PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
14992447-0	2004	Peripheral blood mononuclear cell DNA 6-thioguanine metabolite levels correlate with decreased interferon-gamma production in patients with Crohn"s disease on AZA therapy.	Azathioprine	159-162	interferon gamma	Homo sapiens	95-111
14634700-0	2004	Thiopurine methyltransferase (TPMT) genotype distribution in azathioprine-tolerant and -intolerant patients with various disorders.	Azathioprine	61-73	thiopurine S-methyltransferase	Homo sapiens	0-28
14634700-0	2004	Thiopurine methyltransferase (TPMT) genotype distribution in azathioprine-tolerant and -intolerant patients with various disorders.	Azathioprine	61-73	thiopurine S-methyltransferase	Homo sapiens	30-34
14634700-2	2004	OBJECTIVE: To study the distribution of the thiopurine methyltransferase (TPMT) genotype among azathioprine (Aza)-tolerant and -intolerant patients with various disorders, and to investigate a possible relationship with the Aza metabolite levels.	Azathioprine	95-107	thiopurine S-methyltransferase	Homo sapiens	44-72
14634700-2	2004	OBJECTIVE: To study the distribution of the thiopurine methyltransferase (TPMT) genotype among azathioprine (Aza)-tolerant and -intolerant patients with various disorders, and to investigate a possible relationship with the Aza metabolite levels.	Azathioprine	95-107	thiopurine S-methyltransferase	Homo sapiens	74-78
14634700-2	2004	OBJECTIVE: To study the distribution of the thiopurine methyltransferase (TPMT) genotype among azathioprine (Aza)-tolerant and -intolerant patients with various disorders, and to investigate a possible relationship with the Aza metabolite levels.	Azathioprine	109-112	thiopurine S-methyltransferase	Homo sapiens	44-72
14634700-2	2004	OBJECTIVE: To study the distribution of the thiopurine methyltransferase (TPMT) genotype among azathioprine (Aza)-tolerant and -intolerant patients with various disorders, and to investigate a possible relationship with the Aza metabolite levels.	Azathioprine	109-112	thiopurine S-methyltransferase	Homo sapiens	74-78
14634700-2	2004	OBJECTIVE: To study the distribution of the thiopurine methyltransferase (TPMT) genotype among azathioprine (Aza)-tolerant and -intolerant patients with various disorders, and to investigate a possible relationship with the Aza metabolite levels.	Azathioprine	224-227	thiopurine S-methyltransferase	Homo sapiens	74-78
14634700-4	2004	RESULTS: One non-functional TPMT mutant allele was demonstrated in 2 of the 46 Aza-tolerant patients (4.4%) and one or two non-functional mutant alleles in 2 of the 6 Aza-intolerant patients (33.3%).	Azathioprine	79-82	thiopurine S-methyltransferase	Homo sapiens	28-32
14634700-9	2004	CONCLUSION: Although TPMT genotyping cannot be recommended on behalf of the present study, it is to be expected that half of the patients with one or two non-functional TPMT mutant alleles will develop Aza intolerance leading to withdrawal of therapy.	Azathioprine	202-205	thiopurine S-methyltransferase	Homo sapiens	169-173
14631124-10	2004	Despite some limitations of our study design, the information regarding efficacy, safety and tolerance of the association of AZA and IFN-beta is most encouraging.	Azathioprine	125-128	interferon beta 1	Homo sapiens	133-141
14734128-11	2004	CONCLUSIONS: Changing immunosuppression from a standard AZA-based regimen to MMF resulted in a decrease in systemic inflammatory activity as indicated by levels of high-sensitive CRP.	Azathioprine	56-59	C-reactive protein	Homo sapiens	179-182
15669633-3	2004	Polymorphisms in the thiopurine methyl transferase gene (TPMT) are known to influence the outcome of therapy with azathioprine although pharmacogenetic analysis of outcome has not entered routine clinical use.	Azathioprine	114-126	thiopurine S-methyltransferase	Homo sapiens	21-55
15322947-3	2004	Recently, a polymorphism in the inosine triphosphate pyrophosphatase gene (ITPA) has been associated with severe azathioprine toxicity.	Azathioprine	113-125	inosine triphosphatase	Homo sapiens	75-79
15669633-3	2004	Polymorphisms in the thiopurine methyl transferase gene (TPMT) are known to influence the outcome of therapy with azathioprine although pharmacogenetic analysis of outcome has not entered routine clinical use.	Azathioprine	114-126	thiopurine S-methyltransferase	Homo sapiens	57-61
14566029-0	2004	Relevance of thiopurine methyltransferase status in rheumatology patients receiving azathioprine.	Azathioprine	84-96	thiopurine S-methyltransferase	Homo sapiens	13-41
14566029-3	2004	Severe myelosuppression, associated with abnormal AZA metabolism, is linked to the thiopurine methyltransferase (TPMT) genetic polymorphism.	Azathioprine	50-53	thiopurine S-methyltransferase	Homo sapiens	83-111
14566029-3	2004	Severe myelosuppression, associated with abnormal AZA metabolism, is linked to the thiopurine methyltransferase (TPMT) genetic polymorphism.	Azathioprine	50-53	thiopurine S-methyltransferase	Homo sapiens	113-117
14566029-5	2004	Analysis of recent data suggests that by optimizing the AZA dose on the basis of TPMT status testing (with a substantial reduction in dose for patients homozygous for mutant TPMT alleles), a reduction in drug-induced morbidity and cost savings can be made by avoiding hospitalization and rescue therapy for leucopenic events.	Azathioprine	56-59	thiopurine S-methyltransferase	Homo sapiens	81-85
14566029-5	2004	Analysis of recent data suggests that by optimizing the AZA dose on the basis of TPMT status testing (with a substantial reduction in dose for patients homozygous for mutant TPMT alleles), a reduction in drug-induced morbidity and cost savings can be made by avoiding hospitalization and rescue therapy for leucopenic events.	Azathioprine	56-59	thiopurine S-methyltransferase	Homo sapiens	174-178
14566029-6	2004	In this article we review the pharmacogenetic and clinical implications of the TPMT polymorphism, emphasizing its relevance to rheumatologists managing diseases with AZA.	Azathioprine	166-169	thiopurine S-methyltransferase	Homo sapiens	79-83
14602061-4	2003	The thiopurine methyltransferase (TPMT) enzyme plays a pivotal role in the metabolism of 6-MP and AZA and is critical to the determination of thiopurine toxicity.	Azathioprine	98-101	thiopurine S-methyltransferase	Homo sapiens	4-32
14602061-4	2003	The thiopurine methyltransferase (TPMT) enzyme plays a pivotal role in the metabolism of 6-MP and AZA and is critical to the determination of thiopurine toxicity.	Azathioprine	98-101	thiopurine S-methyltransferase	Homo sapiens	34-38
14556798-0	2003	Synthesis, molecular modeling and biological evaluation of aza-proline and aza-pipecolic derivatives as FKBP12 ligands and their in vivo neuroprotective effects.	Azathioprine	59-62	FKBP prolyl isomerase 1A pseudogene 4	Homo sapiens	104-110
14627413-1	2003	[reaction: see text] Asymmetric reverse-aza-Brook rearrangement of N-Boc-N-trialkylsilyl allylamine yields an enantiomerically enriched alpha-amino allylsilane.	Azathioprine	40-43	BOC cell adhesion associated, oncogene regulated	Homo sapiens	69-72
14560161-2	2003	The measurement of thiopurine methyltransferase (TPMT) activity levels helps to identify the one in 300 patients who are at risk of profound myelosuppression with standard doses of AZA.	Azathioprine	181-184	thiopurine S-methyltransferase	Homo sapiens	19-47
14560161-2	2003	The measurement of thiopurine methyltransferase (TPMT) activity levels helps to identify the one in 300 patients who are at risk of profound myelosuppression with standard doses of AZA.	Azathioprine	181-184	thiopurine S-methyltransferase	Homo sapiens	49-53
14560161-6	2003	However, following severe myelosuppression soon after starting AZA, her genotype was determined, which showed that she was homozygous for low TPMT activity.	Azathioprine	63-66	thiopurine S-methyltransferase	Homo sapiens	142-146
14651577-0	2003	Azathioprine as a treatment for severe atopic eczema in children with a partial thiopurine methyl transferase (TPMT) deficiency.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	80-109
14651577-0	2003	Azathioprine as a treatment for severe atopic eczema in children with a partial thiopurine methyl transferase (TPMT) deficiency.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	111-115
14651577-2	2003	Thiopurine methyl transferase (TPMT) exhibits autosomal codominant polymorphism and plays an important role in the metabolism of azathioprine.	Azathioprine	129-141	thiopurine S-methyltransferase	Homo sapiens	0-29
14651577-2	2003	Thiopurine methyl transferase (TPMT) exhibits autosomal codominant polymorphism and plays an important role in the metabolism of azathioprine.	Azathioprine	129-141	thiopurine S-methyltransferase	Homo sapiens	31-35
14556746-1	2003	In humans, the enzyme thiopurine methyltransferase (TPMT) metabolizes 6-thiopurine (6-TP) medications, including 6-thioguanine, 6-mercaptopurine and azathioprine, commonly used for immune suppression and for the treatment of hematopoietic malignancies.	Azathioprine	149-161	thiopurine S-methyltransferase	Homo sapiens	22-50
14556746-1	2003	In humans, the enzyme thiopurine methyltransferase (TPMT) metabolizes 6-thiopurine (6-TP) medications, including 6-thioguanine, 6-mercaptopurine and azathioprine, commonly used for immune suppression and for the treatment of hematopoietic malignancies.	Azathioprine	149-161	thiopurine S-methyltransferase	Homo sapiens	52-56
14588189-1	2003	BACKGROUND AND OBJECTIVE: The measurement of the activity of thiopurine methyltransferase (TPMT) is useful to monitor, on an individual basis, the dose of azathioprine in order to identify patients at risk of myelotoxicity.	Azathioprine	155-167	thiopurine S-methyltransferase	Homo sapiens	61-89
14588189-1	2003	BACKGROUND AND OBJECTIVE: The measurement of the activity of thiopurine methyltransferase (TPMT) is useful to monitor, on an individual basis, the dose of azathioprine in order to identify patients at risk of myelotoxicity.	Azathioprine	155-167	thiopurine S-methyltransferase	Homo sapiens	91-95
14588189-11	2003	CONCLUSIONS: TPMT activity in patients with autoimmune hepatitis displays a similar distribution to that reported in other populations (approximately 1% of patients have low levels and 9% have intermediate levels) and it does not depend on the age, gender or simultaneous azathioprine treatment.	Azathioprine	272-284	thiopurine S-methyltransferase	Homo sapiens	13-17
13679074-1	2003	Human thiopurine S-methyltransferase (TPMT) is an enzyme responsible for the detoxification of widely used thiopurine drugs such as azathioprine (Aza).	Azathioprine	132-144	thiopurine S-methyltransferase	Homo sapiens	6-36
13679074-1	2003	Human thiopurine S-methyltransferase (TPMT) is an enzyme responsible for the detoxification of widely used thiopurine drugs such as azathioprine (Aza).	Azathioprine	132-144	thiopurine S-methyltransferase	Homo sapiens	38-42
13679074-1	2003	Human thiopurine S-methyltransferase (TPMT) is an enzyme responsible for the detoxification of widely used thiopurine drugs such as azathioprine (Aza).	Azathioprine	146-149	thiopurine S-methyltransferase	Homo sapiens	6-36
13679074-1	2003	Human thiopurine S-methyltransferase (TPMT) is an enzyme responsible for the detoxification of widely used thiopurine drugs such as azathioprine (Aza).	Azathioprine	146-149	thiopurine S-methyltransferase	Homo sapiens	38-42
13679074-3	2003	DNA samples from four leucopenic patients treated with Aza were screened by PCR-SSCP analysis for mutations in the 10 exons of the TPMT gene.	Azathioprine	55-58	thiopurine S-methyltransferase	Homo sapiens	131-135
14668694-4	2003	So it is possible that differences in TPMT activity may influence the bioequivalence of azathioprine products among individuals, especially those patients deficient in TPMT enzyme activity.	Azathioprine	88-100	thiopurine S-methyltransferase	Homo sapiens	38-42
12806628-10	2003	Mucosal biopsies obtained before and 4 months after azathioprine discontinuation showed complete reversal of severe duodenal villus atrophy and marked up-regulation of mucosal dipeptidyl peptidase IV and PepT1 messenger RNA.	Azathioprine	52-64	dipeptidyl peptidase 4	Homo sapiens	176-199
14576848-1	2003	The genetic polymorphism of thiopurine methyltransferase (TPMT) is one of the most developed examples of pharmacogenetics, spanning from molecular genetics to clinical diagnostics for individualizing thiopurine therapy (i.e. azathioprine, mercaptopurine, and thioguanine).	Azathioprine	225-237	thiopurine S-methyltransferase	Homo sapiens	28-56
14576848-1	2003	The genetic polymorphism of thiopurine methyltransferase (TPMT) is one of the most developed examples of pharmacogenetics, spanning from molecular genetics to clinical diagnostics for individualizing thiopurine therapy (i.e. azathioprine, mercaptopurine, and thioguanine).	Azathioprine	225-237	thiopurine S-methyltransferase	Homo sapiens	58-62
12949626-1	2003	Thiopurine methyltransferase (TPMT) catalyzes the inactivation of thiopurine drugs (mercaptopurine, thioguanine and azathioprine) used to treat acute lymphoblastic leukemia, autoimmune diseases and recipients of transplanted organs.	Azathioprine	116-128	thiopurine S-methyltransferase	Homo sapiens	0-28
12949626-1	2003	Thiopurine methyltransferase (TPMT) catalyzes the inactivation of thiopurine drugs (mercaptopurine, thioguanine and azathioprine) used to treat acute lymphoblastic leukemia, autoimmune diseases and recipients of transplanted organs.	Azathioprine	116-128	thiopurine S-methyltransferase	Homo sapiens	30-34
14502119-2	2003	Patients who are deficient in thiopurine methyltransferase (TPMT) are at an increased risk for azathioprine- and 6-mercaptopurine-induced toxicities because of the accumulation of toxic metabolites, and patients with high TPMT activity may not receive maximum benefit because of the increased clearance.	Azathioprine	95-107	thiopurine S-methyltransferase	Homo sapiens	30-58
14502119-2	2003	Patients who are deficient in thiopurine methyltransferase (TPMT) are at an increased risk for azathioprine- and 6-mercaptopurine-induced toxicities because of the accumulation of toxic metabolites, and patients with high TPMT activity may not receive maximum benefit because of the increased clearance.	Azathioprine	95-107	thiopurine S-methyltransferase	Homo sapiens	60-64
14502119-3	2003	Therefore, routine TPMT genotyping prior to the initiation of azathioprine or 6-mercaptopurine therapy should be considered to decrease the risk of severe and possibly preventable adverse effects and to identify patients who might benefit from higher doses.	Azathioprine	62-74	thiopurine S-methyltransferase	Homo sapiens	19-23
12812701-1	2003	BACKGROUND AND OBJECTIVE: We aimed at assessing whether there exists a relationship between thiopurine methyltransferase (TPMT) activity and the incidence of adverse events, especially myelotoxicity, in patients with inflammatory bowel disease treated with azathioprine (AZA) or 6-mercaptopurine (6-MP).	Azathioprine	257-269	thiopurine S-methyltransferase	Homo sapiens	122-126
12812701-1	2003	BACKGROUND AND OBJECTIVE: We aimed at assessing whether there exists a relationship between thiopurine methyltransferase (TPMT) activity and the incidence of adverse events, especially myelotoxicity, in patients with inflammatory bowel disease treated with azathioprine (AZA) or 6-mercaptopurine (6-MP).	Azathioprine	271-274	thiopurine S-methyltransferase	Homo sapiens	122-126
12812701-2	2003	PATIENTS AND METHOD: By means of a radiochemical method, we determined the TPMT activity in erythrocytes of patients with inflammatory bowel disease who had received previously or at the time of the study AZA or 6-MP (n = 97).	Azathioprine	205-208	thiopurine S-methyltransferase	Homo sapiens	75-79
12812701-11	2003	CONCLUSIONS: In this study, the usefulness of the determination of the TPMT activity to identify patients with inflammatory bowel disease at risk of myelotoxicity due to AZA or 6-MP has not been confirmed.	Azathioprine	170-173	thiopurine S-methyltransferase	Homo sapiens	71-75
12794758-12	2003	We demonstrate that in vitro resistance to 5-FU can be overcome by reexpression of hMLH1 protein through 5 aza-dC-induced demethylation in hypermethylated cell lines.	Azathioprine	107-110	mutL homolog 1	Homo sapiens	83-88
12806628-10	2003	Mucosal biopsies obtained before and 4 months after azathioprine discontinuation showed complete reversal of severe duodenal villus atrophy and marked up-regulation of mucosal dipeptidyl peptidase IV and PepT1 messenger RNA.	Azathioprine	52-64	solute carrier family 15 member 1	Homo sapiens	204-209
12762671-1	2003	[reaction: see text] Metalation of a Boc-protected N-silylamine alpha to nitrogen results in migration of the silicon from nitrogen to carbon (reverse aza-Brook rearrangement), yielding an alpha-amino silane.	Azathioprine	151-154	BOC cell adhesion associated, oncogene regulated	Homo sapiens	37-40
12697733-6	2003	The activation of Rac1 target genes such as mitogen-activated protein kinase kinase (MEK), NF-kappaB, and bcl-x(L) was suppressed by azathioprine, leading to a mitochondrial pathway of apoptosis.	Azathioprine	133-145	Rac family small GTPase 1	Homo sapiens	18-22
12777850-11	2003	There were no statistically significant differences among the groups at 5 days after transplantation, although the increase in TGF-beta1 was more pronounced in the HBD groups, especially in azathioprine-treated animals.	Azathioprine	190-202	transforming growth factor beta 1	Sus scrofa	127-136
12692068-0	2003	TPMT in the treatment of inflammatory bowel disease with azathioprine.	Azathioprine	57-69	thiopurine S-methyltransferase	Homo sapiens	0-4
12673023-5	2003	Halogen-substitution effects on AhR ligand activity in aza-polycyclic aromatics were also investigated with quinoline, benzo[f]quinoline (BfQ), benzo[h]quinoline (BhQ) and 1,7-phenanthroline (1,7-Phe).	Azathioprine	55-58	aryl hydrocarbon receptor	Homo sapiens	32-35
12673023-6	2003	Position-specific induction of AhR ligand activity was observed in aza-tricyclic aromatic compounds, BfQ, BhQ, and 1,7-Phe, and the ratio of the ligand activities (lacZ units/microM) of monochlorinated and monobrominated aza-tricyclic aromatic compounds to those of the corresponding parent non-halogenated compounds ranged from 2.2- to 254-fold.	Azathioprine	67-70	aryl hydrocarbon receptor	Homo sapiens	31-34
12697733-0	2003	CD28-dependent Rac1 activation is the molecular target of azathioprine in primary human CD4+ T lymphocytes.	Azathioprine	58-70	CD28 molecule	Homo sapiens	0-4
12697733-0	2003	CD28-dependent Rac1 activation is the molecular target of azathioprine in primary human CD4+ T lymphocytes.	Azathioprine	58-70	Rac family small GTPase 1	Homo sapiens	15-19
12697733-6	2003	The activation of Rac1 target genes such as mitogen-activated protein kinase kinase (MEK), NF-kappaB, and bcl-x(L) was suppressed by azathioprine, leading to a mitochondrial pathway of apoptosis.	Azathioprine	133-145	mitogen-activated protein kinase kinase 7	Homo sapiens	44-83
12697733-0	2003	CD28-dependent Rac1 activation is the molecular target of azathioprine in primary human CD4+ T lymphocytes.	Azathioprine	58-70	CD4 molecule	Homo sapiens	88-91
12697733-3	2003	In the present study, we have identified a unique and unexpected role for azathioprine and its metabolites in the control of T cell apoptosis by modulation of Rac1 activation upon CD28 costimulation.	Azathioprine	74-86	Rac family small GTPase 1	Homo sapiens	159-163
12697733-3	2003	In the present study, we have identified a unique and unexpected role for azathioprine and its metabolites in the control of T cell apoptosis by modulation of Rac1 activation upon CD28 costimulation.	Azathioprine	74-86	CD28 molecule	Homo sapiens	180-184
12697733-6	2003	The activation of Rac1 target genes such as mitogen-activated protein kinase kinase (MEK), NF-kappaB, and bcl-x(L) was suppressed by azathioprine, leading to a mitochondrial pathway of apoptosis.	Azathioprine	133-145	mitogen-activated protein kinase kinase 7	Homo sapiens	85-88
12697733-5	2003	Apoptosis induction required costimulation with CD28 and was mediated by specific blockade of Rac1 activation through binding of azathioprine-generated 6-thioguanine triphosphate (6-Thio-GTP) to Rac1 instead of GTP.	Azathioprine	129-141	CD28 molecule	Homo sapiens	48-52
12697733-6	2003	The activation of Rac1 target genes such as mitogen-activated protein kinase kinase (MEK), NF-kappaB, and bcl-x(L) was suppressed by azathioprine, leading to a mitochondrial pathway of apoptosis.	Azathioprine	133-145	BCL2 like 1	Homo sapiens	106-114
12697733-5	2003	Apoptosis induction required costimulation with CD28 and was mediated by specific blockade of Rac1 activation through binding of azathioprine-generated 6-thioguanine triphosphate (6-Thio-GTP) to Rac1 instead of GTP.	Azathioprine	129-141	Rac family small GTPase 1	Homo sapiens	94-98
12697733-5	2003	Apoptosis induction required costimulation with CD28 and was mediated by specific blockade of Rac1 activation through binding of azathioprine-generated 6-thioguanine triphosphate (6-Thio-GTP) to Rac1 instead of GTP.	Azathioprine	129-141	Rac family small GTPase 1	Homo sapiens	195-199
12697733-7	2003	Azathioprine thus converts a costimulatory signal into an apoptotic signal by modulating Rac1 activity.	Azathioprine	0-12	Rac family small GTPase 1	Homo sapiens	89-93
12665573-8	2003	DNMT1 and -3b displayed the greatest in vivo binding avidity for aza-dC-containing genomic DNA in these cells.	Azathioprine	65-68	DNA methyltransferase 1	Homo sapiens	0-13
12773967-6	2003	The IL-2R mAbs have been used with a variety of maintenance immunosuppression regimens double therapy with cyclosporine and prednisone, triple therapy with cyclosporine, azathioprine and prednisone and with newer regimens such as cyclosporine or tacrolimus, mycophenolate mofetil (MMF) and prednisone, and most recently with sirolimus, MMF and prednisone.	Azathioprine	170-182	interleukin 2 receptor subunit alpha	Homo sapiens	4-9
12643897-0	2003	Synthesis of aza and oxaglutamyl-p-nitroanilide derivatives and their kinetic studies with gamma-glutamyltranspeptidase.	Azathioprine	13-16	gamma-glutamyltransferase 1	Rattus norvegicus	91-119
12558400-0	2003	An asymmetric synthesis of aza analogues of the tricyclic skeleton of daphnane and the ABC ring system of phorbol.	Azathioprine	27-30	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	87-90
12558400-1	2003	An asymmetric synthesis of aza analogues of the ABC ring system of phorbol and related compounds containing the 5-7-6-fused framework of daphnane involved construction of the central seven-membered ring by a regioselective reduction of a chiral imide and cyclization with trifluoromethanesulfonic acid.	Azathioprine	27-30	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	48-51
12492733-1	2003	BACKGROUND: Inter-individual response to azathioprine is partly due to inter-individual variation in the thiopurine methyltransferase (TPMT) activity.	Azathioprine	41-53	thiopurine S-methyltransferase	Homo sapiens	105-133
12492733-1	2003	BACKGROUND: Inter-individual response to azathioprine is partly due to inter-individual variation in the thiopurine methyltransferase (TPMT) activity.	Azathioprine	41-53	thiopurine S-methyltransferase	Homo sapiens	135-139
12492734-1	2003	BACKGROUND: Azathioprine (AZA) and its active metabolite mercaptopurine (MP) are frequently used in the management of inflammatory bowel disease.	Azathioprine	12-24	azurocidin 1	Homo sapiens	26-29
14614765-6	2003	Other agents that nonspecifically inhibit TNFalpha release include methotrexate, azathioprine and pentoxifylline.	Azathioprine	81-93	tumor necrosis factor	Homo sapiens	42-50
12477776-0	2003	Safe treatment of thiopurine S-methyltransferase deficient Crohn"s disease patients with azathioprine.	Azathioprine	89-101	thiopurine S-methyltransferase	Homo sapiens	18-48
12477776-1	2003	Thiopurine S-methyltransferase (TPMT) deficient patients develop life threatening haematotoxicity (for example, pancytopenia) when treated with a standard dose of azathioprine (AZA) and 6-mercaptopurine (6-MP) due to excessive accumulation of cytotoxic metabolites.	Azathioprine	163-175	thiopurine S-methyltransferase	Homo sapiens	0-30
12477776-1	2003	Thiopurine S-methyltransferase (TPMT) deficient patients develop life threatening haematotoxicity (for example, pancytopenia) when treated with a standard dose of azathioprine (AZA) and 6-mercaptopurine (6-MP) due to excessive accumulation of cytotoxic metabolites.	Azathioprine	163-175	thiopurine S-methyltransferase	Homo sapiens	32-36
12477776-1	2003	Thiopurine S-methyltransferase (TPMT) deficient patients develop life threatening haematotoxicity (for example, pancytopenia) when treated with a standard dose of azathioprine (AZA) and 6-mercaptopurine (6-MP) due to excessive accumulation of cytotoxic metabolites.	Azathioprine	177-180	thiopurine S-methyltransferase	Homo sapiens	0-30
12477776-1	2003	Thiopurine S-methyltransferase (TPMT) deficient patients develop life threatening haematotoxicity (for example, pancytopenia) when treated with a standard dose of azathioprine (AZA) and 6-mercaptopurine (6-MP) due to excessive accumulation of cytotoxic metabolites.	Azathioprine	177-180	thiopurine S-methyltransferase	Homo sapiens	32-36
14505127-6	2003	To investigate the frequency of TPMT mutation, findings for 82 patients among 141 patients with UC or CD who were treated with AZA or 6-MP were analyzed retrospectively.	Azathioprine	127-130	thiopurine S-methyltransferase	Homo sapiens	32-36
14505127-16	2003	Seven of 8 patients (88%) who developed bone marrow suppression with a low dose of AZA had a mutant TPMT allele.	Azathioprine	83-86	thiopurine S-methyltransferase	Homo sapiens	100-104
14505127-23	2003	Investigation of the TPMT allele may be useful for predicting the appearance of bone marrow suppression, when low-dose 6-MP or AZA is given.	Azathioprine	127-130	thiopurine S-methyltransferase	Homo sapiens	21-25
14505139-0	2003	Role and side-effects of TPMT polymorphisms of 6-MP and azathioprine in the treatment of steroid-resistant and -dependent ulcerative colitis.	Azathioprine	56-68	thiopurine S-methyltransferase	Homo sapiens	25-29
12616032-14	2003	CONCLUSION: Treatment with prednisolone and azathioprine is beneficial in ameliorating the clinical course of a subset of IgAN patients with heavy proteinuria or impaired renal function.	Azathioprine	44-56	IGAN1	Homo sapiens	122-126
12509149-5	2003	As regards the Franck-Condon excited states of aza-derivatives, our theoretical results show that the first singlet excited state has (piH, piL*) character in all compounds except for E-4,4"-dipyridylethene, where S1 has (n, pi*) character in non-polar solvent.	Azathioprine	47-50	serpin family A member 2 (gene/pseudogene)	Homo sapiens	140-143
12509611-0	2003	Is thiopurine methyltransferase genetic polymorphism a major factor for withdrawal of azathioprine in rheumatoid arthritis patients?	Azathioprine	86-98	thiopurine S-methyltransferase	Homo sapiens	3-31
12509611-1	2003	OBJECTIVE: To determine whether the presence of thiopurine methyltransferase (TPMT) alleles associated with reduced or absent activity of thiopurine methyltransferase is a major factor for withdrawal of azathioprine (AZA) in rheumatoid arthritis (RA) patients.	Azathioprine	203-215	thiopurine S-methyltransferase	Homo sapiens	48-76
12509611-1	2003	OBJECTIVE: To determine whether the presence of thiopurine methyltransferase (TPMT) alleles associated with reduced or absent activity of thiopurine methyltransferase is a major factor for withdrawal of azathioprine (AZA) in rheumatoid arthritis (RA) patients.	Azathioprine	203-215	thiopurine S-methyltransferase	Homo sapiens	78-82
12509611-1	2003	OBJECTIVE: To determine whether the presence of thiopurine methyltransferase (TPMT) alleles associated with reduced or absent activity of thiopurine methyltransferase is a major factor for withdrawal of azathioprine (AZA) in rheumatoid arthritis (RA) patients.	Azathioprine	203-215	thiopurine S-methyltransferase	Homo sapiens	138-166
12509611-1	2003	OBJECTIVE: To determine whether the presence of thiopurine methyltransferase (TPMT) alleles associated with reduced or absent activity of thiopurine methyltransferase is a major factor for withdrawal of azathioprine (AZA) in rheumatoid arthritis (RA) patients.	Azathioprine	217-220	thiopurine S-methyltransferase	Homo sapiens	48-76
12509611-1	2003	OBJECTIVE: To determine whether the presence of thiopurine methyltransferase (TPMT) alleles associated with reduced or absent activity of thiopurine methyltransferase is a major factor for withdrawal of azathioprine (AZA) in rheumatoid arthritis (RA) patients.	Azathioprine	217-220	thiopurine S-methyltransferase	Homo sapiens	78-82
12509611-1	2003	OBJECTIVE: To determine whether the presence of thiopurine methyltransferase (TPMT) alleles associated with reduced or absent activity of thiopurine methyltransferase is a major factor for withdrawal of azathioprine (AZA) in rheumatoid arthritis (RA) patients.	Azathioprine	217-220	thiopurine S-methyltransferase	Homo sapiens	138-166
12509611-8	2003	TPMT genotyping may allow the use of high doses of AZA in patients with normal TPMT alleles to improve the efficacy of this immunosuppressive drug.	Azathioprine	51-54	thiopurine S-methyltransferase	Homo sapiens	0-4
12509611-8	2003	TPMT genotyping may allow the use of high doses of AZA in patients with normal TPMT alleles to improve the efficacy of this immunosuppressive drug.	Azathioprine	51-54	thiopurine S-methyltransferase	Homo sapiens	79-83
12684587-5	2003	Measurement of 6-MP metabolite levels and TPMT molecular analysis provide clinicians with useful tools for optimizing therapeutic response to 6-MP/AZA, as well as for identifying individuals at increased risk for drug-induced toxicity.	Azathioprine	147-150	thiopurine S-methyltransferase	Homo sapiens	42-46
12465143-0	2002	Practical pharmacogenetics: the cost effectiveness of screening for thiopurine s-methyltransferase polymorphisms in patients with rheumatological conditions treated with azathioprine.	Azathioprine	170-182	thiopurine S-methyltransferase	Homo sapiens	68-98
12465143-1	2002	OBJECTIVE: Thiopurine S-methyltransferase (TPMT), which catalyzes the inactivation of azathioprine (AZA), exhibits genetic polymorphism that results in dose related, serious toxicities (mainly hematological cytopenias) in 10-15% of individuals treated with AZA.	Azathioprine	86-98	thiopurine S-methyltransferase	Homo sapiens	11-41
12465143-1	2002	OBJECTIVE: Thiopurine S-methyltransferase (TPMT), which catalyzes the inactivation of azathioprine (AZA), exhibits genetic polymorphism that results in dose related, serious toxicities (mainly hematological cytopenias) in 10-15% of individuals treated with AZA.	Azathioprine	86-98	thiopurine S-methyltransferase	Homo sapiens	43-47
12465143-1	2002	OBJECTIVE: Thiopurine S-methyltransferase (TPMT), which catalyzes the inactivation of azathioprine (AZA), exhibits genetic polymorphism that results in dose related, serious toxicities (mainly hematological cytopenias) in 10-15% of individuals treated with AZA.	Azathioprine	100-103	thiopurine S-methyltransferase	Homo sapiens	11-41
12465143-1	2002	OBJECTIVE: Thiopurine S-methyltransferase (TPMT), which catalyzes the inactivation of azathioprine (AZA), exhibits genetic polymorphism that results in dose related, serious toxicities (mainly hematological cytopenias) in 10-15% of individuals treated with AZA.	Azathioprine	100-103	thiopurine S-methyltransferase	Homo sapiens	43-47
12465143-1	2002	OBJECTIVE: Thiopurine S-methyltransferase (TPMT), which catalyzes the inactivation of azathioprine (AZA), exhibits genetic polymorphism that results in dose related, serious toxicities (mainly hematological cytopenias) in 10-15% of individuals treated with AZA.	Azathioprine	257-260	thiopurine S-methyltransferase	Homo sapiens	11-41
12269967-2	2002	Patients with thiopurine methyltransferase (TPMT) deficiency are intolerant to azathioprine, whilst carriers are at increased risk of side-effects.	Azathioprine	79-91	thiopurine S-methyltransferase	Homo sapiens	14-42
12269967-2	2002	Patients with thiopurine methyltransferase (TPMT) deficiency are intolerant to azathioprine, whilst carriers are at increased risk of side-effects.	Azathioprine	79-91	thiopurine S-methyltransferase	Homo sapiens	44-48
12269967-3	2002	AIM: To evaluate the importance of TPMT activity in the management of azathioprine therapy in inflammatory bowel disease.	Azathioprine	70-82	thiopurine S-methyltransferase	Homo sapiens	35-39
12269967-11	2002	CONCLUSIONS: Inflammatory bowel disease patients with intermediate TPMT activity have an increased risk of azathioprine toxicity.	Azathioprine	107-119	thiopurine S-methyltransferase	Homo sapiens	67-71
12386643-7	2002	When stimulated with 2-micromol/L thrombin receptor-activating peptide, CD62 expression in platelets from patients treated with azathioprine (63% +/- 17%; P <.05), cyclosporine (51% +/- 23%; P <.05), and tacrolimus (50% +/- 22%; P <.05) was elevated compared with control subjects (33% +/- 19%).	Azathioprine	128-140	selectin P	Homo sapiens	72-76
12509149-5	2003	As regards the Franck-Condon excited states of aza-derivatives, our theoretical results show that the first singlet excited state has (piH, piL*) character in all compounds except for E-4,4"-dipyridylethene, where S1 has (n, pi*) character in non-polar solvent.	Azathioprine	47-50	pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included)	Homo sapiens	135-138
12465143-1	2002	OBJECTIVE: Thiopurine S-methyltransferase (TPMT), which catalyzes the inactivation of azathioprine (AZA), exhibits genetic polymorphism that results in dose related, serious toxicities (mainly hematological cytopenias) in 10-15% of individuals treated with AZA.	Azathioprine	257-260	thiopurine S-methyltransferase	Homo sapiens	43-47
12386643-8	2002	PAC1 expression was significantly increased in the patient groups that received azathioprine and cyclosporine.	Azathioprine	80-92	ADCYAP receptor type I	Homo sapiens	0-4
12135816-1	2002	BACKGROUND: Thiopurine S-methyltransferase (TPMT), which exhibits autosomal codominant polymorphism, plays an important role in the metabolism of thiopurine drugs such as mercaptopurine, thioguanine and azathioprine.	Azathioprine	203-215	thiopurine S-methyltransferase	Homo sapiens	12-42
12217596-0	2002	Thiopurine methyltransferase phenotype and genotype in relation to azathioprine therapy in autoimmune hepatitis.	Azathioprine	67-79	thiopurine S-methyltransferase	Homo sapiens	0-28
12217596-1	2002	BACKGROUND/AIMS: Toxicity and efficacy of azathioprine is governed partly by the activity of thiopurine methyltransferase (TPMT).	Azathioprine	42-54	thiopurine S-methyltransferase	Homo sapiens	93-121
12217596-1	2002	BACKGROUND/AIMS: Toxicity and efficacy of azathioprine is governed partly by the activity of thiopurine methyltransferase (TPMT).	Azathioprine	42-54	thiopurine S-methyltransferase	Homo sapiens	123-127
12217596-4	2002	RESULTS: TPMT activities were significantly lower in patients intolerant of azathioprine (group I, n=15) than in those who sustained remission on azathioprine alone (group II, n=28; P=0.003) and those who tolerated azathioprine but continued to require corticosteroids (group III, n=29; P<0.0001), and were higher in group III than in group II (P=0.034).	Azathioprine	76-88	thiopurine S-methyltransferase	Homo sapiens	9-13
12361557-0	2002	[Individualized therapy with azathioprine or 6-mercaptopurine by monitoring thiopurine methyl-transferase (TPMT) activity].	Azathioprine	29-41	thiopurine S-methyltransferase	Homo sapiens	76-105
12361557-0	2002	[Individualized therapy with azathioprine or 6-mercaptopurine by monitoring thiopurine methyl-transferase (TPMT) activity].	Azathioprine	29-41	thiopurine S-methyltransferase	Homo sapiens	107-111
12135816-1	2002	BACKGROUND: Thiopurine S-methyltransferase (TPMT), which exhibits autosomal codominant polymorphism, plays an important role in the metabolism of thiopurine drugs such as mercaptopurine, thioguanine and azathioprine.	Azathioprine	203-215	thiopurine S-methyltransferase	Homo sapiens	44-48
12055182-7	2002	By chromatin immunoprecipitation assays, we observed in vivo binding of MeCP2 and MBD2 to the 5"-end of H-rev107 in WEHI 7.1 cells, which was reduced to undetectable levels upon 5-aza-dC treatment, concluding that MeCP2 and MBD2 might be involved in silencing the methylated H-rev107 gene in lymphoma cells and probably certain tumors.	Azathioprine	180-183	methyl CpG binding protein 2	Mus musculus	72-77
12352910-10	2002	CONCLUSIONS: Replacement of MMF by AZA after 3 months of therapy with ME-CsA and steroids provides comparable efficacy and safety profiles to continuous MMF over 12 months.	Azathioprine	35-38	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	70-76
12192200-0	2002	Determination of thiopurine methyltransferase genotype or phenotype optimizes initial dosing of azathioprine for the treatment of Crohn"s disease.	Azathioprine	96-108	thiopurine S-methyltransferase	Homo sapiens	17-45
12192200-2	2002	Thiopurine methyltransferase (TPMT) is an enzyme responsible for the metabolism of AZA, and its activity is inversely related to the risk of developing acute leukopenia.	Azathioprine	83-86	thiopurine S-methyltransferase	Homo sapiens	0-28
12192200-2	2002	Thiopurine methyltransferase (TPMT) is an enzyme responsible for the metabolism of AZA, and its activity is inversely related to the risk of developing acute leukopenia.	Azathioprine	83-86	thiopurine S-methyltransferase	Homo sapiens	30-34
12192200-3	2002	GOALS: the aim of this retrospective study is to determine whether initial AZA dosing based on TPMT genotype or phenotype alters the likelihood of developing acute leukopenia.	Azathioprine	75-78	thiopurine S-methyltransferase	Homo sapiens	95-99
12055182-7	2002	By chromatin immunoprecipitation assays, we observed in vivo binding of MeCP2 and MBD2 to the 5"-end of H-rev107 in WEHI 7.1 cells, which was reduced to undetectable levels upon 5-aza-dC treatment, concluding that MeCP2 and MBD2 might be involved in silencing the methylated H-rev107 gene in lymphoma cells and probably certain tumors.	Azathioprine	180-183	methyl-CpG binding domain protein 2	Mus musculus	82-86
12055182-7	2002	By chromatin immunoprecipitation assays, we observed in vivo binding of MeCP2 and MBD2 to the 5"-end of H-rev107 in WEHI 7.1 cells, which was reduced to undetectable levels upon 5-aza-dC treatment, concluding that MeCP2 and MBD2 might be involved in silencing the methylated H-rev107 gene in lymphoma cells and probably certain tumors.	Azathioprine	180-183	phospholipase A and acyltransferase 3	Mus musculus	104-112
12117866-0	2002	TPMT in the treatment of Crohn"s disease with azathioprine.	Azathioprine	46-58	thiopurine S-methyltransferase	Homo sapiens	0-4
12117866-2	2002	At the start of azathioprine or mercaptopurine therapy, measurement of TPMT activity has a role in identifying the 1 in 300 patients who are at risk of severe myelosuppression when treated with standard thiopurine dosages.	Azathioprine	16-28	thiopurine S-methyltransferase	Homo sapiens	71-75
12117866-3	2002	During the initial months of azathioprine therapy a knowledge of TPMT status warns of early bone marrow toxicity.	Azathioprine	29-41	thiopurine S-methyltransferase	Homo sapiens	65-69
12172211-0	2002	Azathioprine therapy and adverse drug reactions in patients with inflammatory bowel disease: impact of thiopurine S-methyltransferase polymorphism.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	103-133
12172211-3	2002	Whereas azathioprine-related pancytopenia has been clearly linked to thiopurine S-methyltransferase (TPMT) polymorphism limited data are available to explain gastrointestinal side effects.	Azathioprine	8-20	thiopurine S-methyltransferase	Homo sapiens	69-99
12172211-3	2002	Whereas azathioprine-related pancytopenia has been clearly linked to thiopurine S-methyltransferase (TPMT) polymorphism limited data are available to explain gastrointestinal side effects.	Azathioprine	8-20	thiopurine S-methyltransferase	Homo sapiens	101-105
12172211-4	2002	In a retrospective analysis of 93 adults with IBD and azathioprine therapy both phenotyping and genotyping was used to explore systematically the relationship between TPMT and azathioprine-related adverse reactions.	Azathioprine	54-66	thiopurine S-methyltransferase	Homo sapiens	167-171
12172211-4	2002	In a retrospective analysis of 93 adults with IBD and azathioprine therapy both phenotyping and genotyping was used to explore systematically the relationship between TPMT and azathioprine-related adverse reactions.	Azathioprine	176-188	thiopurine S-methyltransferase	Homo sapiens	167-171
12021625-1	2002	This study examined the role of thiopurine methyltransferase (TPMT) polymorphism in the metabolism and clinical effects of azathioprine and 6-mercaptopurine in the treatment of inflammatory bowel disease and childhood leukemia.	Azathioprine	123-135	thiopurine S-methyltransferase	Homo sapiens	32-60
12168480-8	2002	CONCLUSION: This is the first report of an erythema gyratum repens in association with azathioprine treatment in an autoimmune hepatitis type I patient with proven common polymorphism in the TPMT gene.	Azathioprine	87-99	thiopurine S-methyltransferase	Homo sapiens	191-195
12096148-1	2002	BACKGROUND: Individuals with low activity of a key metabolic enzyme, thiopurine methyl transferase (TPMT), are more susceptible to azathioprine-induced myelosuppression.	Azathioprine	131-143	thiopurine S-methyltransferase	Homo sapiens	69-98
12096148-1	2002	BACKGROUND: Individuals with low activity of a key metabolic enzyme, thiopurine methyl transferase (TPMT), are more susceptible to azathioprine-induced myelosuppression.	Azathioprine	131-143	thiopurine S-methyltransferase	Homo sapiens	100-104
12021625-1	2002	This study examined the role of thiopurine methyltransferase (TPMT) polymorphism in the metabolism and clinical effects of azathioprine and 6-mercaptopurine in the treatment of inflammatory bowel disease and childhood leukemia.	Azathioprine	123-135	thiopurine S-methyltransferase	Homo sapiens	62-66
12021625-4	2002	The authors assayed the TPMT activity in red blood cells from 122 patients treated with azathioprine or 6-mercaptopurine (83 adults with inflammatory bowel disease and 39 children with acute lymphoblastic leukemia) and in 290 untreated controls (219 adult blood donors and 71 children).	Azathioprine	88-100	thiopurine S-methyltransferase	Homo sapiens	24-28
11982569-0	2002	Clinical improvement and significant reduction of total serum IgE in patients suffering from severe atopic dermatitis treated with oral azathioprine.	Azathioprine	136-148	immunoglobulin heavy constant epsilon	Homo sapiens	62-65
11982569-2	2002	The aim of this retrospective case series was to examine the effect of oral azathioprine on the clinical severity and serum IgE levels in 38 patients with severe atopic dermatitis.	Azathioprine	76-88	immunoglobulin heavy constant epsilon	Homo sapiens	124-127
11886398-6	2002	After Azathioprine and corticosteroid treatment, the anti-VWF antibody disappeared and the patient"s haemostatic profile normalized, except for the platelet VWF content which still remained decreased.	Azathioprine	6-18	von Willebrand factor	Homo sapiens	58-61
11834357-3	2002	The results demonstrate that patients taking MMF instead of azathioprine generated significantly fewer de novo anti-vimentin antibodies.	Azathioprine	60-72	vimentin	Homo sapiens	116-124
11579291-2	2001	Allografts obliterate within 3 weeks, the immunosuppression cyclosporine (CsA)-azathioprine (AZA)-methylprednisolone (MP) delays OB, but OB is prevented when AZA is switched to 40-0-(2-hydroxyethyl)-rapamycin (RAD).	Azathioprine	79-91	RRAD, Ras related glycolysis inhibitor and calcium channel regulator	Homo sapiens	210-213
12090325-5	2002	Considering that mild IgAN may be an early stage of the disease and can be reversed by immunosuppressive agents we have used prednisolone and azathioprine in patients with isolated hematuria in a prospective, randomized, controlled study since 1988.	Azathioprine	142-154	IGAN1	Homo sapiens	22-26
12090325-6	2002	In this prospective study we have evaluated the effect of prednisolone with azathioprine on the clinical course of IgAN and its impact on histologic parameters and prevention of progression in patients with isolated hematuria.	Azathioprine	76-88	IGAN1	Homo sapiens	115-119
12090325-17	2002	We conclude that early treatment with prednisolone and azathioprine appears to be beneficial in preventing the progression of immunologic renal injury and in improving histopathological features in IgAN patients with isolated hematuria.	Azathioprine	55-67	IGAN1	Homo sapiens	198-202
11907637-6	2001	We investigated 10 patients receiving immunosuppressive therapy consisting of cyclosporine A, prednisone, and azathioprine who had increased concentrations of LDL-cholesterol (LDL-C), and 10 age-matched healthy controls.	Azathioprine	110-122	component of oligomeric golgi complex 2	Homo sapiens	176-181
11750393-0	2001	Effects of mycophenolate mofetil and azathioprine on the erythropoietin production in renal transplant recipients.	Azathioprine	37-49	erythropoietin	Homo sapiens	57-71
11579291-2	2001	Allografts obliterate within 3 weeks, the immunosuppression cyclosporine (CsA)-azathioprine (AZA)-methylprednisolone (MP) delays OB, but OB is prevented when AZA is switched to 40-0-(2-hydroxyethyl)-rapamycin (RAD).	Azathioprine	93-96	RRAD, Ras related glycolysis inhibitor and calcium channel regulator	Homo sapiens	210-213
11304783-1	2001	PURPOSE: To assess thiopurine S-methyltransferase (TPMT) phenotype and genotype in patients who were intolerant to treatment with mercaptopurine (MP) or azathioprine (AZA), and to evaluate their clinical management.	Azathioprine	153-165	thiopurine S-methyltransferase	Homo sapiens	19-49
11680327-10	2001	CONCLUSION: Early "high-dose" IS therapy using azathioprine and prednisone in GMG resulted in a significant increase in the number of patients in remission and reduced morbidity at 1 and 2 years.	Azathioprine	47-59	angiotensin II receptor type 1	Homo sapiens	178-188
11485170-5	2001	The nitrogen atom attached to the carbon cage formed a "[5,6]open" type aza substructure, which was confirmed by the appearance of 31-32 signals in the region of deltaC 133-148 (carbon shifts of Sp2 carbons of the cage) in the 13C nuclear magnetic resonance spectra.	Azathioprine	72-75	Sp2 transcription factor	Homo sapiens	195-198
11344381-0	2001	High 6-thioguanine nucleotide levels and low thiopurine methyltransferase activity in patients with lupus erythematosus treated with azathioprine.	Azathioprine	133-145	thiopurine S-methyltransferase	Homo sapiens	45-73
11417444-11	2001	In patients treated with azathioprine, the TPMT activity showed a slow increase that declined to pre-treatment values when azathioprine was withdrawn.	Azathioprine	25-37	thiopurine S-methyltransferase	Homo sapiens	43-47
11417444-11	2001	In patients treated with azathioprine, the TPMT activity showed a slow increase that declined to pre-treatment values when azathioprine was withdrawn.	Azathioprine	123-135	thiopurine S-methyltransferase	Homo sapiens	43-47
11417444-15	2001	In patients treated with azathioprine after renal transplantation, the observed increase of TPMT activity could possibly be the result of enzyme induction.	Azathioprine	25-37	thiopurine S-methyltransferase	Homo sapiens	92-96
11383598-8	2001	Under azathioprine, gastroduodenal and intestinal permeability, CDAI, and C-reactive protein decreased.	Azathioprine	6-18	C-reactive protein	Homo sapiens	74-92
11304783-1	2001	PURPOSE: To assess thiopurine S-methyltransferase (TPMT) phenotype and genotype in patients who were intolerant to treatment with mercaptopurine (MP) or azathioprine (AZA), and to evaluate their clinical management.	Azathioprine	153-165	thiopurine S-methyltransferase	Homo sapiens	51-55
11304783-1	2001	PURPOSE: To assess thiopurine S-methyltransferase (TPMT) phenotype and genotype in patients who were intolerant to treatment with mercaptopurine (MP) or azathioprine (AZA), and to evaluate their clinical management.	Azathioprine	167-170	thiopurine S-methyltransferase	Homo sapiens	19-49
11707060-15	2001	Both mercaptopurine and azathioprine have a short t1/2beta (1 to 2 hours), but the t1/2beta of 6-TGN ranges from 3 to 13 days.	Azathioprine	24-36	CD5 molecule	Homo sapiens	50-58
11354662-0	2001	Aza analogues of thalidomide: synthesis and evaluation as inhibitors of tumor necrosis factor-alpha production in vitro.	Azathioprine	0-3	tumor necrosis factor	Homo sapiens	72-99
11337944-1	2001	Polymorphisms at three loci in the thiopurine methyltransferase (TPMT) gene are known to be responsible for azathioprine and 6-mercaptopurine (6MP) toxicity.	Azathioprine	108-120	thiopurine S-methyltransferase	Homo sapiens	35-63
11337944-1	2001	Polymorphisms at three loci in the thiopurine methyltransferase (TPMT) gene are known to be responsible for azathioprine and 6-mercaptopurine (6MP) toxicity.	Azathioprine	108-120	thiopurine S-methyltransferase	Homo sapiens	65-69
11337944-3	2001	The allele frequency was different from that in Caucasians, and investigation of TPMT polymorphisms with consideration of ethnic differences before administration of azathioprine or 6MP may provide clinically useful information.	Azathioprine	166-178	thiopurine S-methyltransferase	Homo sapiens	81-85
11264639-6	2001	As a consequence of the lower clearance of basiliximab, the durations of CD25 saturation were prolonged in the presence of azathioprine (50+/-20 d; range, 13--84) and mycophenolate mofetil (59+/-17 d; range, 28--94) compared with dual therapy (36+/-14 d; range, 12--91).	Azathioprine	123-135	interleukin 2 receptor subunit alpha	Homo sapiens	73-77
11264639-10	2001	The average duration of CD25 saturation was prolonged by 39 and 64% in the presence of azathioprine and mycophenolate mofetil, respectively.	Azathioprine	87-99	interleukin 2 receptor subunit alpha	Homo sapiens	24-28
11480208-2	2001	Azathioprine treatment caused an increase in serum albumin/globin ratio and a decrease in total protein in spleen tissue.	Azathioprine	0-12	albumin	Mus musculus	45-58
11179762-1	2001	The level of expression of the enzyme thiopurine methyltransferase (TPMT) is an important determinant of the metabolism of drugs used both in the treatment of acute leukaemia (6-mercaptopurine and 6-thioguanine) and as an immunosuppressant in patients with autoimmune diseases or following organ transplantation (azathioprine).	Azathioprine	313-325	thiopurine S-methyltransferase	Homo sapiens	38-66
11179762-1	2001	The level of expression of the enzyme thiopurine methyltransferase (TPMT) is an important determinant of the metabolism of drugs used both in the treatment of acute leukaemia (6-mercaptopurine and 6-thioguanine) and as an immunosuppressant in patients with autoimmune diseases or following organ transplantation (azathioprine).	Azathioprine	313-325	thiopurine S-methyltransferase	Homo sapiens	68-72
11707060-13	2001	Both mercaptopurine and its prodrug azathioprine are metabolised to active compounds (6-thioguanine nucleotides; 6-TGN) by hypoxanthine-guanine phosphoribosyltransferase and to inactive metabolites by the polymorphically expressed thiopurine S-methyltransferase (TPMT) and xanthine oxidase.	Azathioprine	36-48	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	123-169
11707060-13	2001	Both mercaptopurine and its prodrug azathioprine are metabolised to active compounds (6-thioguanine nucleotides; 6-TGN) by hypoxanthine-guanine phosphoribosyltransferase and to inactive metabolites by the polymorphically expressed thiopurine S-methyltransferase (TPMT) and xanthine oxidase.	Azathioprine	36-48	thiopurine S-methyltransferase	Homo sapiens	231-261
11707060-13	2001	Both mercaptopurine and its prodrug azathioprine are metabolised to active compounds (6-thioguanine nucleotides; 6-TGN) by hypoxanthine-guanine phosphoribosyltransferase and to inactive metabolites by the polymorphically expressed thiopurine S-methyltransferase (TPMT) and xanthine oxidase.	Azathioprine	36-48	thiopurine S-methyltransferase	Homo sapiens	263-267
11073627-0	2000	Modification of the aza-robinson annulation for the synthesis of 4-methyl-benzo[c]quinolizin-3-ones, potent inhibitors of steroid 5alpha-reductase 1.	Azathioprine	20-24	steroid 5 alpha-reductase 1	Homo sapiens	122-148
11165712-5	2001	Granulysin was studied in phytohemagglutinin (PHA) stimulated cell lines (donor PBL and CD45RO(+) T cells) by FACS, Western blotting, and RT-PCR after pretreating with cyclosporine A (CSA), azathioprine, mycophenolic acid, and steroids.	Azathioprine	190-202	granulysin	Homo sapiens	0-10
11165712-9	2001	Granulysin levels were unchanged after azathioprine and mycophenolic acid treatment, decreased after treating activated PBL with steroids and cyclosporine A (CSA), and paradoxically, increased (p < 0.05) after treating CD45RO(+) CTL with CSA.	Azathioprine	39-51	granulysin	Homo sapiens	0-10
11134264-0	2001	Long-term results of TPMT activity monitoring in azathioprine-treated renal allograft recipients.	Azathioprine	49-61	thiopurine S-methyltransferase	Homo sapiens	21-25
11134264-1	2001	Thiopurine methyltransferase (TPMT) is implicated in the metabolism of azathioprine.	Azathioprine	71-83	thiopurine S-methyltransferase	Homo sapiens	0-28
11134264-1	2001	Thiopurine methyltransferase (TPMT) is implicated in the metabolism of azathioprine.	Azathioprine	71-83	thiopurine S-methyltransferase	Homo sapiens	30-34
11134264-2	2001	The consequences of differential TPMT activity induction by azathioprine on the long-term results after renal transplantation were investigated.	Azathioprine	60-72	thiopurine S-methyltransferase	Homo sapiens	33-37
11134264-14	2001	TPMT activity induction was observed in 57% of renal transplant recipients who received azathioprine.	Azathioprine	88-100	thiopurine S-methyltransferase	Homo sapiens	0-4
11134264-16	2001	The appropriate conversion from azathioprine, which is a pro-drug, into 6-mercaptopurine could explain both better graft outcome and TPMT induction.	Azathioprine	32-44	thiopurine S-methyltransferase	Homo sapiens	133-137
11574780-6	2001	Tumour response to in vivo drug treatment was associated with an early down-regulation of Bcl-2, which was somewhat more marked for the aza compound.	Azathioprine	136-139	BCL2 apoptosis regulator	Homo sapiens	90-95
11149863-0	2000	The aza- The inclusion of a C-2 trialkylsilyl substituent into allylic amine precursors allows the base-induced aza-[2,3]-Wittig sigmatropic rearrangement to proceed in excellent yield and diastereoselectivity.	Azathioprine	4-7	complement C2	Homo sapiens	28-31
11025471-1	2000	BACKGROUND: Thiopurine S-methyltransferase (TPMT) catalyzes the S-methylation (inactivation) of mercaptopurine, azathioprine, and thioguanine, and exhibits genetic variation.	Azathioprine	112-124	thiopurine S-methyltransferase	Homo sapiens	12-42
11048998-4	2000	IL-2 receptor antibodies have been shown to decrease rejection rates when added to a regimen of cyclosporine (CsA), azathioprine and prednisone.	Azathioprine	116-128	interleukin 2 receptor subunit beta	Homo sapiens	0-13
11025471-1	2000	BACKGROUND: Thiopurine S-methyltransferase (TPMT) catalyzes the S-methylation (inactivation) of mercaptopurine, azathioprine, and thioguanine, and exhibits genetic variation.	Azathioprine	112-124	thiopurine S-methyltransferase	Homo sapiens	44-48
11007234-1	2000	OBJECTIVE: Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that catalyzes the inactivation of mercaptopurine, azathioprine, and thioguanine.	Azathioprine	122-134	thiopurine S-methyltransferase	Homo sapiens	11-41
11064448-2	2000	We report two patients who developed the first manifestations of clinically definite multiple sclerosis while on long term (3.5 and 10 years, respectively) treatment with azathioprine for Crohn"s disease.	Azathioprine	171-183	MS	Homo sapiens	85-103
11093885-0	2000	[Aplasia after azathioprine administration: role of the thiopurine methyltransferase genetic polymorphism].	Azathioprine	15-27	thiopurine S-methyltransferase	Homo sapiens	56-84
11093885-2	2000	Adverse effects during treatment are related to the activity of thiopurine methyltransferase (TPMT), an enzyme which plays a role in azathioprine metabolism.	Azathioprine	133-145	thiopurine S-methyltransferase	Homo sapiens	64-92
11093885-2	2000	Adverse effects during treatment are related to the activity of thiopurine methyltransferase (TPMT), an enzyme which plays a role in azathioprine metabolism.	Azathioprine	133-145	thiopurine S-methyltransferase	Homo sapiens	94-98
11093885-3	2000	The presence of the allelic variants of the TPMT gene allows us to classify patients into three different groups: high, moderate and low risk of myelosuppression after receiving standard doses of azathioprine.	Azathioprine	196-208	thiopurine S-methyltransferase	Homo sapiens	44-48
11093885-4	2000	PATIENTS AND METHODS: Study of the allelic variants of the TPMT gene in the positions 460 and 719 with PCR methods in a patient with Crohn"s disease, who developed aplasia after receiving azathioprine.	Azathioprine	188-200	thiopurine S-methyltransferase	Homo sapiens	59-63
11093885-8	2000	CONCLUSIONS: Genotyping the allelic variants of the TPMT gene is a useful method to identify patients at moderate or high risk of myelosuppression after administration of azathioprine.	Azathioprine	171-183	thiopurine S-methyltransferase	Homo sapiens	52-56
11007234-1	2000	OBJECTIVE: Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that catalyzes the inactivation of mercaptopurine, azathioprine, and thioguanine.	Azathioprine	122-134	thiopurine S-methyltransferase	Homo sapiens	43-47
11012112-1	2000	Our objective was to determine if thiopurine methyltransferase (TPMT), the enzyme important in the metabolism of azathioprine in human beings, is detectable in red blood cell lysates (RBCL) of healthy dogs, cats, and horses.	Azathioprine	113-125	thiopurine S-methyltransferase	Homo sapiens	34-62
10993211-1	2000	Thiopurine methyltransferase (TPMT) catalyzes the metabolism of important drugs such as 6-mercaptopurine, 6-thioguanine, and azathioprine.	Azathioprine	125-137	thiopurine S-methyltransferase	Homo sapiens	0-28
10993211-1	2000	Thiopurine methyltransferase (TPMT) catalyzes the metabolism of important drugs such as 6-mercaptopurine, 6-thioguanine, and azathioprine.	Azathioprine	125-137	thiopurine S-methyltransferase	Homo sapiens	30-34
11012112-1	2000	Our objective was to determine if thiopurine methyltransferase (TPMT), the enzyme important in the metabolism of azathioprine in human beings, is detectable in red blood cell lysates (RBCL) of healthy dogs, cats, and horses.	Azathioprine	113-125	thiopurine S-methyltransferase	Homo sapiens	64-68
11012121-3	2000	Adverse reactions to azathioprine in humans have been correlated with reduced activity of thiopurine methyltransferase (TPMT) in erythrocytes.	Azathioprine	21-33	thiopurine S-methyltransferase	Homo sapiens	90-118
11012121-3	2000	Adverse reactions to azathioprine in humans have been correlated with reduced activity of thiopurine methyltransferase (TPMT) in erythrocytes.	Azathioprine	21-33	thiopurine S-methyltransferase	Homo sapiens	120-124
10798786-0	2000	Thiopurine S-methyltransferase gene polymorphism is predictive of azathioprine-induced myelosuppression in heart transplant recipients.	Azathioprine	66-78	thiopurine S-methyltransferase	Homo sapiens	0-30
10833476-0	2000	Genotypic analysis of thiopurine S-methyltransferase in patients with Crohn"s disease and severe myelosuppression during azathioprine therapy.	Azathioprine	121-133	thiopurine S-methyltransferase	Homo sapiens	22-52
10833476-1	2000	BACKGROUND & AIMS: Myelosuppression in patients with Crohn"s disease (CD) treated with azathioprine has been attributed to low activity of thiopurine S-methyltransferase (TPMT).	Azathioprine	87-99	thiopurine S-methyltransferase	Homo sapiens	139-169
10833476-1	2000	BACKGROUND & AIMS: Myelosuppression in patients with Crohn"s disease (CD) treated with azathioprine has been attributed to low activity of thiopurine S-methyltransferase (TPMT).	Azathioprine	87-99	thiopurine S-methyltransferase	Homo sapiens	171-175
10833476-9	2000	CONCLUSIONS: Twenty-seven percent of patients with CD and myelosuppression during azathioprine therapy had mutant alleles of the TPMT gene associated with enzyme deficiency.	Azathioprine	82-94	thiopurine S-methyltransferase	Homo sapiens	129-133
10841498-0	2000	On the total synthesis and preliminary biological evaluations of 15(R) and 15(S) aza-dEpoB: a Mitsunobu inversion at C15 in pre-epothilone fragments.	Azathioprine	81-84	placenta associated 8	Homo sapiens	117-120
10849375-3	2000	Mutations of the hypoxanthine guanine phosphoribosyltransferase (hprt) gene measured by 6-thioguanine (TG) selection were studied in 28 patients (60 determinations) enrolled in a prospective double-blinded placebo-controlled study of azathioprine immunosuppression: 17 patients (34 determinations) were receiving azathioprine and 11 (26 determinations) placebo.	Azathioprine	234-246	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	17-63
