullary thyroid carcinoma burdened genealogy shows a new point mutation TCG(Ser)--&gt;GCG(Ala) in codon 891, in the exon 15 of the protooncogene RET.	TMG-chitotriomycin	87-90	ret proto-oncogene	Homo sapiens	160-163
11313948-1	2001	Tyrosine 1062 of Ret, which represents an intracytoplasmic docking site for multiple signaling molecules, is essential for Ret-mediated activation of phosphatidylinositol 3-Kinase (PI3-K).	Tyrosine	0-8	ret proto-oncogene	Homo sapiens	17-20
11313948-1	2001	Tyrosine 1062 of Ret, which represents an intracytoplasmic docking site for multiple signaling molecules, is essential for Ret-mediated activation of phosphatidylinositol 3-Kinase (PI3-K).	Tyrosine	0-8	ret proto-oncogene	Homo sapiens	123-126
11313948-4	2001	Here we show that the Insulin Receptor Substrate-1 (IRS-1) is tyrosine phosphorylated and associated with the p85 regulatory subunit of PI3-K in response to Ret activation.	Tyrosine	62-70	ret proto-oncogene	Homo sapiens	157-160
11313948-6	2001	The association with the PTB domain of IRS-1 depends on the phosphorylation of tyrosine 1062 of Ret.	Tyrosine	79-87	ret proto-oncogene	Homo sapiens	96-99
11313948-7	2001	The deletion of asparagine 1059 (delN1059) and the substitution of leucine 1061 (L1061P), two Ret mutations identified in families affected by congenital megacolon (Hirschsprung"s disease), impair the binding of IRS-1 to Ret as well as Ret-mediated Akt(PKB) stimulation.	Leucine	67-74	ret proto-oncogene	Homo sapiens	94-97
11280716-9	2001	This finding suggests that all families with a pedigree suggestive of FMTC should be regarded at risk from MEN 2A disease, at least when a critical mutation in the RET cysteine domain is detected.	Cysteine	168-176	ret proto-oncogene	Homo sapiens	107-113
11280716-9	2001	This finding suggests that all families with a pedigree suggestive of FMTC should be regarded at risk from MEN 2A disease, at least when a critical mutation in the RET cysteine domain is detected.	Cysteine	168-176	ret proto-oncogene	Homo sapiens	164-167
12182058-6	2001	We also found one deletion/insertion mutation in RET exon 11 that encompasses cysteine codon 634 and has not been published so far.	Cysteine	78-86	ret proto-oncogene	Homo sapiens	49-52
11338505-3	2001	The familial medullary thyroid carcinoma burdened genealogy shows a new point mutation TCG(Ser)--&gt;GCG(Ala) in codon 891, in the exon 15 of the protooncogene RET.	Serine	91-94	ret proto-oncogene	Homo sapiens	160-163
11338505-3	2001	The familial medullary thyroid carcinoma burdened genealogy shows a new point mutation TCG(Ser)--&gt;GCG(Ala) in codon 891, in the exon 15 of the protooncogene RET.	gallocatechin gallate	101-104	ret proto-oncogene	Homo sapiens	160-163
11338505-3	2001	The familial medullary thyroid carcinoma burdened genealogy shows a new point mutation TCG(Ser)--&gt;GCG(Ala) in codon 891, in the exon 15 of the protooncogene RET.	Alanine	105-108	ret proto-oncogene	Homo sapiens	160-163
11338505-10	2001	The mutation results in substitution of cysteine amino acid residue in the cysteine-rich extracellular domain of protein kinase encoded by the gene RET for arginine.	cysteine amino acid	40-59	ret proto-oncogene	Homo sapiens	148-151
11338505-10	2001	The mutation results in substitution of cysteine amino acid residue in the cysteine-rich extracellular domain of protein kinase encoded by the gene RET for arginine.	Cysteine	40-48	ret proto-oncogene	Homo sapiens	148-151
11338505-10	2001	The mutation results in substitution of cysteine amino acid residue in the cysteine-rich extracellular domain of protein kinase encoded by the gene RET for arginine.	Arginine	156-164	ret proto-oncogene	Homo sapiens	148-151
11156407-1	2000	As part of ongoing studies on the RET rearrangement frequency in children with papillary thyroid carcinoma (PTC) after their exposure to radioactive iodine after the Chernobyl reactor accident, new methods for the detection of novel types of RET rearrangements are being developed.	radioactive iodine	137-155	ret proto-oncogene	Homo sapiens	34-37
11289739-4	2000	The RET proto-oncogene is the causative gene of the MEN2 syndromes and mutations in this gene are found in &gt;90% of inherited cases, allowing easier and more reliable family screening than pentagastrin stimulation tests.	Pentagastrin	191-203	ret proto-oncogene	Homo sapiens	4-7
11106404-3	2000	GDNF family ligands first bind to the glycosylphosphatidylinositol (GPI)-anchored GDNF family receptor alpha (GFRalpha) and then the GDNF family ligand-GFRalpha complex binds to and stimulates autophosphorylation of Ret.	Glycosylphosphatidylinositols	68-71	ret proto-oncogene	Homo sapiens	216-219
11023712-5	2000	However the inhibition of receptor tyrosine kinase, protein kinase C and phosphatidylinositol 3-kinase by genistien, chelerythrine and wortmannin, respectively, had no significant effect on aggregation.	genistien	106-115	ret proto-oncogene	Homo sapiens	26-50
11093842-9	2000	Concerning the diagnostic tests, it must be noted the low sensitivity (60%) of vanillylmandelic acid in MEN 2A.	Vanilmandelic Acid	79-100	ret proto-oncogene	Homo sapiens	104-110
11053775-9	2000	Our data also provide evidence that the H(2)O(2)-induced mitogenic response is, in part, mediated through the receptor tyrosine kinase, PDGF receptor.	Hydrogen Peroxide	40-48	ret proto-oncogene	Homo sapiens	110-134
11061555-0	2000	Tyrosines 1015 and 1062 are in vivo autophosphorylation sites in ret and ret-derived oncoproteins.	Tyrosine	0-9	ret proto-oncogene	Homo sapiens	65-68
11061555-0	2000	Tyrosines 1015 and 1062 are in vivo autophosphorylation sites in ret and ret-derived oncoproteins.	Tyrosine	0-9	ret proto-oncogene	Homo sapiens	73-76
11061555-3	2000	Oncogenic mutations cause constitutive activation of the kinase function of RET, which, in turn, results in the autophosphorylation of RET tyrosine residues critical for signaling.	Tyrosine	139-147	ret proto-oncogene	Homo sapiens	76-79
11061555-3	2000	Oncogenic mutations cause constitutive activation of the kinase function of RET, which, in turn, results in the autophosphorylation of RET tyrosine residues critical for signaling.	Tyrosine	139-147	ret proto-oncogene	Homo sapiens	135-138
11061555-5	2000	The aim of the present study was to assess the phosphorylation of two such residues, tyrosines 1015 and 1062 (Y1015 and Y1062), in the in vivo signaling of RET and RET-derived oncogenes.	Tyrosine	85-94	ret proto-oncogene	Homo sapiens	156-159
11061555-5	2000	The aim of the present study was to assess the phosphorylation of two such residues, tyrosines 1015 and 1062 (Y1015 and Y1062), in the in vivo signaling of RET and RET-derived oncogenes.	Tyrosine	85-94	ret proto-oncogene	Homo sapiens	164-167
10918602-0	2000	A novel type of mutation in the cysteine rich domain of the RET receptor causes ligand independent activation.	Cysteine	32-40	ret proto-oncogene	Homo sapiens	60-63
10998441-1	2000	Pheochromocytoma and its extra-adrenal counterpart paraganglioma are rare catecholamine producing tumors which usually occur sporadically but may also be a part of neuroendocrine tumor syndromes such as multiple endocrine neoplasia type 2A (MEN 2A).	Catecholamines	74-87	ret proto-oncogene	Homo sapiens	203-239
11002419-0	2000	Characterization of intracellular signals via tyrosine 1062 in RET activated by glial cell line-derived neurotrophic factor.	Tyrosine	46-54	ret proto-oncogene	Homo sapiens	63-66
11002419-2	2000	Recently, it was shown that tyrosine 1062 in RET represents a binding site for SHC adaptor proteins and is crucial for both RAS/mitogen activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3-K)/AKT signaling pathways.	Tyrosine	28-36	ret proto-oncogene	Homo sapiens	45-48
11002419-4	2000	In response to GDNF stimulation, SHC bound to GAB1 and GRB2 adaptor proteins as well as RET, and SHC and GAB1 were highly phosphorylated on tyrosine.	Tyrosine	140-148	ret proto-oncogene	Homo sapiens	88-91
11002419-5	2000	The complex formation consisting of SHC, GAB1 and GRB2 was almost abolished by replacement of tyrosine 1062 in RET with phenylalanine.	Tyrosine	94-102	ret proto-oncogene	Homo sapiens	111-114
11002419-5	2000	The complex formation consisting of SHC, GAB1 and GRB2 was almost abolished by replacement of tyrosine 1062 in RET with phenylalanine.	Phenylalanine	120-133	ret proto-oncogene	Homo sapiens	111-114
11002419-7	2000	These results suggested that the RAS and PI3-K pathways activated by GDNF bifurcate mainly through SHC bound to tyrosine 1062 in RET.	Tyrosine	112-120	ret proto-oncogene	Homo sapiens	129-132
10943719-4	2000	However, stimulation with both NT3 and GDNF caused tyrosine-phosphorylation of Ret/GDNF-receptor at a level higher than that caused by GDNF alone.	Tyrosine	51-59	ret proto-oncogene	Homo sapiens	79-82
10943719-6	2000	These results suggest that the actions of NT3 and GDNF converge at the Ret/GDNF-receptor to enhance survival of the developing sympathetic neurons through activation of the phosphatidylinositol (PI) 3-kinase/Akt pathway.	Phosphatidylinositols	173-193	ret proto-oncogene	Homo sapiens	71-74
11000521-5	2000	Furthermore, Ret-9bp increased mitogenic and transforming activity demonstrated by thymidine incorporation as well as colony formation in soft agar.	Thymidine	83-92	ret proto-oncogene	Homo sapiens	13-16
11000521-5	2000	Furthermore, Ret-9bp increased mitogenic and transforming activity demonstrated by thymidine incorporation as well as colony formation in soft agar.	Agar	143-147	ret proto-oncogene	Homo sapiens	13-16
10982477-3	2000	In one family with a joint occurrence of HSCR and FMTC (follicular medullary thyroid carcinoma), we have identified a mutation in codon 609 in one out of 6 cysteine residues encoded in exon 10 of the RET gene.	Cysteine	156-164	ret proto-oncogene	Homo sapiens	200-203
10945862-1	2000	Previous studies showed that human airway smooth muscle (HASM) cells treated with lysophosphatidic acid (LPA), a pertussis toxin (PTX)-sensitive G protein-coupled (GPC) mitogen, simultaneously with epidermal growth factor (EGF), a receptor tyrosine kinase (RTK) mitogen, exhibit markedly synergistic stimulation of mitogenesis.	lysophosphatidic acid	82-103	ret proto-oncogene	Homo sapiens	231-255
10945862-1	2000	Previous studies showed that human airway smooth muscle (HASM) cells treated with lysophosphatidic acid (LPA), a pertussis toxin (PTX)-sensitive G protein-coupled (GPC) mitogen, simultaneously with epidermal growth factor (EGF), a receptor tyrosine kinase (RTK) mitogen, exhibit markedly synergistic stimulation of mitogenesis.	lysophosphatidic acid	82-103	ret proto-oncogene	Homo sapiens	257-260
10945862-1	2000	Previous studies showed that human airway smooth muscle (HASM) cells treated with lysophosphatidic acid (LPA), a pertussis toxin (PTX)-sensitive G protein-coupled (GPC) mitogen, simultaneously with epidermal growth factor (EGF), a receptor tyrosine kinase (RTK) mitogen, exhibit markedly synergistic stimulation of mitogenesis.	lysophosphatidic acid	105-108	ret proto-oncogene	Homo sapiens	231-255
10945862-1	2000	Previous studies showed that human airway smooth muscle (HASM) cells treated with lysophosphatidic acid (LPA), a pertussis toxin (PTX)-sensitive G protein-coupled (GPC) mitogen, simultaneously with epidermal growth factor (EGF), a receptor tyrosine kinase (RTK) mitogen, exhibit markedly synergistic stimulation of mitogenesis.	lysophosphatidic acid	105-108	ret proto-oncogene	Homo sapiens	257-260
10945862-2	2000	We now show that the RTK mitogens basic fibroblast growth factor, insulin-like growth factor-1, insulin, platelet-derived growth factor-AA, and platelet-derived growth factor-BB, as well as transforming growth factor-beta, all induced synergistic stimulation of mitogenesis in the presence of LPA.	lysophosphatidic acid	293-296	ret proto-oncogene	Homo sapiens	21-24
10918602-2	2000	Missense mutations in one of six cysteine codons in the extracellular cysteine-rich domain of the RET proto-oncogene predispose to this disease.	Cysteine	33-41	ret proto-oncogene	Homo sapiens	98-101
10918602-2	2000	Missense mutations in one of six cysteine codons in the extracellular cysteine-rich domain of the RET proto-oncogene predispose to this disease.	Cysteine	70-78	ret proto-oncogene	Homo sapiens	98-101
10728700-0	2000	High levels of tyrosine phosphorylated proto-ret in sporadic phenochromocytomas.	Tyrosine	15-23	ret proto-oncogene	Homo sapiens	45-48
10871866-1	2000	Multiple endocrine neoplasia type 2B (MEN 2B) is a familial cancer syndrome, in which the cardinal feature is medullary thyroid carcinoma (MTC), a malignant tumor arising from the calcitonin producing thyroid C-cells.	thyroid c	201-210	ret proto-oncogene	Homo sapiens	0-36
10871866-1	2000	Multiple endocrine neoplasia type 2B (MEN 2B) is a familial cancer syndrome, in which the cardinal feature is medullary thyroid carcinoma (MTC), a malignant tumor arising from the calcitonin producing thyroid C-cells.	thyroid c	201-210	ret proto-oncogene	Homo sapiens	38-44
10871866-2	2000	MEN 2B is associated with a germline point mutation in the RET proto-oncogene, leading to a Met--&gt;Thr substitution at codon 918 in the kinase domain, which alters the substrate specificity of the protein.	Threonine	101-104	ret proto-oncogene	Homo sapiens	0-6
10871866-2	2000	MEN 2B is associated with a germline point mutation in the RET proto-oncogene, leading to a Met--&gt;Thr substitution at codon 918 in the kinase domain, which alters the substrate specificity of the protein.	Threonine	101-104	ret proto-oncogene	Homo sapiens	59-62
10871866-3	2000	We used the human calcitonin gene (CALC-I) promoter to generate transgenic mice expressing either the human RET oncogene with the MEN2B-specific 918 Met--&gt;Thr mutation (CALC-MEN2B-RET) or the human non-mutated RET proto-oncogene (CALC-WT-RET) in the C-cells.	Threonine	158-161	ret proto-oncogene	Homo sapiens	130-135
10822219-0	2000	Somatic trinucleotide change encompassing codons 882 and 883 of the RET proto-oncogene in a patient with sporadic medullary thyroid carcinoma.	trinucleotide	8-21	ret proto-oncogene	Homo sapiens	68-71
10822219-7	2000	RESULTS: A somatic trinucleotide change encompassing codons 882 and 883 of the RET proto-oncogene (GTA GCT to GTT TTT) was documented.	trinucleotide	19-32	ret proto-oncogene	Homo sapiens	79-82
10850426-9	2000	Finally, we show that in a papillary carcinoma-derived cell line expressing the proto-RET receptor and the related GFRalpha2 co-receptor, GDNF treatment induced RET tyrosine phosphorylation and subsequent signal transduction pathway, indicating that RET could be active in thyroid follicular cells.	Tyrosine	165-173	ret proto-oncogene	Homo sapiens	161-164
10850426-9	2000	Finally, we show that in a papillary carcinoma-derived cell line expressing the proto-RET receptor and the related GFRalpha2 co-receptor, GDNF treatment induced RET tyrosine phosphorylation and subsequent signal transduction pathway, indicating that RET could be active in thyroid follicular cells.	Tyrosine	165-173	ret proto-oncogene	Homo sapiens	161-164
10820165-9	2000	Although PAR-1 is a G protein-coupled receptor, its activation in hPTC, as in other cell systems, resulted in a transient increase in cellular levels of tyrosine-phosphorylated proteins.	Tyrosine	153-161	ret proto-oncogene	Homo sapiens	66-70
10820165-11	2000	Interestingly, thrombin-induced DNA synthesis and MCP-1 gene expression were completely blocked by genistein, a specific tyrosine kinase inhibitor, but not by its inactive analogue daidzein, demonstrating a central role for tyrosine kinase activation in the thrombin effects on hPTC.	Genistein	99-108	ret proto-oncogene	Homo sapiens	278-282
10879045-2	2000	Patients with MEN2A have missense mutations at extracellular cysteine rich domain of c-ret, those with MEN2B have missense mutations at tyrosine kinase domain of c-ret, those with HPRCC have missense mutations at tyrosine kinase domain of c-met, and those with FGIST have in-frame deletion mutations at juxtamembrane domain of c-kit.	Cysteine	61-69	ret proto-oncogene	Homo sapiens	14-19
10734107-2	2000	In some systems, GPCRs stimulate tyrosine phosphorylation by inducing the "transactivation" of a receptor tyrosine kinase (RTK).	Tyrosine	33-41	ret proto-oncogene	Homo sapiens	97-121
10734107-2	2000	In some systems, GPCRs stimulate tyrosine phosphorylation by inducing the "transactivation" of a receptor tyrosine kinase (RTK).	Tyrosine	33-41	ret proto-oncogene	Homo sapiens	123-126
10728700-6	2000	They showed RET transcript, protein amounts as well as Ret-associated phosphotyrosine levels similar to those measured in MEN-2A-associated pheochromocytomas.	Phosphotyrosine	70-85	ret proto-oncogene	Homo sapiens	55-58
10812967-3	2000	RET transduces a signal following activation by ligands of the glial cell line-derived neurotrophic factor (GDNF) family of neurotrophins which currently comprises GDNF, neuturin (NTN), artemin (ART) and persephin (PSP).	neuturin	170-178	ret proto-oncogene	Homo sapiens	0-3
10812967-3	2000	RET transduces a signal following activation by ligands of the glial cell line-derived neurotrophic factor (GDNF) family of neurotrophins which currently comprises GDNF, neuturin (NTN), artemin (ART) and persephin (PSP).	ISONICOTINAMIDINE	180-183	ret proto-oncogene	Homo sapiens	0-3
10637293-4	2000	Before UV irradiation, small percentages of c-Ret (3-4%) and Ret-MEN2B (1-2%) and large percentages of Ret-MEN2A (30-40%) were dimerized through disulfide bonds.	Disulfides	145-154	ret proto-oncogene	Homo sapiens	107-112
10812967-3	2000	RET transduces a signal following activation by ligands of the glial cell line-derived neurotrophic factor (GDNF) family of neurotrophins which currently comprises GDNF, neuturin (NTN), artemin (ART) and persephin (PSP).	art	195-198	ret proto-oncogene	Homo sapiens	0-3
10812967-6	2000	Current evidence indicates that signal transduction by RET activates several second messenger systems including the PLC gamma, Ras, JNK and inositol phosphate pathways.	Inositol Phosphates	140-158	ret proto-oncogene	Homo sapiens	55-58
10679286-1	2000	Multiple endocrine neoplasia (MEN) type 2B mutations have been reported at methionine 918 or alanine 883 in the tyrosine kinase domain of the RET proto-oncogene.	Methionine	75-85	ret proto-oncogene	Homo sapiens	142-145
10679286-2	2000	Recently, a new combination of two germline missense mutations at valine 804 and tyrosine 806 was identified in a patient with MEN 2B-like clinical phenotypes including medullary thyroid carcinoma, mucosal neuroma, and marfanoid habitus.	Valine	66-72	ret proto-oncogene	Homo sapiens	127-133
10679286-2	2000	Recently, a new combination of two germline missense mutations at valine 804 and tyrosine 806 was identified in a patient with MEN 2B-like clinical phenotypes including medullary thyroid carcinoma, mucosal neuroma, and marfanoid habitus.	Tyrosine	81-89	ret proto-oncogene	Homo sapiens	127-133
10679286-7	2000	On the other hand, substitution of phenylalanine for tyrosines 864 and 952 drastically diminished the activity of RET with the V804M/Y806C, M918T or A883F mutation, suggesting that these three mutant proteins have similar biological properties.	Phenylalanine	35-48	ret proto-oncogene	Homo sapiens	114-117
10679286-7	2000	On the other hand, substitution of phenylalanine for tyrosines 864 and 952 drastically diminished the activity of RET with the V804M/Y806C, M918T or A883F mutation, suggesting that these three mutant proteins have similar biological properties.	Tyrosine	53-62	ret proto-oncogene	Homo sapiens	114-117
10656690-3	2000	Phosphorylation of the activation loop tyrosines in RTK"s are essential to activation as well as allosteric changes that facilitate substrate interaction and phosphorylation.	Tyrosine	39-48	ret proto-oncogene	Homo sapiens	52-55
11213488-3	2000	We found that small proportions of c-Ret and Ret-MEN2B and a large proportion of MEN2A were dimerized due to disulfide bonds and that high kinase activity resided in these fractions.	Disulfides	109-118	ret proto-oncogene	Homo sapiens	45-48
11213488-3	2000	We found that small proportions of c-Ret and Ret-MEN2B and a large proportion of MEN2A were dimerized due to disulfide bonds and that high kinase activity resided in these fractions.	Disulfides	109-118	ret proto-oncogene	Homo sapiens	49-54
11213488-3	2000	We found that small proportions of c-Ret and Ret-MEN2B and a large proportion of MEN2A were dimerized due to disulfide bonds and that high kinase activity resided in these fractions.	Disulfides	109-118	ret proto-oncogene	Homo sapiens	81-86
11213488-4	2000	The UV-induced activation of c-Ret and superactivation of Ret-MEN2A and Ret-MEN2B were then shown to be closely associated with promotion of the disulfide bond-mediated dimerization of the Ret proteins.	Disulfides	145-154	ret proto-oncogene	Homo sapiens	31-34
11213488-4	2000	The UV-induced activation of c-Ret and superactivation of Ret-MEN2A and Ret-MEN2B were then shown to be closely associated with promotion of the disulfide bond-mediated dimerization of the Ret proteins.	Disulfides	145-154	ret proto-oncogene	Homo sapiens	58-61
11213488-4	2000	The UV-induced activation of c-Ret and superactivation of Ret-MEN2A and Ret-MEN2B were then shown to be closely associated with promotion of the disulfide bond-mediated dimerization of the Ret proteins.	Disulfides	145-154	ret proto-oncogene	Homo sapiens	62-67
11213488-4	2000	The UV-induced activation of c-Ret and superactivation of Ret-MEN2A and Ret-MEN2B were then shown to be closely associated with promotion of the disulfide bond-mediated dimerization of the Ret proteins.	Disulfides	145-154	ret proto-oncogene	Homo sapiens	58-61
11213488-4	2000	The UV-induced activation of c-Ret and superactivation of Ret-MEN2A and Ret-MEN2B were then shown to be closely associated with promotion of the disulfide bond-mediated dimerization of the Ret proteins.	Disulfides	145-154	ret proto-oncogene	Homo sapiens	76-81
11213488-4	2000	The UV-induced activation of c-Ret and superactivation of Ret-MEN2A and Ret-MEN2B were then shown to be closely associated with promotion of the disulfide bond-mediated dimerization of the Ret proteins.	Disulfides	145-154	ret proto-oncogene	Homo sapiens	58-61
11213488-8	2000	Most importantly, the levels of basal kinase activity and dimerization of Ret-TPC-1-C376A, in which cysteine 376 in the tyrosine kinase domain of Ret-TPC-1 was replaced with alanine, were low and were not increased by UV irradiation.	Alanine	174-181	ret proto-oncogene	Homo sapiens	74-77
11213488-9	2000	These results suggest that the cysteine at this position works as the primary target of dimerization of Ret proteins inside the cell for both the maintenance of the basal kinase activity and its promotion by UV, possibly in co-operation with the cysteine(s) in the extracellular domain of Ret-MEN2A and Rfp-Ret, which is the target of dimerization and polymerization outside the cell.	Cysteine	31-39	ret proto-oncogene	Homo sapiens	104-107
11213488-9	2000	These results suggest that the cysteine at this position works as the primary target of dimerization of Ret proteins inside the cell for both the maintenance of the basal kinase activity and its promotion by UV, possibly in co-operation with the cysteine(s) in the extracellular domain of Ret-MEN2A and Rfp-Ret, which is the target of dimerization and polymerization outside the cell.	Cysteine	31-39	ret proto-oncogene	Homo sapiens	289-292
11213488-9	2000	These results suggest that the cysteine at this position works as the primary target of dimerization of Ret proteins inside the cell for both the maintenance of the basal kinase activity and its promotion by UV, possibly in co-operation with the cysteine(s) in the extracellular domain of Ret-MEN2A and Rfp-Ret, which is the target of dimerization and polymerization outside the cell.	Cysteine	31-39	ret proto-oncogene	Homo sapiens	293-298
11213488-9	2000	These results suggest that the cysteine at this position works as the primary target of dimerization of Ret proteins inside the cell for both the maintenance of the basal kinase activity and its promotion by UV, possibly in co-operation with the cysteine(s) in the extracellular domain of Ret-MEN2A and Rfp-Ret, which is the target of dimerization and polymerization outside the cell.	Cysteine	31-39	ret proto-oncogene	Homo sapiens	289-292
11213488-9	2000	These results suggest that the cysteine at this position works as the primary target of dimerization of Ret proteins inside the cell for both the maintenance of the basal kinase activity and its promotion by UV, possibly in co-operation with the cysteine(s) in the extracellular domain of Ret-MEN2A and Rfp-Ret, which is the target of dimerization and polymerization outside the cell.	Cysteine	246-254	ret proto-oncogene	Homo sapiens	104-107
11213488-9	2000	These results suggest that the cysteine at this position works as the primary target of dimerization of Ret proteins inside the cell for both the maintenance of the basal kinase activity and its promotion by UV, possibly in co-operation with the cysteine(s) in the extracellular domain of Ret-MEN2A and Rfp-Ret, which is the target of dimerization and polymerization outside the cell.	Cysteine	246-254	ret proto-oncogene	Homo sapiens	289-292
11213488-9	2000	These results suggest that the cysteine at this position works as the primary target of dimerization of Ret proteins inside the cell for both the maintenance of the basal kinase activity and its promotion by UV, possibly in co-operation with the cysteine(s) in the extracellular domain of Ret-MEN2A and Rfp-Ret, which is the target of dimerization and polymerization outside the cell.	Cysteine	246-254	ret proto-oncogene	Homo sapiens	293-298
11213488-9	2000	These results suggest that the cysteine at this position works as the primary target of dimerization of Ret proteins inside the cell for both the maintenance of the basal kinase activity and its promotion by UV, possibly in co-operation with the cysteine(s) in the extracellular domain of Ret-MEN2A and Rfp-Ret, which is the target of dimerization and polymerization outside the cell.	Cysteine	246-254	ret proto-oncogene	Homo sapiens	289-292
10637293-6	2000	We found that UV irradiation promotes the disulfide bond-mediated dimerization of the Ret proteins, in close association with activation and superactivation of Ret kinases.	Disulfides	42-51	ret proto-oncogene	Homo sapiens	86-89
10637293-6	2000	We found that UV irradiation promotes the disulfide bond-mediated dimerization of the Ret proteins, in close association with activation and superactivation of Ret kinases.	Disulfides	42-51	ret proto-oncogene	Homo sapiens	160-163
10637293-8	2000	Interestingly, the levels of basic kinase activity and dimerization of Ret-PTC-1-C376A, in which cysteine 376 in the tyrosine kinase domain of Ret-PTC-1 was replaced by alanine, were low and were not increased by UV irradiation.	Alanine	169-176	ret proto-oncogene	Homo sapiens	71-80
10637293-9	2000	These results suggest that Ret-PTC-1 cysteine 376 is one of possibly multiple critical target amino acids of UV for Ret kinase activation.	Cysteine	37-45	ret proto-oncogene	Homo sapiens	27-36
10637293-9	2000	These results suggest that Ret-PTC-1 cysteine 376 is one of possibly multiple critical target amino acids of UV for Ret kinase activation.	Cysteine	37-45	ret proto-oncogene	Homo sapiens	27-30
10774729-1	2000	The GDNF family ligands (GFLs: GDNF, neurturin, persephin, and artemin) signal through RET and a gly-cosyl-phosphatidylinositol (GPI)-anchored coreceptor (GFRalpha1-alpha4) that binds ligand with high affinity and provides specificity.	artemin	63-70	ret proto-oncogene	Homo sapiens	87-90
10774729-3	2000	Here, we report that GPI-anchored GFRalpha1 recruits RET to lipid rafts after GDNF stimulation and results in RET/Src association.	Glycosylphosphatidylinositols	21-24	ret proto-oncogene	Homo sapiens	53-56
10774729-3	2000	Here, we report that GPI-anchored GFRalpha1 recruits RET to lipid rafts after GDNF stimulation and results in RET/Src association.	Glycosylphosphatidylinositols	21-24	ret proto-oncogene	Homo sapiens	110-113
10637293-5	2000	These dimerized Ret proteins were preferentially autophosphorylated, suggesting a close relation between up-regulated kinase activity and disulfide bond-mediated dimerization of Ret proteins.	Disulfides	138-147	ret proto-oncogene	Homo sapiens	16-19
10637293-5	2000	These dimerized Ret proteins were preferentially autophosphorylated, suggesting a close relation between up-regulated kinase activity and disulfide bond-mediated dimerization of Ret proteins.	Disulfides	138-147	ret proto-oncogene	Homo sapiens	178-181
10731788-9	2000	RESULTS: Seven out of nine patients had a mutation on codon 634 of exon 11 of RET (TGC-CGC), leading to cysteine arginine substitution in the codified protein; all gene carriers had biochemical markers of MTC/CCH and four of Pheo.	cysteine arginine	104-121	ret proto-oncogene	Homo sapiens	78-81
10731788-9	2000	RESULTS: Seven out of nine patients had a mutation on codon 634 of exon 11 of RET (TGC-CGC), leading to cysteine arginine substitution in the codified protein; all gene carriers had biochemical markers of MTC/CCH and four of Pheo.	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	209-212	ret proto-oncogene	Homo sapiens	78-81
10731788-12	2000	CONCLUSIONS: Phenotypic penetration of RET mutation was 100% for MTC/CCH, but only 57% of the gene carriers had Pheo.	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	69-72	ret proto-oncogene	Homo sapiens	39-42
10583708-17	1999	The indication from the good correlation between bone-Mg and %Ret and a marked decrease in %Ret in patients after Mg medication was that one can really measure magnesium deficiency.	Magnesium	160-169	ret proto-oncogene	Homo sapiens	62-65
10583708-17	1999	The indication from the good correlation between bone-Mg and %Ret and a marked decrease in %Ret in patients after Mg medication was that one can really measure magnesium deficiency.	Magnesium	160-169	ret proto-oncogene	Homo sapiens	92-95
10628190-4	1999	In 95% of MEN2A families and 85% of FMTC families, the germ-line missense mutations underlying the disease affect one of the five cysteine codons of the extracellular domain of the RET proto-oncogene.	Cysteine	130-138	ret proto-oncogene	Homo sapiens	10-15
10628190-4	1999	In 95% of MEN2A families and 85% of FMTC families, the germ-line missense mutations underlying the disease affect one of the five cysteine codons of the extracellular domain of the RET proto-oncogene.	Cysteine	130-138	ret proto-oncogene	Homo sapiens	181-184
10465268-0	1999	The role of amino acids surrounding tyrosine 1062 in ret in specific binding of the shc phosphotyrosine-binding domain.	Tyrosine	36-44	ret proto-oncogene	Homo sapiens	53-56
10484767-6	1999	A tyrosine residue at position 1062 is an intracytoplasmic docking site that enables RET to recruit several signalling molecules, including the Shc adaptor protein.	Tyrosine	2-10	ret proto-oncogene	Homo sapiens	85-88
10549772-4	1999	RESULTS: Direct sequence DNA analysis of the RET proto-oncogene showed a heterozygosity for a G to C transition at the second nucleotide of codon 620 (exon 10) in the patients, resulting in the replacement of cysteine by a serine residue in the affected Ret protein.	Cysteine	209-217	ret proto-oncogene	Homo sapiens	45-48
10549772-4	1999	RESULTS: Direct sequence DNA analysis of the RET proto-oncogene showed a heterozygosity for a G to C transition at the second nucleotide of codon 620 (exon 10) in the patients, resulting in the replacement of cysteine by a serine residue in the affected Ret protein.	Cysteine	209-217	ret proto-oncogene	Homo sapiens	254-257
10549772-4	1999	RESULTS: Direct sequence DNA analysis of the RET proto-oncogene showed a heterozygosity for a G to C transition at the second nucleotide of codon 620 (exon 10) in the patients, resulting in the replacement of cysteine by a serine residue in the affected Ret protein.	Serine	223-229	ret proto-oncogene	Homo sapiens	45-48
10484798-2	1999	Genetic testing in 2 children from one kindred revealed a mutation in exon 10, codon 618 (TGC to AGC) in the extracellular cysteine-rich region of the RET gene.	Cysteine	123-131	ret proto-oncogene	Homo sapiens	151-154
10465268-0	1999	The role of amino acids surrounding tyrosine 1062 in ret in specific binding of the shc phosphotyrosine-binding domain.	Phosphotyrosine	88-103	ret proto-oncogene	Homo sapiens	53-56
10465268-1	1999	We investigated the role of the I-E-N-K-L (amino acids 1057-1061) sequence amino-terminal to Tyr1062 in Ret for binding of the Shc phosphotyrosine-binding (PTB) domain.	Phosphotyrosine	131-146	ret proto-oncogene	Homo sapiens	104-107
10448070-2	1999	Tyrosine phosphorylation of Grb2-associated binder-1 (Gab1) and activation of phosphatidylinositol 3-kinase (PI 3-kinase) were induced at higher levels by GDNF stimulation or the MEN 2B mutation than by the MEN 2A mutation.	Tyrosine	0-8	ret proto-oncogene	Homo sapiens	179-185
10490816-0	1999	The Glu632-Leu633 deletion in cysteine rich domain of Ret induces constitutive dimerization and alters the processing of the receptor protein.	Cysteine	30-38	ret proto-oncogene	Homo sapiens	54-57
10490816-9	1999	Like other Cys point mutations, this 6 bp deletion affecting two amino acid residues between two adjacent Cys, is capable of activating the transforming ability of Ret by promoting receptor dimerization.	Cysteine	11-14	ret proto-oncogene	Homo sapiens	164-167
