PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
31719901-12	2019	Conclusions: Ultrasound enhanced anti-tumor effect of temozolomide in glioblastoma cells via JNK and p38 pathways.	temozolomide	54-66	mitogen-activated protein kinase 14	Mus musculus	101-104
31758290-7	2020	While TMZ treated cells did not show alteration in any of the Wnt ligands, PI3K inhibitor (LY294002) treatment repressed Akt activation and abolished the TMZ-mediated induction of Wnt/beta-catenin pathway.	temozolomide	154-157	catenin beta 1	Homo sapiens	184-196
31671279-0	2020	Eukaryotic initiation factor 5B (eIF5B) regulates temozolomide-mediated apoptosis in brain tumor stem cells (BTSCs).	temozolomide	50-62	eukaryotic translation initiation factor 5B	Homo sapiens	0-31
31671279-0	2020	Eukaryotic initiation factor 5B (eIF5B) regulates temozolomide-mediated apoptosis in brain tumor stem cells (BTSCs).	temozolomide	50-62	eukaryotic translation initiation factor 5B	Homo sapiens	33-38
31671279-9	2020	We show that silencing eIF5B leads to increased TMZ sensitivity in two BTSC lines, BT25 and BT48.	temozolomide	48-51	eukaryotic translation initiation factor 5B	Homo sapiens	23-28
31671279-10	2020	Depletion of eIF5B decreases levels of anti-apoptotic proteins in BT48 and sensitizes these cells to TMZ-induced activation of caspase-3, cleavage of PARP, and apoptosis.	temozolomide	101-104	eukaryotic translation initiation factor 5B	Homo sapiens	13-18
31671279-10	2020	Depletion of eIF5B decreases levels of anti-apoptotic proteins in BT48 and sensitizes these cells to TMZ-induced activation of caspase-3, cleavage of PARP, and apoptosis.	temozolomide	101-104	caspase 3	Homo sapiens	127-136
31671279-10	2020	Depletion of eIF5B decreases levels of anti-apoptotic proteins in BT48 and sensitizes these cells to TMZ-induced activation of caspase-3, cleavage of PARP, and apoptosis.	temozolomide	101-104	poly(ADP-ribose) polymerase 1	Homo sapiens	150-154
31863352-9	2020	In cases of non-MGMT promoter methylation, systemic therapy with temozolomide is still recommended in many hospitals.	temozolomide	65-77	O-6-methylguanine-DNA methyltransferase	Homo sapiens	16-20
31865606-0	2020	IKBKE enhances TMZ-chemoresistance through upregulation of MGMT expression in glioblastoma.	temozolomide	15-18	inhibitor of nuclear factor kappa B kinase subunit epsilon	Homo sapiens	0-5
31865606-0	2020	IKBKE enhances TMZ-chemoresistance through upregulation of MGMT expression in glioblastoma.	temozolomide	15-18	O-6-methylguanine-DNA methyltransferase	Homo sapiens	59-63
31865606-5	2020	Our study aimed to investigate the mechanism of IKBKE enhancing the resistance of glioma cells to temozolomide.	temozolomide	98-110	inhibitor of nuclear factor kappa B kinase subunit epsilon	Homo sapiens	48-53
31865606-11	2020	RESULTS: In this study, we demonstrated that IKBKE enhances the resistance of glioblastoma cells to temozolomide (TMZ) by activating the AKT/NF-kappaB signaling pathway to upregulate the expression of the DNA repair enzyme o6-methylguanine-dna methyltransferase (MGMT).	temozolomide	100-112	inhibitor of nuclear factor kappa B kinase subunit epsilon	Homo sapiens	45-50
31865606-11	2020	RESULTS: In this study, we demonstrated that IKBKE enhances the resistance of glioblastoma cells to temozolomide (TMZ) by activating the AKT/NF-kappaB signaling pathway to upregulate the expression of the DNA repair enzyme o6-methylguanine-dna methyltransferase (MGMT).	temozolomide	100-112	AKT serine/threonine kinase 1	Homo sapiens	137-140
31865606-11	2020	RESULTS: In this study, we demonstrated that IKBKE enhances the resistance of glioblastoma cells to temozolomide (TMZ) by activating the AKT/NF-kappaB signaling pathway to upregulate the expression of the DNA repair enzyme o6-methylguanine-dna methyltransferase (MGMT).	temozolomide	114-117	inhibitor of nuclear factor kappa B kinase subunit epsilon	Homo sapiens	45-50
31865606-11	2020	RESULTS: In this study, we demonstrated that IKBKE enhances the resistance of glioblastoma cells to temozolomide (TMZ) by activating the AKT/NF-kappaB signaling pathway to upregulate the expression of the DNA repair enzyme o6-methylguanine-dna methyltransferase (MGMT).	temozolomide	114-117	AKT serine/threonine kinase 1	Homo sapiens	137-140
31865606-11	2020	RESULTS: In this study, we demonstrated that IKBKE enhances the resistance of glioblastoma cells to temozolomide (TMZ) by activating the AKT/NF-kappaB signaling pathway to upregulate the expression of the DNA repair enzyme o6-methylguanine-dna methyltransferase (MGMT).	temozolomide	114-117	O-6-methylguanine-DNA methyltransferase	Homo sapiens	223-261
31865606-11	2020	RESULTS: In this study, we demonstrated that IKBKE enhances the resistance of glioblastoma cells to temozolomide (TMZ) by activating the AKT/NF-kappaB signaling pathway to upregulate the expression of the DNA repair enzyme o6-methylguanine-dna methyltransferase (MGMT).	temozolomide	114-117	O-6-methylguanine-DNA methyltransferase	Homo sapiens	263-267
31865606-12	2020	In glioblastoma cells, IKBKE knockdown enhances apoptosis and suppresses cell proliferation, clone formation, and tumor development in vivo induced by TMZ.	temozolomide	151-154	inhibitor of nuclear factor kappa B kinase subunit epsilon	Homo sapiens	23-28
31865606-13	2020	However, overexpression of IKBKE reduces the effects of TMZ.	temozolomide	56-59	inhibitor of nuclear factor kappa B kinase subunit epsilon	Homo sapiens	27-32
31865606-14	2020	CONCLUSION: Our studies suggest that inhibition of IKBKE can enhance the therapeutic effect of TMZ on GBM in vitro and in vivo, providing new research directions and therapeutic targets for the treatment of GBM.	temozolomide	95-98	inhibitor of nuclear factor kappa B kinase subunit epsilon	Homo sapiens	51-56
31916238-0	2020	A Key Role of DNA Damage-Inducible Transcript 4 (DDIT4) Connects Autophagy and GLUT3-Mediated Stemness To Desensitize Temozolomide Efficacy in Glioblastomas.	temozolomide	118-130	DNA damage inducible transcript 4	Homo sapiens	14-47
31916238-0	2020	A Key Role of DNA Damage-Inducible Transcript 4 (DDIT4) Connects Autophagy and GLUT3-Mediated Stemness To Desensitize Temozolomide Efficacy in Glioblastomas.	temozolomide	118-130	DNA damage inducible transcript 4	Homo sapiens	49-54
31916238-0	2020	A Key Role of DNA Damage-Inducible Transcript 4 (DDIT4) Connects Autophagy and GLUT3-Mediated Stemness To Desensitize Temozolomide Efficacy in Glioblastomas.	temozolomide	118-130	solute carrier family 2 member 3	Homo sapiens	79-84
31916238-3	2020	Herein, we investigated DDIT4 signaling in GBM and temozolomide (TMZ) drug resistance.	temozolomide	65-68	DNA damage inducible transcript 4	Homo sapiens	24-29
31916238-4	2020	We identified that TMZ induced DDIT4 upregulation, leading to desensitization against TMZ cytotoxicity in GBM cells.	temozolomide	19-22	DNA damage inducible transcript 4	Homo sapiens	31-36
31916238-4	2020	We identified that TMZ induced DDIT4 upregulation, leading to desensitization against TMZ cytotoxicity in GBM cells.	temozolomide	86-89	DNA damage inducible transcript 4	Homo sapiens	31-36
31916238-6	2020	Furthermore, patients with lower DDIT4 levels, especially O-6-methylguanine-DNA methyltransferase (MGMT)-methylated patients, exhibited better TMZ therapeutic efficacy.	temozolomide	143-146	DNA damage inducible transcript 4	Homo sapiens	33-38
31916238-6	2020	Furthermore, patients with lower DDIT4 levels, especially O-6-methylguanine-DNA methyltransferase (MGMT)-methylated patients, exhibited better TMZ therapeutic efficacy.	temozolomide	143-146	O-6-methylguanine-DNA methyltransferase	Homo sapiens	58-97
31916238-6	2020	Furthermore, patients with lower DDIT4 levels, especially O-6-methylguanine-DNA methyltransferase (MGMT)-methylated patients, exhibited better TMZ therapeutic efficacy.	temozolomide	143-146	O-6-methylguanine-DNA methyltransferase	Homo sapiens	99-103
31916238-8	2020	Among these 5 genes, only GLUT3 was upregulated in both TMZ-treated and DDIT4-overexpressing cells.	temozolomide	56-59	solute carrier family 2 member 3	Homo sapiens	26-31
31916238-9	2020	DDIT4-mediated GLUT3 expression was also identified, and its expression decreased TMZ"s cytotoxicity.	temozolomide	82-85	DNA damage inducible transcript 4	Homo sapiens	0-5
31916238-9	2020	DDIT4-mediated GLUT3 expression was also identified, and its expression decreased TMZ"s cytotoxicity.	temozolomide	82-85	solute carrier family 2 member 3	Homo sapiens	15-20
31916238-13	2020	Finally, we identified TMZ-upregulated activating transcription factor 4 (ATF4) as an upstream regulator of DDIT4-mediated GLUT3/stemness signaling and autophagy.	temozolomide	23-26	activating transcription factor 4	Homo sapiens	39-72
31916238-13	2020	Finally, we identified TMZ-upregulated activating transcription factor 4 (ATF4) as an upstream regulator of DDIT4-mediated GLUT3/stemness signaling and autophagy.	temozolomide	23-26	activating transcription factor 4	Homo sapiens	74-78
31916238-13	2020	Finally, we identified TMZ-upregulated activating transcription factor 4 (ATF4) as an upstream regulator of DDIT4-mediated GLUT3/stemness signaling and autophagy.	temozolomide	23-26	DNA damage inducible transcript 4	Homo sapiens	108-113
31916238-13	2020	Finally, we identified TMZ-upregulated activating transcription factor 4 (ATF4) as an upstream regulator of DDIT4-mediated GLUT3/stemness signaling and autophagy.	temozolomide	23-26	solute carrier family 2 member 3	Homo sapiens	123-128
31916238-14	2020	Consequently, ATF4/DDIT4 signaling was connected to both autophagy and GLUT3-regulated stemness, which are involved in TMZ drug resistance and the poor prognoses of GBM patients.	temozolomide	119-122	activating transcription factor 4	Homo sapiens	14-18
31916238-14	2020	Consequently, ATF4/DDIT4 signaling was connected to both autophagy and GLUT3-regulated stemness, which are involved in TMZ drug resistance and the poor prognoses of GBM patients.	temozolomide	119-122	DNA damage inducible transcript 4	Homo sapiens	19-24
31916238-14	2020	Consequently, ATF4/DDIT4 signaling was connected to both autophagy and GLUT3-regulated stemness, which are involved in TMZ drug resistance and the poor prognoses of GBM patients.	temozolomide	119-122	solute carrier family 2 member 3	Homo sapiens	71-76
31578804-0	2020	Receptor tyrosine kinase AXL is correlated with poor prognosis and induces temozolomide resistance in glioblastoma.	temozolomide	75-87	AXL receptor tyrosine kinase	Homo sapiens	25-28
31578804-1	2020	AIMS: To investigate the functions and underlying mechanisms of AXL receptor tyrosine kinase (AXL) in tumor proliferation and chemoresistance to temozolomide (TMZ) in glioblastoma (GBM).	temozolomide	145-157	AXL receptor tyrosine kinase	Homo sapiens	64-67
31578804-1	2020	AIMS: To investigate the functions and underlying mechanisms of AXL receptor tyrosine kinase (AXL) in tumor proliferation and chemoresistance to temozolomide (TMZ) in glioblastoma (GBM).	temozolomide	145-157	AXL receptor tyrosine kinase	Homo sapiens	94-97
31578804-1	2020	AIMS: To investigate the functions and underlying mechanisms of AXL receptor tyrosine kinase (AXL) in tumor proliferation and chemoresistance to temozolomide (TMZ) in glioblastoma (GBM).	temozolomide	159-162	AXL receptor tyrosine kinase	Homo sapiens	64-67
31578804-1	2020	AIMS: To investigate the functions and underlying mechanisms of AXL receptor tyrosine kinase (AXL) in tumor proliferation and chemoresistance to temozolomide (TMZ) in glioblastoma (GBM).	temozolomide	159-162	AXL receptor tyrosine kinase	Homo sapiens	94-97
31578804-2	2020	METHODS: With a kinome-wide bioinformatics analysis, AXL was found to be an essential kinase candidate in TMZ chemoresistance promotion.	temozolomide	106-109	AXL receptor tyrosine kinase	Homo sapiens	53-56
31578804-3	2020	Additionally, the biological functions of AXL in oncogenesis and TMZ resistance were clarified by using qRT-PCR, Western blotting, and in vivo intracranial GBM xenograft models followed the induction of TMZ resistance in U87 or U251 cells.	temozolomide	203-206	AXL receptor tyrosine kinase	Homo sapiens	42-45
31578804-5	2020	Finally, the Chou-Talalay model was performed to confirm the synergistic effect of AXL inhibitor TP-0903 with TMZ.	temozolomide	110-113	AXL receptor tyrosine kinase	Homo sapiens	83-86
31578804-7	2020	Moreover, AXL knockdown reduced tumorigenesis and TMZ resistance in vitro and in vivo; however, exogenous AXL overexpression induced TMZ resistance in GBM.	temozolomide	50-53	AXL receptor tyrosine kinase	Homo sapiens	10-13
31578804-7	2020	Moreover, AXL knockdown reduced tumorigenesis and TMZ resistance in vitro and in vivo; however, exogenous AXL overexpression induced TMZ resistance in GBM.	temozolomide	133-136	AXL receptor tyrosine kinase	Homo sapiens	106-109
31578804-8	2020	Lastly, a specific AXL inhibitor, TP-0903, dramatically decreased tumor growth and increased sensitivity to TMZ via a synergistic effect.	temozolomide	108-111	AXL receptor tyrosine kinase	Homo sapiens	19-22
31578804-9	2020	CONCLUSION: AXL contributed to chemoresistance to TMZ in GBM and could be used as a novel prognostic biomarker and therapeutic target for GBM.	temozolomide	50-53	AXL receptor tyrosine kinase	Homo sapiens	12-15
31853548-6	2020	Studies in animal models documented that FUS enhanced the delivery of numerous chemotherapeutic and investigational agents across the BBB and into brain tumors, including temozolomide, bevacizumab, 1,3-bis (2-chloroethyl)-1-nitrosourea, doxorubicin, viral vectors, and cells.	temozolomide	171-183	FUS RNA binding protein	Homo sapiens	41-44
31758290-0	2020	Temozolomide induces activation of Wnt/beta-catenin signaling in glioma cells via PI3K/Akt pathway: implications in glioma therapy.	temozolomide	0-12	catenin beta 1	Homo sapiens	39-51