10849375-3	2000	Mutations of the hypoxanthine guanine phosphoribosyltransferase (hprt) gene measured by 6-thioguanine (TG) selection were studied in 28 patients (60 determinations) enrolled in a prospective double-blinded placebo-controlled study of azathioprine immunosuppression: 17 patients (34 determinations) were receiving azathioprine and 11 (26 determinations) placebo.	Azathioprine	234-246	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	65-69
10849375-3	2000	Mutations of the hypoxanthine guanine phosphoribosyltransferase (hprt) gene measured by 6-thioguanine (TG) selection were studied in 28 patients (60 determinations) enrolled in a prospective double-blinded placebo-controlled study of azathioprine immunosuppression: 17 patients (34 determinations) were receiving azathioprine and 11 (26 determinations) placebo.	Azathioprine	313-325	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	17-63
10849375-3	2000	Mutations of the hypoxanthine guanine phosphoribosyltransferase (hprt) gene measured by 6-thioguanine (TG) selection were studied in 28 patients (60 determinations) enrolled in a prospective double-blinded placebo-controlled study of azathioprine immunosuppression: 17 patients (34 determinations) were receiving azathioprine and 11 (26 determinations) placebo.	Azathioprine	313-325	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	65-69
10849375-6	2000	However, azathioprine, which is converted to 6-mercaptopurine in vivo, selects and amplifies the hprt mutants that do arise.	Azathioprine	9-21	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	97-101
10849375-7	2000	Clinical azathioprine resistance may be explained by hprt mutations arising in T cells relevant to the underlying autoimmune process.	Azathioprine	9-21	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	53-57
10798786-1	2000	Azathioprine (AZA) is metabolized via the cytosolic enzyme thiopurine S-methyltransferase (TPMT).	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	59-89
10798786-1	2000	Azathioprine (AZA) is metabolized via the cytosolic enzyme thiopurine S-methyltransferase (TPMT).	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	91-95
10798786-1	2000	Azathioprine (AZA) is metabolized via the cytosolic enzyme thiopurine S-methyltransferase (TPMT).	Azathioprine	14-17	thiopurine S-methyltransferase	Homo sapiens	59-89
10798786-1	2000	Azathioprine (AZA) is metabolized via the cytosolic enzyme thiopurine S-methyltransferase (TPMT).	Azathioprine	14-17	thiopurine S-methyltransferase	Homo sapiens	91-95
10594482-0	1999	Thiopurine methyltransferase activity and its relationship to the occurrence of rejection episodes in paediatric renal transplant recipients treated with azathioprine.	Azathioprine	154-166	thiopurine S-methyltransferase	Homo sapiens	0-28
10594482-3	1999	The aim of this study was to evaluate the inter- and intraindividual variability of red blood cell thiopurine methyltransferase and 6-TGN concentrations and their relationship to the clinical effects of azathioprine in paediatric patients.	Azathioprine	203-215	thiopurine S-methyltransferase	Homo sapiens	99-127
10594482-8	1999	CONCLUSIONS: We report a relationship between TPMT activity and occurrence of rejection in paediatric kidney transplant patients undergoing azathioprine therapy.	Azathioprine	140-152	thiopurine S-methyltransferase	Homo sapiens	46-50
10594482-9	1999	These data suggest a link between high red blood cell TPMT activity and poor clinical outcome probably caused by rapid azathioprine catabolism.	Azathioprine	119-131	thiopurine S-methyltransferase	Homo sapiens	54-58
10727309-1	2000	The risk of azathioprine-induced myelosuppression can be predicted by detecting patients with intermediate or low thiopurine methyltransferase (TPMT) activity.	Azathioprine	12-24	thiopurine S-methyltransferase	Homo sapiens	114-142
10727309-1	2000	The risk of azathioprine-induced myelosuppression can be predicted by detecting patients with intermediate or low thiopurine methyltransferase (TPMT) activity.	Azathioprine	12-24	thiopurine S-methyltransferase	Homo sapiens	144-148
10727309-5	2000	This has led to the development of a technique for TPMT genotype analysis that will identify patients at risk of azathioprine-induced myelosuppression.	Azathioprine	113-125	thiopurine S-methyltransferase	Homo sapiens	51-55
10727309-9	2000	Screening patients for TPMT mutations will reduce the risk of azathioprine-induced myelosuppression, and our study suggests that it may also be a cost-attractive strategy.	Azathioprine	62-74	thiopurine S-methyltransferase	Homo sapiens	23-27
10693638-0	2000	A longitudinal study of TGF-beta1 protein levels in renal allograft recipients converted from CsA to MMF or AZA.	Azathioprine	108-111	transforming growth factor beta 1	Homo sapiens	24-33
11272543-5	2000	[1]3+ was converted to an aza-capped Co4(III)Zn4(II) octanuclear complex, [Zn4O[Co(L)]4]6+ ([2]6+), by reaction with I- in the presence of Zn2+ and ZnO in water.	Azathioprine	26-29	mitochondrially encoded cytochrome c oxidase III	Homo sapiens	41-44
11272543-9	2000	Treatment of [2]6+ with a basic aqueous solution resulted in a cleavage of the Zn-S bonds to produce an aza-capped Co(III) mononuclear complex, [Co(L)] ([3]), from which [1]3+ is readily reproduced by the reaction with Ag+ in water.	Azathioprine	104-107	mitochondrially encoded cytochrome c oxidase III	Homo sapiens	115-122
10631636-3	1999	Statistical correlations significantly showed that: (a) AZA lowers TNF-alpha (P = 0.002) and increases IL-4 production (P = 0.0024), and IFN-beta 1 a increases TNF-alpha and decreases IL-4 levels; (b) CST has a negative effect on TNF-alpha, IL-6, and IL-4 synthesis; and (c) AZA, IFN-beta 1 a, and CST diminish IgG OB synthesis (P = 0.001).	Azathioprine	56-59	tumor necrosis factor	Homo sapiens	67-76
10628931-1	1999	OBJECTIVE: Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that preferentially catalyzes the S-methylation of aromatic and heterocyclic sulfhydryl compounds, including Azathioprine (AZA).	Azathioprine	180-192	thiopurine S-methyltransferase	Homo sapiens	11-41
10628931-1	1999	OBJECTIVE: Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that preferentially catalyzes the S-methylation of aromatic and heterocyclic sulfhydryl compounds, including Azathioprine (AZA).	Azathioprine	180-192	thiopurine S-methyltransferase	Homo sapiens	43-47
10628931-1	1999	OBJECTIVE: Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that preferentially catalyzes the S-methylation of aromatic and heterocyclic sulfhydryl compounds, including Azathioprine (AZA).	Azathioprine	194-197	thiopurine S-methyltransferase	Homo sapiens	11-41
10628931-1	1999	OBJECTIVE: Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that preferentially catalyzes the S-methylation of aromatic and heterocyclic sulfhydryl compounds, including Azathioprine (AZA).	Azathioprine	194-197	thiopurine S-methyltransferase	Homo sapiens	43-47
10628931-2	1999	It has been reported that the level of AZA toxicity is dependent on the TPMT genotypes in Caucasian individuals; we thus investigated this relationship in Japanese.	Azathioprine	39-42	thiopurine S-methyltransferase	Homo sapiens	72-76
10628931-3	1999	METHODS: The TPMT genotype was determined using peripheral blood cell DNA obtained from 36 Japanese patients with rheumatic diseases who were treated with AZA, by polymerase chain reaction (PCR) technique.	Azathioprine	155-158	thiopurine S-methyltransferase	Homo sapiens	13-17
10628931-6	1999	All 3 patients (100%) with the mutant TPMT allele (TPMT*3C) discontinued AZA treatment due to leucopenia while only 4 patients (12%) without mutant TPMT alleles showed leucopenia (p=0.0049, Fisher"s exact test).	Azathioprine	73-76	thiopurine S-methyltransferase	Homo sapiens	38-42
10628931-6	1999	All 3 patients (100%) with the mutant TPMT allele (TPMT*3C) discontinued AZA treatment due to leucopenia while only 4 patients (12%) without mutant TPMT alleles showed leucopenia (p=0.0049, Fisher"s exact test).	Azathioprine	73-76	thiopurine S-methyltransferase	Homo sapiens	51-55
10628931-6	1999	All 3 patients (100%) with the mutant TPMT allele (TPMT*3C) discontinued AZA treatment due to leucopenia while only 4 patients (12%) without mutant TPMT alleles showed leucopenia (p=0.0049, Fisher"s exact test).	Azathioprine	73-76	thiopurine S-methyltransferase	Homo sapiens	51-55
10628931-8	1999	CONCLUSION: The TPMT mutant allele, TPMT*3C, also exists in Japanese individuals, and the bone marrow toxicity of AZA is likely stronger in patients with this mutant allele.	Azathioprine	114-117	thiopurine S-methyltransferase	Homo sapiens	16-20
10628931-8	1999	CONCLUSION: The TPMT mutant allele, TPMT*3C, also exists in Japanese individuals, and the bone marrow toxicity of AZA is likely stronger in patients with this mutant allele.	Azathioprine	114-117	thiopurine S-methyltransferase	Homo sapiens	36-40
10634140-1	1999	Thiopurine methyltransferase (TPMT) degrades 6-mercaptopurine, azathioprine and 6-thioguanine which are commonly used in the treatment of autoimmune diseases, leukaemia and organ transplantation.	Azathioprine	63-75	thiopurine S-methyltransferase	Homo sapiens	0-28
10634140-1	1999	Thiopurine methyltransferase (TPMT) degrades 6-mercaptopurine, azathioprine and 6-thioguanine which are commonly used in the treatment of autoimmune diseases, leukaemia and organ transplantation.	Azathioprine	63-75	thiopurine S-methyltransferase	Homo sapiens	30-34
10631636-3	1999	Statistical correlations significantly showed that: (a) AZA lowers TNF-alpha (P = 0.002) and increases IL-4 production (P = 0.0024), and IFN-beta 1 a increases TNF-alpha and decreases IL-4 levels; (b) CST has a negative effect on TNF-alpha, IL-6, and IL-4 synthesis; and (c) AZA, IFN-beta 1 a, and CST diminish IgG OB synthesis (P = 0.001).	Azathioprine	56-59	interleukin 4	Homo sapiens	103-107
10631636-3	1999	Statistical correlations significantly showed that: (a) AZA lowers TNF-alpha (P = 0.002) and increases IL-4 production (P = 0.0024), and IFN-beta 1 a increases TNF-alpha and decreases IL-4 levels; (b) CST has a negative effect on TNF-alpha, IL-6, and IL-4 synthesis; and (c) AZA, IFN-beta 1 a, and CST diminish IgG OB synthesis (P = 0.001).	Azathioprine	56-59	interleukin 6	Homo sapiens	241-245
10631636-6	1999	The enhanced production of IL-10 detected before or at relapse with AZA and IFN-beta 1 a (trends) may interfere with initiation of the immune reaction and with the development of new CNS lesions.	Azathioprine	68-71	interleukin 10	Homo sapiens	27-32
10025742-5	1999	After adjustment for age, kidney transplant recipients receiving cyclosporine, azathioprine, and prednisolone had a significantly (2.8 times) higher risk of cutaneous SCC relative to those receiving azathioprine and prednisolone.	Azathioprine	79-91	serpin family B member 3	Homo sapiens	167-170
10630693-0	1999	Combined treatment with steroids and azathioprine in IgA nephropathy: design of a prospective randomised multicentre trial.	Azathioprine	37-49	IGAN1	Homo sapiens	53-68
10630693-3	1999	This new randomised trial was designed to prospectively evaluate whether adding low-dose azathioprine to steroids improves long-term renal survival in adult biopsy-proven IgAN patients with proteinuria > or = 1 g/24 h and plasma creatinine < or = 2.0 mg/dl.	Azathioprine	89-101	IGAN1	Homo sapiens	171-175
10424251-4	1999	An involvement of an azathioprine-induced C1-INH gene mutation is hypothised.	Azathioprine	21-33	serpin family G member 1	Homo sapiens	42-48
19078358-10	1999	The average time from AZA initiation to first appearance of an abnormal AST and/or AP value was 27 days (range = 7-62 days).	Azathioprine	22-25	solute carrier family 17 member 5	Homo sapiens	72-75
19078358-12	1999	There were no interventions in response to an abnormal laboratory value, and no patient experienced an adverse clinical outcome attributable to AZA hepatotoxicity during the 10-year study period.AZA use for rheumatic conditions may be associated with elevations in both the serum AST and/or AP values.	Azathioprine	195-198	solute carrier family 17 member 5	Homo sapiens	280-283
9931345-1	1999	Thiopurine methyltransferase (TPMT) catalyses the S-methylation of thiopurine drugs such as 6-mercapto-purine, 6-thioguanine and azathioprine.	Azathioprine	129-141	thiopurine S-methyltransferase	Homo sapiens	0-28
9931345-1	1999	Thiopurine methyltransferase (TPMT) catalyses the S-methylation of thiopurine drugs such as 6-mercapto-purine, 6-thioguanine and azathioprine.	Azathioprine	129-141	thiopurine S-methyltransferase	Homo sapiens	30-34
10461478-1	1999	OBJECTIVE: To determine whether the presence of polymorphisms associated with reduced or absent activity of thiopurine methyltransferase (TPMT), an enzyme involved in azathioprine metabolism, can predict side-effects, particularly myelosuppression, in patients taking this drug.	Azathioprine	167-179	thiopurine S-methyltransferase	Homo sapiens	108-136
10461478-1	1999	OBJECTIVE: To determine whether the presence of polymorphisms associated with reduced or absent activity of thiopurine methyltransferase (TPMT), an enzyme involved in azathioprine metabolism, can predict side-effects, particularly myelosuppression, in patients taking this drug.	Azathioprine	167-179	thiopurine S-methyltransferase	Homo sapiens	138-142
10461478-2	1999	METHODS: The TPMT genotype was determined in 120 patients with systemic lupus erythematosus (SLE) together with 15 patients with inflammatory bowel disease (IBD) and correlated with the effects of clinical exposure to azathioprine.	Azathioprine	218-230	thiopurine S-methyltransferase	Homo sapiens	13-17
10407499-10	1999	Azathioprine (Aza) was the only immunosuppressive drug which had a dose-dependent influence on the relative decrease of Lp(a) levels.	Azathioprine	0-12	lipoprotein(a)	Homo sapiens	120-125
10407499-10	1999	Azathioprine (Aza) was the only immunosuppressive drug which had a dose-dependent influence on the relative decrease of Lp(a) levels.	Azathioprine	0-3	lipoprotein(a)	Homo sapiens	120-125
10505112-10	1999	Down-regulation of FR alpha antigen expression was due, at least in part, to methylation of retroviral vector long terminal repeat promoter since FR alpha expression was partially restored, ex vivo, by treatment with 5-aza-2"-deoxy-cytidine (aza).	Azathioprine	219-222	rabaptin, RAB GTPase binding effector protein 2	Mus musculus	19-27
10505112-10	1999	Down-regulation of FR alpha antigen expression was due, at least in part, to methylation of retroviral vector long terminal repeat promoter since FR alpha expression was partially restored, ex vivo, by treatment with 5-aza-2"-deoxy-cytidine (aza).	Azathioprine	219-222	rabaptin, RAB GTPase binding effector protein 2	Mus musculus	146-154
10213363-3	1999	TPMT, which exhibits autosomal co-dominant polymorphism, plays an important role in metabolism of the antileukemic and immunosuppressive medications, mercaptopurine, thioguanine, and azathioprine.	Azathioprine	183-195	thiopurine S-methyltransferase	Homo sapiens	0-4
9918329-9	1999	Prednisone and azathioprine-treated dogs had significant (P < 0.05) decreases in serum IgG levels and Thy-1+ and CD8+ lymphocyte subpopulations, with an increase in the CD4:CD8.	Azathioprine	15-27	Thy-1 cell surface antigen	Canis lupus familiaris	105-110
9918329-9	1999	Prednisone and azathioprine-treated dogs had significant (P < 0.05) decreases in serum IgG levels and Thy-1+ and CD8+ lymphocyte subpopulations, with an increase in the CD4:CD8.	Azathioprine	15-27	T-cell surface glycoprotein CD4	Canis lupus familiaris	172-175
9836719-1	1998	6-Thioguanine and 6-methylmercaptopurine (Me6-MP) nucleotides are the two major thiopurine metabolites of azathioprine found in erythrocytes.	Azathioprine	106-118	protocadherin gamma subfamily B, 7	Homo sapiens	42-45
9778228-8	1998	Compared with "high" activity, baseline intermediate TPMT activity gave a relative risk of 3.1 (95% confidence interval 1.6-6.2) for the development of severe toxicity with AZA treatment.	Azathioprine	173-176	thiopurine S-methyltransferase	Homo sapiens	53-57
9825816-8	1998	Median serum creatinine was lower in the Aza group (Aza: 119 micromol/L; CsA.	Azathioprine	41-44	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	73-76
9778228-9	1998	CONCLUSION: In RA patients, inherited intermediate TPMT activity seems predictive for the development of severe side effects of AZA.	Azathioprine	128-131	thiopurine S-methyltransferase	Homo sapiens	51-55
9778228-10	1998	Clinicians should consider measuring TPMT prior to treatment initiation to improve the safety of AZA use.	Azathioprine	97-100	thiopurine S-methyltransferase	Homo sapiens	37-41
9529174-9	1998	Both myeloperoxidase activity and the number of neutrophils accumulating in the liver 24 hours after reperfusion in animals treated with AZA, CsA, FK506, and RPM were significantly lower than in untreated animals.	Azathioprine	137-140	myeloperoxidase	Rattus norvegicus	5-20
9780118-4	1998	The pharmacodynamics of AZA are assessed by measurement of the activity of thiopurine methyl transferase (TPMT), which is induced by a metabolite of AZA, 6-mercaptopurine.	Azathioprine	24-27	thiopurine S-methyltransferase	Homo sapiens	75-104
9780118-4	1998	The pharmacodynamics of AZA are assessed by measurement of the activity of thiopurine methyl transferase (TPMT), which is induced by a metabolite of AZA, 6-mercaptopurine.	Azathioprine	24-27	thiopurine S-methyltransferase	Homo sapiens	106-110
9780118-4	1998	The pharmacodynamics of AZA are assessed by measurement of the activity of thiopurine methyl transferase (TPMT), which is induced by a metabolite of AZA, 6-mercaptopurine.	Azathioprine	149-152	thiopurine S-methyltransferase	Homo sapiens	75-104
9780118-4	1998	The pharmacodynamics of AZA are assessed by measurement of the activity of thiopurine methyl transferase (TPMT), which is induced by a metabolite of AZA, 6-mercaptopurine.	Azathioprine	149-152	thiopurine S-methyltransferase	Homo sapiens	106-110
9780118-10	1998	Renal transplant recipients who are treated with AZA and who exhibit an increase in TPMT activity from the time of transplantation experience fewer episodes of active rejection.	Azathioprine	49-52	thiopurine S-methyltransferase	Homo sapiens	84-88
9780130-1	1998	Thiopurine methyltransferase (TPMT) is a cytoplasmic enzyme that preferentially catalyzes the S-methylation of aromatic and heterocyclic sulphydryl compounds, such as the thiopurine drugs azathioprine, mercaptopurine, and thioguanine.	Azathioprine	188-200	thiopurine S-methyltransferase	Homo sapiens	0-28
9780130-1	1998	Thiopurine methyltransferase (TPMT) is a cytoplasmic enzyme that preferentially catalyzes the S-methylation of aromatic and heterocyclic sulphydryl compounds, such as the thiopurine drugs azathioprine, mercaptopurine, and thioguanine.	Azathioprine	188-200	thiopurine S-methyltransferase	Homo sapiens	30-34
9702422-14	1998	DISCUSSION: Severe type B insulin resistance may respond favorably to treatment with plasmapheresis and cyclophosphamide followed by cyclosporin A in combination with azathioprin.	Azathioprine	167-178	insulin	Homo sapiens	26-33
9762674-4	1998	When cytokine levels were analysed independently from MS clinical activity, the use of AZA inhibited IgG OB and TNF-alpha synthesis (P = 0.002) but increased IL-4 (P = 0.0024), whereas IFN-beta 1a stimulated TNF-alpha and inhibited IgG OB and IL-4 production.	Azathioprine	87-90	tumor necrosis factor	Homo sapiens	112-121
9762674-4	1998	When cytokine levels were analysed independently from MS clinical activity, the use of AZA inhibited IgG OB and TNF-alpha synthesis (P = 0.002) but increased IL-4 (P = 0.0024), whereas IFN-beta 1a stimulated TNF-alpha and inhibited IgG OB and IL-4 production.	Azathioprine	87-90	interleukin 4	Homo sapiens	158-162
9762674-4	1998	When cytokine levels were analysed independently from MS clinical activity, the use of AZA inhibited IgG OB and TNF-alpha synthesis (P = 0.002) but increased IL-4 (P = 0.0024), whereas IFN-beta 1a stimulated TNF-alpha and inhibited IgG OB and IL-4 production.	Azathioprine	87-90	tumor necrosis factor	Homo sapiens	208-217
9762674-4	1998	When cytokine levels were analysed independently from MS clinical activity, the use of AZA inhibited IgG OB and TNF-alpha synthesis (P = 0.002) but increased IL-4 (P = 0.0024), whereas IFN-beta 1a stimulated TNF-alpha and inhibited IgG OB and IL-4 production.	Azathioprine	87-90	interleukin 4	Homo sapiens	243-247
9698512-1	1998	BACKGROUND: Recent multicenter reports have demonstrated improved outcome in recipients of cadaveric renal transplants treated with mycophenolate mofetil (MMF) versus azathioprine (AZA) in combination with cyclosporine A (CSA) and prednisone.	Azathioprine	181-184	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	222-225
9695718-1	1998	OBJECTIVE: Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that catalyzes the S-methylation of mercaptopurine, azathioprine, thioguanine and most of their nucleotide metabolites.	Azathioprine	123-135	thiopurine S-methyltransferase	Homo sapiens	11-41
9695718-1	1998	OBJECTIVE: Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that catalyzes the S-methylation of mercaptopurine, azathioprine, thioguanine and most of their nucleotide metabolites.	Azathioprine	123-135	thiopurine S-methyltransferase	Homo sapiens	43-47
9619646-3	1998	Here we report the case of a patient with myasthenia gravis receiving long-term immunosuppression with azathioprine and recurrent well-differentiated thymic carcinoma who developed CD4+ T-cell depletion and CNS cryptococcosis after multiple courses of chemotherapy and mediastinal irradiation.	Azathioprine	103-115	CD4 molecule	Homo sapiens	181-184
9292114-0	1997	The effect of methotrexate and azathioprine on the serum levels of IgA-alpha 1-antitrypsin complex in juvenile chronic arthritis.	Azathioprine	31-43	serpin family A member 1	Homo sapiens	71-90
9336428-0	1997	Azathioprine-induced severe pancytopenia due to a homozygous two-point mutation of the thiopurine methyltransferase gene in a patient with juvenile HLA-B27-associated spondylarthritis.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	87-115
9336428-0	1997	Azathioprine-induced severe pancytopenia due to a homozygous two-point mutation of the thiopurine methyltransferase gene in a patient with juvenile HLA-B27-associated spondylarthritis.	Azathioprine	0-12	major histocompatibility complex, class I, B	Homo sapiens	148-155
9336428-2	1997	We describe a 14-year-old girl with HLA-B27+ spondylarthritis who was treated with AZA 3 mg/kg/day and who suddenly developed severe pancytopenia in the seventh week of treatment.	Azathioprine	83-86	major histocompatibility complex, class I, B	Homo sapiens	36-43
9336428-3	1997	Analysis of the catabolic pathway of AZA revealed a homozygous deficiency of thiopurine methyltransferase (TPMT) on the basis of a combined 2-point mutation at nucleotide positions 460 and 719 in the gene for TPMT, causing a toxic level of the metabolic active 6-thioguanine nucleotides (6-TGN) (2,394 pmoles/8 x 10(8) red blood cells).	Azathioprine	37-40	thiopurine S-methyltransferase	Homo sapiens	77-105
9336428-3	1997	Analysis of the catabolic pathway of AZA revealed a homozygous deficiency of thiopurine methyltransferase (TPMT) on the basis of a combined 2-point mutation at nucleotide positions 460 and 719 in the gene for TPMT, causing a toxic level of the metabolic active 6-thioguanine nucleotides (6-TGN) (2,394 pmoles/8 x 10(8) red blood cells).	Azathioprine	37-40	thiopurine S-methyltransferase	Homo sapiens	107-111
9284961-0	1997	A cyclic GMP- and G-kinase-dependent effect of azathioprine on migration by human neutrophils.	Azathioprine	47-59	guanylate kinase 1	Homo sapiens	9-26
9284961-1	1997	Relatively high concentrations of azathioprine had an inhibitory effect on interleukin 8 (IL-8)- or formyl-methionyl-leucyl-phenylalanine-activated (fMLP)-chemotaxis by human neutrophils.	Azathioprine	34-46	C-X-C motif chemokine ligand 8	Homo sapiens	75-88
9284961-1	1997	Relatively high concentrations of azathioprine had an inhibitory effect on interleukin 8 (IL-8)- or formyl-methionyl-leucyl-phenylalanine-activated (fMLP)-chemotaxis by human neutrophils.	Azathioprine	34-46	C-X-C motif chemokine ligand 8	Homo sapiens	90-94
9284961-1	1997	Relatively high concentrations of azathioprine had an inhibitory effect on interleukin 8 (IL-8)- or formyl-methionyl-leucyl-phenylalanine-activated (fMLP)-chemotaxis by human neutrophils.	Azathioprine	34-46	formyl peptide receptor 1	Homo sapiens	149-153
9284961-6	1997	High concentrations of azathioprine (1 mM) inhibited CD11b expression of fMLP- or IL-8- activated neutrophils; the latter could explain the inhibitory effect of azathioprine.	Azathioprine	23-35	integrin subunit alpha M	Homo sapiens	53-58
9284961-6	1997	High concentrations of azathioprine (1 mM) inhibited CD11b expression of fMLP- or IL-8- activated neutrophils; the latter could explain the inhibitory effect of azathioprine.	Azathioprine	23-35	formyl peptide receptor 1	Homo sapiens	73-77
9284961-6	1997	High concentrations of azathioprine (1 mM) inhibited CD11b expression of fMLP- or IL-8- activated neutrophils; the latter could explain the inhibitory effect of azathioprine.	Azathioprine	23-35	C-X-C motif chemokine ligand 8	Homo sapiens	82-86
9284961-6	1997	High concentrations of azathioprine (1 mM) inhibited CD11b expression of fMLP- or IL-8- activated neutrophils; the latter could explain the inhibitory effect of azathioprine.	Azathioprine	161-173	formyl peptide receptor 1	Homo sapiens	73-77
9284961-6	1997	High concentrations of azathioprine (1 mM) inhibited CD11b expression of fMLP- or IL-8- activated neutrophils; the latter could explain the inhibitory effect of azathioprine.	Azathioprine	161-173	C-X-C motif chemokine ligand 8	Homo sapiens	82-86
9284961-9	1997	The antagonists had only a marginal effect on inhibition of IL-8-activated chemotaxis by high concentrations of azathioprine, thus the G-kinase seems not to be of great importance on the inhibitory effect of azathioprine.	Azathioprine	112-124	C-X-C motif chemokine ligand 8	Homo sapiens	60-64
9510461-6	1998	Due to the risk of fatal myelosuppression we recommend up-front determination of TPMT activity in patients treated with 6MP or azathioprine.	Azathioprine	127-139	thiopurine S-methyltransferase	Homo sapiens	81-85
9869892-5	1998	We showed a significant decrease in uPA plasma concentration in patients treated with azathioprine.	Azathioprine	86-98	proline rich acidic protein 1	Homo sapiens	36-39
9641508-6	1998	Of the 101 patients treated with azathioprine, two out of 15 in remission were HLA B27 positive, whereas as many as 41 out of 86 with still active disease were HLA B27 positive (p = 0.013).	Azathioprine	33-45	major histocompatibility complex, class I, B	Homo sapiens	79-86
9292114-1	1997	In the present study we investigated the influence of methotrexate (MTX) and azathioprine (AZA) on the serum levels of the IgA-alpha 1-antitrypsin (IgA-AT) complex in patients with the systemic form of juvenile chronic arthritis (JCA).	Azathioprine	77-89	serpin family A member 1	Homo sapiens	127-146
9292114-1	1997	In the present study we investigated the influence of methotrexate (MTX) and azathioprine (AZA) on the serum levels of the IgA-alpha 1-antitrypsin (IgA-AT) complex in patients with the systemic form of juvenile chronic arthritis (JCA).	Azathioprine	91-94	serpin family A member 1	Homo sapiens	127-146
9094472-2	1997	He had CD4 lymphocytopenia during azathioprine and topical corticosteroid therapy for atopic dermatitits (AD).	Azathioprine	34-46	CD4 molecule	Homo sapiens	7-10
9200774-1	1997	The objectives of this study were to establish monitoring of azathioprine (AZA) treatment in renal allograft recipients by red blood cell (RBC) 6-thioguanine nucleotide (6-TGN) measurements and to characterize the variability of RBC thiopurine methyltransferase (TPMT) activity and the effects on 6-TGN levels and the incidence of rejection episodes.	Azathioprine	61-73	thiopurine S-methyltransferase	Homo sapiens	233-261
9200774-1	1997	The objectives of this study were to establish monitoring of azathioprine (AZA) treatment in renal allograft recipients by red blood cell (RBC) 6-thioguanine nucleotide (6-TGN) measurements and to characterize the variability of RBC thiopurine methyltransferase (TPMT) activity and the effects on 6-TGN levels and the incidence of rejection episodes.	Azathioprine	61-73	thiopurine S-methyltransferase	Homo sapiens	263-267
9200774-1	1997	The objectives of this study were to establish monitoring of azathioprine (AZA) treatment in renal allograft recipients by red blood cell (RBC) 6-thioguanine nucleotide (6-TGN) measurements and to characterize the variability of RBC thiopurine methyltransferase (TPMT) activity and the effects on 6-TGN levels and the incidence of rejection episodes.	Azathioprine	75-78	thiopurine S-methyltransferase	Homo sapiens	233-261
9200774-1	1997	The objectives of this study were to establish monitoring of azathioprine (AZA) treatment in renal allograft recipients by red blood cell (RBC) 6-thioguanine nucleotide (6-TGN) measurements and to characterize the variability of RBC thiopurine methyltransferase (TPMT) activity and the effects on 6-TGN levels and the incidence of rejection episodes.	Azathioprine	75-78	thiopurine S-methyltransferase	Homo sapiens	263-267
9103127-0	1997	Molecular diagnosis of thiopurine S-methyltransferase deficiency: genetic basis for azathioprine and mercaptopurine intolerance.	Azathioprine	84-96	thiopurine S-methyltransferase	Homo sapiens	23-53
9103127-1	1997	BACKGROUND: Thiopurine S-methyltransferase (TPMT) catalyzes the S-methylation (that is, inactivation) of mercaptopurine, azathioprine, and thioguanine and exhibits genetic polymorphism.	Azathioprine	121-133	thiopurine S-methyltransferase	Homo sapiens	12-42
9103127-1	1997	BACKGROUND: Thiopurine S-methyltransferase (TPMT) catalyzes the S-methylation (that is, inactivation) of mercaptopurine, azathioprine, and thioguanine and exhibits genetic polymorphism.	Azathioprine	121-133	thiopurine S-methyltransferase	Homo sapiens	44-48
9377846-3	1997	The authors describe the drugs employed in the therapy of the PBC: cortisone, azathioprine, metotrexate, chlorambucil, colchicine, D-penicillamine and hydrophilic bile salts; the favourable risk-benefice rate of colchicine, azathioprine and hydrophilic bile salts is outlined, even if they are poorly active on the disease"s course.	Azathioprine	78-90	dihydrolipoamide S-acetyltransferase	Homo sapiens	62-65
9377846-3	1997	The authors describe the drugs employed in the therapy of the PBC: cortisone, azathioprine, metotrexate, chlorambucil, colchicine, D-penicillamine and hydrophilic bile salts; the favourable risk-benefice rate of colchicine, azathioprine and hydrophilic bile salts is outlined, even if they are poorly active on the disease"s course.	Azathioprine	224-236	dihydrolipoamide S-acetyltransferase	Homo sapiens	62-65
9050957-5	1997	The decrease in TNF-alpha levels and the increase in "suppressor-inducer" lymphocytes could reduce chronic inflammation in multiple sclerosis, and paralleled an overall favourable clinical response to azathioprine treatment in our patients.	Azathioprine	201-213	tumor necrosis factor	Homo sapiens	16-25
9713575-6	1997	However, recent reports /4-6/ have indicated that patients with a genetically determined deficiency in thiopurine methyltransferase (TPMT), an important enzyme in azathioprine metabolism, are at high risk for myelosuppression.	Azathioprine	163-175	thiopurine S-methyltransferase	Homo sapiens	103-131
9713575-6	1997	However, recent reports /4-6/ have indicated that patients with a genetically determined deficiency in thiopurine methyltransferase (TPMT), an important enzyme in azathioprine metabolism, are at high risk for myelosuppression.	Azathioprine	163-175	thiopurine S-methyltransferase	Homo sapiens	133-137
8927965-10	1996	Hepatotoxicity has been reported among patients receiving azathioprine (cholestatic hepatitis) and methotrexate (elevated AST levels and, rarely, liver fibrosis or cirrhosis).	Azathioprine	58-70	solute carrier family 17 member 5	Homo sapiens	122-125
8880119-4	1996	Daily treatment with azathioprine and prednisone induced resolution of the intrathoracic abnormalities but was associated with a progressive decrease of circulating IgG and IgA levels and natural killer (NK) lymphocytes that was not related to treatment.	Azathioprine	21-33	CD79a molecule	Homo sapiens	173-176
7575779-9	1995	In this recent group, patients maintained on prednisolone and azathioprine alone had significantly lower fibrinogen levels than those receiving cyA.	Azathioprine	62-74	fibrinogen beta chain	Homo sapiens	105-115
8689814-1	1996	Thiopurine methyltransferase (TPMT) is a cytoplasmic enzyme that catalyzes the S-methylation of the cytotoxic drugs 6-mercaptopurine and azathioprine.	Azathioprine	137-149	thiopurine S-methyltransferase	Homo sapiens	0-28
8689814-1	1996	Thiopurine methyltransferase (TPMT) is a cytoplasmic enzyme that catalyzes the S-methylation of the cytotoxic drugs 6-mercaptopurine and azathioprine.	Azathioprine	137-149	thiopurine S-methyltransferase	Homo sapiens	30-34
8768028-2	1996	METHOD: IFN alpha was used in 18 patients with posterior uveitis, nine with Behcet disease and nine with primary uveitis (mean evolution time 3.8 years) previously treated with corticosteroids (18), CyA (16) and azathioprine (1).	Azathioprine	212-224	interferon alpha 2	Homo sapiens	8-17
8644731-1	1996	The autosomal recessive trait of thiopurine S-methytransferase (TPMT) deficiency is associated with severe hematopoietic toxicity when patients are treated with standard doses of mercaptopurine, azathioprine, or thioguanine.	Azathioprine	195-207	thiopurine S-methyltransferase	Homo sapiens	33-62
8644731-1	1996	The autosomal recessive trait of thiopurine S-methytransferase (TPMT) deficiency is associated with severe hematopoietic toxicity when patients are treated with standard doses of mercaptopurine, azathioprine, or thioguanine.	Azathioprine	195-207	thiopurine S-methyltransferase	Homo sapiens	64-68
8849359-6	1995	After treatment with azathioprine, the proteinuria resolved and the serum albumin level increased from 1.9 mg/dl to normal.	Azathioprine	21-33	albumin	Homo sapiens	74-81
8549944-8	1995	There were significantly greater decreases over the trial period in the median erythrocyte sedimentation rate, C reactive protein, and leucocyte count in the azathioprine group.	Azathioprine	158-170	C-reactive protein	Homo sapiens	111-129
8687298-0	1995	Monitoring of TPMT in heart transplant recipients under immunosuppressive therapy with azathioprine.	Azathioprine	87-99	thiopurine S-methyltransferase	Homo sapiens	14-18
8687298-4	1995	Thiopurine methyltransferase (TPMT) is thought to be the most important enzyme in the catabolism of AZA.	Azathioprine	100-103	thiopurine S-methyltransferase	Homo sapiens	0-28
8687298-4	1995	Thiopurine methyltransferase (TPMT) is thought to be the most important enzyme in the catabolism of AZA.	Azathioprine	100-103	thiopurine S-methyltransferase	Homo sapiens	30-34
8687298-14	1995	We suggest screening for TPMT activity in transplant patients with leukopenia under AZA therapy.	Azathioprine	84-87	thiopurine S-methyltransferase	Homo sapiens	25-29
8738760-8	1996	In this case an excessively high erythrocyte 6-TGN concentration (2,211 pmol/8 x 10(8) RBCs) was associated with a complete deficiency of thiopurine methyltransferase (TPMT), one of the main AZA detoxifying enzymes.	Azathioprine	191-194	thiopurine S-methyltransferase	Homo sapiens	138-166
8738760-8	1996	In this case an excessively high erythrocyte 6-TGN concentration (2,211 pmol/8 x 10(8) RBCs) was associated with a complete deficiency of thiopurine methyltransferase (TPMT), one of the main AZA detoxifying enzymes.	Azathioprine	191-194	thiopurine S-methyltransferase	Homo sapiens	168-172
8834013-7	1996	Reductions in circulating IL-6 and sIL-2R concentrations have also been observed with cyclosporin and corticosteroids, whereas azathioprine reduces IL-6 but not sIL-2R.	Azathioprine	127-139	interleukin 6	Homo sapiens	148-152
7570968-0	1995	Monitoring of azathioprine-induced immunosuppression with thiopurine methyltransferase activity in kidney transplant recipients.	Azathioprine	14-26	thiopurine S-methyltransferase	Homo sapiens	58-86
7570968-1	1995	Thiopurine methyltransferase (TPMT), one of the enzymes involved in azathioprine metabolism, exhibits a wide range of activity in the normal population.	Azathioprine	68-80	thiopurine S-methyltransferase	Homo sapiens	0-28
7570968-1	1995	Thiopurine methyltransferase (TPMT), one of the enzymes involved in azathioprine metabolism, exhibits a wide range of activity in the normal population.	Azathioprine	68-80	thiopurine S-methyltransferase	Homo sapiens	30-34
7570968-2	1995	We prospectively evaluated the monitoring of erythrocyte TPMT activity (using a radiochemical method) in kidney transplant recipients with regard to the efficacy of azathioprine.	Azathioprine	165-177	thiopurine S-methyltransferase	Homo sapiens	57-61
7570968-8	1995	We hypothesized that TPMT activity increase was induced by azathioprine in the patients with the lowest incidence of acute rejection.	Azathioprine	59-71	thiopurine S-methyltransferase	Homo sapiens	21-25
7570968-9	1995	The inducibility of TPMT activity would then appear to be an interesting marker of azathioprine-induced immunosuppression.	Azathioprine	83-95	thiopurine S-methyltransferase	Homo sapiens	20-24
8532165-4	1995	We report here that the aza-substituted analog of 1S,3R-ACPD, 2R,4R-4-aminopyrrolidine-2,4-dicarboxylate (2R,4R-APDC), is a highly selective agonist for negatively-coupled cAMP-linked mGluRs in the rat hippocampus, with similar potency in mGluR2 expressing cells.	Azathioprine	24-27	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	239-245
7857117-1	1995	BACKGROUND: Thiopurine methyltransferase (TPMT) is one of three major enzymes involved in the metabolism of azathioprine and its active metabolite 6-mercaptopurine.	Azathioprine	108-120	thiopurine S-methyltransferase	Homo sapiens	12-40
7640156-0	1995	Sulphasalazine inhibition of thiopurine methyltransferase: possible mechanism for interaction with 6-mercaptopurine and azathioprine.	Azathioprine	120-132	thiopurine S-methyltransferase	Homo sapiens	29-57
7857117-1	1995	BACKGROUND: Thiopurine methyltransferase (TPMT) is one of three major enzymes involved in the metabolism of azathioprine and its active metabolite 6-mercaptopurine.	Azathioprine	108-120	thiopurine S-methyltransferase	Homo sapiens	42-46
7857117-8	1995	OBSERVATIONS: Two patients with TPMT levels of less than 12.5 U/mL RBCs (both TPMTH heterozygotes) experienced leukopenia (white blood count < 4.0 x 10(9)/L) with azathioprine doses around 1.5 mg/kg.	Azathioprine	166-178	thiopurine S-methyltransferase	Homo sapiens	32-36
7857117-14	1995	On the other hand, homozygotes for TPMTH, particularly those with TPMT levels at the upper end of the homozygous range, may have a poor clinical response to azathioprine due to inadequate empiric dosing.	Azathioprine	157-169	thiopurine S-methyltransferase	Homo sapiens	35-39
7810520-10	1995	Graft survival rates were superior in cases treated with combined steroid, cyclosporine and azathioprine or mizoribine, to those treated with other immuno-suppressive regimens, and they decreased as the number of HLA-A, -B and -DR increased.	Azathioprine	92-104	major histocompatibility complex, class I, A	Homo sapiens	213-230
7733148-8	1995	Patients whose immunosuppressive regimen was CsA-based had a 1-year graft survival of 71.5 versus 63.6% in the AZA group.	Azathioprine	111-114	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	45-48
7818564-2	1995	To date, thiopurine methyltransferase (TPMT) deficiency has been reported as a cause of AZA-related bone marrow toxicity in 1 patient with rheumatoid arthritis (RA).	Azathioprine	88-91	thiopurine S-methyltransferase	Homo sapiens	9-37
7818564-2	1995	To date, thiopurine methyltransferase (TPMT) deficiency has been reported as a cause of AZA-related bone marrow toxicity in 1 patient with rheumatoid arthritis (RA).	Azathioprine	88-91	thiopurine S-methyltransferase	Homo sapiens	39-43
7818564-4	1995	METHODS: Lymphocyte activity of purine nucleoside phosphorylase and 5"-nucleotidase (5NT) and erythrocyte activity of TPMT, key enzymes in thiopurine catabolism, were measured in 3 RA patients who had experienced AZA-related bone marrow toxicity and in 16 RA patients without signs of toxicity despite at least 6 months of treatment with AZA.	Azathioprine	213-216	thiopurine S-methyltransferase	Homo sapiens	118-122
7818564-4	1995	METHODS: Lymphocyte activity of purine nucleoside phosphorylase and 5"-nucleotidase (5NT) and erythrocyte activity of TPMT, key enzymes in thiopurine catabolism, were measured in 3 RA patients who had experienced AZA-related bone marrow toxicity and in 16 RA patients without signs of toxicity despite at least 6 months of treatment with AZA.	Azathioprine	338-341	thiopurine S-methyltransferase	Homo sapiens	118-122
7818564-8	1995	Deficiency of purine enzymes, including TPMT and 5NT, may be a cause of AZA-related bone marrow toxicity in patients with RA.	Azathioprine	72-75	thiopurine S-methyltransferase	Homo sapiens	40-44
7973537-1	1994	Insulin secretory reserve assessed by the method of glucose potentiation of arginine induced insulin secretion is decreased in non-diabetic transplant recipients using triple immunosuppressive therapy with prednisone, cyclosporine, and azathioprine.	Azathioprine	236-248	insulin	Homo sapiens	0-7
8582469-1	1995	Red blood cell (RBC) thiopurine methyltransferase (TPMT) metabolizes the cytotoxic drugs 6-mercaptopurine and azathioprine.	Azathioprine	110-122	thiopurine S-methyltransferase	Homo sapiens	21-49
8582469-1	1995	Red blood cell (RBC) thiopurine methyltransferase (TPMT) metabolizes the cytotoxic drugs 6-mercaptopurine and azathioprine.	Azathioprine	110-122	thiopurine S-methyltransferase	Homo sapiens	51-55
7478120-2	1995	The effect of treatment with prednisolone and azathioprine on the clinical course of patients with IgA nephropathy is described in this retrospective study.	Azathioprine	46-58	CD79a molecule	Homo sapiens	99-102
8794271-1	1995	This single center analysis shows further improvement in the already excellent long-term, cadaveric renal allograft survival with Aza since the introduction of CsA.	Azathioprine	130-133	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	160-163
7747620-1	1995	The immunosuppressant agent cyclosporin A (CsA) induces a high turnover osteopenic state, while the effect on bone of the antimetabolite azathioprine, a drug often used in conjunction with CsA in transplant patients, is less clear.	Azathioprine	137-149	chorionic somatomammotropin hormone 1	Homo sapiens	189-192
7747620-2	1995	This study was therefore designed to investigate the outcome of azathioprine administration, with reference to CsA, on bone mineral metabolism using the rat model.	Azathioprine	64-76	chorionic somatomammotropin hormone 1	Homo sapiens	111-114
7481481-12	1995	The addition of low doses of cytotoxic drugs (oral cyclophosphamide or azathioprine) resulted in an improvement in the capacity to absorb IL-2 and a reduction in spontaneous IL-1 production.	Azathioprine	71-83	interleukin 2	Homo sapiens	138-142
7481481-12	1995	The addition of low doses of cytotoxic drugs (oral cyclophosphamide or azathioprine) resulted in an improvement in the capacity to absorb IL-2 and a reduction in spontaneous IL-1 production.	Azathioprine	71-83	interleukin 1 alpha	Homo sapiens	174-178
8035809-5	1994	We demonstrate here that the constitutive HSE-binding activity present in F9 and PCC4.aza.R1 EC cells, as well as a similar activity found to be present in mouse embryonic stem cells, is composed predominantly of HSF2.	Azathioprine	86-89	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	42-45
7533260-10	1994	Proliferation of ZR/AZA cells could be partially inhibited with an EGF receptor-blocking antibody.	Azathioprine	20-23	epidermal growth factor receptor	Homo sapiens	67-79
8082307-7	1994	Considering chemotherapy, the levels of soluble CD8 showed an inverse correlation with the daily dosage of azathioprine.	Azathioprine	107-119	CD8a molecule	Homo sapiens	48-51
20693061-6	1994	Other immunomodulatory compounds such as azathioprine (1 mug/ml) and tributyltin oxide (1 nm) caused a partial inhibition of IL-2 and/or IL-2 receptor mRNA within rodent mixed lymphocyte cultures.	Azathioprine	41-53	interleukin 2	Homo sapiens	125-129
20693061-6	1994	Other immunomodulatory compounds such as azathioprine (1 mug/ml) and tributyltin oxide (1 nm) caused a partial inhibition of IL-2 and/or IL-2 receptor mRNA within rodent mixed lymphocyte cultures.	Azathioprine	41-53	interleukin 2 receptor subunit beta	Homo sapiens	137-150
7520943-1	1994	The synthesis and structure-activity relationships of a series of aza-tricyclic analogs of the quinuclidine substance P (SP) antagonist 1 are described.	Azathioprine	66-69	tachykinin precursor 1	Homo sapiens	108-119
7520943-1	1994	The synthesis and structure-activity relationships of a series of aza-tricyclic analogs of the quinuclidine substance P (SP) antagonist 1 are described.	Azathioprine	66-69	tachykinin precursor 1	Homo sapiens	121-123
8035809-5	1994	We demonstrate here that the constitutive HSE-binding activity present in F9 and PCC4.aza.R1 EC cells, as well as a similar activity found to be present in mouse embryonic stem cells, is composed predominantly of HSF2.	Azathioprine	86-89	heat shock factor 2	Mus musculus	213-217
7914751-0	1994	Interference of circulating azathioprine but not methotrexate or sulfasalazine with measurements of interleukin-6 bioactivity.	Azathioprine	28-40	interleukin 6	Homo sapiens	100-113
20693003-6	1994	Azathioprine (10 mug/ml) inhibited the expression of all mRNAs in rat lymphocyte cultures and inhibited both IL-2 mRNA and actin expression in thymocytes isolated from PVG rats (2 mg/kg/day for 28 days).	Azathioprine	0-12	interleukin 2	Rattus norvegicus	109-113
8393676-6	1993	Both treatments induced decreases in IL-6 concentrations, but circulating AZA (or its metabolites) appears to interfere with the measurement of IL-6 bioactivity.	Azathioprine	74-77	interleukin 6	Homo sapiens	144-148
7914751-5	1994	Addition of exogenous AZA, 6-mercaptopurine (6-MP), and MTX to the IL-6 bioassay resulted in a dose-dependent inhibition of the B9 cell proliferation induced by IL-6, AZA being most potent on a molar basis.	Azathioprine	22-25	interleukin 6	Homo sapiens	67-71
7914751-5	1994	Addition of exogenous AZA, 6-mercaptopurine (6-MP), and MTX to the IL-6 bioassay resulted in a dose-dependent inhibition of the B9 cell proliferation induced by IL-6, AZA being most potent on a molar basis.	Azathioprine	22-25	interleukin 6	Homo sapiens	161-165
7914751-5	1994	Addition of exogenous AZA, 6-mercaptopurine (6-MP), and MTX to the IL-6 bioassay resulted in a dose-dependent inhibition of the B9 cell proliferation induced by IL-6, AZA being most potent on a molar basis.	Azathioprine	167-170	interleukin 6	Homo sapiens	67-71
7914751-8	1994	This study shows that circulating AZA (or its metabolites) exert an inhibitory effect in the IL-6 bioassay.	Azathioprine	34-37	interleukin 6	Homo sapiens	93-97
7936018-2	1994	Erythropoietin improved the anaemia in all patients and raised the RCIT (4 still on azathioprine to 72.2 +/- 9.8, p < 0.003; 7 non-azathioprine patients to 62.7 +/- 5.3, p < 0.01); the IIT remained higher in the azathioprine-treated (85.5 +/- 19.3 vs. 37.1 +/- 5.4; p < 0.013).	Azathioprine	84-96	erythropoietin	Homo sapiens	0-14
7936018-2	1994	Erythropoietin improved the anaemia in all patients and raised the RCIT (4 still on azathioprine to 72.2 +/- 9.8, p < 0.003; 7 non-azathioprine patients to 62.7 +/- 5.3, p < 0.01); the IIT remained higher in the azathioprine-treated (85.5 +/- 19.3 vs. 37.1 +/- 5.4; p < 0.013).	Azathioprine	134-146	erythropoietin	Homo sapiens	0-14
7936018-2	1994	Erythropoietin improved the anaemia in all patients and raised the RCIT (4 still on azathioprine to 72.2 +/- 9.8, p < 0.003; 7 non-azathioprine patients to 62.7 +/- 5.3, p < 0.01); the IIT remained higher in the azathioprine-treated (85.5 +/- 19.3 vs. 37.1 +/- 5.4; p < 0.013).	Azathioprine	134-146	erythropoietin	Homo sapiens	0-14
7936018-4	1994	In summary, azathioprine exacerbates the anaemia of renal failure by augmenting ineffective erythropoiesis, while erythropoietin benefits those on azathioprine as much as other renal patients by stimulating both effective and ineffective erythropoiesis.	Azathioprine	147-159	erythropoietin	Homo sapiens	114-128
7936019-0	1994	Increased serum erythropoietin level during azathioprine treatment in renal transplant recipients.	Azathioprine	44-56	erythropoietin	Homo sapiens	16-30
7936019-9	1994	In conclusion, a switch from Cy to Az 1 year after renal transplantation results in a sustained rise in s-EPO which may in part represent a compensatory phenomenon to bone marrow suppression.	Azathioprine	35-37	erythropoietin	Homo sapiens	106-109
8165444-0	1994	The effect of azathioprine on serum levels of interleukin 6 and soluble interleukin 2 receptor.	Azathioprine	14-26	interleukin 6	Homo sapiens	46-94
8165444-3	1994	This study addressed the effect of AZA on serum IL-6 and soluble IL-2 receptor (sIL-2R) levels in RA.	Azathioprine	35-38	interleukin 6	Homo sapiens	48-52
8212154-5	1993	Since a common variable of all these patients was their use of an angiotensin-converting enzyme (ACE) inhibitor as antihypertensive medication, we speculated that the combination of azathioprine and ACE blocker might be the reason for the anemia.	Azathioprine	182-194	angiotensin I converting enzyme	Homo sapiens	66-95
8212154-5	1993	Since a common variable of all these patients was their use of an angiotensin-converting enzyme (ACE) inhibitor as antihypertensive medication, we speculated that the combination of azathioprine and ACE blocker might be the reason for the anemia.	Azathioprine	182-194	angiotensin I converting enzyme	Homo sapiens	97-100
7507270-5	1994	The effects of CsA abrogated the effects of AZA when both were present during pregnancy.	Azathioprine	44-47	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	15-18
7507270-12	1994	In contrast, among children exposed only to AZA, the majority of CD29hi T cells were CD45R0+.	Azathioprine	44-47	integrin subunit beta 1	Homo sapiens	65-69
7507270-15	1994	This work suggests that the presence of CsA throughout pregnancy has only a minimal effect on fetal immune development and appears to have less impact on T cells than does exposure to AZA only.	Azathioprine	184-187	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	40-43
7694584-4	1993	We found that dexamethasone (4-40 micrograms/mL), the azathioprine metabolite 6-mercaptopurine (10-100 micrograms/mL) and cyclosporine A (0.1-1 microgram/mL) have no effect on the basal and the tumor necrosis factor-alpha- or interleukin-1-stimulated expression of these adhesion molecules.	Azathioprine	54-66	tumor necrosis factor	Homo sapiens	194-221
7694584-4	1993	We found that dexamethasone (4-40 micrograms/mL), the azathioprine metabolite 6-mercaptopurine (10-100 micrograms/mL) and cyclosporine A (0.1-1 microgram/mL) have no effect on the basal and the tumor necrosis factor-alpha- or interleukin-1-stimulated expression of these adhesion molecules.	Azathioprine	54-66	interleukin 1 alpha	Homo sapiens	226-239
8108339-1	1993	Azathioprine immunosuppressive therapy prolongs remissions and stimulates residual beta-cell function, suppresses insulin antibody production, reduces the activity of the complement and CH50 components, reduces initially increased cellular immunity parameters (total T and B cell counts, T helper to T inductor ratio, and the count of DR carrier cells) in patients with newly detected insulin-dependent diabetes mellitus; this makes this drug effective at the first stages of the disease.	Azathioprine	0-12	insulin	Homo sapiens	114-121
8097536-4	1993	In a trial comparing methotrexate with azathioprine significant differences could be found in favor of methotrexate by the variables of pain, DAS, ESR, C-reactive protein, hemoglobin and thrombocytes; not by Ritchie score, number of tender joints and number of swollen joints.	Azathioprine	39-51	C-reactive protein	Homo sapiens	152-170
7685225-4	1993	The DMARDs such as gold salts, D-penicillamine, sulphasalazine and azathioprine have been shown to reduce serum CRP concentrations significantly in patients with RA.	Azathioprine	67-79	C-reactive protein	Homo sapiens	112-115
8472623-5	1993	Introduction of combined immunosuppressive therapy (prednisone plus azathioprine) together with plasmapheresis resulted in rapid lowering of daily insulin requirement and reduction in anti-insulin antibodies.	Azathioprine	68-80	insulin	Homo sapiens	147-154
8472623-5	1993	Introduction of combined immunosuppressive therapy (prednisone plus azathioprine) together with plasmapheresis resulted in rapid lowering of daily insulin requirement and reduction in anti-insulin antibodies.	Azathioprine	68-80	insulin	Homo sapiens	189-196
8432886-0	1993	Effects of azathioprine on response of renal anaemia to subcutaneous recombinant human erythropoietin.	Azathioprine	11-23	erythropoietin	Homo sapiens	87-101
8482489-0	1993	Interaction of AZA analogs of chlorpromazine with the dopamine D2 receptor.	Azathioprine	15-18	dopamine receptor D2	Homo sapiens	54-74
8432886-1	1993	AIMS: To determine the effect of concomitant azathioprine treatment on the response of patients with renal failure to treatment with subcutaneous recombinant human erythropoietin (r-HuEPO).	Azathioprine	45-57	erythropoietin	Homo sapiens	164-178
1960417-2	1991	Here we show that the generation of interferon-gamma producing cells (IFN-gamma pc) in rat spleen cell cultures stimulated with concanavalin A (ConA) is dose-dependently inhibited by a wide variety of immunosuppressants such as cyclosporin A, FK506, hydrocortisone, dexamethasone, azathioprine and ART-18, a monoclonal antibody (mAb) with established immunosuppressive activity in organ transplantation and autoimmunity.	Azathioprine	281-293	interferon gamma	Rattus norvegicus	36-52
1502195-10	1992	IL-1 was shown to stimulate the secretion of thymulin as measured both by its ability to stimulate induction of IL-2 receptor-positive lymphocytes from human peripheral blood lymphocytes and by the azathioprine-sensitive rosette assay.	Azathioprine	198-210	interleukin 1 alpha	Homo sapiens	0-4
1639529-6	1992	Both the CS and AZA groups exhibited significant elevations of factor IX activity, von Willebrand factor (vWF), D-dimer, protein C and tissue type plasminogen activator (t-PA) levels when compared with the normal controls.	Azathioprine	16-19	von Willebrand factor	Homo sapiens	83-104
1639529-6	1992	Both the CS and AZA groups exhibited significant elevations of factor IX activity, von Willebrand factor (vWF), D-dimer, protein C and tissue type plasminogen activator (t-PA) levels when compared with the normal controls.	Azathioprine	16-19	von Willebrand factor	Homo sapiens	106-109
1639529-6	1992	Both the CS and AZA groups exhibited significant elevations of factor IX activity, von Willebrand factor (vWF), D-dimer, protein C and tissue type plasminogen activator (t-PA) levels when compared with the normal controls.	Azathioprine	16-19	plasminogen activator, tissue type	Homo sapiens	135-168
1639529-6	1992	Both the CS and AZA groups exhibited significant elevations of factor IX activity, von Willebrand factor (vWF), D-dimer, protein C and tissue type plasminogen activator (t-PA) levels when compared with the normal controls.	Azathioprine	16-19	plasminogen activator, tissue type	Homo sapiens	170-174
1639529-8	1992	Comparison of data from CS and AZA groups revealed higher factor XII activity and vWF concentration in the former group.	Azathioprine	31-34	von Willebrand factor	Homo sapiens	82-85
1639529-10	1992	In addition, both CS and AZA-treated transplant recipients showed increased plasma concentrations of D-dimer and t-PA.	Azathioprine	25-28	plasminogen activator, tissue type	Homo sapiens	113-117
1374547-6	1992	Patients treated with azathioprine had lower levels of CD5+ B cells than untreated patients and controls.	Azathioprine	22-34	CD5 molecule	Homo sapiens	55-58
1585469-0	1992	The importance of thiopurine methyltransferase activity for the use of azathioprine in transplant recipients.	Azathioprine	71-83	thiopurine S-methyltransferase	Homo sapiens	18-46
1585469-1	1992	The immunosuppressive efficacy of azathioprine is related to its rapid metabolism in vivo to 6-mercaptopurine (6MP), with subsequent conversion to thioguanine nucleotides by an anabolic route involving hypoxanthine-guanine phosphoribosyltransferase.	Azathioprine	34-46	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	202-248
1585469-10	1992	TPMT activity in these 24 patients was also significantly lower than the general group of azathioprine-treated recipients.	Azathioprine	90-102	thiopurine S-methyltransferase	Homo sapiens	0-4
1585469-11	1992	This inverse association between TPMT activity and allograft function was again found among 30 patients receiving triple therapy (azathioprine, CsA, prednisolone).	Azathioprine	130-142	thiopurine S-methyltransferase	Homo sapiens	33-37
1314975-11	1992	Low-dose s.c. Epo effectively corrects anaemia in graft failure despite azathioprine and/or CsA therapy, without obvious acceleration of graft failure.	Azathioprine	72-84	erythropoietin	Homo sapiens	14-17
1585469-13	1992	We conclude that total intolerance to azathioprine is rare and usually appears in patients with very low TPMT activities.	Azathioprine	38-50	thiopurine S-methyltransferase	Homo sapiens	105-109
1585469-14	1992	Our results also suggest that the wide range of TPMT activity may be an important factor in determining long-term graft survival in azathioprine-treated patients; those with high activity might benefit from doses near the upper limit generally recommended.	Azathioprine	132-144	thiopurine S-methyltransferase	Homo sapiens	48-52
1529801-2	1992	A pharmacological survey revealed that as a class the anti-rheumatics (e.g., auranofin, azathioprine, and methotrexate) were the most potent inhibitors of GVH induced splenomegaly.	Azathioprine	88-100	graft versus host regulation	Mus musculus	155-158
14621717-10	1992	CSA/AZA is a good immunosuppressive regime for the first renal transplant in children, but only 75% tolerated AZA/CSA without same damage to their grafts.	Azathioprine	110-113	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	0-3
1960417-2	1991	Here we show that the generation of interferon-gamma producing cells (IFN-gamma pc) in rat spleen cell cultures stimulated with concanavalin A (ConA) is dose-dependently inhibited by a wide variety of immunosuppressants such as cyclosporin A, FK506, hydrocortisone, dexamethasone, azathioprine and ART-18, a monoclonal antibody (mAb) with established immunosuppressive activity in organ transplantation and autoimmunity.	Azathioprine	281-293	interferon gamma	Rattus norvegicus	70-79
1799934-0	1991	Binding position of azathioprine with bovine serum albumin determined by measuring nuclear magnetic resonance relaxation time.	Azathioprine	20-32	albumin	Homo sapiens	45-58
1799934-1	1991	The interaction between azathioprine (AZ) and bovine serum albumin (BSA) is mainly due to hydrophobic binding according to the dependence of the binding constant on the ionic strength obtained by equilibrium dialysis.	Azathioprine	24-36	albumin	Homo sapiens	53-66
1799934-1	1991	The interaction between azathioprine (AZ) and bovine serum albumin (BSA) is mainly due to hydrophobic binding according to the dependence of the binding constant on the ionic strength obtained by equilibrium dialysis.	Azathioprine	38-40	albumin	Homo sapiens	53-66
1864013-3	1991	However, in a study of Northern blotting using cDNA for IL-2R (anti-alpha chain specific), both the 3500 and 1400 bp families of IL-2R mRNA were remarkably decreased in PBMC from CsA-prednisolone-treated recipients compared with azathioprine-prednisolone-treated recipients and normal individuals.	Azathioprine	229-241	interleukin 2 receptor subunit beta	Homo sapiens	56-61
1864013-3	1991	However, in a study of Northern blotting using cDNA for IL-2R (anti-alpha chain specific), both the 3500 and 1400 bp families of IL-2R mRNA were remarkably decreased in PBMC from CsA-prednisolone-treated recipients compared with azathioprine-prednisolone-treated recipients and normal individuals.	Azathioprine	229-241	interleukin 2 receptor subunit beta	Homo sapiens	129-134