10490816-9	1999	Like other Cys point mutations, this 6 bp deletion affecting two amino acid residues between two adjacent Cys, is capable of activating the transforming ability of Ret by promoting receptor dimerization.	Cysteine	106-109	ret proto-oncogene	Homo sapiens	164-167
10448070-2	1999	Tyrosine phosphorylation of Grb2-associated binder-1 (Gab1) and activation of phosphatidylinositol 3-kinase (PI 3-kinase) were induced at higher levels by GDNF stimulation or the MEN 2B mutation than by the MEN 2A mutation.	Tyrosine	0-8	ret proto-oncogene	Homo sapiens	207-213
10380889-8	1999	These findings provide a model for the role of RET/PTC1 in the formation of abnormal follicles with reduced iodide uptake ability observed in human papillary thyroid carcinoma.	Iodides	108-114	ret proto-oncogene	Homo sapiens	47-50
10445755-2	1999	Based on the hypothesis that arsenic sensitizes cells to mitogenic stimulation by affecting the receptor tyrosine kinase (RTK) signal transduction pathway, these studies first examined the response of fibroblasts to specific mitogens using a defined media system.	Arsenic	29-36	ret proto-oncogene	Homo sapiens	96-120
10445755-2	1999	Based on the hypothesis that arsenic sensitizes cells to mitogenic stimulation by affecting the receptor tyrosine kinase (RTK) signal transduction pathway, these studies first examined the response of fibroblasts to specific mitogens using a defined media system.	Arsenic	29-36	ret proto-oncogene	Homo sapiens	122-125
10445755-3	1999	In both rodent and human fibroblasts, DNA synthesis was found to be stimulated in cells exposed to a transient, sub-lethal concentration of sodium arsenite followed by stimulation with known RTK pathway activators.	sodium arsenite	140-155	ret proto-oncogene	Homo sapiens	191-194
10445755-4	1999	This effect is observed for up to 32 h after removal of arsenic, suggesting that the RTK pathway is affected in a sustained manner.	Arsenic	56-63	ret proto-oncogene	Homo sapiens	85-88
10442282-5	1999	DNA sequence analysis of peripheral white blood cells revealed that codon 634 in exon 11 of the RET gene was mutated from TGC (Cys) to TAC (Tyr).	Cysteine	127-130	ret proto-oncogene	Homo sapiens	96-99
10442282-5	1999	DNA sequence analysis of peripheral white blood cells revealed that codon 634 in exon 11 of the RET gene was mutated from TGC (Cys) to TAC (Tyr).	Tyrosine	140-143	ret proto-oncogene	Homo sapiens	96-99
10233362-5	1999	Consistent with this observation, when THP-1 monocytic and HL-60 promyelocytic leukaemia cells expressing Ret were differentiated toward macrophages or granulocytes by treatment of 12-O-tetradecanoylphorbol-13-acetate (TPA) or all-trans retinoic acid (RA), Ret expression strikingly decreased during differentiation.	Tretinoin	237-250	ret proto-oncogene	Homo sapiens	106-109
10414402-5	1999	Measurement of Ptc,O2 underestimated arterial oxygen tension (Pa,O2) and this underestimation increased with the level of Pa,O2 (p&lt;0.01).	Oxygen	46-52	ret proto-oncogene	Homo sapiens	15-18
10414402-5	1999	Measurement of Ptc,O2 underestimated arterial oxygen tension (Pa,O2) and this underestimation increased with the level of Pa,O2 (p&lt;0.01).	Protactinium	62-64	ret proto-oncogene	Homo sapiens	15-18
10414402-5	1999	Measurement of Ptc,O2 underestimated arterial oxygen tension (Pa,O2) and this underestimation increased with the level of Pa,O2 (p&lt;0.01).	Oxygen	65-67	ret proto-oncogene	Homo sapiens	15-18
10414402-5	1999	Measurement of Ptc,O2 underestimated arterial oxygen tension (Pa,O2) and this underestimation increased with the level of Pa,O2 (p&lt;0.01).	Protactinium	122-124	ret proto-oncogene	Homo sapiens	15-18
10414402-5	1999	Measurement of Ptc,O2 underestimated arterial oxygen tension (Pa,O2) and this underestimation increased with the level of Pa,O2 (p&lt;0.01).	Oxygen	65-67	ret proto-oncogene	Homo sapiens	15-18
10233362-5	1999	Consistent with this observation, when THP-1 monocytic and HL-60 promyelocytic leukaemia cells expressing Ret were differentiated toward macrophages or granulocytes by treatment of 12-O-tetradecanoylphorbol-13-acetate (TPA) or all-trans retinoic acid (RA), Ret expression strikingly decreased during differentiation.	Tetradecanoylphorbol Acetate	181-217	ret proto-oncogene	Homo sapiens	106-109
10414402-6	1999	Measurements of Ptc,CO2 overestimated arterial carbon dioxide tension (Pa,CO2) and this overestimation increased with the level of Pa,CO2 (p&lt;0.05).	Carbon Dioxide	47-61	ret proto-oncogene	Homo sapiens	16-19
10323403-8	1999	This new mutation creates an additional cysteine residue in the extracellular cysteine-rich domain of RET.	Cysteine	40-48	ret proto-oncogene	Homo sapiens	102-105
10323403-8	1999	This new mutation creates an additional cysteine residue in the extracellular cysteine-rich domain of RET.	Cysteine	78-86	ret proto-oncogene	Homo sapiens	102-105
10233362-5	1999	Consistent with this observation, when THP-1 monocytic and HL-60 promyelocytic leukaemia cells expressing Ret were differentiated toward macrophages or granulocytes by treatment of 12-O-tetradecanoylphorbol-13-acetate (TPA) or all-trans retinoic acid (RA), Ret expression strikingly decreased during differentiation.	Tetradecanoylphorbol Acetate	219-222	ret proto-oncogene	Homo sapiens	106-109
10233362-5	1999	Consistent with this observation, when THP-1 monocytic and HL-60 promyelocytic leukaemia cells expressing Ret were differentiated toward macrophages or granulocytes by treatment of 12-O-tetradecanoylphorbol-13-acetate (TPA) or all-trans retinoic acid (RA), Ret expression strikingly decreased during differentiation.	Tretinoin	252-254	ret proto-oncogene	Homo sapiens	106-109
10091505-7	1999	We found a ret exon 11 codon 634 mutation, that resulted in the change of TGC to TAC, a cysteine-tyrosine amino acid exchange.	Cysteine	88-96	ret proto-oncogene	Homo sapiens	11-14
10070972-8	1999	Furthermore, we show that Ret is able to associate with the SH2 domain of Src in a phosphotyrosine-dependent fashion.	Phosphotyrosine	83-98	ret proto-oncogene	Homo sapiens	26-29
10208419-0	1999	Rho-dependent and -independent tyrosine phosphorylation of focal adhesion kinase, paxillin and p130Cas mediated by Ret kinase.	Tyrosine	31-39	ret proto-oncogene	Homo sapiens	115-118
10208419-8	1999	These results suggested the presence of Rho-dependent and -independent signaling pathways downstream of PI-3" kinase that mediate tyrosine phosphorylation of FAK, paxillin and p130Cas through Ret kinase.	Tyrosine	130-138	ret proto-oncogene	Homo sapiens	192-195
10049754-0	1999	Mechanism of Ret activation by a mutation at aspartic acid 631 identified in sporadic pheochromocytoma.	Aspartic Acid	45-58	ret proto-oncogene	Homo sapiens	13-16
10049754-1	1999	Mutations at aspartic acid 631 in Ret were reported in sporadic pheochromocytoma and medullary thyroid carcinoma.	Aspartic Acid	13-26	ret proto-oncogene	Homo sapiens	34-37
10049754-3	1999	Among them, RET cDNA with a mutation of aspartic acid to tyrosine (D631Y) that was reported in sporadic pheochromocytoma showed high transforming activity.	Aspartic Acid	40-53	ret proto-oncogene	Homo sapiens	12-15
10049754-3	1999	Among them, RET cDNA with a mutation of aspartic acid to tyrosine (D631Y) that was reported in sporadic pheochromocytoma showed high transforming activity.	Tyrosine	57-65	ret proto-oncogene	Homo sapiens	12-15
10049754-4	1999	The D631Y mutation activated Ret by inducing its disulfide-linked dimerization in the transfectant as observed for multiple endocrine neoplasia (MEN) 2A mutations at cysteine 609, 611, 618, 620, 630, or 634.	Disulfides	49-58	ret proto-oncogene	Homo sapiens	29-32
10049754-4	1999	The D631Y mutation activated Ret by inducing its disulfide-linked dimerization in the transfectant as observed for multiple endocrine neoplasia (MEN) 2A mutations at cysteine 609, 611, 618, 620, 630, or 634.	Disulfides	49-58	ret proto-oncogene	Homo sapiens	124-152
10049754-4	1999	The D631Y mutation activated Ret by inducing its disulfide-linked dimerization in the transfectant as observed for multiple endocrine neoplasia (MEN) 2A mutations at cysteine 609, 611, 618, 620, 630, or 634.	Cysteine	166-174	ret proto-oncogene	Homo sapiens	29-32
10049754-4	1999	The D631Y mutation activated Ret by inducing its disulfide-linked dimerization in the transfectant as observed for multiple endocrine neoplasia (MEN) 2A mutations at cysteine 609, 611, 618, 620, 630, or 634.	Cysteine	166-174	ret proto-oncogene	Homo sapiens	124-152
10049754-5	1999	Further mutation analysis suggested that cysteine 630 or 634 could be involved in the disulfide-linked Ret dimerization induced by the D631Y mutation.	Cysteine	41-49	ret proto-oncogene	Homo sapiens	103-106
10049754-5	1999	Further mutation analysis suggested that cysteine 630 or 634 could be involved in the disulfide-linked Ret dimerization induced by the D631Y mutation.	Disulfides	86-95	ret proto-oncogene	Homo sapiens	103-106
10091505-7	1999	We found a ret exon 11 codon 634 mutation, that resulted in the change of TGC to TAC, a cysteine-tyrosine amino acid exchange.	tyrosine amino acid	97-116	ret proto-oncogene	Homo sapiens	11-14
9840920-0	1998	A 5"-CG-3"-rich region in the promoter of the transcriptionally frequently silenced RET protooncogene lacks methylated cytidine residues.	Cytidine	119-127	ret proto-oncogene	Homo sapiens	84-87
9950371-5	1999	Germline missense mutations in one of six cysteine codons (609, 611, 618, and 620 in exon 10, and codons 630 and 634 in exon 11), which encode part of the extracellular cysteine rich domain of RET, have been detected in the majority of these families: 100% of MEN 2A families, 67% of FMTC families, and 54% of families classified as "other".	Cysteine	42-50	ret proto-oncogene	Homo sapiens	193-196
9950371-5	1999	Germline missense mutations in one of six cysteine codons (609, 611, 618, and 620 in exon 10, and codons 630 and 634 in exon 11), which encode part of the extracellular cysteine rich domain of RET, have been detected in the majority of these families: 100% of MEN 2A families, 67% of FMTC families, and 54% of families classified as "other".	Cysteine	42-50	ret proto-oncogene	Homo sapiens	260-266
9950371-5	1999	Germline missense mutations in one of six cysteine codons (609, 611, 618, and 620 in exon 10, and codons 630 and 634 in exon 11), which encode part of the extracellular cysteine rich domain of RET, have been detected in the majority of these families: 100% of MEN 2A families, 67% of FMTC families, and 54% of families classified as "other".	Cysteine	169-177	ret proto-oncogene	Homo sapiens	193-196
9950371-5	1999	Germline missense mutations in one of six cysteine codons (609, 611, 618, and 620 in exon 10, and codons 630 and 634 in exon 11), which encode part of the extracellular cysteine rich domain of RET, have been detected in the majority of these families: 100% of MEN 2A families, 67% of FMTC families, and 54% of families classified as "other".	Cysteine	169-177	ret proto-oncogene	Homo sapiens	260-266
10335266-3	1998	For this purpose, 4-aminoquinazoline derivatives were prepared and evaluated for their ability to inhibit RTK activity and the autophosphorylation of EGF-R.	4-aminoquinazoline	18-36	ret proto-oncogene	Homo sapiens	106-109
10084649-3	1999	A panel of RTK inhibitors (tyrphostins) have been tested and compared for their antiproliferative effects on the hormone-dependent human breast cancer cell line, MCF-7, in vitro.	Tyrphostins	27-38	ret proto-oncogene	Homo sapiens	11-14
10947080-5	1999	The synthetic glucocorticoid dexamethasone was found to reduce RET expression at both mRNA and protein levels.	Dexamethasone	29-42	ret proto-oncogene	Homo sapiens	63-66
9879991-0	1998	Dual effect on the RET receptor of MEN 2 mutations affecting specific extracytoplasmic cysteines.	Cysteine	87-96	ret proto-oncogene	Homo sapiens	19-22
9879991-2	1998	Germline mutations affecting one of five cysteines (Cys609, 611, 618, 620 and 634) located in the juxtamembrane domain of the RET receptor are responsible for the vast majority of two cancer-prone disorders, multiple endocrine neoplasia type 2A (MEN 2A) and familial medullary thyroid carcinoma (FMTC).	Cysteine	41-50	ret proto-oncogene	Homo sapiens	126-129
9879991-2	1998	Germline mutations affecting one of five cysteines (Cys609, 611, 618, 620 and 634) located in the juxtamembrane domain of the RET receptor are responsible for the vast majority of two cancer-prone disorders, multiple endocrine neoplasia type 2A (MEN 2A) and familial medullary thyroid carcinoma (FMTC).	Cysteine	41-50	ret proto-oncogene	Homo sapiens	208-244
9879991-2	1998	Germline mutations affecting one of five cysteines (Cys609, 611, 618, 620 and 634) located in the juxtamembrane domain of the RET receptor are responsible for the vast majority of two cancer-prone disorders, multiple endocrine neoplasia type 2A (MEN 2A) and familial medullary thyroid carcinoma (FMTC).	Cysteine	41-50	ret proto-oncogene	Homo sapiens	246-252
9879991-7	1998	We now report that each mutation induces a constitutive catalytic activity due to the aberrant disulfide homodimerization of RET.	Disulfides	95-104	ret proto-oncogene	Homo sapiens	125-128
9879991-10	1998	These findings provide a molecular basis explaining the range of phenotype engendered by alterations of RET cysteines and suggest a novel mechanism whereby mutations of cysteines 609, 618 and 620 exert both activating and inactivating effects.	Cysteine	108-117	ret proto-oncogene	Homo sapiens	104-107
9879991-10	1998	These findings provide a molecular basis explaining the range of phenotype engendered by alterations of RET cysteines and suggest a novel mechanism whereby mutations of cysteines 609, 618 and 620 exert both activating and inactivating effects.	Cysteine	169-178	ret proto-oncogene	Homo sapiens	104-107
9840920-5	1998	In a DNA segment starting 790 nucleotides upstream of the transcriptional start site of the RET gene, a few 5-mC residues have been identified.	5-methyldeoxycytidine	108-112	ret proto-oncogene	Homo sapiens	92-95
9858681-6	1998	The Lio RTK is expressed preferentially in the adult CX and MB.	[1-PENTADECANOYL-2-DECANOYL-GLYCEROL-3-YL]PHOSPHONYL CHOLINE	4-7	ret proto-oncogene	Homo sapiens	8-11
9748280-6	1998	Purified, recombinant RGSZ1, RET-RGS1, and GAIP each accelerated the hydrolysis of Galphaz-GTP over 400-fold with Km values of approximately 2 nM.	galphaz-gtp	83-94	ret proto-oncogene	Homo sapiens	29-37
9814501-7	1998	A polyclonal antibody to the carboxyterminus of RET was used for immunohistochemistry on paraffin sections.	Paraffin	89-97	ret proto-oncogene	Homo sapiens	48-51
9798915-4	1998	Treatment with 1 microM 2-(4-morpholinyl)-8-phenylchromone (LY294002) or 100 nM wortmannin, two distinct and potent inhibitors of phosphatidylinositol 3-kinase activity, completely inhibited GDNF-induced phosphatidylinositol 3-kinase activation, but did not affect Ret phosphorylation.	2-(4-morpholinyl)-8-phenylchromone	24-58	ret proto-oncogene	Homo sapiens	265-268
9748280-13	1998	RGSZ1, RET-RGS1, and GAIP share a cysteine string sequence, perhaps targeting them to secretory vesicles and allowing them to participate in the proposed control of secretion by Gz.	Cysteine	34-42	ret proto-oncogene	Homo sapiens	7-15
9748280-13	1998	RGSZ1, RET-RGS1, and GAIP share a cysteine string sequence, perhaps targeting them to secretory vesicles and allowing them to participate in the proposed control of secretion by Gz.	gz	178-180	ret proto-oncogene	Homo sapiens	7-15
9768676-11	1998	RET TK messenger ribonucleic acid expression is common in PTCs, using RT-PCR, and cannot be used to infer the presence of specific RET rearrangements or of RET activation.	ribonucleic	17-28	ret proto-oncogene	Homo sapiens	0-3
9794240-3	1998	These mutations were localized to a group of tandem cysteines which are analogous to activating germline mutations observed in human MEN2A and familial MTC (FMTC).	Cysteine	52-61	ret proto-oncogene	Homo sapiens	133-138
9764818-5	1998	In this study, by performing classical inhibition experiments using synthetic phosphopeptides and by site-directed mutagenesis of the putative docking site, we have determined that for Grb2 the latter is provided by the tyrosine 620 of Ret/ptc2 long isoform (corresponding to Tyr 1096 on proto-Ret).	Tyrosine	220-228	ret proto-oncogene	Homo sapiens	236-239
9764818-5	1998	In this study, by performing classical inhibition experiments using synthetic phosphopeptides and by site-directed mutagenesis of the putative docking site, we have determined that for Grb2 the latter is provided by the tyrosine 620 of Ret/ptc2 long isoform (corresponding to Tyr 1096 on proto-Ret).	Tyrosine	220-228	ret proto-oncogene	Homo sapiens	294-297
9764818-5	1998	In this study, by performing classical inhibition experiments using synthetic phosphopeptides and by site-directed mutagenesis of the putative docking site, we have determined that for Grb2 the latter is provided by the tyrosine 620 of Ret/ptc2 long isoform (corresponding to Tyr 1096 on proto-Ret).	Tyrosine	276-279	ret proto-oncogene	Homo sapiens	236-239
9764818-5	1998	In this study, by performing classical inhibition experiments using synthetic phosphopeptides and by site-directed mutagenesis of the putative docking site, we have determined that for Grb2 the latter is provided by the tyrosine 620 of Ret/ptc2 long isoform (corresponding to Tyr 1096 on proto-Ret).	Tyrosine	276-279	ret proto-oncogene	Homo sapiens	294-297
9764818-7	1998	This possibility is supported by the evidence that the mutant Ret/ptc2Y620F long isoform displays a weak coimmunoprecipitation with Grb2 and that this mutant, lacking the docking site for Grb2 but owing all the others phosphotyrosines, surprisingly displays a reduced transforming activity compared to that of the two WTs oncogenes.	Phosphotyrosine	218-234	ret proto-oncogene	Homo sapiens	62-65
9681851-3	1998	Cysteine mutations detected in MEN-2A and FMTC induced disulphide-linked homodimers of Ret on the cell surface, leading to activation of its intrinsic tyrosine kinase.	Cysteine	0-8	ret proto-oncogene	Homo sapiens	31-37
9881906-9	1998	These results indicate that Korean MEN 2A patients have germ-line mutations in the ret protooncogene at the cysteine residues like patients of other races, and the strategy employing direct sequencing to find mutations at "hot spot" and search for ensuing new restriction sites could be a useful approach for the molecular diagnosis of genetic diseases accompanied by mutations in restricted areas of disease genes such as MEN 2.	Cysteine	108-116	ret proto-oncogene	Homo sapiens	35-41
9881906-9	1998	These results indicate that Korean MEN 2A patients have germ-line mutations in the ret protooncogene at the cysteine residues like patients of other races, and the strategy employing direct sequencing to find mutations at "hot spot" and search for ensuing new restriction sites could be a useful approach for the molecular diagnosis of genetic diseases accompanied by mutations in restricted areas of disease genes such as MEN 2.	Cysteine	108-116	ret proto-oncogene	Homo sapiens	83-86
9642119-0	1998	Skin cancer chemopreventive effects of a flavonoid antioxidant silymarin are mediated via impairment of receptor tyrosine kinase signaling and perturbation in cell cycle progression.	Flavonoids	41-50	ret proto-oncogene	Homo sapiens	104-128
9642119-0	1998	Skin cancer chemopreventive effects of a flavonoid antioxidant silymarin are mediated via impairment of receptor tyrosine kinase signaling and perturbation in cell cycle progression.	Silymarin	63-72	ret proto-oncogene	Homo sapiens	104-128
9745455-3	1998	In this report, we describe a new kindred in which the MEN2 and HSCR phenotypes are associated with a single C620S point mutation at one of the cysteine codons of the extracellular domain of the ret protooncogene.	Cysteine	144-152	ret proto-oncogene	Homo sapiens	195-198
9777362-1	1998	A new point mutation, TCG(Ser)--&gt;GCG(Ala) in codon 891, exon 15 of the RET protooncogene was revealed in two patients from a pedigree with familial medullary thyroid carcinoma (FMTC), but not in healthy persons.	TMG-chitotriomycin	22-25	ret proto-oncogene	Homo sapiens	74-77
9777362-1	1998	A new point mutation, TCG(Ser)--&gt;GCG(Ala) in codon 891, exon 15 of the RET protooncogene was revealed in two patients from a pedigree with familial medullary thyroid carcinoma (FMTC), but not in healthy persons.	Serine	26-29	ret proto-oncogene	Homo sapiens	74-77
9777362-1	1998	A new point mutation, TCG(Ser)--&gt;GCG(Ala) in codon 891, exon 15 of the RET protooncogene was revealed in two patients from a pedigree with familial medullary thyroid carcinoma (FMTC), but not in healthy persons.	gallocatechin gallate	36-39	ret proto-oncogene	Homo sapiens	74-77
9777362-1	1998	A new point mutation, TCG(Ser)--&gt;GCG(Ala) in codon 891, exon 15 of the RET protooncogene was revealed in two patients from a pedigree with familial medullary thyroid carcinoma (FMTC), but not in healthy persons.	Alanine	40-43	ret proto-oncogene	Homo sapiens	74-77
9681851-3	1998	Cysteine mutations detected in MEN-2A and FMTC induced disulphide-linked homodimers of Ret on the cell surface, leading to activation of its intrinsic tyrosine kinase.	Cysteine	0-8	ret proto-oncogene	Homo sapiens	87-90
9681851-3	1998	Cysteine mutations detected in MEN-2A and FMTC induced disulphide-linked homodimers of Ret on the cell surface, leading to activation of its intrinsic tyrosine kinase.	disulphide	55-65	ret proto-oncogene	Homo sapiens	31-37
9681851-3	1998	Cysteine mutations detected in MEN-2A and FMTC induced disulphide-linked homodimers of Ret on the cell surface, leading to activation of its intrinsic tyrosine kinase.	disulphide	55-65	ret proto-oncogene	Homo sapiens	87-90
9681851-4	1998	Of these cysteine-mutated proteins, Ret with a codon 634 mutation had the highest transforming activity.	Cysteine	9-17	ret proto-oncogene	Homo sapiens	36-39
9681851-8	1998	In addition, we investigated the role of tyrosines present in the intracellular domain for the transforming activity of the mutant Ret proteins.	Tyrosine	41-50	ret proto-oncogene	Homo sapiens	131-134
9681851-9	1998	As a result, we found that tyrosine 905 is essential for the transforming activity of the MEN-2A-Ret mutant protein whereas tyrosines 864 and 952 are critical for that of the MEN-2B-Ret mutant protein.	Tyrosine	27-35	ret proto-oncogene	Homo sapiens	90-96
9681851-10	1998	Moreover, it turned out that tyrosine 1062 regulates the activity of both MEN-2A-Ret and MEN-2B-Ret and represents a binding site for the Shc adaptor protein.	Tyrosine	29-37	ret proto-oncogene	Homo sapiens	74-80
9681851-10	1998	Moreover, it turned out that tyrosine 1062 regulates the activity of both MEN-2A-Ret and MEN-2B-Ret and represents a binding site for the Shc adaptor protein.	Tyrosine	29-37	ret proto-oncogene	Homo sapiens	81-84
9681851-10	1998	Moreover, it turned out that tyrosine 1062 regulates the activity of both MEN-2A-Ret and MEN-2B-Ret and represents a binding site for the Shc adaptor protein.	Tyrosine	29-37	ret proto-oncogene	Homo sapiens	89-95
9681851-10	1998	Moreover, it turned out that tyrosine 1062 regulates the activity of both MEN-2A-Ret and MEN-2B-Ret and represents a binding site for the Shc adaptor protein.	Tyrosine	29-37	ret proto-oncogene	Homo sapiens	96-99
9681852-1	1998	In a few patients with Hirschsprung disease (HSCR) and no clinical symptoms of multiple endocrine neoplasia type 2 (MEN-2A) or medullary thyroid carcinoma (MTC), missense mutations in the cysteine residues 609 and 620 of the Ret gene have been identified.	Cysteine	188-196	ret proto-oncogene	Homo sapiens	116-122
9681852-1	1998	In a few patients with Hirschsprung disease (HSCR) and no clinical symptoms of multiple endocrine neoplasia type 2 (MEN-2A) or medullary thyroid carcinoma (MTC), missense mutations in the cysteine residues 609 and 620 of the Ret gene have been identified.	Cysteine	188-196	ret proto-oncogene	Homo sapiens	225-228
9681852-2	1998	In several pedigrees with either MEN-2A or familial MTC (FMTC) a documented germline mutation in cysteine 618 or 620 follows the segregation of the disease phenotype.	Cysteine	97-105	ret proto-oncogene	Homo sapiens	33-39
9627110-8	1998	The pathway leading to the activation of JNK by RET is clearly divergent from that leading to the activation of ERK: substitution of the tyrosine 1062 of Ret, the Shc binding site, for phenylalanine abrogates ERK but not JNK activation.	Tyrosine	137-145	ret proto-oncogene	Homo sapiens	48-51
9627110-8	1998	The pathway leading to the activation of JNK by RET is clearly divergent from that leading to the activation of ERK: substitution of the tyrosine 1062 of Ret, the Shc binding site, for phenylalanine abrogates ERK but not JNK activation.	Tyrosine	137-145	ret proto-oncogene	Homo sapiens	154-157
9627110-8	1998	The pathway leading to the activation of JNK by RET is clearly divergent from that leading to the activation of ERK: substitution of the tyrosine 1062 of Ret, the Shc binding site, for phenylalanine abrogates ERK but not JNK activation.	Phenylalanine	185-198	ret proto-oncogene	Homo sapiens	48-51
9627110-8	1998	The pathway leading to the activation of JNK by RET is clearly divergent from that leading to the activation of ERK: substitution of the tyrosine 1062 of Ret, the Shc binding site, for phenylalanine abrogates ERK but not JNK activation.	Phenylalanine	185-198	ret proto-oncogene	Homo sapiens	154-157
9587071-2	1998	Missense RET proto-oncogene mutations of one of cysteine codons in exons 10 and 11 are found in the majority of families with MEN 2A and or familial MTC.	Cysteine	48-56	ret proto-oncogene	Homo sapiens	9-12
9620546-2	1998	In MEN2A mutations affecting cysteine residues in the extracellular domain of the receptor cause constitutive activation of the tyrosine kinase by the formation of disulfide-bonded homodimers.	Cysteine	29-37	ret proto-oncogene	Homo sapiens	3-8
9620546-2	1998	In MEN2A mutations affecting cysteine residues in the extracellular domain of the receptor cause constitutive activation of the tyrosine kinase by the formation of disulfide-bonded homodimers.	Disulfides	164-173	ret proto-oncogene	Homo sapiens	3-8
9571170-3	1998	The inhibition was competitive to ATP and non-competitive to the phosphate acceptor, poly (Glu, Ala, Tyr) 6:3:1 for EGF receptor tyrosine kinase.	Phosphates	65-74	ret proto-oncogene	Homo sapiens	120-144
9571170-3	1998	The inhibition was competitive to ATP and non-competitive to the phosphate acceptor, poly (Glu, Ala, Tyr) 6:3:1 for EGF receptor tyrosine kinase.	poly (glu, ala, tyr) 6	85-107	ret proto-oncogene	Homo sapiens	120-144
9539247-5	1998	METHODS: Ret protein expression was evaluated immunohistochemically in formalin-fixed, paraffin-embedded whole-prostate sections.	Formaldehyde	71-79	ret proto-oncogene	Homo sapiens	9-12
9539247-5	1998	METHODS: Ret protein expression was evaluated immunohistochemically in formalin-fixed, paraffin-embedded whole-prostate sections.	Paraffin	87-95	ret proto-oncogene	Homo sapiens	9-12
9575150-0	1998	Expression of the receptor tyrosine kinase Ret on the plasma membrane is dependent on calcium.	Calcium	86-93	ret proto-oncogene	Homo sapiens	43-46
9575150-3	1998	Here we show that expression of p170(ret) is dependent on calcium.	Calcium	58-65	ret proto-oncogene	Homo sapiens	37-40
9575150-4	1998	Depletion of extracellular calcium completely blocks p170(ret) expression, which is not caused by a decrease in half-life of p170(ret) at the plasma membrane but by a defect in processing of p150(ret) into p170(ret).	Calcium	27-34	ret proto-oncogene	Homo sapiens	58-61
9575150-6	1998	We propose that a relatively high concentration of luminal calcium is necessary for the proper folding of Ret in the endoplasmic reticulum.	Calcium	59-66	ret proto-oncogene	Homo sapiens	106-109
9582017-4	1998	Phosphorylation of these activation loop tyrosines is postulated to be a conserved event required for complete RTK activation.	Tyrosine	41-50	ret proto-oncogene	Homo sapiens	111-114
9587071-2	1998	Missense RET proto-oncogene mutations of one of cysteine codons in exons 10 and 11 are found in the majority of families with MEN 2A and or familial MTC.	Cysteine	48-56	ret proto-oncogene	Homo sapiens	126-132
9617347-5	1998	Germline RET point mutations were found in six of 40 cases (15%), cysteine residues at codon 618 in two, codon 634 in three and valine residue at codon 804 in one, and were newly identified as heritable MTC.	Valine	128-134	ret proto-oncogene	Homo sapiens	9-12
9589057-6	1998	Genetic testing for ret protooncogene mutation revealed a point mutation at codon 634 (Cys--&gt;Arg) in exon 11.	Cysteine	87-90	ret proto-oncogene	Homo sapiens	20-23
9589057-6	1998	Genetic testing for ret protooncogene mutation revealed a point mutation at codon 634 (Cys--&gt;Arg) in exon 11.	Arginine	96-99	ret proto-oncogene	Homo sapiens	20-23
9641892-4	1998	Patients with PTC had no evidence of macroscopic lymph node invasion during surgery and underwent, in addition to the total thyroidectomy, a PCND.	pcnd	141-145	ret proto-oncogene	Homo sapiens	14-17
9528752-7	1998	PDGF and EGF(Ret) stimulation resulted in binding of p85 to tyrosine-phosphorylated proteins and strong Ras activation.	Tyrosine	60-68	ret proto-oncogene	Homo sapiens	13-16
9528800-5	1998	This localization was mediated by association with Enigma via the Ret/ptc2 sequence containing tyrosine 586.	Tyrosine	95-103	ret proto-oncogene	Homo sapiens	66-69
9528800-7	1998	The PTB domain of Shc also interacted with Ret/ptc2 at tyrosine 586, and this association resulted in tyrosine phosphorylation of Shc.	Tyrosine	55-63	ret proto-oncogene	Homo sapiens	43-46
9528800-7	1998	The PTB domain of Shc also interacted with Ret/ptc2 at tyrosine 586, and this association resulted in tyrosine phosphorylation of Shc.	Tyrosine	102-110	ret proto-oncogene	Homo sapiens	43-46
9467954-0	1998	Calcium-dependent Ret activation by GDNF and neurturin.	Calcium	0-7	ret proto-oncogene	Homo sapiens	18-21
10640177-11	1998	The cell line shows a heterozygous sequence variant TGC (cysteine) to TGG (tryptophan) in codon 611 in exon 10 of the RET proto-oncogene.	Cysteine	57-65	ret proto-oncogene	Homo sapiens	118-121
10640177-11	1998	The cell line shows a heterozygous sequence variant TGC (cysteine) to TGG (tryptophan) in codon 611 in exon 10 of the RET proto-oncogene.	GAMMA-GLUTAMYL-S-(1,2-DICARBOXYETHYL)CYSTEINYLGLYCINE	70-73	ret proto-oncogene	Homo sapiens	118-121
10640177-11	1998	The cell line shows a heterozygous sequence variant TGC (cysteine) to TGG (tryptophan) in codon 611 in exon 10 of the RET proto-oncogene.	Tryptophan	75-85	ret proto-oncogene	Homo sapiens	118-121
9467954-6	1998	These findings thus suggested that, in addition to GPI-linked cell surface proteins, Ca2+ ions are components of the signal transducing complex formed by Ret and GDNF protein family.	Glycosylphosphatidylinositols	51-54	ret proto-oncogene	Homo sapiens	154-157
9502784-8	1998	Finally, the C609W HSCR mutation exerts a dual effect on RET since it leads to a decrease of the receptor at the cell surface and converted RET51 into a constitutively activated kinase due to the formation of disulfide-linked homodimers.	Disulfides	209-218	ret proto-oncogene	Homo sapiens	57-60
9502784-8	1998	Finally, the C609W HSCR mutation exerts a dual effect on RET since it leads to a decrease of the receptor at the cell surface and converted RET51 into a constitutively activated kinase due to the formation of disulfide-linked homodimers.	Disulfides	209-218	ret proto-oncogene	Homo sapiens	140-145
9384613-10	1998	MEN 2A families with RET exon 10 Cys mutations had a substantially greater risk of developing HSCR1 than those with the more common RET exon 11 Cys634 or exon 14 c804 mutations (P = 0.0005).	Cysteine	33-36	ret proto-oncogene	Homo sapiens	0-6
9621513-4	1998	Mutations in nucleotide sequences encoding one of three specific cysteine residues in the extracellular domain of the RET protein were found in 33 of the 34 MEN2A patients and in five of the six FMTC patients examined.	Cysteine	65-73	ret proto-oncogene	Homo sapiens	118-121
9621513-4	1998	Mutations in nucleotide sequences encoding one of three specific cysteine residues in the extracellular domain of the RET protein were found in 33 of the 34 MEN2A patients and in five of the six FMTC patients examined.	Cysteine	65-73	ret proto-oncogene	Homo sapiens	157-162
9621513-5	1998	A mutation at codon 918, causing the substitution of threonine for methionine in the tyrosine kinase domain of the protein, was found in germline DNAs of all four patients with MEN2B and in two of the 22 patients with sporadic MTCs; codon 918 was mutated somatically in tumor DNAs from three other sporadic cases.	Threonine	53-62	ret proto-oncogene	Homo sapiens	177-182
9621513-5	1998	A mutation at codon 918, causing the substitution of threonine for methionine in the tyrosine kinase domain of the protein, was found in germline DNAs of all four patients with MEN2B and in two of the 22 patients with sporadic MTCs; codon 918 was mutated somatically in tumor DNAs from three other sporadic cases.	Methionine	67-77	ret proto-oncogene	Homo sapiens	177-182
9442958-0	1998	Iodine-131 MIBG imaging in multiple endocrine neoplasia type 2B.	iodine-131 mibg	0-15	ret proto-oncogene	Homo sapiens	27-63