31758290-0	2020	Temozolomide induces activation of Wnt/beta-catenin signaling in glioma cells via PI3K/Akt pathway: implications in glioma therapy.	temozolomide	0-12	AKT serine/threonine kinase 1	Homo sapiens	87-90
31758290-5	2020	Gene Set Enrichment Analysis (GSEA) indicated a significant enrichment of Wnt/beta-catenin signaling besides many other pathways in TMZ treated cells.	temozolomide	132-135	catenin beta 1	Homo sapiens	78-90
31758290-6	2020	Further, we demonstrate that TMZ treatment increased the activity from TOPflash reporter, (a Wnt responsive reporter), enhanced the levels of pGSK-3beta (S9) and reduced the levels of p-beta-catenin (S33/37/T41) with a concomitant increase in transcript and protein levels of Wnt targets in a concentration and time-dependent manner.	temozolomide	29-32	catenin beta 1	Homo sapiens	186-198
31758290-8	2020	In addition, we show that Wnt/beta-catenin signaling activation by TMZ is independent of ATM/Chk2 pathway.	temozolomide	67-70	catenin beta 1	Homo sapiens	30-42
31758290-9	2020	Further, we also demonstrate the activation of mTOR pathway after TMZ treatment.	temozolomide	66-69	mechanistic target of rapamycin kinase	Homo sapiens	47-51
31758290-10	2020	Thus, our results demonstrate that activation of Wnt/beta-catenin pathway involves an ATM/Chk2- independent PI3K/Akt/GSK-3 cascade in TMZ treated cells and further provides mechanistic basis for the chemoresistance of glioma to TMZ.	temozolomide	134-137	catenin beta 1	Homo sapiens	53-65
31758290-10	2020	Thus, our results demonstrate that activation of Wnt/beta-catenin pathway involves an ATM/Chk2- independent PI3K/Akt/GSK-3 cascade in TMZ treated cells and further provides mechanistic basis for the chemoresistance of glioma to TMZ.	temozolomide	134-137	ATM serine/threonine kinase	Homo sapiens	86-89
31758290-10	2020	Thus, our results demonstrate that activation of Wnt/beta-catenin pathway involves an ATM/Chk2- independent PI3K/Akt/GSK-3 cascade in TMZ treated cells and further provides mechanistic basis for the chemoresistance of glioma to TMZ.	temozolomide	134-137	checkpoint kinase 2	Homo sapiens	90-94
31758290-10	2020	Thus, our results demonstrate that activation of Wnt/beta-catenin pathway involves an ATM/Chk2- independent PI3K/Akt/GSK-3 cascade in TMZ treated cells and further provides mechanistic basis for the chemoresistance of glioma to TMZ.	temozolomide	134-137	AKT serine/threonine kinase 1	Homo sapiens	113-116
31758290-10	2020	Thus, our results demonstrate that activation of Wnt/beta-catenin pathway involves an ATM/Chk2- independent PI3K/Akt/GSK-3 cascade in TMZ treated cells and further provides mechanistic basis for the chemoresistance of glioma to TMZ.	temozolomide	228-231	catenin beta 1	Homo sapiens	53-65
31758290-10	2020	Thus, our results demonstrate that activation of Wnt/beta-catenin pathway involves an ATM/Chk2- independent PI3K/Akt/GSK-3 cascade in TMZ treated cells and further provides mechanistic basis for the chemoresistance of glioma to TMZ.	temozolomide	228-231	ATM serine/threonine kinase	Homo sapiens	86-89
31987922-7	2020	Moreover, Nano-DOX also suppressed stimulated activation of STAT3 and IL-6 induced by temozolomide, a first-line anti-GBM chemotherapy, resistance to which critically involves STAT3 activation.	temozolomide	86-98	signal transducer and activator of transcription 3	Homo sapiens	60-65
32045717-5	2020	TMZ inhibited mtDNA replication and transcription of mitochondrial genes (ND1 and Cyt b) in NSC by 24 h, whereas the effect of TMZ on neuronal mtDNA transcription was less pronounced.	temozolomide	0-3	mitochondrially encoded NADH dehydrogenase 1	Homo sapiens	74-77
32045717-5	2020	TMZ inhibited mtDNA replication and transcription of mitochondrial genes (ND1 and Cyt b) in NSC by 24 h, whereas the effect of TMZ on neuronal mtDNA transcription was less pronounced.	temozolomide	0-3	mitochondrially encoded cytochrome b	Homo sapiens	82-87
32045717-7	2020	Acute TMZ exposure (4 h) caused a rapid reduction in dendritic branching and loss of postsynaptic density-95 (PSD95) puncta on dendrites.	temozolomide	6-9	discs large MAGUK scaffold protein 4	Homo sapiens	85-108
32045717-7	2020	Acute TMZ exposure (4 h) caused a rapid reduction in dendritic branching and loss of postsynaptic density-95 (PSD95) puncta on dendrites.	temozolomide	6-9	discs large MAGUK scaffold protein 4	Homo sapiens	110-115
32032585-14	2020	Organoids with reduced levels of MGMT and CHFR mRNAs were sensitive to temozolomide and taxane drugs.	temozolomide	71-83	O-6-methylguanine-DNA methyltransferase	Homo sapiens	33-37
32032585-14	2020	Organoids with reduced levels of MGMT and CHFR mRNAs were sensitive to temozolomide and taxane drugs.	temozolomide	71-83	checkpoint with forkhead and ring finger domains	Homo sapiens	42-46
31987922-7	2020	Moreover, Nano-DOX also suppressed stimulated activation of STAT3 and IL-6 induced by temozolomide, a first-line anti-GBM chemotherapy, resistance to which critically involves STAT3 activation.	temozolomide	86-98	interleukin 6	Homo sapiens	70-74
31987922-7	2020	Moreover, Nano-DOX also suppressed stimulated activation of STAT3 and IL-6 induced by temozolomide, a first-line anti-GBM chemotherapy, resistance to which critically involves STAT3 activation.	temozolomide	86-98	signal transducer and activator of transcription 3	Homo sapiens	176-181
31833081-3	2020	The aims of this study were to comprehend the effect of TMZ on nucleus and the underlying mechanism of acquired TMZ resistance in MGMT-deficient GBM.	temozolomide	56-59	O-6-methylguanine-DNA methyltransferase	Homo sapiens	130-134
31900275-7	2020	RESULTS: While having no detectable effect in MSH6 wild-type GBMs, PARPi selectively restored TMZ sensitivity in MSH6-deficient GBM cells.	temozolomide	94-97	mutS homolog 6	Homo sapiens	113-117
31900275-8	2020	This genotype-specific restoration of activity translated in vivo, where combination treatment of veliparib and TMZ showed potent suppression of tumor growth of MSH6-inactivated orthotopic xenografts, compared with TMZ monotherapy.	temozolomide	112-115	mutS homolog 6	Homo sapiens	161-165
31900275-11	2020	CONCLUSIONS: PARPi restoration of TMZ chemosensitivity in MSH6-inactivated glioma represents a promising strategy to overcome acquired chemoresistance caused by MMR deficiency.	temozolomide	34-37	mutS homolog 6	Homo sapiens	58-62
31613002-0	2020	Role of Sonic hedgehog signaling in cell cycle, oxidative stress, and autophagy of temozolomide resistant glioblastoma.	temozolomide	83-95	sonic hedgehog signaling molecule	Homo sapiens	8-22
31613002-2	2020	The Sonic hedgehog (SHH) pathway is involved with GBM tumorigenesis and TMZ chemoresistance.	temozolomide	72-75	sonic hedgehog signaling molecule	Homo sapiens	4-18
31613002-2	2020	The Sonic hedgehog (SHH) pathway is involved with GBM tumorigenesis and TMZ chemoresistance.	temozolomide	72-75	sonic hedgehog signaling molecule	Homo sapiens	20-23
31613002-3	2020	The role of SHH pathway inhibition in the potentiation of TMZ"s effects using T98G, U251, and GBM11 cell lines is investigated herein.	temozolomide	58-61	sonic hedgehog signaling molecule	Homo sapiens	12-15
31613002-9	2020	The selective inhibition of the SHH pathway potentiated the cytotoxic effect of TMZ, thus becoming a promising in vitro strategy for GBM treatment.	temozolomide	80-83	sonic hedgehog signaling molecule	Homo sapiens	32-35
31750728-0	2020	NCK1-AS1 Increases Drug Resistance of Glioma Cells to Temozolomide by Modulating miR-137/TRIM24.	temozolomide	54-66	NCK adaptor protein 1	Homo sapiens	0-4
31750728-0	2020	NCK1-AS1 Increases Drug Resistance of Glioma Cells to Temozolomide by Modulating miR-137/TRIM24.	temozolomide	54-66	prostaglandin D2 receptor	Homo sapiens	5-8
32036239-0	2020	Temozolomide for patients with wild-type isocitrate dehydrogenase (IDH) 1 glioblastoma using propensity score matching.	temozolomide	0-12	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	67-73
32036239-1	2020	OBJECTIVE: The isocitrate dehydrogenase (IDH) 1 wild-type glioblastoma (GBM) is a major population of GBM that should be of concern in terms of the efficacy of using Temozolomide (TMZ) in adjuvant treatment.	temozolomide	166-178	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	15-47
32036239-1	2020	OBJECTIVE: The isocitrate dehydrogenase (IDH) 1 wild-type glioblastoma (GBM) is a major population of GBM that should be of concern in terms of the efficacy of using Temozolomide (TMZ) in adjuvant treatment.	temozolomide	180-183	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	15-47
32036239-13	2020	CONCLUSIONS: The present study revealed that the effect of TMZ with RT in IDH1 wild-type GBM patients had advantages in terms of survival by using multivariable analysis and PS approaches.	temozolomide	59-62	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	74-78
31750728-0	2020	NCK1-AS1 Increases Drug Resistance of Glioma Cells to Temozolomide by Modulating miR-137/TRIM24.	temozolomide	54-66	microRNA 137	Homo sapiens	81-88
31750728-0	2020	NCK1-AS1 Increases Drug Resistance of Glioma Cells to Temozolomide by Modulating miR-137/TRIM24.	temozolomide	54-66	tripartite motif containing 24	Homo sapiens	89-95
31750728-2	2020	The purpose of this study was to investigate the effect and molecular mechanism of long noncoding RNA (lncRNA) NCK1-AS1 on the drug resistance of temozolomide (TMZ) in glioma cells.	temozolomide	146-158	NCK adaptor protein 1	Homo sapiens	111-115
31750728-2	2020	The purpose of this study was to investigate the effect and molecular mechanism of long noncoding RNA (lncRNA) NCK1-AS1 on the drug resistance of temozolomide (TMZ) in glioma cells.	temozolomide	146-158	prostaglandin D2 receptor	Homo sapiens	116-119
31750728-2	2020	The purpose of this study was to investigate the effect and molecular mechanism of long noncoding RNA (lncRNA) NCK1-AS1 on the drug resistance of temozolomide (TMZ) in glioma cells.	temozolomide	160-163	NCK adaptor protein 1	Homo sapiens	111-115
31750728-2	2020	The purpose of this study was to investigate the effect and molecular mechanism of long noncoding RNA (lncRNA) NCK1-AS1 on the drug resistance of temozolomide (TMZ) in glioma cells.	temozolomide	160-163	prostaglandin D2 receptor	Homo sapiens	116-119
31750728-8	2020	Results: NCK1-AS1 expression was increased in regular and recurrent glioma tissues and TMZ-resistant cells.	temozolomide	87-90	NCK adaptor protein 1	Homo sapiens	9-13
31750728-8	2020	Results: NCK1-AS1 expression was increased in regular and recurrent glioma tissues and TMZ-resistant cells.	temozolomide	87-90	prostaglandin D2 receptor	Homo sapiens	14-17
31750728-13	2020	In addition, the decreases of cell viability and IC50 induced by NCK1-AS1 knockdown were reversed after adding TRIM24 in U251/TMZ and A172/TMZ cells.	temozolomide	126-129	NCK adaptor protein 1	Homo sapiens	65-69
31750728-13	2020	In addition, the decreases of cell viability and IC50 induced by NCK1-AS1 knockdown were reversed after adding TRIM24 in U251/TMZ and A172/TMZ cells.	temozolomide	126-129	prostaglandin D2 receptor	Homo sapiens	70-73
31750728-13	2020	In addition, the decreases of cell viability and IC50 induced by NCK1-AS1 knockdown were reversed after adding TRIM24 in U251/TMZ and A172/TMZ cells.	temozolomide	126-129	tripartite motif containing 24	Homo sapiens	111-117
31750728-13	2020	In addition, the decreases of cell viability and IC50 induced by NCK1-AS1 knockdown were reversed after adding TRIM24 in U251/TMZ and A172/TMZ cells.	temozolomide	139-142	NCK adaptor protein 1	Homo sapiens	65-69
31750728-13	2020	In addition, the decreases of cell viability and IC50 induced by NCK1-AS1 knockdown were reversed after adding TRIM24 in U251/TMZ and A172/TMZ cells.	temozolomide	139-142	prostaglandin D2 receptor	Homo sapiens	70-73
31750728-13	2020	In addition, the decreases of cell viability and IC50 induced by NCK1-AS1 knockdown were reversed after adding TRIM24 in U251/TMZ and A172/TMZ cells.	temozolomide	139-142	tripartite motif containing 24	Homo sapiens	111-117
31750728-14	2020	Conclusion: NCK1-AS1 could increase drug resistance of glioma cells to TMZ by modulating miR-137/TRIM24 pathway.	temozolomide	71-74	NCK adaptor protein 1	Homo sapiens	12-16
31750728-14	2020	Conclusion: NCK1-AS1 could increase drug resistance of glioma cells to TMZ by modulating miR-137/TRIM24 pathway.	temozolomide	71-74	prostaglandin D2 receptor	Homo sapiens	17-20
31750728-14	2020	Conclusion: NCK1-AS1 could increase drug resistance of glioma cells to TMZ by modulating miR-137/TRIM24 pathway.	temozolomide	71-74	microRNA 137	Homo sapiens	89-96
31750728-14	2020	Conclusion: NCK1-AS1 could increase drug resistance of glioma cells to TMZ by modulating miR-137/TRIM24 pathway.	temozolomide	71-74	tripartite motif containing 24	Homo sapiens	97-103
31833081-3	2020	The aims of this study were to comprehend the effect of TMZ on nucleus and the underlying mechanism of acquired TMZ resistance in MGMT-deficient GBM.	temozolomide	112-115	O-6-methylguanine-DNA methyltransferase	Homo sapiens	130-134
31833081-4	2020	We show the changes of nuclear proteome in the MGMT-deficient GBM U87 cells treated with TMZ for 1 week.	temozolomide	89-92	O-6-methylguanine-DNA methyltransferase	Homo sapiens	47-51
32070670-10	2020	When the patients were divided into pre and post temozolomide era, the association of MGMT promoter methylation status with PFS was only noted in the patients of temozolomide era (pre, p = 0.432; post, p = 0.015).	temozolomide	49-61	O-6-methylguanine-DNA methyltransferase	Homo sapiens	86-90