1713050-6	1991	Analysis of cell membrane markers showed a loss of the early differentiation antigens CD34 and CD33 from leukaemic bone marrow cells after 7 days of Aza-dC treatment, which is suggestive of leukaemic cell differentiation.	Azathioprine	149-152	CD34 molecule	Homo sapiens	86-90
1655916-5	1991	In the early post Tx period, the administration of antithymocyte globulin (ATG) or OKT3 monoclonal antibody and peak dosages of azathioprine were associated with significantly inhibited in vitro IFN-gamma production.	Azathioprine	128-140	interferon gamma	Homo sapiens	195-204
1713050-6	1991	Analysis of cell membrane markers showed a loss of the early differentiation antigens CD34 and CD33 from leukaemic bone marrow cells after 7 days of Aza-dC treatment, which is suggestive of leukaemic cell differentiation.	Azathioprine	149-152	CD33 molecule	Homo sapiens	95-99
1896399-2	1991	In kidney transplant patients on CyA or azathioprine respectively, plasma erythropoietin levels were significantly higher during the first three months after transplantation than in normals.	Azathioprine	40-52	erythropoietin	Homo sapiens	74-88
1896399-4	1991	As compared with patients on CyA, in azathioprine treated patients plasma erythropoietin levels were significantly higher 12 to 60 months after transplantation.	Azathioprine	37-49	erythropoietin	Homo sapiens	74-88
1896399-5	1991	These elevated erythropoietin levels in azathioprine treated patients seem to be due also to factors other than higher prednisone dosage.	Azathioprine	40-52	erythropoietin	Homo sapiens	15-29
1674429-3	1991	By applying the method of immunocytochemical assay, we have demonstrated the appearance of the multidrug-resistant phenotype (P-glycoprotein+ cells, multidrug-resistant cells) in mononuclear cells of the peripheral blood from 32/49 patients receiving triple-drug (azathioprine, steroids, cyclosporine) immunosuppressive therapy after heart transplantation.	Azathioprine	264-276	ATP binding cassette subfamily B member 1	Homo sapiens	126-140
1829436-2	1991	Longitudinal studies showed reduced numbers of CD45R+CD4+ lymphocytes in patients treated with cyclophosphamide or azathioprine.	Azathioprine	115-127	protein tyrosine phosphatase receptor type C	Homo sapiens	47-52
1906396-1	1991	A study was made of changes in the ratio of CD4+/CD8+ in patients who had received cadaverous kidneys and who were under treatment with a combination of cyclosporin A + azathioprine + cor ticosteroids.	Azathioprine	169-181	CD4 molecule	Homo sapiens	44-47
2024235-4	1991	Administration of azathioprine (AZA), cyclosporine A (CSA) or both as immunosuppressive therapy did not affect HC II levels, but CSA seems to have raised plasma AT III.	Azathioprine	18-30	serpin family C member 1	Homo sapiens	161-167
1723035-4	1991	In patients on azathioprine the absolute number of CD3+CD5--lymphocytes is reduced, along with other lymphoid subpopulations.	Azathioprine	15-27	CD5 molecule	Homo sapiens	55-58
2066352-5	1991	Moreover, the elution rate of DNA fragmentation, even at low dose of AZA that is not cytotoxic, significantly increased in the presence of buthionine sulfoximine, which is a selective inhibitor of gamma-glutamylcysteine synthetase; i.e., depletion of GSH in hepatocytes enhanced the DNA damage by AZA.	Azathioprine	69-72	glutamate-cysteine ligase, catalytic subunit	Rattus norvegicus	197-230
2066352-5	1991	Moreover, the elution rate of DNA fragmentation, even at low dose of AZA that is not cytotoxic, significantly increased in the presence of buthionine sulfoximine, which is a selective inhibitor of gamma-glutamylcysteine synthetase; i.e., depletion of GSH in hepatocytes enhanced the DNA damage by AZA.	Azathioprine	297-300	glutamate-cysteine ligase, catalytic subunit	Rattus norvegicus	197-230
1870754-0	1991	The effect of conversion from cyclosporin to azathioprine on renin-containing cells in renal allograft biopsies.	Azathioprine	45-57	renin	Homo sapiens	61-66
1870754-5	1991	Numbers of renin-containing cells decreased after conversion to azathioprine.	Azathioprine	64-76	renin	Homo sapiens	11-16
2128095-6	1990	The two patients subjected to long-term therapy with a combination of prednisone (initially 2-3 mg/kg BW) and azathioprine (2-3 mg/kg BW) responded positively; the F VIII: C concentration increased.	Azathioprine	110-122	coagulation factor VIII	Homo sapiens	164-170
2128095-10	1990	In conclusion, long-term therapy of an acquired F VIII: C inhibitor with a combination of prednisone and azathioprine may lead to complete disappearance of the inhibitor, normalization of the coagulation tests, and complete remission of the bleeding tendency.	Azathioprine	105-117	coagulation factor VIII	Homo sapiens	48-54
2144431-9	1990	However, 4 og 5 patients with MCTD and 4 of 5 patients receiving Imurel were found to have low E-CR1 expression and capacity to bind IC.	Azathioprine	65-71	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	97-100
2151903-4	1990	Higher basal ANP levels were found in patients of the CyA and Aza group than in normals (significantly higher in patients of the CyA group).	Azathioprine	62-65	natriuretic peptide A	Homo sapiens	13-16
2219281-3	1990	Two of 6 Aza treated patients (33%) developed recurrence of FSGS and nephrotic syndrome (NS).	Azathioprine	9-12	actinin alpha 4	Homo sapiens	60-64
34474172-12	2022	Combination of anti-TNF with immunomodulators (azathioprine, 6-meracptopurine, methotrexate) resulted in an attenuated vaccine response as compared to anti-TNF monotherapy.	Azathioprine	47-59	tumor necrosis factor	Homo sapiens	20-23
2209678-5	1990	CYA and AZA did not influence CD4+/CD8+ ratio of circulating T cells but affected HNK-1+ cells.	Azathioprine	8-11	beta-1,3-glucuronyltransferase 1	Homo sapiens	82-87
2088967-5	1990	CsA, azathioprine and prednisone all appear to have the potential for adverse effects variously on islet engraftment, insulin secretion, and/or peripheral insulin activity.	Azathioprine	5-17	insulin	Homo sapiens	118-125
2088967-5	1990	CsA, azathioprine and prednisone all appear to have the potential for adverse effects variously on islet engraftment, insulin secretion, and/or peripheral insulin activity.	Azathioprine	5-17	insulin	Homo sapiens	155-162
33806932-8	2021	Proinflammatory cytokines, such as interleukin (IL)-1ss and IL-6, increase upon AZA treatment, both systemically and in the aortic tissue.	Azathioprine	80-83	interleukin 6	Rattus norvegicus	60-64
33806932-10	2021	As the AZA effect could be decreased in NLRP3-/- aortic rings in an ex vivo experiment, the signaling pathway might be, at least in part, dependent on the NLRP3 inflammasome.	Azathioprine	7-10	NLR family, pyrin domain containing 3	Rattus norvegicus	40-45
33806932-10	2021	As the AZA effect could be decreased in NLRP3-/- aortic rings in an ex vivo experiment, the signaling pathway might be, at least in part, dependent on the NLRP3 inflammasome.	Azathioprine	7-10	NLR family, pyrin domain containing 3	Rattus norvegicus	155-160
34474172-12	2022	Combination of anti-TNF with immunomodulators (azathioprine, 6-meracptopurine, methotrexate) resulted in an attenuated vaccine response as compared to anti-TNF monotherapy.	Azathioprine	47-59	tumor necrosis factor	Homo sapiens	156-159
34866237-0	2022	Effect of NUDT15 polymorphisms on early hematological safety of low-dose azathioprine in Chinese patients with pemphigus vulgaris: A prospective cohort study.	Azathioprine	73-85	nudix hydrolase 15	Homo sapiens	10-16
34582038-0	2022	TPMT and NUDT15 Variants Predict Discontinuation of Azathioprine for Myelotoxicity in Patients with Inflammatory Disease: Real-World Clinical Results.	Azathioprine	52-64	thiopurine S-methyltransferase	Homo sapiens	0-4
34582038-0	2022	TPMT and NUDT15 Variants Predict Discontinuation of Azathioprine for Myelotoxicity in Patients with Inflammatory Disease: Real-World Clinical Results.	Azathioprine	52-64	nudix hydrolase 15	Homo sapiens	9-15
34582038-3	2022	Thiopurine-S-methyltransferase (TPMT) and nudix hydrolase-15 (NUDT15) are enzymes involved in azathioprine metabolism; variants in the genes encoding these enzymes increase the risk for azathioprine myelotoxicity.	Azathioprine	94-106	thiopurine S-methyltransferase	Homo sapiens	0-30
34582038-3	2022	Thiopurine-S-methyltransferase (TPMT) and nudix hydrolase-15 (NUDT15) are enzymes involved in azathioprine metabolism; variants in the genes encoding these enzymes increase the risk for azathioprine myelotoxicity.	Azathioprine	94-106	thiopurine S-methyltransferase	Homo sapiens	32-36
34582038-3	2022	Thiopurine-S-methyltransferase (TPMT) and nudix hydrolase-15 (NUDT15) are enzymes involved in azathioprine metabolism; variants in the genes encoding these enzymes increase the risk for azathioprine myelotoxicity.	Azathioprine	94-106	nudix hydrolase 15	Homo sapiens	62-68
34582038-3	2022	Thiopurine-S-methyltransferase (TPMT) and nudix hydrolase-15 (NUDT15) are enzymes involved in azathioprine metabolism; variants in the genes encoding these enzymes increase the risk for azathioprine myelotoxicity.	Azathioprine	186-198	thiopurine S-methyltransferase	Homo sapiens	0-30
34582038-3	2022	Thiopurine-S-methyltransferase (TPMT) and nudix hydrolase-15 (NUDT15) are enzymes involved in azathioprine metabolism; variants in the genes encoding these enzymes increase the risk for azathioprine myelotoxicity.	Azathioprine	186-198	thiopurine S-methyltransferase	Homo sapiens	32-36
34582038-3	2022	Thiopurine-S-methyltransferase (TPMT) and nudix hydrolase-15 (NUDT15) are enzymes involved in azathioprine metabolism; variants in the genes encoding these enzymes increase the risk for azathioprine myelotoxicity.	Azathioprine	186-198	nudix hydrolase 15	Homo sapiens	62-68
34582038-6	2022	We hypothesized that in patients with inflammatory diseases, TPMT and NUDT15 genotype data predict the risk of discontinuing azathioprine due to myelotoxicity.	Azathioprine	125-137	thiopurine S-methyltransferase	Homo sapiens	61-65
34582038-6	2022	We hypothesized that in patients with inflammatory diseases, TPMT and NUDT15 genotype data predict the risk of discontinuing azathioprine due to myelotoxicity.	Azathioprine	125-137	nudix hydrolase 15	Homo sapiens	70-76
34582038-14	2022	In conclusion, TPMT and NUDT15 metabolizer status predicts discontinuation due to myelotoxicity for patients taking azathioprine for inflammatory conditions.	Azathioprine	116-128	thiopurine S-methyltransferase	Homo sapiens	15-19
34582038-14	2022	In conclusion, TPMT and NUDT15 metabolizer status predicts discontinuation due to myelotoxicity for patients taking azathioprine for inflammatory conditions.	Azathioprine	116-128	nudix hydrolase 15	Homo sapiens	24-30
2357842-3	1990	Significantly higher levels of C4a anaphylatoxin were found in 16 patients, with more aggressive disease requiring supplementary treatment with azathioprine, while the remaining eight patients, with less severe disease, required purely steroid therapy.	Azathioprine	144-156	complement C4A (Rodgers blood group)	Homo sapiens	31-34
34866237-3	2022	To investigate hematological AE of low-dose AZA based on NUDT15 genotypes among patients with PV, a prospective cohort study was conducted in patients with PV, followed-up for the first 8 weeks after AZA administration.	Azathioprine	44-47	nudix hydrolase 15	Homo sapiens	57-63
34866237-10	2022	Low-dose AZA based on NUDT15 genotypes can reduce the risk of early hematological AE among patients with PV.	Azathioprine	9-12	nudix hydrolase 15	Homo sapiens	22-28
34534644-9	2021	At 2:1 and 5:1 M ratios the alpha-chain was consistently modified at K7, H20, H50, and the beta-chain at C93 and H97 with the aza-Michael adduct.	Azathioprine	126-129	Fc gamma receptor and transporter	Homo sapiens	28-39
33882797-3	2021	This study aimed to evaluate the gene expression of sod1, sod2, cat, nrf2 and gp91phox in CD patients before and after Azathioprine (Aza) consumption.	Azathioprine	119-131	superoxide dismutase 1	Homo sapiens	52-56
33882797-3	2021	This study aimed to evaluate the gene expression of sod1, sod2, cat, nrf2 and gp91phox in CD patients before and after Azathioprine (Aza) consumption.	Azathioprine	119-131	superoxide dismutase 2	Homo sapiens	58-62
33882797-3	2021	This study aimed to evaluate the gene expression of sod1, sod2, cat, nrf2 and gp91phox in CD patients before and after Azathioprine (Aza) consumption.	Azathioprine	119-131	catalase	Homo sapiens	64-67
33882797-3	2021	This study aimed to evaluate the gene expression of sod1, sod2, cat, nrf2 and gp91phox in CD patients before and after Azathioprine (Aza) consumption.	Azathioprine	119-131	NFE2 like bZIP transcription factor 2	Homo sapiens	69-73
33882797-3	2021	This study aimed to evaluate the gene expression of sod1, sod2, cat, nrf2 and gp91phox in CD patients before and after Azathioprine (Aza) consumption.	Azathioprine	119-131	cytochrome b-245 beta chain	Homo sapiens	78-86
33882797-3	2021	This study aimed to evaluate the gene expression of sod1, sod2, cat, nrf2 and gp91phox in CD patients before and after Azathioprine (Aza) consumption.	Azathioprine	133-136	superoxide dismutase 1	Homo sapiens	52-56
33882797-3	2021	This study aimed to evaluate the gene expression of sod1, sod2, cat, nrf2 and gp91phox in CD patients before and after Azathioprine (Aza) consumption.	Azathioprine	133-136	superoxide dismutase 2	Homo sapiens	58-62
33882797-3	2021	This study aimed to evaluate the gene expression of sod1, sod2, cat, nrf2 and gp91phox in CD patients before and after Azathioprine (Aza) consumption.	Azathioprine	133-136	catalase	Homo sapiens	64-67
33882797-3	2021	This study aimed to evaluate the gene expression of sod1, sod2, cat, nrf2 and gp91phox in CD patients before and after Azathioprine (Aza) consumption.	Azathioprine	133-136	NFE2 like bZIP transcription factor 2	Homo sapiens	69-73
33882797-3	2021	This study aimed to evaluate the gene expression of sod1, sod2, cat, nrf2 and gp91phox in CD patients before and after Azathioprine (Aza) consumption.	Azathioprine	133-136	cytochrome b-245 beta chain	Homo sapiens	78-86
33882797-7	2021	Following treatment with Aza, the decreased expression levels of gp91phox (P-value < 0.05), cat (P-value < 0.05), sod1(P-value < 0.001) and nrf2 (P-value < 0.001) were observed in CD patients.	Azathioprine	25-28	cytochrome b-245 beta chain	Homo sapiens	65-73
33882797-7	2021	Following treatment with Aza, the decreased expression levels of gp91phox (P-value < 0.05), cat (P-value < 0.05), sod1(P-value < 0.001) and nrf2 (P-value < 0.001) were observed in CD patients.	Azathioprine	25-28	catalase	Homo sapiens	92-95
33882797-7	2021	Following treatment with Aza, the decreased expression levels of gp91phox (P-value < 0.05), cat (P-value < 0.05), sod1(P-value < 0.001) and nrf2 (P-value < 0.001) were observed in CD patients.	Azathioprine	25-28	superoxide dismutase 1	Homo sapiens	114-118
33882797-7	2021	Following treatment with Aza, the decreased expression levels of gp91phox (P-value < 0.05), cat (P-value < 0.05), sod1(P-value < 0.001) and nrf2 (P-value < 0.001) were observed in CD patients.	Azathioprine	25-28	NFE2 like bZIP transcription factor 2	Homo sapiens	140-144
34732168-11	2021	A more significant reduction of MuSK-ab titers was observed in patients receiving TAC or RTX plus Pred than those receiving AZA plus Pred.	Azathioprine	124-127	muscle associated receptor tyrosine kinase	Homo sapiens	32-36
34797551-8	2022	Meanwhile, the ARR also decreased in all AQP4-Ab groups (from 0.3 to 0.2 in RTX, from 0.9 to 0.5 in AZA, and from 0.9 to 0.4 in MMF).	Azathioprine	100-103	aquaporin 4	Homo sapiens	41-45
34797551-14	2022	CONCLUSIONS: RTX, AZA, and MMF therapies efficiently lowered the relapse frequency and disability in both of the AQP4-Ab seropositive or seronegative patients with NMO.	Azathioprine	18-21	aquaporin 4	Homo sapiens	113-117
34478745-6	2021	In addition, immunohistochemical evaluation of CAM revealed that AZA decreased TGF-beta and VEGF levels, important cytokines involved in the angiogenic process.	Azathioprine	65-68	transforming growth factor alpha	Homo sapiens	79-87
34478745-6	2021	In addition, immunohistochemical evaluation of CAM revealed that AZA decreased TGF-beta and VEGF levels, important cytokines involved in the angiogenic process.	Azathioprine	65-68	vascular endothelial growth factor A	Homo sapiens	92-96
34416244-6	2021	Among the 11 metabolites evaluated, TIMP, TGMP, TGDP, TGTP, MeTIMP, MeTIDP and MeTITP were detectable in HCEC cells treated with azathioprine or mercaptopurine, considering two different incubation times before the addition of the drugs (4 and 48 h).	Azathioprine	129-141	TIMP metallopeptidase inhibitor 1	Homo sapiens	36-40
34466252-0	2021	Azathioprine-induced severe myelosuppression accompanied by massive hair loss and painful oral ulcer in an autoimmune hepatitis patient with NUDT15 minor variant: A case report.	Azathioprine	0-12	nudix hydrolase 15	Homo sapiens	141-147
34931247-1	2021	OBJECTIVES: We retrospectively compared the therapeutic effects of combination therapy with prednisolone (PSL) and oral tacrolimus (TAC) or azathioprine (AZA) on progressive interstitial pneumonia with systemic sclerosis (SSc-PIP).	Azathioprine	140-152	prolactin induced protein	Homo sapiens	226-229
34466252-1	2021	This report highlights azathioprine-induced severe myelosuppression in the patient with NUDT15 minor variant.	Azathioprine	23-35	nudix hydrolase 15	Homo sapiens	88-94
34430579-1	2021	Background: This study aimed to analyze the cost-effectiveness of combining screening for thiopurine methyl transferase (TPMT) and nucleotide triphosphate diphosphatase (NUDT15) defective alleles with therapeutic drug monitoring (TDM) in Chinese patients with inflammatory bowel disease (IBD) treated with azathioprine (AZA).	Azathioprine	306-318	thiopurine S-methyltransferase	Homo sapiens	90-119
34430579-1	2021	Background: This study aimed to analyze the cost-effectiveness of combining screening for thiopurine methyl transferase (TPMT) and nucleotide triphosphate diphosphatase (NUDT15) defective alleles with therapeutic drug monitoring (TDM) in Chinese patients with inflammatory bowel disease (IBD) treated with azathioprine (AZA).	Azathioprine	306-318	thiopurine S-methyltransferase	Homo sapiens	121-125
34430579-1	2021	Background: This study aimed to analyze the cost-effectiveness of combining screening for thiopurine methyl transferase (TPMT) and nucleotide triphosphate diphosphatase (NUDT15) defective alleles with therapeutic drug monitoring (TDM) in Chinese patients with inflammatory bowel disease (IBD) treated with azathioprine (AZA).	Azathioprine	306-318	nudix hydrolase 15	Homo sapiens	170-176
34430579-1	2021	Background: This study aimed to analyze the cost-effectiveness of combining screening for thiopurine methyl transferase (TPMT) and nucleotide triphosphate diphosphatase (NUDT15) defective alleles with therapeutic drug monitoring (TDM) in Chinese patients with inflammatory bowel disease (IBD) treated with azathioprine (AZA).	Azathioprine	320-323	thiopurine S-methyltransferase	Homo sapiens	90-119
34430579-1	2021	Background: This study aimed to analyze the cost-effectiveness of combining screening for thiopurine methyl transferase (TPMT) and nucleotide triphosphate diphosphatase (NUDT15) defective alleles with therapeutic drug monitoring (TDM) in Chinese patients with inflammatory bowel disease (IBD) treated with azathioprine (AZA).	Azathioprine	320-323	thiopurine S-methyltransferase	Homo sapiens	121-125
34430579-1	2021	Background: This study aimed to analyze the cost-effectiveness of combining screening for thiopurine methyl transferase (TPMT) and nucleotide triphosphate diphosphatase (NUDT15) defective alleles with therapeutic drug monitoring (TDM) in Chinese patients with inflammatory bowel disease (IBD) treated with azathioprine (AZA).	Azathioprine	320-323	nudix hydrolase 15	Homo sapiens	170-176
34430579-2	2021	Methods: We evaluated the cost-effectiveness of combining screening for NUDT15 and TPMT deficiency with TDM in patients receiving AZA treatment over a 1-year horizon by developing a decision tree model.	Azathioprine	130-133	nudix hydrolase 15	Homo sapiens	72-78
34430579-11	2021	Conclusions: For Chinese patients with IBD who receive an AZA regimen, a strategy involving combined NUDT15/TPMT genotype screening prior to treatment initiation and incorporating TDM for treatment management is cost-effective compared to strategies involving genotyping of NUDT15 or TPMT alone or genotyping without TDM.	Azathioprine	58-61	nudix hydrolase 15	Homo sapiens	101-107
34137496-10	2021	Addition of Aza and TSA normalized miR-126 and EGFL7 expression levels in SSc-MVECs.	Azathioprine	12-15	microRNA 126	Homo sapiens	35-42
34137496-10	2021	Addition of Aza and TSA normalized miR-126 and EGFL7 expression levels in SSc-MVECs.	Azathioprine	12-15	EGF like domain multiple 7	Homo sapiens	47-52
34084143-6	2021	Only the NUDT15 (415C>T) polymorphism was found to be associated with the adverse effects of azathioprine-induced myelosuppression (odds ratio (OR), 51.818; 95% CI, 5.280-508.556; p = 0.001), which suggested that the NUDT15 (415C>T) polymorphism could be an influencing factor of azathioprine-induced myelosuppression in the Chinese population.	Azathioprine	93-105	nudix hydrolase 15	Homo sapiens	9-15
34141785-2	2021	Bone marrow inhibition is a common side effect of AZA, and severe bone marrow inhibition is related to decreased thiopurine S-methyltransferase (TPMT) activity.	Azathioprine	50-53	thiopurine S-methyltransferase	Homo sapiens	113-143
34141785-2	2021	Bone marrow inhibition is a common side effect of AZA, and severe bone marrow inhibition is related to decreased thiopurine S-methyltransferase (TPMT) activity.	Azathioprine	50-53	thiopurine S-methyltransferase	Homo sapiens	145-149
34084143-6	2021	Only the NUDT15 (415C>T) polymorphism was found to be associated with the adverse effects of azathioprine-induced myelosuppression (odds ratio (OR), 51.818; 95% CI, 5.280-508.556; p = 0.001), which suggested that the NUDT15 (415C>T) polymorphism could be an influencing factor of azathioprine-induced myelosuppression in the Chinese population.	Azathioprine	93-105	nudix hydrolase 15	Homo sapiens	217-223
34084143-6	2021	Only the NUDT15 (415C>T) polymorphism was found to be associated with the adverse effects of azathioprine-induced myelosuppression (odds ratio (OR), 51.818; 95% CI, 5.280-508.556; p = 0.001), which suggested that the NUDT15 (415C>T) polymorphism could be an influencing factor of azathioprine-induced myelosuppression in the Chinese population.	Azathioprine	280-292	nudix hydrolase 15	Homo sapiens	9-15
34084143-6	2021	Only the NUDT15 (415C>T) polymorphism was found to be associated with the adverse effects of azathioprine-induced myelosuppression (odds ratio (OR), 51.818; 95% CI, 5.280-508.556; p = 0.001), which suggested that the NUDT15 (415C>T) polymorphism could be an influencing factor of azathioprine-induced myelosuppression in the Chinese population.	Azathioprine	280-292	nudix hydrolase 15	Homo sapiens	217-223
35120281-0	2022	HLA-variants associated with azathioprine-induced pancreatitis in patients with Crohn"s disease.	Azathioprine	29-41	major histocompatibility complex, class II, DR beta 1	Homo sapiens	0-3
35067667-5	2022	RESULTS: ITPA genotypes and 6-TGN concentration were both associated with the clinical effectiveness of azathioprine (P=0.036 and P=4.6x10-7), with a significant correlation also detected between them (P=0.042).	Azathioprine	104-116	inosine triphosphatase	Homo sapiens	9-13
35607307-7	2022	Also, using the demethylating agents such as AZA on LoVo and Caco-2 cancer cell lines causes induction of transcription level of EYA4, implying the possible mechanism of DNA methylation in the upregulation of EYA4.	Azathioprine	45-48	EYA transcriptional coactivator and phosphatase 4	Homo sapiens	129-133
35607307-7	2022	Also, using the demethylating agents such as AZA on LoVo and Caco-2 cancer cell lines causes induction of transcription level of EYA4, implying the possible mechanism of DNA methylation in the upregulation of EYA4.	Azathioprine	45-48	EYA transcriptional coactivator and phosphatase 4	Homo sapiens	209-213
35584442-0	2022	C-reactive protein levels and prevalence of leukopenia in patients with inflammatory bowel disease treated with azathioprine and/or mesalazine: a real-life study.	Azathioprine	112-124	C-reactive protein	Homo sapiens	0-18
35584442-1	2022	OBJECTIVE: To examine serum C-reactive protein levels and the prevalence of leukopenia in patients with Crohn"s disease or ulcerative colitis undergoing treatment with azathioprine and/or mesalazine.	Azathioprine	168-180	C-reactive protein	Homo sapiens	28-46
34870401-1	2022	Background: In individuals with reduced thiopurine S-methyltransferase activity, undesirable adverse effects can occur during treatment with azathioprine (AZA).	Azathioprine	141-153	thiopurine S-methyltransferase	Homo sapiens	40-70
34870401-1	2022	Background: In individuals with reduced thiopurine S-methyltransferase activity, undesirable adverse effects can occur during treatment with azathioprine (AZA).	Azathioprine	155-158	thiopurine S-methyltransferase	Homo sapiens	40-70
34870401-4	2022	Our goal was to estimate the prevalence of TPMT gene mutations in Czech patients with rheumatic diseases and to assess the adverse effects associated with AZA therapy in these patients.	Azathioprine	155-158	thiopurine S-methyltransferase	Homo sapiens	43-47
34870401-7	2022	Conclusions: Our findings show the importance of testing for variants of the TPMT gene before the administration of AZA in clinical rheumatology practice.	Azathioprine	116-119	thiopurine S-methyltransferase	Homo sapiens	77-81
35120281-8	2022	We conclude that HLA-DQA1*02:01-HLA-DRB1*07:01 is a marker for increased risk of acute pancreatitis in individuals of Swedish genetic origin, treated with azathioprine for Crohn"s disease.	Azathioprine	155-167	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	17-25
35120281-8	2022	We conclude that HLA-DQA1*02:01-HLA-DRB1*07:01 is a marker for increased risk of acute pancreatitis in individuals of Swedish genetic origin, treated with azathioprine for Crohn"s disease.	Azathioprine	155-167	major histocompatibility complex, class II, DR beta 1	Homo sapiens	32-40
35432721-13	2022	DNA methylation analysis in primary myocytes indicated that selenium supplementation or DNMT inhibitor AZA treatment reduced DNA methylation of the GPX1 gene promoter.	Azathioprine	103-106	glutathione peroxidase 1	Rattus norvegicus	148-152
35615323-4	2022	The targeted NGS analysis showed that the VEN/AZA combination led to the eradication of the FLT3-ITD and RUNX1 mutated clone/s primarily associated with AML evolution, and subsequently, the SRSF2, NRAS, and ASXL1 mutated clone/s.	Azathioprine	46-49	fms related receptor tyrosine kinase 3	Homo sapiens	92-96
35615323-4	2022	The targeted NGS analysis showed that the VEN/AZA combination led to the eradication of the FLT3-ITD and RUNX1 mutated clone/s primarily associated with AML evolution, and subsequently, the SRSF2, NRAS, and ASXL1 mutated clone/s.	Azathioprine	46-49	RUNX family transcription factor 1	Homo sapiens	105-110
35615323-4	2022	The targeted NGS analysis showed that the VEN/AZA combination led to the eradication of the FLT3-ITD and RUNX1 mutated clone/s primarily associated with AML evolution, and subsequently, the SRSF2, NRAS, and ASXL1 mutated clone/s.	Azathioprine	46-49	serine and arginine rich splicing factor 2	Homo sapiens	190-195
35615323-4	2022	The targeted NGS analysis showed that the VEN/AZA combination led to the eradication of the FLT3-ITD and RUNX1 mutated clone/s primarily associated with AML evolution, and subsequently, the SRSF2, NRAS, and ASXL1 mutated clone/s.	Azathioprine	46-49	NRAS proto-oncogene, GTPase	Homo sapiens	197-201
35615323-4	2022	The targeted NGS analysis showed that the VEN/AZA combination led to the eradication of the FLT3-ITD and RUNX1 mutated clone/s primarily associated with AML evolution, and subsequently, the SRSF2, NRAS, and ASXL1 mutated clone/s.	Azathioprine	46-49	ASXL transcriptional regulator 1	Homo sapiens	207-212
35432721-14	2022	Selenium supplementation and AZA administration showed synergic inhibitory effect on GPX1 gene promoter methylation.	Azathioprine	29-32	glutathione peroxidase 1	Rattus norvegicus	85-89
35422896-6	2022	Meanwhile, healthy human peripheral blood Treg cells were treated with inhibitor of DNMT3b (AZA and EGCG) or transduced with DNMT3b shRNA.	Azathioprine	92-95	DNA methyltransferase 3 beta	Homo sapiens	84-90
35450035-2	2022	Despite the fact that thiopurine S-methyltransferase (TPMT) polymorphism has been recognized as a major cause of the interindividual variability in the azathioprine response, recent evidence suggests that there might be some yet unknown causes which complicate dosing strategies causing either failure of therapy or toxicity.	Azathioprine	152-164	thiopurine S-methyltransferase	Homo sapiens	22-52
35450035-2	2022	Despite the fact that thiopurine S-methyltransferase (TPMT) polymorphism has been recognized as a major cause of the interindividual variability in the azathioprine response, recent evidence suggests that there might be some yet unknown causes which complicate dosing strategies causing either failure of therapy or toxicity.	Azathioprine	152-164	thiopurine S-methyltransferase	Homo sapiens	54-58
35422896-9	2022	Consistently, inhibition of DNMT3b (AZA and EGCG) decreased the expression levels of DNMT3b, which can increase the expression levels of FOXP3, and increase the levels of TGF-beta and IL-10 and decrease the levels of IL-beta and IFN-gamma.	Azathioprine	36-39	DNA methyltransferase 3B	Mus musculus	28-34
35422896-9	2022	Consistently, inhibition of DNMT3b (AZA and EGCG) decreased the expression levels of DNMT3b, which can increase the expression levels of FOXP3, and increase the levels of TGF-beta and IL-10 and decrease the levels of IL-beta and IFN-gamma.	Azathioprine	36-39	DNA methyltransferase 3B	Mus musculus	85-91
35422896-9	2022	Consistently, inhibition of DNMT3b (AZA and EGCG) decreased the expression levels of DNMT3b, which can increase the expression levels of FOXP3, and increase the levels of TGF-beta and IL-10 and decrease the levels of IL-beta and IFN-gamma.	Azathioprine	36-39	forkhead box P3	Mus musculus	137-142
35422896-9	2022	Consistently, inhibition of DNMT3b (AZA and EGCG) decreased the expression levels of DNMT3b, which can increase the expression levels of FOXP3, and increase the levels of TGF-beta and IL-10 and decrease the levels of IL-beta and IFN-gamma.	Azathioprine	36-39	transforming growth factor alpha	Mus musculus	171-179
35422896-9	2022	Consistently, inhibition of DNMT3b (AZA and EGCG) decreased the expression levels of DNMT3b, which can increase the expression levels of FOXP3, and increase the levels of TGF-beta and IL-10 and decrease the levels of IL-beta and IFN-gamma.	Azathioprine	36-39	interleukin 10	Mus musculus	184-189
35422896-9	2022	Consistently, inhibition of DNMT3b (AZA and EGCG) decreased the expression levels of DNMT3b, which can increase the expression levels of FOXP3, and increase the levels of TGF-beta and IL-10 and decrease the levels of IL-beta and IFN-gamma.	Azathioprine	36-39	interferon gamma	Mus musculus	229-238
34995765-12	2022	Mycophenolate, azathioprine, calcineurin inhibitors and steroids associated with a lower risk of POF compared to CYC.	Azathioprine	15-27	POF1B actin binding protein	Homo sapiens	97-100
35192152-0	2022	Genotype-Guided Prescription of Azathioprine Reduces the Incidence of Adverse Drug Reactions in TPMT Intermediate Metabolizers to a Similar Incidence as Normal Metabolizers.	Azathioprine	32-44	thiopurine S-methyltransferase	Homo sapiens	96-100
35192152-3	2022	We aimed to investigate the influence of TPMT phenotype, concomitant treatments, and demographic characteristics on the incidence of adverse reactions (ADRs) in patients who start treatment with azathioprine (AZA).	Azathioprine	195-207	thiopurine S-methyltransferase	Homo sapiens	41-45
35192152-3	2022	We aimed to investigate the influence of TPMT phenotype, concomitant treatments, and demographic characteristics on the incidence of adverse reactions (ADRs) in patients who start treatment with azathioprine (AZA).	Azathioprine	209-212	thiopurine S-methyltransferase	Homo sapiens	41-45
35356677-0	2022	Fluorine-induced diastereodivergence discovered in an equally rare enantioselective syn-aza-Henry reaction.	Azathioprine	88-91	synemin	Homo sapiens	84-87
35118815-3	2022	We hypothesized that among TPMT and NUDT15 normal metabolizers, a score combining the genetically predicted expression of other proteins in the thiopurine pathway would be associated with a higher risk for azathioprine discontinuation due to myelotoxicity.	Azathioprine	206-218	thiopurine S-methyltransferase	Homo sapiens	27-31
35118815-3	2022	We hypothesized that among TPMT and NUDT15 normal metabolizers, a score combining the genetically predicted expression of other proteins in the thiopurine pathway would be associated with a higher risk for azathioprine discontinuation due to myelotoxicity.	Azathioprine	206-218	nudix hydrolase 15	Homo sapiens	36-42
35118815-4	2022	We conducted a retrospective cohort study of new users of azathioprine who were normal TPMT and NUDT15 metabolizers.	Azathioprine	58-70	thiopurine S-methyltransferase	Homo sapiens	87-91
35118815-4	2022	We conducted a retrospective cohort study of new users of azathioprine who were normal TPMT and NUDT15 metabolizers.	Azathioprine	58-70	nudix hydrolase 15	Homo sapiens	96-102
35118815-12	2022	In conclusion, among patients who were TPMT and NUDT15 normal metabolizers, a score combining the predicted expression of AOX1 and NME1 was associated with an increased risk for discontinuing azathioprine due to myelotoxicity.	Azathioprine	192-204	thiopurine S-methyltransferase	Homo sapiens	39-43
35118815-12	2022	In conclusion, among patients who were TPMT and NUDT15 normal metabolizers, a score combining the predicted expression of AOX1 and NME1 was associated with an increased risk for discontinuing azathioprine due to myelotoxicity.	Azathioprine	192-204	nudix hydrolase 15	Homo sapiens	48-54
35118815-12	2022	In conclusion, among patients who were TPMT and NUDT15 normal metabolizers, a score combining the predicted expression of AOX1 and NME1 was associated with an increased risk for discontinuing azathioprine due to myelotoxicity.	Azathioprine	192-204	aldehyde oxidase 1	Homo sapiens	122-126
35118815-12	2022	In conclusion, among patients who were TPMT and NUDT15 normal metabolizers, a score combining the predicted expression of AOX1 and NME1 was associated with an increased risk for discontinuing azathioprine due to myelotoxicity.	Azathioprine	192-204	NME/NM23 nucleoside diphosphate kinase 1	Homo sapiens	131-135
35584388-1	2022	OBJECTIVES: Azathioprine (AZA)-induced pancreatitis (AIP) is a common, idiosyncratic adverse effect whose incidence and risk factors data in inflammatory bowel disease (IBD) patients are not fully clarified.	Azathioprine	12-24	aryl hydrocarbon receptor interacting protein	Homo sapiens	53-56
35584388-1	2022	OBJECTIVES: Azathioprine (AZA)-induced pancreatitis (AIP) is a common, idiosyncratic adverse effect whose incidence and risk factors data in inflammatory bowel disease (IBD) patients are not fully clarified.	Azathioprine	26-29	aryl hydrocarbon receptor interacting protein	Homo sapiens	53-56
35584388-7	2022	Smoking (P = 0.02), single daily dose of AZA (P < 0.001), and concomitant budesonide (P = 0.001) were risk factors for AIP.	Azathioprine	41-44	aryl hydrocarbon receptor interacting protein	Homo sapiens	119-122
35584388-8	2022	In multivariate analysis, concomitant treatment with budesonide (odds ratio, 5.3; P = 0.002) and single daily dose of AZA (odds ratio, 3.8; P = 0.002) were the only predictors of AIP.	Azathioprine	118-121	aryl hydrocarbon receptor interacting protein	Homo sapiens	179-182
35169948-6	2022	MTX and AZA treatment decreased Hb levels, increased relative liver weight, increased the activity of glutamate pyruvate transaminase (ALT) and glutamate oxaloacetate transaminase (AST) aminotransferase (ALT) and aspartate aminotransferase (AST) values, and displayed histopathological and ultrastructural alterations.	Azathioprine	8-11	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	213-239
35169948-6	2022	MTX and AZA treatment decreased Hb levels, increased relative liver weight, increased the activity of glutamate pyruvate transaminase (ALT) and glutamate oxaloacetate transaminase (AST) aminotransferase (ALT) and aspartate aminotransferase (AST) values, and displayed histopathological and ultrastructural alterations.	Azathioprine	8-11	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	241-244
35118815-1	2022	TPMT and NUDT15 variants explain less than 25% of azathioprine-associated myelotoxicity.	Azathioprine	50-62	thiopurine S-methyltransferase	Homo sapiens	0-4
35118815-1	2022	TPMT and NUDT15 variants explain less than 25% of azathioprine-associated myelotoxicity.	Azathioprine	50-62	nudix hydrolase 15	Homo sapiens	9-15
34751173-0	2022	A novel NUDT15 variant identified in Caucasian TPMT wild type patients with inflammatory bowel disease and azathioprine-related myelotoxicity.	Azathioprine	107-119	nudix hydrolase 15	Homo sapiens	8-14
35034963-0	2022	Association of ITPA gene polymorphisms with adverse effects of AZA/6-MP administration: a systematic review and meta-analysis.	Azathioprine	63-66	inosine triphosphatase	Homo sapiens	15-19
35034963-3	2022	In the present study we performed a systematic review and a meta-analysis, comprising 30 studies and 3582 individuals, to investigate the putative genetic association of two inosine triphosphatase (ITPA) polymorphisms with adverse effects in patients treated with AZA/6-MP.	Azathioprine	264-267	inosine triphosphatase	Homo sapiens	198-202
35159194-3	2022	Recently, thiopurine drug metabolites such as azathioprine have been included in the lists of ITPase substrates.	Azathioprine	46-58	inosine triphosphatase	Homo sapiens	94-100
35052616-1	2022	Hybrids based on an aza-analogue of CGP37157, a mitochondrial Na+/Ca2+ exchanger antagonist, and lipoic acid were obtained in order to combine in a single molecule the antioxidant and NRF2 induction properties of lipoic acid and the neuroprotective activity of CGP37157.	Azathioprine	20-23	NFE2 like bZIP transcription factor 2	Homo sapiens	184-188
34751173-0	2022	A novel NUDT15 variant identified in Caucasian TPMT wild type patients with inflammatory bowel disease and azathioprine-related myelotoxicity.	Azathioprine	107-119	thiopurine S-methyltransferase	Homo sapiens	47-51
35371455-1	2022	Background: A randomized controlled trial demonstrated a beneficial effect of corticosteroids (CS) + cyclophosphamide followed by azathioprine in progressive immunoglobulin A nephropathy (IgAN).	Azathioprine	130-142	IGAN1	Homo sapiens	188-192
2529858-2	1989	Structure-activity studies starting from substituted N-carboxymethyl dipeptide inhibitors resulted in the introduction of a cyclo-alkane P1" residue and in the replacement of the aza-link between P1 and P1" residues by a methylene group, with a net ten-fold potency gain.	Azathioprine	179-182	zinc finger protein 185	Mus musculus	196-206
2474211-6	1989	In the pilot study, GAB (1.0-1.5 mg/kg/day) was given in 12-hr infusions, in association with prednisone (Pred) 1 mg/kg/day and azathioprine (Aza) 2 mg/kg/day, as prophylactic treatment of rejection in 12 kidney-transplanted patients during the first 2 weeks postgrafting.	Azathioprine	128-140	alpha-1-B glycoprotein	Homo sapiens	20-23
2758725-0	1989	Pharmacogenetics of acute azathioprine toxicity: relationship to thiopurine methyltransferase genetic polymorphism.	Azathioprine	26-38	thiopurine S-methyltransferase	Homo sapiens	65-93
2758725-3	1989	The enzyme thiopurine methyltransferase (TPMT) plays an important role in azathioprine catabolism.	Azathioprine	74-86	thiopurine S-methyltransferase	Homo sapiens	11-39
2758725-3	1989	The enzyme thiopurine methyltransferase (TPMT) plays an important role in azathioprine catabolism.	Azathioprine	74-86	thiopurine S-methyltransferase	Homo sapiens	41-45
2758725-10	1989	Inherited low TPMT activity appears to be a major risk factor for acute azathioprine-induced myelosuppression.	Azathioprine	72-84	thiopurine S-methyltransferase	Homo sapiens	14-18
2702102-9	1989	We suggest that treatment with prednisone and azathioprine may be beneficial in children with severe IgAN and that a controlled clinical trial is warranted.	Azathioprine	46-58	IGAN1	Homo sapiens	101-105
2656346-6	1989	Fasting plasma C-peptide was significantly greater in the azathioprine-treated group at 3 and 6 mo, but this difference was not sustained.	Azathioprine	58-70	insulin	Homo sapiens	15-24
2672226-1	1989	We describe a bootstrap investigation of the stability of a Cox proportional hazards regression model resulting from the analysis of a clinical trial of azathioprine versus placebo in patients with primary biliary cirrhosis.	Azathioprine	153-165	cytochrome c oxidase subunit 8A	Homo sapiens	60-63
2495253-3	1989	Following in vitro exposure to IFN-gamma an increase in NK activity from 36 to 44% (P less than 0.05) could be induced during CsA therapy but this was no longer observed after conversion to AZA (19 to 22%, N.S.).	Azathioprine	190-193	interferon gamma	Homo sapiens	31-40
2495253-5	1989	The IFN-gamma production capacity after mitogen stimulation of unprimed lymphocytes was more depressed during CsA than during AZA therapy (median 25 vs 80 U/ml 10(6) cells, P less than 0.05), suggesting a reversible inhibition of CsA on lymphokine production.	Azathioprine	126-129	interferon gamma	Homo sapiens	4-13
2495253-6	1989	Despite the better IFN-gamma production capacity, both the activity, inducibility and number of NK cells were significantly lower under AZA therapy than under CsA therapy.	Azathioprine	136-139	interferon gamma	Homo sapiens	19-28
2626634-3	1989	The second patient, who had been treated with azathioprine (AZ) one year previously, had an apparently balanced translocation 46 XX, t (11; 11) (p 12, p 14) in blood T lymphocytes but not in skin fibroblast culture.	Azathioprine	46-58	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	145-149
2626634-3	1989	The second patient, who had been treated with azathioprine (AZ) one year previously, had an apparently balanced translocation 46 XX, t (11; 11) (p 12, p 14) in blood T lymphocytes but not in skin fibroblast culture.	Azathioprine	46-58	ribonuclease P/MRP subunit p14	Homo sapiens	151-155
2626634-3	1989	The second patient, who had been treated with azathioprine (AZ) one year previously, had an apparently balanced translocation 46 XX, t (11; 11) (p 12, p 14) in blood T lymphocytes but not in skin fibroblast culture.	Azathioprine	60-62	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	145-149
2626634-3	1989	The second patient, who had been treated with azathioprine (AZ) one year previously, had an apparently balanced translocation 46 XX, t (11; 11) (p 12, p 14) in blood T lymphocytes but not in skin fibroblast culture.	Azathioprine	60-62	ribonuclease P/MRP subunit p14	Homo sapiens	151-155
2672532-4	1989	Patients who received cyclosporine A as immunosuppressive treatment excreted little or no EGF during the first month, while patients who received prednisone and azathioprine excreted EGF as early as four days after the transplantation.	Azathioprine	161-173	epidermal growth factor	Homo sapiens	183-186
3047930-3	1988	A significantly increased mIg incidence was observed in heart Tx patients, patients over 40 years of age, and those receiving azathioprine or antithymocyte globulin in addition to prednisolone and cyclosporine as immunosuppressive treatment.	Azathioprine	126-138	chemokine (C-X-C motif) ligand 9	Mus musculus	26-29
3178923-9	1988	The immunosuppressive action of AZA depends on the synergistic cooperation of the relatively weak cytostatic effect of low doses of 6-MP and the chemosensitizing effect of PLD which is induced by highly reactive imidazole derivatives.	Azathioprine	32-35	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	172-175
3070501-0	1988	[Serum gastrin level in patients treated with cyclosporin A or azathioprine with prednisone after kidney transplantation].	Azathioprine	63-75	gastrin	Homo sapiens	7-14
2455447-4	1988	The incidence of diabetes mellitus (DM) requiring insulin therapy was higher in CsA-treated recipients (18/105, 17.1%) than in Az-treated recipients (23/180, 12.8%; P less than 0.05), although both the daily Pred and cumulative doses of methylprednisolone (MP) at the onset of DM were significantly smaller in the CsA group than in the Az group (26.1 +/- 2.2 mg v 41.4 +/- 3.4 mg, P less than 0.01 and 3,086 +/- 626 mg v 7,133 +/- 1,129 mg, P less than 0.01, respectively).	Azathioprine	127-129	insulin	Homo sapiens	50-57
2455447-4	1988	The incidence of diabetes mellitus (DM) requiring insulin therapy was higher in CsA-treated recipients (18/105, 17.1%) than in Az-treated recipients (23/180, 12.8%; P less than 0.05), although both the daily Pred and cumulative doses of methylprednisolone (MP) at the onset of DM were significantly smaller in the CsA group than in the Az group (26.1 +/- 2.2 mg v 41.4 +/- 3.4 mg, P less than 0.01 and 3,086 +/- 626 mg v 7,133 +/- 1,129 mg, P less than 0.01, respectively).	Azathioprine	336-338	insulin	Homo sapiens	50-57
2455447-7	1988	Insulin could be withdrawn within 3 months in six of eight patients who had been converted from CsA to Az.	Azathioprine	103-105	insulin	Homo sapiens	0-7
3285537-3	1988	Serum CRP concentration rose in response to operation in virtually all patients, regardless of immunosuppressive regimen, from mean baselines of 5.9 +/- 2.7 mcg/ml (AZA) and 6.8 +/- 6.5 mcg/ml (CsA) to mean peak levels of 43.8 +/- 33.4 mcg/ml and 65.1 +/- 39.5 mcg/ml, respectively.	Azathioprine	165-168	C-reactive protein	Homo sapiens	6-9
3285537-4	1988	CRP rose during 76% of acute rejection episodes in AZA patients by a mean of 29.7 +/- 37.4 mcg/ml.	Azathioprine	51-54	C-reactive protein	Homo sapiens	0-3
3285537-1	1988	Acute or persistent elevations in serum C-reactive protein (CRP) concentration have been shown to be of value in diagnosing acute rejection episodes in azathioprine (AZA)-treated renal transplant recipients.	Azathioprine	152-164	C-reactive protein	Homo sapiens	40-58
3731110-10	1986	7MB[c]ACR was at least 5-fold more active as a tumor initiator on mouse skin than was the unsubstituted aza-aromatic compound, benz[c]acridine.	Azathioprine	104-107	acrosin prepropeptide	Mus musculus	6-9
3285537-1	1988	Acute or persistent elevations in serum C-reactive protein (CRP) concentration have been shown to be of value in diagnosing acute rejection episodes in azathioprine (AZA)-treated renal transplant recipients.	Azathioprine	152-164	C-reactive protein	Homo sapiens	60-63
3285537-1	1988	Acute or persistent elevations in serum C-reactive protein (CRP) concentration have been shown to be of value in diagnosing acute rejection episodes in azathioprine (AZA)-treated renal transplant recipients.	Azathioprine	166-169	C-reactive protein	Homo sapiens	40-58
3285537-1	1988	Acute or persistent elevations in serum C-reactive protein (CRP) concentration have been shown to be of value in diagnosing acute rejection episodes in azathioprine (AZA)-treated renal transplant recipients.	Azathioprine	166-169	C-reactive protein	Homo sapiens	60-63
3677489-5	1987	The degree of c-myc and c-myb expression was significantly reduced along with or prior to the amelioration of clinical symptoms and improvement as determined by laboratory data under treatment with prednisolone and/or azathioprine administration.	Azathioprine	218-230	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	14-19
3677489-5	1987	The degree of c-myc and c-myb expression was significantly reduced along with or prior to the amelioration of clinical symptoms and improvement as determined by laboratory data under treatment with prednisolone and/or azathioprine administration.	Azathioprine	218-230	MYB proto-oncogene, transcription factor	Homo sapiens	24-29
3300326-4	1987	Upright plasma renin activity was suppressed in cyclosporine-treated patients (cyclosporine 2.9 +/- 0.9, azathioprine 4.7 +/- 0.9, renal insufficiency 5.2 +/- 1.9 ng/ml/hour) but could be stimulated by a four-day period of dietary sodium restriction and diuretic administration (cyclosporine 15.8 +/- 4.4 ng/ml/hour).	Azathioprine	105-117	renin	Homo sapiens	15-20
3547923-0	1987	Interleukin 2 response inhibition following donor specific transfusions given with azathioprine.	Azathioprine	83-95	interleukin 2	Homo sapiens	0-13
2947355-0	1986	Modulation of the response to interleukin 2 in recipients of donor-specific transfusions under azathioprine immunosuppression.	Azathioprine	95-107	interleukin 2	Homo sapiens	30-43
2947355-1	1986	The effect of plasma from recipients of donor-specific transfusions given under azathioprine immunosuppression (DST+A) on the response to IL-2 was examined.	Azathioprine	80-92	interleukin 2	Homo sapiens	138-142
3284065-9	1988	On the other hand, a significant (P less than .01) early maturation of blood-borne monocytes into tissue macrophages was observed in the CsA-treated grafts in context of first rejection, which was lacking from those treated with CsA + MP or Aza + MP.	Azathioprine	241-244	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	137-140
3278431-7	1988	In the CsA group, 71% required either a significant reduction in CsA dosage with the addition of azathioprine or a complete switch to azathioprine, mainly because of CsA-associated nephrotoxicity.	Azathioprine	97-109	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	7-10
3278431-7	1988	In the CsA group, 71% required either a significant reduction in CsA dosage with the addition of azathioprine or a complete switch to azathioprine, mainly because of CsA-associated nephrotoxicity.	Azathioprine	134-146	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	7-10
2977607-4	1988	Proliferative responses and IL2 production were partially restored in mice given immunosuppressive therapy with azathioprine, cyclosporin A or Sch 24937 a drug whose inhibitory effects on cellular and humoral immune responses in mice have recently been described.	Azathioprine	112-124	interleukin 2	Mus musculus	28-31
3495914-0	1987	Initial characterization of humoral IL-2 response inhibition following donor-specific transfusions under azathioprine immunosuppression.	Azathioprine	105-117	interleukin 2	Homo sapiens	36-40
3495914-1	1987	A previous study indicated that noncompetitive humoral inhibition of IL-2-induced proliferation was a frequent consequence of donor-specific transfusions under azathioprine immunosuppression.	Azathioprine	160-172	interleukin 2	Homo sapiens	69-73
3467886-1	1987	Thiopurine methyltransferase (TPMT) catalyzes the S-methylation of thiopurine drugs such as 6-mercaptopurine (6-MP) and azathioprine.	Azathioprine	120-132	thiopurine S-methyltransferase	Homo sapiens	0-28
3467886-1	1987	Thiopurine methyltransferase (TPMT) catalyzes the S-methylation of thiopurine drugs such as 6-mercaptopurine (6-MP) and azathioprine.	Azathioprine	120-132	thiopurine S-methyltransferase	Homo sapiens	30-34
3099440-10	1987	Allograft mononuclear cell infiltrates in cyclosporine (CsA) vs. azathioprine-treated patients revealed significantly fewer Leu 2 (P less than .05) and Leu M1 (P less than .05) cell populations in CsA patients during acute rejection.	Azathioprine	65-77	deleted in lymphocytic leukemia 1	Homo sapiens	124-129
3090376-2	1986	In contrast, transplant patients treated with azathioprine or cyclosporine A have percentages of OKT 8 and Leu 7 positive PBL, similar to control persons (respectively 29 +/- 13, 33 +/- 10, 30 +/- 10 for the OKT 8+ cells and 8 +/- 7, 11 +/- 6 and 15 +/- 9 for the Leu 7+ cells).	Azathioprine	46-58	beta-1,3-glucuronyltransferase 1	Homo sapiens	107-112
3086252-8	1986	Of these agents, only the nonsteroidal drugs reduced serum haptoglobin; hydrocortisone, cyclophosphamide and azathioprine elevated haptoglobin.	Azathioprine	109-121	haptoglobin	Rattus norvegicus	131-142
3090376-2	1986	In contrast, transplant patients treated with azathioprine or cyclosporine A have percentages of OKT 8 and Leu 7 positive PBL, similar to control persons (respectively 29 +/- 13, 33 +/- 10, 30 +/- 10 for the OKT 8+ cells and 8 +/- 7, 11 +/- 6 and 15 +/- 9 for the Leu 7+ cells).	Azathioprine	46-58	beta-1,3-glucuronyltransferase 1	Homo sapiens	264-269
3899841-5	1985	Using Cox multiple regression analysis and adjusting for slight imbalance between the two treatment groups, the therapeutic effect of azathioprine was statistically significant (p = 0.01), with azathioprine reducing the risk of dying to 59% of that observed during placebo treatment (95% confidence interval 40%-90%) or improving survival time by 20 mo in the average patient.	Azathioprine	134-146	cytochrome c oxidase subunit 8A	Homo sapiens	6-9
2934083-3	1985	When both stimulator and responder lymphocytes in the MLR were HGPRT deficient, azathioprine (36 microM) was much more inhibitory than 6-MP (100 microM).	Azathioprine	80-92	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	63-68
2934083-5	1985	The difference in inhibitory activity between azathioprine and 6-MP was reduced when normal stimulator lymphocytes were cultured with HGPRT deficient responder lymphocytes in the MLR.	Azathioprine	46-58	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	134-139
3899841-5	1985	Using Cox multiple regression analysis and adjusting for slight imbalance between the two treatment groups, the therapeutic effect of azathioprine was statistically significant (p = 0.01), with azathioprine reducing the risk of dying to 59% of that observed during placebo treatment (95% confidence interval 40%-90%) or improving survival time by 20 mo in the average patient.	Azathioprine	194-206	cytochrome c oxidase subunit 8A	Homo sapiens	6-9
2931095-0	1985	Effect of interleukin-2 on the inhibition of the human mixed lymphocyte reaction (MLR) by azathioprine.	Azathioprine	90-102	interleukin 2	Homo sapiens	10-23
2931095-1	1985	The effect of interleukin-2 on the response of the human MLR to azathioprine was studied.	Azathioprine	64-76	interleukin 2	Homo sapiens	14-27
2931095-3	1985	Only partial relief (16%) of azathioprine (36 microM) inhibition was found in the interleukin-2 treated MLR compared with azathioprine treatment alone.	Azathioprine	29-41	interleukin 2	Homo sapiens	82-95
2931095-4	1985	However, [3H]-thymidine incorporation by azathioprine (36 microM) + interleukin-2 treated MLR was 4.3 times greater than that exposed to azathioprine alone.	Azathioprine	137-149	interleukin 2	Homo sapiens	68-81
3871612-6	1985	Azathioprine is a competitive inhibitor of glutathione S-transferase, benziodarone is covalently bound to ligandin and TSO is an inducer of liver ligandin.	Azathioprine	0-12	glutathione S-transferase alpha 2	Rattus norvegicus	146-154
2859508-4	1985	Haemostatic tests in cyclosporin-treated and azathioprine-treated patients and normal subjects (10 in each group) showed increased concentrations of factor VIII C, fibrinogen, antithrombin III, and protein C in the cyclosporin-treated patients.	Azathioprine	45-57	fibrinogen beta chain	Homo sapiens	164-174
2859508-4	1985	Haemostatic tests in cyclosporin-treated and azathioprine-treated patients and normal subjects (10 in each group) showed increased concentrations of factor VIII C, fibrinogen, antithrombin III, and protein C in the cyclosporin-treated patients.	Azathioprine	45-57	serpin family C member 1	Homo sapiens	176-192
3920961-0	1985	Effects of treatment with azathioprine and cyclosporin A on interferon-gamma production by peripheral blood leukocytes of renal allograft recipients.	Azathioprine	26-38	interferon gamma	Homo sapiens	60-76
3920961-2	1985	Both under immunosuppressive treatment with azathioprine and with cyclosporin A (CsA) the PBMC of these patients proved deficient for IFN-gamma production when compared to those of healthy controls.	Azathioprine	44-56	interferon gamma	Homo sapiens	134-143
3920961-3	1985	After conversion from conventional azathioprine to CsA medication the ConA-induced IFN-gamma production increased.	Azathioprine	35-47	interferon gamma	Homo sapiens	83-92
3918592-8	1985	AgT-1 antibodies inhibited the biological activity of the active thymic fraction (AFT-6) in recovering the sensitivity of spleen fRFC from thymectomized mice to the inhibitory action of azathioprin.	Azathioprine	186-197	solute carrier family 7, (cationic amino acid transporter, y+ system) member 13	Mus musculus	0-5
3871612-8	1985	As there is published proof that the reaction of MeHg+ with GSH does not require enzymatic help, the inhibitory effect of azathioprine and benziodarone confirms the role of ligandin in the transport of methylmercury or its GSH complex.	Azathioprine	122-134	glutathione S-transferase alpha 2	Rattus norvegicus	173-181
3919749-0	1985	Lack of inhibition of purine nucleoside phosphorylase and adenosine deaminase in patients treated with azathioprine.	Azathioprine	103-115	adenosine deaminase	Homo sapiens	58-77
3004140-0	1985	Aza-substituted omega-side-chain modifications of 7-oxabicyclo[2.2.1]heptane thromboxane A2 receptor antagonists: structure-activity relationships.	Azathioprine	0-3	thromboxane A2 receptor	Homo sapiens	77-100
2864321-1	1985	A highly purified preparation of human prealbumin was shown to potentiate the sensitivity of rosette spleen forming cells of adult thymectomized mice to azathioprine in vitro and in vivo and to induce the appearance of the Thy 1, 2 antigen in vitro on spleen cells of adult thymectomized mice.	Azathioprine	153-165	transthyretin	Mus musculus	39-49
6151783-1	1984	A 26-year-old male with renal allograft, who received immunosuppressive treatment with azathioprine, presented marked elevations of serum biliary tract enzymes, such as gamma-glutamyl transpeptidase (5,609 units/l) and alkaline phosphatase (60.5 Bessey-Lowry units), 14 months after transplantation.	Azathioprine	87-99	inactive glutathione hydrolase 2	Homo sapiens	169-198
6735556-1	1984	A patient with pemphigus vulgaris had lesions on the lip that proved to be refractory to intralesional corticosteroid therapy and to treatment with azathioprine and later to daily administration of 250 mg of prednisone.	Azathioprine	148-160	SMG1 nonsense mediated mRNA decay associated PI3K related kinase	Homo sapiens	53-56
6151783-0	1984	Nonicteric liver damage with a gamma-glutamyl transpeptidase level of 5,609 units/l in a renal-transplant recipient receiving azathioprine.	Azathioprine	126-138	inactive glutathione hydrolase 2	Homo sapiens	31-60
6540565-0	1984	Hypoxanthine-guanine phosphoribosyltransferase-independent toxicity of azathioprine in human lymphoblasts.	Azathioprine	71-83	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	0-46
7136860-0	1982	Alteration of hepatic ornithine decarboxylase and aniline hydroxylase activities following a single dosing of azathioprine to rats.	Azathioprine	110-122	ornithine decarboxylase 1	Rattus norvegicus	22-45
6216997-10	1982	Patients with CAH receiving azathioprine (n = 8) had significantly fewer TSC cells, and a higher TH/TSC ratio (2 .	Azathioprine	28-40	TSC complex subunit 1	Homo sapiens	73-76
6216997-10	1982	Patients with CAH receiving azathioprine (n = 8) had significantly fewer TSC cells, and a higher TH/TSC ratio (2 .	Azathioprine	28-40	TSC complex subunit 1	Homo sapiens	100-103
6359389-9	1983	The fall in IgE levels following transplantation is proposed to be attributable to the combined corticosteroid-azathioprine treatment.	Azathioprine	111-123	immunoglobulin heavy constant epsilon	Homo sapiens	12-15
6288913-4	1982	This assumption was supported by several lines of evidence as follows: (1) rat erythrocytes which are less antigenic for mice caused a relatively low response in terms of increase in cyclic GMP compared with SRBC, (2) this cyclic GMP response was abrogated in animals under immunosuppressive states where X-irradiated, azathioprine-treated or tumor-bearing mice were used.	Azathioprine	319-331	5'-nucleotidase, cytosolic II	Mus musculus	230-233
7026278-3	1981	Prednisolone coupled with azathioprine reduced the toxic action of the latter and raised the concentration of alpha 1-glycoprotein, alpha 2-macroglobin, transferrin, haptoglobin which are responsible for nonspecific defence factors.	Azathioprine	26-38	transferrin	Homo sapiens	153-164
7026278-3	1981	Prednisolone coupled with azathioprine reduced the toxic action of the latter and raised the concentration of alpha 1-glycoprotein, alpha 2-macroglobin, transferrin, haptoglobin which are responsible for nonspecific defence factors.	Azathioprine	26-38	haptoglobin	Homo sapiens	166-177
303241-3	1977	A circulating thymic factor (FTS) has been characterized by a bioassay based on its ability to render theta-negative rosette-forming cells theta-positive and azathioprine-sensitive.	Azathioprine	158-170	AKT interacting protein	Homo sapiens	0-33