9384613-10	1998	MEN 2A families with RET exon 10 Cys mutations had a substantially greater risk of developing HSCR1 than those with the more common RET exon 11 Cys634 or exon 14 c804 mutations (P = 0.0005).	Cysteine	33-36	ret proto-oncogene	Homo sapiens	21-24
9384613-10	1998	MEN 2A families with RET exon 10 Cys mutations had a substantially greater risk of developing HSCR1 than those with the more common RET exon 11 Cys634 or exon 14 c804 mutations (P = 0.0005).	Cysteine	33-36	ret proto-oncogene	Homo sapiens	94-99
9384613-11	1998	These findings suggest that expression of HSCR1 in MEN 2A may be peculiar to RET exon 10 Cys mutations .	Cysteine	89-92	ret proto-oncogene	Homo sapiens	42-47
9384613-11	1998	These findings suggest that expression of HSCR1 in MEN 2A may be peculiar to RET exon 10 Cys mutations .	Cysteine	89-92	ret proto-oncogene	Homo sapiens	51-57
9384613-12	1998	However, HSCR1 in MEN 2A is not exclusive to C618R or C620R RET mutations and can occur with other exon 10 Cys amino acid substitutions.	Cysteine	107-110	ret proto-oncogene	Homo sapiens	9-14
9384613-12	1998	However, HSCR1 in MEN 2A is not exclusive to C618R or C620R RET mutations and can occur with other exon 10 Cys amino acid substitutions.	Cysteine	107-110	ret proto-oncogene	Homo sapiens	18-24
9452046-0	1998	Cys 634 mutations in the RET proto-oncogene in Spanish families affected by MEN 2A.	Cysteine	0-3	ret proto-oncogene	Homo sapiens	25-28
9452046-0	1998	Cys 634 mutations in the RET proto-oncogene in Spanish families affected by MEN 2A.	Cysteine	0-3	ret proto-oncogene	Homo sapiens	76-82
9452064-0	1998	Duplication of 9 base pairs in the critical cysteine-rich domain of the RET proto-oncogene causes multiple endocrine neoplasia type 2A.	Cysteine	44-52	ret proto-oncogene	Homo sapiens	72-75
9539934-4	1998	RESULTS: A heterozygote T--&gt;C (Cys--&gt;Arg) mutation at codon 618 in exon 10 of the RET proto-oncogene was identified in 4 family members who had previously been diagnosed with medullary thyroid cancer.	Cysteine	34-37	ret proto-oncogene	Homo sapiens	88-91
9706252-8	1998	A unique mutation of codon 918 in exon 16, ATG --&gt; ACG (methionine to threonine), was found in both MEN 2B affected patients.	acceleratory factor from growth hormone	54-57	ret proto-oncogene	Homo sapiens	103-109
9706252-8	1998	A unique mutation of codon 918 in exon 16, ATG --&gt; ACG (methionine to threonine), was found in both MEN 2B affected patients.	Methionine	59-69	ret proto-oncogene	Homo sapiens	103-109
9706252-8	1998	A unique mutation of codon 918 in exon 16, ATG --&gt; ACG (methionine to threonine), was found in both MEN 2B affected patients.	Threonine	73-82	ret proto-oncogene	Homo sapiens	103-109
10027003-4	1998	MEN2A mutations involve cysteine residues present in the Ret extracellular domain and induce disulfide-linked Ret dimerization on the cell surface.	Cysteine	24-32	ret proto-oncogene	Homo sapiens	0-5
10027003-4	1998	MEN2A mutations involve cysteine residues present in the Ret extracellular domain and induce disulfide-linked Ret dimerization on the cell surface.	Cysteine	24-32	ret proto-oncogene	Homo sapiens	57-60
10027003-4	1998	MEN2A mutations involve cysteine residues present in the Ret extracellular domain and induce disulfide-linked Ret dimerization on the cell surface.	Disulfides	93-102	ret proto-oncogene	Homo sapiens	0-5
10027003-4	1998	MEN2A mutations involve cysteine residues present in the Ret extracellular domain and induce disulfide-linked Ret dimerization on the cell surface.	Disulfides	93-102	ret proto-oncogene	Homo sapiens	57-60
10027003-4	1998	MEN2A mutations involve cysteine residues present in the Ret extracellular domain and induce disulfide-linked Ret dimerization on the cell surface.	Disulfides	93-102	ret proto-oncogene	Homo sapiens	110-113
10027003-8	1998	More interestingly, ret mutations in cysteines 618 and 620 were reported in several families who developed both MEN2A and HSCR.	Cysteine	37-46	ret proto-oncogene	Homo sapiens	20-23
9539934-4	1998	RESULTS: A heterozygote T--&gt;C (Cys--&gt;Arg) mutation at codon 618 in exon 10 of the RET proto-oncogene was identified in 4 family members who had previously been diagnosed with medullary thyroid cancer.	Arginine	43-46	ret proto-oncogene	Homo sapiens	88-91
10027003-8	1998	More interestingly, ret mutations in cysteines 618 and 620 were reported in several families who developed both MEN2A and HSCR.	Cysteine	37-46	ret proto-oncogene	Homo sapiens	112-117
9398735-2	1997	Mutations in one of five cysteine residues in the extracellular domain have been found in over 95% of families with MEN 2A and 88% of families with FMTC.	Cysteine	25-33	ret proto-oncogene	Homo sapiens	116-122
9426223-2	1997	RET expression is enhanced in vitro by several differentiating agents, including retinoic acid (RA), which up-regulates RET expression in neuroblastoma cell lines.	Tretinoin	81-94	ret proto-oncogene	Homo sapiens	0-3
9426223-2	1997	RET expression is enhanced in vitro by several differentiating agents, including retinoic acid (RA), which up-regulates RET expression in neuroblastoma cell lines.	Tretinoin	81-94	ret proto-oncogene	Homo sapiens	120-123
9426223-2	1997	RET expression is enhanced in vitro by several differentiating agents, including retinoic acid (RA), which up-regulates RET expression in neuroblastoma cell lines.	Tretinoin	96-98	ret proto-oncogene	Homo sapiens	0-3
9426223-2	1997	RET expression is enhanced in vitro by several differentiating agents, including retinoic acid (RA), which up-regulates RET expression in neuroblastoma cell lines.	Tretinoin	96-98	ret proto-oncogene	Homo sapiens	120-123
9426223-5	1997	Finally, our functional analysis of a candidate RA response element present in the RET promoter provides new hints for the understanding of the interaction between nuclear receptors and their specific recognition sites.	Tretinoin	48-50	ret proto-oncogene	Homo sapiens	83-86
9398735-3	1997	In MEN 2B patients, a specific mutation at codon 918, substituting a threonine for a methionine, has been found in 95% of cases.	Threonine	69-78	ret proto-oncogene	Homo sapiens	3-9
9398735-3	1997	In MEN 2B patients, a specific mutation at codon 918, substituting a threonine for a methionine, has been found in 95% of cases.	Methionine	85-95	ret proto-oncogene	Homo sapiens	3-9
9393871-2	1997	Germline mutation of a methionine to a threonine within the RET TK domain predisposes to the Multiple Endocrine Neoplasia type 2B (MEN 2B).	Methionine	23-33	ret proto-oncogene	Homo sapiens	60-63
10462620-4	1997	Pentagastrin testing and surgical pathology findings for patients who had thyroidectomies were correlated with RET sequence analysis findings.	Pentagastrin	0-12	ret proto-oncogene	Homo sapiens	111-114
9393871-2	1997	Germline mutation of a methionine to a threonine within the RET TK domain predisposes to the Multiple Endocrine Neoplasia type 2B (MEN 2B).	Methionine	23-33	ret proto-oncogene	Homo sapiens	93-129
9393871-2	1997	Germline mutation of a methionine to a threonine within the RET TK domain predisposes to the Multiple Endocrine Neoplasia type 2B (MEN 2B).	Methionine	23-33	ret proto-oncogene	Homo sapiens	131-137
9393871-2	1997	Germline mutation of a methionine to a threonine within the RET TK domain predisposes to the Multiple Endocrine Neoplasia type 2B (MEN 2B).	Threonine	39-48	ret proto-oncogene	Homo sapiens	60-63
9393871-2	1997	Germline mutation of a methionine to a threonine within the RET TK domain predisposes to the Multiple Endocrine Neoplasia type 2B (MEN 2B).	Threonine	39-48	ret proto-oncogene	Homo sapiens	93-129
9393871-2	1997	Germline mutation of a methionine to a threonine within the RET TK domain predisposes to the Multiple Endocrine Neoplasia type 2B (MEN 2B).	Threonine	39-48	ret proto-oncogene	Homo sapiens	131-137
9393871-3	1997	It has been demonstrated that, unlike c-Ret, the MEN 2B mutated Ret displays constitutive TK activity, tyrosine autophosphorylation and transforms fibroblasts.	Tyrosine	103-111	ret proto-oncogene	Homo sapiens	49-55
9393871-3	1997	It has been demonstrated that, unlike c-Ret, the MEN 2B mutated Ret displays constitutive TK activity, tyrosine autophosphorylation and transforms fibroblasts.	Tyrosine	103-111	ret proto-oncogene	Homo sapiens	64-67
9393871-5	1997	Change in substrate specificity leads to the tyrosine autophosphorylation of MEN 2B Ret on new sites as well as the phosphorylation of several novel downstream targets.	Tyrosine	45-53	ret proto-oncogene	Homo sapiens	77-83
9393871-5	1997	Change in substrate specificity leads to the tyrosine autophosphorylation of MEN 2B Ret on new sites as well as the phosphorylation of several novel downstream targets.	Tyrosine	45-53	ret proto-oncogene	Homo sapiens	84-87
9393871-8	1997	However, in contrast to the activated WT form, expression of the MEN 2B mutated Ret-ptc 2 results in the tyrosine phosphorylation of a panel of proteins which interestingly interact with Crk and Nck.	Tyrosine	105-113	ret proto-oncogene	Homo sapiens	65-71
9393871-8	1997	However, in contrast to the activated WT form, expression of the MEN 2B mutated Ret-ptc 2 results in the tyrosine phosphorylation of a panel of proteins which interestingly interact with Crk and Nck.	Tyrosine	105-113	ret proto-oncogene	Homo sapiens	80-83
9259272-2	1997	GDNF and its receptor complex of c-RET tyrosine kinase and a glycosyl-phosphatidylinositol linked protein GDNFR-alpha are of great interest due to their potential use in the therapy of Parkinson"s and motoneuron diseases.	Glycosylphosphatidylinositols	61-90	ret proto-oncogene	Homo sapiens	35-38
9325171-4	1997	In addition, in neuronal cells, but not in astrocytes, Tat increased the phosphotyrosine content of Shc, a protein involved in signal transduction downstream of receptor tyrosine kinase activation.	Phosphotyrosine	73-88	ret proto-oncogene	Homo sapiens	161-185
9360560-0	1997	Germline dinucleotide mutation in codon 883 of the RET proto-oncogene in multiple endocrine neoplasia type 2B without codon 918 mutation.	Dinucleoside Phosphates	9-21	ret proto-oncogene	Homo sapiens	51-54
9354331-5	1997	Ret-expressing neurons also express the glycosyl-phosphatidyl inositol-linked (GPI-linked) GDNF binding component GDNFR-alpha and retrogradely transport 125I-GDNF, indicating the presence of a biologically active GDNF receptor complex.	Glycosylphosphatidylinositols	40-70	ret proto-oncogene	Homo sapiens	0-3
9230192-0	1997	Biological properties of Ret with cysteine mutations correlate with multiple endocrine neoplasia type 2A, familial medullary thyroid carcinoma, and Hirschsprung"s disease phenotype.	Cysteine	34-42	ret proto-oncogene	Homo sapiens	25-28
9230192-1	1997	We investigated the transforming activity of the ret proto-oncogene with a mutation in cysteine 609, 611, 618, 620, 630, or 634 detected in patients with multiple endocrine neoplasia type 2A (MEN 2A), familial medullary thyroid carcinoma (FMTC), or Hirschsprung"s disease.	Cysteine	87-95	ret proto-oncogene	Homo sapiens	192-198
9230192-0	1997	Biological properties of Ret with cysteine mutations correlate with multiple endocrine neoplasia type 2A, familial medullary thyroid carcinoma, and Hirschsprung"s disease phenotype.	Cysteine	34-42	ret proto-oncogene	Homo sapiens	68-104
9230192-7	1997	These results thus suggest that mutations in cysteine 609, 611, 618, or 620 may have the potential to develop Hirschsprung"s disease in addition to MEN 2A and FMTC.	Cysteine	45-53	ret proto-oncogene	Homo sapiens	148-154
9230192-1	1997	We investigated the transforming activity of the ret proto-oncogene with a mutation in cysteine 609, 611, 618, 620, 630, or 634 detected in patients with multiple endocrine neoplasia type 2A (MEN 2A), familial medullary thyroid carcinoma (FMTC), or Hirschsprung"s disease.	Cysteine	87-95	ret proto-oncogene	Homo sapiens	49-52
9108413-1	1997	The RET proto-oncogene product is a receptor tyrosine kinase representing the signal-transducing molecule of a multisubunit surface receptor complex for the glial cell line-derived neurotrophic factor (GDNF), in which a novel glycosyl-phosphatidylinositol (PI)-linked protein (termed GDNFR-alpha) acts as the ligand-binding component.	Glycosylphosphatidylinositols	226-255	ret proto-oncogene	Homo sapiens	4-7
9262196-3	1997	Ret mRNA is strongly expressed in dopamine neurons and alpha-motor neurons as well as in thalamus, ruber and occluomotor nuclei, the habenular complex, septum, cerebellum, and brain stem nuclei.	Dopamine	34-42	ret proto-oncogene	Homo sapiens	0-3
9262196-6	1997	The presence of Ret protein was confirmed in adult dopamine neurons using immunohistochemistry.	Dopamine	51-59	ret proto-oncogene	Homo sapiens	16-19
9192898-6	1997	Finally, we show that NTN, in the presence of NTNR-alpha, induces tyrosine-phosphorylation of Ret, and that NTN, NTNR-alpha and Ret form a physical complex on the cell surface.	Tyrosine	66-74	ret proto-oncogene	Homo sapiens	94-97
9192898-6	1997	Finally, we show that NTN, in the presence of NTNR-alpha, induces tyrosine-phosphorylation of Ret, and that NTN, NTNR-alpha and Ret form a physical complex on the cell surface.	Tyrosine	66-74	ret proto-oncogene	Homo sapiens	128-131
9160884-7	1997	Sequencing revealed the deletion of nine bases encompassing a key cysteine at codon 634, often altered in MEN 2A.	Cysteine	66-74	ret proto-oncogene	Homo sapiens	106-112
9242375-3	1997	The majority of MEN2A and FMTC mutations are clustered in the extra-cellular cysteine-rich domain and result in constitutive activation of the tyrosine kinase through the formation of disulfide-bonded RET homodimers.	Cysteine	77-85	ret proto-oncogene	Homo sapiens	16-21
9242375-3	1997	The majority of MEN2A and FMTC mutations are clustered in the extra-cellular cysteine-rich domain and result in constitutive activation of the tyrosine kinase through the formation of disulfide-bonded RET homodimers.	Cysteine	77-85	ret proto-oncogene	Homo sapiens	201-204
9242375-3	1997	The majority of MEN2A and FMTC mutations are clustered in the extra-cellular cysteine-rich domain and result in constitutive activation of the tyrosine kinase through the formation of disulfide-bonded RET homodimers.	Disulfides	184-193	ret proto-oncogene	Homo sapiens	16-21
9242375-3	1997	The majority of MEN2A and FMTC mutations are clustered in the extra-cellular cysteine-rich domain and result in constitutive activation of the tyrosine kinase through the formation of disulfide-bonded RET homodimers.	Disulfides	184-193	ret proto-oncogene	Homo sapiens	201-204
9242375-5	1997	Both mutations occur within the catalytic domain of the RET kinase and lead to the substitution of either glutamic acid 768 or valine 804 by an aspartic acid and a leucine respectively.	Glutamic Acid	106-119	ret proto-oncogene	Homo sapiens	56-59
9242375-5	1997	Both mutations occur within the catalytic domain of the RET kinase and lead to the substitution of either glutamic acid 768 or valine 804 by an aspartic acid and a leucine respectively.	Leucine	164-171	ret proto-oncogene	Homo sapiens	56-59
9262059-4	1997	Autopsy did not reveal the cause of death of the stillborn infant, who was also found to be affected with MEN 2A by molecular study of paraffin-embedded tissue.	Paraffin	135-143	ret proto-oncogene	Homo sapiens	106-112
9223675-2	1997	The majority of patients with multiple endocrine neoplasia type 2A (MEN2A) and familial medullary thyroid carcinoma (FMTC) carry germ-line point mutations that result in the substitution of one of five cysteine residues.	Cysteine	202-210	ret proto-oncogene	Homo sapiens	30-66
9223675-2	1997	The majority of patients with multiple endocrine neoplasia type 2A (MEN2A) and familial medullary thyroid carcinoma (FMTC) carry germ-line point mutations that result in the substitution of one of five cysteine residues.	Cysteine	202-210	ret proto-oncogene	Homo sapiens	68-73
9223675-7	1997	Because the new RET alleles described here involve cysteine residues in a region of protein previously associated with FMTC and MEN2A, it is very likely that they represent mutations that predispose to the development of MTC.	Cysteine	51-59	ret proto-oncogene	Homo sapiens	16-19
9223675-7	1997	Because the new RET alleles described here involve cysteine residues in a region of protein previously associated with FMTC and MEN2A, it is very likely that they represent mutations that predispose to the development of MTC.	Cysteine	51-59	ret proto-oncogene	Homo sapiens	128-133
9108413-1	1997	The RET proto-oncogene product is a receptor tyrosine kinase representing the signal-transducing molecule of a multisubunit surface receptor complex for the glial cell line-derived neurotrophic factor (GDNF), in which a novel glycosyl-phosphatidylinositol (PI)-linked protein (termed GDNFR-alpha) acts as the ligand-binding component.	Glycosylphosphatidylinositols	226-255	ret proto-oncogene	Homo sapiens	36-60
9075701-5	1997	However, also when serine and valine, but not leucine or phenylalanine, were inserted in position 918, the RET TK function was activated and induced, especially in the case of the RET(918Ser), immmediate-early response genes.	Serine	19-25	ret proto-oncogene	Homo sapiens	107-110
9150704-0	1997	Molecular analysis of the RET proto-oncogene in patients with sporadic medullary thyroid carcinoma: a novel point mutation in the extracellular cysteine-rich domain.	Cysteine	144-152	ret proto-oncogene	Homo sapiens	26-29
9098026-1	1997	BACKGROUND &amp; AIMS: Glial cell line-derived neurotrophic factor (GDNF) signals through the product of the ret proto-oncogene, which is known to be mutated in Hirschsprung"s disease and other conditions with gut dysmotility.	Adenosine Monophosphate	12-15	ret proto-oncogene	Homo sapiens	109-112
9075701-5	1997	However, also when serine and valine, but not leucine or phenylalanine, were inserted in position 918, the RET TK function was activated and induced, especially in the case of the RET(918Ser), immmediate-early response genes.	Serine	19-25	ret proto-oncogene	Homo sapiens	180-183
9096326-6	1997	Recombinant RET-RGS-d accelerates single turnover hydrolysis of GTP by transducin.	Guanosine Triphosphate	64-67	ret proto-oncogene	Homo sapiens	12-15
9075701-5	1997	However, also when serine and valine, but not leucine or phenylalanine, were inserted in position 918, the RET TK function was activated and induced, especially in the case of the RET(918Ser), immmediate-early response genes.	Valine	30-36	ret proto-oncogene	Homo sapiens	107-110
9075701-5	1997	However, also when serine and valine, but not leucine or phenylalanine, were inserted in position 918, the RET TK function was activated and induced, especially in the case of the RET(918Ser), immmediate-early response genes.	Valine	30-36	ret proto-oncogene	Homo sapiens	180-183
9075701-7	1997	However, only when a threonine residue is present in position 918, does RET efficiently couple with a transforming pathway.	Threonine	21-30	ret proto-oncogene	Homo sapiens	72-75
9097963-0	1997	A duplication of 12 bp in the critical cysteine rich domain of the RET proto-oncogene results in a distinct phenotype of multiple endocrine neoplasia type 2A.	Cysteine	39-47	ret proto-oncogene	Homo sapiens	67-70
9097963-0	1997	A duplication of 12 bp in the critical cysteine rich domain of the RET proto-oncogene results in a distinct phenotype of multiple endocrine neoplasia type 2A.	Cysteine	39-47	ret proto-oncogene	Homo sapiens	121-157
9097963-6	1997	Genetic analysis revealed the presence of an unusual heterozygous mutation in exon 11 of the RET proto-oncogene representing a duplication of 12 bp resulting in the insertion of four amino acids between codon 634 (Cys) and 635 (Arg), thus creating an additional cysteine residue.	Cysteine	214-217	ret proto-oncogene	Homo sapiens	93-96
9097963-6	1997	Genetic analysis revealed the presence of an unusual heterozygous mutation in exon 11 of the RET proto-oncogene representing a duplication of 12 bp resulting in the insertion of four amino acids between codon 634 (Cys) and 635 (Arg), thus creating an additional cysteine residue.	Arginine	228-231	ret proto-oncogene	Homo sapiens	93-96
9097963-6	1997	Genetic analysis revealed the presence of an unusual heterozygous mutation in exon 11 of the RET proto-oncogene representing a duplication of 12 bp resulting in the insertion of four amino acids between codon 634 (Cys) and 635 (Arg), thus creating an additional cysteine residue.	Cysteine	262-270	ret proto-oncogene	Homo sapiens	93-96
9096326-8	1997	The N-terminal half of RET-RGS1 contains a putative transmembrane domain and a string of nine cysteines that are potential substrates for multiple palmitoylation.	Cysteine	94-103	ret proto-oncogene	Homo sapiens	23-31
9121763-0	1997	Cell scattering of SK-N-MC neuroepithelioma cells in response to Ret and FGF receptor tyrosine kinase activation is correlated with sustained ERK2 activation.	sk-n-mc	19-26	ret proto-oncogene	Homo sapiens	65-68
9096393-5	1997	The majority of MEN2A and FMTC mutations are located in the extracellular domain and cause the replacement of one of five juxtamembrane cysteines by a different amino acid.	Cysteine	136-145	ret proto-oncogene	Homo sapiens	16-21
9111993-1	1997	Germ-line mutations of the RET proto-oncogene, involving five cysteine residues at codons 609, 611, 618, 620 and 634, are associated with two variants of the inherited cancer syndrome multiple endocrine neoplasia type 2: type 2A and familial medullary thyroid carcinoma.	Cysteine	62-70	ret proto-oncogene	Homo sapiens	27-30
9047384-5	1997	Moreover, our analysis has identified the Ret tyrosine residue and the Shc domains involved in the interaction.	Tyrosine	46-54	ret proto-oncogene	Homo sapiens	42-45
9047384-6	1997	In fact, here we show that both the phosphotyrosine binding domains of Shc, PTB and SH2, interact with Ret/ptc2 in vitro.	Phosphotyrosine	36-51	ret proto-oncogene	Homo sapiens	103-106
9047384-9	1997	In keeping with this finding, by using RET/PTC2-Y586F mutant, we have demonstrated that this tyrosine residue, the last amino acid but one before the divergence of the two Ret isoforms, is the docking site for Shc.	Tyrosine	93-101	ret proto-oncogene	Homo sapiens	39-42
9047384-9	1997	In keeping with this finding, by using RET/PTC2-Y586F mutant, we have demonstrated that this tyrosine residue, the last amino acid but one before the divergence of the two Ret isoforms, is the docking site for Shc.	Tyrosine	93-101	ret proto-oncogene	Homo sapiens	172-175
9012462-0	1997	The different RET-activating capability of mutations of cysteine 620 or cysteine 634 correlates with the multiple endocrine neoplasia type 2 disease phenotype.	Cysteine	56-64	ret proto-oncogene	Homo sapiens	14-17
9012462-0	1997	The different RET-activating capability of mutations of cysteine 620 or cysteine 634 correlates with the multiple endocrine neoplasia type 2 disease phenotype.	Cysteine	72-80	ret proto-oncogene	Homo sapiens	14-17
9012462-3	1997	The mutations associated with MEN2A and FMTC affect one of five cysteine residues mapping in the extracellular domain of the Ret protein.	Cysteine	64-72	ret proto-oncogene	Homo sapiens	30-35
9012462-3	1997	The mutations associated with MEN2A and FMTC affect one of five cysteine residues mapping in the extracellular domain of the Ret protein.	Cysteine	64-72	ret proto-oncogene	Homo sapiens	125-128
9012462-5	1997	Mutations of Cys-634 are more frequent in families with MEN2A, whereas Cys-620 mutations are very rarely found in MEN2A patients and, in contrast, are frequently found in FMTC patients.	Cysteine	13-16	ret proto-oncogene	Homo sapiens	56-61
9012462-6	1997	We have reported previously that mutations of Cys-634 constitutively activate the RET transforming potential by causing a disulfide bridge-mediated homodimerization.	Cysteine	46-49	ret proto-oncogene	Homo sapiens	82-85
9012462-6	1997	We have reported previously that mutations of Cys-634 constitutively activate the RET transforming potential by causing a disulfide bridge-mediated homodimerization.	Disulfides	122-131	ret proto-oncogene	Homo sapiens	82-85
9012462-7	1997	Here, we report that the mutation Cys-620 --&gt; Tyr is able to cause a constitutive dimerization of Ret, with consequent activation of its kinase and transforming activities, to a lower extent than mutation of Cys-634.	Cysteine	34-37	ret proto-oncogene	Homo sapiens	101-104
9012462-7	1997	Here, we report that the mutation Cys-620 --&gt; Tyr is able to cause a constitutive dimerization of Ret, with consequent activation of its kinase and transforming activities, to a lower extent than mutation of Cys-634.	Tyrosine	49-52	ret proto-oncogene	Homo sapiens	101-104
9012462-7	1997	Here, we report that the mutation Cys-620 --&gt; Tyr is able to cause a constitutive dimerization of Ret, with consequent activation of its kinase and transforming activities, to a lower extent than mutation of Cys-634.	Cysteine	211-214	ret proto-oncogene	Homo sapiens	101-104
9024637-4	1997	Besides activation by a specific ligand, a newly defined RTK function involves signal integration of a variety of stimuli, including calcium-dependent responses in neuronal cells, activation of G-protein-coupled receptors or cellular stress such as UV irradiation.	Calcium	133-140	ret proto-oncogene	Homo sapiens	57-60
9035202-6	1997	Both missense mutations and gene rearrangements act in a dominant fashion, and cause constitutive phosphorylation on the tyrosine of RET and highly enhance RET kinase activity, leading to transforming or oncogenic activity.	Tyrosine	121-129	ret proto-oncogene	Homo sapiens	133-136
9086571-0	1997	False-positive results of basal and pentagastrin-stimulated calcitonin in non-gene carriers of multiple endocrine neoplasia type 2A.	Pentagastrin	36-48	ret proto-oncogene	Homo sapiens	95-131
9086571-2	1997	The aim of this study was to assess the specificity of basal and pentagastrin stimulated calcitonin levels in 3 family members with MEN 2A.	Pentagastrin	65-77	ret proto-oncogene	Homo sapiens	132-138
9018112-4	1997	In this study, we have introduced a MEN 2A mutation (Cys634--&gt;Arg) and the unique MEN 2B mutation (Met918--&gt;Thr) in two RET isoforms of 1114 and 1072 amino acids which differ in the carboxy-terminus part.	Arginine	65-68	ret proto-oncogene	Homo sapiens	126-129
9018112-4	1997	In this study, we have introduced a MEN 2A mutation (Cys634--&gt;Arg) and the unique MEN 2B mutation (Met918--&gt;Thr) in two RET isoforms of 1114 and 1072 amino acids which differ in the carboxy-terminus part.	Threonine	114-117	ret proto-oncogene	Homo sapiens	85-91
9018112-4	1997	In this study, we have introduced a MEN 2A mutation (Cys634--&gt;Arg) and the unique MEN 2B mutation (Met918--&gt;Thr) in two RET isoforms of 1114 and 1072 amino acids which differ in the carboxy-terminus part.	Threonine	114-117	ret proto-oncogene	Homo sapiens	126-129
9167949-8	1997	Missense mutations affecting conserved cysteine codons adjacent to the transmembrane domain of the RET proto-oncogene have been identified in the germline DNA of patients with MEN-2A and FMTC.	Cysteine	39-47	ret proto-oncogene	Homo sapiens	99-102
9167949-8	1997	Missense mutations affecting conserved cysteine codons adjacent to the transmembrane domain of the RET proto-oncogene have been identified in the germline DNA of patients with MEN-2A and FMTC.	Cysteine	39-47	ret proto-oncogene	Homo sapiens	176-182
9035202-6	1997	Both missense mutations and gene rearrangements act in a dominant fashion, and cause constitutive phosphorylation on the tyrosine of RET and highly enhance RET kinase activity, leading to transforming or oncogenic activity.	Tyrosine	121-129	ret proto-oncogene	Homo sapiens	156-159
8957089-4	1996	RET is affected by germ line and somatic mutations in MEN2A, MEN2B tumor syndromes and in the abnormal developmental Hirschsprung disease, whereas mutations of NTRK1 have been reported very recently in patients with congenital insensitivity to pain with anidrosis (CIPA).	3-(2-carboxyindol-3-yl)propionic acid	265-269	ret proto-oncogene	Homo sapiens	0-3
9003111-12	1996	CONCLUSION: In FMTC families with cysteine codon mutations of the RET proto-oncogene, screening for other endocrinopathies is mandatory, since these may not be MTC-only families.	Cysteine	34-42	ret proto-oncogene	Homo sapiens	66-69
8663426-0	1996	A mutation at tyrosine 1062 in MEN2A-Ret and MEN2B-Ret impairs their transforming activity and association with shc adaptor proteins.	Tyrosine	14-22	ret proto-oncogene	Homo sapiens	31-40
9012117-3	1996	The most frequent hereditary mutation found in MEN 2A and FMTC groups is substitution of thymine for cytosine in position 2095 of the transmembranous domain of the Ret-tyrosine kinase gene.	Thymine	89-96	ret proto-oncogene	Homo sapiens	47-53
9012117-3	1996	The most frequent hereditary mutation found in MEN 2A and FMTC groups is substitution of thymine for cytosine in position 2095 of the transmembranous domain of the Ret-tyrosine kinase gene.	Thymine	89-96	ret proto-oncogene	Homo sapiens	164-167
9012117-3	1996	The most frequent hereditary mutation found in MEN 2A and FMTC groups is substitution of thymine for cytosine in position 2095 of the transmembranous domain of the Ret-tyrosine kinase gene.	Cytosine	101-109	ret proto-oncogene	Homo sapiens	47-53
9012117-3	1996	The most frequent hereditary mutation found in MEN 2A and FMTC groups is substitution of thymine for cytosine in position 2095 of the transmembranous domain of the Ret-tyrosine kinase gene.	Cytosine	101-109	ret proto-oncogene	Homo sapiens	164-167
8917360-4	1996	Sequencing of PCR amplified DNA revealed the deletion of nine bases encompassing a key cysteine codon at position 1831-3, often altered in MEN 2A.	Cysteine	87-95	ret proto-oncogene	Homo sapiens	139-145
8880581-4	1996	The mutational spectrum of MEN 2B is remarkably narrow, with over 95% of cases being caused by a single methionine to threonine substitution in the intracellular tyrosine kinase domain.	Methionine	104-114	ret proto-oncogene	Homo sapiens	27-33
8880581-4	1996	The mutational spectrum of MEN 2B is remarkably narrow, with over 95% of cases being caused by a single methionine to threonine substitution in the intracellular tyrosine kinase domain.	Threonine	118-127	ret proto-oncogene	Homo sapiens	27-33
8884827-5	1996	A codon 918 germ line mutation, which converts a highly conserved methionine to a threonine in the intracellular tyrosine kinase portion of this receptor of RET, has been identified in 95% of patients with MEN 2B.	Methionine	66-76	ret proto-oncogene	Homo sapiens	157-160
8884827-5	1996	A codon 918 germ line mutation, which converts a highly conserved methionine to a threonine in the intracellular tyrosine kinase portion of this receptor of RET, has been identified in 95% of patients with MEN 2B.	Methionine	66-76	ret proto-oncogene	Homo sapiens	206-212
8884827-5	1996	A codon 918 germ line mutation, which converts a highly conserved methionine to a threonine in the intracellular tyrosine kinase portion of this receptor of RET, has been identified in 95% of patients with MEN 2B.	Threonine	82-91	ret proto-oncogene	Homo sapiens	157-160
8884827-5	1996	A codon 918 germ line mutation, which converts a highly conserved methionine to a threonine in the intracellular tyrosine kinase portion of this receptor of RET, has been identified in 95% of patients with MEN 2B.	Threonine	82-91	ret proto-oncogene	Homo sapiens	206-212
8751579-6	1996	RESULTS: The TT: delta Raf-1:ER cells treated with beta-estradiol underwent marked biochemical and morphologic changes, including cell rounding, increase in calcitonin transcription, loss of RET proto-oncogene expression, and cessation of cell growth.	Estradiol	51-65	ret proto-oncogene	Homo sapiens	191-194
8909322-4	1996	RESULTS: One of these kindred"s carried both Hirschsprung"s disease and MEN 2A in conjunction with a cysteine-to-arginine substitution of codon 620 of the RET gene.	Cysteine	101-109	ret proto-oncogene	Homo sapiens	72-78
8909322-4	1996	RESULTS: One of these kindred"s carried both Hirschsprung"s disease and MEN 2A in conjunction with a cysteine-to-arginine substitution of codon 620 of the RET gene.	Cysteine	101-109	ret proto-oncogene	Homo sapiens	155-158
8909322-4	1996	RESULTS: One of these kindred"s carried both Hirschsprung"s disease and MEN 2A in conjunction with a cysteine-to-arginine substitution of codon 620 of the RET gene.	Arginine	113-121	ret proto-oncogene	Homo sapiens	155-158
8855235-2	1996	This report demonstrates that the glial cell line-derived neurotrophic factor (GDNF) activates RET, as measured by tyrosine phosphorylation of the intracellular catalytic domain.	Tyrosine	115-123	ret proto-oncogene	Homo sapiens	95-98
8765374-4	1996	Ten different types of mutations were identified in the MEN 2A/FMTC families (620 Cys--&gt;Arg, 618 Cys--&gt;Ser, Gly, 611 Cys--&gt;Tyr; 634 Cys--&gt;Arg, Tyr, Trp, Phe, Ser, Gly) and all 6 MEN 2B families had a 918 Met--&gt;Thr point mutation.	Cysteine	82-85	ret proto-oncogene	Homo sapiens	56-62
8765374-4	1996	Ten different types of mutations were identified in the MEN 2A/FMTC families (620 Cys--&gt;Arg, 618 Cys--&gt;Ser, Gly, 611 Cys--&gt;Tyr; 634 Cys--&gt;Arg, Tyr, Trp, Phe, Ser, Gly) and all 6 MEN 2B families had a 918 Met--&gt;Thr point mutation.	Arginine	91-94	ret proto-oncogene	Homo sapiens	56-62
8765374-4	1996	Ten different types of mutations were identified in the MEN 2A/FMTC families (620 Cys--&gt;Arg, 618 Cys--&gt;Ser, Gly, 611 Cys--&gt;Tyr; 634 Cys--&gt;Arg, Tyr, Trp, Phe, Ser, Gly) and all 6 MEN 2B families had a 918 Met--&gt;Thr point mutation.	Cysteine	100-103	ret proto-oncogene	Homo sapiens	56-62