32070670-10	2020	When the patients were divided into pre and post temozolomide era, the association of MGMT promoter methylation status with PFS was only noted in the patients of temozolomide era (pre, p = 0.432; post, p = 0.015).	temozolomide	162-174	O-6-methylguanine-DNA methyltransferase	Homo sapiens	86-90
31806377-5	2020	Interestingly, we observed that the addition of four different autophagy inducers, rapamycin (RAP), CCI779, ABT737 and temozolomide (TMZ), induced the differences of DR5 expression and cell apoptosis after irradiation.	temozolomide	119-131	TNF receptor superfamily member 10b	Homo sapiens	166-169
31756732-9	2020	MSI1 was found to promote drug resistance to the combined treatment with TMZ and VPA.	temozolomide	73-76	musashi RNA binding protein 1	Homo sapiens	0-4
31806377-5	2020	Interestingly, we observed that the addition of four different autophagy inducers, rapamycin (RAP), CCI779, ABT737 and temozolomide (TMZ), induced the differences of DR5 expression and cell apoptosis after irradiation.	temozolomide	133-136	TNF receptor superfamily member 10b	Homo sapiens	166-169
31806377-6	2020	Unlike RAP and CCI779, ABT737 and TMZ were able to increase DR5 expression and further induce cell death.	temozolomide	34-37	TNF receptor superfamily member 10b	Homo sapiens	60-63
32020475-7	2020	A Cox proportional hazards model identified extent of resection and MGMT methylation status as significant prognostic factors in the TMZ era; however, these factors were not significant in the TMZ-BEV era.	temozolomide	133-136	O-6-methylguanine-DNA methyltransferase	Homo sapiens	68-72
32028734-1	2020	13a-(S)-3-pivaloyloxyl-6,7-dimethoxyphenanthro(9,10-b)-indolizidine (CAT3) is a novel oral anti-glioma pro-drug with a potent anti-tumor effect against temozolomide-resistant glioma in vivo.	temozolomide	152-164	solute carrier family 7 member 3	Rattus norvegicus	69-73
31841318-8	2020	The DNA repair protein MGMT (O6-methylguanine DNA methyltransferase) protects against environmental mutagenesis by DNA methylating agents and, by removing m6G, limits the therapeutic potential of temozolomide in cancer therapy.	temozolomide	196-208	O-6-methylguanine-DNA methyltransferase	Mus musculus	23-27
31841318-8	2020	The DNA repair protein MGMT (O6-methylguanine DNA methyltransferase) protects against environmental mutagenesis by DNA methylating agents and, by removing m6G, limits the therapeutic potential of temozolomide in cancer therapy.	temozolomide	196-208	O-6-methylguanine-DNA methyltransferase	Mus musculus	29-67
32075134-6	2020	Visualization of active MGMT levels reveals discrete active and inactive MGMT populations with biphasic kinetics for MGMT inactivation in response to TMZ-induced DNA damage.	temozolomide	150-153	O-6-methylguanine-DNA methyltransferase	Homo sapiens	24-28
32075134-6	2020	Visualization of active MGMT levels reveals discrete active and inactive MGMT populations with biphasic kinetics for MGMT inactivation in response to TMZ-induced DNA damage.	temozolomide	150-153	O-6-methylguanine-DNA methyltransferase	Homo sapiens	73-77
32075134-6	2020	Visualization of active MGMT levels reveals discrete active and inactive MGMT populations with biphasic kinetics for MGMT inactivation in response to TMZ-induced DNA damage.	temozolomide	150-153	O-6-methylguanine-DNA methyltransferase	Homo sapiens	73-77
32020475-8	2020	In subgroup analyses, patients with MGMT methylation had improved OS after TMZ introduction (pre-TMZ vs. TMZ, 18.5 vs. 28.1 months; P = 0.13), and those without MGMT methylation had significantly increased OS after BEV approval (TMZ vs. TMZ-BEV, 12.2 vs. 16.7 months; P = 0.04).	temozolomide	97-100	O-6-methylguanine-DNA methyltransferase	Homo sapiens	36-40
32020475-8	2020	In subgroup analyses, patients with MGMT methylation had improved OS after TMZ introduction (pre-TMZ vs. TMZ, 18.5 vs. 28.1 months; P = 0.13), and those without MGMT methylation had significantly increased OS after BEV approval (TMZ vs. TMZ-BEV, 12.2 vs. 16.7 months; P = 0.04).	temozolomide	97-100	O-6-methylguanine-DNA methyltransferase	Homo sapiens	36-40
32020475-8	2020	In subgroup analyses, patients with MGMT methylation had improved OS after TMZ introduction (pre-TMZ vs. TMZ, 18.5 vs. 28.1 months; P = 0.13), and those without MGMT methylation had significantly increased OS after BEV approval (TMZ vs. TMZ-BEV, 12.2 vs. 16.7 months; P = 0.04).	temozolomide	75-78	O-6-methylguanine-DNA methyltransferase	Homo sapiens	36-40
32020475-8	2020	In subgroup analyses, patients with MGMT methylation had improved OS after TMZ introduction (pre-TMZ vs. TMZ, 18.5 vs. 28.1 months; P = 0.13), and those without MGMT methylation had significantly increased OS after BEV approval (TMZ vs. TMZ-BEV, 12.2 vs. 16.7 months; P = 0.04).	temozolomide	97-100	O-6-methylguanine-DNA methyltransferase	Homo sapiens	36-40
32020475-8	2020	In subgroup analyses, patients with MGMT methylation had improved OS after TMZ introduction (pre-TMZ vs. TMZ, 18.5 vs. 28.1 months; P = 0.13), and those without MGMT methylation had significantly increased OS after BEV approval (TMZ vs. TMZ-BEV, 12.2 vs. 16.7 months; P = 0.04).	temozolomide	97-100	O-6-methylguanine-DNA methyltransferase	Homo sapiens	36-40
31896509-0	2020	AR ubiquitination induced by the curcumin analog suppresses growth of temozolomide-resistant glioblastoma through disrupting GPX4-Mediated redox homeostasis.	temozolomide	70-82	androgen receptor	Mus musculus	0-2
31653969-12	2020	In glioblastoma, the TRPV2 is part of an interactome-based signature complex, which is negatively associated with survival, and it is expressed in high risk of recurrence and temozolomide-resistant patients.	temozolomide	175-187	transient receptor potential cation channel subfamily V member 2	Homo sapiens	21-26
31896509-0	2020	AR ubiquitination induced by the curcumin analog suppresses growth of temozolomide-resistant glioblastoma through disrupting GPX4-Mediated redox homeostasis.	temozolomide	70-82	glutathione peroxidase 4	Mus musculus	125-129
31896509-12	2020	Taken together, AR potentiates TMZ resistance for glioblastoma, and ALZ003-mediated AR ubiquitination might open a new insight into therapeutic strategy for TMZ resistant glioblastoma.	temozolomide	157-160	androgen receptor	Mus musculus	84-86
31896509-5	2020	In this study, we found that AR expression is significantly correlated with poor prognosis, and AR obviously induced the resistance to temozolomide (TMZ) treatment.	temozolomide	135-147	androgen receptor	Mus musculus	96-98
31896509-5	2020	In this study, we found that AR expression is significantly correlated with poor prognosis, and AR obviously induced the resistance to temozolomide (TMZ) treatment.	temozolomide	149-152	androgen receptor	Mus musculus	96-98
31896509-12	2020	Taken together, AR potentiates TMZ resistance for glioblastoma, and ALZ003-mediated AR ubiquitination might open a new insight into therapeutic strategy for TMZ resistant glioblastoma.	temozolomide	31-34	androgen receptor	Mus musculus	16-18
32003751-9	2020	Moreover, IL-33 prevented temozolomide induced tumor apoptosis.	temozolomide	26-38	interleukin 33	Homo sapiens	10-15
32001707-0	2020	Dual functionalized brain-targeting nanoinhibitors restrain temozolomide-resistant glioma via attenuating EGFR and MET signaling pathways.	temozolomide	60-72	epidermal growth factor receptor	Homo sapiens	106-110
32001707-2	2020	In this study, the crosstalk activation of epidermal growth factor receptor (EGFR) and mesenchymal-epithelial transition factor (MET) signaling pathways is demonstrated to contribute to temozolomide (TMZ) resistance, resulting in an unfavorable prognosis for patients with glioblastoma.	temozolomide	186-198	epidermal growth factor receptor	Homo sapiens	43-75
32001707-2	2020	In this study, the crosstalk activation of epidermal growth factor receptor (EGFR) and mesenchymal-epithelial transition factor (MET) signaling pathways is demonstrated to contribute to temozolomide (TMZ) resistance, resulting in an unfavorable prognosis for patients with glioblastoma.	temozolomide	186-198	epidermal growth factor receptor	Homo sapiens	77-81
32001707-2	2020	In this study, the crosstalk activation of epidermal growth factor receptor (EGFR) and mesenchymal-epithelial transition factor (MET) signaling pathways is demonstrated to contribute to temozolomide (TMZ) resistance, resulting in an unfavorable prognosis for patients with glioblastoma.	temozolomide	200-203	epidermal growth factor receptor	Homo sapiens	43-75
32001707-2	2020	In this study, the crosstalk activation of epidermal growth factor receptor (EGFR) and mesenchymal-epithelial transition factor (MET) signaling pathways is demonstrated to contribute to temozolomide (TMZ) resistance, resulting in an unfavorable prognosis for patients with glioblastoma.	temozolomide	200-203	epidermal growth factor receptor	Homo sapiens	77-81
32003751-0	2020	The Interleukin-33/ST2 axis promotes glioma mesenchymal transition, stemness and TMZ resistance via JNK activation.	temozolomide	81-84	interleukin 33	Homo sapiens	4-18
32003751-10	2020	Anti-ST2 or knockdown IL-33 increased the sensitivity of tumor to temozolomide.	temozolomide	66-78	ST2	Homo sapiens	5-8
32003751-0	2020	The Interleukin-33/ST2 axis promotes glioma mesenchymal transition, stemness and TMZ resistance via JNK activation.	temozolomide	81-84	ST2	Homo sapiens	19-22
32001707-4	2020	In the presence of BIP-MPC-NP, DNA damage repair is attenuated and TMZ sensitivity is enhanced via the down-regulation of E2F1 mediated by TTP in TMZ resistant glioma.	temozolomide	67-70	growth differentiation factor 10	Homo sapiens	19-22
32001707-4	2020	In the presence of BIP-MPC-NP, DNA damage repair is attenuated and TMZ sensitivity is enhanced via the down-regulation of E2F1 mediated by TTP in TMZ resistant glioma.	temozolomide	67-70	E2F transcription factor 1	Homo sapiens	122-126
32001707-4	2020	In the presence of BIP-MPC-NP, DNA damage repair is attenuated and TMZ sensitivity is enhanced via the down-regulation of E2F1 mediated by TTP in TMZ resistant glioma.	temozolomide	146-149	growth differentiation factor 10	Homo sapiens	19-22
32003751-10	2020	Anti-ST2 or knockdown IL-33 increased the sensitivity of tumor to temozolomide.	temozolomide	66-78	interleukin 33	Homo sapiens	22-27
32001707-4	2020	In the presence of BIP-MPC-NP, DNA damage repair is attenuated and TMZ sensitivity is enhanced via the down-regulation of E2F1 mediated by TTP in TMZ resistant glioma.	temozolomide	146-149	E2F transcription factor 1	Homo sapiens	122-126
32039031-5	2019	SF7761 cells with H3F3A gene mutation showed MGMT promoter methylation, lacked MGMT expression, and sensitivity to TMZ treatment.	temozolomide	115-118	H3.3 histone A	Homo sapiens	18-23
32039031-0	2019	MGMT Expression Contributes to Temozolomide Resistance in H3K27M-Mutant Diffuse Midline Gliomas.	temozolomide	31-43	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-4
32039031-7	2019	We confirmed in vitro that MGMT expression contributes to TMZ resistance in DMG cell lines.	temozolomide	58-61	O-6-methylguanine-DNA methyltransferase	Homo sapiens	27-31
31713817-0	2020	LINC00174 down-regulation decreases chemoresistance to temozolomide in human glioma cells by regulating miR-138-5p/SOX9 axis.	temozolomide	55-67	long intergenic non-protein coding RNA 174	Homo sapiens	0-9
31821983-2	2020	Promising, albeit limited, activity and efficacy of temozolomide have been reported in pretreated patients with metastatic colorectal cancer bearing MGMT promoter methylation.	temozolomide	52-64	O-6-methylguanine-DNA methyltransferase	Homo sapiens	149-153
31821983-3	2020	MGMT silencing and proficiency of the mismatch repair system were considered the major predictive biomarkers of sensitivity to temozolomide.	temozolomide	127-139	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-4
31713817-5	2020	Our results demonstrated that the expression level of LINC00174 was higher in glioma tissues, and LINC00174 down-regulation could remarkably prevent cell proliferation and promote cell apoptosis in both glioma cells and TMZ-resistant glioma cells.	temozolomide	220-223	long intergenic non-protein coding RNA 174	Homo sapiens	54-63
31713817-5	2020	Our results demonstrated that the expression level of LINC00174 was higher in glioma tissues, and LINC00174 down-regulation could remarkably prevent cell proliferation and promote cell apoptosis in both glioma cells and TMZ-resistant glioma cells.	temozolomide	220-223	long intergenic non-protein coding RNA 174	Homo sapiens	98-107
31810938-0	2019	Temozolomide-resistant Glioblastoma Depends on HDAC6 Activity Through Regulation of DNA Mismatch Repair.	temozolomide	0-12	histone deacetylase 6	Homo sapiens	47-52
31964274-2	2020	Temozolomide is typically used in glioblastoma treatment; however, the enzymes alkylpurine-DNA-N-glycosylase (APNG) and methylguanine-DNA-methyltransferase (MGMT) efficiently mediate the repair of DNA damage caused by temozolomide, reducing treatment efficacy.	temozolomide	0-12	N-methylpurine DNA glycosylase	Homo sapiens	79-108
31964274-2	2020	Temozolomide is typically used in glioblastoma treatment; however, the enzymes alkylpurine-DNA-N-glycosylase (APNG) and methylguanine-DNA-methyltransferase (MGMT) efficiently mediate the repair of DNA damage caused by temozolomide, reducing treatment efficacy.	temozolomide	0-12	N-methylpurine DNA glycosylase	Homo sapiens	110-114
31964274-2	2020	Temozolomide is typically used in glioblastoma treatment; however, the enzymes alkylpurine-DNA-N-glycosylase (APNG) and methylguanine-DNA-methyltransferase (MGMT) efficiently mediate the repair of DNA damage caused by temozolomide, reducing treatment efficacy.	temozolomide	0-12	O-6-methylguanine-DNA methyltransferase	Homo sapiens	120-155