43222-8	1979	Differences in AZA and 6-MP kinetics among the monkeys were attributed to differences in individual aldehyde oxidase and xanthine oxidase levels.	Azathioprine	15-18	aldehyde oxidase 1	Macaca mulatta	100-116
273245-0	1978	Thymic hormone-like restoration by human prealbumin of azathioprine sensitivity of spleen cells from thymectomized mice.	Azathioprine	55-67	transthyretin	Mus musculus	41-51
338201-0	1978	Changes in serum and urine lysozyme activity after kidney transplantation: influence of graft function and therapy with azathioprine.	Azathioprine	120-132	lysozyme	Homo sapiens	27-35
338201-2	1978	Resumption of graft function decreases the high serum lysozyme activity by increasing the rate of catabolism in the transplant; at the same time, however, the production is inhibited by therapy with azathioprine.	Azathioprine	199-211	lysozyme	Homo sapiens	54-62
917042-1	1977	Plasmapheresis combined with prednisone and azathioprine therapy produced striking clinical improvement in five patients with myasthenia gravis who still had moderate to severe disability despite thymectomy, high-dose prednisone therapy and optimal doses of cholinesterase inhibitors.	Azathioprine	44-56	butyrylcholinesterase	Homo sapiens	258-272
802685-5	1976	The two aza-analogues of des-His-LHRH were neither agonists nor antagonists in these two test systems.	Azathioprine	8-11	gonadotropin releasing hormone 1	Rattus norvegicus	33-37
4844636-0	1974	The effects of azathioprine on CCl4 induced cirrhosis in the rat.	Azathioprine	15-27	C-C motif chemokine ligand 4	Rattus norvegicus	31-35
1190831-4	1975	After an incubation of 120 min azathioprine (1mM/1) inhibited lactate and glucose-6-phosphate dehydrogenase activities by about 10 per cent only, whereas the corresponding values with methotrexate amounted to 80 and 70 per cent, respectively.	Azathioprine	31-43	glucose-6-phosphate dehydrogenase	Homo sapiens	74-107
4433653-0	1974	Enhanced response of erythropoietin sensitive cells to erythropoietin by low dose prednisolone hemisuccinate and its abolition by azathioprine.	Azathioprine	130-142	erythropoietin	Homo sapiens	21-35
4433653-0	1974	Enhanced response of erythropoietin sensitive cells to erythropoietin by low dose prednisolone hemisuccinate and its abolition by azathioprine.	Azathioprine	130-142	erythropoietin	Homo sapiens	55-69
33840389-0	2021	Blood CD3-(CD56 or 16)+ natural killer cell distributions are heterogeneous in healthy adults and suppressed by azathioprine in patients with ANCA-associated vasculitides.	Azathioprine	112-124	neural cell adhesion molecule 1	Homo sapiens	11-15
33950972-0	2021	Azathioprine-induced toxoplasma gondii infection in a patient with Crohn"s disease with NUDT15 variation: A case report.	Azathioprine	0-12	nudix hydrolase 15	Homo sapiens	88-94
33950972-3	2021	Most of the previous literature focused on the TPMP gene-related adverse reactions, herein, we report a case of Crohn"s disease patient with nucleoside diphosphate-linked moiety X motif 15 gene (NUDT15) variation and wild-type TPMP gene who developed toxoplasma gondii infection after azathioprine treatment.	Azathioprine	285-297	nudix hydrolase 15	Homo sapiens	195-201
33950972-9	2021	CONCLUSION: We report a case of Crohn"s disease in a patient who developed severe pneumonia caused by toxoplasma gondii infection due to the administration of AZA, with normal TPMP gene but NUDT15 gene mutation.	Azathioprine	159-162	nudix hydrolase 15	Homo sapiens	190-196
33950972-10	2021	This indicates that NUDT15 variation may contribute to severe adverse events in patients treated with azathioprine, and we suggest that NUDT15 genotype be detected before the use of azathioprine in order to provide personalized therapy and reduce side effects.	Azathioprine	102-114	nudix hydrolase 15	Homo sapiens	20-26
33929082-1	2021	Xanthine oxidase (XO) competes with thiopurine S-methyltransferase (TPMT) and hypoxanthine guanine phosphoribosyltransferase (HPRT) to metabolize azathioprine (AZA)/6-mercaptopurine (6-MP) in vivo.	Azathioprine	146-158	thiopurine S-methyltransferase	Homo sapiens	36-66
33929082-1	2021	Xanthine oxidase (XO) competes with thiopurine S-methyltransferase (TPMT) and hypoxanthine guanine phosphoribosyltransferase (HPRT) to metabolize azathioprine (AZA)/6-mercaptopurine (6-MP) in vivo.	Azathioprine	146-158	thiopurine S-methyltransferase	Homo sapiens	68-72
33929082-1	2021	Xanthine oxidase (XO) competes with thiopurine S-methyltransferase (TPMT) and hypoxanthine guanine phosphoribosyltransferase (HPRT) to metabolize azathioprine (AZA)/6-mercaptopurine (6-MP) in vivo.	Azathioprine	146-158	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	78-124
33929082-1	2021	Xanthine oxidase (XO) competes with thiopurine S-methyltransferase (TPMT) and hypoxanthine guanine phosphoribosyltransferase (HPRT) to metabolize azathioprine (AZA)/6-mercaptopurine (6-MP) in vivo.	Azathioprine	146-158	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	126-130
33929082-1	2021	Xanthine oxidase (XO) competes with thiopurine S-methyltransferase (TPMT) and hypoxanthine guanine phosphoribosyltransferase (HPRT) to metabolize azathioprine (AZA)/6-mercaptopurine (6-MP) in vivo.	Azathioprine	160-163	thiopurine S-methyltransferase	Homo sapiens	68-72
33929082-1	2021	Xanthine oxidase (XO) competes with thiopurine S-methyltransferase (TPMT) and hypoxanthine guanine phosphoribosyltransferase (HPRT) to metabolize azathioprine (AZA)/6-mercaptopurine (6-MP) in vivo.	Azathioprine	160-163	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	78-124
33929082-1	2021	Xanthine oxidase (XO) competes with thiopurine S-methyltransferase (TPMT) and hypoxanthine guanine phosphoribosyltransferase (HPRT) to metabolize azathioprine (AZA)/6-mercaptopurine (6-MP) in vivo.	Azathioprine	160-163	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	126-130
33968761-13	2021	However, in the presence of Aza despite increased ERV-K113 env expression, an inhibition of HEK293 proliferation and a further restriction of invasion was found.	Azathioprine	28-31	endogenous retrovirus group K member 20	Homo sapiens	59-62
33968761-15	2021	In addition, ERV-K env significantly regulates proliferation and invasion depending on p53 status and Aza treatment.	Azathioprine	102-105	endogenous retrovirus group K member 20	Homo sapiens	19-22
16695929-3	1967	This inability to respond to azathioprine can be directly related to the absence in these patients of the enzyme hypoxanthine-guanine phosphoribosyltransferase which is required for conversion of the drug or its metabolites to the biochemically active ribonucleotide form.	Azathioprine	29-41	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	113-159
33997038-6	2021	Conclusions: A combination of hypoxia, IL-15, and AZA promotes the conversion of pbNK into idNK cells CD56+CD16--expressing KIR receptors and produces VEGF.	Azathioprine	50-53	IDNK gluconokinase	Homo sapiens	91-95
33997038-6	2021	Conclusions: A combination of hypoxia, IL-15, and AZA promotes the conversion of pbNK into idNK cells CD56+CD16--expressing KIR receptors and produces VEGF.	Azathioprine	50-53	neural cell adhesion molecule 1	Homo sapiens	102-106
33997038-6	2021	Conclusions: A combination of hypoxia, IL-15, and AZA promotes the conversion of pbNK into idNK cells CD56+CD16--expressing KIR receptors and produces VEGF.	Azathioprine	50-53	vascular endothelial growth factor A	Homo sapiens	151-155
33272733-0	2021	Optimization of azathioprine dose in combined treatment with anti-TNF-alpha in inflammatory bowel disease.	Azathioprine	16-28	tumor necrosis factor	Homo sapiens	66-75
33923173-8	2021	The induced expression of ZnT1 that remained impervious in cells treated with aza-dC coincided with resistance to Cd cytotoxicity.	Azathioprine	78-81	solute carrier family 30 member 1	Homo sapiens	26-30
33860754-0	2021	Importance of NUDT15 c.415C>T phenotype in treatment of inflammatory bowel disease with azathioprine and occurrence of severe myelosuppression: A case report.	Azathioprine	88-100	nudix hydrolase 15	Homo sapiens	14-20
33860754-5	2021	In this case, the azathioprine-related genotyping test showed that homozygous wild-type TPMT*3 but a c.415C>T homozygous mutation was found in NUDT15.	Azathioprine	18-30	nudix hydrolase 15	Homo sapiens	143-149
34027115-3	2021	Assessment of thiopurine methyltransferase (TPMT), the key enzyme for the inactivation of AZA, as a predictor of AZA toxicity had been a matter of conflict.	Azathioprine	90-93	thiopurine S-methyltransferase	Homo sapiens	14-42
33846471-0	2021	Association of genetic variants in TPMT, ITPA, and NUDT15 with azathioprine-induced myelosuppression in southwest china patients with autoimmune hepatitis.	Azathioprine	63-75	thiopurine S-methyltransferase	Homo sapiens	35-39
33846471-0	2021	Association of genetic variants in TPMT, ITPA, and NUDT15 with azathioprine-induced myelosuppression in southwest china patients with autoimmune hepatitis.	Azathioprine	63-75	nudix hydrolase 15	Homo sapiens	51-57
33846471-1	2021	This study aimed to investigate the influence of TPMT*3C, ITPA, NUDT15, and 6-thioguanine nucleotides (6-TGN) on azathioprine (AZA)-induced myelosuppression in Southwest China patients with autoimmune hepatitis (AIH).	Azathioprine	113-125	nudix hydrolase 15	Homo sapiens	64-70
33846471-10	2021	This study confirmed that NUDT15 variants are a potential independent risk predictor for AZA-induced leukopenia and neutropenia.	Azathioprine	89-92	nudix hydrolase 15	Homo sapiens	26-32
33746983-9	2021	Two of these nodes, Nfkb1 and Rac1, are directly targeted by prednisolone and azathioprine respectively, supporting the idea that the methodology developed here can identify valid therapeutic targets.	Azathioprine	78-90	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	20-25
33150655-11	2021	A dosage guideline for azathioprine was developed based on the PPK model that enables individualised azathioprine dosing in adult patients with different body weights, TPMT*3C genotypes and co-administration with mesalazine.	Azathioprine	23-35	kallikrein B1	Homo sapiens	63-66
33150655-11	2021	A dosage guideline for azathioprine was developed based on the PPK model that enables individualised azathioprine dosing in adult patients with different body weights, TPMT*3C genotypes and co-administration with mesalazine.	Azathioprine	101-113	kallikrein B1	Homo sapiens	63-66
33987044-11	2021	He was started on azathioprine and prednisone and showed a positive response, indicated by a decreasing erythrocyte sedimentation rate and C-reactive protein.	Azathioprine	18-30	C-reactive protein	Homo sapiens	139-157
33821842-0	2021	Pretreatment HLADQA1-HLADRB1 Testing for the Prevention of Azathioprine-Induced Pancreatitis in Inflammatory Bowel Disease: A Prospective Cohort Study.	Azathioprine	59-71	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	13-28
33821842-2	2021	The haplotype HLADQA1-HLADRB1*07:01A>C is strongly associated with azathioprine-induced pancreatitis in IBD.	Azathioprine	67-79	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	14-21
33821842-3	2021	We aimed to evaluate whether pretreatment HLADQA1-HLADRB1*07:01A>C screening will reduce the risk of azathioprine-induced pancreatitis.	Azathioprine	101-113	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	42-49
33821842-7	2021	RESULTS: HLADQA1-HLADRB1*07:01A>C screening resulted in an 11-fold reduction in the incidence of azathioprine-induced pancreatitis (n = 1/328 or 0.30% vs n = 13/373 or 3.4%).	Azathioprine	97-109	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	9-16
33821842-10	2021	DISCUSSION: HLADQA1-HLADRB1*07:01A>C screening reduced the risk of azathioprine-induced pancreatitis; however, using this strategy to guide the use of azathioprine therapy in IBD may eliminate a large proportion of patients from being eligible for treatment with azathioprine.	Azathioprine	67-79	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	12-19
33821842-10	2021	DISCUSSION: HLADQA1-HLADRB1*07:01A>C screening reduced the risk of azathioprine-induced pancreatitis; however, using this strategy to guide the use of azathioprine therapy in IBD may eliminate a large proportion of patients from being eligible for treatment with azathioprine.	Azathioprine	151-163	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	12-19
33821842-10	2021	DISCUSSION: HLADQA1-HLADRB1*07:01A>C screening reduced the risk of azathioprine-induced pancreatitis; however, using this strategy to guide the use of azathioprine therapy in IBD may eliminate a large proportion of patients from being eligible for treatment with azathioprine.	Azathioprine	151-163	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	12-19
33821842-11	2021	In regions where there is access to other IBD therapies, and given the short-term and long-term toxicities associated with azathioprine, HLADQA1-HLADRB1*07:01A>C-screening may be a clinically relevant strategy for enhancing the safe use of azathioprine in IBD.	Azathioprine	123-135	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	137-144
33821842-11	2021	In regions where there is access to other IBD therapies, and given the short-term and long-term toxicities associated with azathioprine, HLADQA1-HLADRB1*07:01A>C-screening may be a clinically relevant strategy for enhancing the safe use of azathioprine in IBD.	Azathioprine	240-252	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	137-144
33746983-9	2021	Two of these nodes, Nfkb1 and Rac1, are directly targeted by prednisolone and azathioprine respectively, supporting the idea that the methodology developed here can identify valid therapeutic targets.	Azathioprine	78-90	Rac family small GTPase 1	Mus musculus	30-34
34027115-3	2021	Assessment of thiopurine methyltransferase (TPMT), the key enzyme for the inactivation of AZA, as a predictor of AZA toxicity had been a matter of conflict.	Azathioprine	90-93	thiopurine S-methyltransferase	Homo sapiens	44-48
34027115-3	2021	Assessment of thiopurine methyltransferase (TPMT), the key enzyme for the inactivation of AZA, as a predictor of AZA toxicity had been a matter of conflict.	Azathioprine	113-116	thiopurine S-methyltransferase	Homo sapiens	14-42
34027115-3	2021	Assessment of thiopurine methyltransferase (TPMT), the key enzyme for the inactivation of AZA, as a predictor of AZA toxicity had been a matter of conflict.	Azathioprine	113-116	thiopurine S-methyltransferase	Homo sapiens	44-48
34027115-4	2021	This work aimed to study the role of TPMT serum level assessment and other host-, disease-, and treatment-related factors in predicting AZA toxicity.	Azathioprine	136-139	thiopurine S-methyltransferase	Homo sapiens	37-41
33748720-4	2021	Through integrative genome-wide analysis and global proteomic analysis, we found that elevated lipid metabolism likely due to hyperactive EGFR/AKT/SREBP-1 signaling was inhibited by azathioprine.	Azathioprine	182-194	epidermal growth factor receptor	Homo sapiens	138-142
33748720-4	2021	Through integrative genome-wide analysis and global proteomic analysis, we found that elevated lipid metabolism likely due to hyperactive EGFR/AKT/SREBP-1 signaling was inhibited by azathioprine.	Azathioprine	182-194	AKT serine/threonine kinase 1	Homo sapiens	143-146
33748720-4	2021	Through integrative genome-wide analysis and global proteomic analysis, we found that elevated lipid metabolism likely due to hyperactive EGFR/AKT/SREBP-1 signaling was inhibited by azathioprine.	Azathioprine	182-194	sterol regulatory element binding transcription factor 1	Homo sapiens	147-154
32617765-6	2021	Variants in two genes, TPMT and NUDT15, are widely recognized, leading drug regulatory agencies and professional organizations to adopt recommendations for testing before initiation of azathioprine therapy.	Azathioprine	185-197	thiopurine S-methyltransferase	Homo sapiens	23-27
33707905-6	2021	In this report, we highlight a case of serious hematological toxicity associated with azathioprine use in a patient with Crohn"s disease with homozygous NUDT 15 variant, thus favoring the implementation of a pharmacogenomic approach before starting azathioprine, particularly in the Asian population.	Azathioprine	86-98	nudix hydrolase 15	Homo sapiens	153-160
33707905-6	2021	In this report, we highlight a case of serious hematological toxicity associated with azathioprine use in a patient with Crohn"s disease with homozygous NUDT 15 variant, thus favoring the implementation of a pharmacogenomic approach before starting azathioprine, particularly in the Asian population.	Azathioprine	249-261	nudix hydrolase 15	Homo sapiens	153-160
33406412-3	2021	The immunosuppressive effect and pancreatitis risk of azathioprine are influenced by the activity of the enzyme thiopurine methyltransferase (TPMT) and by the genetic mutations in HLA-DQA1-HLA-DRB locus, respectively.	Azathioprine	54-66	thiopurine S-methyltransferase	Homo sapiens	112-140
33406412-3	2021	The immunosuppressive effect and pancreatitis risk of azathioprine are influenced by the activity of the enzyme thiopurine methyltransferase (TPMT) and by the genetic mutations in HLA-DQA1-HLA-DRB locus, respectively.	Azathioprine	54-66	thiopurine S-methyltransferase	Homo sapiens	142-146
32617765-6	2021	Variants in two genes, TPMT and NUDT15, are widely recognized, leading drug regulatory agencies and professional organizations to adopt recommendations for testing before initiation of azathioprine therapy.	Azathioprine	185-197	nudix hydrolase 15	Homo sapiens	32-38
32617765-10	2021	Azathioprine is a success story for the clinical implementation of pharmacogenomics, particularly the effects of TPMT and NUDT15 variants on myelosuppression.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	113-117
32617765-10	2021	Azathioprine is a success story for the clinical implementation of pharmacogenomics, particularly the effects of TPMT and NUDT15 variants on myelosuppression.	Azathioprine	0-12	nudix hydrolase 15	Homo sapiens	122-128
33277447-11	2020	Cox proportional hazard models identified older age at the time of transplantation and history of azathioprine consumption seems to be associated with risk for post-transplant malignancy.	Azathioprine	98-110	solute carrier family 35 member G1	Homo sapiens	160-164
33283312-8	2021	Predictors of infections in anti-TNFalpha-exposed patients were concomitant use of systemic steroids (OR 1.9, p=0.02) or azathioprine (OR 2.6, p=0.01) and a BMI<18.5 at time of infection (OR 2.2, p=0.01).	Azathioprine	121-133	tumor necrosis factor	Homo sapiens	33-41
33111378-0	2020	NUDT15 C415T variant compared with TPMT genotyping in predicting azathioprine-induced leucopenia: prospective analysis of 1014 inflammatory bowel disease patients in India.	Azathioprine	65-77	nudix hydrolase 15	Homo sapiens	0-6
33111378-14	2020	CONCLUSION: NUDT15 variant genotyping appears to be a better predictor for azathioprine-induced leucopenia in an Indian population than TPMT with high accuracy and can be useful in optimizing azathioprine dosage.	Azathioprine	75-87	nudix hydrolase 15	Homo sapiens	12-18
33111378-14	2020	CONCLUSION: NUDT15 variant genotyping appears to be a better predictor for azathioprine-induced leucopenia in an Indian population than TPMT with high accuracy and can be useful in optimizing azathioprine dosage.	Azathioprine	192-204	nudix hydrolase 15	Homo sapiens	12-18
33311945-10	2020	After adjustment for sex, age, type of IBD and latent TB, anti-TNFalpha with azathioprine increased the relative risk to 17.8 times more than conventional treatment.	Azathioprine	77-89	tumor necrosis factor	Homo sapiens	63-71
32713039-0	2020	Complete remission of refractory pemphigus vulgaris in a Chinese patient with mutated NUDT15 by combination of minimal doses of azathioprine and prednisone.	Azathioprine	128-140	nudix hydrolase 15	Homo sapiens	86-92
33240902-12	2020	Multivariate analysis revealed C-reactive protein >10 mg/L at disease relapse on AZA monotherapy [adjusted hazard ratio (HR), 4.72; 95% CI, 1.19-18.75, P = 0.027] and 6-thioguanine nucleotides level >=235 pmol/8 x 108 erythrocytes at AZA monotherapy (adjusted HR, 5.32; 95% CI, 1.40-20.14, P = 0.014) were associated with disease relapse on combination therapy.	Azathioprine	81-84	C-reactive protein	Homo sapiens	31-49
33240902-12	2020	Multivariate analysis revealed C-reactive protein >10 mg/L at disease relapse on AZA monotherapy [adjusted hazard ratio (HR), 4.72; 95% CI, 1.19-18.75, P = 0.027] and 6-thioguanine nucleotides level >=235 pmol/8 x 108 erythrocytes at AZA monotherapy (adjusted HR, 5.32; 95% CI, 1.40-20.14, P = 0.014) were associated with disease relapse on combination therapy.	Azathioprine	234-237	C-reactive protein	Homo sapiens	31-49
32713039-1	2020	While azathioprine (AZA) combined with corticosteroids remains the first-line therapy to treat patients with pemphigus vulgaris (PV), there are increasing reports of AZA-induced leukopenia, which provides the rationale for monitoring the blood cell count and testing the genotypes at the thiopurine methyltransferase (TPMT) and the nucleoside diphosphate-linked moiety X-type motif 15 (NUDT15) genes.	Azathioprine	166-169	thiopurine S-methyltransferase	Homo sapiens	288-316
32713039-1	2020	While azathioprine (AZA) combined with corticosteroids remains the first-line therapy to treat patients with pemphigus vulgaris (PV), there are increasing reports of AZA-induced leukopenia, which provides the rationale for monitoring the blood cell count and testing the genotypes at the thiopurine methyltransferase (TPMT) and the nucleoside diphosphate-linked moiety X-type motif 15 (NUDT15) genes.	Azathioprine	166-169	thiopurine S-methyltransferase	Homo sapiens	318-322
32713039-1	2020	While azathioprine (AZA) combined with corticosteroids remains the first-line therapy to treat patients with pemphigus vulgaris (PV), there are increasing reports of AZA-induced leukopenia, which provides the rationale for monitoring the blood cell count and testing the genotypes at the thiopurine methyltransferase (TPMT) and the nucleoside diphosphate-linked moiety X-type motif 15 (NUDT15) genes.	Azathioprine	166-169	nudix hydrolase 15	Homo sapiens	332-384
32713039-1	2020	While azathioprine (AZA) combined with corticosteroids remains the first-line therapy to treat patients with pemphigus vulgaris (PV), there are increasing reports of AZA-induced leukopenia, which provides the rationale for monitoring the blood cell count and testing the genotypes at the thiopurine methyltransferase (TPMT) and the nucleoside diphosphate-linked moiety X-type motif 15 (NUDT15) genes.	Azathioprine	166-169	nudix hydrolase 15	Homo sapiens	386-392
32054992-2	2020	Currently, we use thiopurine methyltransferase (TPMT) testing to predict leukopenia in patients taking azathioprine.	Azathioprine	103-115	thiopurine S-methyltransferase	Homo sapiens	18-46
33081236-3	2020	Azathioprine (AZA) is a well-known immunosuppressant that has been known for many years for its ability to provide long-term disease remission in IBDs, but has important side effects, most of which are related to a single nucleotide polymorphism in the gene for thiopurine methyltransferase (TPMT), which ensures the degradation and efficacy of AZA.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	262-290
33081236-3	2020	Azathioprine (AZA) is a well-known immunosuppressant that has been known for many years for its ability to provide long-term disease remission in IBDs, but has important side effects, most of which are related to a single nucleotide polymorphism in the gene for thiopurine methyltransferase (TPMT), which ensures the degradation and efficacy of AZA.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	292-296
33081236-3	2020	Azathioprine (AZA) is a well-known immunosuppressant that has been known for many years for its ability to provide long-term disease remission in IBDs, but has important side effects, most of which are related to a single nucleotide polymorphism in the gene for thiopurine methyltransferase (TPMT), which ensures the degradation and efficacy of AZA.	Azathioprine	14-17	thiopurine S-methyltransferase	Homo sapiens	262-290
33081236-3	2020	Azathioprine (AZA) is a well-known immunosuppressant that has been known for many years for its ability to provide long-term disease remission in IBDs, but has important side effects, most of which are related to a single nucleotide polymorphism in the gene for thiopurine methyltransferase (TPMT), which ensures the degradation and efficacy of AZA.	Azathioprine	14-17	thiopurine S-methyltransferase	Homo sapiens	292-296
32054992-2	2020	Currently, we use thiopurine methyltransferase (TPMT) testing to predict leukopenia in patients taking azathioprine.	Azathioprine	103-115	thiopurine S-methyltransferase	Homo sapiens	48-52
32054992-7	2020	Compared with TPMT testing alone, additional genetic and clinical variables improve the prediction of azathioprine-associated leukopenia.	Azathioprine	102-114	thiopurine S-methyltransferase	Homo sapiens	14-18
31683056-9	2020	In the longitudinal analysis, exposure to 5-ASAs or methotrexate was not associated with change in eGFR, whereas azathioprine was associated with a slightly higher eGFR (0.32 mL/min/1.73 m2; 95% CI, 0.16-0.48).	Azathioprine	113-125	CD59 molecule (CD59 blood group)	Homo sapiens	178-183
32537908-5	2020	FA selectively reacts with the PrAK residues on EGFP and fLuc through 2-aza-Cope rearrangement, resulting in fluorescence and luminescence turn-on responses, respectively, to FA over potentially interfering reactive species in aqueous buffer.	Azathioprine	72-75	MAPK activated protein kinase 5	Homo sapiens	31-35
32689833-12	2020	In conclusion, our study suggests that maintaining therapeutic levels of anti-TNFalpha drugs without antibodies formation is feasible with lower doses of azathioprine, minimizing its side effects.	Azathioprine	154-166	tumor necrosis factor	Homo sapiens	78-86
32842934-6	2022	DISCUSSION: NUDT15 R139C mutation can be used as a predictive factor for AZA-induced leukopenia in both European and Asian populations.	Azathioprine	73-76	nudix hydrolase 15	Homo sapiens	12-18
32842934-7	2022	The association between TPMT mutations and AZA-induced leukopenia is well established.	Azathioprine	43-46	thiopurine S-methyltransferase	Homo sapiens	24-28
33229787-0	2020	Thiopurine S-methyltransferase Genetic Polymorphism and Its Contribution for Azathioprine-Induced Myelosuppression in Kidney Transplant Recipients: A Summative Analysis.	Azathioprine	77-89	thiopurine S-methyltransferase	Homo sapiens	0-30
32827393-0	2020	NUDT15 polymorphism explains serious toxicity to azathioprine in Indian patients with chronic immune thrombocytopenia and autoimmune hemolytic anemia: a case series.	Azathioprine	49-61	nudix hydrolase 15	Homo sapiens	0-6
28520349-0	2012	Azathioprine Therapy and TPMT Genotype Azathioprine is an immunosuppressant that belongs to the drug class of thiopurines.	Azathioprine	39-51	thiopurine S-methyltransferase	Homo sapiens	25-29
28520349-4	2012	Thiopurine S-methyltransferase (TPMT) inactivates azathioprine, leaving less parent drug available to form TGNs.	Azathioprine	50-62	thiopurine S-methyltransferase	Homo sapiens	0-30
28520349-4	2012	Thiopurine S-methyltransferase (TPMT) inactivates azathioprine, leaving less parent drug available to form TGNs.	Azathioprine	50-62	thiopurine S-methyltransferase	Homo sapiens	32-36
28520349-6	2012	However, patients who carry two nonfunctional TPMT alleles universally experience life-threatening myelosuppression when treated with azathioprine, due to high levels of TGNs.	Azathioprine	134-146	thiopurine S-methyltransferase	Homo sapiens	46-50
28520349-7	2012	Patients who carry one nonfunctional TPMT allele may also be unable to tolerate conventional doses of azathioprine (3, 4).	Azathioprine	102-114	thiopurine S-methyltransferase	Homo sapiens	37-41
28520349-10	2012	The Clinical Pharmacogenetics Implementation Consortium (CPIC) has published recommendations for TPMT genotype-based azathioprine dosing.	Azathioprine	117-129	thiopurine S-methyltransferase	Homo sapiens	97-101
28520349-11	2012	These recommendations include: Consider an alternate agent or extreme dose reduction of azathioprine for patients with low or deficient TPMT activity.	Azathioprine	88-100	thiopurine S-methyltransferase	Homo sapiens	136-140
32598049-0	2020	Adjustment of azathioprine dose should be based on a lower 6-TGN target level to avoid leucopenia in NUDT15 intermediate metabolizers.	Azathioprine	14-26	nudix hydrolase 15	Homo sapiens	101-107
32598049-2	2020	AIM: To investigate the association between NUDT15 polymorphisms and time-to-leucopenia in paediatric patients with inflammatory bowel disease (IBD) receiving azathioprine and to determine the relationship between NUDT15 polymorphisms and 6-thioguanine nucleotide (6-TGN) levels.	Azathioprine	159-171	nudix hydrolase 15	Homo sapiens	44-50
32598049-11	2020	CONCLUSION: NUDT15 polymorphisms were associated with time-to-leucopenia during azathioprine treatment in Korean paediatric patients with IBD.	Azathioprine	80-92	nudix hydrolase 15	Homo sapiens	12-18
32115750-9	2020	The 5"-Aza-treated cells have decreased alpha-SMA expression with reduced MeCP2 association.	Azathioprine	7-10	actin alpha 1, skeletal muscle	Homo sapiens	40-49
32801881-7	2020	Furthermore, treatment with AZA not only promoted the demethylation of RUNX3 but also restored the mRNA and protein expression of RUNX3, and the reactivation of expression of the later exhibited its anti-tumor effects through regulation of the cycle progression in PCa cells.	Azathioprine	28-31	RUNX family transcription factor 3	Homo sapiens	71-76
32801881-7	2020	Furthermore, treatment with AZA not only promoted the demethylation of RUNX3 but also restored the mRNA and protein expression of RUNX3, and the reactivation of expression of the later exhibited its anti-tumor effects through regulation of the cycle progression in PCa cells.	Azathioprine	28-31	RUNX family transcription factor 3	Homo sapiens	130-135
32704308-1	2020	Background: Thiopurine methyltransferase (TPMT) plays a significant role in the metabolism of thiopurines, and, for patients with inflammatory bowel disease (IBD), it is useful to perform TPMT genotyping prior to azathioprine (AZA) treatment.	Azathioprine	213-225	thiopurine S-methyltransferase	Homo sapiens	12-40
32704308-1	2020	Background: Thiopurine methyltransferase (TPMT) plays a significant role in the metabolism of thiopurines, and, for patients with inflammatory bowel disease (IBD), it is useful to perform TPMT genotyping prior to azathioprine (AZA) treatment.	Azathioprine	213-225	thiopurine S-methyltransferase	Homo sapiens	42-46
32704308-1	2020	Background: Thiopurine methyltransferase (TPMT) plays a significant role in the metabolism of thiopurines, and, for patients with inflammatory bowel disease (IBD), it is useful to perform TPMT genotyping prior to azathioprine (AZA) treatment.	Azathioprine	213-225	thiopurine S-methyltransferase	Homo sapiens	188-192
32704308-1	2020	Background: Thiopurine methyltransferase (TPMT) plays a significant role in the metabolism of thiopurines, and, for patients with inflammatory bowel disease (IBD), it is useful to perform TPMT genotyping prior to azathioprine (AZA) treatment.	Azathioprine	227-230	thiopurine S-methyltransferase	Homo sapiens	12-40
32704308-1	2020	Background: Thiopurine methyltransferase (TPMT) plays a significant role in the metabolism of thiopurines, and, for patients with inflammatory bowel disease (IBD), it is useful to perform TPMT genotyping prior to azathioprine (AZA) treatment.	Azathioprine	227-230	thiopurine S-methyltransferase	Homo sapiens	42-46
32704308-1	2020	Background: Thiopurine methyltransferase (TPMT) plays a significant role in the metabolism of thiopurines, and, for patients with inflammatory bowel disease (IBD), it is useful to perform TPMT genotyping prior to azathioprine (AZA) treatment.	Azathioprine	227-230	thiopurine S-methyltransferase	Homo sapiens	188-192
31980448-12	2020	CONCLUSION: In case of immune-mediated LOR to a first anti-TNF, AZA should be associated with the second anti-TNF.	Azathioprine	64-67	tumor necrosis factor	Homo sapiens	59-62
31980448-12	2020	CONCLUSION: In case of immune-mediated LOR to a first anti-TNF, AZA should be associated with the second anti-TNF.	Azathioprine	64-67	tumor necrosis factor	Homo sapiens	110-113
32636225-6	2020	He was also given a trial of steroid and azathioprine for 1 year on the basis of liver biopsy findings, raised IgG and positive ASMA but finding no improvement stopped.	Azathioprine	41-53	actin alpha 1, skeletal muscle	Homo sapiens	128-132
32115750-9	2020	The 5"-Aza-treated cells have decreased alpha-SMA expression with reduced MeCP2 association.	Azathioprine	7-10	methyl-CpG binding protein 2	Homo sapiens	74-79
31855303-10	2020	RESULTS: Thymus and activation-regulated chemokine, CTACK, IL-13 and VEGF showed a significant decrease after treatment with methotrexate or azathioprine.	Azathioprine	141-153	C-C motif chemokine ligand 27	Homo sapiens	52-57
31855303-10	2020	RESULTS: Thymus and activation-regulated chemokine, CTACK, IL-13 and VEGF showed a significant decrease after treatment with methotrexate or azathioprine.	Azathioprine	141-153	interleukin 13	Homo sapiens	59-64
31855303-10	2020	RESULTS: Thymus and activation-regulated chemokine, CTACK, IL-13 and VEGF showed a significant decrease after treatment with methotrexate or azathioprine.	Azathioprine	141-153	vascular endothelial growth factor A	Homo sapiens	69-73
32606331-11	2020	Expression of slug and CD87 genes was activated following treatment with AZA and TGF-beta.	Azathioprine	73-76	snail family zinc finger 2	Mus musculus	14-18
32606331-11	2020	Expression of slug and CD87 genes was activated following treatment with AZA and TGF-beta.	Azathioprine	73-76	plasminogen activator, urokinase receptor	Mus musculus	23-27
33442476-0	2020	NUDT15 genotyping during azathioprine treatment in patients with inflammatory bowel disease: implications for a dose-optimization strategy.	Azathioprine	25-37	nudix hydrolase 15	Homo sapiens	0-6
33442476-1	2020	Background: NUDT15 R139C is an Asian-prevalent genetic variant related to azathioprine (AZA) intolerance in patients with inflammatory bowel disease (IBD).	Azathioprine	74-86	nudix hydrolase 15	Homo sapiens	12-18
33442476-1	2020	Background: NUDT15 R139C is an Asian-prevalent genetic variant related to azathioprine (AZA) intolerance in patients with inflammatory bowel disease (IBD).	Azathioprine	88-91	nudix hydrolase 15	Homo sapiens	12-18
32712634-12	2020	CONCLUSION: Higher initial prednisolone dose and the use of azathioprine in PV desmoglein 1 antibody titre at diagnosis in PV and PF might be prognostic markers for achieving remission.	Azathioprine	60-72	desmoglein 1	Homo sapiens	79-91
32070863-0	2020	Myasthenia gravis and azathioprine treatment: Adverse events related to thiopurine S-methyl-transferase (TPMT) polymorphisms.	Azathioprine	22-34	thiopurine S-methyltransferase	Homo sapiens	72-103
32527447-7	2020	miR-137 methylation was analyzed by bioinformatics, and miR-137 restoration was detected after Aza treatment.	Azathioprine	95-98	microRNA 137	Homo sapiens	56-63
32547497-14	2020	Using a personalized medicine approach, she was started on anti-(TNF)-alpha therapy with infliximab combined with azathioprine, which are indicated for treatment of CD.	Azathioprine	114-126	tumor necrosis factor	Homo sapiens	64-75
32070863-0	2020	Myasthenia gravis and azathioprine treatment: Adverse events related to thiopurine S-methyl-transferase (TPMT) polymorphisms.	Azathioprine	22-34	thiopurine S-methyltransferase	Homo sapiens	105-109
32070863-2	2020	To analyses the prevalence of thiopurine S-methyl-transferase (TPMT) genotypes and their association with adverse events due to azathioprine therapy in MG patients.	Azathioprine	128-140	thiopurine S-methyltransferase	Homo sapiens	30-61
32070863-2	2020	To analyses the prevalence of thiopurine S-methyl-transferase (TPMT) genotypes and their association with adverse events due to azathioprine therapy in MG patients.	Azathioprine	128-140	thiopurine S-methyltransferase	Homo sapiens	63-67
32070863-13	2020	Although TPMT genotype has been associated with AZA-related adverse events, since no statistically significant difference among wild-type and other TPMT genotypes for minor adverse events, our study supports the view that TPMT genotype alone is not enough to adequately personalise the AZA therapy in MG patients.	Azathioprine	48-51	thiopurine S-methyltransferase	Homo sapiens	9-13
32070863-14	2020	In conclusion, these results were important to characterise the prevalence of TPMT gene variants in MG patients treated with AZA and correlate the adverse events of this therapy in a real-world outpatient clinic from Southern Brazil.	Azathioprine	125-128	thiopurine S-methyltransferase	Homo sapiens	78-82
32187056-0	2020	Association of thiopurine S-methyltransferase and NUDT15 polymorphisms with azathioprine-induced myelotoxicity in Chinese patients with rheumatological disease.	Azathioprine	76-88	thiopurine S-methyltransferase	Homo sapiens	15-45
32083540-6	2020	POF was significantly associated with anti-Sm (p=0.0004), anti-RNP (p=0.02), anti-cardiolipin (p=0.0008), lupus anticoagulant (p=0.0002), treatment with cyclophosphamide (p=0.0001), azathioprine (p=0.0001), mycophenolate mofetil (p=0.0001), cyclosporine A (p=0.007).	Azathioprine	182-194	POF1B actin binding protein	Homo sapiens	0-3
31744310-0	2020	First Case of Azathioprine-Induced Severe Hematotoxicity in a Tunisian Patient With Homozygous TT for NUDT15 rs116855232.	Azathioprine	14-26	nudix hydrolase 15	Homo sapiens	102-108
32187056-0	2020	Association of thiopurine S-methyltransferase and NUDT15 polymorphisms with azathioprine-induced myelotoxicity in Chinese patients with rheumatological disease.	Azathioprine	76-88	nudix hydrolase 15	Homo sapiens	50-56
32277014-6	2020	Treatment of K-RasG12D and K-RasG12D/Vav1 mice with azathioprine, an immune-suppressor drug which inhibits Vav1"s activity as a GDP/GTP exchange factor, dramatically reduced the number of malignant lesions.	Azathioprine	52-64	vav 1 oncogene	Mus musculus	37-41
32277014-6	2020	Treatment of K-RasG12D and K-RasG12D/Vav1 mice with azathioprine, an immune-suppressor drug which inhibits Vav1"s activity as a GDP/GTP exchange factor, dramatically reduced the number of malignant lesions.	Azathioprine	52-64	vav 1 oncogene	Mus musculus	107-111
31743483-0	2020	The potential application of human PIG-A assay on azathioprine-treated inflammatory bowel disease patients.	Azathioprine	50-62	phosphatidylinositol glycan anchor biosynthesis class A	Sus scrofa	35-40
32062783-4	2020	Mutations in thiopurine methyltransferase (TPMT) and inosine triphosphate pyrophosphohydrolase (ITPA) genes account for the major genetic polymorphism markers for azathioprine adverse risk factors in Caucasians, but not in Asians.	Azathioprine	163-175	thiopurine S-methyltransferase	Homo sapiens	13-41
32062783-4	2020	Mutations in thiopurine methyltransferase (TPMT) and inosine triphosphate pyrophosphohydrolase (ITPA) genes account for the major genetic polymorphism markers for azathioprine adverse risk factors in Caucasians, but not in Asians.	Azathioprine	163-175	thiopurine S-methyltransferase	Homo sapiens	43-47
32062783-6	2020	The aim of our study was to determine the contribution of NUDT15 mutations in azathioprine-induced neutropenia in Han Chinese patients with dermatologic diseases.	Azathioprine	78-90	nudix hydrolase 15	Homo sapiens	58-64
32062783-16	2020	CONCLUSIONS: Pretreatment screening of NUDT15 might reduce the chance of azathioprine-induced neutropenia in Han Chinese patients with dermatologic diseases.	Azathioprine	73-85	nudix hydrolase 15	Homo sapiens	39-45
31743483-5	2020	The estimated relative risk for the exposed patients was 1.22 which indicated that AZA is a risk factor for inducing PIG-A mutation.	Azathioprine	83-86	phosphatidylinositol glycan anchor biosynthesis class A	Sus scrofa	117-122
31743483-3	2020	In this study, PIG-A mutation frequencies (MFs) were evaluated in 36 azathioprine (AZA; human carcinogen)-treated inflammatory bowel disease (IBD) patients and 36 healthy volunteers.	Azathioprine	69-81	phosphatidylinositol glycan anchor biosynthesis class A	Sus scrofa	15-20
31743483-10	2020	Our findings indicate that AZA-treated IBD patients have only a marginally significant increase in PIG-A MF; in contrast, a much stronger AZA-associated increase in genotoxicity was detected with the lymphocyte MN assay.	Azathioprine	27-30	phosphatidylinositol glycan anchor biosynthesis class A	Sus scrofa	99-104
31532479-8	2020	Initial azathioprine remained the most cost-effective treatment on sensitivity analysis compared with infliximab and combination therapy, with 90% reductions in anti-TNF therapy costs and a 5-year time horizon, although combination therapy had an acceptable cost-effectiveness when costs were reduced in the extended model.	Azathioprine	8-20	tumor necrosis factor	Homo sapiens	166-169
31994212-0	2020	Coexisting mutations in CARD14 and NUTD15 detected in a young female with azathioprine hypersensitivity syndrome manifested as acute generalized exanthematous pustulosis.	Azathioprine	74-86	caspase recruitment domain family member 14	Homo sapiens	24-30
31504957-9	2020	IFN-alpha was used in patients who were refractory to or could not tolerate AZA or had concomitant eye involvement requiring further treatment.	Azathioprine	76-79	interferon alpha 1	Homo sapiens	0-9
31532479-10	2020	CONCLUSIONS: In the biosimilar era, initial azathioprine with escalation to infliximab appeared more cost-effective in the short term compared with infliximab or combination therapy, although initial combination therapy yields acceptable ICERs in the long term with continued reductions in anti-TNF therapy costs and will likely be the preferred treatment strategy in the future.	Azathioprine	44-56	tumor necrosis factor	Homo sapiens	295-298
31209730-9	2019	By injection AZA which was DNA-methylation inhibitor into EAP mice, prostate inflammation was alleviated, expressions of TGF-beta and Foxp3 were increased, and the suppressive function of Tregs was improved in vitro and in vivo.	Azathioprine	13-16	transforming growth factor alpha	Mus musculus	121-129
31816823-10	2019	Immunohistochemical labelling for LC3 revealed azathioprine to induce autophagy in the bone marrow.	Azathioprine	47-59	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	34-37
31788536-2	2019	Thiopurine medications, such as azathioprine and mercaptopurine, are immunosuppressants that suppress Rac1 activation.	Azathioprine	32-44	Rac family small GTPase 1	Homo sapiens	102-106
31694755-0	2019	Treatment of anti-TNF-related paradoxic palmoplantar psoriasis in Behcet"s disease with azathioprine.	Azathioprine	88-100	tumor necrosis factor	Homo sapiens	18-21
31755075-6	2020	Aza-pretreated group showed higher intracellular expression of insulin and the transcription factor "PDX-1".	Azathioprine	0-3	insulin	Homo sapiens	63-70
31755075-6	2020	Aza-pretreated group showed higher intracellular expression of insulin and the transcription factor "PDX-1".	Azathioprine	0-3	pancreatic and duodenal homeobox 1	Homo sapiens	101-106
31755075-11	2020	In conclusion, this additional step with Aza could enhance the response of MSC to the classical differentiation protocol for insulin-secreting cells and may help in establishing a regenerative solution for patients with diabetes.	Azathioprine	41-44	insulin	Homo sapiens	125-132
31464791-5	2019	Variations in the thiopurine S-methyltransferase (TPMT) gene can lead to diminished TPMT enzyme activity and to an increased incidence of myelotoxicity due to high 6-methylmercaptopurine ribonucleotides levels after treatment with azathioprine and mercaptopurine.	Azathioprine	231-243	thiopurine S-methyltransferase	Homo sapiens	18-48
31464791-5	2019	Variations in the thiopurine S-methyltransferase (TPMT) gene can lead to diminished TPMT enzyme activity and to an increased incidence of myelotoxicity due to high 6-methylmercaptopurine ribonucleotides levels after treatment with azathioprine and mercaptopurine.	Azathioprine	231-243	thiopurine S-methyltransferase	Homo sapiens	50-54
31464791-5	2019	Variations in the thiopurine S-methyltransferase (TPMT) gene can lead to diminished TPMT enzyme activity and to an increased incidence of myelotoxicity due to high 6-methylmercaptopurine ribonucleotides levels after treatment with azathioprine and mercaptopurine.	Azathioprine	231-243	thiopurine S-methyltransferase	Homo sapiens	84-88
31646864-2	2019	A new synthetic strategy which features an efficient aza-Michael addition, a ruthenium-catalyzed transfer dehydrogenation, and an intramolecular palladium-catalyzed oxidative coupling was adopted to install the ABC tricycle system.	Azathioprine	53-56	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	211-214
31300821-0	2019	Letter to the Editor: Activated Toxoplasma May Attenuate the Effect of Azathioprine and Deteriorate the Symptoms in IBD Patients via mTORC1 Manipulation.	Azathioprine	71-83	CREB regulated transcription coactivator 1	Mus musculus	133-139
31408737-0	2019	Antimalarial agents diminish while methotrexate, azathioprine and mycophenolic acid increase BAFF levels in systemic lupus erythematosus.	Azathioprine	49-61	TNF superfamily member 13b	Homo sapiens	93-97
29754190-18	2019	Anti-TNF-alpha drugs with or without immunomodulators (azathioprine, 6-mercaptopurine, methotrexate) are often used for the induction and maintenance of remission.	Azathioprine	55-67	tumor necrosis factor	Homo sapiens	5-14
31556692-0	2019	NUDT15 and TPMT Genetic Polymorphisms Are Related to Azathioprine Intolerance in Chinese Patients with Rheumatic Diseases.	Azathioprine	53-65	nudix hydrolase 15	Homo sapiens	0-6
31556692-0	2019	NUDT15 and TPMT Genetic Polymorphisms Are Related to Azathioprine Intolerance in Chinese Patients with Rheumatic Diseases.	Azathioprine	53-65	thiopurine S-methyltransferase	Homo sapiens	11-15
31556692-5	2019	Results: The TPMT*3C and NUDT15*3 genotypes were significantly associated with AZA-induced leukopenia (p = 0.007 and 4.475 x 10-6, respectively).	Azathioprine	79-82	nudix hydrolase 15	Homo sapiens	25-31
31556692-9	2019	Conclusion: This study demonstrated that NUDT15*3 and TPMT*3C are both highly predictive genetic markers for AZA-induced toxicity in Chinese populations with rheumatic diseases.	Azathioprine	109-112	nudix hydrolase 15	Homo sapiens	41-47
31209730-9	2019	By injection AZA which was DNA-methylation inhibitor into EAP mice, prostate inflammation was alleviated, expressions of TGF-beta and Foxp3 were increased, and the suppressive function of Tregs was improved in vitro and in vivo.	Azathioprine	13-16	forkhead box P3	Mus musculus	134-139
31387318-2	2019	The aim of the study was to assess a possible correlation between genetic variability of the enzyme thiopurine S-methyltransferase (TPMT) and the development of toxicity to azathioprine.	Azathioprine	173-185	thiopurine S-methyltransferase	Homo sapiens	100-130
22934314-13	1993	Agents/circumstances to avoid: Azathioprine should be avoided by individuals taking XDH inhibitors.	Azathioprine	31-43	xanthine dehydrogenase	Homo sapiens	84-87
31567972-6	2019	Levels of IL-6, IL-7, and monocyte chemoattractant protein 1 were higher with 5-aminosalicylic acid (5-ASA) + Azathioprine therapy than controls (P &lt; .05).	Azathioprine	110-122	interleukin 6	Homo sapiens	10-14
31567972-6	2019	Levels of IL-6, IL-7, and monocyte chemoattractant protein 1 were higher with 5-aminosalicylic acid (5-ASA) + Azathioprine therapy than controls (P &lt; .05).	Azathioprine	110-122	interleukin 7	Homo sapiens	16-20
31567972-6	2019	Levels of IL-6, IL-7, and monocyte chemoattractant protein 1 were higher with 5-aminosalicylic acid (5-ASA) + Azathioprine therapy than controls (P &lt; .05).	Azathioprine	110-122	C-C motif chemokine ligand 2	Homo sapiens	26-60
30889246-0	2019	The Inflammatory Bowel Disease Drug Azathioprine Induces Autophagy via mTORC1 and the Unfolded Protein Response Sensor PERK.	Azathioprine	36-48	CREB regulated transcription coactivator 1	Mus musculus	71-77
30889246-0	2019	The Inflammatory Bowel Disease Drug Azathioprine Induces Autophagy via mTORC1 and the Unfolded Protein Response Sensor PERK.	Azathioprine	36-48	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	119-123
30889246-7	2019	RESULTS: Azathioprine induces autophagy via mechanisms involving modulation of mechanistic target of rapamycin (mTORC1) signaling and stimulation of the unfolded protein response (UPR) sensor PERK.	Azathioprine	9-21	CREB regulated transcription coactivator 1	Mus musculus	112-118
30889246-7	2019	RESULTS: Azathioprine induces autophagy via mechanisms involving modulation of mechanistic target of rapamycin (mTORC1) signaling and stimulation of the unfolded protein response (UPR) sensor PERK.	Azathioprine	9-21	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	192-196
30889246-8	2019	Induction of autophagy with azathioprine correlated with the enhanced clearance of AIEC and dampened AIEC-induced increases in TNFalpha.	Azathioprine	28-40	tumor necrosis factor	Homo sapiens	127-135
30889246-9	2019	Azathioprine induced significant increase in autophagosome bound LC3-II in PBMC populations ex vivo, supporting in vitro findings.	Azathioprine	0-12	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	65-68
30889246-11	2019	CONCLUSIONS: Modulation of autophagy via mTORC1 and the UPR may contribute to the therapeutic efficacy of azathioprine in IBD.	Azathioprine	106-118	CREB regulated transcription coactivator 1	Mus musculus	41-47
30843183-0	2019	NUDT15 polymorphism identified in a patient with azathioprine hypersensitivity syndrome presenting as erythema nodosum and hepatotoxicity.	Azathioprine	49-61	nudix hydrolase 15	Homo sapiens	0-6
30458698-9	2019	Placental growth factor increased in AZA (24 hours, 10 ng/mL) and CsA (125 ng/mL; P &lt; .05).	Azathioprine	37-40	placental growth factor	Homo sapiens	0-23
31387318-2	2019	The aim of the study was to assess a possible correlation between genetic variability of the enzyme thiopurine S-methyltransferase (TPMT) and the development of toxicity to azathioprine.	Azathioprine	173-185	thiopurine S-methyltransferase	Homo sapiens	132-136
30911150-15	2019	In summary, Aza promotes neutrophil apoptosis by activating DAPK1 to accelerate inflammatory resolution in LPS-induced ARDS.	Azathioprine	12-15	death associated protein kinase 1	Mus musculus	60-65
31427963-12	2019	Indicatively, pre-emptive HLA-B*5701 and TPMT testing before administration of abacavir and azathioprine, respectively, is reimbursed by Medicare based on both economic and efficacy evidence.	Azathioprine	92-104	major histocompatibility complex, class I, B	Homo sapiens	26-31
31427963-12	2019	Indicatively, pre-emptive HLA-B*5701 and TPMT testing before administration of abacavir and azathioprine, respectively, is reimbursed by Medicare based on both economic and efficacy evidence.	Azathioprine	92-104	thiopurine S-methyltransferase	Homo sapiens	41-45
30911150-16	2019	This study provides the first evidence that Aza prevents LPS-induced neutrophil survival by modulating DAPK1 expression.	Azathioprine	44-47	death associated protein kinase 1	Mus musculus	103-108
30911150-3	2019	It has been proved that 5-Aza-2"-deoxycytidine (Aza) can inhibit cancer by activating death-associated protein kinase 1 (DAPK1) to promote apoptosis.	Azathioprine	26-29	death associated protein kinase 1	Mus musculus	86-119
30954555-7	2019	DNMT inhibitor, AZA prevented the H2O2 induced promoter-CpG-island methylation of CDH1.	Azathioprine	16-19	DNA methyltransferase 1	Homo sapiens	0-4
30911150-3	2019	It has been proved that 5-Aza-2"-deoxycytidine (Aza) can inhibit cancer by activating death-associated protein kinase 1 (DAPK1) to promote apoptosis.	Azathioprine	26-29	death associated protein kinase 1	Mus musculus	121-126
30911150-5	2019	Here, we investigated whether Aza can regulate DAPK1 expression to influence the fate of neutrophils in ARDS.	Azathioprine	30-33	death associated protein kinase 1	Mus musculus	47-52
30911150-7	2019	We observed that culturing dHL-60 cells with Aza increased apoptosis by inhibiting NF-kappaB activation to modulate the expression of Bcl-2 family proteins, which was closely related to the levels of DAPK1.	Azathioprine	45-48	B cell leukemia/lymphoma 2	Mus musculus	134-139
30911150-7	2019	We observed that culturing dHL-60 cells with Aza increased apoptosis by inhibiting NF-kappaB activation to modulate the expression of Bcl-2 family proteins, which was closely related to the levels of DAPK1.	Azathioprine	45-48	death associated protein kinase 1	Mus musculus	200-205
30911150-13	2019	However, administration of the DAPK1 inhibitor attenuated the protective effects of Aza.	Azathioprine	84-87	death associated protein kinase 1	Mus musculus	31-36
30911150-14	2019	Similarly, the proapoptotic function of Aza was prevented when DAPK1 was inhibited either in vivo or in vitro.	Azathioprine	40-43	death associated protein kinase 1	Mus musculus	63-68
31117643-5	2019	Isotopic-labeling experiments support a syn amino-palladation mechanism for this new class of aza-Wacker reactions.	Azathioprine	94-97	synemin	Homo sapiens	40-43
30954555-7	2019	DNMT inhibitor, AZA prevented the H2O2 induced promoter-CpG-island methylation of CDH1.	Azathioprine	16-19	cadherin 1	Homo sapiens	82-86
30901719-6	2019	In addition, the elevated mRNA expression of MMP-1, MMP-3 and RAGE induced by TNBS was remarkably inhibited by BJOE, SASP or AZA treatments, while the mRNA expression of PPAR-gamma was significantly enhanced.	Azathioprine	125-128	matrix metallopeptidase 1	Rattus norvegicus	45-50
30748107-13	2019	Expression of TNF-alpha, IL-2, IL-4, IL-5, and IL-13 mRNA in the NPs treated by steroid, AZA, and 6-MP were significantly lower than those of the control (p < 0.001 for all).	Azathioprine	89-92	tumor necrosis factor	Homo sapiens	14-23
30901719-6	2019	In addition, the elevated mRNA expression of MMP-1, MMP-3 and RAGE induced by TNBS was remarkably inhibited by BJOE, SASP or AZA treatments, while the mRNA expression of PPAR-gamma was significantly enhanced.	Azathioprine	125-128	matrix metallopeptidase 3	Rattus norvegicus	52-57
30901719-6	2019	In addition, the elevated mRNA expression of MMP-1, MMP-3 and RAGE induced by TNBS was remarkably inhibited by BJOE, SASP or AZA treatments, while the mRNA expression of PPAR-gamma was significantly enhanced.	Azathioprine	125-128	advanced glycosylation end product-specific receptor	Rattus norvegicus	62-66
30901719-6	2019	In addition, the elevated mRNA expression of MMP-1, MMP-3 and RAGE induced by TNBS was remarkably inhibited by BJOE, SASP or AZA treatments, while the mRNA expression of PPAR-gamma was significantly enhanced.	Azathioprine	125-128	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	170-180
30901719-7	2019	Furthermore, the activation of TLR4/NF-kappaB signaling pathway was significantly inhibited by AZA and BJOE treatment when compared with that of TNBS-treated rats.	Azathioprine	95-98	toll-like receptor 4	Rattus norvegicus	31-35
30748107-12	2019	On immunohistochemistry, IL-13 showed a steady falling tendency in submucosal glands by steroid, AZA, and 6-MP.	Azathioprine	97-100	interleukin 13	Homo sapiens	25-30
30748107-13	2019	Expression of TNF-alpha, IL-2, IL-4, IL-5, and IL-13 mRNA in the NPs treated by steroid, AZA, and 6-MP were significantly lower than those of the control (p < 0.001 for all).	Azathioprine	89-92	interleukin 5	Homo sapiens	37-41
30748107-13	2019	Expression of TNF-alpha, IL-2, IL-4, IL-5, and IL-13 mRNA in the NPs treated by steroid, AZA, and 6-MP were significantly lower than those of the control (p < 0.001 for all).	Azathioprine	89-92	interleukin 13	Homo sapiens	47-52
30748107-14	2019	By ELISA, IL-2 and IL-13 were significantly lower with topical steroid, AZA, and 6-MP treatment (p = 0.012 and p < 0.001).	Azathioprine	72-75	interleukin 2	Homo sapiens	10-14
30748107-14	2019	By ELISA, IL-2 and IL-13 were significantly lower with topical steroid, AZA, and 6-MP treatment (p = 0.012 and p < 0.001).	Azathioprine	72-75	interleukin 13	Homo sapiens	19-24
30987408-0	2019	Azathioprine Biotransformation in Young Patients with Inflammatory Bowel Disease: Contribution of Glutathione-S Transferase M1 and A1 Variants.	Azathioprine	0-12	glutathione S-transferase mu 1	Homo sapiens	98-126
30963516-0	2019	Modeling the Outcome of Systematic TPMT Genotyping or Phenotyping Before Azathioprine Prescription: A Cost-Effectiveness Analysis.	Azathioprine	73-85	thiopurine S-methyltransferase	Homo sapiens	35-39
30963516-1	2019	BACKGROUND: Thiopurine S-methyltransferase (TPMT) testing, either by genotyping or phenotyping, can reduce the incidence of adverse severe myelotoxicity episodes induced by azathioprine.	Azathioprine	173-185	thiopurine S-methyltransferase	Homo sapiens	12-42
30963516-1	2019	BACKGROUND: Thiopurine S-methyltransferase (TPMT) testing, either by genotyping or phenotyping, can reduce the incidence of adverse severe myelotoxicity episodes induced by azathioprine.	Azathioprine	173-185	thiopurine S-methyltransferase	Homo sapiens	44-48
30916983-0	2019	Tandem Rh(II) and Chiral Squaramide Relay Catalysis: Enantioselective Synthesis of Dihydro-beta-carbolines via Insertion to C-H Bond and Aza-Michael Reaction.	Azathioprine	137-140	Rh blood group D antigen	Homo sapiens	7-13
31024313-1	2019	The aim of this study was to investigate the influence of NUDT15 R139C and thiopurine S-methyltransferase (TPMT) on azathioprine (AZA) induced leukopenia in patients with autoimmune hepatitis (AIH) and related cirrhosis.	Azathioprine	116-128	nudix hydrolase 15	Homo sapiens	58-64
31024313-1	2019	The aim of this study was to investigate the influence of NUDT15 R139C and thiopurine S-methyltransferase (TPMT) on azathioprine (AZA) induced leukopenia in patients with autoimmune hepatitis (AIH) and related cirrhosis.	Azathioprine	116-128	thiopurine S-methyltransferase	Homo sapiens	75-105
31024313-1	2019	The aim of this study was to investigate the influence of NUDT15 R139C and thiopurine S-methyltransferase (TPMT) on azathioprine (AZA) induced leukopenia in patients with autoimmune hepatitis (AIH) and related cirrhosis.	Azathioprine	116-128	thiopurine S-methyltransferase	Homo sapiens	107-111
31024313-1	2019	The aim of this study was to investigate the influence of NUDT15 R139C and thiopurine S-methyltransferase (TPMT) on azathioprine (AZA) induced leukopenia in patients with autoimmune hepatitis (AIH) and related cirrhosis.	Azathioprine	130-133	nudix hydrolase 15	Homo sapiens	58-64
31024313-1	2019	The aim of this study was to investigate the influence of NUDT15 R139C and thiopurine S-methyltransferase (TPMT) on azathioprine (AZA) induced leukopenia in patients with autoimmune hepatitis (AIH) and related cirrhosis.	Azathioprine	130-133	thiopurine S-methyltransferase	Homo sapiens	75-105
31024313-1	2019	The aim of this study was to investigate the influence of NUDT15 R139C and thiopurine S-methyltransferase (TPMT) on azathioprine (AZA) induced leukopenia in patients with autoimmune hepatitis (AIH) and related cirrhosis.	Azathioprine	130-133	thiopurine S-methyltransferase	Homo sapiens	107-111
31024313-10	2019	Adjusting the AZA dosage should be considered in patients according to the NUDT15 R139C genotypes.	Azathioprine	14-17	nudix hydrolase 15	Homo sapiens	75-81
30987408-9	2019	TPMT rs1142345 variant (4.8% of patients) was associated with increased TGN (LME p = 0.0042), TGN/dose ratio (LME p &lt; 0.0001), decreased azathioprine dose (LME p = 0.0087), and MMPN (LME p = 0.0011).	Azathioprine	140-152	thiopurine S-methyltransferase	Homo sapiens	0-4
30987408-12	2019	In conclusion, GSTs variants are associated with azathioprine efficacy and pharmacokinetics.	Azathioprine	49-61	glutathione S-transferase kappa 1	Homo sapiens	15-19
30758887-2	2019	The reaction enables dediazotized dicarbonylation of alpha-diazoketones, creating direct C(sp3 )/C(sp2 )-H bond bifunctionalization to access tetracyclic aza-heterocyclic skeletons.	Azathioprine	154-157	Sp2 transcription factor	Homo sapiens	97-102
30368728-10	2019	GEO data analysis indicated that SFRP1 and SFRP2 expression were increased in three CRC cell lines (COLO320, HCT116 and HT29) after 5"-AZA-deoxycytidine treatment, suggesting that DNA methylation played an important role in regulating gene expression of the two genes.	Azathioprine	135-138	secreted frizzled related protein 1	Homo sapiens	33-38
30368728-10	2019	GEO data analysis indicated that SFRP1 and SFRP2 expression were increased in three CRC cell lines (COLO320, HCT116 and HT29) after 5"-AZA-deoxycytidine treatment, suggesting that DNA methylation played an important role in regulating gene expression of the two genes.	Azathioprine	135-138	secreted frizzled related protein 2	Homo sapiens	43-48
30742971-0	2019	Novel multiple heterozygous NUDT15 variants cause an azathioprine-induced severe leukopenia in a patient with systemic lupus erythematosus.	Azathioprine	53-65	nudix hydrolase 15	Homo sapiens	28-34