8765374-4	1996	Ten different types of mutations were identified in the MEN 2A/FMTC families (620 Cys--&gt;Arg, 618 Cys--&gt;Ser, Gly, 611 Cys--&gt;Tyr; 634 Cys--&gt;Arg, Tyr, Trp, Phe, Ser, Gly) and all 6 MEN 2B families had a 918 Met--&gt;Thr point mutation.	Serine	109-112	ret proto-oncogene	Homo sapiens	56-62
8765374-4	1996	Ten different types of mutations were identified in the MEN 2A/FMTC families (620 Cys--&gt;Arg, 618 Cys--&gt;Ser, Gly, 611 Cys--&gt;Tyr; 634 Cys--&gt;Arg, Tyr, Trp, Phe, Ser, Gly) and all 6 MEN 2B families had a 918 Met--&gt;Thr point mutation.	Glycine	114-117	ret proto-oncogene	Homo sapiens	56-62
8765374-4	1996	Ten different types of mutations were identified in the MEN 2A/FMTC families (620 Cys--&gt;Arg, 618 Cys--&gt;Ser, Gly, 611 Cys--&gt;Tyr; 634 Cys--&gt;Arg, Tyr, Trp, Phe, Ser, Gly) and all 6 MEN 2B families had a 918 Met--&gt;Thr point mutation.	Cysteine	100-103	ret proto-oncogene	Homo sapiens	56-62
8765374-4	1996	Ten different types of mutations were identified in the MEN 2A/FMTC families (620 Cys--&gt;Arg, 618 Cys--&gt;Ser, Gly, 611 Cys--&gt;Tyr; 634 Cys--&gt;Arg, Tyr, Trp, Phe, Ser, Gly) and all 6 MEN 2B families had a 918 Met--&gt;Thr point mutation.	Tyrosine	132-135	ret proto-oncogene	Homo sapiens	56-62
8765374-4	1996	Ten different types of mutations were identified in the MEN 2A/FMTC families (620 Cys--&gt;Arg, 618 Cys--&gt;Ser, Gly, 611 Cys--&gt;Tyr; 634 Cys--&gt;Arg, Tyr, Trp, Phe, Ser, Gly) and all 6 MEN 2B families had a 918 Met--&gt;Thr point mutation.	Cysteine	100-103	ret proto-oncogene	Homo sapiens	56-62
8663426-3	1996	In the present study we investigated the role of tyrosine residues present in the carboxyl-terminal sequence for the transforming activity of Ret with the MEN 2A or MEN 2B mutation (MEN2A-Ret or MEN2B-Ret).	Tyrosine	49-57	ret proto-oncogene	Homo sapiens	182-191
8663426-5	1996	The Shc adaptor proteins bound to the MEN2A-Ret and MEN2B-Ret proteins and were phosphorylated on tyrosine in the transfectants.	Tyrosine	98-106	ret proto-oncogene	Homo sapiens	38-47
8663426-5	1996	The Shc adaptor proteins bound to the MEN2A-Ret and MEN2B-Ret proteins and were phosphorylated on tyrosine in the transfectants.	Tyrosine	98-106	ret proto-oncogene	Homo sapiens	52-57
8663426-5	1996	The Shc adaptor proteins bound to the MEN2A-Ret and MEN2B-Ret proteins and were phosphorylated on tyrosine in the transfectants.	Tyrosine	98-106	ret proto-oncogene	Homo sapiens	44-47
8663426-7	1996	In addition, phosphopeptide analysis of MEN2A-Ret demonstrated that tyrosine 1062 represents an autophosphorylation site of the mutant Ret proteins.	Tyrosine	68-76	ret proto-oncogene	Homo sapiens	40-45
8663426-7	1996	In addition, phosphopeptide analysis of MEN2A-Ret demonstrated that tyrosine 1062 represents an autophosphorylation site of the mutant Ret proteins.	Tyrosine	68-76	ret proto-oncogene	Homo sapiens	46-49
8663426-7	1996	In addition, phosphopeptide analysis of MEN2A-Ret demonstrated that tyrosine 1062 represents an autophosphorylation site of the mutant Ret proteins.	Tyrosine	68-76	ret proto-oncogene	Homo sapiens	135-138
8663426-0	1996	A mutation at tyrosine 1062 in MEN2A-Ret and MEN2B-Ret impairs their transforming activity and association with shc adaptor proteins.	Tyrosine	14-22	ret proto-oncogene	Homo sapiens	45-50
8663426-0	1996	A mutation at tyrosine 1062 in MEN2A-Ret and MEN2B-Ret impairs their transforming activity and association with shc adaptor proteins.	Tyrosine	14-22	ret proto-oncogene	Homo sapiens	37-40
8663426-3	1996	In the present study we investigated the role of tyrosine residues present in the carboxyl-terminal sequence for the transforming activity of Ret with the MEN 2A or MEN 2B mutation (MEN2A-Ret or MEN2B-Ret).	Tyrosine	49-57	ret proto-oncogene	Homo sapiens	142-145
8654369-7	1996	The HSCR972 (Arg972--&gt;Gly) mutation, mapping in the intracytoplasmic region of RET, impaired its tyrosine kinase activity, while two extracellular mutations, HSCR32 (Ser32--&gt;Leu) and HSCR393 (Phe393--&gt;Leu), inhibited the biological activity of RET by impairing the correct maturation of the RET protein and its transport to the cell surface.	Glycine	25-28	ret proto-oncogene	Homo sapiens	82-85
8657309-4	1996	We further demonstrate that GDNF promotes the formation of a physical complex between GDNFR-alpha and the orphan tyrosin kinase receptor Ret, thereby inducing its tyrosine phosphorylation.	Tyrosine	163-171	ret proto-oncogene	Homo sapiens	137-140
8752835-5	1996	We have carried out linkage analysis in seven families with cutaneous amyloidosis using four dinucleotide repeat markers from the RET region.	Dinucleoside Phosphates	93-105	ret proto-oncogene	Homo sapiens	130-133
8657281-3	1996	Here we show that GDNF binds to, and induces tyrosine phosphorylation of, the product of the c-ret proto-oncogene, an orphan receptor tyrosine kinase, in a GDNF-responsive motor-neuron cell line.	Tyrosine	45-53	ret proto-oncogene	Homo sapiens	95-98
8663233-11	1996	A peptide corresponding to the carboxyl-terminal 20 amino acids of Ret dissociated Enigma and Ret complexes, while a mutant that changed Asn-Lys-Leu-Tyr in the peptide to Ala-Lys-Leu-Ala or a peptide corresponding to exon16 of InsR failed to disrupt the complexes, indicating the Asn-Lys-Leu-Tyr sequence of Ret is essential to the recognition motif for LIM2 of Enigma.	Asparagine	137-140	ret proto-oncogene	Homo sapiens	67-70
8663233-11	1996	A peptide corresponding to the carboxyl-terminal 20 amino acids of Ret dissociated Enigma and Ret complexes, while a mutant that changed Asn-Lys-Leu-Tyr in the peptide to Ala-Lys-Leu-Ala or a peptide corresponding to exon16 of InsR failed to disrupt the complexes, indicating the Asn-Lys-Leu-Tyr sequence of Ret is essential to the recognition motif for LIM2 of Enigma.	Lys-Leu-Tyr	141-152	ret proto-oncogene	Homo sapiens	67-70
8663233-11	1996	A peptide corresponding to the carboxyl-terminal 20 amino acids of Ret dissociated Enigma and Ret complexes, while a mutant that changed Asn-Lys-Leu-Tyr in the peptide to Ala-Lys-Leu-Ala or a peptide corresponding to exon16 of InsR failed to disrupt the complexes, indicating the Asn-Lys-Leu-Tyr sequence of Ret is essential to the recognition motif for LIM2 of Enigma.	Alanine	171-174	ret proto-oncogene	Homo sapiens	67-70
8663233-11	1996	A peptide corresponding to the carboxyl-terminal 20 amino acids of Ret dissociated Enigma and Ret complexes, while a mutant that changed Asn-Lys-Leu-Tyr in the peptide to Ala-Lys-Leu-Ala or a peptide corresponding to exon16 of InsR failed to disrupt the complexes, indicating the Asn-Lys-Leu-Tyr sequence of Ret is essential to the recognition motif for LIM2 of Enigma.	Lys-Leu-Ala	175-186	ret proto-oncogene	Homo sapiens	67-70
8663233-11	1996	A peptide corresponding to the carboxyl-terminal 20 amino acids of Ret dissociated Enigma and Ret complexes, while a mutant that changed Asn-Lys-Leu-Tyr in the peptide to Ala-Lys-Leu-Ala or a peptide corresponding to exon16 of InsR failed to disrupt the complexes, indicating the Asn-Lys-Leu-Tyr sequence of Ret is essential to the recognition motif for LIM2 of Enigma.	Asparagine	280-283	ret proto-oncogene	Homo sapiens	67-70
8663233-11	1996	A peptide corresponding to the carboxyl-terminal 20 amino acids of Ret dissociated Enigma and Ret complexes, while a mutant that changed Asn-Lys-Leu-Tyr in the peptide to Ala-Lys-Leu-Ala or a peptide corresponding to exon16 of InsR failed to disrupt the complexes, indicating the Asn-Lys-Leu-Tyr sequence of Ret is essential to the recognition motif for LIM2 of Enigma.	Lysine	141-144	ret proto-oncogene	Homo sapiens	67-70
8663233-11	1996	A peptide corresponding to the carboxyl-terminal 20 amino acids of Ret dissociated Enigma and Ret complexes, while a mutant that changed Asn-Lys-Leu-Tyr in the peptide to Ala-Lys-Leu-Ala or a peptide corresponding to exon16 of InsR failed to disrupt the complexes, indicating the Asn-Lys-Leu-Tyr sequence of Ret is essential to the recognition motif for LIM2 of Enigma.	Leucine	145-148	ret proto-oncogene	Homo sapiens	67-70
8663233-11	1996	A peptide corresponding to the carboxyl-terminal 20 amino acids of Ret dissociated Enigma and Ret complexes, while a mutant that changed Asn-Lys-Leu-Tyr in the peptide to Ala-Lys-Leu-Ala or a peptide corresponding to exon16 of InsR failed to disrupt the complexes, indicating the Asn-Lys-Leu-Tyr sequence of Ret is essential to the recognition motif for LIM2 of Enigma.	Tyrosine	149-152	ret proto-oncogene	Homo sapiens	67-70
8675603-8	1996	In this study, we report on a novel kindred with MEN 2A and HSCR phenotype associated with a point mutation (C618R) in one of the cysteine codons at the extracellular domain of the RET proto-oncogene.	Cysteine	130-138	ret proto-oncogene	Homo sapiens	49-55
8675603-8	1996	In this study, we report on a novel kindred with MEN 2A and HSCR phenotype associated with a point mutation (C618R) in one of the cysteine codons at the extracellular domain of the RET proto-oncogene.	Cysteine	130-138	ret proto-oncogene	Homo sapiens	181-184
8740514-0	1996	Ret and trk proto-oncogene activation in thyroid papillary carcinomas in French patients from the Champagne-Ardenne region.	champagne-ardenne	98-115	ret proto-oncogene	Homo sapiens	0-3
8783101-6	1996	The DNA sequence of the PCR products from clinically established MEN 2A patients showed a mutation at codon 634 (TGC--&gt;CGC) that resulted in an amino acid change from cysteine to arginine.	Cysteine	170-178	ret proto-oncogene	Homo sapiens	65-71
8662982-2	1996	Mitogenic activity of Ret/ptc2 required dimerization via the N terminus of RI and a tyrosine residue located C-terminal to the kinase core of Ret, Tyr-586 (Durick, K., Yao, V. J., Borrello, M. G., Bongarzone, I., Pierotti, M. A. and Taylor, S. S. (1995) J. Biol.	Tyrosine	84-92	ret proto-oncogene	Homo sapiens	22-25
8662982-2	1996	Mitogenic activity of Ret/ptc2 required dimerization via the N terminus of RI and a tyrosine residue located C-terminal to the kinase core of Ret, Tyr-586 (Durick, K., Yao, V. J., Borrello, M. G., Bongarzone, I., Pierotti, M. A. and Taylor, S. S. (1995) J. Biol.	Tyrosine	147-150	ret proto-oncogene	Homo sapiens	22-25
8662982-2	1996	Mitogenic activity of Ret/ptc2 required dimerization via the N terminus of RI and a tyrosine residue located C-terminal to the kinase core of Ret, Tyr-586 (Durick, K., Yao, V. J., Borrello, M. G., Bongarzone, I., Pierotti, M. A. and Taylor, S. S. (1995) J. Biol.	bongarzone	197-207	ret proto-oncogene	Homo sapiens	22-25
8662982-12	1996	Although the association with Enigma required Tyr-586 of Ret/ptc2, the interaction was phosphorylation-independent.	Tyrosine	46-49	ret proto-oncogene	Homo sapiens	57-60
8783101-6	1996	The DNA sequence of the PCR products from clinically established MEN 2A patients showed a mutation at codon 634 (TGC--&gt;CGC) that resulted in an amino acid change from cysteine to arginine.	Arginine	182-190	ret proto-oncogene	Homo sapiens	65-71
8662982-13	1996	In contrast to the SH2 interactions, disruption of the interaction with Enigma abolished Ret/ptc2 mitogenic signaling, suggesting that LIM domain recognition of an unphosphorylated tyrosine-based motif is required for Ret signal transduction.	Tyrosine	181-189	ret proto-oncogene	Homo sapiens	89-92
8662982-13	1996	In contrast to the SH2 interactions, disruption of the interaction with Enigma abolished Ret/ptc2 mitogenic signaling, suggesting that LIM domain recognition of an unphosphorylated tyrosine-based motif is required for Ret signal transduction.	Tyrosine	181-189	ret proto-oncogene	Homo sapiens	218-221
8628282-0	1996	The full oncogenic activity of Ret/ptc2 depends on tyrosine 539, a docking site for phospholipase Cgamma.	Tyrosine	51-59	ret proto-oncogene	Homo sapiens	31-34
8626834-8	1996	In all but 1 of 27 familial MTC (FMTC) families, mutations were detected in 1 of 4 cysteines in the extracellular domain of the ret protooncogene.	Cysteine	83-92	ret proto-oncogene	Homo sapiens	128-131
8628282-3	1996	The respective Ret/ptc oncoproteins display constitutive TK activity and tyrosine phosphorylation.	Tyrosine	73-81	ret proto-oncogene	Homo sapiens	15-18
8628282-3	1996	The respective Ret/ptc oncoproteins display constitutive TK activity and tyrosine phosphorylation.	Tyrosine	73-81	ret proto-oncogene	Homo sapiens	19-22
8628282-5	1996	Two putative PLCgamma docking sites, Tyr-505 and Tyr-539, have been identified on Ret/ptc2 by competition experiments using phosphorylated peptides modelled on Ret sequence.	Tyrosine	37-40	ret proto-oncogene	Homo sapiens	82-85
8626874-7	1996	Our results show that, in papillary thyroid carcinoma, the frequency of RET and NTRK1 activation is significantly higher in the group of patients aged 4-30 years, thas supporting the concept that age could be contributing to this thyroid specific carcinogenic process.	3,5-tetrahydroaldosterone sulfate	163-167	ret proto-oncogene	Homo sapiens	72-75
8628282-5	1996	Two putative PLCgamma docking sites, Tyr-505 and Tyr-539, have been identified on Ret/ptc2 by competition experiments using phosphorylated peptides modelled on Ret sequence.	Tyrosine	37-40	ret proto-oncogene	Homo sapiens	160-163
8628282-5	1996	Two putative PLCgamma docking sites, Tyr-505 and Tyr-539, have been identified on Ret/ptc2 by competition experiments using phosphorylated peptides modelled on Ret sequence.	Tyrosine	49-52	ret proto-oncogene	Homo sapiens	82-85
8628282-5	1996	Two putative PLCgamma docking sites, Tyr-505 and Tyr-539, have been identified on Ret/ptc2 by competition experiments using phosphorylated peptides modelled on Ret sequence.	Tyrosine	49-52	ret proto-oncogene	Homo sapiens	160-163
8628282-6	1996	Transfection experiments and biochemical analysis using Tyr--&gt;Phe mutants of Ret/ptc2 allowed us to rule out Tyr-505 and to identify Tyr-539 as a functional PLCgamma docking site in vivo.	Tyrosine	56-59	ret proto-oncogene	Homo sapiens	80-83
8628282-6	1996	Transfection experiments and biochemical analysis using Tyr--&gt;Phe mutants of Ret/ptc2 allowed us to rule out Tyr-505 and to identify Tyr-539 as a functional PLCgamma docking site in vivo.	Phenylalanine	65-68	ret proto-oncogene	Homo sapiens	80-83
8628282-9	1996	In conclusion, this paper demonstrates that Tyr-539 of Ret/ptc2 (Tyr-761 on the proto-RET product) is an essential docking site for the full transforming potential of the oncogene.	Tyrosine	44-47	ret proto-oncogene	Homo sapiens	55-58
8628282-9	1996	In conclusion, this paper demonstrates that Tyr-539 of Ret/ptc2 (Tyr-761 on the proto-RET product) is an essential docking site for the full transforming potential of the oncogene.	Tyrosine	44-47	ret proto-oncogene	Homo sapiens	86-89
8628282-9	1996	In conclusion, this paper demonstrates that Tyr-539 of Ret/ptc2 (Tyr-761 on the proto-RET product) is an essential docking site for the full transforming potential of the oncogene.	Tyrosine	65-68	ret proto-oncogene	Homo sapiens	55-58
8628282-9	1996	In conclusion, this paper demonstrates that Tyr-539 of Ret/ptc2 (Tyr-761 on the proto-RET product) is an essential docking site for the full transforming potential of the oncogene.	Tyrosine	65-68	ret proto-oncogene	Homo sapiens	86-89
12114682-3	1996	In FMTC and MEN2A, point mutations result in the substitution of one of five Cys residues in the extracellular domain of RET.	Cysteine	77-80	ret proto-oncogene	Homo sapiens	12-17
12114682-3	1996	In FMTC and MEN2A, point mutations result in the substitution of one of five Cys residues in the extracellular domain of RET.	Cysteine	77-80	ret proto-oncogene	Homo sapiens	121-124
8670046-1	1996	We demonstrate that a Hirschsprung (HSCR) mutation in the tyrosine kinase domain of the RET proto-oncogene abolishes in cis the tyrosine-phosphorylation associated with the activating mutation in multiple endocrine neoplasia type 2A (MEN2A) in transiently transfected Cos cells.	Tyrosine	58-66	ret proto-oncogene	Homo sapiens	88-91
8733882-7	1996	Recently, we utilized the "Cold SSCP" method, nonradioactive single-stranded conformation polymorphism analysis, to screen for RET mutations and have identified a novel mutation, a 6-bp deletion preceding the cysteine-634, in a sporadic MTC.	Cysteine	209-217	ret proto-oncogene	Homo sapiens	127-130
8708421-0	1996	[Gas6: a ligand for receptor tyrosine kinase containing gamma-carboxyglutamic acids].	1-Carboxyglutamic Acid	56-83	ret proto-oncogene	Homo sapiens	20-44
8621456-2	1996	Multiple endocrine neoplasia type 2B (MEN 2B) is caused by the mutation of a conserved methionine to a threonine in the catalytic domain of the RET kinase.	Methionine	87-97	ret proto-oncogene	Homo sapiens	0-36
8621456-2	1996	Multiple endocrine neoplasia type 2B (MEN 2B) is caused by the mutation of a conserved methionine to a threonine in the catalytic domain of the RET kinase.	Methionine	87-97	ret proto-oncogene	Homo sapiens	38-44
8621456-2	1996	Multiple endocrine neoplasia type 2B (MEN 2B) is caused by the mutation of a conserved methionine to a threonine in the catalytic domain of the RET kinase.	Methionine	87-97	ret proto-oncogene	Homo sapiens	144-147
8621456-2	1996	Multiple endocrine neoplasia type 2B (MEN 2B) is caused by the mutation of a conserved methionine to a threonine in the catalytic domain of the RET kinase.	Threonine	103-112	ret proto-oncogene	Homo sapiens	0-36
8621456-2	1996	Multiple endocrine neoplasia type 2B (MEN 2B) is caused by the mutation of a conserved methionine to a threonine in the catalytic domain of the RET kinase.	Threonine	103-112	ret proto-oncogene	Homo sapiens	38-44
8621456-2	1996	Multiple endocrine neoplasia type 2B (MEN 2B) is caused by the mutation of a conserved methionine to a threonine in the catalytic domain of the RET kinase.	Threonine	103-112	ret proto-oncogene	Homo sapiens	144-147
8621380-5	1996	Among the 6 autophosphorylation sites found in the wild-type RET receptor, the MEN2B mutant lacked phosphorylation at Tyr-1096, leading to decreased Grb2 binding, while simultaneously creating a new phosphorylation site.	Tyrosine	118-121	ret proto-oncogene	Homo sapiens	61-64
8621380-5	1996	Among the 6 autophosphorylation sites found in the wild-type RET receptor, the MEN2B mutant lacked phosphorylation at Tyr-1096, leading to decreased Grb2 binding, while simultaneously creating a new phosphorylation site.	Tyrosine	118-121	ret proto-oncogene	Homo sapiens	79-84
8670046-1	1996	We demonstrate that a Hirschsprung (HSCR) mutation in the tyrosine kinase domain of the RET proto-oncogene abolishes in cis the tyrosine-phosphorylation associated with the activating mutation in multiple endocrine neoplasia type 2A (MEN2A) in transiently transfected Cos cells.	Tyrosine	58-66	ret proto-oncogene	Homo sapiens	196-232
8670046-1	1996	We demonstrate that a Hirschsprung (HSCR) mutation in the tyrosine kinase domain of the RET proto-oncogene abolishes in cis the tyrosine-phosphorylation associated with the activating mutation in multiple endocrine neoplasia type 2A (MEN2A) in transiently transfected Cos cells.	Tyrosine	58-66	ret proto-oncogene	Homo sapiens	234-239
8670046-5	1996	Finally, analysis of the enzymic activity of MEN2A and MEN2B tumours confirmed the relative levels of tyrosine phosphorylation observed in Cos cells, indicating that this condition, in vivo, may account for the RET transforming potential.	Tyrosine	102-110	ret proto-oncogene	Homo sapiens	45-50
8732448-2	1996	We report an MEN 2A family in which serine (AGC) substitutes for cysteine (TGC) at codon 618 in exon 10 of the RET proto-oncogene.	Serine	36-42	ret proto-oncogene	Homo sapiens	13-19
8849576-14	1996	Three individuals from different MEN 2A kindreds, who were subsequently shown not to be gene carriers, had false positive pentagastrin stimulation tests.	Pentagastrin	122-134	ret proto-oncogene	Homo sapiens	33-39
8849577-0	1996	The identification of false positive responses to the pentagastrin stimulation test in RET mutation negative members of MEN 2A families.	Pentagastrin	54-66	ret proto-oncogene	Homo sapiens	87-90
8849577-0	1996	The identification of false positive responses to the pentagastrin stimulation test in RET mutation negative members of MEN 2A families.	Pentagastrin	54-66	ret proto-oncogene	Homo sapiens	120-126
8849577-8	1996	Two RET mutation negative males had thyroidectomy based on prior pentagastrin test results.	Pentagastrin	65-77	ret proto-oncogene	Homo sapiens	4-7
8849577-13	1996	False positive responses to pentagastrin stimulation were identified in seven individuals who were RET mutation negative in two of the 16 families.	Pentagastrin	28-40	ret proto-oncogene	Homo sapiens	99-102
8732448-2	1996	We report an MEN 2A family in which serine (AGC) substitutes for cysteine (TGC) at codon 618 in exon 10 of the RET proto-oncogene.	Serine	36-42	ret proto-oncogene	Homo sapiens	111-114
8732448-2	1996	We report an MEN 2A family in which serine (AGC) substitutes for cysteine (TGC) at codon 618 in exon 10 of the RET proto-oncogene.	agc	44-47	ret proto-oncogene	Homo sapiens	13-19
8732448-2	1996	We report an MEN 2A family in which serine (AGC) substitutes for cysteine (TGC) at codon 618 in exon 10 of the RET proto-oncogene.	agc	44-47	ret proto-oncogene	Homo sapiens	111-114
8732448-2	1996	We report an MEN 2A family in which serine (AGC) substitutes for cysteine (TGC) at codon 618 in exon 10 of the RET proto-oncogene.	Cysteine	65-73	ret proto-oncogene	Homo sapiens	13-19
8732448-2	1996	We report an MEN 2A family in which serine (AGC) substitutes for cysteine (TGC) at codon 618 in exon 10 of the RET proto-oncogene.	Cysteine	65-73	ret proto-oncogene	Homo sapiens	111-114
9074721-5	1996	The RET gene encodes a receptor tyrosine kinase, which displays a cadherin-like domain and a cysteine rich motif in its extracellular part.	Cysteine	93-101	ret proto-oncogene	Homo sapiens	4-7
8637703-0	1996	Identification of tyrosine residues that are essential for transforming activity of the ret proto-oncogene with MEN2A or MEN2B mutation.	Tyrosine	18-26	ret proto-oncogene	Homo sapiens	88-91
8637703-0	1996	Identification of tyrosine residues that are essential for transforming activity of the ret proto-oncogene with MEN2A or MEN2B mutation.	Tyrosine	18-26	ret proto-oncogene	Homo sapiens	112-117
8637703-0	1996	Identification of tyrosine residues that are essential for transforming activity of the ret proto-oncogene with MEN2A or MEN2B mutation.	Tyrosine	18-26	ret proto-oncogene	Homo sapiens	121-126
8637703-3	1996	In the present study, we investigated the role of tyrosine residues present in the kinase domain for the transforming activity of the mutant Ret proteins.	Tyrosine	50-58	ret proto-oncogene	Homo sapiens	141-144
8637703-4	1996	Substitution of phenylalanine for tyrosine 905 (Y905F) that corresponds to tyrosine 416 of the Src protein abolished the transforming activity of Ret with the MEN2A mutation (MEN2A-Ret) but not with the MEN2B mutation (MEN2B-Ret).	Tyrosine	34-42	ret proto-oncogene	Homo sapiens	146-149
8637703-4	1996	Substitution of phenylalanine for tyrosine 905 (Y905F) that corresponds to tyrosine 416 of the Src protein abolished the transforming activity of Ret with the MEN2A mutation (MEN2A-Ret) but not with the MEN2B mutation (MEN2B-Ret).	Tyrosine	34-42	ret proto-oncogene	Homo sapiens	159-164
8637703-4	1996	Substitution of phenylalanine for tyrosine 905 (Y905F) that corresponds to tyrosine 416 of the Src protein abolished the transforming activity of Ret with the MEN2A mutation (MEN2A-Ret) but not with the MEN2B mutation (MEN2B-Ret).	Tyrosine	34-42	ret proto-oncogene	Homo sapiens	175-184
8637703-4	1996	Substitution of phenylalanine for tyrosine 905 (Y905F) that corresponds to tyrosine 416 of the Src protein abolished the transforming activity of Ret with the MEN2A mutation (MEN2A-Ret) but not with the MEN2B mutation (MEN2B-Ret).	Tyrosine	34-42	ret proto-oncogene	Homo sapiens	203-208
8637703-4	1996	Substitution of phenylalanine for tyrosine 905 (Y905F) that corresponds to tyrosine 416 of the Src protein abolished the transforming activity of Ret with the MEN2A mutation (MEN2A-Ret) but not with the MEN2B mutation (MEN2B-Ret).	Tyrosine	34-42	ret proto-oncogene	Homo sapiens	219-224
8637703-4	1996	Substitution of phenylalanine for tyrosine 905 (Y905F) that corresponds to tyrosine 416 of the Src protein abolished the transforming activity of Ret with the MEN2A mutation (MEN2A-Ret) but not with the MEN2B mutation (MEN2B-Ret).	Tyrosine	34-42	ret proto-oncogene	Homo sapiens	181-184
8637703-5	1996	On the other hand, the transforming activity of MEN2B-Ret but not MEN2A-Ret significantly decreased by changing tyrosine 864 or 952 to phenylalanine.	Tyrosine	112-120	ret proto-oncogene	Homo sapiens	48-53
8637703-5	1996	On the other hand, the transforming activity of MEN2B-Ret but not MEN2A-Ret significantly decreased by changing tyrosine 864 or 952 to phenylalanine.	Tyrosine	112-120	ret proto-oncogene	Homo sapiens	54-57
8637703-5	1996	On the other hand, the transforming activity of MEN2B-Ret but not MEN2A-Ret significantly decreased by changing tyrosine 864 or 952 to phenylalanine.	Phenylalanine	135-148	ret proto-oncogene	Homo sapiens	48-53
8637703-5	1996	On the other hand, the transforming activity of MEN2B-Ret but not MEN2A-Ret significantly decreased by changing tyrosine 864 or 952 to phenylalanine.	Phenylalanine	135-148	ret proto-oncogene	Homo sapiens	54-57
8637703-6	1996	In addition, double mutations of these tyrosines (Y864/952F) completely abolished the activity of MEN2B-Ret.	Tyrosine	39-48	ret proto-oncogene	Homo sapiens	98-107
8637703-8	1996	These results thus indicated that tyrosine residues essential for the transforming activity are different between MEN2A-Ret and MEN2B-Ret.	Tyrosine	34-42	ret proto-oncogene	Homo sapiens	114-123
8637703-8	1996	These results thus indicated that tyrosine residues essential for the transforming activity are different between MEN2A-Ret and MEN2B-Ret.	Tyrosine	34-42	ret proto-oncogene	Homo sapiens	128-137
8561803-1	1996	Using transfection of NIH 3T3 cells, we have recently demonstrated that multiple endocrine neoplasia (MEN) 2A mutations activate the c-Ret protein by inducing its disulfide-linked homodimerization on the cell surface.	Disulfides	163-172	ret proto-oncogene	Homo sapiens	135-138
8561803-4	1996	By labeling the c-Ret protein immunoprecipitated from tumor tissues with [gamma-32P]ATP in vitro, its homodimers were detected in pheochromocytomas from MEN 2A patients but not in a sporadic tumor.	gamma-32p	74-83	ret proto-oncogene	Homo sapiens	18-21
8561803-4	1996	By labeling the c-Ret protein immunoprecipitated from tumor tissues with [gamma-32P]ATP in vitro, its homodimers were detected in pheochromocytomas from MEN 2A patients but not in a sporadic tumor.	Adenosine Triphosphate	84-87	ret proto-oncogene	Homo sapiens	18-21
8734283-4	1996	In 97% of MEN 2A patients, the germline mutation affects one of five cysteine codons within exons 10 and 11 in the extracellular domain.	Cysteine	69-77	ret proto-oncogene	Homo sapiens	10-16
8734285-5	1996	In members of a MEN2 family, carrying a RET mutation, CCH is constant and associated with micro-MTC.	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	54-57	ret proto-oncogene	Homo sapiens	40-43
9074721-6	1996	Missense mutations at one of five cysteines clustered in the extra-cytoplasmic domain of RET have been identified in the majority of the MEN 2A families and in two-thirds of FMTC.	Cysteine	34-43	ret proto-oncogene	Homo sapiens	89-92
9074721-6	1996	Missense mutations at one of five cysteines clustered in the extra-cytoplasmic domain of RET have been identified in the majority of the MEN 2A families and in two-thirds of FMTC.	Cysteine	34-43	ret proto-oncogene	Homo sapiens	137-143
9074721-7	1996	A single point mutation leading to the replacement of a methionine by a threonine within the tyrosine kinase domain has been detected in almost all cases of MEN 2B.	Methionine	56-66	ret proto-oncogene	Homo sapiens	157-163
9074721-7	1996	A single point mutation leading to the replacement of a methionine by a threonine within the tyrosine kinase domain has been detected in almost all cases of MEN 2B.	Threonine	72-81	ret proto-oncogene	Homo sapiens	157-163
8829625-2	1996	To date, the sequence variations occur in RET exons 10 and 11 and alter highly conserved cysteine residues in the proposed extracellular domain at codons 609, 611, 618, 620, and 634.	Cysteine	89-97	ret proto-oncogene	Homo sapiens	42-45
8981015-8	1996	Four family members of MEN 2A families have had thyroidectomy on the basis of pentagastrin testing and now proved not to be gene carriers.	Pentagastrin	78-90	ret proto-oncogene	Homo sapiens	23-29
8715023-0	1996	Silicone oil"s properties make it a versatile tool for vit/ret surgery.	Silicone Oils	0-12	ret proto-oncogene	Homo sapiens	59-62
8557249-5	1996	All MEN 2A families had a mutation involving one of five cysteine codons in exons 10 and 11 of RET.	Cysteine	57-65	ret proto-oncogene	Homo sapiens	4-10
8557249-5	1996	All MEN 2A families had a mutation involving one of five cysteine codons in exons 10 and 11 of RET.	Cysteine	57-65	ret proto-oncogene	Homo sapiens	95-98
8557249-8	1996	All MEN 2B probands carried a Met to Thr mutation in exon 16.	Threonine	37-40	ret proto-oncogene	Homo sapiens	4-10
7495285-6	1995	Six MEN-2A-associated hyperplastic glands exhibited identical band shifts in the polymerase chain reaction single-strand conformation polymorphism analysis of exon 11, which corresponded to a Cys 634--&gt;Arg substitution in the nucleotide sequence analysis (TGC--&gt;CGC), whereas in the MEN 2B parathyroid specimen a point mutation was found at codon 918 of exon 16 (ATG--&gt;ACG), causing a Met 918--&gt;Thr substitution.	Cysteine	192-195	ret proto-oncogene	Homo sapiens	4-10
8570194-5	1995	The Ret (MEN2A) and Ret (MEN2B) proteins were constitutively phosphorylated on tyrosine, and their in vitro kinase activity was significantly higher than that of the wild type protein.	Tyrosine	79-87	ret proto-oncogene	Homo sapiens	4-7
8570194-5	1995	The Ret (MEN2A) and Ret (MEN2B) proteins were constitutively phosphorylated on tyrosine, and their in vitro kinase activity was significantly higher than that of the wild type protein.	Tyrosine	79-87	ret proto-oncogene	Homo sapiens	9-14
8570194-5	1995	The Ret (MEN2A) and Ret (MEN2B) proteins were constitutively phosphorylated on tyrosine, and their in vitro kinase activity was significantly higher than that of the wild type protein.	Tyrosine	79-87	ret proto-oncogene	Homo sapiens	20-23
8570194-5	1995	The Ret (MEN2A) and Ret (MEN2B) proteins were constitutively phosphorylated on tyrosine, and their in vitro kinase activity was significantly higher than that of the wild type protein.	Tyrosine	79-87	ret proto-oncogene	Homo sapiens	25-30
8570194-6	1995	The MTC cell line TT carries a CYs634-> Trp MEN2A mutation, and we have shown by immunoelectronmicroscopy that Ret is clustered on the cell surface in a manner reminiscent of ligand-induced aggregation of cell surface receptors.	Tryptophan	40-43	ret proto-oncogene	Homo sapiens	111-114
7495285-6	1995	Six MEN-2A-associated hyperplastic glands exhibited identical band shifts in the polymerase chain reaction single-strand conformation polymorphism analysis of exon 11, which corresponded to a Cys 634--&gt;Arg substitution in the nucleotide sequence analysis (TGC--&gt;CGC), whereas in the MEN 2B parathyroid specimen a point mutation was found at codon 918 of exon 16 (ATG--&gt;ACG), causing a Met 918--&gt;Thr substitution.	Arginine	205-208	ret proto-oncogene	Homo sapiens	4-10
7495285-6	1995	Six MEN-2A-associated hyperplastic glands exhibited identical band shifts in the polymerase chain reaction single-strand conformation polymorphism analysis of exon 11, which corresponded to a Cys 634--&gt;Arg substitution in the nucleotide sequence analysis (TGC--&gt;CGC), whereas in the MEN 2B parathyroid specimen a point mutation was found at codon 918 of exon 16 (ATG--&gt;ACG), causing a Met 918--&gt;Thr substitution.	Threonine	407-410	ret proto-oncogene	Homo sapiens	4-10
7495285-8	1995	Furthermore, our results are in accordance with the observation that MEN 2A patients with Cys 634--&gt;Arg (germline) mutations have a higher risk of developing parathyroid disease than those with other mutations at codon 634.	Cysteine	90-93	ret proto-oncogene	Homo sapiens	69-75
7495285-8	1995	Furthermore, our results are in accordance with the observation that MEN 2A patients with Cys 634--&gt;Arg (germline) mutations have a higher risk of developing parathyroid disease than those with other mutations at codon 634.	Arginine	103-106	ret proto-oncogene	Homo sapiens	69-75
8666102-5	1995	The order of sensitivity of the techniques to assess methacholine-induced changes in lung function was ZIOS &gt; sRaw &gt; Ptc,O2 &gt; FEV1 &gt; Rint.	Methacholine Chloride	53-65	ret proto-oncogene	Homo sapiens	123-126
8563482-5	1995	The majority of the mutations associated with MEN 2A and FMTC are tightly clustered in a cysteine-rich region of the RET receptor.	Cysteine	89-97	ret proto-oncogene	Homo sapiens	46-52
8635999-1	1995	We examined whether the novel point mutation from GCC (Ala) to GAC (Asp) at codon 664 in exon 11 of RET proto-oncogene, which we had found in two small cell lung carcinoma (SCLC) cell lines, existed in genomic DNA of tumor tissues of the two SCLC patients from whom these SCLC cell lines were derived.	Alanine	55-58	ret proto-oncogene	Homo sapiens	100-103