31964274-2	2020	Temozolomide is typically used in glioblastoma treatment; however, the enzymes alkylpurine-DNA-N-glycosylase (APNG) and methylguanine-DNA-methyltransferase (MGMT) efficiently mediate the repair of DNA damage caused by temozolomide, reducing treatment efficacy.	temozolomide	0-12	O-6-methylguanine-DNA methyltransferase	Homo sapiens	157-161
31964274-2	2020	Temozolomide is typically used in glioblastoma treatment; however, the enzymes alkylpurine-DNA-N-glycosylase (APNG) and methylguanine-DNA-methyltransferase (MGMT) efficiently mediate the repair of DNA damage caused by temozolomide, reducing treatment efficacy.	temozolomide	218-230	N-methylpurine DNA glycosylase	Homo sapiens	79-108
31964274-2	2020	Temozolomide is typically used in glioblastoma treatment; however, the enzymes alkylpurine-DNA-N-glycosylase (APNG) and methylguanine-DNA-methyltransferase (MGMT) efficiently mediate the repair of DNA damage caused by temozolomide, reducing treatment efficacy.	temozolomide	218-230	N-methylpurine DNA glycosylase	Homo sapiens	110-114
31964274-2	2020	Temozolomide is typically used in glioblastoma treatment; however, the enzymes alkylpurine-DNA-N-glycosylase (APNG) and methylguanine-DNA-methyltransferase (MGMT) efficiently mediate the repair of DNA damage caused by temozolomide, reducing treatment efficacy.	temozolomide	218-230	O-6-methylguanine-DNA methyltransferase	Homo sapiens	120-155
31964274-2	2020	Temozolomide is typically used in glioblastoma treatment; however, the enzymes alkylpurine-DNA-N-glycosylase (APNG) and methylguanine-DNA-methyltransferase (MGMT) efficiently mediate the repair of DNA damage caused by temozolomide, reducing treatment efficacy.	temozolomide	218-230	O-6-methylguanine-DNA methyltransferase	Homo sapiens	157-161
31906036-0	2019	Histone 2A Family Member J Drives Mesenchymal Transition and Temozolomide Resistance in Glioblastoma Multiforme.	temozolomide	61-73	H2A.J histone	Homo sapiens	0-26
31906036-3	2019	By using The Cancer Genome Atlas (TCGA) database, we found that the upregulation of histone 2A family member J (H2AFJ), but not other H2AFs, is extensively detected in the therapeutic-insensitive mesenchymal, IDH wildtype, MGMT unmethylated, or non-G-CIMP GBM and is associated with poor TMZ responsiveness independent of radiation.	temozolomide	288-291	H2A.J histone	Homo sapiens	84-110
31906036-3	2019	By using The Cancer Genome Atlas (TCGA) database, we found that the upregulation of histone 2A family member J (H2AFJ), but not other H2AFs, is extensively detected in the therapeutic-insensitive mesenchymal, IDH wildtype, MGMT unmethylated, or non-G-CIMP GBM and is associated with poor TMZ responsiveness independent of radiation.	temozolomide	288-291	H2A.J histone	Homo sapiens	112-117
31906036-5	2019	Whereas H2AFJ knockdown diminished TMZ resistance, H2AFJ overexpression promoted TMZ resistance in a panel of GBM cell lines.	temozolomide	81-84	H2A.J histone	Homo sapiens	51-56
31906036-8	2019	Moreover, we found that therapeutic targeting HADC3 by tacedinaline or NF-kappaB by ML029 is likely able to overcome the TMZ resistance in GBM cells with H2AFJ upregulation.	temozolomide	121-124	nuclear factor kappa B subunit 1	Homo sapiens	71-80
31906036-8	2019	Moreover, we found that therapeutic targeting HADC3 by tacedinaline or NF-kappaB by ML029 is likely able to overcome the TMZ resistance in GBM cells with H2AFJ upregulation.	temozolomide	121-124	H2A.J histone	Homo sapiens	154-159
31906036-9	2019	Significantly, the GBM cohorts harboring a high-level H2AFJ transcript combined with high-level expression of TNF-alpha/NF-kappaB geneset, IL-6/STAT3 geneset or HADC3 were associated with a shorter time to tumor repopulation after initial treatment with TMZ.	temozolomide	254-257	H2A.J histone	Homo sapiens	54-59
31906036-10	2019	These findings not only provide H2AFJ as a biomarker to predict TMZ therapeutic effectiveness but also suggest a new strategy to combat TMZ-insensitive GBM by targeting the interaction network constructed by TNF-alpha/NF-kappaB, IL-6/STAT3, HDAC3, and H2AFJ.	temozolomide	64-67	H2A.J histone	Homo sapiens	32-37
31906036-10	2019	These findings not only provide H2AFJ as a biomarker to predict TMZ therapeutic effectiveness but also suggest a new strategy to combat TMZ-insensitive GBM by targeting the interaction network constructed by TNF-alpha/NF-kappaB, IL-6/STAT3, HDAC3, and H2AFJ.	temozolomide	64-67	tumor necrosis factor	Homo sapiens	208-217
31906036-10	2019	These findings not only provide H2AFJ as a biomarker to predict TMZ therapeutic effectiveness but also suggest a new strategy to combat TMZ-insensitive GBM by targeting the interaction network constructed by TNF-alpha/NF-kappaB, IL-6/STAT3, HDAC3, and H2AFJ.	temozolomide	64-67	interleukin 6	Homo sapiens	229-233
31906036-10	2019	These findings not only provide H2AFJ as a biomarker to predict TMZ therapeutic effectiveness but also suggest a new strategy to combat TMZ-insensitive GBM by targeting the interaction network constructed by TNF-alpha/NF-kappaB, IL-6/STAT3, HDAC3, and H2AFJ.	temozolomide	64-67	signal transducer and activator of transcription 3	Homo sapiens	234-239
31906036-10	2019	These findings not only provide H2AFJ as a biomarker to predict TMZ therapeutic effectiveness but also suggest a new strategy to combat TMZ-insensitive GBM by targeting the interaction network constructed by TNF-alpha/NF-kappaB, IL-6/STAT3, HDAC3, and H2AFJ.	temozolomide	64-67	histone deacetylase 3	Homo sapiens	241-246
31906036-10	2019	These findings not only provide H2AFJ as a biomarker to predict TMZ therapeutic effectiveness but also suggest a new strategy to combat TMZ-insensitive GBM by targeting the interaction network constructed by TNF-alpha/NF-kappaB, IL-6/STAT3, HDAC3, and H2AFJ.	temozolomide	64-67	H2A.J histone	Homo sapiens	252-257
31906036-10	2019	These findings not only provide H2AFJ as a biomarker to predict TMZ therapeutic effectiveness but also suggest a new strategy to combat TMZ-insensitive GBM by targeting the interaction network constructed by TNF-alpha/NF-kappaB, IL-6/STAT3, HDAC3, and H2AFJ.	temozolomide	136-139	tumor necrosis factor	Homo sapiens	208-217
31906036-10	2019	These findings not only provide H2AFJ as a biomarker to predict TMZ therapeutic effectiveness but also suggest a new strategy to combat TMZ-insensitive GBM by targeting the interaction network constructed by TNF-alpha/NF-kappaB, IL-6/STAT3, HDAC3, and H2AFJ.	temozolomide	136-139	interleukin 6	Homo sapiens	229-233
31906036-10	2019	These findings not only provide H2AFJ as a biomarker to predict TMZ therapeutic effectiveness but also suggest a new strategy to combat TMZ-insensitive GBM by targeting the interaction network constructed by TNF-alpha/NF-kappaB, IL-6/STAT3, HDAC3, and H2AFJ.	temozolomide	136-139	signal transducer and activator of transcription 3	Homo sapiens	234-239
31906036-10	2019	These findings not only provide H2AFJ as a biomarker to predict TMZ therapeutic effectiveness but also suggest a new strategy to combat TMZ-insensitive GBM by targeting the interaction network constructed by TNF-alpha/NF-kappaB, IL-6/STAT3, HDAC3, and H2AFJ.	temozolomide	136-139	histone deacetylase 3	Homo sapiens	241-246
31906036-10	2019	These findings not only provide H2AFJ as a biomarker to predict TMZ therapeutic effectiveness but also suggest a new strategy to combat TMZ-insensitive GBM by targeting the interaction network constructed by TNF-alpha/NF-kappaB, IL-6/STAT3, HDAC3, and H2AFJ.	temozolomide	136-139	H2A.J histone	Homo sapiens	252-257
31921673-1	2019	The Pediatric Preclinical Testing Program previously identified the PARP inhibitor talazoparib (TLZ) as a means to potentiate temozolomide (TMZ) activity for the treatment of Ewing sarcoma.	temozolomide	126-138	poly(ADP-ribose) polymerase 1	Homo sapiens	68-72
31921673-1	2019	The Pediatric Preclinical Testing Program previously identified the PARP inhibitor talazoparib (TLZ) as a means to potentiate temozolomide (TMZ) activity for the treatment of Ewing sarcoma.	temozolomide	140-143	poly(ADP-ribose) polymerase 1	Homo sapiens	68-72
31791385-13	2019	CONCLUSIONS: The two novel EZH2i MC4040 and MC4041 impaired primary GBM cell viability, showing even stronger effects in combination with TMZ.	temozolomide	138-141	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	27-31
31889239-10	2020	To our knowledge, ours is the second study (Hoffman et al., J Neurooncol 145: 321-328, 2019) to evaluate the prognostic impact of EGFR CN gain specifically in young adults with IDH-WT GBM and in the era of modern radiation and Temozolomide, but is the first one to compares this impact with a population of adults over 45, and correlates this date with clinical onset, dimension and localization of disease between this groups.	temozolomide	227-239	epidermal growth factor receptor	Homo sapiens	130-134
31810002-0	2020	Inhibition of Casein Kinase II by CX-4945, But Not Yes-associated protein (YAP) by Verteporfin, Enhances the Antitumor Efficacy of Temozolomide in Glioblastoma.	temozolomide	131-143	Yes1 associated transcriptional regulator	Homo sapiens	75-78
31810002-3	2020	O6-methylguanine-DNA-methyltransferase (MGMT) overexpression is associated with TMZ resistance, and low MGMT is a positive response marker for TMZ therapy.	temozolomide	80-83	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-38
31810002-3	2020	O6-methylguanine-DNA-methyltransferase (MGMT) overexpression is associated with TMZ resistance, and low MGMT is a positive response marker for TMZ therapy.	temozolomide	80-83	O-6-methylguanine-DNA methyltransferase	Homo sapiens	40-44
31810002-3	2020	O6-methylguanine-DNA-methyltransferase (MGMT) overexpression is associated with TMZ resistance, and low MGMT is a positive response marker for TMZ therapy.	temozolomide	143-146	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-38
31810002-3	2020	O6-methylguanine-DNA-methyltransferase (MGMT) overexpression is associated with TMZ resistance, and low MGMT is a positive response marker for TMZ therapy.	temozolomide	143-146	O-6-methylguanine-DNA methyltransferase	Homo sapiens	104-108
31810002-5	2020	We found TMZ sensitivity is positively correlated with MGMT expression and multidrug-resistance protein ABC subfamily G member 2 (ABCG2) in these cells.	temozolomide	9-12	O-6-methylguanine-DNA methyltransferase	Homo sapiens	55-59
31810002-5	2020	We found TMZ sensitivity is positively correlated with MGMT expression and multidrug-resistance protein ABC subfamily G member 2 (ABCG2) in these cells.	temozolomide	9-12	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	104-128
31810002-5	2020	We found TMZ sensitivity is positively correlated with MGMT expression and multidrug-resistance protein ABC subfamily G member 2 (ABCG2) in these cells.	temozolomide	9-12	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	130-135
31878276-6	2019	Depletion of CD11b+Ly6G-Ly6C- MDCs in mice bearing ALTS1C1-tk tumors and receiving ganciclovir (GCV) prolonged the mean survival time for mice from 30.7 to 37.8 days, but not the controls, while the effectiveness of temozolomide was enhanced.	temozolomide	216-228	integrin alpha M	Mus musculus	13-18
31878276-6	2019	Depletion of CD11b+Ly6G-Ly6C- MDCs in mice bearing ALTS1C1-tk tumors and receiving ganciclovir (GCV) prolonged the mean survival time for mice from 30.7 to 37.8 days, but not the controls, while the effectiveness of temozolomide was enhanced.	temozolomide	216-228	lymphocyte antigen 6 complex, locus G	Mus musculus	19-23
31878276-6	2019	Depletion of CD11b+Ly6G-Ly6C- MDCs in mice bearing ALTS1C1-tk tumors and receiving ganciclovir (GCV) prolonged the mean survival time for mice from 30.7 to 37.8 days, but not the controls, while the effectiveness of temozolomide was enhanced.	temozolomide	216-228	lymphocyte antigen 6 complex, locus C1	Mus musculus	24-28
31810938-6	2019	RESULTS: We showed that HDAC6-selecitve inhibitors block activation of the EGFR and p53 pathways in TMZ-resistant GBM cells.	temozolomide	100-103	histone deacetylase 6	Homo sapiens	24-29
31810938-6	2019	RESULTS: We showed that HDAC6-selecitve inhibitors block activation of the EGFR and p53 pathways in TMZ-resistant GBM cells.	temozolomide	100-103	epidermal growth factor receptor	Homo sapiens	75-79
31810938-6	2019	RESULTS: We showed that HDAC6-selecitve inhibitors block activation of the EGFR and p53 pathways in TMZ-resistant GBM cells.	temozolomide	100-103	tumor protein p53	Homo sapiens	84-87
31810938-7	2019	Importantly, the inhibition of HDAC6 correlates with increased levels of MSH2 and MSH6, key DNA mismatch repair proteins, in TMZ-resistant GBM cells.	temozolomide	125-128	histone deacetylase 6	Homo sapiens	31-36
31810938-7	2019	Importantly, the inhibition of HDAC6 correlates with increased levels of MSH2 and MSH6, key DNA mismatch repair proteins, in TMZ-resistant GBM cells.	temozolomide	125-128	mutS homolog 2	Homo sapiens	73-77
31810938-7	2019	Importantly, the inhibition of HDAC6 correlates with increased levels of MSH2 and MSH6, key DNA mismatch repair proteins, in TMZ-resistant GBM cells.	temozolomide	125-128	mutS homolog 6	Homo sapiens	82-86
31810938-8	2019	In addition to the MSH, HDAC6 inhibitors decrease MGMT expression in TMZ-resistant GBM cells.	temozolomide	69-72	msh homeobox 2	Homo sapiens	19-22
31810938-8	2019	In addition to the MSH, HDAC6 inhibitors decrease MGMT expression in TMZ-resistant GBM cells.	temozolomide	69-72	histone deacetylase 6	Homo sapiens	24-29
31810938-8	2019	In addition to the MSH, HDAC6 inhibitors decrease MGMT expression in TMZ-resistant GBM cells.	temozolomide	69-72	O-6-methylguanine-DNA methyltransferase	Homo sapiens	50-54
31810938-9	2019	Furthermore, HDAC6 inhibitors increase TMZ sensitivity and efficiently induce apoptosis in TMZ-resistant GBM cells.	temozolomide	39-42	histone deacetylase 6	Homo sapiens	13-18