30867438-0	2019	The immunosuppressant drug azathioprine restrains adipogenesis of muscle Fibro/Adipogenic Progenitors from dystrophic mice by affecting AKT signaling.	Azathioprine	27-39	thymoma viral proto-oncogene 1	Mus musculus	136-139
30867438-6	2019	We show here that AZA negatively affects the adipogenic propensity of FAPs purified from wild type and mdx mice by impairing the expression of the master adipogenic regulator, peroxisome proliferator-activated receptor gamma (PPARgamma).	Azathioprine	18-21	peroxisome proliferator activated receptor gamma	Mus musculus	176-224
30867438-6	2019	We show here that AZA negatively affects the adipogenic propensity of FAPs purified from wild type and mdx mice by impairing the expression of the master adipogenic regulator, peroxisome proliferator-activated receptor gamma (PPARgamma).	Azathioprine	18-21	peroxisome proliferator activated receptor gamma	Mus musculus	226-235
30840585-0	2019	Combined evaluation of genotype and phenotype of thiopurine S-methyltransferase (TPMT) in the clinical management of patients in chronic therapy with azathioprine.	Azathioprine	150-162	thiopurine S-methyltransferase	Homo sapiens	49-79
30840585-0	2019	Combined evaluation of genotype and phenotype of thiopurine S-methyltransferase (TPMT) in the clinical management of patients in chronic therapy with azathioprine.	Azathioprine	150-162	thiopurine S-methyltransferase	Homo sapiens	81-85
30840585-1	2019	Background The thiopurine S-methyltransferase (TPMT)/azathioprine (AZA) gene-drug pair is one of the most well-known pharmacogenetic markers.	Azathioprine	53-65	thiopurine S-methyltransferase	Homo sapiens	15-45
30840585-1	2019	Background The thiopurine S-methyltransferase (TPMT)/azathioprine (AZA) gene-drug pair is one of the most well-known pharmacogenetic markers.	Azathioprine	53-65	thiopurine S-methyltransferase	Homo sapiens	47-51
30840585-1	2019	Background The thiopurine S-methyltransferase (TPMT)/azathioprine (AZA) gene-drug pair is one of the most well-known pharmacogenetic markers.	Azathioprine	67-70	thiopurine S-methyltransferase	Homo sapiens	15-45
30840585-1	2019	Background The thiopurine S-methyltransferase (TPMT)/azathioprine (AZA) gene-drug pair is one of the most well-known pharmacogenetic markers.	Azathioprine	67-70	thiopurine S-methyltransferase	Homo sapiens	47-51
30984441-2	2019	The new sensor, labelled as GrO-IL-AuNPs-Chit/CSE, exhibited an improved electrocatalytic response to cancer drugs such as purine antimetabolites (6-thioguanine, 6-mercaptopurine, and azathioprine) in a wide concentration range with a low detection limit (20-40 nmol L-1, S/N = 3), and satisfactory recoveries (97.1-103.0%).	Azathioprine	184-196	choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity)	Homo sapiens	46-49
30760238-9	2019	The CXCR4 was activated by either the hypoxic condition or treatment with AZA.	Azathioprine	74-77	C-X-C motif chemokine receptor 4	Homo sapiens	4-9
30629316-12	2019	One patient was treated with azathioprine after rituximab failure, obtaining a progressive increase of ADAMTS-13 activity to more than 40%.	Azathioprine	29-41	adamts-13	None	103-112
30368003-14	2019	CONCLUSIONS: Azathioprine hypersensitivity syndrome is strikingly common in ANCA-associated vasculitis, might be associated with reduced TPMT activity, is accompanied by an increase in neutrophil counts, and may occur even during concomitant prednisolone therapy.	Azathioprine	13-25	thiopurine S-methyltransferase	Homo sapiens	137-141
30610229-3	2019	Steroid therapy remains the first line therapy for moderate/severe and severe vision threatening TED The use of some traditional nonspecific immunosuppressant such as mycophenolate, cyclosporine and azathioprine seems useful in combination with steroid therapy to achieve stable results in the long term; methotrexate is useful as steroid-sparing medications and in steroid resistant or intolerant patients.	Azathioprine	199-211	NALCN channel auxiliary factor 2	Homo sapiens	97-100
30746133-0	2019	Azathioprine hypersensitivity syndrome in anti-myeloperoxidase anti-neutrophil cytoplasmic antibody-associated vasculitis.	Azathioprine	0-12	myeloperoxidase	Homo sapiens	47-62
30746133-1	2019	Two patients with anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) and rapid onset of high fever, tachycardia and systemic hypotension accompanied by elevated laboratory markers of infection were diagnosed with azathioprine hypersensitivity syndrome only after repeat exposure.	Azathioprine	227-239	adeno-associated virus integration site 1	Homo sapiens	78-81
30746133-2	2019	Azathioprine hypersensitivity can closely mimic sepsis and/or vasculitis activity and should be considered in AAV, a condition with frequent use of this drug.	Azathioprine	0-12	adeno-associated virus integration site 1	Homo sapiens	110-113
30035323-0	2019	Azathioprine-induced myelosuppression in two pemphigus vulgaris patients with homozygous polymorphism of NUDT15.	Azathioprine	0-12	nudix hydrolase 15	Homo sapiens	105-111
31631819-7	2019	An association between TPMT genotypes 1/3A and 3B/3B and azathioprine related bone marrow suppression was found (P value &lt;= 0.05).	Azathioprine	57-69	thiopurine S-methyltransferase	Homo sapiens	23-27
30634695-6	2019	Both azathioprine and 6-mercaptopurine showed comparable EC50 values against cells expressing ABCC4 (G187W) and those expressing ABCC4 (WT).	Azathioprine	5-17	ATP binding cassette subfamily C member 4	Homo sapiens	94-99
30686035-1	2019	INTRODUCTION: Genetic polymorphism of thiopurine S-methyltransferase, the key enzyme in metabolism of thiopurines (azathioprine and 6-mercaptopurine) used in the treatment of inflammatory bowel disease, results in different enzyme activities.	Azathioprine	115-127	thiopurine S-methyltransferase	Homo sapiens	38-68
31631819-8	2019	CONCLUSION: The findings suggest that there was significant association between TPMT genotypes 1/3A and 3B/3B and azathioprine related bone marrow suppression.	Azathioprine	114-126	thiopurine S-methyltransferase	Homo sapiens	80-84
30451123-1	2019	BACKGROUND: Thiopurine S-methyltransferase (TPMT) is a cytoplasmic enzyme that catalyzes thiopurine drugs such as 6-mercaptopurine, 6-thioguanine, and azathioprine.	Azathioprine	151-163	thiopurine S-methyltransferase	Homo sapiens	12-42
30451123-1	2019	BACKGROUND: Thiopurine S-methyltransferase (TPMT) is a cytoplasmic enzyme that catalyzes thiopurine drugs such as 6-mercaptopurine, 6-thioguanine, and azathioprine.	Azathioprine	151-163	thiopurine S-methyltransferase	Homo sapiens	44-48
30451123-3	2019	The aim of this study is to assess TPMT genetic polymorphisms activity and metabolic products of AZA in patients with IBD.	Azathioprine	97-100	thiopurine S-methyltransferase	Homo sapiens	35-39
30451123-13	2019	CONCLUSIONS: Our results showed that TPMT polymorphisms are associated with 6-TGN levels in patients using AZA.	Azathioprine	107-110	thiopurine S-methyltransferase	Homo sapiens	37-41
30451123-14	2019	This study suggests that AZA dosage may be determined according to the high or low prevalence of a TPMT genotype.	Azathioprine	25-28	thiopurine S-methyltransferase	Homo sapiens	99-103
30577778-3	2018	CASE PRESENTATION: We describe the case of a 45-year-old man with MOG-IgG1-positive highly relapsing optic neuritis who had experienced 5 attacks over 21 months and had monocular blindness despite prednisolone and azathioprine therapy.	Azathioprine	214-226	myelin oligodendrocyte glycoprotein	Homo sapiens	66-69
31198067-9	2019	mtTFA expression in CSE-treated HUVECs was restored by the methylation inhibitor, 5-aza-2"-deoxycytidine(AZA).	Azathioprine	105-108	transcription factor A, mitochondrial	Homo sapiens	0-5
30371086-2	2018	The reaction proceeds via the generation of the aza-Breslow intermediates from imines and NHC, which under oxidative conditions form the key imidoyl azoliums and a subsequent intramolecular cyclization furnishes the product.	Azathioprine	48-51	high mobility group nucleosomal binding domain 4	Homo sapiens	90-93
30106365-0	2018	Neutropenia related to an azathioprine metabolic disorder induced by an inosine triphosphate pyrophosphohydrolase (ITPA) gene mutation in a patient with PR3-ANCA-positive microscopic polyangiitis : .	Azathioprine	26-38	inosine triphosphatase	Homo sapiens	115-119
30048737-6	2018	IL-2 production was reduced in response to treatment with well-known immunotoxicants cyclosporin A (CYA), dexamethasone (DEX), azathioprine (AZPR), methotrexate (MOT) and benzo(a)pyrene (BAP) but was not affected by treatment with cyclophosphamide (CYPH).	Azathioprine	127-139	interleukin 2	Homo sapiens	0-4
30048737-6	2018	IL-2 production was reduced in response to treatment with well-known immunotoxicants cyclosporin A (CYA), dexamethasone (DEX), azathioprine (AZPR), methotrexate (MOT) and benzo(a)pyrene (BAP) but was not affected by treatment with cyclophosphamide (CYPH).	Azathioprine	141-145	interleukin 2	Homo sapiens	0-4
30577288-0	2018	Azathioprine-induced Agranulocytosis and Severe Alopecia After Kidney Transplantation Associated With a NUDT15 Polymorphism: A Case Report.	Azathioprine	0-12	nudix hydrolase 15	Homo sapiens	104-110
30577288-4	2018	Genetic testing revealed a homozygous polymorphism of NUDT15 (rs116855232, NM_018283.3:c.415C&gt;T: p.Arg139Cys), which has previously been identified as a risk factor for AZA-related complications in patients with inflammatory bowel disease.	Azathioprine	172-175	nudix hydrolase 15	Homo sapiens	54-60
30577288-5	2018	CONCLUSION: Genetic screening for NUDT15 could contribute to the prevention of serious adverse reactions to AZA and provide the opportunity for personalized medicine.	Azathioprine	108-111	nudix hydrolase 15	Homo sapiens	34-40
30106365-0	2018	Neutropenia related to an azathioprine metabolic disorder induced by an inosine triphosphate pyrophosphohydrolase (ITPA) gene mutation in a patient with PR3-ANCA-positive microscopic polyangiitis : .	Azathioprine	26-38	proteinase 3	Homo sapiens	153-156
30106365-14	2018	Therefore, we analyzed three AZA metabolism-associated genes for mutations: thiopurine S-methyltransferase (TPMT), inosine triphosphate pyrophosphohydrolase (ITPA), and nucleoside diphosphate linked moiety X-type motif 15 (NUDT15), and we identified ITPA 94C&gt;A mutation.	Azathioprine	29-32	thiopurine S-methyltransferase	Homo sapiens	76-106
30106365-14	2018	Therefore, we analyzed three AZA metabolism-associated genes for mutations: thiopurine S-methyltransferase (TPMT), inosine triphosphate pyrophosphohydrolase (ITPA), and nucleoside diphosphate linked moiety X-type motif 15 (NUDT15), and we identified ITPA 94C&gt;A mutation.	Azathioprine	29-32	thiopurine S-methyltransferase	Homo sapiens	108-112
30106365-14	2018	Therefore, we analyzed three AZA metabolism-associated genes for mutations: thiopurine S-methyltransferase (TPMT), inosine triphosphate pyrophosphohydrolase (ITPA), and nucleoside diphosphate linked moiety X-type motif 15 (NUDT15), and we identified ITPA 94C&gt;A mutation.	Azathioprine	29-32	nudix hydrolase 15	Homo sapiens	223-229
30106365-14	2018	Therefore, we analyzed three AZA metabolism-associated genes for mutations: thiopurine S-methyltransferase (TPMT), inosine triphosphate pyrophosphohydrolase (ITPA), and nucleoside diphosphate linked moiety X-type motif 15 (NUDT15), and we identified ITPA 94C&gt;A mutation.	Azathioprine	29-32	inosine triphosphatase	Homo sapiens	250-254
30106365-15	2018	This was a rare case of PR3-positive MPA with AZA-induced severe neutropenia that was possibly due to an ITPA gene mutation.	Azathioprine	46-49	proteinase 3	Homo sapiens	24-27
30106365-15	2018	This was a rare case of PR3-positive MPA with AZA-induced severe neutropenia that was possibly due to an ITPA gene mutation.	Azathioprine	46-49	inosine triphosphatase	Homo sapiens	105-109
30106365-16	2018	This case suggests that ITPA gene mutation is related to the adverse reactions of AZA in Japanese patients.	Azathioprine	82-85	inosine triphosphatase	Homo sapiens	24-28
30101994-2	2018	We tried to see whether NUDT15 gene polymorphism can be the most susceptible genetic factor for AZA toxicity and the gene screening is beneficial to avoid the adverse events of AZA for the treatment of skin diseases.	Azathioprine	96-99	nudix hydrolase 15	Homo sapiens	24-30
29455435-7	2018	RESULTS: Among 10 miRNAs specifically up-regulated in microarray analysis of AZA-treated SCC090 cells, we observed significantly decreased expression of hsa-miR-181c-5p, hsa-miR-132-5p, hsa-miR-658 in HPV +ve HNC cohort, TCGA tissue samples, and cell lines as compared to their HPV -ve counterpart, and their promoter region also possesses CpG islands.	Azathioprine	77-80	microRNA 132	Homo sapiens	170-181
29455435-7	2018	RESULTS: Among 10 miRNAs specifically up-regulated in microarray analysis of AZA-treated SCC090 cells, we observed significantly decreased expression of hsa-miR-181c-5p, hsa-miR-132-5p, hsa-miR-658 in HPV +ve HNC cohort, TCGA tissue samples, and cell lines as compared to their HPV -ve counterpart, and their promoter region also possesses CpG islands.	Azathioprine	77-80	microRNA 658	Homo sapiens	186-197
30631001-20	2018	She additionally received azathioprine 50 mg tab BID.	Azathioprine	26-38	BH3 interacting domain death agonist	Homo sapiens	49-52
29704867-0	2018	Azathioprine-induced alopecia and leukopenia associated with NUDT15 polymorphisms.	Azathioprine	0-12	nudix hydrolase 15	Homo sapiens	61-67
30976415-0	2019	Erratum: Azathioprine hypersensitivity syndrome in anti-myeloperoxidase anti-neutrophil cytoplasmic antibody-associated vasculitis.	Azathioprine	9-21	myeloperoxidase	Homo sapiens	56-71
30101994-2	2018	We tried to see whether NUDT15 gene polymorphism can be the most susceptible genetic factor for AZA toxicity and the gene screening is beneficial to avoid the adverse events of AZA for the treatment of skin diseases.	Azathioprine	177-180	nudix hydrolase 15	Homo sapiens	24-30
29939442-0	2018	A Novel Sc(OTf)3 -Catalyzed (2+2+1)-Cycloannulation/Aza-Friedel-Crafts Alkylation Sequence toward Multicyclic 2-Pyrrolines.	Azathioprine	52-55	POU class 5 homeobox 1	Homo sapiens	8-16
30313113-0	2018	Successful azathioprine treatment in an adolescent with chronic enteropathy associated with SLCO2A1 gene: A case report.	Azathioprine	11-23	solute carrier organic anion transporter family member 2A1	Homo sapiens	92-99
29936783-7	2018	Methylation of PRG2 gene was significantly decreasedin K562-R+5-Aza cells compared to other cells (p=0.021).	Azathioprine	63-67	proteoglycan 2, pro eosinophil major basic protein	Homo sapiens	15-19
29356833-2	2018	Discontinuation of azathioprine only resulted in a mild increase in CD4+ T cell numbers; however, therapy with the TNFalpha inhibitor adalimumab was initiated for a clinical flare and resulted in long-lasting clinical remission and rapid normalization of the lymphocytopenia including the respective lymphocyte subsets.	Azathioprine	19-31	CD4 molecule	Homo sapiens	68-71
30064482-12	2018	Both in vitro and in vivo assays showed that CD133+/CD44+ cells with high OPN levels were more sensitive to DNA methylation inhibitor, 5 Azacytidine (5 Aza).	Azathioprine	137-140	CD44 molecule (Indian blood group)	Homo sapiens	52-56
30064482-12	2018	Both in vitro and in vivo assays showed that CD133+/CD44+ cells with high OPN levels were more sensitive to DNA methylation inhibitor, 5 Azacytidine (5 Aza).	Azathioprine	137-140	secreted phosphoprotein 1	Homo sapiens	74-77
30185363-0	2018	Azathioprine-induced interstitial nephritis in an anti-neutrophil cytoplasmic antibody (ANCA) myeloperoxidase (MPO) vasculitis patient.	Azathioprine	0-12	myeloperoxidase	Homo sapiens	94-109
30185363-0	2018	Azathioprine-induced interstitial nephritis in an anti-neutrophil cytoplasmic antibody (ANCA) myeloperoxidase (MPO) vasculitis patient.	Azathioprine	0-12	myeloperoxidase	Homo sapiens	111-114
30185363-3	2018	We report the case of a 50-year-old Caucasian man with kidney-limited ANCA myeloperoxidase (MPO) vasculitis who presented with general malaise, fever, worsening renal function, and elevated inflammatory markers 2 weeks after the initiation of therapy with oral AZA.	Azathioprine	261-264	myeloperoxidase	Homo sapiens	92-95
30185363-6	2018	A diagnosis of allergic interstitial nephritis secondary to AZA was established, corresponding to the first biopsy-proven case described in an ANCA MPO vasculitis patient.	Azathioprine	60-63	myeloperoxidase	Homo sapiens	148-151
30223827-7	2018	Moreover, testicular tissue from the AZA-treated group had increased levels of oxidative stress indicator, MDA, and decreased activity of the antioxidant enzymes as superoxide dismutase (SOD), reduced glutathione (GSH) and catalase (CAT) levels.	Azathioprine	37-40	catalase	Rattus norvegicus	223-231
30223827-7	2018	Moreover, testicular tissue from the AZA-treated group had increased levels of oxidative stress indicator, MDA, and decreased activity of the antioxidant enzymes as superoxide dismutase (SOD), reduced glutathione (GSH) and catalase (CAT) levels.	Azathioprine	37-40	catalase	Rattus norvegicus	233-236
29745420-3	2018	Azathioprine (AZA) directly targets BCL-2 family-mediated apoptosis.	Azathioprine	0-12	B cell leukemia/lymphoma 2	Mus musculus	36-41
29745420-3	2018	Azathioprine (AZA) directly targets BCL-2 family-mediated apoptosis.	Azathioprine	14-17	B cell leukemia/lymphoma 2	Mus musculus	36-41
29745420-10	2018	BCL-2 inhibitor initiated cell death in T cells from patients refractory to AZA and reduced lymphocyte count in Il10-/- mice.	Azathioprine	76-79	BCL2 apoptosis regulator	Homo sapiens	0-5
29745420-15	2018	BCL-2 inhibition could be a new therapy option for patients refractory to AZA.	Azathioprine	74-77	BCL2 apoptosis regulator	Homo sapiens	0-5
30225153-0	2018	Anti-CD20 Treatment of Autoimmune Hemolytic Anemia Refractory to Corticosteroids and Azathioprine: A Pediatric Case Report and Mini Review.	Azathioprine	85-97	keratin 20	Homo sapiens	5-9
29802687-1	2018	A number of aza-heterocyclic compounds, which share the 5,6-dihydropyrrolo[2,1-a]isoquinoline (DHPIQ) scaffold with members of the lamellarin alkaloid family, were synthesized and evaluated for their ability to reverse in vitro multidrug resistance in cancer cells through inhibition of P-glycoprotein (P-gp) and/or multidrug-resistance-associated protein 1.	Azathioprine	12-15	ATP binding cassette subfamily B member 1	Homo sapiens	287-301
29802687-1	2018	A number of aza-heterocyclic compounds, which share the 5,6-dihydropyrrolo[2,1-a]isoquinoline (DHPIQ) scaffold with members of the lamellarin alkaloid family, were synthesized and evaluated for their ability to reverse in vitro multidrug resistance in cancer cells through inhibition of P-glycoprotein (P-gp) and/or multidrug-resistance-associated protein 1.	Azathioprine	12-15	ATP binding cassette subfamily B member 1	Homo sapiens	303-307
29661590-5	2018	She relapsed under treatment with AZA when CD19 cells reappeared 6 months after the first rituximab infusion.	Azathioprine	34-37	CD19 molecule	Homo sapiens	43-47
29370945-0	2018	[Usefulness of thiopurine methyltransferase polymorphism study and metabolites measurement for patients treated by azathioprine].	Azathioprine	115-127	thiopurine S-methyltransferase	Homo sapiens	15-43
29327413-0	2018	ITPA Activity in Children Treated by Azathioprine: Relationship to the Occurrence of Adverse Drug Reactions and Inflammatory Response.	Azathioprine	37-49	inosine triphosphatase	Homo sapiens	0-4
29327413-2	2018	This study investigated (i) the relationships between inosine triphosphate pyrophosphatase (ITPA) activity, an enzyme involved in thiopurine metabolism, and the occurrence of ADRs in children with immunological disease on AZA therapy, and (ii) the relationship between ITPA activity and the inflammatory activity observed in children with IBD.	Azathioprine	222-225	inosine triphosphatase	Homo sapiens	54-90
29327413-2	2018	This study investigated (i) the relationships between inosine triphosphate pyrophosphatase (ITPA) activity, an enzyme involved in thiopurine metabolism, and the occurrence of ADRs in children with immunological disease on AZA therapy, and (ii) the relationship between ITPA activity and the inflammatory activity observed in children with IBD.	Azathioprine	222-225	inosine triphosphatase	Homo sapiens	92-96
29327413-9	2018	Therefore, measurement of ITPA activity may help to identify children with IBD predisposed to residual inflammation on AZA therapy.	Azathioprine	119-122	inosine triphosphatase	Homo sapiens	26-30
29370945-3	2018	Severe myelosuppression, associated with abnormal AZA metabolism, is linked to the thiopurine methyltransferase (TPMT) genetic polymorphism that results in a high variability of its activity with 89% of patients with a normal activity, 11% with an intermediate activity, and 0.3% with very low activity leading to a very high risk of bonne marrow suppression.	Azathioprine	50-53	thiopurine S-methyltransferase	Homo sapiens	83-111
29370945-3	2018	Severe myelosuppression, associated with abnormal AZA metabolism, is linked to the thiopurine methyltransferase (TPMT) genetic polymorphism that results in a high variability of its activity with 89% of patients with a normal activity, 11% with an intermediate activity, and 0.3% with very low activity leading to a very high risk of bonne marrow suppression.	Azathioprine	50-53	thiopurine S-methyltransferase	Homo sapiens	113-117
29867468-0	2018	NUDT15 R139C Variants Increase the Risk of Azathioprine-Induced Leukopenia in Chinese Autoimmune Patients.	Azathioprine	43-55	nudix hydrolase 15	Homo sapiens	0-6
30083334-8	2018	Notably, necrostatin-1, the specific inhibitor of the RIP3 signaling pathway, and 6-thioguanine (6-TG), the active metabolite of azathioprine, predominantly reduced IL-6 production compared to other cytokines.	Azathioprine	129-141	interleukin 6	Homo sapiens	165-169
29867468-1	2018	The aim of this study was to investigate the influence of NUDT15 R139C, thiopurine S-methyltransferase (TPMT), and 6-TGN on azathioprine (AZA) induced leukopenia in Chinese autoimmune patients.	Azathioprine	124-136	nudix hydrolase 15	Homo sapiens	58-64
29867468-1	2018	The aim of this study was to investigate the influence of NUDT15 R139C, thiopurine S-methyltransferase (TPMT), and 6-TGN on azathioprine (AZA) induced leukopenia in Chinese autoimmune patients.	Azathioprine	124-136	thiopurine S-methyltransferase	Homo sapiens	104-108
29867468-1	2018	The aim of this study was to investigate the influence of NUDT15 R139C, thiopurine S-methyltransferase (TPMT), and 6-TGN on azathioprine (AZA) induced leukopenia in Chinese autoimmune patients.	Azathioprine	138-141	nudix hydrolase 15	Homo sapiens	58-64
29867468-1	2018	The aim of this study was to investigate the influence of NUDT15 R139C, thiopurine S-methyltransferase (TPMT), and 6-TGN on azathioprine (AZA) induced leukopenia in Chinese autoimmune patients.	Azathioprine	138-141	thiopurine S-methyltransferase	Homo sapiens	104-108
29867468-7	2018	Therefore, the variant of NUDT15 R139C is strongly associated with AZA-induced leukopenia in Chinese patients with various autoimmune diseases such as systemic lupus erythematosus, Sjogren"s syndrome, etc.	Azathioprine	67-70	nudix hydrolase 15	Homo sapiens	26-32
29270995-0	2018	HLA-DQA1-HLA-DRB1 polymorphism is a major predictor of azathioprine-induced pancreatitis in patients with inflammatory bowel disease.	Azathioprine	55-67	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	0-17
29630648-2	2018	Genetic polymorphisms and activity of the enzyme thiopurine methyltransferase (TPMT) have been associated with azathioprine efficacy and toxicity in several populations.	Azathioprine	111-123	thiopurine S-methyltransferase	Homo sapiens	49-77
29630648-2	2018	Genetic polymorphisms and activity of the enzyme thiopurine methyltransferase (TPMT) have been associated with azathioprine efficacy and toxicity in several populations.	Azathioprine	111-123	thiopurine S-methyltransferase	Homo sapiens	79-83
29421584-3	2018	Much of the side effect profile of AZA can be linked to a single nucleotide polymorphism (SNP) in the thiopurine methyltransferase (TPMT) gene which ensures the breakdown and efficacy of AZA.	Azathioprine	35-38	thiopurine S-methyltransferase	Homo sapiens	102-130
29421584-3	2018	Much of the side effect profile of AZA can be linked to a single nucleotide polymorphism (SNP) in the thiopurine methyltransferase (TPMT) gene which ensures the breakdown and efficacy of AZA.	Azathioprine	35-38	thiopurine S-methyltransferase	Homo sapiens	132-136
29421584-3	2018	Much of the side effect profile of AZA can be linked to a single nucleotide polymorphism (SNP) in the thiopurine methyltransferase (TPMT) gene which ensures the breakdown and efficacy of AZA.	Azathioprine	187-190	thiopurine S-methyltransferase	Homo sapiens	102-130
29421584-3	2018	Much of the side effect profile of AZA can be linked to a single nucleotide polymorphism (SNP) in the thiopurine methyltransferase (TPMT) gene which ensures the breakdown and efficacy of AZA.	Azathioprine	187-190	thiopurine S-methyltransferase	Homo sapiens	132-136
30206554-9	2018	Conventional therapy of HLA-B27-associated AAU with local or systemic glucocorticoids and immunosuppressive drugs (sulfasalazine, methotrexate, azathioprine, etc.)	Azathioprine	144-156	major histocompatibility complex, class I, B	Homo sapiens	24-31
30477053-2	2018	However, azathioprine has low therapeutic index with myelosuppression as its predominant toxicity which is linked with thiopurine S-methyltransferase (TPMT) enzyme activity, which is involved in drug metabolism.	Azathioprine	9-21	thiopurine S-methyltransferase	Homo sapiens	119-149
30477053-2	2018	However, azathioprine has low therapeutic index with myelosuppression as its predominant toxicity which is linked with thiopurine S-methyltransferase (TPMT) enzyme activity, which is involved in drug metabolism.	Azathioprine	9-21	thiopurine S-methyltransferase	Homo sapiens	151-155
28836866-7	2018	Importantly, variant allele frequency (VAF) of some mutated genes (RET, SF3B1, ASXL1) decreased after 9 months of treatment in Aza-responder patients.	Azathioprine	127-130	ret proto-oncogene	Homo sapiens	67-70
28836866-7	2018	Importantly, variant allele frequency (VAF) of some mutated genes (RET, SF3B1, ASXL1) decreased after 9 months of treatment in Aza-responder patients.	Azathioprine	127-130	splicing factor 3b subunit 1	Homo sapiens	72-77
28836866-7	2018	Importantly, variant allele frequency (VAF) of some mutated genes (RET, SF3B1, ASXL1) decreased after 9 months of treatment in Aza-responder patients.	Azathioprine	127-130	ASXL transcriptional regulator 1	Homo sapiens	79-84
29702976-0	2018	NUDT15 R139C variation increases the risk of azathioprine-induced toxicity in Chinese subjects: Case report and literature review.	Azathioprine	45-57	nudix hydrolase 15	Homo sapiens	0-6
29702976-3	2018	Recent studies found that NUDT15 R139C polymorphism is strongly associated with AZA-induced leukopenia in Koreans.	Azathioprine	80-83	nudix hydrolase 15	Homo sapiens	26-32
29702976-5	2018	Here, we report a case of a Chinese patient with Sjogren syndrome (SS) with wild-type TPMT*3C who was diagnosed with AZA-induced severe toxicity due to NUDT15 mutation based on clinical and laboratory characteristics.	Azathioprine	117-120	thiopurine S-methyltransferase	Homo sapiens	86-90
29702976-5	2018	Here, we report a case of a Chinese patient with Sjogren syndrome (SS) with wild-type TPMT*3C who was diagnosed with AZA-induced severe toxicity due to NUDT15 mutation based on clinical and laboratory characteristics.	Azathioprine	117-120	nudix hydrolase 15	Homo sapiens	152-158
29702976-10	2018	CONCLUSION: In this report, we first provide detailed clinical and laboratory characteristics of AZA-induced leukopenia in a patient with SS with a mutant NUDT15 R139C genotype (TT allele) and normal TPMT activity.	Azathioprine	97-100	nudix hydrolase 15	Homo sapiens	155-161
29702976-10	2018	CONCLUSION: In this report, we first provide detailed clinical and laboratory characteristics of AZA-induced leukopenia in a patient with SS with a mutant NUDT15 R139C genotype (TT allele) and normal TPMT activity.	Azathioprine	97-100	thiopurine S-methyltransferase	Homo sapiens	200-204
29614587-0	2018	[Role of Rac1 signaling pathway of azathioprine and peptidoglycan in the regulation of monocyte-macrophage apoptosis in Crohn"s disease].	Azathioprine	35-47	Rac family small GTPase 1	Homo sapiens	9-13
29270995-9	2018	CONCLUSIONS: The class II HLA region (at rs2647087) is an important marker of AZA-induced pancreatitis risk.	Azathioprine	78-81	major histocompatibility complex, class II, DR beta 1	Homo sapiens	26-29
29270995-10	2018	We propose a simple and clinically implementable algorithm based on rs2647087 and TPMT genotypes for AZA selection and dosing for patients with IBD.	Azathioprine	101-104	thiopurine S-methyltransferase	Homo sapiens	82-86
29720911-0	2018	Association Between Thiopurine S-Methyltransferase (TPMT) Genetic Variants and Infection in Pediatric Heart Transplant Recipients Treated With Azathioprine: A Multi-Institutional Analysis.	Azathioprine	143-155	thiopurine S-methyltransferase	Homo sapiens	20-50
29720911-0	2018	Association Between Thiopurine S-Methyltransferase (TPMT) Genetic Variants and Infection in Pediatric Heart Transplant Recipients Treated With Azathioprine: A Multi-Institutional Analysis.	Azathioprine	143-155	thiopurine S-methyltransferase	Homo sapiens	52-56
29720911-2	2018	Polymorphisms in the gene encoding thiopurine S-methyltransferase (TPMT) can alter the metabolism of azathioprine, resulting in marrow toxicity and life-threatening infection.	Azathioprine	101-113	thiopurine S-methyltransferase	Homo sapiens	35-65
29720911-2	2018	Polymorphisms in the gene encoding thiopurine S-methyltransferase (TPMT) can alter the metabolism of azathioprine, resulting in marrow toxicity and life-threatening infection.	Azathioprine	101-113	thiopurine S-methyltransferase	Homo sapiens	67-71
29720911-3	2018	In a multicenter cohort of pediatric heart transplant (HT) recipients, we determined the frequency of TPMT genetic variation and assessed whether azathioprine-treated recipients with TPMT variants were at increased risk of infection.	Azathioprine	146-158	thiopurine S-methyltransferase	Homo sapiens	183-187
29491687-1	2018	AIM: To observe gene polymorphisms of TPMT and NUDT15, and compare their predictive value for azathioprine (AZA)-induced leukopenia in inflammatory bowel disease (IBD).	Azathioprine	108-111	thiopurine S-methyltransferase	Homo sapiens	38-42
29491687-9	2018	There were 44 patients (20.1%) with mutant genotype of NUDT15 (C/T); among them, 16 received AZA, and 8 (50%) developed leukopenia.	Azathioprine	93-96	nudix hydrolase 15	Homo sapiens	55-61
29491687-10	2018	There were 175 patients (79.7%) with wild genotype of NUDT15 (C/C); among them, 64 received AZA, and 11 (17.2%) developed leukopenia.	Azathioprine	92-95	nudix hydrolase 15	Homo sapiens	54-60
29491687-13	2018	The remaining 216 patients (98.6%) were found to bear the wild genotype of TPMT (A/A); among them, 79 patients received AZA, and 18 (22.8%) developed leukopenia, and there was no significant difference from those with A/G (P = 0.071).	Azathioprine	120-123	thiopurine S-methyltransferase	Homo sapiens	75-79
29491687-15	2018	Therefore, NUDT15 gene polymorphism was obviously a better biomarker than TPMT gene polymorphism in the prediction of AZA-induced leukopenia.	Azathioprine	118-121	nudix hydrolase 15	Homo sapiens	11-17
29491687-15	2018	Therefore, NUDT15 gene polymorphism was obviously a better biomarker than TPMT gene polymorphism in the prediction of AZA-induced leukopenia.	Azathioprine	118-121	thiopurine S-methyltransferase	Homo sapiens	74-78
29491687-17	2018	NUDT15 polymorphism is a better predictor for AZA-induced leukopenia than TPMT polymorphism.	Azathioprine	46-49	nudix hydrolase 15	Homo sapiens	0-6
29406904-7	2018	Compared with the AZA group, the MMF group and the RTX group decreased the AQP-4-IgG titre evidently and caused fewer adverse events.	Azathioprine	18-21	aquaporin 4	Homo sapiens	75-80
28929558-3	2018	The configuration at C3a in 1 was controlled by the stereocenter at C9a, which was selectively generated (91 % ee) by an organocatalytic enantioselective aza-Friedel-Crafts reaction developed by our research group.	Azathioprine	154-157	complement C3	Homo sapiens	21-24
29272584-3	2018	Dimetallic aza[80]fullerenes M2@C79N (M = Y or Gd) possess an unpaired electron located between two metal ions, offering an opportunity to manipulate spin(s) protected in the cage for quantum information processing.	Azathioprine	11-14	spindlin 1	Homo sapiens	150-154
29193730-5	2018	After treating the cells with demethylation agent Aza and TSA, ADAMTS9 expression was dramatically increased.	Azathioprine	50-53	ADAM metallopeptidase with thrombospondin type 1 motif 9	Homo sapiens	63-70
29232840-3	2017	The enzymatic chemo- and enantioselective synthesis of (R)-(-)-N-benzyl-3-(benzylamino)butanamide is reported, showing the influence of the solvent on the chemoselectivity of the aza-Michael addition and the subsequent kinetic resolution of the Michael adduct; both processes are catalyzed by CalB and both are influenced by the nature of the solvent medium.	Azathioprine	179-182	calbindin 1	Homo sapiens	293-297
29283382-7	2017	Two other thiopurine drugs, mercaptopurine and azathioprine, were also evaluated for their tyrosinase inhibition; mercaptopurine caused stronger inhibition than thioguanine did, whereas azathioprine was a poor inhibitor.	Azathioprine	186-198	tyrosinase	Homo sapiens	91-101
28045129-1	2018	The conversion of azathioprine (AZA) to mercaptopurine (MP) is mediated by glutathione transferase Mu1 (GSTM1), alpha1 (GSTA1) and alpha2 (GSTA2).	Azathioprine	18-30	glutathione S-transferase mu 1	Homo sapiens	99-102
28045129-1	2018	The conversion of azathioprine (AZA) to mercaptopurine (MP) is mediated by glutathione transferase Mu1 (GSTM1), alpha1 (GSTA1) and alpha2 (GSTA2).	Azathioprine	18-30	glutathione S-transferase mu 1	Homo sapiens	104-109
28045129-1	2018	The conversion of azathioprine (AZA) to mercaptopurine (MP) is mediated by glutathione transferase Mu1 (GSTM1), alpha1 (GSTA1) and alpha2 (GSTA2).	Azathioprine	18-30	adrenoceptor alpha 1D	Homo sapiens	112-118
28045129-1	2018	The conversion of azathioprine (AZA) to mercaptopurine (MP) is mediated by glutathione transferase Mu1 (GSTM1), alpha1 (GSTA1) and alpha2 (GSTA2).	Azathioprine	18-30	glutathione S-transferase alpha 1	Homo sapiens	120-125
28045129-1	2018	The conversion of azathioprine (AZA) to mercaptopurine (MP) is mediated by glutathione transferase Mu1 (GSTM1), alpha1 (GSTA1) and alpha2 (GSTA2).	Azathioprine	18-30	glutathione S-transferase alpha 2	Homo sapiens	139-144
28045129-1	2018	The conversion of azathioprine (AZA) to mercaptopurine (MP) is mediated by glutathione transferase Mu1 (GSTM1), alpha1 (GSTA1) and alpha2 (GSTA2).	Azathioprine	32-35	glutathione S-transferase mu 1	Homo sapiens	99-102
28045129-1	2018	The conversion of azathioprine (AZA) to mercaptopurine (MP) is mediated by glutathione transferase Mu1 (GSTM1), alpha1 (GSTA1) and alpha2 (GSTA2).	Azathioprine	32-35	glutathione S-transferase mu 1	Homo sapiens	104-109
28045129-1	2018	The conversion of azathioprine (AZA) to mercaptopurine (MP) is mediated by glutathione transferase Mu1 (GSTM1), alpha1 (GSTA1) and alpha2 (GSTA2).	Azathioprine	32-35	adrenoceptor alpha 1D	Homo sapiens	112-118
28045129-1	2018	The conversion of azathioprine (AZA) to mercaptopurine (MP) is mediated by glutathione transferase Mu1 (GSTM1), alpha1 (GSTA1) and alpha2 (GSTA2).	Azathioprine	32-35	glutathione S-transferase alpha 1	Homo sapiens	120-125
28045129-1	2018	The conversion of azathioprine (AZA) to mercaptopurine (MP) is mediated by glutathione transferase Mu1 (GSTM1), alpha1 (GSTA1) and alpha2 (GSTA2).	Azathioprine	32-35	glutathione S-transferase alpha 2	Homo sapiens	139-144
28045129-4	2018	GSTM1-null genotype carriers on AZA had two-fold lower 6-MMPR levels than AZA users carrying one or two copies of GSTM1 (2239 (1006-4587) versus 4371 (1897-7369) pmol/8 x 108 RBCs; P&lt;0.01).	Azathioprine	32-35	glutathione S-transferase mu 1	Homo sapiens	0-5
28045129-4	2018	GSTM1-null genotype carriers on AZA had two-fold lower 6-MMPR levels than AZA users carrying one or two copies of GSTM1 (2239 (1006-4587) versus 4371 (1897-7369) pmol/8 x 108 RBCs; P&lt;0.01).	Azathioprine	74-77	glutathione S-transferase mu 1	Homo sapiens	0-5
28045129-4	2018	GSTM1-null genotype carriers on AZA had two-fold lower 6-MMPR levels than AZA users carrying one or two copies of GSTM1 (2239 (1006-4587) versus 4371 (1897-7369) pmol/8 x 108 RBCs; P&lt;0.01).	Azathioprine	74-77	glutathione S-transferase mu 1	Homo sapiens	114-119
29212102-1	2017	A 24-year old woman with a history of Crohn"s disease developed bloody diarrhea and multiple abdominal abscesses, daily fever, leukocytosis, and elevated CRP several months after her immunosuppressive therapy with azathioprine was stopped.	Azathioprine	214-226	C-reactive protein	Homo sapiens	154-157
28922253-14	2017	Antidrug antibody positivity rates were significantly higher throughout patients with previous anti-TNF exposure; concomitant azathioprine prevented antidrug antibody formation in anti-TNF-naive patients with CD.	Azathioprine	126-138	tumor necrosis factor	Homo sapiens	185-188
29264467-7	2017	We tried high-dose steroids, azathioprine, and intravenous immunoglobulins, which resulted in improvement and barely detectable insulin receptor antibody.	Azathioprine	29-41	insulin receptor	Homo sapiens	128-144
28857898-1	2017	BACKGROUND: There is evidence that genotyping for the thiopurine S-methyltransferase (TPMT) gene variants is useful for the prediction of response to thiopurine analogs (azathioprine and 6-mercaptopurine) in patients with inflammatory bowel disease (IBD).	Azathioprine	170-182	thiopurine S-methyltransferase	Homo sapiens	54-84
28857898-1	2017	BACKGROUND: There is evidence that genotyping for the thiopurine S-methyltransferase (TPMT) gene variants is useful for the prediction of response to thiopurine analogs (azathioprine and 6-mercaptopurine) in patients with inflammatory bowel disease (IBD).	Azathioprine	170-182	thiopurine S-methyltransferase	Homo sapiens	86-90
28650902-0	2017	ITPA Activity in Adults and Children Treated With or Without Azathioprine: Relationship Between TPMT Activity, Thiopurine Metabolites, and Co-medications.	Azathioprine	61-73	inosine triphosphatase	Homo sapiens	0-4
29019504-0	2017	Synthesis of functionalized imidazolidine-2-thiones via NHC/base-promoted aza-benzoin/aza-acetalization domino reactions.	Azathioprine	74-77	high mobility group nucleosomal binding domain 4	Homo sapiens	56-59
29019504-2	2017	A novel class of alpha-sulfonylamines have been suitably prepared (46-81% yield) as precursors of formal benzylidenethiourea acceptors; these are generated in situ and intercepted by N-heterocyclic carbene (NHC)-activated aldehydes affording open-chain aza-benzoin-type adducts, which in turn undergo an intramolecular aza-acetalization reaction in a one-pot fashion.	Azathioprine	253-256	high mobility group nucleosomal binding domain 4	Homo sapiens	183-205
29019504-2	2017	A novel class of alpha-sulfonylamines have been suitably prepared (46-81% yield) as precursors of formal benzylidenethiourea acceptors; these are generated in situ and intercepted by N-heterocyclic carbene (NHC)-activated aldehydes affording open-chain aza-benzoin-type adducts, which in turn undergo an intramolecular aza-acetalization reaction in a one-pot fashion.	Azathioprine	253-256	high mobility group nucleosomal binding domain 4	Homo sapiens	207-210
28966507-1	2017	BACKGROUND: Thiopurine S-methyltransferase (TPMT) is an important enzyme in the metabolism of thiopurines including azathioprine (AZA), 6-mercaptopurine, and 6-thioguanine.	Azathioprine	116-128	thiopurine S-methyltransferase	Homo sapiens	12-42
28966507-1	2017	BACKGROUND: Thiopurine S-methyltransferase (TPMT) is an important enzyme in the metabolism of thiopurines including azathioprine (AZA), 6-mercaptopurine, and 6-thioguanine.	Azathioprine	116-128	thiopurine S-methyltransferase	Homo sapiens	44-48
28966507-1	2017	BACKGROUND: Thiopurine S-methyltransferase (TPMT) is an important enzyme in the metabolism of thiopurines including azathioprine (AZA), 6-mercaptopurine, and 6-thioguanine.	Azathioprine	130-133	thiopurine S-methyltransferase	Homo sapiens	12-42
28966507-1	2017	BACKGROUND: Thiopurine S-methyltransferase (TPMT) is an important enzyme in the metabolism of thiopurines including azathioprine (AZA), 6-mercaptopurine, and 6-thioguanine.	Azathioprine	130-133	thiopurine S-methyltransferase	Homo sapiens	44-48
28966507-2	2017	TPMT genotyping is widely used for screening of AZA-related toxicity during routine clinical practice in Korea.	Azathioprine	48-51	thiopurine S-methyltransferase	Homo sapiens	0-4
28966507-3	2017	However, the data of TPMT genotypes and its AZA-related toxicity have not been studied in the field of dermatology.	Azathioprine	44-47	thiopurine S-methyltransferase	Homo sapiens	21-25
28966507-4	2017	OBJECTIVE: The aim of this study was to evaluate the genetic basis of TPMT polymorphism in Korean dermatologic patients and subsequently to investigate the relationship between mutant TPMT and adverse responses to AZA treatment.	Azathioprine	214-217	thiopurine S-methyltransferase	Homo sapiens	70-74
28966507-4	2017	OBJECTIVE: The aim of this study was to evaluate the genetic basis of TPMT polymorphism in Korean dermatologic patients and subsequently to investigate the relationship between mutant TPMT and adverse responses to AZA treatment.	Azathioprine	214-217	thiopurine S-methyltransferase	Homo sapiens	184-188
28966507-14	2017	CONCLUSION: Our results suggest that 1) TPMT polymorphisms in Korean dermatologic patients are similar to those previously reported in Asian patients with the most common mutant allele being TPMT*3C and 2) AZA can be used in the patients with these polymorphisms under a careful dosing regimen.	Azathioprine	206-209	thiopurine S-methyltransferase	Homo sapiens	40-44
28650902-2	2017	The ability of ITPA to modify the thiopurine metabolite levels is currently used to optimize azathioprine (AZA) therapy in relation to thiopurine S-methyltransferase (TPMT) activity, the aim of this study is to investigate ITPA phenotype in a large population and to evaluate the relation between ITPA and TPMT activities and thiopurine metabolites.	Azathioprine	93-105	inosine triphosphatase	Homo sapiens	15-19
28650902-2	2017	The ability of ITPA to modify the thiopurine metabolite levels is currently used to optimize azathioprine (AZA) therapy in relation to thiopurine S-methyltransferase (TPMT) activity, the aim of this study is to investigate ITPA phenotype in a large population and to evaluate the relation between ITPA and TPMT activities and thiopurine metabolites.	Azathioprine	93-105	thiopurine S-methyltransferase	Homo sapiens	135-165
28650902-2	2017	The ability of ITPA to modify the thiopurine metabolite levels is currently used to optimize azathioprine (AZA) therapy in relation to thiopurine S-methyltransferase (TPMT) activity, the aim of this study is to investigate ITPA phenotype in a large population and to evaluate the relation between ITPA and TPMT activities and thiopurine metabolites.	Azathioprine	107-110	inosine triphosphatase	Homo sapiens	15-19
28650902-2	2017	The ability of ITPA to modify the thiopurine metabolite levels is currently used to optimize azathioprine (AZA) therapy in relation to thiopurine S-methyltransferase (TPMT) activity, the aim of this study is to investigate ITPA phenotype in a large population and to evaluate the relation between ITPA and TPMT activities and thiopurine metabolites.	Azathioprine	107-110	thiopurine S-methyltransferase	Homo sapiens	135-165
28650902-2	2017	The ability of ITPA to modify the thiopurine metabolite levels is currently used to optimize azathioprine (AZA) therapy in relation to thiopurine S-methyltransferase (TPMT) activity, the aim of this study is to investigate ITPA phenotype in a large population and to evaluate the relation between ITPA and TPMT activities and thiopurine metabolites.	Azathioprine	107-110	thiopurine S-methyltransferase	Homo sapiens	167-171
28650902-0	2017	ITPA Activity in Adults and Children Treated With or Without Azathioprine: Relationship Between TPMT Activity, Thiopurine Metabolites, and Co-medications.	Azathioprine	61-73	thiopurine S-methyltransferase	Homo sapiens	96-100
28650902-2	2017	The ability of ITPA to modify the thiopurine metabolite levels is currently used to optimize azathioprine (AZA) therapy in relation to thiopurine S-methyltransferase (TPMT) activity, the aim of this study is to investigate ITPA phenotype in a large population and to evaluate the relation between ITPA and TPMT activities and thiopurine metabolites.	Azathioprine	107-110	inosine triphosphatase	Homo sapiens	223-227
28650902-2	2017	The ability of ITPA to modify the thiopurine metabolite levels is currently used to optimize azathioprine (AZA) therapy in relation to thiopurine S-methyltransferase (TPMT) activity, the aim of this study is to investigate ITPA phenotype in a large population and to evaluate the relation between ITPA and TPMT activities and thiopurine metabolites.	Azathioprine	107-110	inosine triphosphatase	Homo sapiens	223-227
28650902-2	2017	The ability of ITPA to modify the thiopurine metabolite levels is currently used to optimize azathioprine (AZA) therapy in relation to thiopurine S-methyltransferase (TPMT) activity, the aim of this study is to investigate ITPA phenotype in a large population and to evaluate the relation between ITPA and TPMT activities and thiopurine metabolites.	Azathioprine	107-110	thiopurine S-methyltransferase	Homo sapiens	306-310
28650902-3	2017	METHODS: ITPA activity was determined in 183 adults and 138 children with or without AZA therapy.	Azathioprine	85-88	inosine triphosphatase	Homo sapiens	9-13
28924385-9	2017	Conversely, treatment with the DNA methylation inhibitor AZA caused induction of miR-449c.	Azathioprine	57-60	microRNA 449c	Homo sapiens	81-89
28659184-13	2017	The down-regulation of RERG was restored in NPC cells treated with Aza and TSA.	Azathioprine	67-70	RAS like estrogen regulated growth inhibitor	Homo sapiens	23-27
28556421-11	2017	There was a significant increase in the frequency of contractions after ciclosporin, tacrolimus, azathioprine and sirolimus treatment compared with control animals (4.6 +- 0.3 cycles min-1 ).	Azathioprine	97-109	CD59 molecule (CD59 blood group)	Homo sapiens	183-188
28621934-3	2017	In comparison with TQOPEN, the thia and aza derivatives TQSPEN and TQNPEN exhibit improved Cd2+/Zn2+ selectivity and higher Cd2+-binding affinity, respectively.	Azathioprine	40-43	CD2 molecule	Homo sapiens	91-94
28621934-3	2017	In comparison with TQOPEN, the thia and aza derivatives TQSPEN and TQNPEN exhibit improved Cd2+/Zn2+ selectivity and higher Cd2+-binding affinity, respectively.	Azathioprine	40-43	CD2 molecule	Homo sapiens	124-127
28670229-8	2017	However, NUDT15 p.Arg139Cys was significantly associated with the interval between initiation and discontinuation of AZA among patients with gastrointestinal intolerance.	Azathioprine	117-120	nudix hydrolase 15	Homo sapiens	9-15
28699600-12	2017	CONCLUSION: The TT genotype of ECM1 gene rs3737240 SNP significantly increased susceptibility for UC and azathioprine use in UC patients in a Turkish population.	Azathioprine	105-117	extracellular matrix protein 1	Homo sapiens	31-35
28566182-0	2017	NUDT15 p.R139C variant is common and strongly associated with azathioprine-induced early leukopenia and severe alopecia in Korean patients with various neurological diseases.	Azathioprine	62-74	nudix hydrolase 15	Homo sapiens	0-6
28566182-2	2017	In addition to variation in TPMT (thiopurine S-methyltransferase), the NUDT15 p.R139C variant was recently identified to have a strong association with AZA-induced leukopenia.	Azathioprine	152-155	nudix hydrolase 15	Homo sapiens	71-77
28566182-10	2017	Therefore, the NUDT15 p.R139C variant is common and strongly associated with AZA-induced early leukopenia and severe alopecia in Korean patients with various neurological diseases.	Azathioprine	77-80	nudix hydrolase 15	Homo sapiens	15-21
28679512-4	2017	We present the case of a patient who developed GBS while undergoing treatment with adalimumab in combination with azathioprine for severe fistulising Crohn"s disease, and review the literature on neurological adverse events that occur in association with anti-TNF therapy.	Azathioprine	114-126	tumor necrosis factor	Homo sapiens	260-263
28677646-4	2017	3-(4,5-Dimethyl-2-thiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay clearly indicated that the EC50 values of azathioprine against cells expressing ABCC4 (WT) were 1.4-1.7-fold higher than those against cells expressing SNP variants of ABCC4 (M184K; N297S; K304N or E757K).	Azathioprine	122-134	ATP binding cassette subfamily C member 4	Homo sapiens	160-165
28677646-4	2017	3-(4,5-Dimethyl-2-thiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay clearly indicated that the EC50 values of azathioprine against cells expressing ABCC4 (WT) were 1.4-1.7-fold higher than those against cells expressing SNP variants of ABCC4 (M184K; N297S; K304N or E757K).	Azathioprine	122-134	ATP binding cassette subfamily C member 4	Homo sapiens	248-253
28584644-8	2017	By comparison, the TNF-alpha mRNA expression level was evaluated in patients with a history of taking medications and demonstrated a significant association in the group that received the 5-ASA + Pred + AZA,5.	Azathioprine	203-206	tumor necrosis factor	Homo sapiens	19-28
27769591-5	2017	Two transient increases in sUA (maximal sUA 1.0 and 6.2mg/dL, respectively), were associated with azathioprine non-compliance and resolved with azathioprine reinstitution.	Azathioprine	98-110	SUMO1 activating enzyme subunit 1	Homo sapiens	40-45
27769591-5	2017	Two transient increases in sUA (maximal sUA 1.0 and 6.2mg/dL, respectively), were associated with azathioprine non-compliance and resolved with azathioprine reinstitution.	Azathioprine	144-156	SUMO1 activating enzyme subunit 1	Homo sapiens	40-45
28404876-6	2017	Results demonstrated that AZA- and DAC-treated AML cells reduce the release of sNKG2DL, preventing downregulation of NKG2D receptor on the cell surface and promoting immune recognition mediated by NKG2D-NKG2DL engagement.	Azathioprine	26-29	killer cell lectin like receptor K1	Homo sapiens	117-131
28404876-6	2017	Results demonstrated that AZA- and DAC-treated AML cells reduce the release of sNKG2DL, preventing downregulation of NKG2D receptor on the cell surface and promoting immune recognition mediated by NKG2D-NKG2DL engagement.	Azathioprine	26-29	killer cell lectin like receptor K1	Homo sapiens	80-85
28111033-0	2017	Azathioprine therapy in a case of pediatric multiple sclerosis that was seropositive for MOG-IgG.	Azathioprine	0-12	myelin oligodendrocyte glycoprotein	Homo sapiens	89-92
28373537-0	2017	Structure-metabolism relationships in human-AOX: Chemical insights from a large database of aza-aromatic and amide compounds.	Azathioprine	92-95	aldehyde oxidase 1	Homo sapiens	44-47
28539830-7	2017	Moreover, osteosarcoma cells treated with 5-AZA-2"-deoxycytidine (AZA), a DNA methylation inhibitor, exhibited increased levels of miR-370 and decreased levels of beta-catenin downstream targets, which resulted in inhibition of cell proliferation and colony formation ability.	Azathioprine	44-47	microRNA 370	Homo sapiens	131-138
28539830-7	2017	Moreover, osteosarcoma cells treated with 5-AZA-2"-deoxycytidine (AZA), a DNA methylation inhibitor, exhibited increased levels of miR-370 and decreased levels of beta-catenin downstream targets, which resulted in inhibition of cell proliferation and colony formation ability.	Azathioprine	44-47	catenin beta 1	Homo sapiens	163-175
28111033-3	2017	A 10-year-old boy with multiple sclerosis who was seropositive for antibodies against myelin oligodendrocyte glycoprotein (MOG)-IgG was treated with azathioprine plus oral methylprednisolone.	Azathioprine	149-161	myelin oligodendrocyte glycoprotein	Homo sapiens	86-121
28111033-3	2017	A 10-year-old boy with multiple sclerosis who was seropositive for antibodies against myelin oligodendrocyte glycoprotein (MOG)-IgG was treated with azathioprine plus oral methylprednisolone.	Azathioprine	149-161	myelin oligodendrocyte glycoprotein	Homo sapiens	123-126
28111033-6	2017	Azathioprine may be a treatment option, particularly in poor medical resource areas, for pediatric patients with multiple sclerosis who are seropositive for MOG-IgG.	Azathioprine	0-12	myelin oligodendrocyte glycoprotein	Homo sapiens	157-160
27922550-0	2017	A novel ABCC6 haplotype is associated with azathioprine drug response in myasthenia gravis.	Azathioprine	43-55	ATP binding cassette subfamily C member 6	Homo sapiens	8-13
28813730-0	2017	Point-Counterpoint: TPMT Genotyping for Azathioprine in Adult Medicine.	Azathioprine	40-52	thiopurine S-methyltransferase	Homo sapiens	20-24
28273887-7	2017	When we analyzed clinical parameters, patients treated with azathioprine had the highest CSF-1 levels and CCR5 expression.	Azathioprine	60-72	colony stimulating factor 1	Homo sapiens	89-94
28273887-7	2017	When we analyzed clinical parameters, patients treated with azathioprine had the highest CSF-1 levels and CCR5 expression.	Azathioprine	60-72	C-C motif chemokine receptor 5	Homo sapiens	106-110
28611998-5	2017	Systemic treatment with corticosteroids and azathioprine led to complete resolution of mucocutaneous lesions as well as nail manifestations.	Azathioprine	44-56	CD244 molecule	Homo sapiens	120-124
28119098-12	2017	In addition, the mRNA expression of MPO, iNOS and COX-2 induced by DSS treatment was remarkably inhibited by BJOE, SASP or AZA treatments.	Azathioprine	123-126	myeloperoxidase	Mus musculus	36-39
28119098-12	2017	In addition, the mRNA expression of MPO, iNOS and COX-2 induced by DSS treatment was remarkably inhibited by BJOE, SASP or AZA treatments.	Azathioprine	123-126	nitric oxide synthase 2, inducible	Mus musculus	41-45
28119098-12	2017	In addition, the mRNA expression of MPO, iNOS and COX-2 induced by DSS treatment was remarkably inhibited by BJOE, SASP or AZA treatments.	Azathioprine	123-126	cytochrome c oxidase II, mitochondrial	Mus musculus	50-55
28119098-13	2017	Furthermore, when compared with DSS-treated mice, the activation of NF-kappaB was significantly inhibited by AZA and BJOE treatment.	Azathioprine	109-112	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	68-77
28099404-9	2017	Fair skin type, multiple tumors before retransplantation, treatment with azathioprine, T cell-depleting antibodies, and delayed revision of immunosuppression were associated with an increased risk of aggressive cutaneous SCC after retransplantation.	Azathioprine	73-85	serpin family B member 3	Homo sapiens	221-224
28217896-3	2017	Herein, we report the identification and characterization of a dimeric PdI species in two prototypical Pd-catalyzed aerobic oxidation reactions: allylic C-H acetoxylation of terminal alkenes and intramolecular aza-Wacker cyclization.	Azathioprine	210-213	prolyl 4-hydroxylase subunit beta	Homo sapiens	71-74
27922550-6	2017	We showed that two SNPs (rs8058694 and rs8058696) found in ATP-binding cassette subfamily C member 6, a subfamily member of ATP-binding cassette genes, constituted a new haplotype associated with AZA response in MG patients in the discovery cohort (P=0.011; odds ratio: 0.40; 95% confidence interval: 0.20-0.83) and in the combined cohort (P=0.04; odds ratio: 1.58).	Azathioprine	196-199	ATP binding cassette subfamily C member 6	Homo sapiens	59-100
27922550-7	2017	CONCLUSION: These findings highlight the role that the ATP-binding cassette subfamily C member 6 haplotype may play in AZA drug response.	Azathioprine	119-122	ATP binding cassette subfamily C member 6	Homo sapiens	55-96
28081040-1	2017	We describe the case of a pediatric patient on azathioprine therapy with previously undiagnosed homozygote thiopurine S-methyltransferase (TPMT) deficiency, resulting in myelotoxic thiopurine metabolite levels.	Azathioprine	47-59	thiopurine S-methyltransferase	Homo sapiens	107-137
28081040-1	2017	We describe the case of a pediatric patient on azathioprine therapy with previously undiagnosed homozygote thiopurine S-methyltransferase (TPMT) deficiency, resulting in myelotoxic thiopurine metabolite levels.	Azathioprine	47-59	thiopurine S-methyltransferase	Homo sapiens	139-143
28081040-0	2017	Azathioprine Therapy in a Pediatric TPMT-Deficient Patient-Still an Option.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	36-40
28081040-3	2017	We demonstrate that azathioprine therapy still might be an effective and safe therapeutic option in pediatric thiopurine S-methyltransferase-deficient IBD patients.	Azathioprine	20-32	thiopurine S-methyltransferase	Homo sapiens	110-140
29441893-3	2017	Inflammatory bowel disease (IBD) and systemic lupus erythematosus (SLE) patients with low thiopurine (S)-methyltransferase (TPMT) activity tend to respond well to AZA therapy.	Azathioprine	163-166	thiopurine S-methyltransferase	Homo sapiens	90-122
29441893-3	2017	Inflammatory bowel disease (IBD) and systemic lupus erythematosus (SLE) patients with low thiopurine (S)-methyltransferase (TPMT) activity tend to respond well to AZA therapy.	Azathioprine	163-166	thiopurine S-methyltransferase	Homo sapiens	124-128
27521513-2	2016	Patients with PSC also can have inflammatory bowel diseases (IBDs) or features of autoimmune hepatitis (AIH), and therefore are treated with azathioprine.	Azathioprine	141-153	PSC	Homo sapiens	14-17
27163483-5	2016	The overall summary estimate showed a significantly increased risk of SCC in relation to azathioprine exposure (1.56, 95% confidence interval [CI] 1.11-2.18).	Azathioprine	89-101	serpin family B member 3	Homo sapiens	70-73
27163483-8	2016	The pooled findings of available evidence support the contention that treatment with azathioprine increases the risk of SCC in OTRs.	Azathioprine	85-97	serpin family B member 3	Homo sapiens	120-123
27931816-2	2016	Using this Pig-a assay, the in vivo mutagenicity of a single dose of azathioprine (Aza) was investigated in red blood cells (RBC Pig-a assay) and reticulocytes (PIGRET) of rats.	Azathioprine	69-81	phosphatidylinositol glycan anchor biosynthesis class A	Sus scrofa	11-16
27705931-4	2016	Intriguingly, treatment with the DNA methylation inhibitors 5-Aza-CdR (Aza) and 4-phenylbutyric acid (PBA) resulted in miR128-1 upregulation in both GBM cells and GSCs.	Azathioprine	62-65	microRNA 128-1	Homo sapiens	119-127
27931816-2	2016	Using this Pig-a assay, the in vivo mutagenicity of a single dose of azathioprine (Aza) was investigated in red blood cells (RBC Pig-a assay) and reticulocytes (PIGRET) of rats.	Azathioprine	69-81	phosphatidylinositol glycan anchor biosynthesis class A	Sus scrofa	129-134
27931816-2	2016	Using this Pig-a assay, the in vivo mutagenicity of a single dose of azathioprine (Aza) was investigated in red blood cells (RBC Pig-a assay) and reticulocytes (PIGRET) of rats.	Azathioprine	83-86	phosphatidylinositol glycan anchor biosynthesis class A	Sus scrofa	11-16
27931816-2	2016	Using this Pig-a assay, the in vivo mutagenicity of a single dose of azathioprine (Aza) was investigated in red blood cells (RBC Pig-a assay) and reticulocytes (PIGRET) of rats.	Azathioprine	83-86	phosphatidylinositol glycan anchor biosynthesis class A	Sus scrofa	129-134
27931816-7	2016	In contrast, with Aza small effects that were not statistically significant were observed in rats at 21 and 14days in the RBC Pig-a and PIGRET assays respectively.	Azathioprine	18-21	phosphatidylinositol glycan anchor biosynthesis class A	Sus scrofa	126-131
27480670-7	2016	While this intramolecular aza-Buchner cyclization prevents isolation of [Cp*Co(CNAr(Dipp2))], the dinitrogen complex Cp*Co(N2)(CNAr(Dipp2)) is shown to serve as a reliable synthon for this 16e(-) species upon reaction with small molecule substrates.	Azathioprine	26-29	nudix hydrolase 4	Homo sapiens	84-89
28598109-3	2016	RESULTS: Inhibitory rate in AZA+DDP group was the highest,and the lowest was AZA group.RASSF1A gene promoter region methylation levels of AZA,AZA+DDP and AZA+MPA groups significantly reduced and showed obvious demethylation stripes while other groups mainly showed the methylation stripes.The differences of RASSF1A protein expression between AZA,AZA+DDP and AZA+MPA groups were not statistical significant (P&gt;0.05),but the three were higher than model group (P&lt;0.05);there was no statistically significant difference respectively in the DDP,MPA,DDP+ MPA groups compared with that of model group (P&gt;0.05).In the comparison of apoptosis index,model group was the lowest,followed by the three single medicine groups,and the highest was three combination groups (P&lt;0.05).	Azathioprine	28-31	Ras association (RalGDS/AF-6) domain family member 1	Mus musculus	87-94