8635999-1	1995	We examined whether the novel point mutation from GCC (Ala) to GAC (Asp) at codon 664 in exon 11 of RET proto-oncogene, which we had found in two small cell lung carcinoma (SCLC) cell lines, existed in genomic DNA of tumor tissues of the two SCLC patients from whom these SCLC cell lines were derived.	Aspartic Acid	68-71	ret proto-oncogene	Homo sapiens	100-103
7478540-4	1995	CCK-4 cDNA encodes a chicken KLG-related, 1071 amino acid-long transmembrane glycoprotein containing several genetic alterations within the RTK consensus sequences.	CHEMBL2385480	29-32	ret proto-oncogene	Homo sapiens	140-143
8538031-2	1995	In patients with MEN 2A and FMTC different point mutations have been identified in exons 10 and 11 of the cysteine rich regions of RET.	Cysteine	106-114	ret proto-oncogene	Homo sapiens	17-23
8538031-2	1995	In patients with MEN 2A and FMTC different point mutations have been identified in exons 10 and 11 of the cysteine rich regions of RET.	Cysteine	106-114	ret proto-oncogene	Homo sapiens	131-134
7559902-1	1995	The hereditary multiple endocrine neoplasia syndromes types 2A and B (MEN 2A and B) were recently linked to germline mutations in the RET proto-oncogene, altering one of five cysteine residues in exon 10 or 11 (MEN 2A), or substituting a methionine for a threonine at codon 918 in exon 16 (MEN 2B).	Cysteine	175-183	ret proto-oncogene	Homo sapiens	70-82
7559902-1	1995	The hereditary multiple endocrine neoplasia syndromes types 2A and B (MEN 2A and B) were recently linked to germline mutations in the RET proto-oncogene, altering one of five cysteine residues in exon 10 or 11 (MEN 2A), or substituting a methionine for a threonine at codon 918 in exon 16 (MEN 2B).	Cysteine	175-183	ret proto-oncogene	Homo sapiens	134-137
7559902-1	1995	The hereditary multiple endocrine neoplasia syndromes types 2A and B (MEN 2A and B) were recently linked to germline mutations in the RET proto-oncogene, altering one of five cysteine residues in exon 10 or 11 (MEN 2A), or substituting a methionine for a threonine at codon 918 in exon 16 (MEN 2B).	Cysteine	175-183	ret proto-oncogene	Homo sapiens	70-76
7491529-5	1995	The ret mutations were detected by DNA analysis of exons 10, 11, and 16 by using nonradioactive labeling method based on digoxigenin DNA sequencing technique.	Digoxigenin	121-132	ret proto-oncogene	Homo sapiens	4-7
7595167-4	1995	Altogether, we and others found 21 missense mutations in five cysteines clustered in the extra-cellular domain of RET (exons 10 and 11) associated with 111 MEN 2A and FMTC families.	Cysteine	62-71	ret proto-oncogene	Homo sapiens	114-117
7595167-4	1995	Altogether, we and others found 21 missense mutations in five cysteines clustered in the extra-cellular domain of RET (exons 10 and 11) associated with 111 MEN 2A and FMTC families.	Cysteine	62-71	ret proto-oncogene	Homo sapiens	156-162
7595167-5	1995	In contrast, a single point mutation that results in the substitution of threonine for methionine within the catalytic core of the tyrosine kinase domain (codon 918, exon 16) is responsible for all 66 reported cases of MEN 2B.	Threonine	73-82	ret proto-oncogene	Homo sapiens	219-225
7595167-5	1995	In contrast, a single point mutation that results in the substitution of threonine for methionine within the catalytic core of the tyrosine kinase domain (codon 918, exon 16) is responsible for all 66 reported cases of MEN 2B.	Methionine	87-97	ret proto-oncogene	Homo sapiens	219-225
7595170-4	1995	Over 93% of MEN 2B families had the RET 918 ATG--&gt;ACG mutation, while the most frequent mutation detected in MEN 2A families was cysteine codon 634 (87% of all mutations).	acceleratory factor from growth hormone	53-56	ret proto-oncogene	Homo sapiens	12-18
7595170-4	1995	Over 93% of MEN 2B families had the RET 918 ATG--&gt;ACG mutation, while the most frequent mutation detected in MEN 2A families was cysteine codon 634 (87% of all mutations).	acceleratory factor from growth hormone	53-56	ret proto-oncogene	Homo sapiens	36-39
8563482-5	1995	The majority of the mutations associated with MEN 2A and FMTC are tightly clustered in a cysteine-rich region of the RET receptor.	Cysteine	89-97	ret proto-oncogene	Homo sapiens	117-120
8625130-7	1995	RESULTS: Six different missense germline mutations were identified at cysteine residues 618, 630, and 634 of the cysteine-rich extracellular RET domain encoded by exons 10 and 11 in all patients with FMTC and MEN 2A.	Cysteine	70-78	ret proto-oncogene	Homo sapiens	141-144
8579892-3	1995	Activating mutations of a cysteine-rich extracellular region cause enhanced dimerization of the RET tyrosine kinase receptor and autophosphorylation, and are causative for MEN 2A and familial medullary thyroid carcinoma (FMTC).	Cysteine	26-34	ret proto-oncogene	Homo sapiens	96-99
8579892-3	1995	Activating mutations of a cysteine-rich extracellular region cause enhanced dimerization of the RET tyrosine kinase receptor and autophosphorylation, and are causative for MEN 2A and familial medullary thyroid carcinoma (FMTC).	Cysteine	26-34	ret proto-oncogene	Homo sapiens	172-178
8625130-7	1995	RESULTS: Six different missense germline mutations were identified at cysteine residues 618, 630, and 634 of the cysteine-rich extracellular RET domain encoded by exons 10 and 11 in all patients with FMTC and MEN 2A.	Cysteine	70-78	ret proto-oncogene	Homo sapiens	209-215
8625130-7	1995	RESULTS: Six different missense germline mutations were identified at cysteine residues 618, 630, and 634 of the cysteine-rich extracellular RET domain encoded by exons 10 and 11 in all patients with FMTC and MEN 2A.	Cysteine	113-121	ret proto-oncogene	Homo sapiens	141-144
8625130-7	1995	RESULTS: Six different missense germline mutations were identified at cysteine residues 618, 630, and 634 of the cysteine-rich extracellular RET domain encoded by exons 10 and 11 in all patients with FMTC and MEN 2A.	Cysteine	113-121	ret proto-oncogene	Homo sapiens	209-215
8625130-9	1995	A germline Met--&gt;Thr point mutation at codon 918 of the RET tyrosine kinase domain was identified in all three patients with MEN 2B.	Threonine	20-23	ret proto-oncogene	Homo sapiens	59-62
8625130-9	1995	A germline Met--&gt;Thr point mutation at codon 918 of the RET tyrosine kinase domain was identified in all three patients with MEN 2B.	Threonine	20-23	ret proto-oncogene	Homo sapiens	128-134
8556059-0	1995	Mutations in the cysteine-rich region of the RET proto-oncogene in patients diagnosed as having sporadic medullary thyroid carcinoma.	Cysteine	17-25	ret proto-oncogene	Homo sapiens	45-48
8556059-3	1995	To elucidate the etiological roles in tumorigenesis of sporadic MTCs and pheochromocytomas, mutations in the cysteine-rich region of the RET proto-oncogene were analyzed by using polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis.	Cysteine	109-117	ret proto-oncogene	Homo sapiens	137-140
8556060-10	1995	Two MEN 2A patients with a cysteine for a tyrosine substitution at codon 634 in the exon 11 had parathyroid hyperplasia.	Cysteine	27-35	ret proto-oncogene	Homo sapiens	4-10
8556060-10	1995	Two MEN 2A patients with a cysteine for a tyrosine substitution at codon 634 in the exon 11 had parathyroid hyperplasia.	Tyrosine	42-50	ret proto-oncogene	Homo sapiens	4-10
7716719-10	1995	CONCLUSIONS: The RET codon 618 Ser mutation could predispose patients with MEN 2A to HD.	Serine	31-34	ret proto-oncogene	Homo sapiens	17-20
7608256-9	1995	We describe new types of molecular defects of the RET protooncogene in the MEN 2A region that involve noncysteine residues and loss of exon 10.	noncysteine	102-113	ret proto-oncogene	Homo sapiens	50-53
7608256-9	1995	We describe new types of molecular defects of the RET protooncogene in the MEN 2A region that involve noncysteine residues and loss of exon 10.	noncysteine	102-113	ret proto-oncogene	Homo sapiens	75-81
7627271-2	1995	All tumors of 4 MEN 2B patients were confirmed to contain a heterozygous missense mutation at codon 918 (ATG--&gt;ACG; Met--&gt;Thr) of the RET proto-oncogene as well as their leukocytes.	acceleratory factor from growth hormone	114-117	ret proto-oncogene	Homo sapiens	16-22
7627271-2	1995	All tumors of 4 MEN 2B patients were confirmed to contain a heterozygous missense mutation at codon 918 (ATG--&gt;ACG; Met--&gt;Thr) of the RET proto-oncogene as well as their leukocytes.	acceleratory factor from growth hormone	114-117	ret proto-oncogene	Homo sapiens	140-143
7627271-2	1995	All tumors of 4 MEN 2B patients were confirmed to contain a heterozygous missense mutation at codon 918 (ATG--&gt;ACG; Met--&gt;Thr) of the RET proto-oncogene as well as their leukocytes.	Methionine	119-122	ret proto-oncogene	Homo sapiens	16-22
7627271-2	1995	All tumors of 4 MEN 2B patients were confirmed to contain a heterozygous missense mutation at codon 918 (ATG--&gt;ACG; Met--&gt;Thr) of the RET proto-oncogene as well as their leukocytes.	Methionine	119-122	ret proto-oncogene	Homo sapiens	140-143
7627271-2	1995	All tumors of 4 MEN 2B patients were confirmed to contain a heterozygous missense mutation at codon 918 (ATG--&gt;ACG; Met--&gt;Thr) of the RET proto-oncogene as well as their leukocytes.	Threonine	128-131	ret proto-oncogene	Homo sapiens	16-22
7627271-2	1995	All tumors of 4 MEN 2B patients were confirmed to contain a heterozygous missense mutation at codon 918 (ATG--&gt;ACG; Met--&gt;Thr) of the RET proto-oncogene as well as their leukocytes.	Threonine	128-131	ret proto-oncogene	Homo sapiens	140-143
7705835-4	1995	In MEN 2B patients, a single point mutation at codon 918 has recently been characterized, leading to the replacement of a methionine by a threonine within the RET tyrosine kinase domain.	Threonine	138-147	ret proto-oncogene	Homo sapiens	3-9
7705835-4	1995	In MEN 2B patients, a single point mutation at codon 918 has recently been characterized, leading to the replacement of a methionine by a threonine within the RET tyrosine kinase domain.	Threonine	138-147	ret proto-oncogene	Homo sapiens	159-162
7670926-3	1995	In MEN 2A, RET mutations are detectable in one of five cysteine codons within exons 10 and 11 and in MEN 2B in codon 918 (exon 16).	Cysteine	55-63	ret proto-oncogene	Homo sapiens	3-9
7670926-3	1995	In MEN 2A, RET mutations are detectable in one of five cysteine codons within exons 10 and 11 and in MEN 2B in codon 918 (exon 16).	Cysteine	55-63	ret proto-oncogene	Homo sapiens	11-14
7705835-3	1995	Missense mutations at cysteine residues in the extra-cytoplasmic domain are exclusively associated with MEN 2A and FMTC.	Cysteine	22-30	ret proto-oncogene	Homo sapiens	104-110
7705835-4	1995	In MEN 2B patients, a single point mutation at codon 918 has recently been characterized, leading to the replacement of a methionine by a threonine within the RET tyrosine kinase domain.	Methionine	122-132	ret proto-oncogene	Homo sapiens	3-9
7705835-4	1995	In MEN 2B patients, a single point mutation at codon 918 has recently been characterized, leading to the replacement of a methionine by a threonine within the RET tyrosine kinase domain.	Methionine	122-132	ret proto-oncogene	Homo sapiens	159-162
7716719-10	1995	CONCLUSIONS: The RET codon 618 Ser mutation could predispose patients with MEN 2A to HD.	Serine	31-34	ret proto-oncogene	Homo sapiens	75-81
7867726-3	1995	A marked increase in RET mRNA levels was observed in all the cell lines examined shortly after retinoic acid (RA) treatment and before the onset of detectable morphological changes.	Tretinoin	95-108	ret proto-oncogene	Homo sapiens	21-24
7867726-3	1995	A marked increase in RET mRNA levels was observed in all the cell lines examined shortly after retinoic acid (RA) treatment and before the onset of detectable morphological changes.	Tretinoin	110-112	ret proto-oncogene	Homo sapiens	21-24
7867726-4	1995	Upregulation of RET expression was also found in SK-N-BE cells induced to differentiate by 12-O-tetradecanoylphorbol-13-acetate, glial cell-conditioned medium, alpha or gamma interferon, and in SH-SY-5Y cells exposed to nerve growth factor.	sk-n	49-53	ret proto-oncogene	Homo sapiens	16-19
7867726-4	1995	Upregulation of RET expression was also found in SK-N-BE cells induced to differentiate by 12-O-tetradecanoylphorbol-13-acetate, glial cell-conditioned medium, alpha or gamma interferon, and in SH-SY-5Y cells exposed to nerve growth factor.	Tetradecanoylphorbol Acetate	91-127	ret proto-oncogene	Homo sapiens	16-19
7867726-5	1995	Induction of RET expression by RA occurred in the absence of de novo protein synthesis.	Tretinoin	31-33	ret proto-oncogene	Homo sapiens	13-16
7867726-6	1995	On the other hand, cycloheximide treatment by itself caused upregulation of RET transcripts.	Cycloheximide	19-32	ret proto-oncogene	Homo sapiens	76-79
7867726-8	1995	Finally, anti-Ret antibodies immunoprecipitated four bands with apparent molecular weights of 150, 155, 170, and 175 kDa in RA-induced SK-N-BE cells.	sk-n-be	135-142	ret proto-oncogene	Homo sapiens	14-17
7867726-9	1995	These bands likely represent differently glycosylated forms of the two RET primary products (117 and 122 kDa) detected in tunicamycin-treated cells.	Tunicamycin	122-133	ret proto-oncogene	Homo sapiens	71-74
7567689-1	1995	An antibody to the ret proto-oncogene product (RET) was raised and applied to formalin-fixed, paraffin-embedded neuroblastic tumors (NBTs) to investigate its usefulness in diagnosis and evaluation of cell differentiation.	Formaldehyde	78-86	ret proto-oncogene	Homo sapiens	19-22
7532281-3	1995	The 170-kDa Ret protein present on the cell surface of transformed cells was highly phosphorylated on tyrosine and formed disulfide-linked homodimers.	Tyrosine	102-110	ret proto-oncogene	Homo sapiens	12-15
7532281-3	1995	The 170-kDa Ret protein present on the cell surface of transformed cells was highly phosphorylated on tyrosine and formed disulfide-linked homodimers.	Disulfides	122-131	ret proto-oncogene	Homo sapiens	12-15
7536460-2	1995	In MEN 2A, germline missense mutations are found in one of five cysteine codons within exons 10 and 11 in the extracellular domain of the RET protooncogene.	Cysteine	64-72	ret proto-oncogene	Homo sapiens	3-9
7536460-2	1995	In MEN 2A, germline missense mutations are found in one of five cysteine codons within exons 10 and 11 in the extracellular domain of the RET protooncogene.	Cysteine	64-72	ret proto-oncogene	Homo sapiens	138-141
7864888-3	1995	Here we report that a human medullary thyroid carcinoma cell line, the TT cell line, harbours a MEN2A-type mutation, specifically a cysteine to triptophan substitution at the level of the RET codon 634.	Cysteine	132-140	ret proto-oncogene	Homo sapiens	96-101
7864888-3	1995	Here we report that a human medullary thyroid carcinoma cell line, the TT cell line, harbours a MEN2A-type mutation, specifically a cysteine to triptophan substitution at the level of the RET codon 634.	Cysteine	132-140	ret proto-oncogene	Homo sapiens	188-191
7864888-3	1995	Here we report that a human medullary thyroid carcinoma cell line, the TT cell line, harbours a MEN2A-type mutation, specifically a cysteine to triptophan substitution at the level of the RET codon 634.	triptophan	144-154	ret proto-oncogene	Homo sapiens	96-101
7864888-3	1995	Here we report that a human medullary thyroid carcinoma cell line, the TT cell line, harbours a MEN2A-type mutation, specifically a cysteine to triptophan substitution at the level of the RET codon 634.	triptophan	144-154	ret proto-oncogene	Homo sapiens	188-191
7567689-1	1995	An antibody to the ret proto-oncogene product (RET) was raised and applied to formalin-fixed, paraffin-embedded neuroblastic tumors (NBTs) to investigate its usefulness in diagnosis and evaluation of cell differentiation.	Formaldehyde	78-86	ret proto-oncogene	Homo sapiens	47-50
7567689-1	1995	An antibody to the ret proto-oncogene product (RET) was raised and applied to formalin-fixed, paraffin-embedded neuroblastic tumors (NBTs) to investigate its usefulness in diagnosis and evaluation of cell differentiation.	Paraffin	94-102	ret proto-oncogene	Homo sapiens	19-22
7567689-1	1995	An antibody to the ret proto-oncogene product (RET) was raised and applied to formalin-fixed, paraffin-embedded neuroblastic tumors (NBTs) to investigate its usefulness in diagnosis and evaluation of cell differentiation.	Paraffin	94-102	ret proto-oncogene	Homo sapiens	47-50
7567689-7	1995	Thus, RET was considered to be a new marker that would be implemented in diagnosis and estimation of neuronal differentiation of NBTs.	nbts	129-133	ret proto-oncogene	Homo sapiens	6-9
7845675-2	1995	MEN 2A and FMTC mutations characterised thus far occur exclusively in the cysteine-rich domain of the extracellular region of RET.	Cysteine	74-82	ret proto-oncogene	Homo sapiens	0-6
7845675-2	1995	MEN 2A and FMTC mutations characterised thus far occur exclusively in the cysteine-rich domain of the extracellular region of RET.	Cysteine	74-82	ret proto-oncogene	Homo sapiens	126-129
7845675-3	1995	We now report a missense mutation in the intracellular tyrosine kinase domain of RET in the germline of a family with FMTC that does not have a cysteine codon mutation.	Cysteine	144-152	ret proto-oncogene	Homo sapiens	81-84
7889627-8	1995	RESULTS: A heterozygous TGC to CGC mutation of codon 634 (cysteine to arginine) was found in the PHAEO and medullary thyroid cancer from the MEN 2A patient.	Cysteine	58-66	ret proto-oncogene	Homo sapiens	141-147
7860065-3	1995	The majority of mutations found so far in MEN2A patients have been located in nucleotide sequences encoding cysteine residues in the extracellular domain of RET.	Cysteine	108-116	ret proto-oncogene	Homo sapiens	42-47
7860065-3	1995	The majority of mutations found so far in MEN2A patients have been located in nucleotide sequences encoding cysteine residues in the extracellular domain of RET.	Cysteine	108-116	ret proto-oncogene	Homo sapiens	157-160
7860065-4	1995	To characterize MEN2A germline alterations in the Japanese population, we screened DNA from eight unrelated patients for mutations in exons 10 and 11 of the RET proto-oncogene and found mutations in all eight patients, at codons 618, 620, or 634; each of these sites encodes a cysteine residue in the extracellular domain of RET.	Cysteine	277-285	ret proto-oncogene	Homo sapiens	157-160
7889627-8	1995	RESULTS: A heterozygous TGC to CGC mutation of codon 634 (cysteine to arginine) was found in the PHAEO and medullary thyroid cancer from the MEN 2A patient.	Arginine	70-78	ret proto-oncogene	Homo sapiens	141-147
7889627-11	1995	CONCLUSION: Mutations of key cysteine codons of the ret proto-oncogene may be specific to MEN 2A.	Cysteine	29-37	ret proto-oncogene	Homo sapiens	52-55
7889627-11	1995	CONCLUSION: Mutations of key cysteine codons of the ret proto-oncogene may be specific to MEN 2A.	Cysteine	29-37	ret proto-oncogene	Homo sapiens	90-96
8600671-3	1995	Recently, germline point-mutations in RET cysteine codons of the extracellular cysteine-rich domain (encoded by exons 10 and 11) and in the tyrosine-kinase domain (encoded by exon 16) at codon 918, have been associated with the syndromes of multiple endocrine neoplasia (MEN) type 2A, MEN type 2B and familial medullary thyroid carcinoma (FMTC).	Cysteine	42-50	ret proto-oncogene	Homo sapiens	38-41
8573606-3	1995	MEN 2A mutations involved cysteine residues in the extracellular domain and induced disulfide-linked homodimerization of the Ret protein on the cell surface, leading to activation of its intrinsic tyrosine kinase.	Cysteine	26-34	ret proto-oncogene	Homo sapiens	0-6
8573606-3	1995	MEN 2A mutations involved cysteine residues in the extracellular domain and induced disulfide-linked homodimerization of the Ret protein on the cell surface, leading to activation of its intrinsic tyrosine kinase.	Disulfides	84-93	ret proto-oncogene	Homo sapiens	0-6
8573606-3	1995	MEN 2A mutations involved cysteine residues in the extracellular domain and induced disulfide-linked homodimerization of the Ret protein on the cell surface, leading to activation of its intrinsic tyrosine kinase.	Disulfides	84-93	ret proto-oncogene	Homo sapiens	125-128
12114809-4	1995	We found six different missense germ line mutations at cysteine residues encoded by exons 10 and 11 in all patients with MEN 2A or familial medullary thyroid carcinoma (FMTC).	Cysteine	55-63	ret proto-oncogene	Homo sapiens	121-127
12114809-6	1995	A germline Met -* Thr point mutation at codon 918 of the RETtyrosine kinase domain encoded by exon 16 was identified in all MEN 2B patients.	Threonine	18-21	ret proto-oncogene	Homo sapiens	124-130
8600671-3	1995	Recently, germline point-mutations in RET cysteine codons of the extracellular cysteine-rich domain (encoded by exons 10 and 11) and in the tyrosine-kinase domain (encoded by exon 16) at codon 918, have been associated with the syndromes of multiple endocrine neoplasia (MEN) type 2A, MEN type 2B and familial medullary thyroid carcinoma (FMTC).	Cysteine	79-87	ret proto-oncogene	Homo sapiens	38-41
8600671-7	1995	In all 19 MEN 2A patients we found RET germline point-mutations either at cysteine codons 634 (14), 630 (1) in exon 11 or at codon 618 (4) in exon 10.	Cysteine	74-82	ret proto-oncogene	Homo sapiens	35-38
7849700-3	1994	We have recently shown an unexpected correlation between one particular RET mutation, cys634--&gt;arg, and the probability of parathyroid involvement in families with MEN 2A.	Arginine	98-101	ret proto-oncogene	Homo sapiens	72-75
7874109-4	1994	All were missense mutations affecting one of three cysteines in the extracellular domain of the RET tyrosine kinase receptor.	Cysteine	51-60	ret proto-oncogene	Homo sapiens	96-99
7881414-2	1994	In HSCR these mutations are dispersed throughout the gene, while in MEN 2A and FMTC, they are tightly clustered in five cysteine codons of the RET extracellular domain.	Cysteine	120-128	ret proto-oncogene	Homo sapiens	68-74
7881414-2	1994	In HSCR these mutations are dispersed throughout the gene, while in MEN 2A and FMTC, they are tightly clustered in five cysteine codons of the RET extracellular domain.	Cysteine	120-128	ret proto-oncogene	Homo sapiens	143-146
7881414-4	1994	In each of five families with HSCR with or without MEN 2A or FMTC, we have identified a nucleotide substitution in one of the five cysteine codons previously associated with MEN 2A or FMTC.	Cysteine	131-139	ret proto-oncogene	Homo sapiens	51-57
7881414-4	1994	In each of five families with HSCR with or without MEN 2A or FMTC, we have identified a nucleotide substitution in one of the five cysteine codons previously associated with MEN 2A or FMTC.	Cysteine	131-139	ret proto-oncogene	Homo sapiens	174-180
7881414-6	1994	In three families, both HSCR and MEN 2A were associated with a single Cys-->Arg mutation at either codon 618 or 620 of RET.	Cysteine	70-73	ret proto-oncogene	Homo sapiens	33-39
7881414-6	1994	In three families, both HSCR and MEN 2A were associated with a single Cys-->Arg mutation at either codon 618 or 620 of RET.	Cysteine	70-73	ret proto-oncogene	Homo sapiens	119-122
7881414-6	1994	In three families, both HSCR and MEN 2A were associated with a single Cys-->Arg mutation at either codon 618 or 620 of RET.	Arginine	76-79	ret proto-oncogene	Homo sapiens	33-39
7881414-6	1994	In three families, both HSCR and MEN 2A were associated with a single Cys-->Arg mutation at either codon 618 or 620 of RET.	Arginine	76-79	ret proto-oncogene	Homo sapiens	119-122
7881414-8	1994	We suggest that specific mutations in cysteine codons 618 and 620 result in MEN 2A or FMTC, but can also predispose to HSCR with low penetrance.	Cysteine	38-46	ret proto-oncogene	Homo sapiens	76-82
7943181-0	1994	Detection of RET proto-oncogene point mutations in paraffin-embedded pheochromocytoma specimens by nonradioactive single-strand conformation polymorphism analysis and direct sequencing.	Paraffin	51-59	ret proto-oncogene	Homo sapiens	13-16
7943181-3	1994	All MEN 2A-associated pheochromocytomas contained a heterozygous missense germline mutation within cystine codons of the cysteine-rich extracellular domain encoded by exons 10 and 11.	Cystine	99-106	ret proto-oncogene	Homo sapiens	4-10
7943181-3	1994	All MEN 2A-associated pheochromocytomas contained a heterozygous missense germline mutation within cystine codons of the cysteine-rich extracellular domain encoded by exons 10 and 11.	Cysteine	121-129	ret proto-oncogene	Homo sapiens	4-10
7943181-6	1994	These data support recent findings that germline point mutations that are clustered in distinct cysteine codons of the RET proto-oncogene are involved in the neoplastic phenotype of the MEN 2A syndrome.	Cysteine	96-104	ret proto-oncogene	Homo sapiens	119-122
7943181-6	1994	These data support recent findings that germline point mutations that are clustered in distinct cysteine codons of the RET proto-oncogene are involved in the neoplastic phenotype of the MEN 2A syndrome.	Cysteine	96-104	ret proto-oncogene	Homo sapiens	186-192
7849700-3	1994	We have recently shown an unexpected correlation between one particular RET mutation, cys634--&gt;arg, and the probability of parathyroid involvement in families with MEN 2A.	Arginine	98-101	ret proto-oncogene	Homo sapiens	167-173
7961113-3	1994	Tumors of four MEN 2A patients had missense mutations in Cys 634 in the extracellular domain of the ret proto-oncogene.	Cysteine	57-60	ret proto-oncogene	Homo sapiens	15-21
7961113-3	1994	Tumors of four MEN 2A patients had missense mutations in Cys 634 in the extracellular domain of the ret proto-oncogene.	Cysteine	57-60	ret proto-oncogene	Homo sapiens	100-103
7981703-0	1994	Three dinucleotide repeat polymorphisms closely linked to the RET protooncogene D10S1098, D10S1099 and D10S1100.	Dinucleoside Phosphates	6-18	ret proto-oncogene	Homo sapiens	62-65
7987299-1	1994	Mutations in FMTC and MEN 2A exclusively affect cysteine residues in exon 10 and 11 of RET, whereas in MEN 2B codon 918 in exon 16 is involved.	Cysteine	48-56	ret proto-oncogene	Homo sapiens	22-28
7987299-1	1994	Mutations in FMTC and MEN 2A exclusively affect cysteine residues in exon 10 and 11 of RET, whereas in MEN 2B codon 918 in exon 16 is involved.	Cysteine	48-56	ret proto-oncogene	Homo sapiens	87-90
7910861-5	1994	Point mutations in the cysteine-rich domain of the RET were demonstrated in patients with MEN 2A.	Cysteine	23-31	ret proto-oncogene	Homo sapiens	51-54
8183561-3	1994	Chimeric Ret and Trk oncoproteins, encoded by different rearrangements of proto-TRK and proto-RET genes, display a constitutive phosphorylation on tyrosine.	Tyrosine	147-155	ret proto-oncogene	Homo sapiens	9-12
8183561-3	1994	Chimeric Ret and Trk oncoproteins, encoded by different rearrangements of proto-TRK and proto-RET genes, display a constitutive phosphorylation on tyrosine.	Tyrosine	147-155	ret proto-oncogene	Homo sapiens	94-97
8183561-8	1994	In addition, in cells containing either Ret or Trk oncoproteins, Shc proteins are constitutively phosphorylated on tyrosine and bound to Grb2.	Tyrosine	115-123	ret proto-oncogene	Homo sapiens	40-43
7915165-4	1994	Each of the mutations involves a cysteine residue in the extracellular cysteine-rich domain of the RET receptor tyrosine kinase.	Cysteine	33-41	ret proto-oncogene	Homo sapiens	99-127
7915165-4	1994	Each of the mutations involves a cysteine residue in the extracellular cysteine-rich domain of the RET receptor tyrosine kinase.	Cysteine	71-79	ret proto-oncogene	Homo sapiens	99-127
7910861-5	1994	Point mutations in the cysteine-rich domain of the RET were demonstrated in patients with MEN 2A.	Cysteine	23-31	ret proto-oncogene	Homo sapiens	90-96
7906866-6	1994	All mutations occurred within codons specifying cysteine residues in the transition point between the RET protein extracellular and transmembrane domains.	Cysteine	48-56	ret proto-oncogene	Homo sapiens	102-105
7914213-0	1994	Identification of the Cys634--&gt;Tyr mutation of the RET proto-oncogene in a pedigree with multiple endocrine neoplasia type 2A and localized cutaneous lichen amyloidosis.	Tyrosine	34-37	ret proto-oncogene	Homo sapiens	54-57
7914213-0	1994	Identification of the Cys634--&gt;Tyr mutation of the RET proto-oncogene in a pedigree with multiple endocrine neoplasia type 2A and localized cutaneous lichen amyloidosis.	Tyrosine	34-37	ret proto-oncogene	Homo sapiens	92-128
7914213-3	1994	A cys634--&gt;tyr missense mutation, already reported as causative in MEN2A patients, was identified after SSCP analysis and direct sequencing of exon 11 of the RET protooncogene in one individual affected with both MEN2A and CLA, thus suggesting a common etiology for the two disorders.	Tyrosine	14-17	ret proto-oncogene	Homo sapiens	70-75
7914213-3	1994	A cys634--&gt;tyr missense mutation, already reported as causative in MEN2A patients, was identified after SSCP analysis and direct sequencing of exon 11 of the RET protooncogene in one individual affected with both MEN2A and CLA, thus suggesting a common etiology for the two disorders.	Tyrosine	14-17	ret proto-oncogene	Homo sapiens	161-164
7914213-3	1994	A cys634--&gt;tyr missense mutation, already reported as causative in MEN2A patients, was identified after SSCP analysis and direct sequencing of exon 11 of the RET protooncogene in one individual affected with both MEN2A and CLA, thus suggesting a common etiology for the two disorders.	Tyrosine	14-17	ret proto-oncogene	Homo sapiens	216-221
7911697-2	1994	The majority of MEN 2A and familial medullary thyroid carcinoma results from missense mutations within one of five cysteine codons in the extracellular domain of the RET proto-oncogene.	Cysteine	115-123	ret proto-oncogene	Homo sapiens	16-22
7911697-2	1994	The majority of MEN 2A and familial medullary thyroid carcinoma results from missense mutations within one of five cysteine codons in the extracellular domain of the RET proto-oncogene.	Cysteine	115-123	ret proto-oncogene	Homo sapiens	166-169
7911697-3	1994	We now report a missense mutation, resulting in the substitution of a threonine for a methionine at codon 918 in the tyrosine kinase catalytic domain, in the germline of 26 of 28 apparently distinct families with MEN 2B.	Threonine	70-79	ret proto-oncogene	Homo sapiens	213-219
7510705-9	1994	Activation of the activity of FGF receptor tyrosine kinase in smooth muscle cells by ligand binding resulted in tyrosine phosphorylation of one of the FGF receptors and a 90-kDa-protein as well as increased tyrosine phosphorylation of phospholipase C-gamma.	Tyrosine	112-120	ret proto-oncogene	Homo sapiens	34-58
7510340-5	1994	Inhibitory activity against EGF receptor tyrosine kinase was chain-length dependent, with the propanamides being the most effective.	propionamide	94-106	ret proto-oncogene	Homo sapiens	32-56
8114938-6	1994	Mutations in the extracellular cysteine-rich domain of Ret have been identified previously in patients with multiple endocrine neoplasia type 2A, and a targeted mutation in the tyrosine kinase domain of the same gene produces intestinal aganglionosis and kidney agenesis in homozygous transgenic mice.	Cysteine	31-39	ret proto-oncogene	Homo sapiens	55-58
7906866-8	1994	A mutation in codon 664, causing the substitution of a threonine for a methionine in the tyrosine kinase domain of the protein, was found in all nine unrelated MEN 2B patients studied.	Threonine	55-64	ret proto-oncogene	Homo sapiens	160-166
7906866-8	1994	A mutation in codon 664, causing the substitution of a threonine for a methionine in the tyrosine kinase domain of the protein, was found in all nine unrelated MEN 2B patients studied.	Methionine	71-81	ret proto-oncogene	Homo sapiens	160-166
7907913-3	1994	Mutations at one of 5 cysteines in the extracellular domain were found in 97% of patients with MEN 2A and 86% with FMTC but not in MEN 2B patients or normal controls.	Cysteine	22-31	ret proto-oncogene	Homo sapiens	95-101
7584011-9	1994	RET, a transmembrane receptor protein, has a large glycosylated extracellular domain containing clustered cysteine residues and calcium-binding motifs, a single hydrophobic transmembrane domain, and a cytoplasmic domain with tyrosine kinase catalytic activity.	Cysteine	106-114	ret proto-oncogene	Homo sapiens	0-3
7584011-9	1994	RET, a transmembrane receptor protein, has a large glycosylated extracellular domain containing clustered cysteine residues and calcium-binding motifs, a single hydrophobic transmembrane domain, and a cytoplasmic domain with tyrosine kinase catalytic activity.	Calcium	128-135	ret proto-oncogene	Homo sapiens	0-3
7584011-10	1994	Several germline missense mutations in a codon specifying one of these highly conserved cysteine residues have been detected in patients affected with MEN-2A.	Cysteine	88-96	ret proto-oncogene	Homo sapiens	151-157
7685595-2	1993	The 150 kDa and 170 kDa proto-Ret proteins immunoprecipitated with antibodies against their carboxy-terminal 20 amino acids were shown to be phosphorylated predominantly on tyrosine residues in immunocomplex kinase assay.	Tyrosine	173-181	ret proto-oncogene	Homo sapiens	30-33
8363602-0	1993	Inhibition of ret tyrosine kinase activity by herbimycin A.	herbimycin	46-58	ret proto-oncogene	Homo sapiens	14-17
8363602-2	1993	Herbimycin A reversed the morphology of NIH(ret) cells to flat cells with a concomitant reassembly of microfilament bundles.	herbimycin	0-12	ret proto-oncogene	Homo sapiens	44-47