31810938-9	2019	Furthermore, HDAC6 inhibitors increase TMZ sensitivity and efficiently induce apoptosis in TMZ-resistant GBM cells.	temozolomide	91-94	histone deacetylase 6	Homo sapiens	13-18
31810938-10	2019	CONCLUSION: Selective inhibition of HDAC6 may be a promising strategy for the treatment of TMZ-resistant GBM.	temozolomide	91-94	histone deacetylase 6	Homo sapiens	36-41
31770107-1	2019	OBJECTIVE: This study was conducted to elucidate the long non-coding RNA FOXD2-AS1 (lncRNA FOXD2-AS1) expression in glioma and its mechanism on the biological features of glioma cells and the drug resistance of temozolomide (TMZ).	temozolomide	211-223	forkhead box D2	Mus musculus	73-78
31725331-0	2019	SNAP reverses temozolomide resistance in human glioblastoma multiforme cells through down-regulation of MGMT.	temozolomide	14-26	O-6-methylguanine-DNA methyltransferase	Homo sapiens	104-108
31725331-3	2019	Down-regulation of O-6-methylguanine-DNA methyltransferase (MGMT) expression in GBM cells is an attractive strategy for overcoming TMZ resistance and improving outcomes.	temozolomide	131-134	O-6-methylguanine-DNA methyltransferase	Homo sapiens	19-58
31725331-3	2019	Down-regulation of O-6-methylguanine-DNA methyltransferase (MGMT) expression in GBM cells is an attractive strategy for overcoming TMZ resistance and improving outcomes.	temozolomide	131-134	O-6-methylguanine-DNA methyltransferase	Homo sapiens	60-64
31725331-6	2019	SNAP acted principally through post-translational modification of p53, phosphorylated N-myc downstream regulated gene 1, and MGMT protein stability in TMZ-R GBM cells.	temozolomide	151-154	O-6-methylguanine-DNA methyltransferase	Homo sapiens	125-129
31725331-9	2019	SNAP reverses temozolomide resistance in human glioblastoma multiforme cells through down-regulation of MGMT.	temozolomide	14-26	O-6-methylguanine-DNA methyltransferase	Homo sapiens	104-108
31783653-0	2019	On the Critical Issues in Temozolomide Research in Glioblastoma: Clinically Relevant Concentrations and MGMT-independent Resistance.	temozolomide	26-38	O-6-methylguanine-DNA methyltransferase	Homo sapiens	104-108
31783653-8	2019	However, the clinically relevant concentrations of TMZ are sufficient to radiosensitize both MGMT-positive and -negative cell lines in vitro.	temozolomide	51-54	O-6-methylguanine-DNA methyltransferase	Homo sapiens	93-97
31783653-9	2019	It is speculated that a single DNA repair protein, MGMT, is highly efficient in protecting cells against TMZ toxicity.	temozolomide	105-108	O-6-methylguanine-DNA methyltransferase	Homo sapiens	51-55
31783653-10	2019	However, an endogenous level of MGMT protein expression is not universally correlated with TMZ responsiveness, and MGMT-independent mechanisms of TMZ resistance exist.	temozolomide	146-149	O-6-methylguanine-DNA methyltransferase	Homo sapiens	115-119
31639772-11	2019	Temozolomide therapy was well tolerated and most toxicities were limited to grade G1-2 according to WHO criteria.	temozolomide	0-12	proline rich protein BstNI subfamily 3	Homo sapiens	82-86
31721137-0	2019	Is MGMT the best marker to predict response of temozolomide in aggressive pituitary tumors?	temozolomide	47-59	O-6-methylguanine-DNA methyltransferase	Homo sapiens	3-7
31807171-8	2019	The stimulation of glioma cells by IGF1 in vitro was found to decreased the viability of the cells following treatment with temozolomide (TMZ).	temozolomide	124-136	insulin like growth factor 1	Homo sapiens	35-39
31807171-8	2019	The stimulation of glioma cells by IGF1 in vitro was found to decreased the viability of the cells following treatment with temozolomide (TMZ).	temozolomide	138-141	insulin like growth factor 1	Homo sapiens	35-39
31807171-9	2019	In addition, the expression level of IGF1R was increased in glioma cells treated with TMZ.	temozolomide	86-89	insulin like growth factor 1 receptor	Homo sapiens	37-42
31571099-2	2019	Administration of TMZ results in clinical response and improvement in survival of many of these patients depending upon the expression of the DNA repair enzyme O-6 methylguanine DNA transferase (MGMT).	temozolomide	18-21	O-6-methylguanine-DNA methyltransferase	Homo sapiens	195-199
31571099-3	2019	Low or negative MGMT immunoreactivity predicts responsiveness to TMZ therapy.	temozolomide	65-68	O-6-methylguanine-DNA methyltransferase	Homo sapiens	16-20
31571099-8	2019	CONCLUSIONS: These findings could explain lack of response to TMZ treatment in patients with false negative MGMT immunohistochemistry.	temozolomide	62-65	O-6-methylguanine-DNA methyltransferase	Homo sapiens	108-112
31571099-9	2019	Evaluation of tumor samples for MGMT expression should carefully be carried-out using the optimum immunohistochemical protocol to obtain consistent and reliable results that help to identify patients that could respond to TMZ therapy.	temozolomide	222-225	O-6-methylguanine-DNA methyltransferase	Homo sapiens	32-36
31770107-1	2019	OBJECTIVE: This study was conducted to elucidate the long non-coding RNA FOXD2-AS1 (lncRNA FOXD2-AS1) expression in glioma and its mechanism on the biological features of glioma cells and the drug resistance of temozolomide (TMZ).	temozolomide	211-223	arylsulfatase B	Mus musculus	79-82
31770107-1	2019	OBJECTIVE: This study was conducted to elucidate the long non-coding RNA FOXD2-AS1 (lncRNA FOXD2-AS1) expression in glioma and its mechanism on the biological features of glioma cells and the drug resistance of temozolomide (TMZ).	temozolomide	211-223	forkhead box D2	Mus musculus	73-82
31770107-1	2019	OBJECTIVE: This study was conducted to elucidate the long non-coding RNA FOXD2-AS1 (lncRNA FOXD2-AS1) expression in glioma and its mechanism on the biological features of glioma cells and the drug resistance of temozolomide (TMZ).	temozolomide	225-228	forkhead box D2	Mus musculus	73-78
31770107-1	2019	OBJECTIVE: This study was conducted to elucidate the long non-coding RNA FOXD2-AS1 (lncRNA FOXD2-AS1) expression in glioma and its mechanism on the biological features of glioma cells and the drug resistance of temozolomide (TMZ).	temozolomide	225-228	arylsulfatase B	Mus musculus	79-82
31770107-1	2019	OBJECTIVE: This study was conducted to elucidate the long non-coding RNA FOXD2-AS1 (lncRNA FOXD2-AS1) expression in glioma and its mechanism on the biological features of glioma cells and the drug resistance of temozolomide (TMZ).	temozolomide	225-228	forkhead box D2	Mus musculus	73-82
31771235-1	2019	Recently, we found that temozolomide (TMZ) can upregulate the expression of the multidrug-resistance protein ABCC3 in NK cells from both glioma-bearing mice and glioblastoma patients treated with dendritic cell immunotherapy combined with TMZ, allowing NK cells to escape apoptosis and favoring their role as antitumor effector cells.	temozolomide	24-36	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	109-114
31771235-1	2019	Recently, we found that temozolomide (TMZ) can upregulate the expression of the multidrug-resistance protein ABCC3 in NK cells from both glioma-bearing mice and glioblastoma patients treated with dendritic cell immunotherapy combined with TMZ, allowing NK cells to escape apoptosis and favoring their role as antitumor effector cells.	temozolomide	38-41	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	109-114
31771235-1	2019	Recently, we found that temozolomide (TMZ) can upregulate the expression of the multidrug-resistance protein ABCC3 in NK cells from both glioma-bearing mice and glioblastoma patients treated with dendritic cell immunotherapy combined with TMZ, allowing NK cells to escape apoptosis and favoring their role as antitumor effector cells.	temozolomide	239-242	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	109-114
31819508-0	2019	Induction Of XLF And 53BP1 Expression Is Associated With Temozolomide Resistance In Glioblastoma Cells.	temozolomide	57-69	tumor protein p53 binding protein 1	Homo sapiens	21-26
31771235-4	2019	Notably, not only basal but also TMZ-induced ABCC3 expression was related to a strong, long-term NK cell response and a better prognosis of patients.	temozolomide	33-36	ATP binding cassette subfamily C member 3	Homo sapiens	45-50
31819508-7	2019	The TMZ-induced apoptosis was detected by the Caspase 3/7 activity kit.	temozolomide	4-7	caspase 3	Homo sapiens	46-55
31819508-12	2019	Canonical NHEJ key factors, XLF and 53BP1, are upregulated in TMZ-resistant GBM cells.	temozolomide	62-65	tumor protein p53 binding protein 1	Homo sapiens	36-41
31771235-6	2019	ABCC3 expression in patients carrying DelC compared to patients with reference haplotype was higher and modulated by TMZ.	temozolomide	117-120	ATP binding cassette subfamily C member 3	Homo sapiens	0-5
31819508-13	2019	Depletion of XLF or 53BP1 in TMZ-resistant cells significantly improve the potency of TMZ against GBM cell growth.	temozolomide	29-32	tumor protein p53 binding protein 1	Homo sapiens	20-25
31819508-13	2019	Depletion of XLF or 53BP1 in TMZ-resistant cells significantly improve the potency of TMZ against GBM cell growth.	temozolomide	86-89	tumor protein p53 binding protein 1	Homo sapiens	20-25
31771235-7	2019	The transcription factor NRF2, involved in ABCC3 induction, was phosphorylated in CD56dim CD16+ NK cells expressing ABCC3 under TMZ treatment.	temozolomide	128-131	NFE2 like bZIP transcription factor 2	Homo sapiens	25-29
31771235-7	2019	The transcription factor NRF2, involved in ABCC3 induction, was phosphorylated in CD56dim CD16+ NK cells expressing ABCC3 under TMZ treatment.	temozolomide	128-131	ATP binding cassette subfamily C member 3	Homo sapiens	43-48
31771235-7	2019	The transcription factor NRF2, involved in ABCC3 induction, was phosphorylated in CD56dim CD16+ NK cells expressing ABCC3 under TMZ treatment.	temozolomide	128-131	neural cell adhesion molecule 1	Homo sapiens	82-86
31771235-7	2019	The transcription factor NRF2, involved in ABCC3 induction, was phosphorylated in CD56dim CD16+ NK cells expressing ABCC3 under TMZ treatment.	temozolomide	128-131	Fc gamma receptor IIIa	Homo sapiens	90-94
31771235-7	2019	The transcription factor NRF2, involved in ABCC3 induction, was phosphorylated in CD56dim CD16+ NK cells expressing ABCC3 under TMZ treatment.	temozolomide	128-131	ATP binding cassette subfamily C member 3	Homo sapiens	116-121
31798454-0	2019	Corrigendum: SCD1 Confers Temozolomide Resistance to Human Glioma Cells Via the Akt/GSK3beta/beta-Catenin Signaling Axis.	temozolomide	26-38	stearoyl-CoA desaturase	Homo sapiens	13-17
31542479-0	2019	DHFR/TYMS are positive regulators of glioma cell growth and modulate chemo-sensitivity to temozolomide.	temozolomide	90-102	dihydrofolate reductase	Homo sapiens	0-4
31542479-0	2019	DHFR/TYMS are positive regulators of glioma cell growth and modulate chemo-sensitivity to temozolomide.	temozolomide	90-102	thymidylate synthetase	Homo sapiens	5-9
31542479-5	2019	Notably, inhibition of DHFR/TYMS by pemetrexed exhibited synergistic anti-glioma activity with TMZ in both cell lines and U251 xenografts, which suggested potential combined chemotherapy for glioma.	temozolomide	95-98	dihydrofolate reductase	Homo sapiens	23-27
31542479-6	2019	Mechanistically, the synergistic effect of inhibition of DHFR/TYMS with TMZ was due to activated AMPK and subsequently suppressed mTOR signaling pathway.	temozolomide	72-75	dihydrofolate reductase	Homo sapiens	57-61
31542479-6	2019	Mechanistically, the synergistic effect of inhibition of DHFR/TYMS with TMZ was due to activated AMPK and subsequently suppressed mTOR signaling pathway.	temozolomide	72-75	thymidylate synthetase	Homo sapiens	62-66
31542479-7	2019	Taken together, these findings identify an uncharacterized role of DHFR/TYMS in glioma growth and TMZ sensitivity mediated by AMPK-mTOR signal pathway, and provide a prospective approach for improving the anti-tumor activity of TMZ in glioma.	temozolomide	98-101	dihydrofolate reductase	Homo sapiens	67-71
31542479-7	2019	Taken together, these findings identify an uncharacterized role of DHFR/TYMS in glioma growth and TMZ sensitivity mediated by AMPK-mTOR signal pathway, and provide a prospective approach for improving the anti-tumor activity of TMZ in glioma.	temozolomide	98-101	thymidylate synthetase	Homo sapiens	72-76
31542479-7	2019	Taken together, these findings identify an uncharacterized role of DHFR/TYMS in glioma growth and TMZ sensitivity mediated by AMPK-mTOR signal pathway, and provide a prospective approach for improving the anti-tumor activity of TMZ in glioma.	temozolomide	228-231	dihydrofolate reductase	Homo sapiens	67-71
31542479-7	2019	Taken together, these findings identify an uncharacterized role of DHFR/TYMS in glioma growth and TMZ sensitivity mediated by AMPK-mTOR signal pathway, and provide a prospective approach for improving the anti-tumor activity of TMZ in glioma.	temozolomide	228-231	thymidylate synthetase	Homo sapiens	72-76
31798454-0	2019	Corrigendum: SCD1 Confers Temozolomide Resistance to Human Glioma Cells Via the Akt/GSK3beta/beta-Catenin Signaling Axis.	temozolomide	26-38	AKT serine/threonine kinase 1	Homo sapiens	80-83
31798454-0	2019	Corrigendum: SCD1 Confers Temozolomide Resistance to Human Glioma Cells Via the Akt/GSK3beta/beta-Catenin Signaling Axis.	temozolomide	26-38	glycogen synthase kinase 3 beta	Homo sapiens	84-92
31798454-0	2019	Corrigendum: SCD1 Confers Temozolomide Resistance to Human Glioma Cells Via the Akt/GSK3beta/beta-Catenin Signaling Axis.	temozolomide	26-38	catenin beta 1	Homo sapiens	93-105
31814867-9	2019	Additionally, a combination assay of PP7 with temozolomide (TMZ), the most used chemotherapy for glioma patients, was performed resulting in synergism, while PP7 reduced TMZ resistance through inhibition of MGMT expression.	temozolomide	60-63	protein phosphatase with EF-hand domain 1	Homo sapiens	37-40