28598109-3	2016	RESULTS: Inhibitory rate in AZA+DDP group was the highest,and the lowest was AZA group.RASSF1A gene promoter region methylation levels of AZA,AZA+DDP and AZA+MPA groups significantly reduced and showed obvious demethylation stripes while other groups mainly showed the methylation stripes.The differences of RASSF1A protein expression between AZA,AZA+DDP and AZA+MPA groups were not statistical significant (P&gt;0.05),but the three were higher than model group (P&lt;0.05);there was no statistically significant difference respectively in the DDP,MPA,DDP+ MPA groups compared with that of model group (P&gt;0.05).In the comparison of apoptosis index,model group was the lowest,followed by the three single medicine groups,and the highest was three combination groups (P&lt;0.05).	Azathioprine	77-80	Ras association (RalGDS/AF-6) domain family member 1	Mus musculus	87-94
27480670-7	2016	While this intramolecular aza-Buchner cyclization prevents isolation of [Cp*Co(CNAr(Dipp2))], the dinitrogen complex Cp*Co(N2)(CNAr(Dipp2)) is shown to serve as a reliable synthon for this 16e(-) species upon reaction with small molecule substrates.	Azathioprine	26-29	nudix hydrolase 4	Homo sapiens	132-137
27723211-3	2016	The high value of the aza-Piancatelli rearrangement was demonstrated by the synthesis of a cyclopentane-based hNK1 antagonist analogue.	Azathioprine	22-25	beta-1,3-glucuronyltransferase 1	Homo sapiens	110-114
27783843-18	2016	Sixty-four per cent (47/163) of azathioprine patients were able to reduce their prednisone dose to &lt; 10 mg/day compared to 46% (32/70) of placebo patients (RR 1.34, 95% CI 1.02 to 1.77).	Azathioprine	32-44	ribonucleotide reductase catalytic subunit M1	Homo sapiens	159-163
27783843-22	2016	Serious adverse events were reported in 14% of patients receiving azathioprine compared to 4% of placebo patients (2 studies, 216 patients; RR 2.57, 95% CI 0.92 to 7.13).	Azathioprine	66-78	ribonucleotide reductase regulatory subunit M2	Homo sapiens	140-144
27720019-5	2016	Evaluations for glucose-6-phosphate dehydrogenase and thiopurine S-methyltransferase are commonplace clinical tests to reduce hematologic problems associated with drugs, such as dapsone and azathioprine, respectively.	Azathioprine	190-202	thiopurine S-methyltransferase	Homo sapiens	54-84
27787562-10	2016	Direct Dnmt targeting by Aza during the reversal period benefited methylation status of mtDNA and MMP-9 DNA.	Azathioprine	25-28	DNA methyltransferase 1	Homo sapiens	7-11
27787562-10	2016	Direct Dnmt targeting by Aza during the reversal period benefited methylation status of mtDNA and MMP-9 DNA.	Azathioprine	25-28	matrix metallopeptidase 9	Rattus norvegicus	98-103
27720019-5	2016	Evaluations for glucose-6-phosphate dehydrogenase and thiopurine S-methyltransferase are commonplace clinical tests to reduce hematologic problems associated with drugs, such as dapsone and azathioprine, respectively.	Azathioprine	190-202	glucose-6-phosphate dehydrogenase	Homo sapiens	16-49
27307154-1	2016	Thiopurine methyltransferase (TPMT) and inosine triphosphatase (ITPA) are crucial enzymes involved in the metabolism of thiopurine drugs: azathioprine and 6-mercaptopurine, used in the treatment of leukemia or inflammatory bowel diseases (IBD).	Azathioprine	138-150	thiopurine S-methyltransferase	Homo sapiens	0-28
27381176-0	2016	Further evidence that a variant of the gene NUDT15 may be an important predictor of azathioprine-induced toxicity in Chinese subjects: a case report.	Azathioprine	84-96	nudix hydrolase 15	Homo sapiens	44-50
27381176-1	2016	WHAT IS KNOWN AND OBJECTIVE: Thiopurine methyltransferase (TPMT) enzyme is an important component in the metabolism of azathioprine (AZA).	Azathioprine	119-131	thiopurine S-methyltransferase	Homo sapiens	29-57
27381176-1	2016	WHAT IS KNOWN AND OBJECTIVE: Thiopurine methyltransferase (TPMT) enzyme is an important component in the metabolism of azathioprine (AZA).	Azathioprine	119-131	thiopurine S-methyltransferase	Homo sapiens	59-63
27381176-1	2016	WHAT IS KNOWN AND OBJECTIVE: Thiopurine methyltransferase (TPMT) enzyme is an important component in the metabolism of azathioprine (AZA).	Azathioprine	133-136	thiopurine S-methyltransferase	Homo sapiens	29-57
27381176-1	2016	WHAT IS KNOWN AND OBJECTIVE: Thiopurine methyltransferase (TPMT) enzyme is an important component in the metabolism of azathioprine (AZA).	Azathioprine	133-136	thiopurine S-methyltransferase	Homo sapiens	59-63
27381176-4	2016	Moreover, AZA-induced toxicity still occurs in some patients with normal TPMT activity.	Azathioprine	10-13	thiopurine S-methyltransferase	Homo sapiens	73-77
27381176-7	2016	We report the first case of a Chinese patient with AZA-induced severe toxicity with no clinically significant TPMT variant but with the NUDT15 c.415C&gt;T allele.	Azathioprine	51-54	nudix hydrolase 15	Homo sapiens	136-142
27381176-12	2016	WHAT IS NEW AND CONCLUSION: NUDT15 c.415C&gt;T may be another predictor of AZA-induced leukocytopenia.	Azathioprine	75-78	nudix hydrolase 15	Homo sapiens	28-34
27307154-1	2016	Thiopurine methyltransferase (TPMT) and inosine triphosphatase (ITPA) are crucial enzymes involved in the metabolism of thiopurine drugs: azathioprine and 6-mercaptopurine, used in the treatment of leukemia or inflammatory bowel diseases (IBD).	Azathioprine	138-150	thiopurine S-methyltransferase	Homo sapiens	30-34
27307154-1	2016	Thiopurine methyltransferase (TPMT) and inosine triphosphatase (ITPA) are crucial enzymes involved in the metabolism of thiopurine drugs: azathioprine and 6-mercaptopurine, used in the treatment of leukemia or inflammatory bowel diseases (IBD).	Azathioprine	138-150	inosine triphosphatase	Homo sapiens	40-62
27307154-1	2016	Thiopurine methyltransferase (TPMT) and inosine triphosphatase (ITPA) are crucial enzymes involved in the metabolism of thiopurine drugs: azathioprine and 6-mercaptopurine, used in the treatment of leukemia or inflammatory bowel diseases (IBD).	Azathioprine	138-150	inosine triphosphatase	Homo sapiens	64-68
27529730-2	2016	The key core of this alkaloid was constructed through a phosphoric acid promoted and highly stereocontrolled alkyne aza-Prins cyclization reaction, synchronously establishing the bridged B-ring and the C13 quaternary stereocenter.	Azathioprine	116-119	homeobox C13	Homo sapiens	202-205
27666544-9	2016	The expression level of SOCS3 significantly increased in H2228 cells after 5"-Aza-dC treatment.	Azathioprine	78-81	suppressor of cytokine signaling 3	Homo sapiens	24-29
27623738-4	2016	AZA is an antiepileptic drug that has been shown to inhibit AQP4 expression and in this study we investigate the drug as a therapeutic to mitigate the extent of mTBI induced cellular edema.	Azathioprine	0-3	aquaporin 4	Homo sapiens	60-64
27623738-10	2016	Cell death and expression of S100B was significantly reduced when AZA was added shortly before mTBI stretch.	Azathioprine	66-69	S100 calcium binding protein B	Homo sapiens	29-34
27297792-9	2016	This growth was inhibited by azathioprine, a clinically available RAC1 inhibitor.	Azathioprine	29-41	Rac family small GTPase 1	Homo sapiens	66-70
27242368-1	2016	BACKGROUND: Cytoplasmic anti-neutrophil cytoplasmic antibody (C-ANCA) positivity at remission has been associated with an increased relapse rate in patients with proteinase 3 anti-neutrophil cytoplasmic antibody-associated vasculitis (PR3-AAV) after a switch to azathioprine maintenance therapy.	Azathioprine	262-274	proteinase 3	Homo sapiens	62-68
27242368-11	2016	CONCLUSIONS: This randomized trial suggests that extended azathioprine maintenance therapy has only a limited effect on the prevention of relapse in patients with PR3-AAV at 4 years after diagnosis.	Azathioprine	58-70	proteinase 3	Homo sapiens	163-166
27185957-6	2016	There was an increased risk of NMSC in patients taking CSA (RR = 2.51, 95% CI: 1.23, 5.13) and D-Pen (RR 3.49, 95% CI: 1.34, 4.63) in addition to MTX, but not for patients taking AZA or LEF.	Azathioprine	179-182	proprotein convertase subtilisin/kexin type 1 inhibitor	Homo sapiens	97-100
27311871-0	2016	Anaplastic lymphoma kinase (ALK)-positive large B-cell lymphoma in a patient treated with azathioprine for ulcerative colitis.	Azathioprine	90-102	ALK receptor tyrosine kinase	Homo sapiens	0-26
27545130-18	2016	CONCLUSION: Aza can inhibit the activity of DNMT1, reduce DDAH2 promoter methylation level, increase the expression of DDAH2, decrease the content of ADMA, increase eNOS activity and content of nitric oxide, thus lead to the improvement of endothelial dysfunction in mesenteric artery of Hyperhomocysteinemia rats.	Azathioprine	12-15	DNA methyltransferase 1	Rattus norvegicus	44-49
27545130-18	2016	CONCLUSION: Aza can inhibit the activity of DNMT1, reduce DDAH2 promoter methylation level, increase the expression of DDAH2, decrease the content of ADMA, increase eNOS activity and content of nitric oxide, thus lead to the improvement of endothelial dysfunction in mesenteric artery of Hyperhomocysteinemia rats.	Azathioprine	12-15	dimethylarginine dimethylaminohydrolase 2	Rattus norvegicus	58-63
27545130-18	2016	CONCLUSION: Aza can inhibit the activity of DNMT1, reduce DDAH2 promoter methylation level, increase the expression of DDAH2, decrease the content of ADMA, increase eNOS activity and content of nitric oxide, thus lead to the improvement of endothelial dysfunction in mesenteric artery of Hyperhomocysteinemia rats.	Azathioprine	12-15	dimethylarginine dimethylaminohydrolase 2	Rattus norvegicus	119-124
27311871-0	2016	Anaplastic lymphoma kinase (ALK)-positive large B-cell lymphoma in a patient treated with azathioprine for ulcerative colitis.	Azathioprine	90-102	ALK receptor tyrosine kinase	Homo sapiens	28-31
27258810-0	2016	A syn-Selective Aza-Aldol Reaction of Boron Aza-Enolates Generated from N-Sulfonyl-1,2,3-Triazoles and 9-BBN-H.	Azathioprine	16-19	synemin	Homo sapiens	2-5
27258810-1	2016	A syn-selective aza-aldol reaction of boron aza-enolates, generated from N-sulfonyl-1,2,3-triazoles and 9-BBN-H, is reported.	Azathioprine	16-19	synemin	Homo sapiens	2-5
26297310-3	2016	TPMT is one of the important metabolic enzymes of phase II metabolic pathway and catalyzes methylation of thiopurine drugs such as azathioprine, 6-thioguanine and 6-mercaptopurine, which are used to treat patients with neoplasia and autoimmune disease as well as transplant recipients.	Azathioprine	131-143	thiopurine S-methyltransferase	Homo sapiens	0-4
27214117-2	2016	Using 5 mol % of AlCl3 as the catalyst and 2 equiv of trimethylsilyl halides as the halide sources, aza-Prins cyclization of N-tosyl homoallylamine or Prins cyclization of homoallylic alcohol with carbonyl compounds could be readily realized, giving the corresponding trans-2-substituted-4-halopiperidines or cis-2-substituted-4-halotetrahydropyrans in high yields and satisfactory diastereoselectivity.	Azathioprine	100-103	suppressor of cytokine signaling 2	Homo sapiens	309-314
26621483-8	2016	CONCLUSIONS: Patients with PR3-AAV respond better to RTX than to CYC/AZA.	Azathioprine	69-72	proteinase 3	Homo sapiens	27-30
26876431-7	2016	For the introduction of aldehyde oxidase (AOX) into clinical practice, the association between AOX activity and AZA dose requirements should be positively confirmed.	Azathioprine	112-115	aldehyde oxidase 1	Homo sapiens	42-45
26794448-4	2016	METHODS: We have analyzed CAV1 gene expression and associated epigenetic marks (DNA methylation and histone 3 modifications) in the CAV1 promoter in two colon cancer cell lines, under treatment with well established epigenetic modulators, AZA, SAM, TSA and SFN at varying concentrations.	Azathioprine	239-242	caveolin 1	Homo sapiens	132-136
27123083-6	2016	The DNA demethylation drug 5-Aza-2"-deoxycytidine (Aza) was used to treat several ccRCC cell lines, and it was observed that the expression of miR-200c was significantly increased following Aza treatment.	Azathioprine	29-32	microRNA 200c	Homo sapiens	143-151
27123083-6	2016	The DNA demethylation drug 5-Aza-2"-deoxycytidine (Aza) was used to treat several ccRCC cell lines, and it was observed that the expression of miR-200c was significantly increased following Aza treatment.	Azathioprine	51-54	microRNA 200c	Homo sapiens	143-151
27123083-8	2016	In addition, Aza treatment significantly promoted expression of E-cadherin and inhibited the expression of N-cadherin, while the inhibition of miR-200c downregulated E-cadherin and upregulated the expression of N-cadherin, suggesting that miR-200c has a suppressive role in epithelial-mesenchymal transition (EMT) of ccRCC cells.	Azathioprine	13-16	cadherin 1	Homo sapiens	64-74
27123083-8	2016	In addition, Aza treatment significantly promoted expression of E-cadherin and inhibited the expression of N-cadherin, while the inhibition of miR-200c downregulated E-cadherin and upregulated the expression of N-cadherin, suggesting that miR-200c has a suppressive role in epithelial-mesenchymal transition (EMT) of ccRCC cells.	Azathioprine	13-16	cadherin 2	Homo sapiens	107-117
27123083-8	2016	In addition, Aza treatment significantly promoted expression of E-cadherin and inhibited the expression of N-cadherin, while the inhibition of miR-200c downregulated E-cadherin and upregulated the expression of N-cadherin, suggesting that miR-200c has a suppressive role in epithelial-mesenchymal transition (EMT) of ccRCC cells.	Azathioprine	13-16	microRNA 200c	Homo sapiens	143-151
27123083-8	2016	In addition, Aza treatment significantly promoted expression of E-cadherin and inhibited the expression of N-cadherin, while the inhibition of miR-200c downregulated E-cadherin and upregulated the expression of N-cadherin, suggesting that miR-200c has a suppressive role in epithelial-mesenchymal transition (EMT) of ccRCC cells.	Azathioprine	13-16	cadherin 1	Homo sapiens	166-176
27123083-8	2016	In addition, Aza treatment significantly promoted expression of E-cadherin and inhibited the expression of N-cadherin, while the inhibition of miR-200c downregulated E-cadherin and upregulated the expression of N-cadherin, suggesting that miR-200c has a suppressive role in epithelial-mesenchymal transition (EMT) of ccRCC cells.	Azathioprine	13-16	cadherin 2	Homo sapiens	211-221
27123083-8	2016	In addition, Aza treatment significantly promoted expression of E-cadherin and inhibited the expression of N-cadherin, while the inhibition of miR-200c downregulated E-cadherin and upregulated the expression of N-cadherin, suggesting that miR-200c has a suppressive role in epithelial-mesenchymal transition (EMT) of ccRCC cells.	Azathioprine	13-16	microRNA 200c	Homo sapiens	239-247
27123083-9	2016	In conclusion, it was suggested that demethylation drug Aza-induced upregulation of miR-200c may inhibit migration, invasion and EMT in ccRCC cells.	Azathioprine	56-59	microRNA 200c	Homo sapiens	84-92
26876431-7	2016	For the introduction of aldehyde oxidase (AOX) into clinical practice, the association between AOX activity and AZA dose requirements should be positively confirmed.	Azathioprine	112-115	aldehyde oxidase 1	Homo sapiens	24-40
26876431-7	2016	For the introduction of aldehyde oxidase (AOX) into clinical practice, the association between AOX activity and AZA dose requirements should be positively confirmed.	Azathioprine	112-115	aldehyde oxidase 1	Homo sapiens	95-98
26756170-4	2016	Thiopurine methyltransferase (TPMT) deficiency as a cause of severe myelosuppression upon treatment with azathioprine or mercaptopurine is found as a heterozygous trait in only ~ 10% of patients, and homozygous (deficiency) carriers are even more rare--occurring in fewer than 1 in 300 patients.	Azathioprine	105-117	thiopurine S-methyltransferase	Homo sapiens	0-28
26735160-12	2016	Three patients with the NUDT15 heterozygous variant are currently treated with AZA at a dose of 0.76 mg/kg/day.	Azathioprine	79-82	nudix hydrolase 15	Homo sapiens	24-30
26674571-11	2016	Among patients who had AZA-related myelotoxicity, 11.1% were TPMT compound heterozygous, 44.4% had heterozygous genotype (P&lt;0.01).	Azathioprine	23-26	thiopurine S-methyltransferase	Homo sapiens	61-65
27082580-11	2016	TPMT*3C had a specificity of 100%, but a sensitivity of 8% for predicting leucopenia.A 6-TGN level between 225 and 420 pmol/8 x 10(8) RBC could be a therapeutic window in patients receiving AZA therapy, and it could likely predict leucopenia in the initial 12 weeks of AZA therapy and a reasonable chance of successful clinical response in CD patients.	Azathioprine	190-193	thiopurine S-methyltransferase	Homo sapiens	0-4
27082580-11	2016	TPMT*3C had a specificity of 100%, but a sensitivity of 8% for predicting leucopenia.A 6-TGN level between 225 and 420 pmol/8 x 10(8) RBC could be a therapeutic window in patients receiving AZA therapy, and it could likely predict leucopenia in the initial 12 weeks of AZA therapy and a reasonable chance of successful clinical response in CD patients.	Azathioprine	269-272	thiopurine S-methyltransferase	Homo sapiens	0-4
26674571-0	2016	TPMT and ITPA genetic variants in Lithuanian inflammatory bowel disease patients: Prevalence and azathioprine-related side effects.	Azathioprine	97-109	thiopurine S-methyltransferase	Homo sapiens	0-4
26674571-0	2016	TPMT and ITPA genetic variants in Lithuanian inflammatory bowel disease patients: Prevalence and azathioprine-related side effects.	Azathioprine	97-109	inosine triphosphatase	Homo sapiens	9-13
26674571-2	2016	Genetic polymorphisms in thiopurine methyltransferase (TPMT) and inosine triphosphate pyrophosphatase (ITPA) were linked with toxicity of azathioprine (AZA).	Azathioprine	138-150	thiopurine S-methyltransferase	Homo sapiens	55-59
26674571-2	2016	Genetic polymorphisms in thiopurine methyltransferase (TPMT) and inosine triphosphate pyrophosphatase (ITPA) were linked with toxicity of azathioprine (AZA).	Azathioprine	138-150	inosine triphosphatase	Homo sapiens	65-101
26674571-2	2016	Genetic polymorphisms in thiopurine methyltransferase (TPMT) and inosine triphosphate pyrophosphatase (ITPA) were linked with toxicity of azathioprine (AZA).	Azathioprine	138-150	inosine triphosphatase	Homo sapiens	103-107
26674571-2	2016	Genetic polymorphisms in thiopurine methyltransferase (TPMT) and inosine triphosphate pyrophosphatase (ITPA) were linked with toxicity of azathioprine (AZA).	Azathioprine	152-155	thiopurine S-methyltransferase	Homo sapiens	55-59
26674571-2	2016	Genetic polymorphisms in thiopurine methyltransferase (TPMT) and inosine triphosphate pyrophosphatase (ITPA) were linked with toxicity of azathioprine (AZA).	Azathioprine	152-155	inosine triphosphatase	Homo sapiens	65-101
26959719-4	2016	Finally, a very interesting, and never observed before, palladium-catalyzed syn beta-elimination occurred, leading to the selective nitro group reduction reaction on the syn-alpha-amino ester functionalized aza-Henry adducts and obtaining more stable optically pure trifluoromethyl conjugated imines.	Azathioprine	207-210	synemin	Homo sapiens	76-79
26959719-4	2016	Finally, a very interesting, and never observed before, palladium-catalyzed syn beta-elimination occurred, leading to the selective nitro group reduction reaction on the syn-alpha-amino ester functionalized aza-Henry adducts and obtaining more stable optically pure trifluoromethyl conjugated imines.	Azathioprine	207-210	synemin	Homo sapiens	170-173
26674571-2	2016	Genetic polymorphisms in thiopurine methyltransferase (TPMT) and inosine triphosphate pyrophosphatase (ITPA) were linked with toxicity of azathioprine (AZA).	Azathioprine	152-155	inosine triphosphatase	Homo sapiens	103-107
26674571-14	2016	Polymorphisms in TPMT might be associated with myelotoxicity and leukopenia in AZA treated patients, while ITPA variant alleles appear not to be linked with treatment-related side effects.	Azathioprine	79-82	thiopurine S-methyltransferase	Homo sapiens	17-21
26935390-8	2016	A clear role of GSTM1 in modulating azathioprine cytotoxicity, with a close dependency on superoxide anion production, has been recently demonstrated.	Azathioprine	36-48	glutathione S-transferase mu 1	Homo sapiens	16-21
26864060-11	2016	CARD15 expression significantly decreased in CD patients treated with anti-TNFalpha agents compared to azathioprine or steroid treatment groups.	Azathioprine	103-115	nucleotide binding oligomerization domain containing 2	Homo sapiens	0-6
26935390-9	2016	Interestingly, recent genome-wide association studies have shown that, for both azathioprine in inflammatory bowel disease and mercaptopurine in acute lymphoblastic leukemia, treatment effects on patients" white blood cells are related to variants of a gene, NUDT15, involved in biotransformation of oxidated nucleotides.	Azathioprine	80-92	nudix hydrolase 15	Homo sapiens	259-265
25936353-1	2015	OBJECTIVES: Thiopurine S-methyltransferase (TPMT) is the key enzyme inactivating azathioprine (AZA), an immunosuppressive agent commonly used for treating inflammatory diseases including Behcet"s disease (BD), systemic lupus erythematosus (SLE) and systemic vasculitis.	Azathioprine	81-93	thiopurine S-methyltransferase	Homo sapiens	12-42
27416704-10	2016	Although his PR3-ANCA level was still high after discharge, the administration of azathioprine led to a decrease in the PR-3 ANCA levels.	Azathioprine	82-94	proteinase 3	Homo sapiens	13-16
26633017-0	2015	Association between Thiopurine S-Methyltransferase Polymorphisms and Azathioprine-Induced Adverse Drug Reactions in Patients with Autoimmune Diseases: A Meta-Analysis.	Azathioprine	69-81	thiopurine S-methyltransferase	Homo sapiens	20-50
26633017-2	2015	Thiopurine S-methyltransferase (TPMT) is an important enzyme involved in AZA metabolism.	Azathioprine	73-76	thiopurine S-methyltransferase	Homo sapiens	0-30
26633017-2	2015	Thiopurine S-methyltransferase (TPMT) is an important enzyme involved in AZA metabolism.	Azathioprine	73-76	thiopurine S-methyltransferase	Homo sapiens	32-36
26633017-4	2015	Although several studies have investigated the association between TPMT polymorphisms and AZA-induced ADRs, the results are inconsistent.	Azathioprine	90-93	thiopurine S-methyltransferase	Homo sapiens	67-71
26633017-5	2015	The purpose of this study is to evaluate whether there is an association between TPMT polymorphisms and AZA-induced ADRs using meta-analysis.	Azathioprine	104-107	thiopurine S-methyltransferase	Homo sapiens	81-85
26633017-9	2015	RESULTS: Eleven published studies, with a total of 651 patients with autoimmune diseases, investigated associations between TPMT polymorphisms and AZA-induced ADRs, were included in this meta-analysis.	Azathioprine	147-150	thiopurine S-methyltransferase	Homo sapiens	124-128
26633017-10	2015	Our meta-analysis demonstrated that TPMT polymorphisms were significantly associated with AZA-induced overall ADRs, bone marrow toxicity and gastric intolerance; pooled ORs were 3.12 (1.48-6.56), 3.76 (1.97-7.17) and 6.43 (2.04-20.25), respectively.	Azathioprine	90-93	thiopurine S-methyltransferase	Homo sapiens	36-40
26633017-14	2015	CONCLUSIONS: Our meta-analysis demonstrated an association of TPMT polymorphisms with overall AZA-induced ADRs, bone marrow toxicity and gastric intolerance, but not with hepatotoxicity.	Azathioprine	94-97	thiopurine S-methyltransferase	Homo sapiens	62-66
27548499-8	2016	An additional role for azathioprine in combo therapy with TNF antibodies has been indicated by several trials revealing a substantial benefit on response.	Azathioprine	23-35	tumor necrosis factor	Homo sapiens	58-61
26889216-11	2016	The present meta-analysis, which is based on IgAN patients, suggested that AZA, MMF, LET and CTX are effective in reducing proteinuria levels, with acceptable side effects.	Azathioprine	75-78	IGAN1	Homo sapiens	45-49
26863601-2	2016	Although xanthine dehydrogenase (XDH) is the second major contributor to azathioprine breakdown, polymorphisms in XDH have rarely been studied in IBD patients.	Azathioprine	73-85	xanthine dehydrogenase	Homo sapiens	9-31
26863601-2	2016	Although xanthine dehydrogenase (XDH) is the second major contributor to azathioprine breakdown, polymorphisms in XDH have rarely been studied in IBD patients.	Azathioprine	73-85	xanthine dehydrogenase	Homo sapiens	33-36
26434698-6	2015	KEY FINDINGS: Expression of heparanase, Hsp70 and NF-kappaB and oxidative stress were increased by inflammatory process and differentially modulated by sulphasalazine, prednisolone and azathioprine treatments.	Azathioprine	185-197	heparanase	Rattus norvegicus	28-38
26434698-6	2015	KEY FINDINGS: Expression of heparanase, Hsp70 and NF-kappaB and oxidative stress were increased by inflammatory process and differentially modulated by sulphasalazine, prednisolone and azathioprine treatments.	Azathioprine	185-197	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	40-45
26434698-9	2015	In addition, current drugs used to treat IBD (sulphasalazine, prednisolone and azathioprine) differentially modulate heparanase, NF-kappaB and Hsp70 gene expression, cytokine production and oxidative stress.	Azathioprine	79-91	heparanase	Rattus norvegicus	117-127
26434698-9	2015	In addition, current drugs used to treat IBD (sulphasalazine, prednisolone and azathioprine) differentially modulate heparanase, NF-kappaB and Hsp70 gene expression, cytokine production and oxidative stress.	Azathioprine	79-91	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	143-148
26488447-1	2015	An unprecedented multicomponent organocatalyzed Knoevenagel-aza-Michael-cyclocondensation reaction between Meldrum"s acid, hydroxylamines, and aldehydes afforded a straightforward entry to a large array of racemic and syn-diastereoenriched isoxazolidinones as synthetically useful scaffolds.	Azathioprine	60-63	synemin	Homo sapiens	218-221
25936353-1	2015	OBJECTIVES: Thiopurine S-methyltransferase (TPMT) is the key enzyme inactivating azathioprine (AZA), an immunosuppressive agent commonly used for treating inflammatory diseases including Behcet"s disease (BD), systemic lupus erythematosus (SLE) and systemic vasculitis.	Azathioprine	81-93	thiopurine S-methyltransferase	Homo sapiens	44-48
25936353-1	2015	OBJECTIVES: Thiopurine S-methyltransferase (TPMT) is the key enzyme inactivating azathioprine (AZA), an immunosuppressive agent commonly used for treating inflammatory diseases including Behcet"s disease (BD), systemic lupus erythematosus (SLE) and systemic vasculitis.	Azathioprine	95-98	thiopurine S-methyltransferase	Homo sapiens	12-42
25936353-1	2015	OBJECTIVES: Thiopurine S-methyltransferase (TPMT) is the key enzyme inactivating azathioprine (AZA), an immunosuppressive agent commonly used for treating inflammatory diseases including Behcet"s disease (BD), systemic lupus erythematosus (SLE) and systemic vasculitis.	Azathioprine	95-98	thiopurine S-methyltransferase	Homo sapiens	44-48
25936353-2	2015	Low TPMT levels facilitate occurrence of AZA-related adverse effects.	Azathioprine	41-44	thiopurine S-methyltransferase	Homo sapiens	4-8
25936353-7	2015	Receiver operating characteristic (ROC) analysis was used to determine whether a cut-off TPMT level could be found to predict AZA-related adverse effects.	Azathioprine	126-129	thiopurine S-methyltransferase	Homo sapiens	89-93
25936353-9	2015	TPMT levels in 130 patients receiving AZA were similar to the rest of the group.	Azathioprine	38-41	thiopurine S-methyltransferase	Homo sapiens	0-4
25936353-13	2015	Although low plasma TPMT level is not the only factor determining AZA toxicity, a TPMT cut-off value may help to predict AZA-related adverse effects in BD.	Azathioprine	121-124	thiopurine S-methyltransferase	Homo sapiens	82-86
26491367-4	2015	The results suggest that DNA methylation is not directly involved in the regulation of MT1-MMP in placental tissue; however, remodeling of chromatin by a pharmacologic agent such as AZA potentiates an infection-related increase in MT1-MMP.	Azathioprine	182-185	matrix metallopeptidase 14	Homo sapiens	231-238
26299326-5	2015	Silencing of DNMT1 expression by AZA or RNA interference (RNAi) restored AChE production and inhibition of AChE expression by RNAi protected HCC cells from anticancer drugs-induced apoptosis.	Azathioprine	33-36	DNA methyltransferase 1	Homo sapiens	13-18
26141991-7	2015	SIGNIFICANCE: Mapk1, Mapk3,Mapk6 and Mapk9 gene expressionswere affected by colonic inflammation induced by TNBS in rats and counteracted by sulphasalazine, prednisolone and azathioprine treatments, suggesting that these genes participate in the pharmacological response produced for these drugs.	Azathioprine	174-186	mitogen-activated protein kinase 6	Rattus norvegicus	27-32
26432087-0	2015	The impact of glutathione S-transferase genotype and phenotype on the adverse drug reactions to azathioprine in patients with inflammatory bowel diseases.	Azathioprine	96-108	glutathione S-transferase kappa 1	Homo sapiens	14-39
26432087-3	2015	It has been considered that the polymorphic enzyme thiopurine S-methyltransferase (TPMT) plays an important role in the in vivo process of AZA and the occurrence of its myelotoxicity.	Azathioprine	139-142	thiopurine S-methyltransferase	Homo sapiens	51-81
26432087-3	2015	It has been considered that the polymorphic enzyme thiopurine S-methyltransferase (TPMT) plays an important role in the in vivo process of AZA and the occurrence of its myelotoxicity.	Azathioprine	139-142	thiopurine S-methyltransferase	Homo sapiens	83-87
26432087-4	2015	Glutathione S-transferase (GST) mutation is another pharmacogenetic polymorphism which is probably involved in AZA metabolism and tolerance.	Azathioprine	111-114	glutathione S-transferase kappa 1	Homo sapiens	0-25
26432087-4	2015	Glutathione S-transferase (GST) mutation is another pharmacogenetic polymorphism which is probably involved in AZA metabolism and tolerance.	Azathioprine	111-114	glutathione S-transferase kappa 1	Homo sapiens	27-30
26432087-5	2015	The aim of this study was to investigate the association among GST polymorphism, enzyme activity and AZA-related ADRs in Chinese Han patients with IBD.	Azathioprine	101-104	glutathione S-transferase kappa 1	Homo sapiens	63-66
26432087-8	2015	The patients with higher GST activity constituted a pharmacogenetic high risk group for leucopenia during AZA treatment.	Azathioprine	106-109	glutathione S-transferase kappa 1	Homo sapiens	25-28
26432087-9	2015	GST-P1 Ile105/Ile105 genotype appeared to be a promising marker indicating predisposition to AZA-related ADRs.	Azathioprine	93-96	glutathione S-transferase pi 1	Homo sapiens	0-6
26141991-7	2015	SIGNIFICANCE: Mapk1, Mapk3,Mapk6 and Mapk9 gene expressionswere affected by colonic inflammation induced by TNBS in rats and counteracted by sulphasalazine, prednisolone and azathioprine treatments, suggesting that these genes participate in the pharmacological response produced for these drugs.	Azathioprine	174-186	mitogen activated protein kinase 1	Rattus norvegicus	14-19
26311276-0	2015	TPMT Testing Before Starting Azathioprine or Mercaptopurine: Surely Just Do It?	Azathioprine	29-41	thiopurine S-methyltransferase	Homo sapiens	0-4
26327213-4	2015	Over two years, Aza was administered to mice that were wild type, null or heterozygous for the MMR gene Msh2.	Azathioprine	16-19	mutS homolog 2	Mus musculus	104-108
26327213-7	2015	Msh2(+/-) mice were found more tolerant than Msh2(wt) mice to the cytotoxicity of Aza.	Azathioprine	82-85	mutS homolog 2	Mus musculus	0-4
26327213-7	2015	Msh2(+/-) mice were found more tolerant than Msh2(wt) mice to the cytotoxicity of Aza.	Azathioprine	82-85	mutS homolog 2	Mus musculus	45-49
26327213-8	2015	In Msh2(+/-) mice, Aza induced a high incidence of MSI lymphomas in a dose-dependent manner.	Azathioprine	19-22	mutS homolog 2	Mus musculus	3-7
26327213-9	2015	In Msh2(wt) mice, a substantial lifespan was only observed at the lowest Aza dose.	Azathioprine	73-76	mutS homolog 2	Mus musculus	3-7
26141991-7	2015	SIGNIFICANCE: Mapk1, Mapk3,Mapk6 and Mapk9 gene expressionswere affected by colonic inflammation induced by TNBS in rats and counteracted by sulphasalazine, prednisolone and azathioprine treatments, suggesting that these genes participate in the pharmacological response produced for these drugs.	Azathioprine	174-186	mitogen activated protein kinase 3	Rattus norvegicus	21-26
26141991-7	2015	SIGNIFICANCE: Mapk1, Mapk3,Mapk6 and Mapk9 gene expressionswere affected by colonic inflammation induced by TNBS in rats and counteracted by sulphasalazine, prednisolone and azathioprine treatments, suggesting that these genes participate in the pharmacological response produced for these drugs.	Azathioprine	174-186	mitogen-activated protein kinase 9	Rattus norvegicus	37-42
26101014-7	2015	RESULTS: miR-137 was reactivated by treatment with either AZA and/or TSA in lung cancer cell lines.	Azathioprine	58-61	microRNA 137	Homo sapiens	9-16
26116574-2	2015	Here, we examined the efficacy the DNA methyl transferase (DNMT) inhibitor 5-Aza 2-deoxycytidine (Aza), the histone deacetylase (HDAC) inhibitor Trichostatin A (TSA), as well as the combination therapy of Aza and TSA (Aza+TSA) provides in the protection of ALI.	Azathioprine	77-80	DNA methyltransferase 1	Homo sapiens	35-57
26116574-2	2015	Here, we examined the efficacy the DNA methyl transferase (DNMT) inhibitor 5-Aza 2-deoxycytidine (Aza), the histone deacetylase (HDAC) inhibitor Trichostatin A (TSA), as well as the combination therapy of Aza and TSA (Aza+TSA) provides in the protection of ALI.	Azathioprine	77-80	DNA methyltransferase 1	Homo sapiens	59-63
26116574-2	2015	Here, we examined the efficacy the DNA methyl transferase (DNMT) inhibitor 5-Aza 2-deoxycytidine (Aza), the histone deacetylase (HDAC) inhibitor Trichostatin A (TSA), as well as the combination therapy of Aza and TSA (Aza+TSA) provides in the protection of ALI.	Azathioprine	98-101	DNA methyltransferase 1	Homo sapiens	59-63
26116574-2	2015	Here, we examined the efficacy the DNA methyl transferase (DNMT) inhibitor 5-Aza 2-deoxycytidine (Aza), the histone deacetylase (HDAC) inhibitor Trichostatin A (TSA), as well as the combination therapy of Aza and TSA (Aza+TSA) provides in the protection of ALI.	Azathioprine	98-101	DNA methyltransferase 1	Homo sapiens	59-63
26252649-9	2015	Only AZA+ASA group showed increased anti-inflammatory cytokines (IL-10 and TGF-beta).	Azathioprine	5-8	interleukin 10	Homo sapiens	65-70
26252649-9	2015	Only AZA+ASA group showed increased anti-inflammatory cytokines (IL-10 and TGF-beta).	Azathioprine	5-8	transforming growth factor beta 1	Homo sapiens	75-83
26252649-11	2015	UC groups were compared and women treated with azathioprine showed reduction of total protein, globulin, ESR, and lymphocytes, with increased IL-6, TNF, IL-10, and TGF-beta.	Azathioprine	47-59	interleukin 6	Homo sapiens	142-146
26252649-11	2015	UC groups were compared and women treated with azathioprine showed reduction of total protein, globulin, ESR, and lymphocytes, with increased IL-6, TNF, IL-10, and TGF-beta.	Azathioprine	47-59	tumor necrosis factor	Homo sapiens	148-151
26252649-11	2015	UC groups were compared and women treated with azathioprine showed reduction of total protein, globulin, ESR, and lymphocytes, with increased IL-6, TNF, IL-10, and TGF-beta.	Azathioprine	47-59	interleukin 10	Homo sapiens	153-158
26252649-11	2015	UC groups were compared and women treated with azathioprine showed reduction of total protein, globulin, ESR, and lymphocytes, with increased IL-6, TNF, IL-10, and TGF-beta.	Azathioprine	47-59	transforming growth factor beta 1	Homo sapiens	164-172
25977335-6	2015	The purine analogue azathioprine, well known for its function as an anti-inflammatory compound, was recently shown to function by inhibiting Vav1 signaling in immune cells.	Azathioprine	20-32	vav 1 oncogene	Mus musculus	141-145
26557831-6	2015	In patients with chronic disease activity, treatment with anti-TNF antibodies has a higher level of evidence than azathioprine therapy and should therefore be preferred.	Azathioprine	114-126	tumor necrosis factor	Homo sapiens	63-66
25977335-7	2015	We therefore hypothesized that azathioprine could also inhibit Vav1 in pancreatic tumor cells to reduce its proinvasive functions.	Azathioprine	31-43	vav 1 oncogene	Mus musculus	63-67
25977335-8	2015	Indeed, we have found that treatment of cultured pancreatic tumor cells with azathioprine inhibited Vav1-dependent invasive cell migration and matrix degradation, through inhibition of Rac and Cdc42 signaling.	Azathioprine	77-89	vav 1 oncogene	Mus musculus	100-104
25977335-8	2015	Indeed, we have found that treatment of cultured pancreatic tumor cells with azathioprine inhibited Vav1-dependent invasive cell migration and matrix degradation, through inhibition of Rac and Cdc42 signaling.	Azathioprine	77-89	thymoma viral proto-oncogene 1	Mus musculus	185-188
25977335-8	2015	Indeed, we have found that treatment of cultured pancreatic tumor cells with azathioprine inhibited Vav1-dependent invasive cell migration and matrix degradation, through inhibition of Rac and Cdc42 signaling.	Azathioprine	77-89	cell division cycle 42	Mus musculus	193-198
25977335-11	2015	These inhibitory effects were mediated through Vav1, as Vav1-negative cell lines and tumors were largely resistant to azathioprine treatment.	Azathioprine	118-130	vav 1 oncogene	Mus musculus	47-51
25977335-11	2015	These inhibitory effects were mediated through Vav1, as Vav1-negative cell lines and tumors were largely resistant to azathioprine treatment.	Azathioprine	118-130	vav 1 oncogene	Mus musculus	56-60
25977335-12	2015	These findings demonstrate that azathioprine and related compounds could be potent antimetastatic agents for Vav1-positive pancreatic tumors.	Azathioprine	32-44	vav 1 oncogene	Mus musculus	109-113
26095377-6	2015	Our findings showed that using aza-isosteres of bioactive peptide sequences imbue the residue with imperviousness to proteolysis; underscoring a potential approach for developing a new generation of Smac-derived Aza-peptidomimetics.	Azathioprine	31-34	diablo IAP-binding mitochondrial protein	Homo sapiens	199-203
25999375-10	2015	For all of these reasons, the author believes that CYC/AZA should be reserved for patients with newly diagnosed, MPO-ANCA-positive disease who raise no fertility, compliance or malignancy concerns.	Azathioprine	55-58	myeloperoxidase	Homo sapiens	113-116
26095377-6	2015	Our findings showed that using aza-isosteres of bioactive peptide sequences imbue the residue with imperviousness to proteolysis; underscoring a potential approach for developing a new generation of Smac-derived Aza-peptidomimetics.	Azathioprine	212-215	diablo IAP-binding mitochondrial protein	Homo sapiens	199-203
25638157-9	2015	Mutyh-/- mice survived better than wild-type during a 12-month chronicexposure to Aza/UVA treatments that significantly increased levels of skin DNA 8-oxoG.	Azathioprine	82-85	mutY DNA glycosylase	Mus musculus	0-5
25928802-3	2015	The aim of this study is to explain, from a mechanistic point of view, the clinical evidence showing a significant role of glutathione-S-transferase (GST)-M1 genotype on AZA toxicity in inflammatory bowel disease patients.	Azathioprine	170-173	glutathione S-transferase kappa 1	Homo sapiens	123-148
25928802-3	2015	The aim of this study is to explain, from a mechanistic point of view, the clinical evidence showing a significant role of glutathione-S-transferase (GST)-M1 genotype on AZA toxicity in inflammatory bowel disease patients.	Azathioprine	170-173	glutathione S-transferase kappa 1	Homo sapiens	150-153
25928802-7	2015	In this study, an in vitro model to study thiopurines" metabolism has been set up and helped us to demonstrate, for the first time, a clear role of GST-M1 in modulating AZA cytotoxicity, with a close dependency on superoxide anion production.	Azathioprine	169-172	glutathione S-transferase kappa 1	Homo sapiens	148-151
25928802-8	2015	These results provide the molecular basis to shed light on the clinical evidence suggesting a role of GST-M1 genotype in influencing the toxic effects of AZA treatment.	Azathioprine	154-157	glutathione S-transferase kappa 1	Homo sapiens	102-105
26041941-1	2015	Inexpensive and readily available cinchonidinium acetate is an effective catalyst for the syn-selective aza-Henry reaction of arylnitromethanes and aryl imines.	Azathioprine	104-107	synemin	Homo sapiens	90-93
25804610-5	2015	Pharmacologic Nrf2 activation by topical biweekly applications of small (40 nmol) quantities of the potent bis(cyano enone) inducer TBE-31 has a similar protective effect against solar-simulated UV radiation in animals receiving long-term treatment with the immunosuppressive agent azathioprine.	Azathioprine	282-294	NFE2 like bZIP transcription factor 2	Homo sapiens	14-18
26029356-7	2015	X-ray crystal structures of these molecules bound in the GALC active site reveal which residues participate in stabilizing interactions, show how potency is achieved and illustrate the penalties of aza/iminosugar ring distortion.	Azathioprine	198-201	galactosylceramidase	Homo sapiens	57-61
25638157-10	2015	Two squamous cell skin carcinomas arose in Aza/UVA treated Mutyh-/- mice whereas similarly treated wild-type animals remained tumor-free.	Azathioprine	43-46	mutY DNA glycosylase	Mus musculus	59-64
25789922-0	2015	Concomitant use of azathioprine/6-mercaptopurine decreases the risk of anti-TNF-induced skin lesions.	Azathioprine	19-31	tumor necrosis factor	Homo sapiens	76-79
25874518-0	2015	Azathioprine discontinuation earlier than 6 months in Crohn"s disease patients started on anti-TNF therapy is associated with loss of response and the need for anti-TNF dose escalation.	Azathioprine	0-12	tumor necrosis factor	Homo sapiens	95-98
25874518-0	2015	Azathioprine discontinuation earlier than 6 months in Crohn"s disease patients started on anti-TNF therapy is associated with loss of response and the need for anti-TNF dose escalation.	Azathioprine	0-12	tumor necrosis factor	Homo sapiens	165-168
25874518-8	2015	Factors associated with loss of response and therefore the need for anti-TNF dose escalation were azathioprine discontinuation earlier than 6 months and smoking.	Azathioprine	98-110	tumor necrosis factor	Homo sapiens	73-76
25874518-10	2015	CONCLUSION: Azathioprine discontinuation earlier than 6 months and smoking in CD patients started on anti-TNF therapy is associated with loss of response and the need for anti-TNF dose escalation.	Azathioprine	12-24	tumor necrosis factor	Homo sapiens	106-109
25874518-10	2015	CONCLUSION: Azathioprine discontinuation earlier than 6 months and smoking in CD patients started on anti-TNF therapy is associated with loss of response and the need for anti-TNF dose escalation.	Azathioprine	12-24	tumor necrosis factor	Homo sapiens	176-179
25789922-10	2015	CONCLUSIONS: Concomitant use of AZA/6 MP may decrease the occurrence of adverse skin lesions in patients receiving anti-TNF therapy.	Azathioprine	32-35	tumor necrosis factor	Homo sapiens	120-123
25819542-1	2015	BACKGROUND: Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that catalyses the S-methylation of 6-mercaptopurine and azathioprine.	Azathioprine	129-141	thiopurine S-methyltransferase	Homo sapiens	12-42
25819542-1	2015	BACKGROUND: Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that catalyses the S-methylation of 6-mercaptopurine and azathioprine.	Azathioprine	129-141	thiopurine S-methyltransferase	Homo sapiens	44-48
25599836-2	2015	We describe our efforts to identify analogs of thumb pocket 1 HCV NS5B inhibitor 1 (aza-analog of BI 207524) with improved plasma to liver partitioning and a predicted human half-life consistent with achieving a strong antiviral effect at a reasonable dose in HCV-infected patients.	Azathioprine	84-87	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	66-82
25798450-0	2015	Prednisolone and azathioprine are effective in DPPX antibody-positive autoimmune encephalitis.	Azathioprine	17-29	dipeptidyl peptidase like 6	Homo sapiens	47-51
25756665-4	2015	The aim of this study was to evaluate MSC viability, nuclear morphometry, cell polarity, F-actin and focal adhesion kinase (FAK) distribution, and cell migratory properties in the presence of the immunosuppressive drugs azathioprine (AZA) and dexamethasone (DEX).	Azathioprine	220-232	protein tyrosine kinase 2	Homo sapiens	101-122
25756665-4	2015	The aim of this study was to evaluate MSC viability, nuclear morphometry, cell polarity, F-actin and focal adhesion kinase (FAK) distribution, and cell migratory properties in the presence of the immunosuppressive drugs azathioprine (AZA) and dexamethasone (DEX).	Azathioprine	220-232	protein tyrosine kinase 2	Homo sapiens	124-127
25756665-5	2015	After an initial characterization, MSCs were treated with DEX (10 muM) or AZA (1 muM) for 24 hrs or 7 days.	Azathioprine	74-77	latexin	Homo sapiens	81-84
25636121-10	2015	Elevated CRP at diagnosis was associated with a higher risk of progression to surgery in patients with CD (P &lt; 0.0001) and the need for azathioprine in the overall PIBD cohort (P = 0.002).	Azathioprine	139-151	C-reactive protein	Homo sapiens	9-12
25707965-4	2015	Compared to biologic monotherapy, concomitant use of immunomodulators (methotrexate, azathioprine, and 6-mercaptopurine) often increases the systemic exposure of the anti-TNFalpha agent and decreases the formation of antibodies to the anti-TNFalpha agent, consequently enhancing clinical efficacy.	Azathioprine	85-97	tumor necrosis factor	Homo sapiens	171-179
25707965-4	2015	Compared to biologic monotherapy, concomitant use of immunomodulators (methotrexate, azathioprine, and 6-mercaptopurine) often increases the systemic exposure of the anti-TNFalpha agent and decreases the formation of antibodies to the anti-TNFalpha agent, consequently enhancing clinical efficacy.	Azathioprine	85-97	tumor necrosis factor	Homo sapiens	240-248
25332071-6	2015	After an initial decline, absolute CD5+ B cell numbers progressively increased in patients in the RTX treatment arm, but remained low in CYC/AZA-treated patients.	Azathioprine	141-144	CD5 molecule	Homo sapiens	35-38
25343938-3	2015	RT-PCR showed that a stable higher level expression of DLL4 and Notch1 gene in 5-aza-induced group was observed compared to that in the control group.	Azathioprine	81-84	delta like canonical Notch ligand 4	Homo sapiens	55-59
25496025-3	2015	A [2,3]- or [1,2]-rearrangement occurs to give a 2-allylpyrrolidinyl-2-carbimine intermediate which undergoes Cu(OTf)2 catalyzed aza-Friedel-Crafts cyclization to finish a highly functionalized tricyclic system decorated with a synthetically difficult quaternary carbon center, a sulfonamide group, and an allyl segment.	Azathioprine	129-132	POU class 2 homeobox 2	Homo sapiens	113-118
26788381-3	2015	We report a case of 62-year-old male with long history of CD treated with azathioprine (AZA) and aminosalicylic acid (ASA) who was incidentally diagnosed with HCC, for which left hepatectomy was done.	Azathioprine	74-86	HCC	Homo sapiens	159-162
26788381-3	2015	We report a case of 62-year-old male with long history of CD treated with azathioprine (AZA) and aminosalicylic acid (ASA) who was incidentally diagnosed with HCC, for which left hepatectomy was done.	Azathioprine	88-91	HCC	Homo sapiens	159-162
26788381-6	2015	AZA was reported in all case reports of CD that developed HCC.	Azathioprine	0-3	HCC	Homo sapiens	58-61
25343938-3	2015	RT-PCR showed that a stable higher level expression of DLL4 and Notch1 gene in 5-aza-induced group was observed compared to that in the control group.	Azathioprine	81-84	notch receptor 1	Homo sapiens	64-70
26282728-6	2015	Our findings showed that using aza-isosteres of bioactive peptide sequences imbue the residue with imperviousness to proteolysis; underscoring a potential approach for developing a new generation of Smac-derived Aza-peptidomimetics.	Azathioprine	31-34	diablo IAP-binding mitochondrial protein	Homo sapiens	199-203
26328657-5	2015	After switching from AZ to MMF, her symptoms of NPSLE completely resolved with marked improvement of the IL-6 level in her spinal fluid, suggesting that MMF was effective.	Azathioprine	21-23	interleukin 6	Homo sapiens	105-109
28349793-1	2015	Background Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that catalyses the S-methylation of 6-mercaptopurine and azathioprine.	Azathioprine	128-140	thiopurine S-methyltransferase	Homo sapiens	11-41
28349793-1	2015	Background Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that catalyses the S-methylation of 6-mercaptopurine and azathioprine.	Azathioprine	128-140	thiopurine S-methyltransferase	Homo sapiens	43-47
26282728-6	2015	Our findings showed that using aza-isosteres of bioactive peptide sequences imbue the residue with imperviousness to proteolysis; underscoring a potential approach for developing a new generation of Smac-derived Aza-peptidomimetics.	Azathioprine	212-215	diablo IAP-binding mitochondrial protein	Homo sapiens	199-203
25182201-6	2014	Nonsteroidal anti-inflammatory drugs, corticosteroids and immunosuppressive drugs, such as methotrexate or azathioprine, may be helpful; when patients are unresponsive to the combination of corticosteroids and immunosuppressant agents, the tumor necrosis factor-alpha inhibitor infliximab should be considered.	Azathioprine	107-119	tumor necrosis factor	Homo sapiens	240-267
25383471-0	2014	Unprecedented synthesis of aza-bridged benzodioxepine derivatives through a tandem Rh(II)-catalyzed 1,3-rearrangement/[3+2] cycloaddition of carbonyltriazoles.	Azathioprine	27-30	Rh blood group D antigen	Homo sapiens	83-89
25383471-1	2014	Rh(II)-catalyzed novel tandem intramolecular cycloisomerizations of aldehydes or ketones with 1-sulfonyl 1,2,3-triazoles have been disclosed, providing a facile protocol to access a series of functionalized aza-bridged benzodioxepine heterocycles.	Azathioprine	207-210	Rh blood group D antigen	Homo sapiens	0-6
25105206-9	2014	CONCLUSIONS: TB risk with anti-TNF agents appeared to be increased when these agents were used in combination with methotrexate or azathioprine as compared with monotherapy regimen.	Azathioprine	131-143	tumor necrosis factor	Homo sapiens	31-34
25036765-0	2014	Safe azathioprine treatment in a pediatric ulcerative colitis patient with TPMT*16 by thiopurine metabolite monitoring.	Azathioprine	5-17	thiopurine S-methyltransferase	Homo sapiens	75-79
25549677-8	2014	When using azathioprine (AZA), the percentage of relapse was significantly higher in NMO/NMOSD-CTD patients (50.0%) versus NMO/NMOSD ones (18.5%, P = 0.064); When using cyclophosphamide (CTX), there was no such significant difference.	Azathioprine	11-23	CTD	Homo sapiens	95-98
25549677-8	2014	When using azathioprine (AZA), the percentage of relapse was significantly higher in NMO/NMOSD-CTD patients (50.0%) versus NMO/NMOSD ones (18.5%, P = 0.064); When using cyclophosphamide (CTX), there was no such significant difference.	Azathioprine	25-28	CTD	Homo sapiens	95-98
25549677-11	2014	AZA and CTX may effectively reduce relapses in both NMO/NMOSD and NMO/NMOSD-CTD patients.	Azathioprine	0-3	CTD	Homo sapiens	76-79
25225968-9	2014	The SAR observed for these aza analogues are consistent with those previously observed with various phenyl substituted 3-hydroxypyridin-2(1H)-ones.	Azathioprine	27-30	sarcosine dehydrogenase	Homo sapiens	4-7
24647557-4	2014	RESULTS: This is the largest reported cohort of AQP4-Ab positive patients treated with AZA.	Azathioprine	87-90	aquaporin 4	Homo sapiens	48-52
25543600-7	2014	The relative expression level of RECK protein in 5-aza-dC treated group was significantly higher than that in the control group,the invasion ability of SCC-4 cell was decreased gradually.	Azathioprine	51-54	reversion inducing cysteine rich protein with kazal motifs	Homo sapiens	33-37
24085685-5	2014	RESULTS: Incubation with AZA increased constitutive POMC expression and ACTH secretion by human corticotrope adenomas.	Azathioprine	25-28	proopiomelanocortin	Homo sapiens	52-56
24085685-5	2014	RESULTS: Incubation with AZA increased constitutive POMC expression and ACTH secretion by human corticotrope adenomas.	Azathioprine	25-28	proopiomelanocortin	Homo sapiens	72-76
24085685-8	2014	CONCLUSIONS: The present study shows that AZA increases POMC gene expression and ACTH secretion in human pituitary ACTH-secreting tumors.	Azathioprine	42-45	proopiomelanocortin	Homo sapiens	56-60
24085685-8	2014	CONCLUSIONS: The present study shows that AZA increases POMC gene expression and ACTH secretion in human pituitary ACTH-secreting tumors.	Azathioprine	42-45	proopiomelanocortin	Homo sapiens	81-85
24085685-8	2014	CONCLUSIONS: The present study shows that AZA increases POMC gene expression and ACTH secretion in human pituitary ACTH-secreting tumors.	Azathioprine	42-45	proopiomelanocortin	Homo sapiens	115-119
24085685-9	2014	This can be taken to indicate that mechanisms set into motion by AZA play a role in the regulation of ACTH secretion/POMC expression in tumoral corticotropes and paves the way to further studies in Cushing"s disease.	Azathioprine	65-68	proopiomelanocortin	Homo sapiens	102-106
24085685-9	2014	This can be taken to indicate that mechanisms set into motion by AZA play a role in the regulation of ACTH secretion/POMC expression in tumoral corticotropes and paves the way to further studies in Cushing"s disease.	Azathioprine	65-68	proopiomelanocortin	Homo sapiens	117-121
25543600-7	2014	The relative expression level of RECK protein in 5-aza-dC treated group was significantly higher than that in the control group,the invasion ability of SCC-4 cell was decreased gradually.	Azathioprine	51-54	MAU2 sister chromatid cohesion factor	Homo sapiens	152-157
24878269-0	2014	Novel aza-analogous ergoline derived scaffolds as potent serotonin 5-HT6 and dopamine D2 receptor ligands.	Azathioprine	6-9	dopamine receptor D2	Homo sapiens	77-97
25048487-1	2014	PURPOSE: This study aimed to assess the role of thiopurine S-methyltransferase (TPMT) and 6-thioguanine nucleotide (6-TGN) as predictors of clinical response and side effects to azathioprine (AZA), and estimate the optimal AZA dose in Korean pediatric inflammatory bowel disease (IBD) patients.	Azathioprine	178-190	thiopurine S-methyltransferase	Homo sapiens	48-78
25048487-1	2014	PURPOSE: This study aimed to assess the role of thiopurine S-methyltransferase (TPMT) and 6-thioguanine nucleotide (6-TGN) as predictors of clinical response and side effects to azathioprine (AZA), and estimate the optimal AZA dose in Korean pediatric inflammatory bowel disease (IBD) patients.	Azathioprine	178-190	thiopurine S-methyltransferase	Homo sapiens	80-84
25048487-10	2014	CONCLUSION: TPMT genotype and thiopurine metabolite monitoring could be helpful to examine TPMT genotypes before administering AZA and to measure 6-TGN concentrations during prescribing AZA in IBD patients.	Azathioprine	127-130	thiopurine S-methyltransferase	Homo sapiens	12-16
25048487-10	2014	CONCLUSION: TPMT genotype and thiopurine metabolite monitoring could be helpful to examine TPMT genotypes before administering AZA and to measure 6-TGN concentrations during prescribing AZA in IBD patients.	Azathioprine	186-189	thiopurine S-methyltransferase	Homo sapiens	12-16
24884302-7	2014	When certolizumab pegol, infliximab, or adalimumab were collectively compared with azathioprine, patients initiated on an anti-TNF agent avoided further prescriptions for corticosteroids at a greater rate than patients receiving azathioprine at 12 (43% vs. 27%, respectively; P &lt; 0.0001) and 24 months (33% vs. 23%, respectively; P = 0.028).	Azathioprine	229-241	tumor necrosis factor	Homo sapiens	127-130
24884302-8	2014	Individually, all anti-TNF agents showed higher rates of corticosteroid-sparing compared with azathioprine at 12 (P &lt; 0.0001-0.011), but not 24 months (P = 0.0086-0.24).	Azathioprine	94-106	tumor necrosis factor	Homo sapiens	23-26
25029617-4	2014	Azathioprine and 6-MP have been shown to affect small GTPase Rac1 in T cells and endothelial cells, whereas the effect on macrophages and gut epithelial cells is unknown.	Azathioprine	0-12	Rac family small GTPase 1	Homo sapiens	61-65
24810467-0	2014	Synthesis of beta-C-galactosyl ceramide and its new aza variant via the Horner-Wadsworth-Emmons reaction.	Azathioprine	52-55	colony stimulating factor 2 receptor subunit beta	Homo sapiens	13-19
25268669-7	2014	Finally, in a pilot study of 7 patients with relapsing posterior uveitis refractory to azathioprine and/or cyclosporine, the anti-IL-1beta antibody Gevokizumab was beneficial.	Azathioprine	87-99	interleukin 1 beta	Homo sapiens	130-138
24696000-4	2014	We show that combined Aza/GF incubation can increase expression of miR-218, miR-150, and miR-451.	Azathioprine	22-25	microRNA 150	Homo sapiens	76-83
24696000-4	2014	We show that combined Aza/GF incubation can increase expression of miR-218, miR-150, and miR-451.	Azathioprine	22-25	microRNA 451a	Homo sapiens	89-96
24796767-9	2014	Monotherapy with azathioprine before phenotype change as well as combination therapy with azathioprine/anti-TNFalpha before phenotype change delayed disease progression (B1-B2 or B3) in comparison with patients who did not receive treatment (P&lt;0.001).	Azathioprine	90-102	immunoglobulin kappa variable 7-3 (pseudogene)	Homo sapiens	170-181
24810467-1	2014	A simple strategy for the synthesis of beta-C-galactosyl ceramide and its new aza-variant analogue is described using the Horner-Wadsworth-Emmons reaction as the key step in combining the sugar and aglycone portions.	Azathioprine	78-81	colony stimulating factor 2 receptor subunit beta	Homo sapiens	39-45
24703255-7	2014	Although cyclosporine, azathioprine, and methotrexate increased muscle Daf levels when used alone, upon co-treatment with prednisone only azathioprine maintained myotube Daf levels close to basal.	Azathioprine	23-35	CD55 molecule, decay accelerating factor for complement	Mus musculus	71-74
24703255-7	2014	Although cyclosporine, azathioprine, and methotrexate increased muscle Daf levels when used alone, upon co-treatment with prednisone only azathioprine maintained myotube Daf levels close to basal.	Azathioprine	138-150	CD55 molecule, decay accelerating factor for complement	Mus musculus	170-173
24710034-1	2014	Thiopurine S-methyltransferase (TPMT) is a key enzyme in the methylation of the thiopurine drugs azathioprine and 6-mercaptopurine.	Azathioprine	97-109	thiopurine S-methyltransferase	Homo sapiens	0-30
24710034-1	2014	Thiopurine S-methyltransferase (TPMT) is a key enzyme in the methylation of the thiopurine drugs azathioprine and 6-mercaptopurine.	Azathioprine	97-109	thiopurine S-methyltransferase	Homo sapiens	32-36
24603304-6	2014	To test whether Aza-dC inhibits proliferation of differentiated teratocarcinoma cells, we depleted OCT4 expression in N2102Ep and TERA1 cells treated with Aza-dC.	Azathioprine	155-158	POU class 5 homeobox 1	Homo sapiens	99-103
24762746-2	2014	AZA is catabolized by thiopurine S-methyltransferase (TPMT), which exhibits genetic polymorphisms.	Azathioprine	0-3	thiopurine S-methyltransferase	Homo sapiens	22-52
24762746-2	2014	AZA is catabolized by thiopurine S-methyltransferase (TPMT), which exhibits genetic polymorphisms.	Azathioprine	0-3	thiopurine S-methyltransferase	Homo sapiens	54-58
24707136-4	2014	Indeed, in pediatric patients with IBD, deletion of GST-M1, which determines reduced enzymatic activity, was recently associated with reduced sensitivity to azathioprine and reduced production of azathioprine active metabolites.	Azathioprine	157-169	glutathione S-transferase mu 1	Homo sapiens	52-58
24707136-4	2014	Indeed, in pediatric patients with IBD, deletion of GST-M1, which determines reduced enzymatic activity, was recently associated with reduced sensitivity to azathioprine and reduced production of azathioprine active metabolites.	Azathioprine	196-208	glutathione S-transferase mu 1	Homo sapiens	52-58
24707136-5	2014	In addition to increase the activation of azathioprine to mercaptopurine, GSTs may contribute to azathioprine effects even by modulating GSH consumption, oxidative stress and apoptosis.	Azathioprine	97-109	glutathione S-transferase kappa 1	Homo sapiens	74-78
24707136-6	2014	Therefore, genetic polymorphisms in genes for GSTs may be useful to predict response to azathioprine even if more in vitro and clinical validation studies are needed.	Azathioprine	88-100	glutathione S-transferase kappa 1	Homo sapiens	46-50
23962279-3	2014	The thiopurine drugs azathioprine, mercaptopurine and thioguanine are substrates for TPMT; these drugs exhibit well documented myelosuppressive effects on haematopoietic cells and have a track record of idiosyncratic drug reactions.	Azathioprine	21-33	thiopurine S-methyltransferase	Homo sapiens	85-89
24074969-3	2014	Immunosuppressive drugs such as azathioprine, cyclophosphamide and tumor necrosis factor blockers (anti-TNFalpha) are commonly used as second-line therapy with varying degrees of success.	Azathioprine	32-44	tumor necrosis factor	Homo sapiens	104-112
24322830-0	2014	Association of thiopurine methyltransferase status with azathioprine side effects in Chinese patients with systemic lupus erythematosus.	Azathioprine	56-68	thiopurine S-methyltransferase	Homo sapiens	15-43