8363602-4	1993	When tyrosine kinase activities of the active ret gene products in herbimycin A-treated NIH(ret) and TPC-1 cells were examined in immunocomplex kinase assays, they drastically decreased in both cells as compared with untreated cells.	herbimycin	67-79	ret proto-oncogene	Homo sapiens	46-49
8363602-4	1993	When tyrosine kinase activities of the active ret gene products in herbimycin A-treated NIH(ret) and TPC-1 cells were examined in immunocomplex kinase assays, they drastically decreased in both cells as compared with untreated cells.	herbimycin	67-79	ret proto-oncogene	Homo sapiens	92-95
8363602-5	1993	In addition, herbimycin A strongly inhibited tyrosine phosphorylation of 40 kDa and 31 kDa proteins present in the immunoprecipitates of both cells, suggesting that these proteins could associate with the Ret proteins.	herbimycin	13-25	ret proto-oncogene	Homo sapiens	205-208
8363602-5	1993	In addition, herbimycin A strongly inhibited tyrosine phosphorylation of 40 kDa and 31 kDa proteins present in the immunoprecipitates of both cells, suggesting that these proteins could associate with the Ret proteins.	Tyrosine	45-53	ret proto-oncogene	Homo sapiens	205-208
7685595-3	1993	The level of tyrosine phosphorylation of the 150 kDa proto-Ret protein was approximately 10-fold higher than that of the 170 kDa proto-Ret protein, although both proteins were expressed at similar levels in neuroblastoma cells.	Tyrosine	13-21	ret proto-oncogene	Homo sapiens	59-62
7685595-4	1993	This result was confirmed by using a lysate of SK-N-MC human primitive neuroectodermal tumor cells transfected with the ret proto-oncogene.	sk-n-mc	47-54	ret proto-oncogene	Homo sapiens	120-123
1766678-0	1991	Expression of the ret proto-oncogene in human neuroblastoma cell lines and its increase during neuronal differentiation induced by retinoic acid.	Tretinoin	131-144	ret proto-oncogene	Homo sapiens	18-21
8487750-1	1993	We have tested the hypothesis that activation of the insulin receptor tyrosine kinase is due to autophosphorylation of tyrosines 1146, 1150 and 1151 within a putative autoinhibitory domain.	Tyrosine	119-128	ret proto-oncogene	Homo sapiens	61-85
8487750-3	1993	This synthetic peptide gave inhibition of the insulin receptor tyrosine kinase autophosphorylation and phosphorylation of the exogenous substrate poly(Glu, Tyr) with an approximate IC50 of 100 microM.	poly	146-150	ret proto-oncogene	Homo sapiens	54-78
8487750-3	1993	This synthetic peptide gave inhibition of the insulin receptor tyrosine kinase autophosphorylation and phosphorylation of the exogenous substrate poly(Glu, Tyr) with an approximate IC50 of 100 microM.	Glutamic Acid	151-154	ret proto-oncogene	Homo sapiens	54-78
8487750-3	1993	This synthetic peptide gave inhibition of the insulin receptor tyrosine kinase autophosphorylation and phosphorylation of the exogenous substrate poly(Glu, Tyr) with an approximate IC50 of 100 microM.	Tyrosine	156-159	ret proto-oncogene	Homo sapiens	54-78
7678053-8	1993	RI alpha-ret transcripts encode two isoforms of the chimeric protein (p76 and p81), which display constitutive tyrosine phosphorylation as well as a tyrosine kinase enzymatic activity.	Tyrosine	111-119	ret proto-oncogene	Homo sapiens	9-12
1390993-5	1992	This differences were also found when we compare the number of RET and REA after the incubation of LN with SP and SN respectively (p less than 0.01, p less than 0.05).	Tin	114-116	ret proto-oncogene	Homo sapiens	63-66
1572907-5	1992	Tyrosine phosphorylation and TGF-alpha mRNA accumulation in response to EGF and TGF-alpha were both inhibited by a monoclonal antibody against the EGF receptor and by the EGF receptor tyrosine kinase inhibitor RG50864, demonstrating the involvement of the tyrosine kinase activity of the receptor in TGF-alpha autoinduction.	Tyrosine	0-8	ret proto-oncogene	Homo sapiens	175-199
8099202-7	1993	Further, 19 of these 20 mutations affect the same conserved cysteine residue at the boundary of the RET extracellular and transmembrane domains.	Cysteine	60-68	ret proto-oncogene	Homo sapiens	100-103
1437145-5	1992	An additional set of experiments led us to conclude that, whereas the normal product of the RET proto-oncogene is a membrane-associated receptor-like molecule not intrinsically phosphorylated on tyrosine, both oncogenic forms of RET, ptc-1 and ptc-2, are constitutively phosphorylated on tyrosine, display an "in vitro" autophosphorylation activity, are translocated from the membrane to the cytoplasm and are apparently unaffected by protein kinase C modulation.	Tyrosine	288-296	ret proto-oncogene	Homo sapiens	92-95
1766678-3	1991	Expression of proto-ret was detected in the neuronal subline, named SH-4305, but not in three non-neuronal sublines.	sh-4305	68-75	ret proto-oncogene	Homo sapiens	20-23
1766678-4	1991	Expression of proto-ret in the SH-4305 cells increased markedly after treatment with retinoic acid for 1 day, with concomitant morphological change, namely neurite outgrowth, and induction of neurofilament mRNA expression.	Tretinoin	85-98	ret proto-oncogene	Homo sapiens	20-23
34762884-6	2022	The fluorescence quenching of Fe3+ were mainly due to the competitive absorption of excitation source and RET, while the ACE mechanism was mostly responsible for the enhancement of As5+.	ferric sulfate	30-34	ret proto-oncogene	Homo sapiens	106-109
2000222-3	1991	When the neuroblastoma cells were treated with tunicamycin, a protein with an apparent molecular weight of 120 kd, which is consistent with that of the c-ret protein predicted from the cDNA sequence, appeared on immunoblots.	Tunicamycin	47-58	ret proto-oncogene	Homo sapiens	154-157
33771190-5	2021	Selpercatinib (LOXO-292) and pralsetinib (BLU-667) are potent and selective inhibitors that target RET alterations, including fusions and mutations, irrespective of the tissue of origin.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	99-102
33771190-6	2021	Recently, the results from the LIBRETTO-001 and ARROW clinical trials demonstrated significant clinical benefits with selpercatinib and pralsetinib respectively, in NSCLC patients with RET gene fusions, with tolerable toxicity profiles.	Selpercatinib	118-131	ret proto-oncogene	Homo sapiens	34-37
20148858-4	2010	Polystyrene microbeads barcoded by fluoresceine isothiocyanate fluorescence as high brightness and low brightness microspheres were coated with receptor tyrosine kinase (RTK) ligand-epidermal growth factor (EGF)/stem cell factor (SCF) and ATP/GTP, respectively.	Polystyrenes	0-11	ret proto-oncogene	Homo sapiens	144-168
20148858-4	2010	Polystyrene microbeads barcoded by fluoresceine isothiocyanate fluorescence as high brightness and low brightness microspheres were coated with receptor tyrosine kinase (RTK) ligand-epidermal growth factor (EGF)/stem cell factor (SCF) and ATP/GTP, respectively.	Polystyrenes	0-11	ret proto-oncogene	Homo sapiens	170-173
2107492-0	1990	2-Aminopurine abolishes EGF- and TPA-stimulated pp33 phosphorylation and c-fos induction without affecting the activation of protein kinase C. Epidermal Growth Factor (EGF) and Tetradecanoyl Phorbol Acetate (TPA) initiate signalling cascades in C3H 10T1/2 fibroblasts by primarily activating distinct protein kinases, the EGF receptor tyrosine kinase and protein kinase C respectively; there is no signal crossover at the initiation of signalling.	2-Aminopurine	0-13	ret proto-oncogene	Homo sapiens	326-350
2107492-0	1990	2-Aminopurine abolishes EGF- and TPA-stimulated pp33 phosphorylation and c-fos induction without affecting the activation of protein kinase C. Epidermal Growth Factor (EGF) and Tetradecanoyl Phorbol Acetate (TPA) initiate signalling cascades in C3H 10T1/2 fibroblasts by primarily activating distinct protein kinases, the EGF receptor tyrosine kinase and protein kinase C respectively; there is no signal crossover at the initiation of signalling.	Tetradecanoylphorbol Acetate	33-36	ret proto-oncogene	Homo sapiens	326-350
33768672-8	2021	The tyrosine phosphorylation patterns differed between ALK, ROS1 and RET fusions, suggesting that oncogenic signaling induced by these kinases involves the modulation of different cellular processes.	Tyrosine	4-12	ret proto-oncogene	Homo sapiens	69-72
34762884-6	2022	The fluorescence quenching of Fe3+ were mainly due to the competitive absorption of excitation source and RET, while the ACE mechanism was mostly responsible for the enhancement of As5+.	arsenic(5+)	181-185	ret proto-oncogene	Homo sapiens	106-109
34822305-4	2022	Multiple linear regression was used to analyze the correlation of risk factors (PCT or ATF4 expression, RET mutation, tumor differentiation, SMTC stage, lymphatic metastasis) for 5-year recurrence and survival of SMTC.	smtc	213-217	ret proto-oncogene	Homo sapiens	104-107
34710947-2	2022	Approval of Retevmo (Selpercatinib) for treatment of lung and thyroid cancer with RET gene mutations or fusions, calls for studies to explore RET fusion partners and their eligibility for RET based targeted therapy.	Selpercatinib	21-34	ret proto-oncogene	Homo sapiens	82-85
34400874-6	2022	Subsequently, the PEI-Ru@Ti3C2@AuNPs-S7 probes were used to combine with the excised hairpin part of TDNAs on the surface of Au-g-C3N4, and the signal change was realized employing electrochemiluminescence resonance energy transfer (ECL-RET).	Gold	125-127	ret proto-oncogene	Homo sapiens	237-240
34822305-8	2022	ATF4 and PCT expressions combined with RET mutation are related to the clinical prognosis of SMTC and can predict SMTC staging.	smtc	93-97	ret proto-oncogene	Homo sapiens	39-42
34822305-8	2022	ATF4 and PCT expressions combined with RET mutation are related to the clinical prognosis of SMTC and can predict SMTC staging.	smtc	114-118	ret proto-oncogene	Homo sapiens	39-42
34743497-9	2021	Pralsetinib and selpercatinib have been developed as tyrosine kinase inhibitors (TKI) selectively targeting RET variation of fusions or mutations, and both agents significantly improved the prognosis of patients with RET fusion-positive NSCLC.	Selpercatinib	16-29	ret proto-oncogene	Homo sapiens	108-111
34246540-0	2022	Central Nervous System Response to Selpercartinib in Patient With RET-rearranged Non-small Cell Lung Cancer After Developing Leptomeningeal Disease on Pralsetinib.	selpercartinib	35-49	ret proto-oncogene	Homo sapiens	66-69
34743497-9	2021	Pralsetinib and selpercatinib have been developed as tyrosine kinase inhibitors (TKI) selectively targeting RET variation of fusions or mutations, and both agents significantly improved the prognosis of patients with RET fusion-positive NSCLC.	Selpercatinib	16-29	ret proto-oncogene	Homo sapiens	217-220
34921013-5	2022	To identify strategies that can improve PDAC sensitivity to HCQ, we applied a CRISPR-Cas9 loss-of-function screen and found that a top sensitizer was the receptor tyrosine kinase (RTK) insulin-like growth factor 1 receptor (IGF1R).	Hydroxychloroquine	60-63	ret proto-oncogene	Homo sapiens	154-178
34921013-5	2022	To identify strategies that can improve PDAC sensitivity to HCQ, we applied a CRISPR-Cas9 loss-of-function screen and found that a top sensitizer was the receptor tyrosine kinase (RTK) insulin-like growth factor 1 receptor (IGF1R).	Hydroxychloroquine	60-63	ret proto-oncogene	Homo sapiens	180-183
34957368-12	2021	Moreover, RET-CCDC6 fusion and EGFR mutation were detected following crizotinib treatment in two patients, suggesting novel mechanisms of resistance.	Crizotinib	69-79	ret proto-oncogene	Homo sapiens	10-13
34913799-6	2021	Ret-He and IRF have been established as the marker of iron deficiency and iron-deficiency anaemia in different age groups and as a marker of response to iron therapy.	Iron	153-157	ret proto-oncogene	Homo sapiens	0-3
34925234-0	2021	Germline RET Leu56Met Variant Is Likely Not Causative of Multiple Endocrine Neoplasia Type 2.	leu56met	13-21	ret proto-oncogene	Homo sapiens	9-12
34894066-2	2022	Imatinib, a receptor tyrosine kinase (RTK) inhibitor, has been used in Penttinen syndrome (PS) patients with good results.	Imatinib Mesylate	0-8	ret proto-oncogene	Homo sapiens	12-36
34894066-2	2022	Imatinib, a receptor tyrosine kinase (RTK) inhibitor, has been used in Penttinen syndrome (PS) patients with good results.	Imatinib Mesylate	0-8	ret proto-oncogene	Homo sapiens	38-41
34944663-8	2021	Based on this finding, we tested the efficacy of hydrazostat in combination with RTK inhibitor imatinib.	Imatinib Mesylate	95-103	ret proto-oncogene	Homo sapiens	81-84
34741450-11	2021	In those with microsatellite-stable mCRC, patients with RET mutations had a higher median TMB than patients with wild-type RET (9.4 vs. 6.7 mutations/Mb, respectively, p = 0.001).	1,2,4,5-tetramethoxybenzene	90-93	ret proto-oncogene	Homo sapiens	56-59
34925234-2	2021	The variant c.166C>A, p.Leu56Met in RET was recently reported in two patients with medullary thyroid cancer (MTC).	leu56met	24-32	ret proto-oncogene	Homo sapiens	36-39
34925234-4	2021	Here, we present clinical follow up of a Danish RET Leu56Met cohort.	leu56met	52-60	ret proto-oncogene	Homo sapiens	48-51
34517600-3	2021	The absorption spectrum of Cu2S and the ECL emission spectrum of the donor could be highly matched, which ensured the occurrence of electrochemiluminescence resonance energy transfer (ECL-RET).	Copper(I) sulfide	27-31	ret proto-oncogene	Homo sapiens	188-191
34216952-3	2021	The prepared catalyst exhibited superior catalytic activity towards oxygen reduction reaction (ORR) such as the more positive onset potential of 0.96 V, half-wave potential of 0.86 V and smaller Tafel slope of 67.9 mV dec-1, outperforming those of commercial Pt/C.	Oxygen	68-74	ret proto-oncogene	Homo sapiens	259-263
34517600-6	2021	Furthermore, the ECL-RET system based on this has shown excellent performance in the detection of florfenicol.	florfenicol	98-109	ret proto-oncogene	Homo sapiens	21-24
34803090-4	2021	We conducted an investigator-initiated trial of alectinib, which also has RET kinase-inhibitory activity, against RET-rearranged NSCLC.	alectinib	48-57	ret proto-oncogene	Homo sapiens	74-77
34900714-0	2021	Zotatifin, an eIF4A-Selective Inhibitor, Blocks Tumor Growth in Receptor Tyrosine Kinase Driven Tumors.	Zotatifin	0-9	ret proto-oncogene	Homo sapiens	64-88
34391699-5	2021	Recently, highly potent and RET-specific inhibitors selpercatinib and pralsetinib were successfully translated to the clinic and FDA approved.	Selpercatinib	52-65	ret proto-oncogene	Homo sapiens	28-31
34803090-4	2021	We conducted an investigator-initiated trial of alectinib, which also has RET kinase-inhibitory activity, against RET-rearranged NSCLC.	alectinib	48-57	ret proto-oncogene	Homo sapiens	114-117
34803090-5	2021	Two RET-rearranged NSCLC patients experienced severe skin toxicity with alectinib after first undergoing anti-PD-1 antibody treatment with an ICI.	alectinib	72-81	ret proto-oncogene	Homo sapiens	4-7
34858321-6	2021	Genetic testing revealed heterozygosity for a mutation at codon 634 in exon 11 (TGC-TTC mutation; p.Cys634Phe) of the Ret gene.	cys634phe	100-109	ret proto-oncogene	Homo sapiens	118-121
34830178-4	2021	Cabozantinib is a receptor tyrosine kinase (RTK) inhibitor, already approved for the treatment of non-skin-related cancers.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	18-42
34830178-4	2021	Cabozantinib is a receptor tyrosine kinase (RTK) inhibitor, already approved for the treatment of non-skin-related cancers.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	44-47
34830178-9	2021	The phosphorylated RTKs p-PDGF-Ralpha, p-IGF-1R, p-MERTK and p-DDR1 were found to be downregulated in the p-RTK array of the MBM cells after cabozantinib treatment.	cabozantinib	141-153	ret proto-oncogene	Homo sapiens	108-111
34858321-7	2021	Intracranial vascular stenosis may have been caused by a genetic mutation of RNF213 and hypersecretion of catecholamines by MEN2A.	Catecholamines	106-120	ret proto-oncogene	Homo sapiens	124-129
34729775-4	2022	The presence of KIT proto-oncogene, receptor tyrosine kinase (KIT)D816V predicted response in adv-SM: 17 (90%) of 19 with and none of three without the mutation responded (P < 0 01).	adv-sm	94-100	ret proto-oncogene	Homo sapiens	36-60
34725737-0	2021	How does nintedanib overcome cancer drug-resistant mutation of RET protein-tyrosine kinase: insights from molecular dynamics simulations.	nintedanib	9-19	ret proto-oncogene	Homo sapiens	63-66
34725737-5	2021	Nintedanib can effectively inhibit the RET L881V mutant, whereas its analog compound 1 is unable to combat this mutant.	nintedanib	0-10	ret proto-oncogene	Homo sapiens	39-42
34725737-7	2021	Here, molecular dynamics (MD) simulations, binding free energy calculations, and structural analysis were performed to uncover the mechanism of overcoming the resistance of RET L881V mutant to nintedanib.	nintedanib	193-203	ret proto-oncogene	Homo sapiens	173-176
34713899-11	2022	In a subset of 19 patients with aggressive disease who had molecular testing as part of clinical care we detected RET fusions in nearly all DSV compared to a minority of N-PTC (83% vs. 15.4%, P = .0095).	dsv	140-143	ret proto-oncogene	Homo sapiens	114-117
34419556-0	2021	Significant response of medullary thyroid cancer choroidal metastases to highly selective RET inhibitor selpercatinib: a case report.	Selpercatinib	104-117	ret proto-oncogene	Homo sapiens	90-93
34826838-6	2021	Oncogenic mutations in the RET protooncogene occur in ~25 % of patients as part of the multiple endocrine neoplasia type 2 syndromes and are present as somatic mutations in 60 % of all MTC and up to 90 % of metastatic cases.The multi-tyrosine kinase inhibitors vandetanib and cabozantinib have been approved for progressive advanced disease but have low specificity for the RET tyrosine kinase.	cabozantinib	276-288	ret proto-oncogene	Homo sapiens	27-30
34826838-7	2021	With the advent of highly selective RET inhibitors selpercatinib and pralsetinib, the treatment landscape has profoundly changed.	Selpercatinib	51-64	ret proto-oncogene	Homo sapiens	36-39
34994624-0	2021	Divergent RET- and BRAF-Mediated Resistance to Osimertinib in EGFR-Mutant NSCLC: A Case Report.	osimertinib	47-58	ret proto-oncogene	Homo sapiens	10-13
34994633-0	2021	Novel RET Fusion RET-SEPTIN9 Predicts Response to Selective RET Inhibition With Selpercatinib in Malignant Pheochromocytoma.	Selpercatinib	80-93	ret proto-oncogene	Homo sapiens	6-9
34994633-0	2021	Novel RET Fusion RET-SEPTIN9 Predicts Response to Selective RET Inhibition With Selpercatinib in Malignant Pheochromocytoma.	Selpercatinib	80-93	ret proto-oncogene	Homo sapiens	17-20
34994633-0	2021	Novel RET Fusion RET-SEPTIN9 Predicts Response to Selective RET Inhibition With Selpercatinib in Malignant Pheochromocytoma.	Selpercatinib	80-93	ret proto-oncogene	Homo sapiens	60-63
34792279-1	2021	Herein, a label-free and immobilization-free electrochemiluminescence resonance energy transfer (ECL-RET) system based on graphitic carbon nitride nanosheets (GCNNs)/Ru(phen)3 2+ donor/acceptor pair is developed, in which the ECL-RET is regulated by regulating the diffusivity of Ru(phen)3 2+ molecules toward the negatively charged GCNNs through logically programmed DNA hybridization reactions.	cyanogen	132-146	ret proto-oncogene	Homo sapiens	101-104
34792279-1	2021	Herein, a label-free and immobilization-free electrochemiluminescence resonance energy transfer (ECL-RET) system based on graphitic carbon nitride nanosheets (GCNNs)/Ru(phen)3 2+ donor/acceptor pair is developed, in which the ECL-RET is regulated by regulating the diffusivity of Ru(phen)3 2+ molecules toward the negatively charged GCNNs through logically programmed DNA hybridization reactions.	cyanogen	132-146	ret proto-oncogene	Homo sapiens	230-233
34792279-1	2021	Herein, a label-free and immobilization-free electrochemiluminescence resonance energy transfer (ECL-RET) system based on graphitic carbon nitride nanosheets (GCNNs)/Ru(phen)3 2+ donor/acceptor pair is developed, in which the ECL-RET is regulated by regulating the diffusivity of Ru(phen)3 2+ molecules toward the negatively charged GCNNs through logically programmed DNA hybridization reactions.	ru(phen)	166-174	ret proto-oncogene	Homo sapiens	101-104
34792279-1	2021	Herein, a label-free and immobilization-free electrochemiluminescence resonance energy transfer (ECL-RET) system based on graphitic carbon nitride nanosheets (GCNNs)/Ru(phen)3 2+ donor/acceptor pair is developed, in which the ECL-RET is regulated by regulating the diffusivity of Ru(phen)3 2+ molecules toward the negatively charged GCNNs through logically programmed DNA hybridization reactions.	ru(phen)	166-174	ret proto-oncogene	Homo sapiens	230-233
34792279-1	2021	Herein, a label-free and immobilization-free electrochemiluminescence resonance energy transfer (ECL-RET) system based on graphitic carbon nitride nanosheets (GCNNs)/Ru(phen)3 2+ donor/acceptor pair is developed, in which the ECL-RET is regulated by regulating the diffusivity of Ru(phen)3 2+ molecules toward the negatively charged GCNNs through logically programmed DNA hybridization reactions.	ru(phen)	280-288	ret proto-oncogene	Homo sapiens	101-104
34792279-1	2021	Herein, a label-free and immobilization-free electrochemiluminescence resonance energy transfer (ECL-RET) system based on graphitic carbon nitride nanosheets (GCNNs)/Ru(phen)3 2+ donor/acceptor pair is developed, in which the ECL-RET is regulated by regulating the diffusivity of Ru(phen)3 2+ molecules toward the negatively charged GCNNs through logically programmed DNA hybridization reactions.	ru(phen)	280-288	ret proto-oncogene	Homo sapiens	230-233
34834190-2	2021	Multiple kinase inhibitors vandetanib and cabozantinib are commonly used in the treatment of RET-positive NSCLC.	vandetanib	27-37	ret proto-oncogene	Homo sapiens	93-96
34834190-2	2021	Multiple kinase inhibitors vandetanib and cabozantinib are commonly used in the treatment of RET-positive NSCLC.	cabozantinib	42-54	ret proto-oncogene	Homo sapiens	93-96
34649088-2	2021	Therefore, in children with MEN2 and advanced MTC, the RET tyrosine kinase (TK) pathway is a target for treatment with selpercatinib, a selective RET TK inhibitor.	Selpercatinib	119-132	ret proto-oncogene	Homo sapiens	146-149
34649088-12	2021	CONCLUSION: Selpercatinib has shown excellent therapeutic efficacy with minimal toxicity in children with MEN2 and progressive metastatic RET-mutated MTC.	Selpercatinib	12-25	ret proto-oncogene	Homo sapiens	138-141
34713870-0	2021	Selpercatinib for lung and thyroid cancers with RET gene mutations or fusions.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	48-51
34225542-1	2021	Introduction: Alectinib is a second-generation inhibitor of anaplastic lymphoma kinase (ALK) and RET.	alectinib	14-23	ret proto-oncogene	Homo sapiens	97-100
34405703-0	2021	Selpercatinib-Enhanced Radioiodine Uptake in RET-Rearranged Thyroid Cancer.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	45-48
34493590-2	2021	The recent FDA approvals of highly potent and selective RET inhibitors, selpercatinib and pralsetinib, has altered the therapeutic management of RET aberrant tumors.	Selpercatinib	72-85	ret proto-oncogene	Homo sapiens	56-59
34493590-2	2021	The recent FDA approvals of highly potent and selective RET inhibitors, selpercatinib and pralsetinib, has altered the therapeutic management of RET aberrant tumors.	Selpercatinib	72-85	ret proto-oncogene	Homo sapiens	145-148
34405703-5	2021	Selpercatinib a highly selective RET inhibitor, was recently approved by the FDA for the treatment of RET fusion-positive lung and thyroid cancers.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	33-36
34405703-5	2021	Selpercatinib a highly selective RET inhibitor, was recently approved by the FDA for the treatment of RET fusion-positive lung and thyroid cancers.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	102-105
34405703-6	2021	We had the unprecedented opportunity to observe restoration of iodine-131 uptake after selpercatinib treatment for a non-radioiodine avid metastatic thyroid cancer with a RET/PTC3 fusion gene.	Iodine	63-69	ret proto-oncogene	Homo sapiens	171-174
34405703-6	2021	We had the unprecedented opportunity to observe restoration of iodine-131 uptake after selpercatinib treatment for a non-radioiodine avid metastatic thyroid cancer with a RET/PTC3 fusion gene.	Selpercatinib	87-100	ret proto-oncogene	Homo sapiens	171-174
34405703-7	2021	CONCLUSION: This finding of a redifferentiation effect with selpercatinib targeting a RET fusion gene, reinforces the proof of concept of this new therapeutic opportunity.	Selpercatinib	60-73	ret proto-oncogene	Homo sapiens	86-89
34405703-9	2021	Furthermore, the combined approach with a targeted therapy and radioactive iodine may increase anti-tumor efficacy and minimize acquired resistance to RET inhibitors.	radioactive iodine	63-81	ret proto-oncogene	Homo sapiens	151-154
34237031-0	2021	NTRK- and RET-fusion-directed therapy in pediatric thyroid cancer yields a tumor response and radioiodine uptake.	Iodine-131	94-105	ret proto-oncogene	Homo sapiens	10-13
34583388-7	2022	For this reason, two selective RET inhibitors (selpercatinib, pralsetinib) for differentiated thyroid carcinomas were approved by the FDA in 2020.	Selpercatinib	47-60	ret proto-oncogene	Homo sapiens	31-34
34551970-3	2022	Vandetanib, an inhibitor of VEGFR/RET/EGFR, was found to target ACVR1 (Kd=150nM) and reduce DIPG cell viability in vitro, but has limited ability to cross the blood-brain-barrier.	vandetanib	0-10	ret proto-oncogene	Homo sapiens	34-37
34523607-4	2021	Lee, H. Lee, and colleagues showed that oncogenic fusions were more commonly associated with invasive disease, increased expression of MAPK signaling pathway genes (ERK score), and decreased expression of the sodium-iodine symporter, which was restored by RET- and NTRK-inhibitory therapy.	Sodium iodine	209-222	ret proto-oncogene	Homo sapiens	256-259
34523767-14	2022	In a phase 1/2 trial, improvements in HRQoL were observed in over 60% of patients with advanced RET fusion-positive NSCLC who received selpercatinib, a highly selective RET inhibitor.	Selpercatinib	135-148	ret proto-oncogene	Homo sapiens	96-99
34523767-14	2022	In a phase 1/2 trial, improvements in HRQoL were observed in over 60% of patients with advanced RET fusion-positive NSCLC who received selpercatinib, a highly selective RET inhibitor.	Selpercatinib	135-148	ret proto-oncogene	Homo sapiens	169-172
34237031-7	2021	Two girls with progressive 131I-refractory lung metastases harboring a TPR-NTRK1 or CCDC6-RET fusion received fusion-targeted therapy; larotrectinib and selpercatinib decreased the tumor extent and restored radioiodine uptake.	larotrectinib	135-148	ret proto-oncogene	Homo sapiens	90-93
34237031-7	2021	Two girls with progressive 131I-refractory lung metastases harboring a TPR-NTRK1 or CCDC6-RET fusion received fusion-targeted therapy; larotrectinib and selpercatinib decreased the tumor extent and restored radioiodine uptake.	Selpercatinib	153-166	ret proto-oncogene	Homo sapiens	90-93
34237031-8	2021	The girl with the CCDC6-RET fusion received 131I therapy combined with selpercatinib, leading to a tumor response.	Selpercatinib	71-84	ret proto-oncogene	Homo sapiens	24-27
34190716-9	2021	In vandetanib treated patients, Ki-67 was reduced 0.3% in RET-positive tumors compared with increased 1.0% in RET-negative tumors, P=0.43 and TUNEL was increased 0.77 in RET-positive tumors and 0.2 in RET-negative tumors, P=0.21.	vandetanib	3-13	ret proto-oncogene	Homo sapiens	58-61
34516023-16	2022	Over 40% of patients with RET-mutant MTC who received selpercatinib, a highly selective RET inhibitor, reported clinical meaningful improvements in diarrhea in a phase I/2 study.	Selpercatinib	54-67	ret proto-oncogene	Homo sapiens	88-91
34477517-8	2022	Other pathways like MAPKs and COMT and receptor tyrosine kinase are also affected by catechin and EGCG that alter their action and barge the cellular activity.	Catechin	85-93	ret proto-oncogene	Homo sapiens	39-63
34477517-8	2022	Other pathways like MAPKs and COMT and receptor tyrosine kinase are also affected by catechin and EGCG that alter their action and barge the cellular activity.	epigallocatechin gallate	98-102	ret proto-oncogene	Homo sapiens	39-63
34190716-9	2021	In vandetanib treated patients, Ki-67 was reduced 0.3% in RET-positive tumors compared with increased 1.0% in RET-negative tumors, P=0.43 and TUNEL was increased 0.77 in RET-positive tumors and 0.2 in RET-negative tumors, P=0.21.	vandetanib	3-13	ret proto-oncogene	Homo sapiens	170-173
34190716-9	2021	In vandetanib treated patients, Ki-67 was reduced 0.3% in RET-positive tumors compared with increased 1.0% in RET-negative tumors, P=0.43 and TUNEL was increased 0.77 in RET-positive tumors and 0.2 in RET-negative tumors, P=0.21.	vandetanib	3-13	ret proto-oncogene	Homo sapiens	201-204
34190716-11	2021	In accordance with the investigational hypothesis, there was a nonsignificant trend with vandetanib treatment of reduction in p-ERK and increased effects in Ret expressing tumors.	vandetanib	89-99	ret proto-oncogene	Homo sapiens	157-160
34428101-5	2021	Lenvatinib is a multitargeted tyrosine kinase inhibitor of VEGFR1-3, FGFR1-4, PDGFRalpha, RET, and KIT signaling networks implicated in tumor angiogenesis, approved in locally recurrent or metastatic, progressive, RAI-refractory DTC.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	90-93
34503226-5	2021	More recently, two selective RET inhibitors, selpercatinib and pralsetinib, demonstrated higher efficacy rates and good tolerability and they were approved for the treatment of patients with metastatic RET fusion-positive NSCLC on the bases of the results of phase II studies.	Selpercatinib	45-58	ret proto-oncogene	Homo sapiens	29-32
34503226-5	2021	More recently, two selective RET inhibitors, selpercatinib and pralsetinib, demonstrated higher efficacy rates and good tolerability and they were approved for the treatment of patients with metastatic RET fusion-positive NSCLC on the bases of the results of phase II studies.	Selpercatinib	45-58	ret proto-oncogene	Homo sapiens	202-205
34733735-4	2021	Multikinase inhibitors (MKIs) such as cabozantinib, vandetanib and lenvatinib, as well as selective inhibitors of RET alterations like selpercatinib (LOXO-292) and pralsetinib (BLU-667) have been approved by the Food and Drug Administration (FDA) for patients with RET fusion-positive tumors, such as thyroid cancer, renal cell, NSCLC, and so on.	cabozantinib	38-50	ret proto-oncogene	Homo sapiens	265-268
34733735-4	2021	Multikinase inhibitors (MKIs) such as cabozantinib, vandetanib and lenvatinib, as well as selective inhibitors of RET alterations like selpercatinib (LOXO-292) and pralsetinib (BLU-667) have been approved by the Food and Drug Administration (FDA) for patients with RET fusion-positive tumors, such as thyroid cancer, renal cell, NSCLC, and so on.	Selpercatinib	135-148	ret proto-oncogene	Homo sapiens	114-117
34733735-4	2021	Multikinase inhibitors (MKIs) such as cabozantinib, vandetanib and lenvatinib, as well as selective inhibitors of RET alterations like selpercatinib (LOXO-292) and pralsetinib (BLU-667) have been approved by the Food and Drug Administration (FDA) for patients with RET fusion-positive tumors, such as thyroid cancer, renal cell, NSCLC, and so on.	Selpercatinib	135-148	ret proto-oncogene	Homo sapiens	265-268
34733735-9	2021	In this study, we reported an ERC1-RET fusion in a 60-year-old female patient with PDAC.	pdac	83-87	ret proto-oncogene	Homo sapiens	35-38
34733735-10	2021	To the best of our knowledge, this case was the first report about ERC1-RET fusion in a patient with PDAC.	pdac	101-105	ret proto-oncogene	Homo sapiens	72-75
34445927-3	2021	AREAS COVERED: We present an up-to-date evaluation of preclinical evidence for RTK inhibition with cabozantinib, specifically VEGFR, MET, KIT, RET, AXL, FLT3, and associated antitumor effects.	cabozantinib	99-111	ret proto-oncogene	Homo sapiens	79-82
34445927-3	2021	AREAS COVERED: We present an up-to-date evaluation of preclinical evidence for RTK inhibition with cabozantinib, specifically VEGFR, MET, KIT, RET, AXL, FLT3, and associated antitumor effects.	cabozantinib	99-111	ret proto-oncogene	Homo sapiens	143-146
33691844-3	2021	As a result, higher electrochemical surface area (ECSA) and methanol oxidation reactions were obtained, and the electrochemical properties of Pt-c(NH2-MIL-101)@NCNT are better than pristine Pt-c(NH2-MIL-101).	Methanol	60-68	ret proto-oncogene	Homo sapiens	142-146
34402300-4	2021	In 2020, RET-selective inhibitors pralsetinib and selpercatinib achieved clinical approval, which marked the first approvals for kinase inhibitors specifically developed to target the RET oncoprotein.	Selpercatinib	50-63	ret proto-oncogene	Homo sapiens	9-12
34402300-4	2021	In 2020, RET-selective inhibitors pralsetinib and selpercatinib achieved clinical approval, which marked the first approvals for kinase inhibitors specifically developed to target the RET oncoprotein.	Selpercatinib	50-63	ret proto-oncogene	Homo sapiens	184-187
34342436-5	2021	Because of the specific recognition of the aptamer toward ATX-a, an intricate design of the DNA sequence enabled the exposure of the Ag+-dependent DNAzyme sequence and H2O2 in situ generated Ag+ triggering a catalytic cleavage reaction to freely release the two ECL-RET energy acceptors, thus switching the ECL signal significantly and achieving ultrasensitive detection.	Hydrogen Peroxide	168-172	ret proto-oncogene	Homo sapiens	266-269