31814867-9	2019	Additionally, a combination assay of PP7 with temozolomide (TMZ), the most used chemotherapy for glioma patients, was performed resulting in synergism, while PP7 reduced TMZ resistance through inhibition of MGMT expression.	temozolomide	170-173	protein phosphatase with EF-hand domain 1	Homo sapiens	158-161
31814867-9	2019	Additionally, a combination assay of PP7 with temozolomide (TMZ), the most used chemotherapy for glioma patients, was performed resulting in synergism, while PP7 reduced TMZ resistance through inhibition of MGMT expression.	temozolomide	170-173	O-6-methylguanine-DNA methyltransferase	Homo sapiens	207-211
31717924-0	2019	ANGPTL4 Induces TMZ Resistance of Glioblastoma by Promoting Cancer Stemness Enrichment via the EGFR/AKT/4E-BP1 Cascade.	temozolomide	16-19	angiopoietin like 4	Homo sapiens	0-7
31717973-5	2019	In experimental settings, high doses of the agent are often used, which are likely to activate responses triggered by base N-alkylations instead of O6-methylguanine (O6MeG), which is the primary cytotoxic lesion induced by low doses of temozolomide and other methylating drugs in O6-methylguanine-DNA methyltransferase (MGMT) repair incompetent cells.	temozolomide	236-248	O-6-methylguanine-DNA methyltransferase	Homo sapiens	280-318
31717973-5	2019	In experimental settings, high doses of the agent are often used, which are likely to activate responses triggered by base N-alkylations instead of O6-methylguanine (O6MeG), which is the primary cytotoxic lesion induced by low doses of temozolomide and other methylating drugs in O6-methylguanine-DNA methyltransferase (MGMT) repair incompetent cells.	temozolomide	236-248	O-6-methylguanine-DNA methyltransferase	Homo sapiens	320-324
31717973-7	2019	MGMT, repairing the lesion through methyl group transfer, is a key node in protecting cells against all these effects and has a significant impact on patient"s survival following temozolomide therapy, supporting the notion that findings obtained on a molecular and cellular level can be translated to the therapeutic setting in vivo.	temozolomide	179-191	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-4
31717924-0	2019	ANGPTL4 Induces TMZ Resistance of Glioblastoma by Promoting Cancer Stemness Enrichment via the EGFR/AKT/4E-BP1 Cascade.	temozolomide	16-19	epidermal growth factor receptor	Homo sapiens	95-99
31717924-0	2019	ANGPTL4 Induces TMZ Resistance of Glioblastoma by Promoting Cancer Stemness Enrichment via the EGFR/AKT/4E-BP1 Cascade.	temozolomide	16-19	AKT serine/threonine kinase 1	Homo sapiens	100-103
31717924-0	2019	ANGPTL4 Induces TMZ Resistance of Glioblastoma by Promoting Cancer Stemness Enrichment via the EGFR/AKT/4E-BP1 Cascade.	temozolomide	16-19	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	104-110
31717924-6	2019	The overexpression of ANGPTL4 induced GSC enrichment that was characterized by polycomb complex protein BMI-1 and SRY (sex determining region Y)-box 2 (SOX2) expression, resulting in TMZ resistance in GBM.	temozolomide	183-186	angiopoietin like 4	Homo sapiens	22-29
31717924-6	2019	The overexpression of ANGPTL4 induced GSC enrichment that was characterized by polycomb complex protein BMI-1 and SRY (sex determining region Y)-box 2 (SOX2) expression, resulting in TMZ resistance in GBM.	temozolomide	183-186	SRY-box transcription factor 2	Homo sapiens	152-156
31680769-0	2019	FoxD2-AS1 is a prognostic factor in glioma and promotes temozolomide resistance in a O6-methylguanine-DNA methyltransferase-dependent manner.	temozolomide	56-68	FOXD2 adjacent opposite strand RNA 1	Homo sapiens	0-9
31708690-7	2019	Then, we found that overexpression of p62 promoted glioma progression by promoting proliferation, migration, glycolysis, temozolomide (TMZ) resistance and nuclear factor kappaB (NF-kappaB) signalling pathway, and repressing autophagic flux and reactive oxygen species (ROS) in vitro.	temozolomide	121-133	nucleoporin 62	Homo sapiens	38-41
31708690-7	2019	Then, we found that overexpression of p62 promoted glioma progression by promoting proliferation, migration, glycolysis, temozolomide (TMZ) resistance and nuclear factor kappaB (NF-kappaB) signalling pathway, and repressing autophagic flux and reactive oxygen species (ROS) in vitro.	temozolomide	135-138	nucleoporin 62	Homo sapiens	38-41
31586022-1	2019	OBJECTIVE: To determine the efficacy of the thrombopoietin receptor agonist romiplostim for the prevention of temozolomide-induced thrombocytopenia in newly diagnosed glioblastoma.	temozolomide	110-122	MPL proto-oncogene, thrombopoietin receptor	Homo sapiens	44-67
31586022-10	2019	CONCLUSION: The thrombopoietin receptor agonist romiplostim improves exposure to chemotherapy in patients with glioblastoma experiencing temozolomide-induced thrombocytopenia.	temozolomide	137-149	MPL proto-oncogene, thrombopoietin receptor	Homo sapiens	16-39
31815044-0	2019	BRCA1 identified as a modulator of temozolomide resistance in P53 wild-type GBM using a high-throughput shRNA-based synthetic lethality screening.	temozolomide	35-47	BRCA1 DNA repair associated	Homo sapiens	0-5
31815044-0	2019	BRCA1 identified as a modulator of temozolomide resistance in P53 wild-type GBM using a high-throughput shRNA-based synthetic lethality screening.	temozolomide	35-47	tumor protein p53	Homo sapiens	62-65
31815044-5	2019	Using an unbiased bioinformatical analysis, we identified BRCA1 as a potential promising candidate gene that induced synthetic lethality with TMZ in glioma sphere-forming cells (GSCs).	temozolomide	142-145	BRCA1 DNA repair associated	Homo sapiens	58-63
31815044-6	2019	BRCA1 knockdown resulted in antitumor activity with TMZ in P53 wild-type GSCs but not in P53 mutant GSCs.	temozolomide	52-55	BRCA1 DNA repair associated	Homo sapiens	0-5
31815044-6	2019	BRCA1 knockdown resulted in antitumor activity with TMZ in P53 wild-type GSCs but not in P53 mutant GSCs.	temozolomide	52-55	tumor protein p53	Homo sapiens	59-62
31815044-7	2019	TMZ treatment induced a DNA damage repair response; the activation of BRCA1 DNA repair pathway targets and knockdown of BRCA1, together with TMZ, led to increased DNA damage and cell death in P53 wild-type GSCs.	temozolomide	0-3	BRCA1 DNA repair associated	Homo sapiens	70-75
31815044-7	2019	TMZ treatment induced a DNA damage repair response; the activation of BRCA1 DNA repair pathway targets and knockdown of BRCA1, together with TMZ, led to increased DNA damage and cell death in P53 wild-type GSCs.	temozolomide	0-3	BRCA1 DNA repair associated	Homo sapiens	120-125
31815044-7	2019	TMZ treatment induced a DNA damage repair response; the activation of BRCA1 DNA repair pathway targets and knockdown of BRCA1, together with TMZ, led to increased DNA damage and cell death in P53 wild-type GSCs.	temozolomide	0-3	tumor protein p53	Homo sapiens	192-195
31815044-7	2019	TMZ treatment induced a DNA damage repair response; the activation of BRCA1 DNA repair pathway targets and knockdown of BRCA1, together with TMZ, led to increased DNA damage and cell death in P53 wild-type GSCs.	temozolomide	141-144	tumor protein p53	Homo sapiens	192-195
31815044-8	2019	Our study identified BRCA1 as a potential target that sensitizes TMZ-induced cell death in P53 wild-type GBM, suggesting that the combined inhibition of BRCA1 and TMZ treatment will be a successful targeted therapy for GBM patients.	temozolomide	65-68	BRCA1 DNA repair associated	Homo sapiens	21-26
31815044-8	2019	Our study identified BRCA1 as a potential target that sensitizes TMZ-induced cell death in P53 wild-type GBM, suggesting that the combined inhibition of BRCA1 and TMZ treatment will be a successful targeted therapy for GBM patients.	temozolomide	65-68	tumor protein p53	Homo sapiens	91-94
31815044-8	2019	Our study identified BRCA1 as a potential target that sensitizes TMZ-induced cell death in P53 wild-type GBM, suggesting that the combined inhibition of BRCA1 and TMZ treatment will be a successful targeted therapy for GBM patients.	temozolomide	65-68	BRCA1 DNA repair associated	Homo sapiens	153-158
31815044-8	2019	Our study identified BRCA1 as a potential target that sensitizes TMZ-induced cell death in P53 wild-type GBM, suggesting that the combined inhibition of BRCA1 and TMZ treatment will be a successful targeted therapy for GBM patients.	temozolomide	163-166	BRCA1 DNA repair associated	Homo sapiens	21-26
31815044-8	2019	Our study identified BRCA1 as a potential target that sensitizes TMZ-induced cell death in P53 wild-type GBM, suggesting that the combined inhibition of BRCA1 and TMZ treatment will be a successful targeted therapy for GBM patients.	temozolomide	163-166	tumor protein p53	Homo sapiens	91-94
31614149-0	2019	Nuclear factor I A promotes temozolomide resistance in glioblastoma via activation of nuclear factor kappaB pathway.	temozolomide	28-40	nuclear factor I A	Homo sapiens	0-18
31614149-2	2019	MAIN METHODS: A genome-wide hierarchical bi-clustering based on previously published microarray databases identified Nuclear Factor I A (NFIA) as one of the most significantly upregulated genes correlated to TMZ resistance in GBM.	temozolomide	208-211	nuclear factor I A	Homo sapiens	117-135
31614149-2	2019	MAIN METHODS: A genome-wide hierarchical bi-clustering based on previously published microarray databases identified Nuclear Factor I A (NFIA) as one of the most significantly upregulated genes correlated to TMZ resistance in GBM.	temozolomide	208-211	nuclear factor I A	Homo sapiens	137-141
31614149-3	2019	Then, the potential biological functions of NFIA in oncogenesis and chemoresistance were clarified by qRT-PCR, Western blotting and in vivo xenograft models with artificially induced TMZ-resistant U87 cells.	temozolomide	183-186	nuclear factor I A	Homo sapiens	44-48
31614149-6	2019	KEY FINDINGS: NFIA was correlated with TMZ resistance in GBM.	temozolomide	39-42	nuclear factor I A	Homo sapiens	14-18
31680769-0	2019	FoxD2-AS1 is a prognostic factor in glioma and promotes temozolomide resistance in a O6-methylguanine-DNA methyltransferase-dependent manner.	temozolomide	56-68	O-6-methylguanine-DNA methyltransferase	Homo sapiens	85-123
31614149-8	2019	Moreover, NFIA contributed to the acquired TMZ resistance of GBM cells, while suppression of NFIA via lentivirus reduced cell proliferation, tumorigenesis and resistance to TMZ of GBM.	temozolomide	173-176	nuclear factor I A	Homo sapiens	93-97
31680769-3	2019	Overexpression of long-noncoding RNA (LncRNA) FoxD2 adjacent opposite strand RNA 1 (FoxD2-AS1) was identified to promote glioma development, but the role in TMZ resistance remains unclear.	temozolomide	157-160	forkhead box D2	Homo sapiens	46-51
31614149-10	2019	Last, NFIA induced phosphorylation of NF-kB p65 at serine 536, thus inducing TMZ resistance in GBM cells.	temozolomide	77-80	nuclear factor I A	Homo sapiens	6-10
31680769-3	2019	Overexpression of long-noncoding RNA (LncRNA) FoxD2 adjacent opposite strand RNA 1 (FoxD2-AS1) was identified to promote glioma development, but the role in TMZ resistance remains unclear.	temozolomide	157-160	FOXD2 adjacent opposite strand RNA 1	Homo sapiens	84-93
31614149-10	2019	Last, NFIA induced phosphorylation of NF-kB p65 at serine 536, thus inducing TMZ resistance in GBM cells.	temozolomide	77-80	RELA proto-oncogene, NF-kB subunit	Homo sapiens	44-47
31614149-11	2019	Altogether, our study suggests that NFIA-dependent transcriptional regulation of NF-kB contributes to acquired TMZ resistance in GBM.	temozolomide	111-114	nuclear factor I A	Homo sapiens	36-40
31680769-6	2019	Knockdown of FoxD2-AS1 decreased the proliferation, metastatic ability of glioma cells and promote the sensitivity to TMZ in glioma cells.	temozolomide	118-121	FOXD2 adjacent opposite strand RNA 1	Homo sapiens	13-22
31614149-12	2019	SIGNIFICANCE: Abnormally activated NFIA-NF-kB signaling was strongly correlated with acquired TMZ resistance and poor prognosis in GBM, and it could be a new therapeutic target for TMZ-resistant GBM.	temozolomide	94-97	nuclear factor I A	Homo sapiens	35-39
31614149-12	2019	SIGNIFICANCE: Abnormally activated NFIA-NF-kB signaling was strongly correlated with acquired TMZ resistance and poor prognosis in GBM, and it could be a new therapeutic target for TMZ-resistant GBM.	temozolomide	181-184	nuclear factor I A	Homo sapiens	35-39
31680769-8	2019	Our data suggested that FoxD2-AS1 is a clinical relevance LncRNA and mediates TMZ resistance by regulating the methylation status of the MGMT promoter region.	temozolomide	78-81	forkhead box D2	Homo sapiens	24-29
31680769-8	2019	Our data suggested that FoxD2-AS1 is a clinical relevance LncRNA and mediates TMZ resistance by regulating the methylation status of the MGMT promoter region.	temozolomide	78-81	prostaglandin D2 receptor	Homo sapiens	30-33
31680769-8	2019	Our data suggested that FoxD2-AS1 is a clinical relevance LncRNA and mediates TMZ resistance by regulating the methylation status of the MGMT promoter region.	temozolomide	78-81	O-6-methylguanine-DNA methyltransferase	Homo sapiens	137-141
31563286-0	2019	Targeting Aurora kinase B attenuates chemoresistance in glioblastoma via a synergistic manner with temozolomide.	temozolomide	99-111	aurora kinase B	Homo sapiens	10-25
31563286-3	2019	In this study, we investigate the underlying mechanism by which glioblastoma (GBM) cells acquire resistance to Temozolomide (TMZ) through Aurora kinase B (AURKB) thus to identify novel therapeutic targets and prognostic biomarkers for GBM.	temozolomide	111-123	aurora kinase B	Homo sapiens	138-153