24322830-2	2014	Thiopurine methyltransferase (TPMT) is the rate-limiting enzyme in the steps of AZA metabolization.	Azathioprine	80-83	thiopurine S-methyltransferase	Homo sapiens	0-28
24322830-2	2014	Thiopurine methyltransferase (TPMT) is the rate-limiting enzyme in the steps of AZA metabolization.	Azathioprine	80-83	thiopurine S-methyltransferase	Homo sapiens	30-34
24322830-16	2014	AZA-induced leukopenia and alopecia were partly correlated to TPMT*3C heterozygotes and low TPMT activity.	Azathioprine	0-3	thiopurine S-methyltransferase	Homo sapiens	62-66
24322830-16	2014	AZA-induced leukopenia and alopecia were partly correlated to TPMT*3C heterozygotes and low TPMT activity.	Azathioprine	0-3	thiopurine S-methyltransferase	Homo sapiens	92-96
24918007-8	2014	TT carriers of ABCB1 C3435T SNP had a higher chance of responding to azathioprine (OR 2.38, p = 0.01), while carriers of ABCB1 G2677T/A SNP, as well as responding better to azathioprine (OR 1.89, p = 0.07), had a lower chance of responding to biologicals (OR 0.31, p = 0.07), which became significant after adjusting for gender (OR 0.75, p = 0.005).	Azathioprine	69-81	ATP binding cassette subfamily B member 1	Homo sapiens	15-20
24498324-10	2014	Upon AZA-mediated DNA demethylation of human AML blasts, CTCF and SMARCA5 are recruited to the -14.4 Enhancer of SPI1 gene and block its expression.	Azathioprine	5-8	CCCTC-binding factor	Homo sapiens	57-61
24498324-10	2014	Upon AZA-mediated DNA demethylation of human AML blasts, CTCF and SMARCA5 are recruited to the -14.4 Enhancer of SPI1 gene and block its expression.	Azathioprine	5-8	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 5	Homo sapiens	66-73
24498324-10	2014	Upon AZA-mediated DNA demethylation of human AML blasts, CTCF and SMARCA5 are recruited to the -14.4 Enhancer of SPI1 gene and block its expression.	Azathioprine	5-8	Spi-1 proto-oncogene	Homo sapiens	113-117
23978487-7	2014	RESULTS: Through November 2012, 35 customized pharmacogenetic rules have been implemented, including rules for TPMT with azathioprine, thioguanine, and mercaptopurine, and for CYP2D6 with codeine, tramadol, amitriptyline, fluoxetine, and paroxetine.	Azathioprine	121-133	thiopurine S-methyltransferase	Homo sapiens	111-115
24918007-8	2014	TT carriers of ABCB1 C3435T SNP had a higher chance of responding to azathioprine (OR 2.38, p = 0.01), while carriers of ABCB1 G2677T/A SNP, as well as responding better to azathioprine (OR 1.89, p = 0.07), had a lower chance of responding to biologicals (OR 0.31, p = 0.07), which became significant after adjusting for gender (OR 0.75, p = 0.005).	Azathioprine	173-185	ATP binding cassette subfamily B member 1	Homo sapiens	15-20
24974183-3	2014	Among five genotypes of GST A2-2, the variant A2*E has threefold-fourfold higher catalytic efficiency with azathioprine, suggesting that the expression of A2*E could boost 6-mercaptopurine release and adverse side effects in treated patients.	Azathioprine	107-119	glutathione S-transferase alpha 2	Homo sapiens	24-32
24184165-7	2014	After AZA administration, the plasma levels of alanine aminotransferase and aspartate aminotransferase were increased, and liver damage was confirmed through a histological evaluation.	Azathioprine	6-9	glutamic--pyruvic transaminase	Homo sapiens	47-71
23888958-4	2014	AZA demethylated promoters of genes related to ionizing radiation response, such as p16 and hMLH1.	Azathioprine	0-3	cyclin dependent kinase inhibitor 2A	Homo sapiens	84-87
23888958-4	2014	AZA demethylated promoters of genes related to ionizing radiation response, such as p16 and hMLH1.	Azathioprine	0-3	mutL homolog 1	Homo sapiens	92-97
23974954-10	2014	CONCLUSIONS: Half the patients under azathioprine and/or infliximab in clinical remission have endoscopic and/or CRP evidence of residual active CD, whereas other patients with endoscopic and CRP normalisation have persistent clinical symptoms.	Azathioprine	37-49	C-reactive protein	Homo sapiens	113-116
24826966-8	2014	In the third part, in vitro effects of drugs containing azathioprine, methylprednisolone and colchicine that have already been used for the treatment of Behcet"s disease were tested on the PON enzymes of the patients with Behcet"s disease and control group.	Azathioprine	56-68	paraoxonase 1	Homo sapiens	189-192
25531359-5	2014	Long-term follow up of patients in a single centre reported responders to azathioprine having a reduced risk of perianal surgery (OR = 0.36; 95% CI: 0.27-0.46), but complex perianal fistulising Crohn"s disease generally requires combination therapy with anti-TNF and azathioprine.	Azathioprine	74-86	tumor necrosis factor	Homo sapiens	259-262
24826966-0	2014	Purification of paraoxonase enzyme from the sera of patients with Behcet"s disease and analyzing the effects of the drugs containing imuran (azathioprine), prednisolone (methylprednisolone) and colchium (colchicine).	Azathioprine	133-139	paraoxonase 1	Homo sapiens	16-27
24826966-0	2014	Purification of paraoxonase enzyme from the sera of patients with Behcet"s disease and analyzing the effects of the drugs containing imuran (azathioprine), prednisolone (methylprednisolone) and colchium (colchicine).	Azathioprine	141-153	paraoxonase 1	Homo sapiens	16-27
24168842-10	2014	Carriers of the mutant allele for IL23R SNPs had a significantly higher probability of developing EIMs (P&lt;0.05), a higher probability of being refractory to 5-ASA (P&lt;0.03), but a higher likelihood of responding to AZT (P=0.05).	Azathioprine	220-223	interleukin 23 receptor	Homo sapiens	34-39
23974954-10	2014	CONCLUSIONS: Half the patients under azathioprine and/or infliximab in clinical remission have endoscopic and/or CRP evidence of residual active CD, whereas other patients with endoscopic and CRP normalisation have persistent clinical symptoms.	Azathioprine	37-49	C-reactive protein	Homo sapiens	192-195
23787247-0	2014	Deletion of glutathione-s-transferase m1 reduces azathioprine metabolite concentrations in young patients with inflammatory bowel disease.	Azathioprine	49-61	glutathione S-transferase mu 2	Homo sapiens	12-40
23996738-1	2014	BACKGROUND: Thiopurine methyltransferase (TPMT) enzyme plays a key role in the metabolism of azathioprine/6-mercaptopurine (6-MP).	Azathioprine	93-105	thiopurine S-methyltransferase	Homo sapiens	12-40
23996738-1	2014	BACKGROUND: Thiopurine methyltransferase (TPMT) enzyme plays a key role in the metabolism of azathioprine/6-mercaptopurine (6-MP).	Azathioprine	93-105	thiopurine S-methyltransferase	Homo sapiens	42-46
23996738-4	2014	AIMS: The aim of this research is to study the prevalence of TPMT mutation in Indian patients requiring immunomodulator therapy and its relation to the development of neutropenia on azathioprine therapy.	Azathioprine	182-194	thiopurine S-methyltransferase	Homo sapiens	61-65
23787247-9	2014	CONCLUSIONS: This study describes the effect of candidate genetic polymorphisms in TPMT, ITPA, and GST-M1 on azathioprine pharmacokinetics in IBD patients, showing, for the first time, relevant effects of GST-M1 genotype on azathioprine metabolites concentration.	Azathioprine	109-121	thiopurine S-methyltransferase	Homo sapiens	83-87
23787247-9	2014	CONCLUSIONS: This study describes the effect of candidate genetic polymorphisms in TPMT, ITPA, and GST-M1 on azathioprine pharmacokinetics in IBD patients, showing, for the first time, relevant effects of GST-M1 genotype on azathioprine metabolites concentration.	Azathioprine	109-121	inosine triphosphatase	Homo sapiens	89-93
24438714-0	2014	The cost-effectiveness of a pharmacogenetic test: a trial-based evaluation of TPMT genotyping for azathioprine.	Azathioprine	98-110	thiopurine S-methyltransferase	Homo sapiens	78-82
23216663-9	2014	Patients with SCC had a higher cumulative dose of azathioprine (&gt;= 500 g: OR 30.0 [95% CI 2.6-345.1]) and longer treatment duration (&gt;= 11 years: OR 13.5 [95% CI 1.3-143.6]).	Azathioprine	50-62	serpin family B member 3	Homo sapiens	14-17
23216663-11	2014	CONCLUSIONS: In this cohort of patients with AIRD treated with azathioprine for at least 1 year, the risk of SCC was increased, as compared with the general population.	Azathioprine	63-75	serpin family B member 3	Homo sapiens	109-112
24174222-3	2014	In the present study, luciferase reporter assay results indicated that the sequences -485 - +73 and -486 - -530 of the S100A4 promoter may harbor the positive and negative cis-acting elements, respectively; and moreover, the luciferase activity promoted by the sequence -485 - +73 increased and the S100A4 gene was significantly upregulated in 5-Aza-induced HEp2 cells.	Azathioprine	346-349	S100 calcium binding protein A4	Homo sapiens	119-125
24438714-1	2014	BACKGROUND: Thiopurine-methyl transferase (TPMT) testing prior to the prescription of azathioprine in autoimmune diseases is one of the few examples of a pharmacogenetic test that has made the transition from research into clinical practice.	Azathioprine	86-98	thiopurine S-methyltransferase	Homo sapiens	12-41
24438714-1	2014	BACKGROUND: Thiopurine-methyl transferase (TPMT) testing prior to the prescription of azathioprine in autoimmune diseases is one of the few examples of a pharmacogenetic test that has made the transition from research into clinical practice.	Azathioprine	86-98	thiopurine S-methyltransferase	Homo sapiens	43-47
24438714-2	2014	TPMT testing could lead to improved prescribing of azathioprine resulting in a reduction in adverse drug reactions as well as an improvement in effectiveness.	Azathioprine	51-63	thiopurine S-methyltransferase	Homo sapiens	0-4
24438714-4	2014	OBJECTIVE: This study aimed to evaluate the cost-effectiveness of a TPMT genotyping test to inform azathioprine prescribing in autoimmune diseases.	Azathioprine	99-111	thiopurine S-methyltransferase	Homo sapiens	68-72
24438714-6	2014	METHODS: A prospective economic evaluation was conducted alongside the TARGET (TPMT: Azathioprine Response to Genotype and Enzyme Testing) study, a pragmatic controlled trial that randomized (1:1) patients to undergo TPMT genotyping before azathioprine (n = 167) or current practice (n = 166).	Azathioprine	85-97	thiopurine S-methyltransferase	Homo sapiens	79-83
24379584-10	2013	Consistent with this observation, mesalazine and azathioprine induced, in primary fibroblasts, IL10RB and TNFRII over-expression and TNFRI and TNFalpha under-expression.	Azathioprine	49-61	interleukin 10 receptor subunit beta	Homo sapiens	95-101
24379584-10	2013	Consistent with this observation, mesalazine and azathioprine induced, in primary fibroblasts, IL10RB and TNFRII over-expression and TNFRI and TNFalpha under-expression.	Azathioprine	49-61	TNF receptor superfamily member 1B	Homo sapiens	106-112
24379584-10	2013	Consistent with this observation, mesalazine and azathioprine induced, in primary fibroblasts, IL10RB and TNFRII over-expression and TNFRI and TNFalpha under-expression.	Azathioprine	49-61	TNF receptor superfamily member 1A	Homo sapiens	106-111
24379584-10	2013	Consistent with this observation, mesalazine and azathioprine induced, in primary fibroblasts, IL10RB and TNFRII over-expression and TNFRI and TNFalpha under-expression.	Azathioprine	49-61	tumor necrosis factor	Homo sapiens	143-151
24121523-0	2013	TPMT genetic variants are associated with increased rejection with azathioprine use in heart transplantation.	Azathioprine	67-79	thiopurine S-methyltransferase	Homo sapiens	0-4
24029750-2	2013	We report a case of a 53-year-old female with a normal thiopurine S-methyltransferase (TPMT) level who developed aplastic anemia within 4 weeks of azathioprine initiation, resulting in death.	Azathioprine	147-159	thiopurine S-methyltransferase	Homo sapiens	55-85
24029750-2	2013	We report a case of a 53-year-old female with a normal thiopurine S-methyltransferase (TPMT) level who developed aplastic anemia within 4 weeks of azathioprine initiation, resulting in death.	Azathioprine	147-159	thiopurine S-methyltransferase	Homo sapiens	87-91
24121523-2	2013	Consensus guidelines recommend that patients with thiopurine S-methyltransferase (TPMT) genetic variants be started on lower AZA dose because of higher active metabolite levels and risk of adverse events.	Azathioprine	125-128	thiopurine S-methyltransferase	Homo sapiens	50-80
24121523-2	2013	Consensus guidelines recommend that patients with thiopurine S-methyltransferase (TPMT) genetic variants be started on lower AZA dose because of higher active metabolite levels and risk of adverse events.	Azathioprine	125-128	thiopurine S-methyltransferase	Homo sapiens	82-86
24121523-3	2013	However, in-vitro lymphocyte proliferation assays performed in participants with inactive TPMT alleles have suggested that AZA use may result in decreased immunosuppressant efficacy as compared with wild-type (WT) individuals.	Azathioprine	123-126	thiopurine S-methyltransferase	Homo sapiens	90-94
24121523-4	2013	The objective of this study was therefore to determine the effect of TPMT genetic variation on AZA efficacy or prevention of rejection in HTX recipients treated with AZA.	Azathioprine	95-98	thiopurine S-methyltransferase	Homo sapiens	69-73
24121523-4	2013	The objective of this study was therefore to determine the effect of TPMT genetic variation on AZA efficacy or prevention of rejection in HTX recipients treated with AZA.	Azathioprine	166-169	thiopurine S-methyltransferase	Homo sapiens	69-73
24121523-12	2013	CONCLUSION: HTX recipients with TPMT genetic variant alleles who are treated with AZA develop acute rejection earlier, more frequently, and of greater severity.	Azathioprine	82-85	thiopurine S-methyltransferase	Homo sapiens	32-36
23871720-9	2013	CONCLUSIONS: These results show that cathelicidin and KLK5 decrease in association with AZA exposure.	Azathioprine	88-91	kallikrein related peptidase 5	Homo sapiens	54-58
24113235-1	2013	Thiopurine efficacy is partly reflected by the genetic polymorphism of the thiopurine methyltransferase (TPMT) enzyme, which is responsible for variation in the metabolism, toxicity and therapeutic efficacy of the thiopurines azathioprine (AZA), 6-mercaptopurine (6-MP) and 6-thioguanine (6-TG).	Azathioprine	226-238	thiopurine S-methyltransferase	Homo sapiens	75-103
24113235-1	2013	Thiopurine efficacy is partly reflected by the genetic polymorphism of the thiopurine methyltransferase (TPMT) enzyme, which is responsible for variation in the metabolism, toxicity and therapeutic efficacy of the thiopurines azathioprine (AZA), 6-mercaptopurine (6-MP) and 6-thioguanine (6-TG).	Azathioprine	226-238	thiopurine S-methyltransferase	Homo sapiens	105-109
24113235-1	2013	Thiopurine efficacy is partly reflected by the genetic polymorphism of the thiopurine methyltransferase (TPMT) enzyme, which is responsible for variation in the metabolism, toxicity and therapeutic efficacy of the thiopurines azathioprine (AZA), 6-mercaptopurine (6-MP) and 6-thioguanine (6-TG).	Azathioprine	240-243	thiopurine S-methyltransferase	Homo sapiens	75-103
24113235-1	2013	Thiopurine efficacy is partly reflected by the genetic polymorphism of the thiopurine methyltransferase (TPMT) enzyme, which is responsible for variation in the metabolism, toxicity and therapeutic efficacy of the thiopurines azathioprine (AZA), 6-mercaptopurine (6-MP) and 6-thioguanine (6-TG).	Azathioprine	240-243	thiopurine S-methyltransferase	Homo sapiens	105-109
23958494-0	2013	Azathioprine desensitizes liver cancer cells to insulin-like growth factor 1 and causes apoptosis when it is combined with bafilomycin A1.	Azathioprine	0-12	insulin like growth factor 1	Homo sapiens	48-76
23958494-2	2013	In this paper we show that azathioprine (AZA) is capable of inhibiting IGF1-mediated signaling cascade in HepG2 cells.	Azathioprine	27-39	insulin like growth factor 1	Homo sapiens	71-75
23958494-2	2013	In this paper we show that azathioprine (AZA) is capable of inhibiting IGF1-mediated signaling cascade in HepG2 cells.	Azathioprine	41-44	insulin like growth factor 1	Homo sapiens	71-75
23958494-3	2013	The efficiency of AZA on inhibition of proliferation differs in the evaluated cell lines as follows: HepG2 (an experimental model of hepatoblastoma)&gt;Hep3B (derived from a hepatocellular carcinoma)&gt;HuH6 (derived from a hepatoblastoma)&gt;&gt;HuH7 (derived from a hepatocellular carcinoma)=Chang Liver cells (a non-malignant cellular model).	Azathioprine	18-21	MIR7-3 host gene	Homo sapiens	247-251
23958494-4	2013	The effect of AZA in HepG2 cells has been proven to derive from activation of Ras/ERK/TSC2, leading to activation of mTOR/p70S6K in a sustained manner.	Azathioprine	14-17	mitogen-activated protein kinase 1	Homo sapiens	82-85
23958494-4	2013	The effect of AZA in HepG2 cells has been proven to derive from activation of Ras/ERK/TSC2, leading to activation of mTOR/p70S6K in a sustained manner.	Azathioprine	14-17	TSC complex subunit 2	Homo sapiens	86-90
23958494-4	2013	The effect of AZA in HepG2 cells has been proven to derive from activation of Ras/ERK/TSC2, leading to activation of mTOR/p70S6K in a sustained manner.	Azathioprine	14-17	ribosomal protein S6 kinase B1	Homo sapiens	122-128
23958494-6	2013	As a consequence, proliferation induced by IGF-1 is inhibited by AZA and autophagy increases leading to senescence of HepG2 cells.	Azathioprine	65-68	insulin like growth factor 1	Homo sapiens	43-48
23958494-8	2013	However, when simultaneous to AZA treatment the autophagy was inhibited by bafilomycin A1 and the degradation of regulatory proteins of cell cycle (e.g. Rb, E2F, and cyclin D1) provoked apoptosis.	Azathioprine	30-33	cyclin D1	Homo sapiens	166-175
23958494-9	2013	In conclusion, AZA induces resistance in hepatoblastoma cells to IGF-1, which leads to autophagy activation, and causes apoptosis when it is combined with bafilomycin A1.	Azathioprine	15-18	insulin like growth factor 1	Homo sapiens	65-70
23958494-10	2013	We are presenting here a novel mechanism of action of azathioprine, which could be useful in treatment of IGF-1 dependent tumors, especially in its combination with other drugs.	Azathioprine	54-66	insulin like growth factor 1	Homo sapiens	106-111
23845595-1	2013	This study was undertaken to examine the effect on the rat embryonic heart of two experimental drugs (AZA and AZB) which are known to block the sodium channel Nav1.5, the hERG potassium channel and the l-type calcium channel.	Azathioprine	102-105	sodium voltage-gated channel alpha subunit 5	Rattus norvegicus	159-165
24014462-5	2013	In addition, we demonstrate that a C-3 reverse prenylated indole can undergo a nonenzymatic aza-Cope rearrangement at 37  C to give an N-1 normal prenylated product.	Azathioprine	92-95	complement C3	Homo sapiens	35-38
23950142-0	2013	Immunosuppressive drug azathioprine reduces aneurysm progression through inhibition of Rac1 and c-Jun-terminal-N-kinase in endothelial cells.	Azathioprine	23-35	Rac family small GTPase 1	Mus musculus	87-91
23950142-0	2013	Immunosuppressive drug azathioprine reduces aneurysm progression through inhibition of Rac1 and c-Jun-terminal-N-kinase in endothelial cells.	Azathioprine	23-35	jun proto-oncogene	Mus musculus	96-101
23950142-9	2013	In line with the in vitro observations, Aza-treated mice showed less c-Jun-terminal-N-kinase activation in ECs and reduced leukocyte influx in the aortic wall.	Azathioprine	40-43	jun proto-oncogene	Mus musculus	69-74
23950142-10	2013	CONCLUSIONS: The immunosuppressive drug Aza has an anti-inflammatory effect and in ECs inhibits Rac1 and c-Jun-terminal-N-kinase activation, which may explain the protective effect of Aza in aneurysm development and, most importantly for clinical implications, aneurysm severity.	Azathioprine	40-43	Rac family small GTPase 1	Mus musculus	96-100
23950142-10	2013	CONCLUSIONS: The immunosuppressive drug Aza has an anti-inflammatory effect and in ECs inhibits Rac1 and c-Jun-terminal-N-kinase activation, which may explain the protective effect of Aza in aneurysm development and, most importantly for clinical implications, aneurysm severity.	Azathioprine	40-43	jun proto-oncogene	Mus musculus	105-110
23950142-10	2013	CONCLUSIONS: The immunosuppressive drug Aza has an anti-inflammatory effect and in ECs inhibits Rac1 and c-Jun-terminal-N-kinase activation, which may explain the protective effect of Aza in aneurysm development and, most importantly for clinical implications, aneurysm severity.	Azathioprine	184-187	Rac family small GTPase 1	Mus musculus	96-100
23950142-10	2013	CONCLUSIONS: The immunosuppressive drug Aza has an anti-inflammatory effect and in ECs inhibits Rac1 and c-Jun-terminal-N-kinase activation, which may explain the protective effect of Aza in aneurysm development and, most importantly for clinical implications, aneurysm severity.	Azathioprine	184-187	jun proto-oncogene	Mus musculus	105-110
24162015-7	2013	In concert with these events, AZA up-regulates PD-L1 transcripts and protein, a key ligand-mediator of immune tolerance.	Azathioprine	30-33	CD274 molecule	Homo sapiens	47-52
24162015-8	2013	Analysis of TCGA samples demonstrates that a significant proportion of primary NSCLC have low expression of AZA-induced immune genes, including PD-L1.	Azathioprine	108-111	CD274 molecule	Homo sapiens	144-149
24142665-0	2013	Successful azathioprine treatment with metabolite monitoring in a pediatric inflammatory bowel disease patient homozygous for TPMT*3C.	Azathioprine	11-23	thiopurine S-methyltransferase	Homo sapiens	126-130
24142665-10	2013	To our knowledge, this is the first case of a patient homozygous for TPMT*3C successfully treated with azathioprine in Korea.	Azathioprine	103-115	thiopurine S-methyltransferase	Homo sapiens	69-73
23770441-5	2013	Additionally, certain variations in the human ITPA gene have been linked to adverse reactions to the immunosuppressive prodrugs azathioprine and 6-mercaptopurine and protection against ribavirin-induced hemolytic anemia.	Azathioprine	128-140	inosine triphosphatase	Homo sapiens	46-50
23706268-3	2013	Inhibition of the enzymatic activity by application of specific chemical CA9 inhibitor sulphonamides (CAI) like Acetazolamide (Aza.	Azathioprine	127-130	carbonic anhydrase 9	Homo sapiens	73-76
23770457-1	2013	Up to 1/5 of patients with wildtype thiopurine-S-methyltransferase (TPMT) activity prescribed azathioprine (AZA) or mercaptopurine (MP) demonstrate a skewed drug metabolism in which MP is preferentially methylated to yield methylmercaptopurine (MeMP).	Azathioprine	94-106	thiopurine S-methyltransferase	Homo sapiens	36-66
23770457-1	2013	Up to 1/5 of patients with wildtype thiopurine-S-methyltransferase (TPMT) activity prescribed azathioprine (AZA) or mercaptopurine (MP) demonstrate a skewed drug metabolism in which MP is preferentially methylated to yield methylmercaptopurine (MeMP).	Azathioprine	94-106	thiopurine S-methyltransferase	Homo sapiens	68-72
23770457-1	2013	Up to 1/5 of patients with wildtype thiopurine-S-methyltransferase (TPMT) activity prescribed azathioprine (AZA) or mercaptopurine (MP) demonstrate a skewed drug metabolism in which MP is preferentially methylated to yield methylmercaptopurine (MeMP).	Azathioprine	94-106	azurocidin 1	Homo sapiens	132-134
23770457-1	2013	Up to 1/5 of patients with wildtype thiopurine-S-methyltransferase (TPMT) activity prescribed azathioprine (AZA) or mercaptopurine (MP) demonstrate a skewed drug metabolism in which MP is preferentially methylated to yield methylmercaptopurine (MeMP).	Azathioprine	94-106	azurocidin 1	Homo sapiens	182-184
23770457-1	2013	Up to 1/5 of patients with wildtype thiopurine-S-methyltransferase (TPMT) activity prescribed azathioprine (AZA) or mercaptopurine (MP) demonstrate a skewed drug metabolism in which MP is preferentially methylated to yield methylmercaptopurine (MeMP).	Azathioprine	108-111	thiopurine S-methyltransferase	Homo sapiens	36-66
23770457-1	2013	Up to 1/5 of patients with wildtype thiopurine-S-methyltransferase (TPMT) activity prescribed azathioprine (AZA) or mercaptopurine (MP) demonstrate a skewed drug metabolism in which MP is preferentially methylated to yield methylmercaptopurine (MeMP).	Azathioprine	108-111	thiopurine S-methyltransferase	Homo sapiens	68-72
23770457-1	2013	Up to 1/5 of patients with wildtype thiopurine-S-methyltransferase (TPMT) activity prescribed azathioprine (AZA) or mercaptopurine (MP) demonstrate a skewed drug metabolism in which MP is preferentially methylated to yield methylmercaptopurine (MeMP).	Azathioprine	108-111	azurocidin 1	Homo sapiens	182-184
23706268-18	2013	Aza., SU.D2, Chetomin or CA9-siRNA possesses functional CA9 inhibitory characteristics when applied against human cancers with hypoxic regions like GBM.	Azathioprine	0-4	carbonic anhydrase 9	Homo sapiens	56-59
22840925-0	2013	"In vitro" azathioprine-induced changes in peripheral T cell apoptosis and IFN-gamma production associate with drug response in patients with Crohn"s Disease.	Azathioprine	11-23	interferon gamma	Homo sapiens	75-84
23845145-4	2013	METHODS: A retrospective cohort of 176 Crohn"s Disease (CD) patients treated with thiopurines (131 with 6MP and 45 with azathioprine) was genotyped for common polymorphisms in GSTM1, GSTT1 and TPMT.	Azathioprine	120-132	glutathione S-transferase mu 1	Homo sapiens	176-181
23649517-7	2013	The compounds showed strong inhibitory activity against hCA I, being more effective as compared to the clinically used AZA (KI: 36.2 mM), but rather less activity against hCA II.	Azathioprine	119-122	carbonic anhydrase 1	Homo sapiens	56-61
23461975-8	2013	Additional studies showed that silibinin alone as well as in combination with TSA or Aza downmodulate the expression of Zeb1, which is a major transcriptional repressor of E-cadherin.	Azathioprine	85-88	zinc finger E-box binding homeobox 1	Homo sapiens	120-124
23461975-8	2013	Additional studies showed that silibinin alone as well as in combination with TSA or Aza downmodulate the expression of Zeb1, which is a major transcriptional repressor of E-cadherin.	Azathioprine	85-88	cadherin 1	Homo sapiens	172-182
22626508-7	2013	RESULTS: The incremental cost-effectiveness ratio (ICER) of combination therapy with IFX plus AZA is 24,917 GBP/QALY when compared with IFX monotherapy.	Azathioprine	94-97	hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit alpha	Homo sapiens	108-111
23534991-0	2013	Lipase-catalyzed aza-Michael reaction on acrylate derivatives.	Azathioprine	17-20	DUF4389 domain-containing protein	Pseudomonas stutzeri	0-6
23534991-1	2013	A methodology has been developed for an efficient and selective lipase-catalyzed aza-Michael reaction of various amines (primary and secondary) with a series of acrylates and alkylacrylates.	Azathioprine	81-84	DUF4389 domain-containing protein	Pseudomonas stutzeri	64-70
23534991-2	2013	Reaction parameters were tuned, and under the optimal conditions it was found that Pseudomonas stutzeri lipase and Chromobacterium viscosum lipase showed the highest selectivity for the aza-Michael addition to substituted alkyl acrylates.	Azathioprine	186-189	DUF4389 domain-containing protein	Pseudomonas stutzeri	104-110
23534991-2	2013	Reaction parameters were tuned, and under the optimal conditions it was found that Pseudomonas stutzeri lipase and Chromobacterium viscosum lipase showed the highest selectivity for the aza-Michael addition to substituted alkyl acrylates.	Azathioprine	186-189	DUF4389 domain-containing protein	Pseudomonas stutzeri	140-146
23633304-19	2013	Sixty-four per cent (47/163) of azathioprine patients were able to reduce their prednisone dose to &lt; 10 mg/day compared to 46% (32/70) of placebo patients (RR 1.34, 95% CI 1.02 to 1.77).	Azathioprine	32-44	ribonucleotide reductase catalytic subunit M1	Homo sapiens	159-163
23633304-23	2013	Serious adverse events were reported in 14% of patients receiving azathioprine compared to 4% of placebo patients (2 studies, 216 patients; RR 2.57, 95% CI 0.92 to 7.13).	Azathioprine	66-78	ribonucleotide reductase regulatory subunit M2	Homo sapiens	140-144
23407052-2	2013	TPMT metabolizes the thiopurines 6-mercaptopurine, 6-thioguanine, and azathioprine, drugs that are widely used for treatment of acute leukemias, inflammatory bowel diseases, and other disorders of immune regulation.	Azathioprine	70-82	thiopurine S-methyltransferase	Homo sapiens	0-4
22626508-9	2013	Assuming that policy makers are willing to pay 30,000 GBP/QALY, the probability that combination therapy with IFX plus AZA is cost-effective is 0.750.	Azathioprine	119-122	hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit alpha	Homo sapiens	54-57
23223314-1	2013	BACKGROUND: Conversion to sirolimus from calcineurin inhibitor- (CNI), azathioprine- (AZA) and mycophenolate-based regimens reduces the risk of development of squamous cell carcinoma of the skin (SCC) in kidney transplant recipients (KTRs).	Azathioprine	71-83	serpin family B member 3	Homo sapiens	196-199
23844534-1	2013	BACKGROUND: Thiopurine S-Methyltransferase (TPMT) catalyses the S-methylation of thiopurine drugs, such as 6-mercaptopurine, 6-thioguanine and azathioprine, leading to their inactivation.	Azathioprine	143-155	thiopurine S-methyltransferase	Homo sapiens	12-42
23844534-1	2013	BACKGROUND: Thiopurine S-Methyltransferase (TPMT) catalyses the S-methylation of thiopurine drugs, such as 6-mercaptopurine, 6-thioguanine and azathioprine, leading to their inactivation.	Azathioprine	143-155	thiopurine S-methyltransferase	Homo sapiens	44-48
23252704-1	2013	The thiopurine S-methyltransferase (TPMT) gene encoding thiopurine methyltransferase is a crucial enzyme in metabolism of thiopurine drugs: azathioprine and 6-mercoptopurine, which are used in the treatment of leukemia or inflammatory bowel diseases.	Azathioprine	140-152	thiopurine S-methyltransferase	Homo sapiens	4-34
23252704-1	2013	The thiopurine S-methyltransferase (TPMT) gene encoding thiopurine methyltransferase is a crucial enzyme in metabolism of thiopurine drugs: azathioprine and 6-mercoptopurine, which are used in the treatment of leukemia or inflammatory bowel diseases.	Azathioprine	140-152	thiopurine S-methyltransferase	Homo sapiens	36-40
23223314-1	2013	BACKGROUND: Conversion to sirolimus from calcineurin inhibitor- (CNI), azathioprine- (AZA) and mycophenolate-based regimens reduces the risk of development of squamous cell carcinoma of the skin (SCC) in kidney transplant recipients (KTRs).	Azathioprine	86-89	serpin family B member 3	Homo sapiens	196-199
23190446-2	2013	Recently, heterocyclic analogues of PIMs in which the inositol is replaced by a piperidine (aza-PIM mimics) or a tetrahydropyran moiety (oxa-PIM mimics) have been prepared by short synthetic sequences and shown to retain the biological activity of the parent PIM structures.	Azathioprine	92-95	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	96-99
23190446-2	2013	Recently, heterocyclic analogues of PIMs in which the inositol is replaced by a piperidine (aza-PIM mimics) or a tetrahydropyran moiety (oxa-PIM mimics) have been prepared by short synthetic sequences and shown to retain the biological activity of the parent PIM structures.	Azathioprine	92-95	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	36-39
23142267-6	2013	We found that blockade of AQP-4 with TEA and AZA produced an increase in S100B secretion in young rats, compatible with an astroglial activation observed in many conditions of brain injury.	Azathioprine	45-48	aquaporin 4	Rattus norvegicus	26-31
23142267-6	2013	We found that blockade of AQP-4 with TEA and AZA produced an increase in S100B secretion in young rats, compatible with an astroglial activation observed in many conditions of brain injury.	Azathioprine	45-48	S100 calcium binding protein B	Rattus norvegicus	73-78
23190446-2	2013	Recently, heterocyclic analogues of PIMs in which the inositol is replaced by a piperidine (aza-PIM mimics) or a tetrahydropyran moiety (oxa-PIM mimics) have been prepared by short synthetic sequences and shown to retain the biological activity of the parent PIM structures.	Azathioprine	92-95	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	96-99
23335936-2	2012	As it relates to thiopurine therapy, genetic polymorphisms of TPMT are strongly associated with the pharmacokinetics and clinical effects of thiopurines (mercaptopurine and azathioprine), influencing their toxicity and efficacy.	Azathioprine	173-185	thiopurine S-methyltransferase	Homo sapiens	62-66
23001722-6	2013	The reduced WNT5A expression could be restored by treatment with Aza, a methyltransferase inhibitor.	Azathioprine	65-68	Wnt family member 5A	Homo sapiens	12-17
23641277-3	2013	Harmonized steroids and cyclophosphamide or azathioprine are effective for active AAV.	Azathioprine	44-56	adeno-associated virus integration site 1	Homo sapiens	82-85
23400745-0	2013	A new thiopurine s-methyltransferase haplotype associated with intolerance to azathioprine.	Azathioprine	78-90	thiopurine S-methyltransferase	Homo sapiens	6-36
23514552-0	2013	The impact of thiopurine-S-methyltransferase genotype on the adverse drug reactions to azathioprine in patients with inflammatory bowel diseases.	Azathioprine	87-99	thiopurine S-methyltransferase	Homo sapiens	14-44
23514552-2	2013	Polymorphisms in thiopurine S-methyltransferase (TPMT) gene have been associated with adverse drug reactions (ADRs) to AZA.	Azathioprine	119-122	thiopurine S-methyltransferase	Homo sapiens	17-47
23514552-2	2013	Polymorphisms in thiopurine S-methyltransferase (TPMT) gene have been associated with adverse drug reactions (ADRs) to AZA.	Azathioprine	119-122	thiopurine S-methyltransferase	Homo sapiens	49-53
23514552-3	2013	METHODS: The aim of this study was to evaluate TPMT polymorphisms and AZA-related toxicity in a Slovak cohort of 220 IBD patients treated with AZA.	Azathioprine	143-146	thiopurine S-methyltransferase	Homo sapiens	47-51
23400745-6	2013	Nevertheless, in view of the highly significant association (Psim = 0.0026) between TPMT*3E and AZA intolerance in the study, this new haplotype should be taken into consideration in pharmacogenetic profiling for AZA.	Azathioprine	213-216	thiopurine S-methyltransferase	Homo sapiens	84-88
23689569-6	2013	In progressive IgAN patients whose clinical and pathological manifestations are more severe, active therapy may be considered including glucocorticoid therapy, cyclophosphamide, azathioprine, mycophenolate mofetil, tacrolimus, and other immunosuppressants.	Azathioprine	178-190	IGAN1	Homo sapiens	15-19
23400745-1	2013	The authors have analyzed single nucleotide polymorphisms in the thiopurine S-methyltransferase (TPMT) gene in the context of efficacy and toxicity of azathioprine (AZA) to determine possible genotype-phenotype correlations between TPMT allelic variants and response to AZA treatment in 76 Italian patients with myasthenia gravis.	Azathioprine	151-163	thiopurine S-methyltransferase	Homo sapiens	65-95
23400745-1	2013	The authors have analyzed single nucleotide polymorphisms in the thiopurine S-methyltransferase (TPMT) gene in the context of efficacy and toxicity of azathioprine (AZA) to determine possible genotype-phenotype correlations between TPMT allelic variants and response to AZA treatment in 76 Italian patients with myasthenia gravis.	Azathioprine	151-163	thiopurine S-methyltransferase	Homo sapiens	97-101
23400745-1	2013	The authors have analyzed single nucleotide polymorphisms in the thiopurine S-methyltransferase (TPMT) gene in the context of efficacy and toxicity of azathioprine (AZA) to determine possible genotype-phenotype correlations between TPMT allelic variants and response to AZA treatment in 76 Italian patients with myasthenia gravis.	Azathioprine	165-168	thiopurine S-methyltransferase	Homo sapiens	65-95
23400745-1	2013	The authors have analyzed single nucleotide polymorphisms in the thiopurine S-methyltransferase (TPMT) gene in the context of efficacy and toxicity of azathioprine (AZA) to determine possible genotype-phenotype correlations between TPMT allelic variants and response to AZA treatment in 76 Italian patients with myasthenia gravis.	Azathioprine	165-168	thiopurine S-methyltransferase	Homo sapiens	97-101
23400745-1	2013	The authors have analyzed single nucleotide polymorphisms in the thiopurine S-methyltransferase (TPMT) gene in the context of efficacy and toxicity of azathioprine (AZA) to determine possible genotype-phenotype correlations between TPMT allelic variants and response to AZA treatment in 76 Italian patients with myasthenia gravis.	Azathioprine	270-273	thiopurine S-methyltransferase	Homo sapiens	65-95
23400745-1	2013	The authors have analyzed single nucleotide polymorphisms in the thiopurine S-methyltransferase (TPMT) gene in the context of efficacy and toxicity of azathioprine (AZA) to determine possible genotype-phenotype correlations between TPMT allelic variants and response to AZA treatment in 76 Italian patients with myasthenia gravis.	Azathioprine	270-273	thiopurine S-methyltransferase	Homo sapiens	97-101
23400745-3	2013	Most importantly, they show that of the 22 AZA-intolerant patients, all 5 who carried mutations of the intolerance-linked haplotype TPMT*3A also carried the intronic T140+114A (rs3931660), all 3 mutations being part of a new haplotype designated TMPT*3E.	Azathioprine	43-46	thiopurine S-methyltransferase	Homo sapiens	132-136
23400745-5	2013	The association of TPMT*3E with AZA intolerance and its frequency must be ascertained in larger, ethnically different cohorts.	Azathioprine	32-35	thiopurine S-methyltransferase	Homo sapiens	19-23
23400745-6	2013	Nevertheless, in view of the highly significant association (Psim = 0.0026) between TPMT*3E and AZA intolerance in the study, this new haplotype should be taken into consideration in pharmacogenetic profiling for AZA.	Azathioprine	96-99	thiopurine S-methyltransferase	Homo sapiens	84-88
23392829-0	2013	Thiopurine methyltransferase screening before azathioprine prescription: a physician survey.	Azathioprine	46-58	thiopurine S-methyltransferase	Homo sapiens	0-28
23392829-1	2013	BACKGROUND: In patients treated with azathioprine, deficient thiopurine methyltransferase (TPMT) activity has been associated with haematologic toxicity.	Azathioprine	37-49	thiopurine S-methyltransferase	Homo sapiens	61-89
23392829-1	2013	BACKGROUND: In patients treated with azathioprine, deficient thiopurine methyltransferase (TPMT) activity has been associated with haematologic toxicity.	Azathioprine	37-49	thiopurine S-methyltransferase	Homo sapiens	91-95
23149442-7	2012	Two (1%) patients carrying TPMT*3C developed leucopenia at week 4 of azathioprine treatment.	Azathioprine	69-81	thiopurine S-methyltransferase	Homo sapiens	27-31
23285477-9	2012	On univariate analysis, male gender, patient age, older age at diagnosis, higher serum CRP levels, greater proteinuria and higher mean cumulative azathioprine dose were associated with thickened CIMT (P&lt;0.05).	Azathioprine	146-158	CIMT	Homo sapiens	195-199
22910063-12	2012	CONCLUSIONS: IFN-beta as add-on to azathioprine decreases relapse activity in active multiple sclerosis.	Azathioprine	35-47	interferon beta 1	Homo sapiens	13-21
22910063-13	2012	In contrast, azathioprine add-on in patients with suboptimal response to IFN-beta does not improve the control over the disease activity.	Azathioprine	13-25	interferon beta 1	Homo sapiens	73-81
22533640-3	2012	In the present study we have explored individual mutational steps leading to a triple-point-mutated human GST (glutathione transferase) A2-2 displaying enhanced activity with azathioprine.	Azathioprine	175-187	immunoglobulin kappa variable 3-25 (pseudogene)	Homo sapiens	136-140
29776234-2	2012	In clinical practice the best example of this is TPMT testing, which is used to rationalize the starting dose of azathioprine and mercaptopurine.	Azathioprine	113-125	thiopurine S-methyltransferase	Homo sapiens	49-53
22673202-4	2012	Here, we report a weak anion exchange high-performance liquid chromatography method to determine ITPase activity in red blood cells and to investigate the relationship with the occurrence of adverse events during azathioprine therapy.	Azathioprine	213-225	inosine triphosphatase	Homo sapiens	97-103
22493988-1	2012	Thiopurine S-methyltransferase (TPMT) catalyzes the methylation of thiopurine drugs, such as azathioprine and mercaptopurine, which are used in a variety of diseases.	Azathioprine	93-105	thiopurine S-methyltransferase	Homo sapiens	0-30
22493988-1	2012	Thiopurine S-methyltransferase (TPMT) catalyzes the methylation of thiopurine drugs, such as azathioprine and mercaptopurine, which are used in a variety of diseases.	Azathioprine	93-105	thiopurine S-methyltransferase	Homo sapiens	32-36
23075721-0	2012	Thiopurine methyltransferase gene polymorphisms and activity in Chinese patients with inflammatory bowel disease treated with azathioprine.	Azathioprine	126-138	thiopurine S-methyltransferase	Homo sapiens	0-28
23075721-4	2012	The aim of this study was to investigate the association of TPMT polymorphisms and activity with azathioprine (AZA)-related adverse events and clinical efficacy in Chinese Han patients with IBD.	Azathioprine	97-109	thiopurine S-methyltransferase	Homo sapiens	60-64
23075721-4	2012	The aim of this study was to investigate the association of TPMT polymorphisms and activity with azathioprine (AZA)-related adverse events and clinical efficacy in Chinese Han patients with IBD.	Azathioprine	111-114	thiopurine S-methyltransferase	Homo sapiens	60-64
23075721-6	2012	Then, using reverse-phase high-performance liquid chromatography, TPMT activity was measured in 13 patients to analyze its correlation with AZA-related toxicity and clinical efficacy.	Azathioprine	140-143	thiopurine S-methyltransferase	Homo sapiens	66-70
23075721-12	2012	One patient who had higher TPMT activity (28.8 U/ml pRBC) suffered from hepatotoxicity during AZA therapy.	Azathioprine	94-97	thiopurine S-methyltransferase	Homo sapiens	27-31
21912888-0	2012	Aza-derivatives of resveratrol are potent macrophage migration inhibitory factor inhibitors.	Azathioprine	0-3	macrophage migration inhibitory factor	Homo sapiens	53-80
22535280-4	2012	OBJECTIVE: The objective of this study was to assess the relationship between variant alleles of thiopurine S-methyltransferase (SNPs 238G &gt; C, 460G &gt; A and 719A &gt; G), inosine triphosphate diphosphatase (SNPs 94C &gt; A and IVS2 + 21A &gt; C), and xanthine dehydrogenase (837C &gt; T) and the occurrence of adverse drug reactions to azathioprine therapy.	Azathioprine	342-354	thiopurine S-methyltransferase	Homo sapiens	97-127
22612279-2	2012	In this work, four pyridine-containing aza-macrocyclic copper(II) complexes were prepared (CuL1-CuL4) varying in ring size and/or substituents and their superoxide scavenging activity evaluated.	Azathioprine	39-42	cullin 1	Homo sapiens	91-95
22081542-8	2012	Elevated hs-CRP at diagnosis was associated with disease location (P = 0.002), noninflammatory disease behavior (P = 0.058), and a subsequent need for later azathioprine/biological therapy (P &lt; 0.001 and P = 0.024), respectively.	Azathioprine	157-169	C-reactive protein	Homo sapiens	12-15
22612479-4	2012	Multiple examples are provided with full characterization and analyses, including a novel aza-variant of the C-O-D ring system of vancomycin.	Azathioprine	90-93	small nuclear ribonucleoprotein polypeptides B and B1	Homo sapiens	109-114
22853939-0	2012	Improvement of anti-TNFalpha antibody-induced pustular psoriasis by azathioprine.	Azathioprine	68-80	tumor necrosis factor	Homo sapiens	20-28
23117946-6	2012	Acetylcholinesterase inhibitors are often the first modality of therapy for MG. As an immune-mediated disorder, MG can respond to several immunosuppressive agents, such as corticosteroids, azathioprine, mycophenolate mofetil, and cyclosporin.	Azathioprine	189-201	acetylcholinesterase (Cartwright blood group)	Homo sapiens	0-20
23052178-0	2012	EML4-ALK-positive non-small cell lung cancer  in a patient treated with azathioprine  for ulcerative colitis.	Azathioprine	72-84	EMAP like 4	Homo sapiens	0-4
23052178-0	2012	EML4-ALK-positive non-small cell lung cancer  in a patient treated with azathioprine  for ulcerative colitis.	Azathioprine	72-84	ALK receptor tyrosine kinase	Homo sapiens	5-8
23052178-4	2012	We describe a case of lung cancer in a 36-year-old nonsmoking woman with ulcerative colitis treated with azathioprine, who was diagnosed with EML4-ALK-positive, metastatic lung cancer two months postpartum.	Azathioprine	105-117	EMAP like 4	Homo sapiens	142-146
23052178-4	2012	We describe a case of lung cancer in a 36-year-old nonsmoking woman with ulcerative colitis treated with azathioprine, who was diagnosed with EML4-ALK-positive, metastatic lung cancer two months postpartum.	Azathioprine	105-117	ALK receptor tyrosine kinase	Homo sapiens	147-150
22594254-1	2012	Thiopurine S-methyltransferase (TPMT) is an enzyme that catalyzes the S-methylation of thiopurine drugs such as 6-mercaptopurine, 6-thioguanine, and azathioprine.	Azathioprine	149-161	thiopurine S-methyltransferase	Homo sapiens	0-30
22495427-4	2012	RESULTS: AOX1 rs55754655 variant allele carriers received a higher mean AZA dose 3, 6, and 12 months after transplantation (P &lt; 0.05).	Azathioprine	72-75	aldehyde oxidase 1	Homo sapiens	9-13
22495427-5	2012	The patients inheriting rs594445 MOCOS minor allele required significantly lower doses of AZA for efficient treatment compared with wild-type heterozygotes at 3, 6, and 12 months from the transplantation (mean values: 1.39 versus 1.59, 1.38 versus 1.58, and 1.33 versus 1.53 mg kg 24 h) and displayed lower mean RBC count at the time points evaluated.	Azathioprine	90-93	molybdenum cofactor sulfurase	Homo sapiens	33-38
22495427-6	2012	Multivariate analysis has shown that the effect of MOCOS rs594445 polymorphism is independent of other investigated gene variations and might influence AZA dosage, similarly to TPMT heterozygosity.	Azathioprine	152-155	molybdenum cofactor sulfurase	Homo sapiens	51-56
22495427-9	2012	However, if the observed association between SNPs: AOX1 rs55754655, MOCOS rs594445, and AZA dose requirements would be positively confirmed in further independent studies, it could be introduced into clinical practice to individualize thiopurine treatment.	Azathioprine	88-91	aldehyde oxidase 1	Homo sapiens	51-55
22495427-9	2012	However, if the observed association between SNPs: AOX1 rs55754655, MOCOS rs594445, and AZA dose requirements would be positively confirmed in further independent studies, it could be introduced into clinical practice to individualize thiopurine treatment.	Azathioprine	88-91	molybdenum cofactor sulfurase	Homo sapiens	68-73
22489952-1	2012	A series of novel 4-phenylquinazoline-2-carboxamides (1-58) were designed as aza-isosters of PK11195, the well-known 18 kDa translocator protein (TSPO) reference ligand, and synthesized by means of a very simple and efficient procedure.	Azathioprine	77-80	translocator protein	Homo sapiens	124-144
22495427-0	2012	Polymorphism of genes involved in purine metabolism (XDH, AOX1, MOCOS) in kidney transplant recipients receiving azathioprine.	Azathioprine	113-125	xanthine dehydrogenase	Homo sapiens	53-56
22495427-0	2012	Polymorphism of genes involved in purine metabolism (XDH, AOX1, MOCOS) in kidney transplant recipients receiving azathioprine.	Azathioprine	113-125	aldehyde oxidase 1	Homo sapiens	58-62
22495427-0	2012	Polymorphism of genes involved in purine metabolism (XDH, AOX1, MOCOS) in kidney transplant recipients receiving azathioprine.	Azathioprine	113-125	molybdenum cofactor sulfurase	Homo sapiens	64-69
22495427-2	2012	The aim of this study was to investigate single nucleotide polymorphisms (SNPs) in XDH, AOX1, and MOCOS genes in relation to clinical parameters and risk of drug side effects in a cohort of kidney transplant recipients treated with azathioprine (AZA) as a part of standard immunosuppressive regimen.	Azathioprine	232-244	xanthine dehydrogenase	Homo sapiens	83-86
22495427-2	2012	The aim of this study was to investigate single nucleotide polymorphisms (SNPs) in XDH, AOX1, and MOCOS genes in relation to clinical parameters and risk of drug side effects in a cohort of kidney transplant recipients treated with azathioprine (AZA) as a part of standard immunosuppressive regimen.	Azathioprine	246-249	xanthine dehydrogenase	Homo sapiens	83-86
22594254-1	2012	Thiopurine S-methyltransferase (TPMT) is an enzyme that catalyzes the S-methylation of thiopurine drugs such as 6-mercaptopurine, 6-thioguanine, and azathioprine.	Azathioprine	149-161	thiopurine S-methyltransferase	Homo sapiens	32-36
21960178-7	2012	Furthermore, the expression of receptor activator of nuclear factor kappa B ligand (RANKL) in femoral stromal/osteoblastic cells of 5-month-old offspring of 5-AZA-treated females was found to be increased.	Azathioprine	159-162	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	31-82
22279051-3	2012	AO has an important role in the metabolism of drugs based on its broad substrate specificity oxidizing aromatic aza-heterocycles, for example, N(1)-methylnicotinamide and N-methylphthalazinium, or aldehydes, such as benzaldehyde, retinal, and vanillin.	Azathioprine	112-115	aldehyde oxidase 1	Homo sapiens	0-2
21960178-7	2012	Furthermore, the expression of receptor activator of nuclear factor kappa B ligand (RANKL) in femoral stromal/osteoblastic cells of 5-month-old offspring of 5-AZA-treated females was found to be increased.	Azathioprine	159-162	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	84-89
22233693-11	2012	Early AZA use was significantly associated with the time to intestinal surgery in CD patients; in a multivariate Cox analysis (HR: 0.43, 95% confidence interval (CI): 0.28-0.65) and after matching on propensity scores for AZA use (HR: 0.42, 95% CI: 0.26-0.67).	Azathioprine	6-9	cytochrome c oxidase subunit 8A	Homo sapiens	113-116
22450143-9	2012	Early azathioprine use was significantly associated with the time to intestinal surgery in Crohn"s disease patients; in a multivariate Cox analysis (HR: 0.43, 95% confidence interval (CI): 0.28-0.65) and after matching on propensity scores for azathioprine use (HR: 0.42,95% CI:0.26-0.67).	Azathioprine	6-18	cytochrome c oxidase subunit 8A	Homo sapiens	135-138
22407464-4	2012	The results suggested that the aza-caged scaffold provides a suitable modification site and the introduction of a hydrophobic moiety leads to improvement in the cytotoxicity and IKKbeta inhibitory activity.	Azathioprine	31-34	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	178-185
22407464-5	2012	The aza-caged compound 6c exhibited an IC(50) value of 2.68, 2.10, 8.02 muM against the HepG2, A549 cells and IKKbeta, respectively.	Azathioprine	4-7	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	110-117
22421577-1	2012	BACKGROUND: Thiopurine methyltransferase (TPMT) catalyzes the methylation of thiopurine drugs such as azathioprine and 6-mercaptopurine.	Azathioprine	102-114	thiopurine S-methyltransferase	Homo sapiens	42-46
22577154-4	2012	We generated AZA-resistant myeloid cell line (SKM1-R) that exhibited increased expression of BCL2L10 an anti-apoptotic Bcl-2 member.	Azathioprine	13-16	sodium voltage-gated channel alpha subunit 4	Homo sapiens	46-50
22421577-1	2012	BACKGROUND: Thiopurine methyltransferase (TPMT) catalyzes the methylation of thiopurine drugs such as azathioprine and 6-mercaptopurine.	Azathioprine	102-114	thiopurine S-methyltransferase	Homo sapiens	12-40
22147245-9	2012	NOD2 carriers were more often treated with systemic and locally active steroids and with an immunosuppressant (Azathioprine/6-MP).	Azathioprine	111-123	nucleotide binding oligomerization domain containing 2	Homo sapiens	0-4
22385887-9	2012	Six out of 27 (22%) current or past users of azathioprine developed ADR, with three (50%) displaying TPMT genotype and/or phenotype alterations.	Azathioprine	45-57	thiopurine S-methyltransferase	Homo sapiens	101-105
22577154-4	2012	We generated AZA-resistant myeloid cell line (SKM1-R) that exhibited increased expression of BCL2L10 an anti-apoptotic Bcl-2 member.	Azathioprine	13-16	BCL2 like 10	Homo sapiens	93-100
22577154-4	2012	We generated AZA-resistant myeloid cell line (SKM1-R) that exhibited increased expression of BCL2L10 an anti-apoptotic Bcl-2 member.	Azathioprine	13-16	BCL2 apoptosis regulator	Homo sapiens	119-124
22577154-5	2012	Importantly, BCL2L10 knockdown sensitized SKM1-R cells to AZA effect suggesting that increased BCL2L10 expression is linked to AZA resistance in SKM1-R. We next established in 77 MDS patients that resistance to AZA is significantly correlated with the percentage of MDS or AML cells expressing BCL2L10.	Azathioprine	58-61	BCL2 like 10	Homo sapiens	13-20
22577154-5	2012	Importantly, BCL2L10 knockdown sensitized SKM1-R cells to AZA effect suggesting that increased BCL2L10 expression is linked to AZA resistance in SKM1-R. We next established in 77 MDS patients that resistance to AZA is significantly correlated with the percentage of MDS or AML cells expressing BCL2L10.	Azathioprine	58-61	sodium voltage-gated channel alpha subunit 4	Homo sapiens	42-46
22577154-5	2012	Importantly, BCL2L10 knockdown sensitized SKM1-R cells to AZA effect suggesting that increased BCL2L10 expression is linked to AZA resistance in SKM1-R. We next established in 77 MDS patients that resistance to AZA is significantly correlated with the percentage of MDS or AML cells expressing BCL2L10.	Azathioprine	58-61	BCL2 like 10	Homo sapiens	95-102
22577154-5	2012	Importantly, BCL2L10 knockdown sensitized SKM1-R cells to AZA effect suggesting that increased BCL2L10 expression is linked to AZA resistance in SKM1-R. We next established in 77 MDS patients that resistance to AZA is significantly correlated with the percentage of MDS or AML cells expressing BCL2L10.	Azathioprine	58-61	BCL2 like 10	Homo sapiens	95-102
22577154-5	2012	Importantly, BCL2L10 knockdown sensitized SKM1-R cells to AZA effect suggesting that increased BCL2L10 expression is linked to AZA resistance in SKM1-R. We next established in 77 MDS patients that resistance to AZA is significantly correlated with the percentage of MDS or AML cells expressing BCL2L10.	Azathioprine	127-130	BCL2 like 10	Homo sapiens	95-102
22577154-5	2012	Importantly, BCL2L10 knockdown sensitized SKM1-R cells to AZA effect suggesting that increased BCL2L10 expression is linked to AZA resistance in SKM1-R. We next established in 77 MDS patients that resistance to AZA is significantly correlated with the percentage of MDS or AML cells expressing BCL2L10.	Azathioprine	127-130	sodium voltage-gated channel alpha subunit 4	Homo sapiens	145-149
22577154-5	2012	Importantly, BCL2L10 knockdown sensitized SKM1-R cells to AZA effect suggesting that increased BCL2L10 expression is linked to AZA resistance in SKM1-R. We next established in 77 MDS patients that resistance to AZA is significantly correlated with the percentage of MDS or AML cells expressing BCL2L10.	Azathioprine	127-130	BCL2 like 10	Homo sapiens	95-102
22577154-5	2012	Importantly, BCL2L10 knockdown sensitized SKM1-R cells to AZA effect suggesting that increased BCL2L10 expression is linked to AZA resistance in SKM1-R. We next established in 77 MDS patients that resistance to AZA is significantly correlated with the percentage of MDS or AML cells expressing BCL2L10.	Azathioprine	127-130	BCL2 like 10	Homo sapiens	95-102
22577154-5	2012	Importantly, BCL2L10 knockdown sensitized SKM1-R cells to AZA effect suggesting that increased BCL2L10 expression is linked to AZA resistance in SKM1-R. We next established in 77 MDS patients that resistance to AZA is significantly correlated with the percentage of MDS or AML cells expressing BCL2L10.	Azathioprine	127-130	sodium voltage-gated channel alpha subunit 4	Homo sapiens	145-149
22334756-1	2012	Glutathione transferase (GST) A2-2 is the human enzyme displaying the highest catalytic activity with the prodrug azathioprine (Aza).	Azathioprine	114-126	glutathione S-transferase alpha 2	Homo sapiens	0-34
22577154-5	2012	Importantly, BCL2L10 knockdown sensitized SKM1-R cells to AZA effect suggesting that increased BCL2L10 expression is linked to AZA resistance in SKM1-R. We next established in 77 MDS patients that resistance to AZA is significantly correlated with the percentage of MDS or AML cells expressing BCL2L10.	Azathioprine	127-130	BCL2 like 10	Homo sapiens	95-102
22334756-1	2012	Glutathione transferase (GST) A2-2 is the human enzyme displaying the highest catalytic activity with the prodrug azathioprine (Aza).	Azathioprine	128-131	glutathione S-transferase alpha 2	Homo sapiens	0-34
22334756-5	2012	Chimeric GSTs were previously generated by DNA shuffling and two peptide segments, one N-terminal and one C-terminal, were identified as primary determinants of Aza activity.	Azathioprine	161-164	glutathione S-transferase alpha 1	Rattus norvegicus	9-13
22577154-7	2012	We propose a convenient assay in which the percentage of BCL2L10 expressing cells as assessed by flow cytometry is predictive of whether or not a patient will become resistant to AZA.	Azathioprine	179-182	BCL2 like 10	Homo sapiens	57-64
22577154-8	2012	Therefore, systematic determination of BCL2L10 expression could be of great interest in newly diagnosed and AZA-treated MDS patients.	Azathioprine	108-111	BCL2 like 10	Homo sapiens	39-46
22334756-7	2012	Substitution of the corresponding two small regions in the low-activity human GST A3-3 or rat GST A3-3 by the human GST A2-2 segments generated chimeras with ~10-fold enhanced Aza activity.	Azathioprine	176-179	glutathione S-transferase alpha 3	Homo sapiens	78-86
22616502-6	2012	The analysis of polymorphisms of the gene coding for the enzyme thiopurine methyl transferase (TPMT) helps in the reduction of the risks associated with the use of azathioprine in the treatment of inflammatory bowel disease.	Azathioprine	164-176	thiopurine S-methyltransferase	Homo sapiens	95-99
22334756-7	2012	Substitution of the corresponding two small regions in the low-activity human GST A3-3 or rat GST A3-3 by the human GST A2-2 segments generated chimeras with ~10-fold enhanced Aza activity.	Azathioprine	176-179	glutathione S-transferase alpha 1	Rattus norvegicus	94-102
22334756-7	2012	Substitution of the corresponding two small regions in the low-activity human GST A3-3 or rat GST A3-3 by the human GST A2-2 segments generated chimeras with ~10-fold enhanced Aza activity.	Azathioprine	176-179	glutathione S-transferase alpha 2	Homo sapiens	116-124
22444596-0	2012	Structure-based redesign of GST A2-2 for enhanced catalytic efficiency with azathioprine.	Azathioprine	76-88	glutathione S-transferase alpha 2	Homo sapiens	28-36
22444596-1	2012	Glutathione transferase (GST) A2-2 is the most efficient human enzyme in the biotransformation of the prodrug azathioprine (Aza).	Azathioprine	110-122	glutathione S-transferase alpha 2	Homo sapiens	0-34
22444596-1	2012	Glutathione transferase (GST) A2-2 is the most efficient human enzyme in the biotransformation of the prodrug azathioprine (Aza).	Azathioprine	124-127	glutathione S-transferase alpha 2	Homo sapiens	0-34
22444596-2	2012	The activation of Aza has therapeutic potential for possible use of GSTs in targeted enzyme-prodrug treatment of diseases.	Azathioprine	18-21	hematopoietic prostaglandin D synthase	Homo sapiens	68-72
24714152-2	2012	Genetic variations in thiopurine S-methyltranfarase (TPMT) gene have been correlated with enzyme activity and with the occurrence of adverse events to AZA and 6MP.	Azathioprine	151-154	thiopurine S-methyltransferase	Homo sapiens	22-51
22054202-7	2012	Gender-stratified tertiles of age-corrected EPO were positively associated with waist circumference (but not BMI), CVD history, time since transplantation, diuretics, azathioprine, CRP, mean corpuscular volume and triglyceride levels, and inversely with CrCl, RAAS-inhibition, cyclosporine, hemoglobin, total- and HDL-cholesterol.	Azathioprine	167-179	erythropoietin	Homo sapiens	44-47
22243962-0	2012	Synthesis and evaluation of aza-peptidyl inhibitors of the lysosomal asparaginyl endopeptidase, legumain.	Azathioprine	28-31	legumain	Mus musculus	96-104
22243962-6	2012	We synthesized a library of aza-peptidyl inhibitors with various non-natural amino acids and different electrophilic warheads, and characterized the kinetic properties of inactivation of legumain.	Azathioprine	28-31	legumain	Mus musculus	187-195
24714152-2	2012	Genetic variations in thiopurine S-methyltranfarase (TPMT) gene have been correlated with enzyme activity and with the occurrence of adverse events to AZA and 6MP.	Azathioprine	151-154	thiopurine S-methyltransferase	Homo sapiens	53-57
21967657-7	2011	AZ dosing was correlated to TPMT levels successfully, with comparable levels of improvement in the heterozygous and homozygous wild-type groups.	Azathioprine	0-2	thiopurine S-methyltransferase	Homo sapiens	28-32
22508060-7	2012	Azathioprine (10 muM) did not significantly alter the Na(+)/H(+) exchanger activity, cell volume and ROS formation prior to LPS exposure but significantly blunted the LPS-induced stimulation of Na(+)/H(+) exchanger activity, ROS formation, cell swelling, TNFalpha production and cell migration.	Azathioprine	0-12	tumor necrosis factor	Mus musculus	255-263