34387474-2	2021	By studying the binding interactions between RNA folds and known small-molecule medicines and mining the resultant dataset across human RNAs, we identified that Dovitinib, a receptor tyrosine kinase (RTK) inhibitor, binds the precursor to microRNA-21 (pre-miR-21).	4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one	161-170	ret proto-oncogene	Homo sapiens	174-198
34505490-2	2021	Selpercatinib and pralsetinib are tyrosine kinase inhibitors selectively targeting RET and with clinical activity in RET-positive NSCLC.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	83-86
34505490-2	2021	Selpercatinib and pralsetinib are tyrosine kinase inhibitors selectively targeting RET and with clinical activity in RET-positive NSCLC.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	117-120
34497761-3	2021	Clinical trials of multikinase inhibitors, including cabozantinib, vandetanib, sorafenib, and lenvatinib, that inhibit RET oncogene activity have shown their antitumor efficacy.	cabozantinib	53-65	ret proto-oncogene	Homo sapiens	119-122
34497761-3	2021	Clinical trials of multikinase inhibitors, including cabozantinib, vandetanib, sorafenib, and lenvatinib, that inhibit RET oncogene activity have shown their antitumor efficacy.	vandetanib	67-77	ret proto-oncogene	Homo sapiens	119-122
34497761-3	2021	Clinical trials of multikinase inhibitors, including cabozantinib, vandetanib, sorafenib, and lenvatinib, that inhibit RET oncogene activity have shown their antitumor efficacy.	lenvatinib	94-104	ret proto-oncogene	Homo sapiens	119-122
34497761-4	2021	Recently, RET inhibitors such as pralsetinib and selpercatinib that are specialized for RET kinase have also been developed, and their efficacy was investigated in previous clinical trials (BLU-667 and LOXO-292).	Selpercatinib	49-62	ret proto-oncogene	Homo sapiens	10-13
34497761-4	2021	Recently, RET inhibitors such as pralsetinib and selpercatinib that are specialized for RET kinase have also been developed, and their efficacy was investigated in previous clinical trials (BLU-667 and LOXO-292).	Selpercatinib	49-62	ret proto-oncogene	Homo sapiens	88-91
34522862-4	2021	Until now, ECL-RET biosensors have been designed for sensing short single-stranded oligonucleotides of less than 45 nucleotides.	Oligonucleotides	83-99	ret proto-oncogene	Homo sapiens	15-18
34522862-5	2021	In this work, an ECL-RET biosensor comprising graphitic carbon nitride quantum dots was assessed for the amplification-free detection in the blood plasma of DNA molecules coding for the EGFR L858R mutation, which is associated with non-small-cell lung cancer.	cyanogen	56-70	ret proto-oncogene	Homo sapiens	21-24
34283563-4	2021	The ECL resonance energy transfer (ECL-RET) between the hollow manganese dioxide nanospheres and luminol results in a conspicuously decreased ECL signal response, and in the presence of glutathione (GSH), effective redox reaction between manganese dioxide and GSH restores the ECL signal.	manganese dioxide	63-80	ret proto-oncogene	Homo sapiens	39-42
34373541-0	2021	Targeted activity of the small molecule kinase inhibitor Pz-1 towards RET and TRK kinases.	Pz-1	57-61	ret proto-oncogene	Homo sapiens	70-73
34373541-1	2021	We have recently described Pz-1, a benzimidazole-based type-2 RET and VEGFR2 inhibitor.	Pz-1	27-31	ret proto-oncogene	Homo sapiens	62-65
34373541-1	2021	We have recently described Pz-1, a benzimidazole-based type-2 RET and VEGFR2 inhibitor.	benzimidazole	35-48	ret proto-oncogene	Homo sapiens	62-65
34373541-3	2021	Pz-1 potently inhibited proliferation of human cancer cells carrying either RET- or TRKA oncoproteins (IC50 ~ 1 nM), with a negligible effect against RET- and TRKA-negative cells.	Pz-1	0-4	ret proto-oncogene	Homo sapiens	76-79
34373541-6	2021	In xenograft models, orally administered Pz-1 almost completely inhibited RET- and TRKA-mutant tumours at 1-3 mg/kg/day but showed a reduced effect on RET/TRKA-negative cancer models.	Pz-1	41-45	ret proto-oncogene	Homo sapiens	74-77
34283563-4	2021	The ECL resonance energy transfer (ECL-RET) between the hollow manganese dioxide nanospheres and luminol results in a conspicuously decreased ECL signal response, and in the presence of glutathione (GSH), effective redox reaction between manganese dioxide and GSH restores the ECL signal.	Luminol	97-104	ret proto-oncogene	Homo sapiens	39-42
34283563-4	2021	The ECL resonance energy transfer (ECL-RET) between the hollow manganese dioxide nanospheres and luminol results in a conspicuously decreased ECL signal response, and in the presence of glutathione (GSH), effective redox reaction between manganese dioxide and GSH restores the ECL signal.	Glutathione	186-197	ret proto-oncogene	Homo sapiens	39-42
34283563-4	2021	The ECL resonance energy transfer (ECL-RET) between the hollow manganese dioxide nanospheres and luminol results in a conspicuously decreased ECL signal response, and in the presence of glutathione (GSH), effective redox reaction between manganese dioxide and GSH restores the ECL signal.	manganese dioxide	238-255	ret proto-oncogene	Homo sapiens	39-42
34283563-4	2021	The ECL resonance energy transfer (ECL-RET) between the hollow manganese dioxide nanospheres and luminol results in a conspicuously decreased ECL signal response, and in the presence of glutathione (GSH), effective redox reaction between manganese dioxide and GSH restores the ECL signal.	Glutathione	260-263	ret proto-oncogene	Homo sapiens	39-42
34283563-5	2021	As a consequence, the designed sensor based on ECL-RET-assisted Au/VO2 signal amplification showed outstanding performance for "signal-on" detection of GSH in the concentration range of 10-3 to 10-10 M, and the detection limit was as low as 0.03 nM.	Glutathione	152-155	ret proto-oncogene	Homo sapiens	51-54
34088726-0	2021	Intracranial efficacy of selpercatinib in RET fusion-positive non-small cell lung cancers on the LIBRETTO-001 trial.	Selpercatinib	25-38	ret proto-oncogene	Homo sapiens	42-45
34344199-0	2022	Combination EGFR and RET Inhibition in Acquired Resistance to Osimertinib in EGFR-Mutant NSCLC.	osimertinib	62-73	ret proto-oncogene	Homo sapiens	21-24
34088726-1	2021	PURPOSE: We report the intracranial efficacy of selpercatinib, a highly potent and selective RET inhibitor, approved in the US for RET fusion-positive non-small cell lung cancers (NSCLCs).	Selpercatinib	48-61	ret proto-oncogene	Homo sapiens	93-96
34088726-1	2021	PURPOSE: We report the intracranial efficacy of selpercatinib, a highly potent and selective RET inhibitor, approved in the US for RET fusion-positive non-small cell lung cancers (NSCLCs).	Selpercatinib	48-61	ret proto-oncogene	Homo sapiens	131-134
34088726-13	2021	CONCLUSIONS: Selpercatinib has robust and durable intracranial efficacy in RET fusion-positive NSCLC patients.	Selpercatinib	13-26	ret proto-oncogene	Homo sapiens	75-78
34232984-3	2022	Selpercatinib (RETEVMO), a targeted inhibitor of RET, was approved by the US Food and Drug Administration for the treatment of RET fusion-positive nonsmall cell lung cancer and nonmedullary thyroid cancer emphasizing the need for rapid and accurate diagnosis of RET fusions.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	49-52
34232984-3	2022	Selpercatinib (RETEVMO), a targeted inhibitor of RET, was approved by the US Food and Drug Administration for the treatment of RET fusion-positive nonsmall cell lung cancer and nonmedullary thyroid cancer emphasizing the need for rapid and accurate diagnosis of RET fusions.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	127-130
34232984-3	2022	Selpercatinib (RETEVMO), a targeted inhibitor of RET, was approved by the US Food and Drug Administration for the treatment of RET fusion-positive nonsmall cell lung cancer and nonmedullary thyroid cancer emphasizing the need for rapid and accurate diagnosis of RET fusions.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	262-265
34203261-2	2021	Here, we show that the receptor tyrosine kinase inhibitor imatinib (also known as STI571, Gleevec) can inhibit the expression of the endogenous ACE2 gene at both the transcript and protein levels.	Imatinib Mesylate	58-66	ret proto-oncogene	Homo sapiens	23-47
34154791-0	2021	Acquired Tertiary MET Resistance (MET D1228N and a Novel LSM8-MET Fusion) to Selpercatinib and Capmatinib in a Patient With KIF5B-RET-positive NSCLC With Secondary MET Amplification as Initial Resistance to Selpercatinib.	Selpercatinib	77-90	ret proto-oncogene	Homo sapiens	130-133
34154791-0	2021	Acquired Tertiary MET Resistance (MET D1228N and a Novel LSM8-MET Fusion) to Selpercatinib and Capmatinib in a Patient With KIF5B-RET-positive NSCLC With Secondary MET Amplification as Initial Resistance to Selpercatinib.	capmatinib	95-105	ret proto-oncogene	Homo sapiens	130-133
34154791-0	2021	Acquired Tertiary MET Resistance (MET D1228N and a Novel LSM8-MET Fusion) to Selpercatinib and Capmatinib in a Patient With KIF5B-RET-positive NSCLC With Secondary MET Amplification as Initial Resistance to Selpercatinib.	Selpercatinib	207-220	ret proto-oncogene	Homo sapiens	130-133
34319869-6	2021	Lenvatinib is a broadly-acting host receptor tyrosine kinase (RTK) inhibitor, but the synergistic effect with remdesivir was not observed with other approved RTK inhibitors (such as pazopanib or sunitinib), suggesting that the mechanism-of-action is independent of host RTKs.	lenvatinib	0-10	ret proto-oncogene	Homo sapiens	36-60
34319869-6	2021	Lenvatinib is a broadly-acting host receptor tyrosine kinase (RTK) inhibitor, but the synergistic effect with remdesivir was not observed with other approved RTK inhibitors (such as pazopanib or sunitinib), suggesting that the mechanism-of-action is independent of host RTKs.	remdesivir	110-120	ret proto-oncogene	Homo sapiens	36-60
34209165-0	2021	Selective Antitumor Activity of Datelliptium toward Medullary Thyroid Carcinoma by Downregulating RET Transcriptional Activity.	detalliptinium	32-44	ret proto-oncogene	Homo sapiens	98-101
34178121-0	2021	Selpercatinib in RET fusion-positive non-small-cell lung cancer (SIREN): a retrospective analysis of patients treated through an access program.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	17-20
34165651-3	2021	Selpercatinib and pralsetinib are RET-selective tyrosine kinase inhibitors (TKIs) with encouraging efficacy, intracranial activity, and tolerability that we recommend as first-line therapy.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	34-37
34117374-1	2021	Cabozantinib is a potent tyrosine kinase inhibitor with multiple targets including MET, VEGFR2, RET, KIT, and FLT3.	cabozantinib	0-12	ret proto-oncogene	Homo sapiens	96-99
34203709-2	2021	Multiple receptor tyrosine kinase (RTK) pathways contribute to the resistance of NSCLC to first- and third-generation EGFR-TKIs, such as erlotinib and osimertinib.	Erlotinib Hydrochloride	137-146	ret proto-oncogene	Homo sapiens	9-33
34203709-2	2021	Multiple receptor tyrosine kinase (RTK) pathways contribute to the resistance of NSCLC to first- and third-generation EGFR-TKIs, such as erlotinib and osimertinib.	Erlotinib Hydrochloride	137-146	ret proto-oncogene	Homo sapiens	35-38
34203709-2	2021	Multiple receptor tyrosine kinase (RTK) pathways contribute to the resistance of NSCLC to first- and third-generation EGFR-TKIs, such as erlotinib and osimertinib.	osimertinib	151-162	ret proto-oncogene	Homo sapiens	9-33
34203709-2	2021	Multiple receptor tyrosine kinase (RTK) pathways contribute to the resistance of NSCLC to first- and third-generation EGFR-TKIs, such as erlotinib and osimertinib.	osimertinib	151-162	ret proto-oncogene	Homo sapiens	35-38
34178121-16	2021	Conclusions: In this real-world setting, the selective RET-inhibitor selpercatinib demonstrated durable systemic and intracranial antitumor activity in RET fusion-positive NSCLC and was well tolerated.	Selpercatinib	69-82	ret proto-oncogene	Homo sapiens	55-58
34178121-2	2021	Selective RET-inhibitors such as selpercatinib have shown therapeutic activity in early clinical trials; however, their efficacy in the real-world setting is unknown.	Selpercatinib	33-46	ret proto-oncogene	Homo sapiens	10-13
34178121-3	2021	Methods: A retrospective efficacy and safety analysis was performed on data from RET fusion-positive NSCLC patients who participated in a selpercatinib access program (named patient protocol) between August 2019 and January 2021.	Selpercatinib	138-151	ret proto-oncogene	Homo sapiens	81-84
34178121-4	2021	Results: Data from 50 patients with RET fusion-positive advanced NSCLC treated with selpercatinib at 27 centers in 12 countries was analyzed.	Selpercatinib	84-97	ret proto-oncogene	Homo sapiens	36-39
34178121-16	2021	Conclusions: In this real-world setting, the selective RET-inhibitor selpercatinib demonstrated durable systemic and intracranial antitumor activity in RET fusion-positive NSCLC and was well tolerated.	Selpercatinib	69-82	ret proto-oncogene	Homo sapiens	152-155
35183775-2	2022	We explored the risk for hypersensitivity with selpercatinib, a first-in-class highly selective and potent, CNS-active RET inhibitor, in prior ICI-treated patients with RET fusion-positive non-small-cell lung cancer (NSCLC) compared with their ICI-naive counterparts.	Selpercatinib	47-60	ret proto-oncogene	Homo sapiens	119-122
34099825-0	2021	The L730V/I RET roof mutations display different activities toward pralsetinib and selpercatinib.	Selpercatinib	83-96	ret proto-oncogene	Homo sapiens	12-15
34099825-1	2021	Recently Food and Drug Administration (FDA)-approved pralsetinib (BLU-667) and selpercatinib (LOXO-292) are RET-selective protein tyrosine kinase inhibitors for treating RET-altered cancers, but whether they have distinct activity was unknown.	Selpercatinib	79-92	ret proto-oncogene	Homo sapiens	108-111
34099825-3	2021	Selpercatinib effectively inhibited these mutants and the KIF5B-RET(L730V/I) oncogene-driven tumors.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	64-67
34107639-7	2021	Immature reticulocyte fraction (IRF) and reticulocyte hemoglobin equivalent (Ret-He) were significantly higher in the iron deficient group as compared to alpha and beta thalassemia.	Iron	118-122	ret proto-oncogene	Homo sapiens	77-80
34107639-9	2021	Sig-nificantly reduced levels of Ret-He were observed in alpha thalassemia and beta thalassemia in comparison to iron deficient group.	Iron	113-117	ret proto-oncogene	Homo sapiens	33-36
34107639-10	2021	While iron deficient group was characterized by increased values of RDW-SD, RDW-CV, IRF, and Ret-He.	Iron	6-10	ret proto-oncogene	Homo sapiens	93-96
34350378-1	2021	Background: We hypothesized that the addition of receptor tyrosine kinase inhibitors (RTKis, e.g., lapatinib, erlotinib, cetuximab, bevacizumab, panitumumab) to radiotherapy-based treatment for solid tumors does not increase overall survival but may increase toxicity.	Lapatinib	99-108	ret proto-oncogene	Homo sapiens	49-73
34350378-1	2021	Background: We hypothesized that the addition of receptor tyrosine kinase inhibitors (RTKis, e.g., lapatinib, erlotinib, cetuximab, bevacizumab, panitumumab) to radiotherapy-based treatment for solid tumors does not increase overall survival but may increase toxicity.	Erlotinib Hydrochloride	110-119	ret proto-oncogene	Homo sapiens	49-73
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
35363275-2	2022	We investigate the role of lenvatinib, a multi-kinase inhibitor with potent activity against RET, in patients with metastatic breast cancer.	lenvatinib	27-37	ret proto-oncogene	Homo sapiens	93-96
35582984-1	2022	We characterized the anti-E2, syn-E2, inv-SN2, and ret-SN2 reaction channels for the reaction of microsolvated HO-(H2O)n anions with CH3CH2X (X = Cl, Br, I), using the CCSD(T)/PP/t//MP2/ECP/d level method, to understand how a solvent influences the competing E2 and SN2 reactions.	Holmium	111-113	ret proto-oncogene	Homo sapiens	51-54
35582984-1	2022	We characterized the anti-E2, syn-E2, inv-SN2, and ret-SN2 reaction channels for the reaction of microsolvated HO-(H2O)n anions with CH3CH2X (X = Cl, Br, I), using the CCSD(T)/PP/t//MP2/ECP/d level method, to understand how a solvent influences the competing E2 and SN2 reactions.	Water	115-118	ret proto-oncogene	Homo sapiens	51-54
35582984-1	2022	We characterized the anti-E2, syn-E2, inv-SN2, and ret-SN2 reaction channels for the reaction of microsolvated HO-(H2O)n anions with CH3CH2X (X = Cl, Br, I), using the CCSD(T)/PP/t//MP2/ECP/d level method, to understand how a solvent influences the competing E2 and SN2 reactions.	ch3ch2x	133-140	ret proto-oncogene	Homo sapiens	51-54
35582984-1	2022	We characterized the anti-E2, syn-E2, inv-SN2, and ret-SN2 reaction channels for the reaction of microsolvated HO-(H2O)n anions with CH3CH2X (X = Cl, Br, I), using the CCSD(T)/PP/t//MP2/ECP/d level method, to understand how a solvent influences the competing E2 and SN2 reactions.	Bromine	150-152	ret proto-oncogene	Homo sapiens	51-54
35582984-1	2022	We characterized the anti-E2, syn-E2, inv-SN2, and ret-SN2 reaction channels for the reaction of microsolvated HO-(H2O)n anions with CH3CH2X (X = Cl, Br, I), using the CCSD(T)/PP/t//MP2/ECP/d level method, to understand how a solvent influences the competing E2 and SN2 reactions.	ccsd	168-172	ret proto-oncogene	Homo sapiens	51-54
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
35612671-2	2022	TPX-0046 is designed to overcome resistance to FDA approved RET inhibitors Selpercatinib and Pralsetinib.	Selpercatinib	75-88	ret proto-oncogene	Homo sapiens	60-63
35497936-2	2022	The present study was designed to explore the effects of tepotinib, a selective tyrosine kinase inhibitor of MET proto-oncogene, receptor tyrosine kinase (MET), on the progression of melanoma.	EMD1214063	57-66	ret proto-oncogene	Homo sapiens	129-153
35579617-7	2022	Additionally, manganese oxide nanoparticles (MnOx) modified with Ab2 can further quench the ECL signal of Ru@DMSNs via the RET between Ru@DMSNs and MnOx.	manganese oxide	14-29	ret proto-oncogene	Homo sapiens	123-126
35579617-7	2022	Additionally, manganese oxide nanoparticles (MnOx) modified with Ab2 can further quench the ECL signal of Ru@DMSNs via the RET between Ru@DMSNs and MnOx.	Ruthenium	106-108	ret proto-oncogene	Homo sapiens	123-126
35579617-7	2022	Additionally, manganese oxide nanoparticles (MnOx) modified with Ab2 can further quench the ECL signal of Ru@DMSNs via the RET between Ru@DMSNs and MnOx.	Ruthenium	135-137	ret proto-oncogene	Homo sapiens	123-126
35616103-0	2022	Somatic Ret Indels In Sporadic Medullary Thyroid Cancer: Prevalence And Response To Selpercatinib.	Selpercatinib	84-97	ret proto-oncogene	Homo sapiens	8-11
35521769-7	2022	New generation TKIs, such as selpercatinib or pralsetinib, that exhibit selective activity against RET, have recently been approved as a second-line treatment option, and they exhibit a more favourable side-effect profile.	Selpercatinib	29-42	ret proto-oncogene	Homo sapiens	99-102
35612671-6	2022	We used as reference literary examples of resistance mechanisms to other macrocyclic inhibitors (Lorlatinib on ALK/ROS1) to construct RET secondary resistance mutations.	lorlatinib	97-107	ret proto-oncogene	Homo sapiens	134-137
35616103-3	2022	OBJECTIVE: To present an update on the prevalence of RET indels in MTC and describe the efficacy of selpercatinib in patients with advanced RET indels MTC.	Selpercatinib	100-113	ret proto-oncogene	Homo sapiens	53-56
35612671-11	2022	Our findings suggest that development of second generation RET inhibitors focused mainly on Solventfront G810X mutations granting resistance to selective RET inhibitors Selpercatinib and Pralsetinib.	Selpercatinib	169-182	ret proto-oncogene	Homo sapiens	59-62
35616103-3	2022	OBJECTIVE: To present an update on the prevalence of RET indels in MTC and describe the efficacy of selpercatinib in patients with advanced RET indels MTC.	Selpercatinib	100-113	ret proto-oncogene	Homo sapiens	140-143
35612671-11	2022	Our findings suggest that development of second generation RET inhibitors focused mainly on Solventfront G810X mutations granting resistance to selective RET inhibitors Selpercatinib and Pralsetinib.	Selpercatinib	169-182	ret proto-oncogene	Homo sapiens	154-157
35582772-3	2022	The prepared Co@NC-800 catalyst has a half-wave potential (E 1/2= 0.835V) close to Pt/C and good stability in excess of Pt/C for oxygen reduction reaction (ORR).	Oxygen	129-135	ret proto-oncogene	Homo sapiens	120-124
35616103-7	2022	Two patients with a RET indel have been treated with selpercatinib.	Selpercatinib	53-66	ret proto-oncogene	Homo sapiens	20-23
35621672-1	2022	Selpercatinib, a RET kinase inhibitor, is an effective treatment for patients with medullary thyroid cancer with RET mutations.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	17-20
35595215-2	2022	METHODS-OBJECTIVE: Here we demonstrate by applying an integrated structural, computational and biochemical approach that the druggability landscape of the RET active site is determined by the conformational setting of the ATP-binding (P-) loop and its coordination with the alphaC helix.	Adenosine Triphosphate	222-225	ret proto-oncogene	Homo sapiens	155-158
35595215-8	2022	CONCLUSIONS: The identification of the post-lysine pocket as a cryptic druggable vulnerability in the RET kinase and its exploitation by second generation RET inhibitors has important implications for future drug design and the development of personalized therapies for patients with RET-driven cancers.	Lysine	44-50	ret proto-oncogene	Homo sapiens	102-105
35595215-8	2022	CONCLUSIONS: The identification of the post-lysine pocket as a cryptic druggable vulnerability in the RET kinase and its exploitation by second generation RET inhibitors has important implications for future drug design and the development of personalized therapies for patients with RET-driven cancers.	Lysine	44-50	ret proto-oncogene	Homo sapiens	155-158
35595215-8	2022	CONCLUSIONS: The identification of the post-lysine pocket as a cryptic druggable vulnerability in the RET kinase and its exploitation by second generation RET inhibitors has important implications for future drug design and the development of personalized therapies for patients with RET-driven cancers.	Lysine	44-50	ret proto-oncogene	Homo sapiens	284-287
35569068-0	2022	Cutaneous Rosai Dorfman disease harboring RET and MAP2K1 mutations, successfully treated with methotrexate.	Methotrexate	94-106	ret proto-oncogene	Homo sapiens	42-45
35621672-1	2022	Selpercatinib, a RET kinase inhibitor, is an effective treatment for patients with medullary thyroid cancer with RET mutations.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	113-116
35530342-3	2022	Anlotinib is a new oral small molecular multi-targeted receptor tyrosine kinase (RTK) inhibitor.	anlotinib	0-9	ret proto-oncogene	Homo sapiens	55-79
35513458-4	2022	As an ECL accelerator, TiO2 nanoparticles (TiO2 NPs) promoted the oxidation of tri-n-propylamine (TPA) to generate more TPA ; in addition, it also acted as a donor to improve the ECL intensity of TPETTZ (acceptor) through electrochemiluminescence resonance energy transfer (ECL-RET).	titanium dioxide	23-27	ret proto-oncogene	Homo sapiens	278-281
35513458-4	2022	As an ECL accelerator, TiO2 nanoparticles (TiO2 NPs) promoted the oxidation of tri-n-propylamine (TPA) to generate more TPA ; in addition, it also acted as a donor to improve the ECL intensity of TPETTZ (acceptor) through electrochemiluminescence resonance energy transfer (ECL-RET).	titanium dioxide	43-47	ret proto-oncogene	Homo sapiens	278-281
35513458-4	2022	As an ECL accelerator, TiO2 nanoparticles (TiO2 NPs) promoted the oxidation of tri-n-propylamine (TPA) to generate more TPA ; in addition, it also acted as a donor to improve the ECL intensity of TPETTZ (acceptor) through electrochemiluminescence resonance energy transfer (ECL-RET).	tripropylamine	79-96	ret proto-oncogene	Homo sapiens	278-281
35513458-4	2022	As an ECL accelerator, TiO2 nanoparticles (TiO2 NPs) promoted the oxidation of tri-n-propylamine (TPA) to generate more TPA ; in addition, it also acted as a donor to improve the ECL intensity of TPETTZ (acceptor) through electrochemiluminescence resonance energy transfer (ECL-RET).	tripropylamine	98-101	ret proto-oncogene	Homo sapiens	278-281
35513458-4	2022	As an ECL accelerator, TiO2 nanoparticles (TiO2 NPs) promoted the oxidation of tri-n-propylamine (TPA) to generate more TPA ; in addition, it also acted as a donor to improve the ECL intensity of TPETTZ (acceptor) through electrochemiluminescence resonance energy transfer (ECL-RET).	tripropylamine	120-123	ret proto-oncogene	Homo sapiens	278-281
35587858-2	2022	Pralsetinib (Gavreto ) is an orally-administered, next-generation, small-molecule selective RET inhibitor that is approved for the treatment of RET fusion-positive metastatic NSCLC.	CRY1 protein, Arabidopsis	13-20	ret proto-oncogene	Homo sapiens	92-95
35587858-2	2022	Pralsetinib (Gavreto ) is an orally-administered, next-generation, small-molecule selective RET inhibitor that is approved for the treatment of RET fusion-positive metastatic NSCLC.	CRY1 protein, Arabidopsis	13-20	ret proto-oncogene	Homo sapiens	144-147
35530342-3	2022	Anlotinib is a new oral small molecular multi-targeted receptor tyrosine kinase (RTK) inhibitor.	anlotinib	0-9	ret proto-oncogene	Homo sapiens	81-84
35571397-2	2022	Before the emergence of specific RET inhibitors, multikinase inhibitors such as cabozantinib and vandetanib were tried for RET fusion-positive NSCLC, but their efficacies were poor, and the U.S. Food and Drug Administration did not approve the application of these drugs for such patients.	vandetanib	97-107	ret proto-oncogene	Homo sapiens	123-126
35462930-7	2022	The other patient acquired EGFR T790M and MET amplification post-dacomitinib and acquired CCDC6-RET fusion after osimertinib treatment.	osimertinib	113-124	ret proto-oncogene	Homo sapiens	96-99
35385843-12	2022	Oxygen free radicals are capable of causing DNA damage via stimulation of the mitogen activating protein (MAP) kinase or phosphatidylinositol-3-kinase (PI3K/Akt) and/or nuclear factor kB (NFkB) pathways resulting in TC-associated-gene mutations such as RET/PTC, AKAP9-BRAF, NTRK1, RAASF, PIK3CA, and PTEN.	Oxygen	0-6	ret proto-oncogene	Homo sapiens	253-256
35066105-7	2022	RESULTS: Among the 45 patients included in MATCH-R who progressed on osimertinib, nine developed a second targetable alteration (n = 2 FGFR3-TACC3, n = 1 KIF5B-RET, n = 1 STRN-ALK fusions; n = 2 BRAFV600E, n = 1 KRASG12V, n = 1 KRASG12R, n = 1 KRASG12D mutations).	osimertinib	69-80	ret proto-oncogene	Homo sapiens	160-163
35359901-5	2022	Methods: We performed RET rs2435357 genotyping from 73 HSCR formalin-fixed and paraffin-embedded (FFPE) rectal and 60 non-HSCR controls using the PCR-RFLP method.	Formaldehyde	60-68	ret proto-oncogene	Homo sapiens	22-25
35038965-2	2022	INTRODUCTION: The most common altered signaling found in aggressive iodine-refractory thyroid cancers derived from follicular cells (RAI-TC) are RTK, MAPK, PI3K, WNT, BRAF, RAS, RET, and TP53.	Iodine	68-74	ret proto-oncogene	Homo sapiens	178-181
35304457-1	2022	The efficacy of the highly selective RET inhibitor selpercatinib is now established in RET-driven cancers, and we sought to characterize the molecular determinants of response and resistance.	Selpercatinib	51-64	ret proto-oncogene	Homo sapiens	37-40
35304457-1	2022	The efficacy of the highly selective RET inhibitor selpercatinib is now established in RET-driven cancers, and we sought to characterize the molecular determinants of response and resistance.	Selpercatinib	51-64	ret proto-oncogene	Homo sapiens	87-90
35328215-11	2022	Noteworthy are BRAF and RET/PTC alterations already validated as targets of Dabrafenib-mesylate, Pralsetinib and Selpercatinib.	Dabrafenib mesylate	76-95	ret proto-oncogene	Homo sapiens	24-27
35328215-11	2022	Noteworthy are BRAF and RET/PTC alterations already validated as targets of Dabrafenib-mesylate, Pralsetinib and Selpercatinib.	Dabrafenib mesylate	76-95	ret proto-oncogene	Homo sapiens	28-31
35328215-11	2022	Noteworthy are BRAF and RET/PTC alterations already validated as targets of Dabrafenib-mesylate, Pralsetinib and Selpercatinib.	Selpercatinib	113-126	ret proto-oncogene	Homo sapiens	24-27
35328215-11	2022	Noteworthy are BRAF and RET/PTC alterations already validated as targets of Dabrafenib-mesylate, Pralsetinib and Selpercatinib.	Selpercatinib	113-126	ret proto-oncogene	Homo sapiens	28-31
35443540-3	2022	RET-He measure the recent functional availability of iron and the correlation well with iron deficient / restricted erythropoiesis, and it is not affected by infection and inflammation related to cancer so it can be useful marker to rapidly rule out iron deficiency in cancer patients.	Iron	53-57	ret proto-oncogene	Homo sapiens	0-3
35443540-3	2022	RET-He measure the recent functional availability of iron and the correlation well with iron deficient / restricted erythropoiesis, and it is not affected by infection and inflammation related to cancer so it can be useful marker to rapidly rule out iron deficiency in cancer patients.	Iron	88-92	ret proto-oncogene	Homo sapiens	0-3
35443540-10	2022	Observation: At a cut off of 28.4 pg, RET-He achieved sensitivity of 96.77 % and specificity of 81.66% with NPV of 99.3% and PPV of 49.2% for iron deficient state in cancer patients.	Iron	142-146	ret proto-oncogene	Homo sapiens	38-41
35443540-13	2022	Conclusion: RET-He is better indicator of IDA in cancer patients as compared to other conventional methods of diagnosing IDA.This study also revealed a direct correlation between RET-He and bone marrow iron stores.	Iron	202-206	ret proto-oncogene	Homo sapiens	12-15
35443540-13	2022	Conclusion: RET-He is better indicator of IDA in cancer patients as compared to other conventional methods of diagnosing IDA.This study also revealed a direct correlation between RET-He and bone marrow iron stores.	Iron	202-206	ret proto-oncogene	Homo sapiens	179-182
35469014-3	2022	More than 500 therapeutic bAbs generated against Wingless-related integration site (WNT) and receptor tyrosine kinase (RTK) targets were functionally evaluated by high-content imaging to capture the complexity of PDO responses.	Antibodies, Bispecific	26-30	ret proto-oncogene	Homo sapiens	93-117
35469014-3	2022	More than 500 therapeutic bAbs generated against Wingless-related integration site (WNT) and receptor tyrosine kinase (RTK) targets were functionally evaluated by high-content imaging to capture the complexity of PDO responses.	Antibodies, Bispecific	26-30	ret proto-oncogene	Homo sapiens	119-122
35368876-4	2022	We are the first to investigate PEITC effects on the receptor tyrosine kinase (RTK) signaling pathway and the effects of proinflammatory cytokines on glioblastoma.	phenethyl isothiocyanate	32-37	ret proto-oncogene	Homo sapiens	53-77
35368876-4	2022	We are the first to investigate PEITC effects on the receptor tyrosine kinase (RTK) signaling pathway and the effects of proinflammatory cytokines on glioblastoma.	phenethyl isothiocyanate	32-37	ret proto-oncogene	Homo sapiens	79-82
35324532-1	2022	Selpercatinib has been approved by most major regulatory bodies in 2020 and become the standard therapy for rearranged during transfection (RET)-rearranged nonsmall-cell lung cancer (NSCLC).	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	140-143
35324532-10	2022	In addition, the apparent lack of response to selpercatinib plus crizotinib in this case highlights the need for future cohort studies for examining the value of combining RET and MET inhibitors in treating RET-rearranged, MET-amplified NSCLC.	Crizotinib	65-75	ret proto-oncogene	Homo sapiens	172-175
35359901-7	2022	Results: The frequencies of genotypes for RET rs2435357 in HSCR paraffin-embedded rectal were CC 0, CT 11 (15%), and TT 62 (85%), whereas their frequencies in HSCR blood samples were CC 4 (4.3%), CT 22 (23.7%), and TT 67 (72%).	Paraffin	64-72	ret proto-oncogene	Homo sapiens	42-45
35007206-3	2022	Selpercatinib (LOXO-292) is a highly selective RET kinase inhibitor indicated in advanced RET-mutant MTC patients.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	47-50
35084096-6	2022	Importantly, the ZnCo-NC based Zn-H2 O2 batteries achieve the superior power density of 442 mW cm-2 , much higher than 238 and 198 mW cm-2 of Zn-air batteries with ZnCo-NC based catalyst and Pt/C respectively.	znco	17-21	ret proto-oncogene	Homo sapiens	191-195
35235141-0	2022	A patent review on efficient strategies for the total synthesis of pazopanib, regorafenib and lenvatinib as novel anti-angiogenesis receptor tyrosine kinase inhibitors for cancer therapy.	pazopanib	67-76	ret proto-oncogene	Homo sapiens	132-156
35235141-0	2022	A patent review on efficient strategies for the total synthesis of pazopanib, regorafenib and lenvatinib as novel anti-angiogenesis receptor tyrosine kinase inhibitors for cancer therapy.	regorafenib	78-89	ret proto-oncogene	Homo sapiens	132-156
35235141-0	2022	A patent review on efficient strategies for the total synthesis of pazopanib, regorafenib and lenvatinib as novel anti-angiogenesis receptor tyrosine kinase inhibitors for cancer therapy.	lenvatinib	94-104	ret proto-oncogene	Homo sapiens	132-156