31563286-3	2019	In this study, we investigate the underlying mechanism by which glioblastoma (GBM) cells acquire resistance to Temozolomide (TMZ) through Aurora kinase B (AURKB) thus to identify novel therapeutic targets and prognostic biomarkers for GBM.	temozolomide	111-123	aurora kinase B	Homo sapiens	155-160
31563286-3	2019	In this study, we investigate the underlying mechanism by which glioblastoma (GBM) cells acquire resistance to Temozolomide (TMZ) through Aurora kinase B (AURKB) thus to identify novel therapeutic targets and prognostic biomarkers for GBM.	temozolomide	125-128	aurora kinase B	Homo sapiens	138-153
31563286-3	2019	In this study, we investigate the underlying mechanism by which glioblastoma (GBM) cells acquire resistance to Temozolomide (TMZ) through Aurora kinase B (AURKB) thus to identify novel therapeutic targets and prognostic biomarkers for GBM.	temozolomide	125-128	aurora kinase B	Homo sapiens	155-160
31563286-8	2019	RESULTS: AURKB was among the most significantly up-regulated kinase-coding genes in TMZ resistant GBM cells according to database GSE68029, moreover, an increased expression of AURKB was closely associated with poor prognosis in glioma and GBM patients.	temozolomide	84-87	aurora kinase B	Homo sapiens	9-14
31563286-8	2019	RESULTS: AURKB was among the most significantly up-regulated kinase-coding genes in TMZ resistant GBM cells according to database GSE68029, moreover, an increased expression of AURKB was closely associated with poor prognosis in glioma and GBM patients.	temozolomide	84-87	aurora kinase B	Homo sapiens	177-182
31563286-9	2019	AURKB knock-down resensitized U87 resistant cells to TMZ both in vitro and in vivo.	temozolomide	53-56	aurora kinase B	Homo sapiens	0-5
31563286-10	2019	Additionally, the combination of TMZ and Hesperadin, a specific AURKB inhibitor, significantly suppressed the proliferation of TMZ resistant GBM cells thus dramatically prolonged the survival of xenograft mice viaa synergistic effect with TMZ.	temozolomide	33-36	aurora kinase B	Mus musculus	64-69
31563286-10	2019	Additionally, the combination of TMZ and Hesperadin, a specific AURKB inhibitor, significantly suppressed the proliferation of TMZ resistant GBM cells thus dramatically prolonged the survival of xenograft mice viaa synergistic effect with TMZ.	temozolomide	127-130	aurora kinase B	Mus musculus	64-69
31563286-10	2019	Additionally, the combination of TMZ and Hesperadin, a specific AURKB inhibitor, significantly suppressed the proliferation of TMZ resistant GBM cells thus dramatically prolonged the survival of xenograft mice viaa synergistic effect with TMZ.	temozolomide	127-130	aurora kinase B	Mus musculus	64-69
31563286-11	2019	CONCLUSION: Elevated AURKB expression was strongly correlated to TMZ resistant acquisition and poor prognosis, furthermore, targeting AURKB would be a potential therapeutic target for GBM patients.	temozolomide	65-68	aurora kinase B	Homo sapiens	21-26
31563286-11	2019	CONCLUSION: Elevated AURKB expression was strongly correlated to TMZ resistant acquisition and poor prognosis, furthermore, targeting AURKB would be a potential therapeutic target for GBM patients.	temozolomide	65-68	aurora kinase B	Homo sapiens	134-139
31629402-0	2019	Enrichment of superoxide dismutase 2 in glioblastoma confers to acquisition of temozolomide resistance that is associated with tumor-initiating cell subsets.	temozolomide	79-91	superoxide dismutase 2	Homo sapiens	14-36
31601097-7	2019	Besides, tFNA-TMZ was able to attenuate drug resistance in TMZ-resistant cells (T98G and LN-18) via downregulating the expression of O6-methylguanine-DNA-methyltransferase (MGMT).	temozolomide	14-17	O-6-methylguanine-DNA methyltransferase	Mus musculus	133-171
31601097-7	2019	Besides, tFNA-TMZ was able to attenuate drug resistance in TMZ-resistant cells (T98G and LN-18) via downregulating the expression of O6-methylguanine-DNA-methyltransferase (MGMT).	temozolomide	14-17	O-6-methylguanine-DNA methyltransferase	Mus musculus	173-177
31601097-7	2019	Besides, tFNA-TMZ was able to attenuate drug resistance in TMZ-resistant cells (T98G and LN-18) via downregulating the expression of O6-methylguanine-DNA-methyltransferase (MGMT).	temozolomide	59-62	O-6-methylguanine-DNA methyltransferase	Mus musculus	133-171
31601097-7	2019	Besides, tFNA-TMZ was able to attenuate drug resistance in TMZ-resistant cells (T98G and LN-18) via downregulating the expression of O6-methylguanine-DNA-methyltransferase (MGMT).	temozolomide	59-62	O-6-methylguanine-DNA methyltransferase	Mus musculus	173-177
31629402-7	2019	SOD2 in the resistant cells functionally determined the cell fate by limiting TMZ-stimulated superoxide reaction and cleavage of caspase-3.	temozolomide	78-81	superoxide dismutase 2	Homo sapiens	0-4
31629402-12	2019	Finally, co-treatment with TMZ and the SOD inhibitor sodium diethyldithiocarbamate trihydrate in xenograft mouse models with the TMZ-resistant primary tumor resulted in lower tumor proliferation, longer survival, and less CD133, Bmi-1, and SOD2 expression.	temozolomide	27-30	prominin 1	Mus musculus	222-227
31629402-12	2019	Finally, co-treatment with TMZ and the SOD inhibitor sodium diethyldithiocarbamate trihydrate in xenograft mouse models with the TMZ-resistant primary tumor resulted in lower tumor proliferation, longer survival, and less CD133, Bmi-1, and SOD2 expression.	temozolomide	27-30	Bmi1 polycomb ring finger oncogene	Mus musculus	229-234
31639020-0	2019	The Chk1 inhibitor SAR-020106 sensitizes human glioblastoma cells to irradiation, to temozolomide, and to decitabine treatment.	temozolomide	85-97	checkpoint kinase 1	Homo sapiens	4-8
31639020-0	2019	The Chk1 inhibitor SAR-020106 sensitizes human glioblastoma cells to irradiation, to temozolomide, and to decitabine treatment.	temozolomide	85-97	sarcosine dehydrogenase	Homo sapiens	19-29
31629402-12	2019	Finally, co-treatment with TMZ and the SOD inhibitor sodium diethyldithiocarbamate trihydrate in xenograft mouse models with the TMZ-resistant primary tumor resulted in lower tumor proliferation, longer survival, and less CD133, Bmi-1, and SOD2 expression.	temozolomide	27-30	superoxide dismutase 2, mitochondrial	Mus musculus	240-244
31629402-12	2019	Finally, co-treatment with TMZ and the SOD inhibitor sodium diethyldithiocarbamate trihydrate in xenograft mouse models with the TMZ-resistant primary tumor resulted in lower tumor proliferation, longer survival, and less CD133, Bmi-1, and SOD2 expression.	temozolomide	129-132	prominin 1	Mus musculus	222-227
31629402-12	2019	Finally, co-treatment with TMZ and the SOD inhibitor sodium diethyldithiocarbamate trihydrate in xenograft mouse models with the TMZ-resistant primary tumor resulted in lower tumor proliferation, longer survival, and less CD133, Bmi-1, and SOD2 expression.	temozolomide	129-132	Bmi1 polycomb ring finger oncogene	Mus musculus	229-234
31629402-12	2019	Finally, co-treatment with TMZ and the SOD inhibitor sodium diethyldithiocarbamate trihydrate in xenograft mouse models with the TMZ-resistant primary tumor resulted in lower tumor proliferation, longer survival, and less CD133, Bmi-1, and SOD2 expression.	temozolomide	129-132	superoxide dismutase 2, mitochondrial	Mus musculus	240-244
31629402-13	2019	CONCLUSION: SOD2 plays crucial roles in the tumor-initiating features that are related to TMZ resistance.	temozolomide	90-93	superoxide dismutase 2	Homo sapiens	12-16
31681604-7	2019	Moreover, miR-199a renders tumor cells more sensitive to temozolomide (TMZ) via targeting K-RAS.	temozolomide	57-69	KRAS proto-oncogene, GTPase	Homo sapiens	90-95
31681604-7	2019	Moreover, miR-199a renders tumor cells more sensitive to temozolomide (TMZ) via targeting K-RAS.	temozolomide	71-74	KRAS proto-oncogene, GTPase	Homo sapiens	90-95
31561595-6	2019	Bioinformatics data have indicated that dopamine receptor (DRD) 2, DRD4, CD133 and Nestin were elevated in GBM clinical samples and correlated to Temozolomide (TMZ) resistance and increased aldehyde dehydrogenase (ALDH) activity (3.5-8.9%) as well as enhanced (2.1-2.4-fold) neurosphere formation efficiency in U87MG and D54MG GBM cell lines.	temozolomide	146-158	dopamine receptor D4	Homo sapiens	67-71
31632968-0	2019	Novel Function of lncRNA ADAMTS9-AS2 in Promoting Temozolomide Resistance in Glioblastoma via Upregulating the FUS/MDM2 Ubiquitination Axis.	temozolomide	50-62	ADAM metallopeptidase with thrombospondin type 1 motif 9	Homo sapiens	25-32
31632968-0	2019	Novel Function of lncRNA ADAMTS9-AS2 in Promoting Temozolomide Resistance in Glioblastoma via Upregulating the FUS/MDM2 Ubiquitination Axis.	temozolomide	50-62	FUS RNA binding protein	Homo sapiens	111-114
31632968-0	2019	Novel Function of lncRNA ADAMTS9-AS2 in Promoting Temozolomide Resistance in Glioblastoma via Upregulating the FUS/MDM2 Ubiquitination Axis.	temozolomide	50-62	MDM2 proto-oncogene	Homo sapiens	115-119
31632968-4	2019	LncRNAs from four public datasets were reanalyzed, and the candidate lncRNA ADAMTS9-AS2 was evaluated in TMZ-treated GBM patients and in vitro cell lines.	temozolomide	105-108	ADAM metallopeptidase with thrombospondin type 1 motif 9	Homo sapiens	76-83
31632968-5	2019	Results: Reanalysis of lncRNA expression profiles identified ADAMTS9-AS2 as significantly overexpressed in TMZ-resistant GBM cells and as positively associated with the IC50 of TMZ in GBM cells.	temozolomide	107-110	ADAM metallopeptidase with thrombospondin type 1 motif 9	Homo sapiens	61-68
31632968-5	2019	Results: Reanalysis of lncRNA expression profiles identified ADAMTS9-AS2 as significantly overexpressed in TMZ-resistant GBM cells and as positively associated with the IC50 of TMZ in GBM cells.	temozolomide	177-180	ADAM metallopeptidase with thrombospondin type 1 motif 9	Homo sapiens	61-68
31632968-6	2019	Overexpression of ADAMTS9-AS2 was also significantly associated with poor TMZ response and shorter progression-free survival (PFS) in TMZ-treated GBM patients.	temozolomide	74-77	ADAM metallopeptidase with thrombospondin type 1 motif 9	Homo sapiens	18-25
31632968-6	2019	Overexpression of ADAMTS9-AS2 was also significantly associated with poor TMZ response and shorter progression-free survival (PFS) in TMZ-treated GBM patients.	temozolomide	134-137	ADAM metallopeptidase with thrombospondin type 1 motif 9	Homo sapiens	18-25
31632968-7	2019	Knockdown of ADAMTS9-AS2 inhibited proliferation and attenuated the IC50 of TMZ, as well as mitigating invasion and migration in TMZ-resistant GBM cells.	temozolomide	76-79	ADAM metallopeptidase with thrombospondin type 1 motif 9	Homo sapiens	13-20
31632968-7	2019	Knockdown of ADAMTS9-AS2 inhibited proliferation and attenuated the IC50 of TMZ, as well as mitigating invasion and migration in TMZ-resistant GBM cells.	temozolomide	129-132	ADAM metallopeptidase with thrombospondin type 1 motif 9	Homo sapiens	13-20
31632968-9	2019	Expression trends of FUS were directly correlated with those of ADAMTS9-AS2, as shown by increasing concentrations and prolonged treatment with TMZ.	temozolomide	144-147	FUS RNA binding protein	Homo sapiens	21-24
31632968-9	2019	Expression trends of FUS were directly correlated with those of ADAMTS9-AS2, as shown by increasing concentrations and prolonged treatment with TMZ.	temozolomide	144-147	ADAM metallopeptidase with thrombospondin type 1 motif 9	Homo sapiens	64-71
31632968-14	2019	Additionally, knockdown of the ADAMTS9-AS2/FUS signaling axis significantly alleviated progression and metastasis in TMZ-resistant cells.	temozolomide	117-120	ADAM metallopeptidase with thrombospondin type 1 motif 9	Homo sapiens	31-38
31632968-14	2019	Additionally, knockdown of the ADAMTS9-AS2/FUS signaling axis significantly alleviated progression and metastasis in TMZ-resistant cells.	temozolomide	117-120	FUS RNA binding protein	Homo sapiens	43-46
31632968-15	2019	Conclusion: ADAMTS9-AS2 possessed a novel function that promotes TMZ resistance via upregulating the FUS/MDM2 axis in GBM cells.	temozolomide	65-68	ADAM metallopeptidase with thrombospondin type 1 motif 9	Homo sapiens	12-19
31632968-15	2019	Conclusion: ADAMTS9-AS2 possessed a novel function that promotes TMZ resistance via upregulating the FUS/MDM2 axis in GBM cells.	temozolomide	65-68	FUS RNA binding protein	Homo sapiens	101-104
31632968-15	2019	Conclusion: ADAMTS9-AS2 possessed a novel function that promotes TMZ resistance via upregulating the FUS/MDM2 axis in GBM cells.	temozolomide	65-68	MDM2 proto-oncogene	Homo sapiens	105-109
31632968-16	2019	The RRM or Znf_RanBP2 domains of FUS facilitate the combination of ADAMTS9-AS2 and FUS, competitively inhibiting MDM2-dependent FUS K48 ubiquitination and resulting in enhanced FUS stability and TMZ resistance.	temozolomide	195-198	FUS RNA binding protein	Homo sapiens	33-36
31632968-16	2019	The RRM or Znf_RanBP2 domains of FUS facilitate the combination of ADAMTS9-AS2 and FUS, competitively inhibiting MDM2-dependent FUS K48 ubiquitination and resulting in enhanced FUS stability and TMZ resistance.	temozolomide	195-198	ADAM metallopeptidase with thrombospondin type 1 motif 9	Homo sapiens	67-74
31632968-16	2019	The RRM or Znf_RanBP2 domains of FUS facilitate the combination of ADAMTS9-AS2 and FUS, competitively inhibiting MDM2-dependent FUS K48 ubiquitination and resulting in enhanced FUS stability and TMZ resistance.	temozolomide	195-198	FUS RNA binding protein	Homo sapiens	83-86
31632968-16	2019	The RRM or Znf_RanBP2 domains of FUS facilitate the combination of ADAMTS9-AS2 and FUS, competitively inhibiting MDM2-dependent FUS K48 ubiquitination and resulting in enhanced FUS stability and TMZ resistance.	temozolomide	195-198	MDM2 proto-oncogene	Homo sapiens	113-117