35235141-5	2022	In the current review, we aim to track the advancements in the total synthesis of three receptor tyrosine kinase inhibitors (pazopanib, regorafenib and lenvatinib).	pazopanib	125-134	ret proto-oncogene	Homo sapiens	88-112
35235141-5	2022	In the current review, we aim to track the advancements in the total synthesis of three receptor tyrosine kinase inhibitors (pazopanib, regorafenib and lenvatinib).	regorafenib	136-147	ret proto-oncogene	Homo sapiens	88-112
35235141-5	2022	In the current review, we aim to track the advancements in the total synthesis of three receptor tyrosine kinase inhibitors (pazopanib, regorafenib and lenvatinib).	lenvatinib	152-162	ret proto-oncogene	Homo sapiens	88-112
35404189-2	2022	Recently, RET fusion-positive metastatic thyroid cancers have attracted much attention owing to the FDA approval of two highly selective anti-RET tyrosine kinase inhibitors, namely, selpercatinib, and pralsetinib.	Selpercatinib	182-195	ret proto-oncogene	Homo sapiens	10-13
35084096-5	2022	Therefore, the ZnCo-NC based catalyst exhibits outstanding bifunctional electrocatalytic activities for ORR with a high Eonset (1.02 V) and E1/2 (0.91 V) and OER with low Ej=10 (1.56 V), better than Pt/C and RuO2 .	znco-nc	15-22	ret proto-oncogene	Homo sapiens	199-203
35007206-3	2022	Selpercatinib (LOXO-292) is a highly selective RET kinase inhibitor indicated in advanced RET-mutant MTC patients.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	90-93
35007206-4	2022	CASE PRESENTATION: We report two observations of RET-mutant progressive metastatic and symptomatic MTC patients who were treated with selpercatinib.	Selpercatinib	134-147	ret proto-oncogene	Homo sapiens	49-52
35081714-0	2022	Discovery of N-Trisubstituted Pyrimidine Derivatives as Type I RET and RET Gatekeeper Mutant Inhibitors with a Novel Kinase Binding Pose.	n-trisubstituted	13-29	ret proto-oncogene	Homo sapiens	63-66
35091706-12	2022	MiR-146b-5p inhibited RET expression.	mir-146b-5p	0-11	ret proto-oncogene	Homo sapiens	22-25
35081714-0	2022	Discovery of N-Trisubstituted Pyrimidine Derivatives as Type I RET and RET Gatekeeper Mutant Inhibitors with a Novel Kinase Binding Pose.	n-trisubstituted	13-29	ret proto-oncogene	Homo sapiens	71-74
35081714-0	2022	Discovery of N-Trisubstituted Pyrimidine Derivatives as Type I RET and RET Gatekeeper Mutant Inhibitors with a Novel Kinase Binding Pose.	pyrimidine	30-40	ret proto-oncogene	Homo sapiens	63-66
35081714-0	2022	Discovery of N-Trisubstituted Pyrimidine Derivatives as Type I RET and RET Gatekeeper Mutant Inhibitors with a Novel Kinase Binding Pose.	pyrimidine	30-40	ret proto-oncogene	Homo sapiens	71-74
35081714-2	2022	Herein, we discovered a series of N-trisubstituted pyrimidine derivatives as potent inhibitors for both wild-type (wt) RET and RETV804M, which is a resistant mutant for several FDA-approved inhibitors.	n-trisubstituted pyrimidine	34-61	ret proto-oncogene	Homo sapiens	119-122
35081714-7	2022	Collectively, N-trisubstituted pyrimidine derivatives could serve as scaffolds for the discovery and development of potent inhibitors of type I RET and its gatekeeper mutant for the treatment of RET-driven cancers.	n-trisubstituted	14-30	ret proto-oncogene	Homo sapiens	144-147
35081714-7	2022	Collectively, N-trisubstituted pyrimidine derivatives could serve as scaffolds for the discovery and development of potent inhibitors of type I RET and its gatekeeper mutant for the treatment of RET-driven cancers.	n-trisubstituted	14-30	ret proto-oncogene	Homo sapiens	195-198
35081714-7	2022	Collectively, N-trisubstituted pyrimidine derivatives could serve as scaffolds for the discovery and development of potent inhibitors of type I RET and its gatekeeper mutant for the treatment of RET-driven cancers.	pyrimidine	31-41	ret proto-oncogene	Homo sapiens	144-147
35081714-7	2022	Collectively, N-trisubstituted pyrimidine derivatives could serve as scaffolds for the discovery and development of potent inhibitors of type I RET and its gatekeeper mutant for the treatment of RET-driven cancers.	pyrimidine	31-41	ret proto-oncogene	Homo sapiens	195-198
35425232-3	2022	In the methanol electrooxidation reaction, the particles showed high catalytic activity and strong resistance to the poisoning carbonaceous species in comparison with those of commercial Pt/C and the as-prepared Pt/C catalysts.	Methanol	7-15	ret proto-oncogene	Homo sapiens	187-191
34985881-4	2022	Moreover, an ECL resonance energy transfer (ECL-RET) biosensor with AgMOF as a donor and BHQ2 as an acceptor was fabricated by duplex-specific nuclease (DSN)-assisted target recycling amplification to detect miRNA-107.	agmof	68-73	ret proto-oncogene	Homo sapiens	48-51
34985881-5	2022	The biosensor exhibited a strong ECL-RET effect due to the higher ECL emission of the AgMOF and perfect match of spectra between the AgMOF and BHQ2.	agmof	86-91	ret proto-oncogene	Homo sapiens	37-40
34985881-5	2022	The biosensor exhibited a strong ECL-RET effect due to the higher ECL emission of the AgMOF and perfect match of spectra between the AgMOF and BHQ2.	agmof	133-138	ret proto-oncogene	Homo sapiens	37-40
34985881-5	2022	The biosensor exhibited a strong ECL-RET effect due to the higher ECL emission of the AgMOF and perfect match of spectra between the AgMOF and BHQ2.	bhq2	143-147	ret proto-oncogene	Homo sapiens	37-40
34931211-1	2022	Herein, a novel and facile dual-wavelength ratiometric electrochemiluminescence-resonance energy transfer (ECL-RET) sensor for hydrogen sulfide (H2S) detection was constructed based on the interaction between S2- and Cd2+-doped g-C3N4 nanosheets (NSs).	Hydrogen Sulfide	127-143	ret proto-oncogene	Homo sapiens	111-114
34931211-1	2022	Herein, a novel and facile dual-wavelength ratiometric electrochemiluminescence-resonance energy transfer (ECL-RET) sensor for hydrogen sulfide (H2S) detection was constructed based on the interaction between S2- and Cd2+-doped g-C3N4 nanosheets (NSs).	Deuterium	145-148	ret proto-oncogene	Homo sapiens	111-114
34931211-4	2022	Furthermore, the overlapping of the absorption spectrum of the formed CdS and the ECL emission spectrum of g-C3N4 NSs led to a feasible RET, thus quenching the ECL intensity from g-C3N4 at 435 nm.	Cadmium	70-73	ret proto-oncogene	Homo sapiens	136-139
34931211-5	2022	Through an ECL decrease at 435 nm and an increase at 515 nm, a dual-wavelength ratiometric ECL-RET system for H2S was designed.	Deuterium	110-113	ret proto-oncogene	Homo sapiens	95-98
35425232-3	2022	In the methanol electrooxidation reaction, the particles showed high catalytic activity and strong resistance to the poisoning carbonaceous species in comparison with those of commercial Pt/C and the as-prepared Pt/C catalysts.	Methanol	7-15	ret proto-oncogene	Homo sapiens	212-216
35012575-0	2022	Edaravone activates the GDNF/RET neurotrophic signaling pathway and protects mRNA-induced motor neurons from iPS cells.	Edaravone	0-9	ret proto-oncogene	Homo sapiens	29-32
35052646-6	2022	Under conditions of OS, N-DDA also increased TRKB, TRKC and RET mRNA levels.	n-dda	24-29	ret proto-oncogene	Homo sapiens	60-63
35252556-2	2022	In this preclinical study, vorolanib demonstrated competitive binding and inhibitory activities with KDR, PDGFRbeta, FLT3, and C-Kit, and inhibited RET and AMPKalpha1 more weakly than sunitinib, indicating more stringent kinase selectivity.	20,21-epoxyresibufogenin-3-formate	27-36	ret proto-oncogene	Homo sapiens	148-151
35070994-2	2021	In addition, certain gene rearrangements (e.g., ALK, ROS1, RET) appear to especially benefit from the use of pemetrexed.	Pemetrexed	109-119	ret proto-oncogene	Homo sapiens	59-62
35012575-9	2022	Guided by the transcriptomic analysis, we show a previously unrecognized effect of edaravone to induce the GDNF receptor RET and the GDNF/RET neurotrophic signaling in vitro and in vivo, suggesting a clinically translatable strategy to activate this key neuroprotective signaling.	Edaravone	83-92	ret proto-oncogene	Homo sapiens	121-124
35012575-9	2022	Guided by the transcriptomic analysis, we show a previously unrecognized effect of edaravone to induce the GDNF receptor RET and the GDNF/RET neurotrophic signaling in vitro and in vivo, suggesting a clinically translatable strategy to activate this key neuroprotective signaling.	Edaravone	83-92	ret proto-oncogene	Homo sapiens	138-141
34738874-7	2022	Mechanistically, the receptor tyrosine kinase signaling antibody array revealed that Janus kinase-1 (JAK1) was specifically inhibited by AZD3759, but not by osimertinib.	AZD3759	137-144	ret proto-oncogene	Homo sapiens	21-45
35425116-3	2021	The "gain of function" mutations in the RET gate-keeper residue, Val804, confers resistance to the majority of known RET inhibitors, including vandetanib.	vandetanib	143-153	ret proto-oncogene	Homo sapiens	40-43
35425116-3	2021	The "gain of function" mutations in the RET gate-keeper residue, Val804, confers resistance to the majority of known RET inhibitors, including vandetanib.	vandetanib	143-153	ret proto-oncogene	Homo sapiens	117-120
35425116-4	2021	To curtail this resistance, researchers developed selpercatinib (LOXO-292) against the RET gate-keeper mutant forms - V804M and V804L.	Selpercatinib	50-63	ret proto-oncogene	Homo sapiens	87-90
35425116-7	2021	The resulting 2696 drug-like NPs were subjected to molecular docking with the RET WT kinase domain and a total of 27 molecules displayed better dock scores than the reference inhibitors - vandetanib and selpercatinib.	vandetanib	188-198	ret proto-oncogene	Homo sapiens	78-81
35425116-7	2021	The resulting 2696 drug-like NPs were subjected to molecular docking with the RET WT kinase domain and a total of 27 molecules displayed better dock scores than the reference inhibitors - vandetanib and selpercatinib.	Selpercatinib	203-216	ret proto-oncogene	Homo sapiens	78-81
34669647-6	2022	Selpercatinib and pralsetinib are kinase inhibitors with high specificity for RET; phase I and II studies showed overall response rates of 73% and 71% in first line, and 69% and 60% in second line treatment, respectively.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	78-81
7159390-2	1982	Rat liver microsomal fraction synthesized Ret-P-Man (retinyl phosphate mannose) and Dol-P-Man (dolichyl phosphate mannose) from endogenous Ret-P (retinyl phosphate) and Dol-P (dolichyl phosphate).	dolichol monophosphate	84-89	ret proto-oncogene	Homo sapiens	139-142
3001107-4	1985	In an attempt to find a protein that might link the receptor tyrosine kinase to these serine/threonine phosphorylation reactions, we have studied the interaction of a partially purified preparation of insulin receptor with purified preparations of serine/threonine kinases known to phosphorylate glycogen synthase.	Serine	86-92	ret proto-oncogene	Homo sapiens	52-76
3001107-4	1985	In an attempt to find a protein that might link the receptor tyrosine kinase to these serine/threonine phosphorylation reactions, we have studied the interaction of a partially purified preparation of insulin receptor with purified preparations of serine/threonine kinases known to phosphorylate glycogen synthase.	Threonine	93-102	ret proto-oncogene	Homo sapiens	52-76
7159390-2	1982	Rat liver microsomal fraction synthesized Ret-P-Man (retinyl phosphate mannose) and Dol-P-Man (dolichyl phosphate mannose) from endogenous Ret-P (retinyl phosphate) and Dol-P (dolichyl phosphate).	mannosylretinylphosphate	53-78	ret proto-oncogene	Homo sapiens	42-45
35022207-2	2022	In this issue of Cancer Discovery, Song and colleagues report that the related PI3Kalpha inhibitors taselisib and inavolisib trigger receptor tyrosine kinase (RTK)-dependent degradation of the mutant p110alpha protein in breast cancer cells that are positive for HER2 RTK, limiting feedback-mediated drug resistance and potentially widening the therapeutic index of PI3Kalpha inhibition.See related article by Song et al., p. 204.	2-(3-(2-(1-isopropyl-3-methyl-1H-1,2-4-triazol-5-yl)-5,6-dihydrobenzo(f)imidazo(1,2-d)(1,4)oxazepin-9-yl)-1H-pyrazol-1-yl)-2-methylpropanamide	100-109	ret proto-oncogene	Homo sapiens	133-157
35022207-2	2022	In this issue of Cancer Discovery, Song and colleagues report that the related PI3Kalpha inhibitors taselisib and inavolisib trigger receptor tyrosine kinase (RTK)-dependent degradation of the mutant p110alpha protein in breast cancer cells that are positive for HER2 RTK, limiting feedback-mediated drug resistance and potentially widening the therapeutic index of PI3Kalpha inhibition.See related article by Song et al., p. 204.	2-(3-(2-(1-isopropyl-3-methyl-1H-1,2-4-triazol-5-yl)-5,6-dihydrobenzo(f)imidazo(1,2-d)(1,4)oxazepin-9-yl)-1H-pyrazol-1-yl)-2-methylpropanamide	100-109	ret proto-oncogene	Homo sapiens	159-162
35022207-2	2022	In this issue of Cancer Discovery, Song and colleagues report that the related PI3Kalpha inhibitors taselisib and inavolisib trigger receptor tyrosine kinase (RTK)-dependent degradation of the mutant p110alpha protein in breast cancer cells that are positive for HER2 RTK, limiting feedback-mediated drug resistance and potentially widening the therapeutic index of PI3Kalpha inhibition.See related article by Song et al., p. 204.	2-(3-(2-(1-isopropyl-3-methyl-1H-1,2-4-triazol-5-yl)-5,6-dihydrobenzo(f)imidazo(1,2-d)(1,4)oxazepin-9-yl)-1H-pyrazol-1-yl)-2-methylpropanamide	100-109	ret proto-oncogene	Homo sapiens	268-271
35079630-7	2022	Following OPBM treatment, significant changes were observed in HIF-1alpha expression, intracellular reactive oxygen species levels, activation of the receptor tyrosine kinase, and glycolytic pathways in hADSCs.	opbm	10-14	ret proto-oncogene	Homo sapiens	150-174
2575183-3	1989	In the individual at risk for developing MEN IIa, annual screening should include measurement of the basal and stimulated plasma CT levels, and determination of plasma levels of calcium, PTH, and CEA.	Calcium	178-185	ret proto-oncogene	Homo sapiens	41-48
2686181-1	1989	On the basis of numerous pharmacological, clinical pharmacological and clinical investigations it could be proved, that Venostasin ret., standardized on 50 mg triterpenglycosides, calculated as escine, has effects on the venous system: It has tonical effects on the veins, decreases permeability and has protective and curative properties.	triterpenglycosides	159-178	ret proto-oncogene	Homo sapiens	131-134
2892276-8	1988	Bilateral adrenal accumulation of the radionuclide was demonstrated in seven of eight MEN IIa gene carriers who had not undergone adrenalectomy.	Radioisotopes	38-50	ret proto-oncogene	Homo sapiens	86-93
2861094-5	1985	The concentrations of serotonin in sera from patients with MTC or MEN-IIa without pheochromocytomas were not different from the concentrations measured in healthy subjects (P greater than 0.10).	Serotonin	22-31	ret proto-oncogene	Homo sapiens	66-73
7159390-2	1982	Rat liver microsomal fraction synthesized Ret-P-Man (retinyl phosphate mannose) and Dol-P-Man (dolichyl phosphate mannose) from endogenous Ret-P (retinyl phosphate) and Dol-P (dolichyl phosphate).	mannosylretinylphosphate	53-78	ret proto-oncogene	Homo sapiens	139-142
7159390-2	1982	Rat liver microsomal fraction synthesized Ret-P-Man (retinyl phosphate mannose) and Dol-P-Man (dolichyl phosphate mannose) from endogenous Ret-P (retinyl phosphate) and Dol-P (dolichyl phosphate).	dolichol monophosphate	95-113	ret proto-oncogene	Homo sapiens	139-142
7159390-2	1982	Rat liver microsomal fraction synthesized Ret-P-Man (retinyl phosphate mannose) and Dol-P-Man (dolichyl phosphate mannose) from endogenous Ret-P (retinyl phosphate) and Dol-P (dolichyl phosphate).	dolichyl phosphate mannose	95-121	ret proto-oncogene	Homo sapiens	139-142
7159390-2	1982	Rat liver microsomal fraction synthesized Ret-P-Man (retinyl phosphate mannose) and Dol-P-Man (dolichyl phosphate mannose) from endogenous Ret-P (retinyl phosphate) and Dol-P (dolichyl phosphate).	retinol phosphate	53-70	ret proto-oncogene	Homo sapiens	42-45
7159390-3	1982	Ret-P-Man synthesis displayed an absolute requirement for a bivalent cation, and also Dol-P-Man synthesis was stimulated by bivalent metal ions.	Metals	133-138	ret proto-oncogene	Homo sapiens	0-3
7159390-4	1982	Mn2+ and Co2+ were the most active, with maximum synthesis of Ret-P-Man occurring at 5-10 mM: Mg2+ was also active, but at higher concentrations.	Manganese(2+)	0-4	ret proto-oncogene	Homo sapiens	62-65
7159390-4	1982	Mn2+ and Co2+ were the most active, with maximum synthesis of Ret-P-Man occurring at 5-10 mM: Mg2+ was also active, but at higher concentrations.	Cobalt(2+)	9-13	ret proto-oncogene	Homo sapiens	62-65
7159390-4	1982	Mn2+ and Co2+ were the most active, with maximum synthesis of Ret-P-Man occurring at 5-10 mM: Mg2+ was also active, but at higher concentrations.	magnesium ion	94-98	ret proto-oncogene	Homo sapiens	62-65
7159390-5	1982	At 5mM-Mn2+ the amount of endogenous Ret-P mannosylated in incubation mixtures containing 5 microM-GDP-mannose in 15 min at 37 degrees C was approx.	Guanosine Diphosphate Mannose	99-110	ret proto-oncogene	Homo sapiens	37-40
7159390-8	1982	Bivalentcation requirement for Ret-P-Man synthesis from exogenous Ret-P showed maximum synthesis at 2.5 mM-Mn2+ or -Co2+.	Manganese(2+)	107-111	ret proto-oncogene	Homo sapiens	31-34
7159390-8	1982	Bivalentcation requirement for Ret-P-Man synthesis from exogenous Ret-P showed maximum synthesis at 2.5 mM-Mn2+ or -Co2+.	Manganese(2+)	107-111	ret proto-oncogene	Homo sapiens	66-69
7159390-8	1982	Bivalentcation requirement for Ret-P-Man synthesis from exogenous Ret-P showed maximum synthesis at 2.5 mM-Mn2+ or -Co2+.	Cobalt(2+)	116-120	ret proto-oncogene	Homo sapiens	31-34
7159390-8	1982	Bivalentcation requirement for Ret-P-Man synthesis from exogenous Ret-P showed maximum synthesis at 2.5 mM-Mn2+ or -Co2+.	Cobalt(2+)	116-120	ret proto-oncogene	Homo sapiens	66-69
7159390-10	1982	Triton X-100 (0.5%) abolished Ret-P-Man synthesis from endogenous Ret-P and caused a 99% inhibition of Ret-P-Man synthesis from exogenous Ret-P.	Octoxynol	0-12	ret proto-oncogene	Homo sapiens	30-33
7159390-10	1982	Triton X-100 (0.5%) abolished Ret-P-Man synthesis from endogenous Ret-P and caused a 99% inhibition of Ret-P-Man synthesis from exogenous Ret-P.	Octoxynol	0-12	ret proto-oncogene	Homo sapiens	66-69
7159390-10	1982	Triton X-100 (0.5%) abolished Ret-P-Man synthesis from endogenous Ret-P and caused a 99% inhibition of Ret-P-Man synthesis from exogenous Ret-P.	Octoxynol	0-12	ret proto-oncogene	Homo sapiens	66-69
7159390-10	1982	Triton X-100 (0.5%) abolished Ret-P-Man synthesis from endogenous Ret-P and caused a 99% inhibition of Ret-P-Man synthesis from exogenous Ret-P.	Octoxynol	0-12	ret proto-oncogene	Homo sapiens	66-69
7159390-13	1982	Since GDP-mannose: Ret-P and GDP-mannose: Dol-P mannosyltransferase activities were not affected, depletion of vitamin A must affect Ret-P and Dol-P pools in opposite ways.	Vitamin A	111-120	ret proto-oncogene	Homo sapiens	133-136
950371-2	1976	Patients with MEN 2a may be normocalcemic, with normal basal serum immunoreactive parathyroid hormone (iPTH) levels, yet have parathyroid hyperplasia discovered during thyroid surgery.	ipth	103-107	ret proto-oncogene	Homo sapiens	14-20
950371-10	1976	Calcium infusion combined with the measurement of serum iPTH levels may detect occult parathyroid hyperplasia in patients with MEN 2a, normocalcemia, and normal basal iPTH values.	Calcium	0-7	ret proto-oncogene	Homo sapiens	127-133
950371-10	1976	Calcium infusion combined with the measurement of serum iPTH levels may detect occult parathyroid hyperplasia in patients with MEN 2a, normocalcemia, and normal basal iPTH values.	ipth	56-60	ret proto-oncogene	Homo sapiens	127-133
33617938-0	2021	Patient-driven discovery and post-clinical validation of NTRK3 fusion as an acquired resistance mechanism to selpercatinib in RET fusion-positive lung cancer.	Selpercatinib	109-122	ret proto-oncogene	Homo sapiens	126-129
33737118-0	2021	Novel drugs, familiar interactions: ciprofloxacin may increase exposure to the RET-inhibitor pralsetinib.	Ciprofloxacin	36-49	ret proto-oncogene	Homo sapiens	79-82
33933276-4	2021	Here, we discuss the two RET-inhibitors selpercatinib and pralsetinib, and the management of patients with RET-fusion positive NSCLC.	Selpercatinib	40-53	ret proto-oncogene	Homo sapiens	25-28
33184860-7	2021	Receptor tyrosine kinase array analysis revealed that morphine selectively induced the transactivation of EGFR.	Morphine	54-62	ret proto-oncogene	Homo sapiens	0-24
33728771-6	2021	In addition, treatment with either alectinib or ceritinib modulated the activation of various molecules downstream of RTK signaling and induced caspase-dependent/independent cell death mainly by inhibiting signal transducer and activator of transcription 3 activation in human GBM cells.	alectinib	35-44	ret proto-oncogene	Homo sapiens	118-121
34058344-2	2021	Currently, several approved multikinase inhibitors such as vandetanib and cabozantinib demonstrate clinical activity in patients with RET-rearranged or RET-mutant cancers.	vandetanib	59-69	ret proto-oncogene	Homo sapiens	134-137
34058344-2	2021	Currently, several approved multikinase inhibitors such as vandetanib and cabozantinib demonstrate clinical activity in patients with RET-rearranged or RET-mutant cancers.	vandetanib	59-69	ret proto-oncogene	Homo sapiens	152-155
34058344-2	2021	Currently, several approved multikinase inhibitors such as vandetanib and cabozantinib demonstrate clinical activity in patients with RET-rearranged or RET-mutant cancers.	cabozantinib	74-86	ret proto-oncogene	Homo sapiens	134-137
34058344-2	2021	Currently, several approved multikinase inhibitors such as vandetanib and cabozantinib demonstrate clinical activity in patients with RET-rearranged or RET-mutant cancers.	cabozantinib	74-86	ret proto-oncogene	Homo sapiens	152-155
33559353-0	2021	Pyrazoloadenine Inhibitors of the RET Lung Cancer Oncoprotein Discovered via a Fragment Optimization Approach.	1H-Pyrazolo[3,4-d]pyrimidin-4-amine	0-15	ret proto-oncogene	Homo sapiens	34-37
33559353-1	2021	A fragment-based drug discovery approach using a pyrazoloadenine fragment library was utilized to uncover new molecules that target the RET (REarranged during Transfection) oncoprotein, which is a driver oncoprotein in ~2% of non-small cell lung cancer.	1H-Pyrazolo[3,4-d]pyrimidin-4-amine	49-64	ret proto-oncogene	Homo sapiens	136-139
33559353-1	2021	A fragment-based drug discovery approach using a pyrazoloadenine fragment library was utilized to uncover new molecules that target the RET (REarranged during Transfection) oncoprotein, which is a driver oncoprotein in ~2% of non-small cell lung cancer.	1H-Pyrazolo[3,4-d]pyrimidin-4-amine	49-64	ret proto-oncogene	Homo sapiens	141-171
33559353-3	2021	An unsubstituted pyrazoloadenine fragment was found active on RET in a biochemical assay but reduced cell viability in non-RET driven cell lines (EC50 = 1 microM and 3 microM, respectively).	1H-Pyrazolo[3,4-d]pyrimidin-4-amine	17-32	ret proto-oncogene	Homo sapiens	62-65
33559353-3	2021	An unsubstituted pyrazoloadenine fragment was found active on RET in a biochemical assay but reduced cell viability in non-RET driven cell lines (EC50 = 1 microM and 3 microM, respectively).	1H-Pyrazolo[3,4-d]pyrimidin-4-amine	17-32	ret proto-oncogene	Homo sapiens	123-126
33559353-4	2021	To increase selectivity for RET, the pyrazoloadenine was modeled in the RET active site, and two domains were identified that were probed with pyrazoloadenine fragment derivatives to improve RET affinity.	1H-Pyrazolo[3,4-d]pyrimidin-4-amine	143-158	ret proto-oncogene	Homo sapiens	28-31
33758332-1	2021	Two RET inhibitors, selpercatinib and pralsetinib, recently received approval for the treatment of advanced RET fusion-positive lung cancer.	Selpercatinib	20-33	ret proto-oncogene	Homo sapiens	4-7
33758332-1	2021	Two RET inhibitors, selpercatinib and pralsetinib, recently received approval for the treatment of advanced RET fusion-positive lung cancer.	Selpercatinib	20-33	ret proto-oncogene	Homo sapiens	108-111
33923880-1	2021	A tyrosine kinase inhibitor, vandetanib (Van), is an anticancer drug affecting the signaling of VEGFR, EGFR and RET protooncogenes.	vandetanib	29-39	ret proto-oncogene	Homo sapiens	112-115
33923880-1	2021	A tyrosine kinase inhibitor, vandetanib (Van), is an anticancer drug affecting the signaling of VEGFR, EGFR and RET protooncogenes.	vandetanib	41-44	ret proto-oncogene	Homo sapiens	112-115
33239432-0	2021	FDA Approval Summary: Selpercatinib for the Treatment of Lung and Thyroid cancers with RET Gene Mutations or Fusions.	Selpercatinib	22-35	ret proto-oncogene	Homo sapiens	87-90
33239432-3	2021	ORRs within the approved patient populations ranged from 64% (95% CI: 54, 73) in prior platinum treated RET fusion-positive NSCLC to 100% (95% CI: 63, 100) in systemic therapy naive RET fusion-positive thyroid cancer, with the majority of responders across indications demonstrating responses of at least 6 months.	Platinum	87-95	ret proto-oncogene	Homo sapiens	104-107
33086236-10	2021	Utilizing combined HE, calponin immunofluorescence, and RET FISH imaging, we demonstrated that IDCs with RET fusions harbored this alteration in both the ductal and myoepithelial cells.	Helium	19-21	ret proto-oncogene	Homo sapiens	105-108
33606922-3	2021	GSK3352589 is an RET kinase inhibitor that was administered in double-blind, randomized, placebo-controlled single-dose (SD) and repeat-dose (RD) studies in healthy subjects to investigate its safety/tolerability and pharmacokinetics.	gsk3352589	0-10	ret proto-oncogene	Homo sapiens	17-20
33754314-0	2021	Kidney malformations and Hirschsprung"s disease in carriers of cysteine mutations in exon 10 of the RET proto-oncogene.	Cysteine	63-71	ret proto-oncogene	Homo sapiens	100-103
33754314-7	2021	CONCLUSION: Hirschsprung"s disease and kidney malformations are the more penetrant, the closer the cysteine mutations are located to the transmembrane domain (codon 636-657) of the RET kinase receptor.	Cysteine	99-107	ret proto-oncogene	Homo sapiens	181-184
34045295-3	2021	ORRs within the approved patient populations ranged from 57% (95% CI: 46, 68) in patients with RET fusion-positive NSCLC previously treated with platinum chemotherapy to 89% (95% CI: 52, 100) in patients with RET fusion-positive thyroid cancer, with response duration of at least 6 months in most responders.	Platinum	145-153	ret proto-oncogene	Homo sapiens	95-98
34024902-6	2021	FDA approval has now been given for selpercatinib for RET fusion-positive NSCLC and papillary thyroid cancer, and RET mutation-positive thyroid cancer.	Selpercatinib	36-49	ret proto-oncogene	Homo sapiens	54-57
33952394-10	2021	CONCLUSION: Data from CBC and RET-He can identify patients with IDA, determine need for and responsiveness to intravenous iron, and reduce time for therapeutic decisions.	Iron	122-126	ret proto-oncogene	Homo sapiens	30-33
33561664-1	2021	Herein, we report a novel dual-quenching electrochemiluminescence (ECL) immunosensor for detecting protein induced by vitamin K absence or antagonist-II (PIVKA-II) based on ECL resonance energy transfer (ECL-RET).	Vitamin K	118-127	ret proto-oncogene	Homo sapiens	208-211
33561664-5	2021	The dual quenching labels of Ag nanocubes modified with vitamin B2 (AgNCs-VB2) were firstly proposed towards g-C3N4 NSs/S2O82- ECL system by ECL-RET, resulting in the remarkable ECL decrease for "signal off" state.	Riboflavin	56-66	ret proto-oncogene	Homo sapiens	145-148
33561664-5	2021	The dual quenching labels of Ag nanocubes modified with vitamin B2 (AgNCs-VB2) were firstly proposed towards g-C3N4 NSs/S2O82- ECL system by ECL-RET, resulting in the remarkable ECL decrease for "signal off" state.	c3n4	111-115	ret proto-oncogene	Homo sapiens	145-148
33561664-5	2021	The dual quenching labels of Ag nanocubes modified with vitamin B2 (AgNCs-VB2) were firstly proposed towards g-C3N4 NSs/S2O82- ECL system by ECL-RET, resulting in the remarkable ECL decrease for "signal off" state.	s2o82	120-125	ret proto-oncogene	Homo sapiens	145-148
33725547-0	2021	Final survival results for the LURET phase II study of vandetanib in previously treated patients with RET-rearranged advanced non-small cell lung cancer.	vandetanib	55-65	ret proto-oncogene	Homo sapiens	33-36
33913953-1	2021	A facile strategy to design a highly efficient electrochemiluminescence resonance energy transfer (ECL-RET) system was proposed by using an AIEgen-based 2D ultrathin metal-organic layer (MOL) to coordinatively immobilize energy donors and acceptors simultaneously, in which the distance between adjacent donor-acceptor pairs was precise and short for obtaining high ECL-RET efficiency.	Metals	166-171	ret proto-oncogene	Homo sapiens	103-106
33655698-7	2021	RESULTS: EGFR-sensitizing mutations, ALK, RET, and ROS1 rearrangements were associated with lower TMB and PD-L1+/TMB-H proportions, whereas KRAS, ALK, RET, and ROS1 substitutions/indels correlated with higher TMB and PD-L1+/TMB-H proportions than wild-type genotypes.	Trimedoxime	98-101	ret proto-oncogene	Homo sapiens	42-45
33655698-7	2021	RESULTS: EGFR-sensitizing mutations, ALK, RET, and ROS1 rearrangements were associated with lower TMB and PD-L1+/TMB-H proportions, whereas KRAS, ALK, RET, and ROS1 substitutions/indels correlated with higher TMB and PD-L1+/TMB-H proportions than wild-type genotypes.	Trimedoxime	98-101	ret proto-oncogene	Homo sapiens	151-154
33655698-7	2021	RESULTS: EGFR-sensitizing mutations, ALK, RET, and ROS1 rearrangements were associated with lower TMB and PD-L1+/TMB-H proportions, whereas KRAS, ALK, RET, and ROS1 substitutions/indels correlated with higher TMB and PD-L1+/TMB-H proportions than wild-type genotypes.	Trimedoxime	113-118	ret proto-oncogene	Homo sapiens	42-45
33655698-7	2021	RESULTS: EGFR-sensitizing mutations, ALK, RET, and ROS1 rearrangements were associated with lower TMB and PD-L1+/TMB-H proportions, whereas KRAS, ALK, RET, and ROS1 substitutions/indels correlated with higher TMB and PD-L1+/TMB-H proportions than wild-type genotypes.	Trimedoxime	113-116	ret proto-oncogene	Homo sapiens	42-45
33721621-1	2021	BACKGROUND: Preclinical studies suggest that combining vandetanib (VAN), a multi-tyrosine kinase inhibitor of rearranged during transfection (RET) proto-oncogene, vascular endothelial growth factor receptor (VEGFR), and epidermal growth factor receptor (EGFR), with everolimus (EV), a mammalian target of rapamycin (mTOR) inhibitor, may improve antitumor activity.	vandetanib	55-65	ret proto-oncogene	Homo sapiens	142-145
33721621-1	2021	BACKGROUND: Preclinical studies suggest that combining vandetanib (VAN), a multi-tyrosine kinase inhibitor of rearranged during transfection (RET) proto-oncogene, vascular endothelial growth factor receptor (VEGFR), and epidermal growth factor receptor (EGFR), with everolimus (EV), a mammalian target of rapamycin (mTOR) inhibitor, may improve antitumor activity.	vandetanib	67-70	ret proto-oncogene	Homo sapiens	142-145
33382428-11	2021	RET+ PTC with a BA signal pattern was more frequently found in unifocal lesions than in multifocal/bilateral tumors (p=0.049).	Barium	16-18	ret proto-oncogene	Homo sapiens	0-3
33728771-6	2021	In addition, treatment with either alectinib or ceritinib modulated the activation of various molecules downstream of RTK signaling and induced caspase-dependent/independent cell death mainly by inhibiting signal transducer and activator of transcription 3 activation in human GBM cells.	ceritinib	48-57	ret proto-oncogene	Homo sapiens	118-121
33748479-10	2021	Both fusions were found in papillary thyroid cancers of follicular histologic subtype with node metastases, one of them (NCOA4-RET) for the radioactive iodine resistant tumor.	radioactive iodine	140-158	ret proto-oncogene	Homo sapiens	127-130
33455880-4	2021	To overcome these issues, new selective RET inhibitors such as pralsetinib (BLU-667) and selpercatinib (LOXO-292) have been developed in clinical trials, with selpercatinib recently approved by the Food and Drug Administration (FDA).	Selpercatinib	89-102	ret proto-oncogene	Homo sapiens	40-43
33455880-4	2021	To overcome these issues, new selective RET inhibitors such as pralsetinib (BLU-667) and selpercatinib (LOXO-292) have been developed in clinical trials, with selpercatinib recently approved by the Food and Drug Administration (FDA).	Selpercatinib	159-172	ret proto-oncogene	Homo sapiens	40-43
33150799-1	2021	Selpercatinib, a novel, highly selective and potent, inhibitor of RET, demonstrated clinically meaningful antitumor activity with manageable toxicity in heavily pretreated and treatment-naive RET fusion-positive non-small-cell lung cancer patients in a Phase I/II clinical trial.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	66-69
33272981-1	2021	PURPOSE: Selpercatinib and pralsetinib induce deep and durable responses in advanced RET fusion-positive lung and thyroid cancer patients.	Selpercatinib	9-22	ret proto-oncogene	Homo sapiens	85-88
33150799-1	2021	Selpercatinib, a novel, highly selective and potent, inhibitor of RET, demonstrated clinically meaningful antitumor activity with manageable toxicity in heavily pretreated and treatment-naive RET fusion-positive non-small-cell lung cancer patients in a Phase I/II clinical trial.	Selpercatinib	0-13	ret proto-oncogene	Homo sapiens	192-195