31632968-16	2019	The RRM or Znf_RanBP2 domains of FUS facilitate the combination of ADAMTS9-AS2 and FUS, competitively inhibiting MDM2-dependent FUS K48 ubiquitination and resulting in enhanced FUS stability and TMZ resistance.	temozolomide	195-198	FUS RNA binding protein	Homo sapiens	83-86
31632968-16	2019	The RRM or Znf_RanBP2 domains of FUS facilitate the combination of ADAMTS9-AS2 and FUS, competitively inhibiting MDM2-dependent FUS K48 ubiquitination and resulting in enhanced FUS stability and TMZ resistance.	temozolomide	195-198	FUS RNA binding protein	Homo sapiens	83-86
31632968-17	2019	Our results suggest that the ADAMTS9-AS2/FUS/MDM2 axis may represent a suitable prognostic biomarker and a potential target in TMZ-resistant GBM therapy.	temozolomide	127-130	ADAM metallopeptidase with thrombospondin type 1 motif 9	Homo sapiens	29-36
31632968-17	2019	Our results suggest that the ADAMTS9-AS2/FUS/MDM2 axis may represent a suitable prognostic biomarker and a potential target in TMZ-resistant GBM therapy.	temozolomide	127-130	FUS RNA binding protein	Homo sapiens	41-44
31632968-17	2019	Our results suggest that the ADAMTS9-AS2/FUS/MDM2 axis may represent a suitable prognostic biomarker and a potential target in TMZ-resistant GBM therapy.	temozolomide	127-130	MDM2 proto-oncogene	Homo sapiens	45-49
31611911-0	2019	A Novel DNA Methylation-Based Signature Can Predict the Responses of MGMT Promoter Unmethylated Glioblastomas to Temozolomide.	temozolomide	113-125	O-6-methylguanine-DNA methyltransferase	Homo sapiens	69-73
31611911-3	2019	DNA methylation profiling holds great promise for further stratifying the responses of MGMT promoter unmethylated GBMs to TMZ.	temozolomide	122-125	O-6-methylguanine-DNA methyltransferase	Homo sapiens	87-91
31611911-4	2019	In this study, we studied 147 TMZ-treated MGMT promoter unmethylated GBM, whose methylation information was obtained from the HumanMethylation27 (HM-27K) BeadChips (n = 107) and the HumanMethylation450 (HM-450K) BeadChips (n = 40) for training and validation, respectively.	temozolomide	30-33	O-6-methylguanine-DNA methyltransferase	Homo sapiens	42-46
31611911-5	2019	In the training set, we performed univariate Cox regression and identified that 3,565 CpGs were significantly associated with the OS of the TMZ-treated MGMT promoter unmethylated GBMs.	temozolomide	140-143	O-6-methylguanine-DNA methyltransferase	Homo sapiens	152-156
31611911-8	2019	In both training and validation datasets, the signature identified the TMZ-sensitive GBMs in the MGMT promoter unmethylated GBMs, and only the patients in the low-risk group appear to benefit from the TMZ treatment.	temozolomide	71-74	O-6-methylguanine-DNA methyltransferase	Homo sapiens	97-101
31611911-8	2019	In both training and validation datasets, the signature identified the TMZ-sensitive GBMs in the MGMT promoter unmethylated GBMs, and only the patients in the low-risk group appear to benefit from the TMZ treatment.	temozolomide	201-204	O-6-methylguanine-DNA methyltransferase	Homo sapiens	97-101
31611911-9	2019	Furthermore, these identified TMZ-sensitive MGMT promoter unmethylated GBMs have a similar OS when compared with the MGMT promoter methylated GBMs after TMZ treatment in both two datasets.	temozolomide	30-33	O-6-methylguanine-DNA methyltransferase	Homo sapiens	44-48
31611911-10	2019	Multivariate Cox regression demonstrated the independent prognostic value of the signature in TMZ-treated MGMT promoter unmethylated GBMs.	temozolomide	94-97	O-6-methylguanine-DNA methyltransferase	Homo sapiens	106-110
31611911-11	2019	Moreover, we also noticed that the hallmark of epithelial-mesenchymal transition, ECM related biological processes and pathways were highly enriched in the MGMT unmethylated GBMs with the high-risk score, indicating that enhanced ECM activities could be involved in the TMZ-resistance of GBM.	temozolomide	270-273	multimerin 1	Homo sapiens	82-85
31611911-11	2019	Moreover, we also noticed that the hallmark of epithelial-mesenchymal transition, ECM related biological processes and pathways were highly enriched in the MGMT unmethylated GBMs with the high-risk score, indicating that enhanced ECM activities could be involved in the TMZ-resistance of GBM.	temozolomide	270-273	O-6-methylguanine-DNA methyltransferase	Homo sapiens	156-160
31611911-11	2019	Moreover, we also noticed that the hallmark of epithelial-mesenchymal transition, ECM related biological processes and pathways were highly enriched in the MGMT unmethylated GBMs with the high-risk score, indicating that enhanced ECM activities could be involved in the TMZ-resistance of GBM.	temozolomide	270-273	multimerin 1	Homo sapiens	230-233
31602000-6	2019	Further, BMP pathway activation confers relative resistance to radiation and temozolomide chemotherapy.	temozolomide	77-89	bone morphogenetic protein 1	Homo sapiens	9-12
31686436-8	2019	After molecular and histological examinations, patients with anaplastic astrocytoma, isocitrate dehydrogenase (IDH)-mutant should be primary treated by standard brain radiotherapy and adjuvant temozolomide chemotherapy whereas those with anaplastic astrocytoma, NOS, and anaplastic astrocytoma, IDH-wildtype should be treated following the protocol for glioblastomas.	temozolomide	193-205	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	85-109
31686436-8	2019	After molecular and histological examinations, patients with anaplastic astrocytoma, isocitrate dehydrogenase (IDH)-mutant should be primary treated by standard brain radiotherapy and adjuvant temozolomide chemotherapy whereas those with anaplastic astrocytoma, NOS, and anaplastic astrocytoma, IDH-wildtype should be treated following the protocol for glioblastomas.	temozolomide	193-205	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	111-114
31561595-6	2019	Bioinformatics data have indicated that dopamine receptor (DRD) 2, DRD4, CD133 and Nestin were elevated in GBM clinical samples and correlated to Temozolomide (TMZ) resistance and increased aldehyde dehydrogenase (ALDH) activity (3.5-8.9%) as well as enhanced (2.1-2.4-fold) neurosphere formation efficiency in U87MG and D54MG GBM cell lines.	temozolomide	160-163	dopamine receptor D4	Homo sapiens	67-71
31561595-7	2019	In addition, TMZ-resistant GSC phenotype was associated with up-regulated DRD4, Akt, mTOR, beta-catenin, CDK6, NF-kappaB and Erk1/2 expression.	temozolomide	13-16	dopamine receptor D4	Homo sapiens	74-78
31561595-7	2019	In addition, TMZ-resistant GSC phenotype was associated with up-regulated DRD4, Akt, mTOR, beta-catenin, CDK6, NF-kappaB and Erk1/2 expression.	temozolomide	13-16	AKT serine/threonine kinase 1	Homo sapiens	80-83
31561595-7	2019	In addition, TMZ-resistant GSC phenotype was associated with up-regulated DRD4, Akt, mTOR, beta-catenin, CDK6, NF-kappaB and Erk1/2 expression.	temozolomide	13-16	mechanistic target of rapamycin kinase	Homo sapiens	85-89
31561595-7	2019	In addition, TMZ-resistant GSC phenotype was associated with up-regulated DRD4, Akt, mTOR, beta-catenin, CDK6, NF-kappaB and Erk1/2 expression.	temozolomide	13-16	catenin beta 1	Homo sapiens	91-103
31561595-7	2019	In addition, TMZ-resistant GSC phenotype was associated with up-regulated DRD4, Akt, mTOR, beta-catenin, CDK6, NF-kappaB and Erk1/2 expression.	temozolomide	13-16	cyclin dependent kinase 6	Homo sapiens	105-109
31561595-7	2019	In addition, TMZ-resistant GSC phenotype was associated with up-regulated DRD4, Akt, mTOR, beta-catenin, CDK6, NF-kappaB and Erk1/2 expression.	temozolomide	13-16	nuclear factor kappa B subunit 1	Homo sapiens	111-120
31561595-7	2019	In addition, TMZ-resistant GSC phenotype was associated with up-regulated DRD4, Akt, mTOR, beta-catenin, CDK6, NF-kappaB and Erk1/2 expression.	temozolomide	13-16	mitogen-activated protein kinase 3	Homo sapiens	125-131
31561595-8	2019	LCC-09 alone, or combined with TMZ, suppressed the tumorigenic and stemness traits of TMZ-resistant GBM cells while concomitantly down-regulating DRD4, Akt, mTOR, beta-catenin, Erk1/2, NF-kappaB, and CDK6 expression.	temozolomide	31-34	dopamine receptor D4	Homo sapiens	146-150
31561595-8	2019	LCC-09 alone, or combined with TMZ, suppressed the tumorigenic and stemness traits of TMZ-resistant GBM cells while concomitantly down-regulating DRD4, Akt, mTOR, beta-catenin, Erk1/2, NF-kappaB, and CDK6 expression.	temozolomide	31-34	AKT serine/threonine kinase 1	Homo sapiens	152-155
31561595-8	2019	LCC-09 alone, or combined with TMZ, suppressed the tumorigenic and stemness traits of TMZ-resistant GBM cells while concomitantly down-regulating DRD4, Akt, mTOR, beta-catenin, Erk1/2, NF-kappaB, and CDK6 expression.	temozolomide	31-34	mechanistic target of rapamycin kinase	Homo sapiens	157-161
31561595-8	2019	LCC-09 alone, or combined with TMZ, suppressed the tumorigenic and stemness traits of TMZ-resistant GBM cells while concomitantly down-regulating DRD4, Akt, mTOR, beta-catenin, Erk1/2, NF-kappaB, and CDK6 expression.	temozolomide	31-34	catenin beta 1	Homo sapiens	163-175
31750824-0	2019	[RAD51 promotes proliferation and migration of glioblastoma cells and decreases sensitivity of cells to temozolomide].	temozolomide	104-116	RAD51 recombinase	Homo sapiens	1-6
31750824-1	2019	Objective To investigate the role of RAD51 in cell proliferation, migration and chemosensitivity to temozolomide (TMZ) using U251 glioma cell line, and to clarify the underlying molecular mechanism.	temozolomide	100-112	RAD51 recombinase	Homo sapiens	37-42
31750824-1	2019	Objective To investigate the role of RAD51 in cell proliferation, migration and chemosensitivity to temozolomide (TMZ) using U251 glioma cell line, and to clarify the underlying molecular mechanism.	temozolomide	114-117	RAD51 recombinase	Homo sapiens	37-42
31750824-7	2019	RAD51 enhanced the proliferation and migration ability of U251 glioma cells; knockdown of RAD51 enhanced the sensitivity of U251 glioma cells to temozolomide.	temozolomide	145-157	RAD51 recombinase	Homo sapiens	90-95
31750824-11	2019	RAD51 knockdown increases the sensitivity of glioma cells to temozolomide.	temozolomide	61-73	RAD51 recombinase	Homo sapiens	0-5
31818145-3	2019	We describe a case of CD10-positive PCNSL presenting with multiple posterior fossa enhancing lesions in an immunocompetent older woman with a history of breast cancer successfully treated by the RTOG 0227 protocol consisting of pre-irradiation chemotherapy with high-dose methotrexate, rituximab, and temozolomide for 6 cycles, followed by low-dose whole-brain radiation and post-irradiation temozolomide.	temozolomide	301-313	membrane metalloendopeptidase	Homo sapiens	22-26
31818145-3	2019	We describe a case of CD10-positive PCNSL presenting with multiple posterior fossa enhancing lesions in an immunocompetent older woman with a history of breast cancer successfully treated by the RTOG 0227 protocol consisting of pre-irradiation chemotherapy with high-dose methotrexate, rituximab, and temozolomide for 6 cycles, followed by low-dose whole-brain radiation and post-irradiation temozolomide.	temozolomide	392-404	membrane metalloendopeptidase	Homo sapiens	22-26
31798765-2	2019	O6-methyl-guanine DNA methyltransferase (MGMT) repairs DNA damage induced by TMZ; hence, elevated MGMT levels usually correlate with TMZ resistance.	temozolomide	77-80	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-39
31798765-2	2019	O6-methyl-guanine DNA methyltransferase (MGMT) repairs DNA damage induced by TMZ; hence, elevated MGMT levels usually correlate with TMZ resistance.	temozolomide	77-80	O-6-methylguanine-DNA methyltransferase	Homo sapiens	41-45
31798765-2	2019	O6-methyl-guanine DNA methyltransferase (MGMT) repairs DNA damage induced by TMZ; hence, elevated MGMT levels usually correlate with TMZ resistance.	temozolomide	77-80	O-6-methylguanine-DNA methyltransferase	Homo sapiens	98-102
31798765-2	2019	O6-methyl-guanine DNA methyltransferase (MGMT) repairs DNA damage induced by TMZ; hence, elevated MGMT levels usually correlate with TMZ resistance.	temozolomide	133-136	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-39
31798765-2	2019	O6-methyl-guanine DNA methyltransferase (MGMT) repairs DNA damage induced by TMZ; hence, elevated MGMT levels usually correlate with TMZ resistance.	temozolomide	133-136	O-6-methylguanine-DNA methyltransferase	Homo sapiens	41-45
31798765-2	2019	O6-methyl-guanine DNA methyltransferase (MGMT) repairs DNA damage induced by TMZ; hence, elevated MGMT levels usually correlate with TMZ resistance.	temozolomide	133-136	O-6-methylguanine-DNA methyltransferase	Homo sapiens	98-102
31798765-3	2019	MGMT promoter methylation is a key regulatory mechanism for MGMT expression and is important in overcoming TMZ therapy resistance.	temozolomide	107-110	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-4
31798765-3	2019	MGMT promoter methylation is a key regulatory mechanism for MGMT expression and is important in overcoming TMZ therapy resistance.	temozolomide	107-110	O-6-methylguanine-DNA methyltransferase	Homo sapiens	60-64
31798765-8	2019	Interestingly, this interaction is disrupted by TMZ exclusively in TMZ sensitive cells, suggesting that this MGMT regulatory pathway might be inactivated in TMZ resistant cells.	temozolomide	48-51	O-6-methylguanine-DNA methyltransferase	Homo sapiens	109-113
31798765-8	2019	Interestingly, this interaction is disrupted by TMZ exclusively in TMZ sensitive cells, suggesting that this MGMT regulatory pathway might be inactivated in TMZ resistant cells.	temozolomide	67-70	O-6-methylguanine-DNA methyltransferase	Homo sapiens	109-113
31798765-8	2019	Interestingly, this interaction is disrupted by TMZ exclusively in TMZ sensitive cells, suggesting that this MGMT regulatory pathway might be inactivated in TMZ resistant cells.	temozolomide	67-70	O-6-methylguanine-DNA methyltransferase	Homo sapiens	109-113