22536046-2	2012	A 68-year-old male patient with anti-proteinase-3 ANCA-positive Wegener"s granulomatosis who was receiving immunosuppressive therapy with methylprednisolone, cyclophosphamide, and azathioprine developed CMV retinitis.	Azathioprine	180-192	proteinase 3	Homo sapiens	37-49
21824328-0	2011	Metabolic stability of peptidomimetics: N-methyl and aza heptapeptide analogs of a PKB/Akt inhibitor.	Azathioprine	53-56	AKT serine/threonine kinase 1	Homo sapiens	83-86
21803983-0	2011	Oral azathioprine leads to higher incorporation of 6-thioguanine in DNA of skin than liver: the protective role of the Keap1/Nrf2/ARE pathway.	Azathioprine	5-17	kelch like ECH associated protein 1	Homo sapiens	119-124
21803983-0	2011	Oral azathioprine leads to higher incorporation of 6-thioguanine in DNA of skin than liver: the protective role of the Keap1/Nrf2/ARE pathway.	Azathioprine	5-17	NFE2 like bZIP transcription factor 2	Homo sapiens	125-129
21803983-6	2011	Genetic upregulation of the Keap1/Nrf2/ARE pathway, a major cellular regulator of the expression of a network of cytoprotective genes, reduces the incorporation of 6-thioguanine in DNA of both skin and liver following treatment with azathioprine.	Azathioprine	233-245	kelch like ECH associated protein 1	Homo sapiens	28-33
21803983-6	2011	Genetic upregulation of the Keap1/Nrf2/ARE pathway, a major cellular regulator of the expression of a network of cytoprotective genes, reduces the incorporation of 6-thioguanine in DNA of both skin and liver following treatment with azathioprine.	Azathioprine	233-245	NFE2 like bZIP transcription factor 2	Homo sapiens	34-38
21803983-9	2011	Our findings suggest that activation of the Keap1/Nrf2/ARE pathway could reduce the risk for skin cancer in patients receiving long-term azathioprine therapy.	Azathioprine	137-149	kelch like ECH associated protein 1	Homo sapiens	44-49
21803983-9	2011	Our findings suggest that activation of the Keap1/Nrf2/ARE pathway could reduce the risk for skin cancer in patients receiving long-term azathioprine therapy.	Azathioprine	137-149	NFE2 like bZIP transcription factor 2	Homo sapiens	50-54
21815707-8	2011	In general, however, AChE inhibitors provide only partial benefit and most patients eventually switch to long-term immunosuppressive therapies, most frequently corticosteroids and/or azathioprine.	Azathioprine	183-195	acetylcholinesterase (Cartwright blood group)	Homo sapiens	21-25
21723857-12	2011	CONCLUSIONS: One quarter of MS episodes during AZA were associated with TPMT deficient genotype.	Azathioprine	47-50	thiopurine S-methyltransferase	Homo sapiens	72-76
21641978-7	2011	In addition, using the epigenetic modifiers, 5-Aza-2"-deoxycytidine (Aza) and Trichostatin A (TSA), we found that modifications of histone acetylation reversed the inhibition of BTD, suggesting that Cr(VI) may cause down regulation of BTD by modifications of histone acetylation.	Azathioprine	47-50	biotinidase	Homo sapiens	178-181
21402617-13	2011	CONCLUSIONS: Clinically progressive PSC requiring LT is associated with a milder course of UC (reduced disease activity and less use of steroids, azathioprine and surgery).	Azathioprine	146-158	PSC	Homo sapiens	36-39
21961091-0	2011	A pharmacogenetics study of TPMT and ITPA genes detects a relationship with side effects and clinical response in patients with inflammatory bowel disease receiving Azathioprine.	Azathioprine	165-177	thiopurine S-methyltransferase	Homo sapiens	28-32
21961091-0	2011	A pharmacogenetics study of TPMT and ITPA genes detects a relationship with side effects and clinical response in patients with inflammatory bowel disease receiving Azathioprine.	Azathioprine	165-177	inosine triphosphatase	Homo sapiens	37-41
21961091-3	2011	Variants in the Thiopurine S-methyltransferase (TPMT) and Inosine triphosphate pyrophosphatase (ITPA) genes have been associated with AZA toxicity, but also can contribute to the lack of response.	Azathioprine	134-137	thiopurine S-methyltransferase	Homo sapiens	16-46
21961091-3	2011	Variants in the Thiopurine S-methyltransferase (TPMT) and Inosine triphosphate pyrophosphatase (ITPA) genes have been associated with AZA toxicity, but also can contribute to the lack of response.	Azathioprine	134-137	thiopurine S-methyltransferase	Homo sapiens	48-52
21961091-3	2011	Variants in the Thiopurine S-methyltransferase (TPMT) and Inosine triphosphate pyrophosphatase (ITPA) genes have been associated with AZA toxicity, but also can contribute to the lack of response.	Azathioprine	134-137	inosine triphosphatase	Homo sapiens	58-94
21961091-3	2011	Variants in the Thiopurine S-methyltransferase (TPMT) and Inosine triphosphate pyrophosphatase (ITPA) genes have been associated with AZA toxicity, but also can contribute to the lack of response.	Azathioprine	134-137	inosine triphosphatase	Homo sapiens	96-100
21961091-4	2011	The aims of this study were to determine the contribution of TPMT and ITPA variants in the development of AZA-related toxicity and response.	Azathioprine	106-109	thiopurine S-methyltransferase	Homo sapiens	61-65
21961091-4	2011	The aims of this study were to determine the contribution of TPMT and ITPA variants in the development of AZA-related toxicity and response.	Azathioprine	106-109	inosine triphosphatase	Homo sapiens	70-74
21961091-5	2011	METHODS: Variants associated with the decrease of enzyme activity in TPMT and ITPA genes were genotyped with the Snapshot system in 232 IBD patients treated with AZA, and correlated with the clinical response and development of adverse drug reactions in a retrospective case-control study.	Azathioprine	162-165	thiopurine S-methyltransferase	Homo sapiens	69-73
21961091-5	2011	METHODS: Variants associated with the decrease of enzyme activity in TPMT and ITPA genes were genotyped with the Snapshot system in 232 IBD patients treated with AZA, and correlated with the clinical response and development of adverse drug reactions in a retrospective case-control study.	Azathioprine	162-165	inosine triphosphatase	Homo sapiens	78-82
21961091-6	2011	RESULTS: Genotypic analysis showed that there is a statistical significance between c.94C &gt; A variant on ITPA gene with non response to AZA treatment (p=0.005) and arthralgia (OR 8.2353; 95%CI 1.752-38.87, p=0.0041), as well as between mutant TPMT alleles and myelosuppression (OR 7.5; 95%CI 1.4456-38.91, p=0.0304).	Azathioprine	139-142	inosine triphosphatase	Homo sapiens	108-112
21961091-6	2011	RESULTS: Genotypic analysis showed that there is a statistical significance between c.94C &gt; A variant on ITPA gene with non response to AZA treatment (p=0.005) and arthralgia (OR 8.2353; 95%CI 1.752-38.87, p=0.0041), as well as between mutant TPMT alleles and myelosuppression (OR 7.5; 95%CI 1.4456-38.91, p=0.0304).	Azathioprine	139-142	thiopurine S-methyltransferase	Homo sapiens	246-250
21961091-8	2011	Mutant alleles on TPMT and the variant c.94C &gt; A on ITPA gene predict side effects induced by AZA in our population (myelosuppression and arthralgia).	Azathioprine	97-100	inosine triphosphatase	Homo sapiens	55-59
21641978-7	2011	In addition, using the epigenetic modifiers, 5-Aza-2"-deoxycytidine (Aza) and Trichostatin A (TSA), we found that modifications of histone acetylation reversed the inhibition of BTD, suggesting that Cr(VI) may cause down regulation of BTD by modifications of histone acetylation.	Azathioprine	47-50	biotinidase	Homo sapiens	235-238
21351239-1	2011	After liver transplantation (LT), hepatic veno-occlusive disease (VOD), which is also known as sinusoidal obstruction syndrome (SOS), has been reported initially in relation to azathioprine use and subsequently in relation to acute rejection (AR).	Azathioprine	177-189	xylosyltransferase 2	Homo sapiens	128-131
21819368-1	2011	OBJECTIVES: Thiopurine S-methyltransferase is an enzyme that catalyzes S-methylation of azathioprine as an immunosuppressive drug.	Azathioprine	88-100	thiopurine S-methyltransferase	Homo sapiens	12-42
21819368-9	2011	During subsequent days, mean azathioprine dosage administered to thiopurine S-methyltransferase wild-type homozygous patients was similar to heterozygous patients, but with no statistical difference (P = .28).	Azathioprine	29-41	thiopurine S-methyltransferase	Homo sapiens	65-95
21819368-15	2011	The incidence of adverse reactions to azathioprine was also low, even in patients carrying a variant of thiopurine S-methyltransferase.	Azathioprine	38-50	thiopurine S-methyltransferase	Homo sapiens	104-134
21677600-6	2011	The levels of C-reactive protein and vascular cell adhesion molecule-1 declined significantly with AZA+everolimus, whereas MMF+everolimus patients demonstrated a significant increase in levels of C-reactive protein, vascular cell adhesion molecule-1, and von Willebrand factor.	Azathioprine	99-102	C-reactive protein	Homo sapiens	14-32
21677600-6	2011	The levels of C-reactive protein and vascular cell adhesion molecule-1 declined significantly with AZA+everolimus, whereas MMF+everolimus patients demonstrated a significant increase in levels of C-reactive protein, vascular cell adhesion molecule-1, and von Willebrand factor.	Azathioprine	99-102	vascular cell adhesion molecule 1	Homo sapiens	37-70
21712851-0	2011	Azathioprine-related myelosuppression in a patient homozygous for TPMT*3A.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	66-70
21712851-3	2011	DIAGNOSIS: Severe myelosuppression as a consequence of azathioprine therapy in a patient homozygous for the TPMT*3A allele.	Azathioprine	55-67	thiopurine S-methyltransferase	Homo sapiens	108-112
21410283-0	2011	Microwave-assisted solid-phase aza-peptide synthesis: aza scan of a PKB/Akt inhibitor using aza-arginine and aza-proline precursors.	Azathioprine	31-34	AKT serine/threonine kinase 1	Homo sapiens	68-71
20726808-4	2011	Genetic analysis revealed heterozygous genotype (*1/*3A) of thiopurine S-methyltransferase (TPMT), a key enzyme of thiopurines" metabolism, which results in lower activity of TPMT enzyme, thereby making our patient more susceptible to azathioprine-related hepato and myelotoxicity development.	Azathioprine	235-247	thiopurine S-methyltransferase	Homo sapiens	60-90
20726808-4	2011	Genetic analysis revealed heterozygous genotype (*1/*3A) of thiopurine S-methyltransferase (TPMT), a key enzyme of thiopurines" metabolism, which results in lower activity of TPMT enzyme, thereby making our patient more susceptible to azathioprine-related hepato and myelotoxicity development.	Azathioprine	235-247	thiopurine S-methyltransferase	Homo sapiens	92-96
20726808-4	2011	Genetic analysis revealed heterozygous genotype (*1/*3A) of thiopurine S-methyltransferase (TPMT), a key enzyme of thiopurines" metabolism, which results in lower activity of TPMT enzyme, thereby making our patient more susceptible to azathioprine-related hepato and myelotoxicity development.	Azathioprine	235-247	thiopurine S-methyltransferase	Homo sapiens	175-179
20726808-8	2011	Our Case Study highlights the clinical difficulties and challenges associated with diagnosing of azathioprine-induced NRH, as well as, supports previous observations that hypercoagulability disorders and abnormal TPMT activity may contribute to NRH development.	Azathioprine	97-109	thiopurine S-methyltransferase	Homo sapiens	213-217
21401729-4	2011	MMF versus Aza treatment was proven to be an independent variable associated with suppression of CD4 cell IL-10 responses (P=0.008), B-cell IL-6R expression (P&lt;0.0001) and ISC formation [P=0.020, staphylococcus cowan strain I (SAC I); P=0.021, pokeweed mitogen (PWM)].	Azathioprine	11-14	CD4 molecule	Homo sapiens	97-100
21401729-4	2011	MMF versus Aza treatment was proven to be an independent variable associated with suppression of CD4 cell IL-10 responses (P=0.008), B-cell IL-6R expression (P&lt;0.0001) and ISC formation [P=0.020, staphylococcus cowan strain I (SAC I); P=0.021, pokeweed mitogen (PWM)].	Azathioprine	11-14	interleukin 10	Homo sapiens	106-111
21301920-0	2011	Steroids and azathioprine in the treatment of IgA nephropathy.	Azathioprine	13-25	IGAN1	Homo sapiens	46-61
21301920-6	2011	In the MP + Aza group, eGFR slightly increased from 57.4 +- 28.7 to 66 +- 31 ml/min/1.73 m(2), p = NS, and Upr decreased from 2.4 +- 1 to 0.7 +- 0.7 g/24 h, p &lt; 0.001.	Azathioprine	12-15	epidermal growth factor receptor	Homo sapiens	23-27
21301920-9	2011	CONCLUSIONS: Both, steroid treatment alone and steroids in combination with azathioprine seem to be effective in reducing the severity of proteinuria and stabilizing renal function in IgAN.	Azathioprine	76-88	IGAN1	Homo sapiens	184-188
21372752-4	2011	Recently, the small guanosine triphosphatase, Rac1, was identified as an important molecular target of 6-thioguanine triphosphate, one of the active metabolite of thiopurines such as azathioprine.	Azathioprine	183-195	Rac family small GTPase 1	Homo sapiens	46-50
21372752-6	2011	OBJECTIVES: Evidence for functional genetic polymorphisms of the human Rac1 gene and to investigate their relative contribution to the development of toxicity induced by azathioprine treatment in patients with inflammatory bowel disease.	Azathioprine	170-182	Rac family small GTPase 1	Homo sapiens	71-75
20970225-0	2011	[Azathioprine-associated severe myelosuppression: indication of routine determination of thiopurine S-methyltransferase variant?].	Azathioprine	1-13	thiopurine S-methyltransferase	Homo sapiens	89-119
20970225-7	2011	CONCLUSION: Routine measurement of TPMT activity or determination of TPMT variant allele may be useful tests, in order to identify the subgroup of patients who are at risk to develop azathioprine induced severe myelosuppression.	Azathioprine	183-195	thiopurine S-methyltransferase	Homo sapiens	69-73
21544018-0	2011	Association between adverse effects under azathioprine therapy and inosine triphosphate pyrophosphatase activity in patients with chronic inflammatory bowel disease.	Azathioprine	42-54	inosine triphosphatase	Homo sapiens	67-103
21545711-13	2011	Both thiopurine derivatives reduced the proportion of apoptotic T helper cells, but a high production of both IL-6 and TGF-beta was observed only in colon of AZA-treated mice.	Azathioprine	158-161	interleukin 6	Mus musculus	110-114
21410283-0	2011	Microwave-assisted solid-phase aza-peptide synthesis: aza scan of a PKB/Akt inhibitor using aza-arginine and aza-proline precursors.	Azathioprine	31-34	AKT serine/threonine kinase 1	Homo sapiens	72-75
21410283-4	2011	We report here an aza-scan of a potent, peptide-based PKB/Akt inhibitor, PTR6154.	Azathioprine	18-21	AKT serine/threonine kinase 1	Homo sapiens	54-57
21545711-13	2011	Both thiopurine derivatives reduced the proportion of apoptotic T helper cells, but a high production of both IL-6 and TGF-beta was observed only in colon of AZA-treated mice.	Azathioprine	158-161	transforming growth factor, beta 1	Mus musculus	119-127
21410283-4	2011	We report here an aza-scan of a potent, peptide-based PKB/Akt inhibitor, PTR6154.	Azathioprine	18-21	AKT serine/threonine kinase 1	Homo sapiens	58-61
21235538-9	2011	In addition, azathioprine-associated lymphopenia was characterized by decreased absolute numbers of CD4(+) CD69(+) and CD4(+) interleukin (IL)-17(+) cells compared to disease activity-associated lymphopenia.	Azathioprine	13-25	CD4 molecule	Homo sapiens	100-103
21235538-9	2011	In addition, azathioprine-associated lymphopenia was characterized by decreased absolute numbers of CD4(+) CD69(+) and CD4(+) interleukin (IL)-17(+) cells compared to disease activity-associated lymphopenia.	Azathioprine	13-25	CD4 molecule	Homo sapiens	119-122
21235538-12	2011	Furthermore, azathioprine treatment was associated with decreased numbers of CD4(+) CD69(+) and CD4(+) IL-17(+) cells and diminished T(reg) suppressive activity.	Azathioprine	13-25	CD4 molecule	Homo sapiens	77-80
21235538-12	2011	Furthermore, azathioprine treatment was associated with decreased numbers of CD4(+) CD69(+) and CD4(+) IL-17(+) cells and diminished T(reg) suppressive activity.	Azathioprine	13-25	CD4 molecule	Homo sapiens	96-99
20863672-8	2011	Significant rises in liver tumor necrosis factor-alpha (TNF-alpha) and caspase-3 levels were noticed in AZA-intoxicated rats.	Azathioprine	104-107	tumor necrosis factor	Rattus norvegicus	27-54
20863672-8	2011	Significant rises in liver tumor necrosis factor-alpha (TNF-alpha) and caspase-3 levels were noticed in AZA-intoxicated rats.	Azathioprine	104-107	tumor necrosis factor	Rattus norvegicus	56-65
20863672-8	2011	Significant rises in liver tumor necrosis factor-alpha (TNF-alpha) and caspase-3 levels were noticed in AZA-intoxicated rats.	Azathioprine	104-107	caspase 3	Rattus norvegicus	71-80
20863672-9	2011	Treatment of the AZA-intoxicated rats with GTP significantly prevented the elevations of sALT, sAST and sALP, inhibited depletion of hepatic GSH, GPx, CAT and GSSG and inhibited MDA accumulation.	Azathioprine	17-20	microtubule associated serine/threonine kinase 1	Rattus norvegicus	95-99
20863672-9	2011	Treatment of the AZA-intoxicated rats with GTP significantly prevented the elevations of sALT, sAST and sALP, inhibited depletion of hepatic GSH, GPx, CAT and GSSG and inhibited MDA accumulation.	Azathioprine	17-20	catalase	Rattus norvegicus	151-154
23126559-0	2010	Assessment of thiopurine methyltransferase activity in patients prescribed azathioprine or other thiopurine-based drugs.	Azathioprine	75-87	thiopurine S-methyltransferase	Homo sapiens	14-42
21537417-8	2011	CONCLUSION: We treated a patient with type B insulin resistance syndrome showing recurrent fasting hypoglycemia with steroids and azathioprine.	Azathioprine	130-142	insulin	Homo sapiens	45-52
21083588-6	2011	Azathioprine therapy was associated with a reduction in total natural killer cells in blood and lamina propria, preferentially of the CD16(+) subset.	Azathioprine	0-12	Fc gamma receptor IIIa	Homo sapiens	134-138
21083588-7	2011	Azathioprine therapy did not impair natural killer degranulation, but reduced natural and cytokine-activated cytotoxicity and interferon-gamma (IFN-gamma) production.	Azathioprine	0-12	interferon gamma	Homo sapiens	126-142
21083588-7	2011	Azathioprine therapy did not impair natural killer degranulation, but reduced natural and cytokine-activated cytotoxicity and interferon-gamma (IFN-gamma) production.	Azathioprine	0-12	interferon gamma	Homo sapiens	144-153
21083588-8	2011	Culture of resting peripheral blood mononuclear cells with azathioprine resulted in loss of natural killer cells and inhibition of activation and IFN-gamma production.	Azathioprine	59-71	interferon gamma	Homo sapiens	146-155
21083588-9	2011	Azathioprine preferentially inhibited proliferation of CD16(+) natural killer cells and induced apoptosis in resting but not in pre-activated natural killer cells.	Azathioprine	0-12	Fc gamma receptor IIIa	Homo sapiens	55-59
21080722-6	2010	2004 , 14 , 6083 - 6087) as a potent inhibitor (IC50 = 30 nM) of DNA-dependent protein kinase (DNA-PK), we have investigated analogues in which the chromen-4-one core template has been replaced by aza-heterocyclic systems: 9-substituted 2-morpholin-4-ylpyrido[1,2-a]pyrimidin-4-ones and 8-substituted 2-morpholin-4-yl-1H-quinolin-4-ones.	Azathioprine	197-200	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	65-93
21080722-6	2010	2004 , 14 , 6083 - 6087) as a potent inhibitor (IC50 = 30 nM) of DNA-dependent protein kinase (DNA-PK), we have investigated analogues in which the chromen-4-one core template has been replaced by aza-heterocyclic systems: 9-substituted 2-morpholin-4-ylpyrido[1,2-a]pyrimidin-4-ones and 8-substituted 2-morpholin-4-yl-1H-quinolin-4-ones.	Azathioprine	197-200	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	95-101
21165581-8	2011	WNT5A expression was up-regulated after exposure to the demethylating agent 5-Aza-2"-deoxycytidine (Aza) in the K562, U937, Jurkat leukemic cell lines and in 83.3% (10/12) of CR patients after cure, respectively.	Azathioprine	78-81	Wnt family member 5A	Homo sapiens	0-5
21165581-9	2011	The increased Wnt5a protein can inhibit K562 malignant proliferation and arrest cell cycle at the G2/M phase after exposure to Aza.	Azathioprine	127-130	Wnt family member 5A	Homo sapiens	14-19
22160088-1	2011	Ongoing analysis of the seminal AZA-001 study has taught many important lessons in the use of DNA methyltransferase (DNMT) inhibitors.	Azathioprine	32-35	DNA methyltransferase 1	Homo sapiens	94-115
22160088-1	2011	Ongoing analysis of the seminal AZA-001 study has taught many important lessons in the use of DNA methyltransferase (DNMT) inhibitors.	Azathioprine	32-35	DNA methyltransferase 1	Homo sapiens	117-121
21082772-2	2010	Linear hydroformylation of N-protected allyl- or homoallylamines (cyclohydrocarbonylation: CHC), followed by a reductive amination constitute the two key steps toward convenient routes to aza-heterocycles.	Azathioprine	188-191	clathrin heavy chain	Homo sapiens	91-94
20923998-11	2010	Azathioprine-treated Msh2(+/)- mice developed diffuse lymphomas lacking Msh2 expression and displaying MSI due to somatic inactivation of the functional Msh2 allele by loss of heterozygosity or mutation.	Azathioprine	0-12	mutS homolog 2	Mus musculus	21-25
21348397-11	2010	CONCLUSIONS: It is advisable that Druze patients be tested for the TPMT enzyme before starting treatment with 6-MP or azathioprine.	Azathioprine	118-130	thiopurine S-methyltransferase	Homo sapiens	67-71
20972624-0	2010	Azathioprine-induced severe cholestatic hepatitis in patient carrying TPMT*3C polymorphism.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	70-74
20923998-0	2010	Azathioprine-induced carcinogenesis in mice according to Msh2 genotype.	Azathioprine	0-12	mutS homolog 2	Mus musculus	57-61
20864690-6	2010	In an additional 33 patients, glomerular and tubular NEP protein levels from renal graft biopsies were significantly higher among the 13 patients receiving cyclosporine + EC-MPS than among the 12 patients receiving cyclosporine + azathioprine or 8 patients receiving cyclosporine alone.	Azathioprine	230-242	membrane metalloendopeptidase	Homo sapiens	53-56
20923998-11	2010	Azathioprine-treated Msh2(+/)- mice developed diffuse lymphomas lacking Msh2 expression and displaying MSI due to somatic inactivation of the functional Msh2 allele by loss of heterozygosity or mutation.	Azathioprine	0-12	mutS homolog 2	Mus musculus	72-76
20923998-11	2010	Azathioprine-treated Msh2(+/)- mice developed diffuse lymphomas lacking Msh2 expression and displaying MSI due to somatic inactivation of the functional Msh2 allele by loss of heterozygosity or mutation.	Azathioprine	0-12	mutS homolog 2	Mus musculus	72-76
20923998-12	2010	By contrast, azathioprine-treated Msh2(WT) mice displayed no obvious tumor phenotype, but histological examination showed microscopic splenic foci of neoplastic lymphoid cells that retained Msh2 expression and did not display MSI.	Azathioprine	13-25	mutS homolog 2	Mus musculus	34-38
20923998-12	2010	By contrast, azathioprine-treated Msh2(WT) mice displayed no obvious tumor phenotype, but histological examination showed microscopic splenic foci of neoplastic lymphoid cells that retained Msh2 expression and did not display MSI.	Azathioprine	13-25	mutS homolog 2	Mus musculus	190-194
20923998-13	2010	Both untreated and azathioprine-treated Msh2-(/)- mice had a reduced lifespan compared with untreated Msh2(WT) mice (median survival of 127 and 107 days of age, respectively) and developed lymphomas with MSI.	Azathioprine	19-31	mutS homolog 2	Mus musculus	40-44
20923998-13	2010	Both untreated and azathioprine-treated Msh2-(/)- mice had a reduced lifespan compared with untreated Msh2(WT) mice (median survival of 127 and 107 days of age, respectively) and developed lymphomas with MSI.	Azathioprine	19-31	mutS homolog 2	Mus musculus	102-106
20923998-14	2010	CONCLUSION: Azathioprine-induced carcinogenesis in mice depends on the number of functional copies of the Msh2 gene.	Azathioprine	12-24	mutS homolog 2	Mus musculus	106-110
20564510-7	2010	Aza induced hepatic damage as indicated by pronounced changes in the histological structure, a significant increase in serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP), and MDA content in the liver tissue.	Azathioprine	0-3	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	153-156
20308917-2	2010	The purpose of this study was to investigate the relative risk of the thiopurine methyltransferase (TPMT) and inosine triphosphate pyrophosphatase (ITPA) genotypes and TPMT activity for the development of leukopenia in Korean IBD patients during AZA/6-MP treatment.	Azathioprine	246-249	inosine triphosphatase	Homo sapiens	148-152
20564510-7	2010	Aza induced hepatic damage as indicated by pronounced changes in the histological structure, a significant increase in serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP), and MDA content in the liver tissue.	Azathioprine	0-3	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	125-151
20953224-2	2010	Due to individual variation of the metabolism of AZA, related to genetic polymorphism of the thiopurine methyl transferase (TPMT), serious toxic effects can result if inappropriate dose is administered.	Azathioprine	49-52	thiopurine S-methyltransferase	Homo sapiens	93-122
20881512-2	2010	TPMT is involved in the detoxification and activation of thiopurines such as 6-mercaptopurine, 6-thioguanine, and azathioprine.	Azathioprine	114-126	thiopurine S-methyltransferase	Homo sapiens	0-4
21094840-8	2010	Administration of azathioprine (P &lt; .0001) or a calcineurin inhibitor (CNI) (P = .02) for more than 1 year was associated with development of malignancy, whereas significantly fewer malignancies were noticed in patients receiving an mTOR-inhibitor (P &lt; .0001).	Azathioprine	18-30	mechanistic target of rapamycin kinase	Homo sapiens	236-240
20953224-2	2010	Due to individual variation of the metabolism of AZA, related to genetic polymorphism of the thiopurine methyl transferase (TPMT), serious toxic effects can result if inappropriate dose is administered.	Azathioprine	49-52	thiopurine S-methyltransferase	Homo sapiens	124-128
20953224-3	2010	AZA dosing according to patients TPMT status can reduce drug-induced morbidity and can be cost effective.	Azathioprine	0-3	thiopurine S-methyltransferase	Homo sapiens	33-37
20140691-7	2010	It is noticeable that serum IL-18 levels in the patients treated with glucocorticoids and cyclophosphamide was lower than those treated with glucocorticoids only or glucocorticoids and other immune inhibitors such as chloroquine/hydroxychloroquine and azathioprine.	Azathioprine	252-264	interleukin 18	Homo sapiens	28-33
20186929-12	2010	UC activity, anemia, and treatment with azathioprine negatively affected catalase.	Azathioprine	40-52	catalase	Homo sapiens	73-81
20434437-5	2010	In the present study, we studied the five known allelic variants of human glutathione transferase A2-2 (GST A2-2) (EC 2.5.1.18), abundantly expressed in liver and efficiently catalyzing the bioactivation of azathioprine to release 6-mercaptopurine.	Azathioprine	207-219	glutathione S-transferase alpha 2	Homo sapiens	104-112
20434437-6	2010	All five variants exhibited high activity with azathioprine, but allelic variant E of GST A2-2 displayed a 3-4-fold elevated catalytic efficiency compared to the other variants.	Azathioprine	47-59	glutathione S-transferase alpha 2	Homo sapiens	86-94
20434437-7	2010	High GST activity can lead to overproduction of 6-mercaptopurine, and the nature of the multiple forms of GSTs in a patient will obviously affect the metabolism of azathioprine.	Azathioprine	164-176	glutathione S-transferase alpha 2	Homo sapiens	106-110
20970593-11	2010	Different immunosuppressive agents have different risks of nonmelanoma skin cancer, as AZA increases the risk of SCC and MMF is a protective factor.	Azathioprine	87-90	serpin family B member 3	Homo sapiens	113-116
20814124-10	2010	Combination therapy with micro-emulsion form of cyclosporine A, prednisolone and azathioprine developed more UTI (P= 0.0418).	Azathioprine	81-93	alpha-1-microglobulin/bikunin precursor	Homo sapiens	109-112
20510207-5	2010	Moreover, increased transcription activity of c-Jun by the JNK activation contributed to the down-regulation of MDR1, thus indicating a central role of JNK signalling to suppress P-gp level in 5-Aza-treated Caki-1 cells.	Azathioprine	195-198	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	46-51
20510207-5	2010	Moreover, increased transcription activity of c-Jun by the JNK activation contributed to the down-regulation of MDR1, thus indicating a central role of JNK signalling to suppress P-gp level in 5-Aza-treated Caki-1 cells.	Azathioprine	195-198	mitogen-activated protein kinase 8	Homo sapiens	59-62
20510207-5	2010	Moreover, increased transcription activity of c-Jun by the JNK activation contributed to the down-regulation of MDR1, thus indicating a central role of JNK signalling to suppress P-gp level in 5-Aza-treated Caki-1 cells.	Azathioprine	195-198	ATP binding cassette subfamily B member 1	Homo sapiens	112-116
20510207-5	2010	Moreover, increased transcription activity of c-Jun by the JNK activation contributed to the down-regulation of MDR1, thus indicating a central role of JNK signalling to suppress P-gp level in 5-Aza-treated Caki-1 cells.	Azathioprine	195-198	mitogen-activated protein kinase 8	Homo sapiens	152-155
20510207-5	2010	Moreover, increased transcription activity of c-Jun by the JNK activation contributed to the down-regulation of MDR1, thus indicating a central role of JNK signalling to suppress P-gp level in 5-Aza-treated Caki-1 cells.	Azathioprine	195-198	ATP binding cassette subfamily B member 1	Homo sapiens	179-183
20367526-0	2010	Inosine triphosphate pyrophosphatase 94C&gt;A polymorphism: clinical implications for patients with systemic lupus erythematosus treated with azathioprine.	Azathioprine	142-154	inosine triphosphatase	Homo sapiens	0-36
19882154-4	2010	We demonstrate that in vitro exposure of freshly excised mouse tumors to DNA methyltransferase inhibitor 5-aza-2"-deoxycytidine (decitabine, AZA) results in selective elimination of tumor cells, but, surprisingly it also enriches CD45(+) tumor-infiltrated cells.	Azathioprine	141-144	protein tyrosine phosphatase, receptor type, C	Mus musculus	230-234
19882154-5	2010	The majority of "post-AZA" surviving CD45(+) tumor-infiltrated cells were represented by CD11b myeloid cells.	Azathioprine	22-25	protein tyrosine phosphatase receptor type C	Homo sapiens	37-41
19882154-5	2010	The majority of "post-AZA" surviving CD45(+) tumor-infiltrated cells were represented by CD11b myeloid cells.	Azathioprine	22-25	integrin subunit alpha M	Homo sapiens	89-94
19882154-6	2010	A culture of isolated tumor-infiltrated CD11b cells in the presence of AZA and GM-CSF promoted their differentiation into mature F4/80/CD11c/MHC class II-positive APCs.	Azathioprine	71-74	integrin subunit alpha M	Homo sapiens	40-45
19882154-6	2010	A culture of isolated tumor-infiltrated CD11b cells in the presence of AZA and GM-CSF promoted their differentiation into mature F4/80/CD11c/MHC class II-positive APCs.	Azathioprine	71-74	integrin subunit alpha X	Homo sapiens	135-140
20236031-9	2010	Thus inulin containing ES, EL and CAP (1:1:1) polymer-coated formulation system can be used for the targeted delivery of azathioprine with desired release pattern.	Azathioprine	121-133	cyclase associated actin cytoskeleton regulatory protein 1	Rattus norvegicus	34-44
19693669-2	2010	We aimed to evaluate the relationships between NOD2/CARD15 mutations, disease phenotype and age of CD diagnosis and response to medical treatment with systemic steroids, azathioprine (AZA) or 6-mercaptopurine (6-MP), and infliximab.	Azathioprine	170-182	nucleotide binding oligomerization domain containing 2	Homo sapiens	47-51
19693669-2	2010	We aimed to evaluate the relationships between NOD2/CARD15 mutations, disease phenotype and age of CD diagnosis and response to medical treatment with systemic steroids, azathioprine (AZA) or 6-mercaptopurine (6-MP), and infliximab.	Azathioprine	184-187	nucleotide binding oligomerization domain containing 2	Homo sapiens	47-51
19682085-2	2010	The aim of this study is to explore in patients with kidney transplantation whether AZA-related side effects can be explained by the inosine triphophate pyrophosphatase (ITPA) or thiopurine S-methyltransferase (TPMT) polymorphisms using both pheno-and genotyping.	Azathioprine	84-87	inosine triphosphatase	Homo sapiens	133-168
19682085-2	2010	The aim of this study is to explore in patients with kidney transplantation whether AZA-related side effects can be explained by the inosine triphophate pyrophosphatase (ITPA) or thiopurine S-methyltransferase (TPMT) polymorphisms using both pheno-and genotyping.	Azathioprine	84-87	inosine triphosphatase	Homo sapiens	170-174
19682085-2	2010	The aim of this study is to explore in patients with kidney transplantation whether AZA-related side effects can be explained by the inosine triphophate pyrophosphatase (ITPA) or thiopurine S-methyltransferase (TPMT) polymorphisms using both pheno-and genotyping.	Azathioprine	84-87	thiopurine S-methyltransferase	Homo sapiens	179-209
19682085-2	2010	The aim of this study is to explore in patients with kidney transplantation whether AZA-related side effects can be explained by the inosine triphophate pyrophosphatase (ITPA) or thiopurine S-methyltransferase (TPMT) polymorphisms using both pheno-and genotyping.	Azathioprine	84-87	thiopurine S-methyltransferase	Homo sapiens	211-215
19682085-13	2010	Patients with ITPA 94C&gt;A homozygous allele are at high risk to develop AZA-related gastrointestinal toxicity and flu-like symptoms (P &lt; 0.01).	Azathioprine	74-77	inosine triphosphatase	Homo sapiens	14-18
19682085-14	2010	TPMT wild-type/ITPA variant (homozygote) is closely related to the AZA-induced side effects (P &lt; 0.01).	Azathioprine	67-70	thiopurine S-methyltransferase	Homo sapiens	0-4
19682085-14	2010	TPMT wild-type/ITPA variant (homozygote) is closely related to the AZA-induced side effects (P &lt; 0.01).	Azathioprine	67-70	inosine triphosphatase	Homo sapiens	15-19
20413314-3	2010	Combination of ligand- and structure-based design resulted in heterocyclic substituted biphenylols and their aza-analogs as new 17beta-HSD1 inhibitors.	Azathioprine	109-112	hydroxysteroid 17-beta dehydrogenase 1	Homo sapiens	128-139
20367526-3	2010	Under AZA therapy, inosine triphosphate pyrophosphatase (ITPA) deficiency presumably leads to accumulation of unusual thioinosine metabolites with the potential for ADRs.	Azathioprine	6-9	inosine triphosphatase	Homo sapiens	19-55
20367526-3	2010	Under AZA therapy, inosine triphosphate pyrophosphatase (ITPA) deficiency presumably leads to accumulation of unusual thioinosine metabolites with the potential for ADRs.	Azathioprine	6-9	inosine triphosphatase	Homo sapiens	57-61
20367526-8	2010	In studies using higher doses, ITPA deficiency appears to increase the risk for AZA toxicity.	Azathioprine	80-83	inosine triphosphatase	Homo sapiens	31-35
20367526-10	2010	It is important to maintain the dose of AZA &lt; 1.5 mg/kg/day for Asian patients with ITPA 94A allele, with careful monitoring of the therapeutic efficacy.	Azathioprine	40-43	inosine triphosphatase	Homo sapiens	87-91
20216118-4	2010	The aim of this work was to investigate simultaneously individual 6-thioguanosine phosphate levels and NDPK activity in red blood cells (RBCs) of patients on azathioprine therapy.	Azathioprine	158-170	cytidine/uridine monophosphate kinase 2	Homo sapiens	103-107
28839543-2	2010	Pretreatment measurement of thiopurine methyltransferase (TPMT) activity is recommended and although conventional practice is to use a dose of 2 mg/kg AZA (1 mg/kg 6-MP), higher doses of 2.5 mg/kg AZA or more may be required in some patients, particularly if TPMT activity is high.	Azathioprine	151-154	thiopurine S-methyltransferase	Homo sapiens	58-62
28839543-2	2010	Pretreatment measurement of thiopurine methyltransferase (TPMT) activity is recommended and although conventional practice is to use a dose of 2 mg/kg AZA (1 mg/kg 6-MP), higher doses of 2.5 mg/kg AZA or more may be required in some patients, particularly if TPMT activity is high.	Azathioprine	197-200	thiopurine S-methyltransferase	Homo sapiens	58-62
20066544-3	2010	A genotypic assay, thiopurine S-methyltransferase (TPMT), has been developed that can potentially identify those at risk for developing leukopenia with azathioprine, and thereby limit its toxicity.	Azathioprine	152-164	thiopurine S-methyltransferase	Homo sapiens	19-49
20066544-3	2010	A genotypic assay, thiopurine S-methyltransferase (TPMT), has been developed that can potentially identify those at risk for developing leukopenia with azathioprine, and thereby limit its toxicity.	Azathioprine	152-164	thiopurine S-methyltransferase	Homo sapiens	51-55
20066544-4	2010	In those with abnormal TPMT activity, azathioprine can be started at lower dose or an alternate regimen selected.	Azathioprine	38-50	thiopurine S-methyltransferase	Homo sapiens	23-27
20066544-9	2010	TPMT testing before azathioprine, NAC, and steroids was the most effective and most costly strategy.	Azathioprine	20-32	thiopurine S-methyltransferase	Homo sapiens	0-4
19663853-0	2010	An audit of thiopurine methyltransferase genotyping and phenotyping before intended azathioprine treatment for dermatological conditions.	Azathioprine	84-96	thiopurine S-methyltransferase	Homo sapiens	12-40
19733946-4	2010	Remission was induced with prednisolone and intravenous cyclophosphamide, followed by maintenance therapy with azathioprine, during which MPO-ANCA results became negative.	Azathioprine	111-123	myeloperoxidase	Homo sapiens	138-141
19663853-2	2010	AIM: To evaluate the course of azathioprine treatment in people with TPMT heterozygosity and whether this deterred clinicians in prescribing the drug.	Azathioprine	31-43	thiopurine S-methyltransferase	Homo sapiens	69-73
19663853-3	2010	METHODS: This was a retrospective analysis on patients who had TPMT assays undertaken with the intention of treating their skin disorder with azathioprine.	Azathioprine	142-154	thiopurine S-methyltransferase	Homo sapiens	63-67
19663853-14	2010	CONCLUSIONS: TPMT heterozygosity was a deterring factor for the prescription of azathioprine in our department, and the dose for wild-type patients was lower than recommended guidelines.	Azathioprine	80-92	thiopurine S-methyltransferase	Homo sapiens	13-17
20408054-2	2010	Subjects with intermediate or no TPMT activity are at risk of azathioprines toxicity treated with conventional dosages of thiopurine drugs.	Azathioprine	62-75	thiopurine S-methyltransferase	Homo sapiens	33-37
20175817-2	2010	Genetic variations in thiopurine S-methyltranfarase (TPMT) gene have been correlated with enzyme activity and with the occurrence of adverse events to AZA and 6MP.	Azathioprine	151-154	thiopurine S-methyltransferase	Homo sapiens	22-51
19914375-5	2010	Furthermore, the ITPA 94C&gt;A [P32T] variant is associated with an increased risk of adverse drug reactions for patients treated with azathioprine.	Azathioprine	135-147	inosine triphosphatase	Homo sapiens	17-21
20175817-2	2010	Genetic variations in thiopurine S-methyltranfarase (TPMT) gene have been correlated with enzyme activity and with the occurrence of adverse events to AZA and 6MP.	Azathioprine	151-154	thiopurine S-methyltransferase	Homo sapiens	53-57
20175817-3	2010	The aim of the present study was to investigate the frequency of the functional TPMT polymorphisms and their association with the occurrence of adverse events during azathioprine therapy in a paediatric IBD cohort.	Azathioprine	166-178	thiopurine S-methyltransferase	Homo sapiens	80-84
20136357-1	2010	UNLABELLED: Thiopurine S-methyltransferase (TPMT) metabolizes thiopurine medications, including azathioprine and 6-mercaptopurine.	Azathioprine	96-108	thiopurine S-methyltransferase	Homo sapiens	12-42
20136357-1	2010	UNLABELLED: Thiopurine S-methyltransferase (TPMT) metabolizes thiopurine medications, including azathioprine and 6-mercaptopurine.	Azathioprine	96-108	thiopurine S-methyltransferase	Homo sapiens	44-48
19866449-9	2010	rPBC was associated independently with nonuse/discontinuation of azathioprine (P = 0.015, hazard ratio = 0.046, 95% confidence interval = 0.008-0.261).	Azathioprine	65-77	dihydrolipoamide S-acetyltransferase	Rattus norvegicus	0-4
20926883-12	2010	Strategies to reduce immunogenicity of anti-TNF agents include combination therapy with azathioprine and administration of a loading dose followed by systematic maintenance dosing.	Azathioprine	88-100	tumor necrosis factor	Homo sapiens	44-47
23136604-1	2010	Thiopurine S-methyltransferase (TPMT) catalyzes the S-methylation of aromatic and heterocyclic sulfhydryl compounds including thiopurine drugs such as 6-mercaptopurine, 6-thioguanine and azathioprine.	Azathioprine	187-199	thiopurine S-methyltransferase	Homo sapiens	0-30
23136604-1	2010	Thiopurine S-methyltransferase (TPMT) catalyzes the S-methylation of aromatic and heterocyclic sulfhydryl compounds including thiopurine drugs such as 6-mercaptopurine, 6-thioguanine and azathioprine.	Azathioprine	187-199	thiopurine S-methyltransferase	Homo sapiens	32-36
20120429-4	2010	This patient has remained clear for two years with this combination and has tolerated a tapering of the azathioprine from the initial dose of 250 mg. Etanercept is a recombinant human dimeric fusion protein which acts as a competitive inhibitor of TNF-alpha by binding to both soluble and receptor-bound molecules of TNF-alpha.	Azathioprine	104-116	tumor necrosis factor	Homo sapiens	248-257
19866449-11	2010	Cyclosporine or tacrolimus alone had no impact on rPBC, but cyclosporine with azathioprine was protective for rPBC in comparison with tacrolimus/azathioprine (0/18 versus 7/25, respectively; P &lt; 0.001).	Azathioprine	78-90	dihydrolipoamide S-acetyltransferase	Rattus norvegicus	110-114
19866449-13	2010	Azathioprine use in PBC patients who underwent transplantation was associated with less disease recurrence and a longer time to rPBC.	Azathioprine	0-12	dihydrolipoamide S-acetyltransferase	Rattus norvegicus	20-23
19866449-13	2010	Azathioprine use in PBC patients who underwent transplantation was associated with less disease recurrence and a longer time to rPBC.	Azathioprine	0-12	dihydrolipoamide S-acetyltransferase	Rattus norvegicus	128-132
19866449-14	2010	Tacrolimus or cyclosporine individually had no effect, but cyclosporine and azathioprine in combination resulted in the least rPBC.	Azathioprine	76-88	dihydrolipoamide S-acetyltransferase	Rattus norvegicus	126-130
19884213-10	2010	In the multivariate analysis, community-based infections associated with mucocutaneous, renal, or central nervous system disease activity as well as fever, and Mex-SLEDAI at admission and nosocomial infections to azathioprine use, infection at admission, disease duration, and hospitalization &gt;7 days.	Azathioprine	213-225	zinc finger SWIM-type containing 2	Homo sapiens	160-163
19542890-4	2009	Use of mycophenolate is superior when compared with azathioprine to allow for CNI reduction.	Azathioprine	52-64	calcineurin binding protein 1	Homo sapiens	78-81
21794679-1	2010	Male with diagnosis of Wegener"s granulomatosis associated to anti-proteinase 3 antibodies that improved initially to the treatment with high dose glucocorticoids and ciclophosphamide, but in a relapse he did not have good response to glucocorticoid treatment, ciclophosphamide, methotrexate nor azathioprine.	Azathioprine	296-308	proteinase 3	Homo sapiens	67-79
19917002-0	2009	Characterization of a novel TPMT mutation associated with azathioprine-induced myelosuppression.	Azathioprine	58-70	thiopurine S-methyltransferase	Homo sapiens	28-32
19445929-6	2009	In contrast, only minimal cTnT protein was found in 5-aza-treated cells.	Azathioprine	54-57	troponin T2, cardiac type	Rattus norvegicus	26-30
19500084-3	2009	Xanthine oxidase/dehydrogenase (XDH) and aldehyde oxidase (AO) compete with TPMT to inactivate AZA.	Azathioprine	95-98	xanthine dehydrogenase	Homo sapiens	0-30
19706768-4	2009	ANOVA and regression were performed to assess relationships among the frequency and spectra of HPRT mutations with disease, duration of illness, duration of treatment, and total therapeutic dose of azathioprine and 6-MP.	Azathioprine	198-210	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	95-99
19569070-0	2009	Fragmentation pathways of new aza derivatives of 16-membered macrolide antibiotic--analog of Josamycin investigated by ESI and FAB mass spectrometric methods.	Azathioprine	30-33	FA complementation group B	Homo sapiens	127-130
20151022-0	2009	A Stereodivergent Approach for Accessing Both C2,8a-Syn and C2,8a-Anti Relative Stereochemical Manifolds in the Lepadin Family via a TiCL(4)-Promoted Aza-[3 + 3] Annulation.	Azathioprine	150-153	synemin	Homo sapiens	52-55
19500084-3	2009	Xanthine oxidase/dehydrogenase (XDH) and aldehyde oxidase (AO) compete with TPMT to inactivate AZA.	Azathioprine	95-98	xanthine dehydrogenase	Homo sapiens	32-35
19500084-3	2009	Xanthine oxidase/dehydrogenase (XDH) and aldehyde oxidase (AO) compete with TPMT to inactivate AZA.	Azathioprine	95-98	aldehyde oxidase 1	Homo sapiens	41-57
19500084-3	2009	Xanthine oxidase/dehydrogenase (XDH) and aldehyde oxidase (AO) compete with TPMT to inactivate AZA.	Azathioprine	95-98	aldehyde oxidase 1	Homo sapiens	59-61
19500084-3	2009	Xanthine oxidase/dehydrogenase (XDH) and aldehyde oxidase (AO) compete with TPMT to inactivate AZA.	Azathioprine	95-98	thiopurine S-methyltransferase	Homo sapiens	76-80
19500084-4	2009	AIM: To assess whether genetic polymorphism in AOX1, XDH and MOCOS (the product of which activates the essential cofactor for AO and XDH) is associated with AZA treatment outcome in IBD.	Azathioprine	157-160	aldehyde oxidase 1	Homo sapiens	47-51
19500084-4	2009	AIM: To assess whether genetic polymorphism in AOX1, XDH and MOCOS (the product of which activates the essential cofactor for AO and XDH) is associated with AZA treatment outcome in IBD.	Azathioprine	157-160	molybdenum cofactor sulfurase	Homo sapiens	61-66
19500084-4	2009	AIM: To assess whether genetic polymorphism in AOX1, XDH and MOCOS (the product of which activates the essential cofactor for AO and XDH) is associated with AZA treatment outcome in IBD.	Azathioprine	157-160	aldehyde oxidase 1	Homo sapiens	47-49
19500084-4	2009	AIM: To assess whether genetic polymorphism in AOX1, XDH and MOCOS (the product of which activates the essential cofactor for AO and XDH) is associated with AZA treatment outcome in IBD.	Azathioprine	157-160	xanthine dehydrogenase	Homo sapiens	133-136
19500084-6	2009	RESULTS: Single nucleotide polymorphism AOX1 c.3404A &gt; G (Asn1135Ser, rs55754655) predicted lack of AZA response (P = 0.035, OR 2.54, 95%CI 1.06-6.13) and when combined with TPMT activity, this information allowed stratification of a patient"s chance of AZA response, ranging from 86% in patients where both markers were favourable to 33% where they were unfavourable (P &lt; 0.0001).	Azathioprine	103-106	aldehyde oxidase 1	Homo sapiens	40-44
19500084-6	2009	RESULTS: Single nucleotide polymorphism AOX1 c.3404A &gt; G (Asn1135Ser, rs55754655) predicted lack of AZA response (P = 0.035, OR 2.54, 95%CI 1.06-6.13) and when combined with TPMT activity, this information allowed stratification of a patient"s chance of AZA response, ranging from 86% in patients where both markers were favourable to 33% where they were unfavourable (P &lt; 0.0001).	Azathioprine	257-260	aldehyde oxidase 1	Homo sapiens	40-44
19223932-1	2009	Thiopurine S-methyltransferase (TPMT) is the rate-limiting step in the conversion of thiopurine drugs including azathioprine (AZA) to inactive metabolites.	Azathioprine	112-124	thiopurine S-methyltransferase	Homo sapiens	0-30
19223932-1	2009	Thiopurine S-methyltransferase (TPMT) is the rate-limiting step in the conversion of thiopurine drugs including azathioprine (AZA) to inactive metabolites.	Azathioprine	112-124	thiopurine S-methyltransferase	Homo sapiens	32-36
19223932-1	2009	Thiopurine S-methyltransferase (TPMT) is the rate-limiting step in the conversion of thiopurine drugs including azathioprine (AZA) to inactive metabolites.	Azathioprine	126-129	thiopurine S-methyltransferase	Homo sapiens	0-30
19223932-1	2009	Thiopurine S-methyltransferase (TPMT) is the rate-limiting step in the conversion of thiopurine drugs including azathioprine (AZA) to inactive metabolites.	Azathioprine	126-129	thiopurine S-methyltransferase	Homo sapiens	32-36
19223932-5	2009	There are some data that support routine TPMT testing before AZA prescribing for reducing AZA-related adverse events.	Azathioprine	90-93	thiopurine S-methyltransferase	Homo sapiens	41-45
19223932-6	2009	Key data include evidence in favor of TPMT testing in addition to the current practice of routine monitoring for reducing the number of AZA-related episodes of myelosuppression, averting deaths from neutropenic sepsis and improving health-related quality of life.	Azathioprine	136-139	thiopurine S-methyltransferase	Homo sapiens	38-42
19660010-4	2009	Our aim was to investigate if azathioprine-related myelosuppression is associated with TPMT polymorphism, which in turn affects its enzyme activity.	Azathioprine	30-42	thiopurine S-methyltransferase	Homo sapiens	87-91
19596925-4	2009	MATERIALS AND METHODS: Two MGMT hypermethylated Ch27 and H1355 lung cancer cell lines were treated with or without 17beta-estradiol and the status of hypermethylation was examined by methylated specific methylation (MSP) as compared with both cells treated with demethylating agents, 5-AZA-dC (AZA) or TSA.	Azathioprine	286-289	O-6-methylguanine-DNA methyltransferase	Homo sapiens	27-31
19596925-5	2009	RESULTS: Our data showed that 17beta-estradiol, similar to AZA, diminished the MGMT hypermethylation and restored MGMT mRNA expression, which was not observed in the case of TSA.	Azathioprine	59-62	O-6-methylguanine-DNA methyltransferase	Homo sapiens	79-83
19596925-5	2009	RESULTS: Our data showed that 17beta-estradiol, similar to AZA, diminished the MGMT hypermethylation and restored MGMT mRNA expression, which was not observed in the case of TSA.	Azathioprine	59-62	O-6-methylguanine-DNA methyltransferase	Homo sapiens	114-118
19392869-2	2009	AIM: To review systematically the efficacy of azathioprine (AZA) and mercaptopurine (MP) in UC, and to conduct a meta-analysis of randomized clinical trials evaluating the efficacy of AZA/MP for the induction or maintenance of UC clinical remission.	Azathioprine	46-58	azurocidin 1	Homo sapiens	60-63
19477696-1	2009	Thiopurine S-methyltransferase (TPMT) catalyzes methylation of thiopurine drugs (e.g. 6-mercaptopurine, azathioprine).	Azathioprine	104-116	thiopurine S-methyltransferase	Homo sapiens	0-30
19695401-0	2009	Impact of the heterozygous TPMT*1/*3C genotype on azathioprine-induced myelosuppression in kidney transplant recipients in Thailand.	Azathioprine	50-62	thiopurine S-methyltransferase	Homo sapiens	27-31
19695401-1	2009	BACKGROUND: Thiopurine S-methyltransferase (TPMT) is a polymorphic enzyme associated with detoxification of azathioprine, an immunosuppressant used after renal transplantation in several Asian countries.	Azathioprine	108-120	thiopurine S-methyltransferase	Homo sapiens	12-42
19695401-1	2009	BACKGROUND: Thiopurine S-methyltransferase (TPMT) is a polymorphic enzyme associated with detoxification of azathioprine, an immunosuppressant used after renal transplantation in several Asian countries.	Azathioprine	108-120	thiopurine S-methyltransferase	Homo sapiens	44-48
19695401-4	2009	OBJECTIVE: The aim of this study was to assess the impact of the heterozygous TPMT*1/*3C genotype on azathioprine-induced myelosuppression in kidney transplant recipients in Thailand.	Azathioprine	101-113	thiopurine S-methyltransferase	Homo sapiens	78-82
19695401-14	2009	The risk for azathioprine-induced myelosuppression in the patients with the heterozygous TPMT*1/*3C genotype was significantly higher than that in patients with the wild-type genotype (adjusted OR, 14.18 [95% CI, 3.07-65.40]; P &lt; 0.005).	Azathioprine	13-25	thiopurine S-methyltransferase	Homo sapiens	89-93
19695401-15	2009	The sensitivity and specificity of TPMT*3C genotyping for the prediction of azathioprine-induced myelosuppression in these kidney transplant recipients were 27% and 97%, respectively.	Azathioprine	76-88	thiopurine S-methyltransferase	Homo sapiens	35-39
19695401-17	2009	CONCLUSION: In these kidney transplant recipients, patients who carried the TPMT*3C allele were at a higher risk for azathioprine-induced myelosuppression than noncarriers.	Azathioprine	117-129	thiopurine S-methyltransferase	Homo sapiens	76-80
19477696-1	2009	Thiopurine S-methyltransferase (TPMT) catalyzes methylation of thiopurine drugs (e.g. 6-mercaptopurine, azathioprine).	Azathioprine	104-116	thiopurine S-methyltransferase	Homo sapiens	32-36
19485949-11	2009	On the first post-transplant day CrCl was higher in AZA group (24,3+/-10 vs. 17,5+/-7,3; p=0,01), next six days situation is reversed CrCl is significantly higher in the MMF group (43,7+/-15 vs. 53, 4+/-22, 8 p=0,006).	Azathioprine	52-55	CRCL	Homo sapiens	33-37
19584951-8	2009	Prednisone and azathioprine treatment decreased total serum IgG, IgE, IFN-gamma and IL-4 levels, and blood CD19+ and CD23+ cells; however serum IL-12, TNFalpha and blood CD4+ T cells increased with treatment.	Azathioprine	15-27	immunoglobulin heavy constant epsilon	Homo sapiens	65-68
19584951-8	2009	Prednisone and azathioprine treatment decreased total serum IgG, IgE, IFN-gamma and IL-4 levels, and blood CD19+ and CD23+ cells; however serum IL-12, TNFalpha and blood CD4+ T cells increased with treatment.	Azathioprine	15-27	interferon gamma	Homo sapiens	70-79
19584951-8	2009	Prednisone and azathioprine treatment decreased total serum IgG, IgE, IFN-gamma and IL-4 levels, and blood CD19+ and CD23+ cells; however serum IL-12, TNFalpha and blood CD4+ T cells increased with treatment.	Azathioprine	15-27	interleukin 4	Homo sapiens	84-88
19584951-8	2009	Prednisone and azathioprine treatment decreased total serum IgG, IgE, IFN-gamma and IL-4 levels, and blood CD19+ and CD23+ cells; however serum IL-12, TNFalpha and blood CD4+ T cells increased with treatment.	Azathioprine	15-27	CD19 molecule	Homo sapiens	107-111
19584951-8	2009	Prednisone and azathioprine treatment decreased total serum IgG, IgE, IFN-gamma and IL-4 levels, and blood CD19+ and CD23+ cells; however serum IL-12, TNFalpha and blood CD4+ T cells increased with treatment.	Azathioprine	15-27	Fc epsilon receptor II	Homo sapiens	117-121
19584951-8	2009	Prednisone and azathioprine treatment decreased total serum IgG, IgE, IFN-gamma and IL-4 levels, and blood CD19+ and CD23+ cells; however serum IL-12, TNFalpha and blood CD4+ T cells increased with treatment.	Azathioprine	15-27	tumor necrosis factor	Homo sapiens	151-159
19167267-2	2009	L is a 30-membered [N(10)] macrocycle with tetraamide functions bind metal ions through aza donors forming hexa-coordinate geometry.	Azathioprine	88-91	hexosaminidase subunit alpha	Homo sapiens	107-111
19682195-2	2009	We examined polymorphism of the thiopurine S-methyltransferase (TPMT) gene to determine whether the TPMT genotype would be a predictive marker for the development of adverse reactions to AZA.	Azathioprine	187-190	thiopurine S-methyltransferase	Homo sapiens	32-62
19682195-2	2009	We examined polymorphism of the thiopurine S-methyltransferase (TPMT) gene to determine whether the TPMT genotype would be a predictive marker for the development of adverse reactions to AZA.	Azathioprine	187-190	thiopurine S-methyltransferase	Homo sapiens	64-68
19682195-2	2009	We examined polymorphism of the thiopurine S-methyltransferase (TPMT) gene to determine whether the TPMT genotype would be a predictive marker for the development of adverse reactions to AZA.	Azathioprine	187-190	thiopurine S-methyltransferase	Homo sapiens	100-104
19682195-14	2009	The incidence of adverse reactions to AZA was high, even in patients carrying wild-type TPMT.	Azathioprine	38-41	thiopurine S-methyltransferase	Homo sapiens	88-92
19218878-11	2009	Indeed, demethylation with 5-Aza-2"-deoxycytidine (Aza) resulted in upregulation of EpoR mRNA.	Azathioprine	29-32	erythropoietin receptor	Homo sapiens	84-88
19404953-6	2009	RESULTS: Based on the mean-mean common or the mean-max CIMT as the dependent variable, univariable analysis showed significant associations of the following variables with increased CIMT: increasing age, longer SLE duration, minority status, higher body mass index (BMI), male sex, increased creatinine clearance, higher lipoprotein(a) level, proteinuria, azathioprine treatment, and prednisone dose.	Azathioprine	356-368	CIMT	Homo sapiens	182-186
19404953-7	2009	In multivariable modeling, both azathioprine use (P=0.005 for the mean-mean model and P=0.102 for the mean-max model) and male sex (P&lt;0.001) were associated with increases in the mean-max CIMT.	Azathioprine	32-44	CIMT	Homo sapiens	191-195
19404953-11	2009	Azathioprine treatment was associated with increased CIMT.	Azathioprine	0-12	CIMT	Homo sapiens	53-57
19485949-11	2009	On the first post-transplant day CrCl was higher in AZA group (24,3+/-10 vs. 17,5+/-7,3; p=0,01), next six days situation is reversed CrCl is significantly higher in the MMF group (43,7+/-15 vs. 53, 4+/-22, 8 p=0,006).	Azathioprine	52-55	CRCL	Homo sapiens	134-138
19381059-8	2009	With the treatment with antibiotics, 5-aminosalicylic acid, steroid, and azathioprine, as a whole, decreasing pattern and intermittent fine coordinated fluctuation of the levels of amylase and lipase along with the decrease of Crohn"s disease activity index (CDAI) and the CRP levels were observed.	Azathioprine	73-85	C-reactive protein	Homo sapiens	273-276
19129747-0	2009	Pro32Thr polymorphism of inosine triphosphate pyrophosphatase gene predicts efficacy of low-dose azathioprine for patients with systemic lupus erythematosus.	Azathioprine	97-109	inosine triphosphatase	Homo sapiens	25-61
19129747-1	2009	We evaluated the relationship between the efficacy of low-dose azathioprine (AZA) therapy and the inosine triphosphate pyrophosphatase (ITPA) 94C&gt;A (Pro32Thr) polymorphism in patients with systemic lupus erythematosus (SLE).	Azathioprine	63-75	inosine triphosphatase	Homo sapiens	98-134
19129747-1	2009	We evaluated the relationship between the efficacy of low-dose azathioprine (AZA) therapy and the inosine triphosphate pyrophosphatase (ITPA) 94C&gt;A (Pro32Thr) polymorphism in patients with systemic lupus erythematosus (SLE).	Azathioprine	63-75	inosine triphosphatase	Homo sapiens	136-140
19129747-1	2009	We evaluated the relationship between the efficacy of low-dose azathioprine (AZA) therapy and the inosine triphosphate pyrophosphatase (ITPA) 94C&gt;A (Pro32Thr) polymorphism in patients with systemic lupus erythematosus (SLE).	Azathioprine	77-80	inosine triphosphatase	Homo sapiens	98-134
19129747-1	2009	We evaluated the relationship between the efficacy of low-dose azathioprine (AZA) therapy and the inosine triphosphate pyrophosphatase (ITPA) 94C&gt;A (Pro32Thr) polymorphism in patients with systemic lupus erythematosus (SLE).	Azathioprine	77-80	inosine triphosphatase	Homo sapiens	136-140
19229528-0	2009	TPMT but not ITPA gene polymorphism influences the risk of azathioprine intolerance in renal transplant recipients.	Azathioprine	59-71	thiopurine S-methyltransferase	Homo sapiens	0-4
19229528-3	2009	METHODS: The aim of the current study was to evaluate an association between TPMT and ITPA gene polymorphisms and drug intolerance in a cohort of 157 renal transplant recipients treated with azathioprine (AZA).	Azathioprine	191-203	thiopurine S-methyltransferase	Homo sapiens	77-81
19229528-3	2009	METHODS: The aim of the current study was to evaluate an association between TPMT and ITPA gene polymorphisms and drug intolerance in a cohort of 157 renal transplant recipients treated with azathioprine (AZA).	Azathioprine	191-203	inosine triphosphatase	Homo sapiens	86-90
19229528-3	2009	METHODS: The aim of the current study was to evaluate an association between TPMT and ITPA gene polymorphisms and drug intolerance in a cohort of 157 renal transplant recipients treated with azathioprine (AZA).	Azathioprine	205-208	thiopurine S-methyltransferase	Homo sapiens	77-81
19229528-3	2009	METHODS: The aim of the current study was to evaluate an association between TPMT and ITPA gene polymorphisms and drug intolerance in a cohort of 157 renal transplant recipients treated with azathioprine (AZA).	Azathioprine	205-208	inosine triphosphatase	Homo sapiens	86-90
19229528-5	2009	RESULTS: Mean AZA dose, mean white-blood-cell count, and platelet count in the course of treatment were lower in carriers of variant TPMT alleles compared to patients with TPMT wild-type genotype.	Azathioprine	14-17	thiopurine S-methyltransferase	Homo sapiens	133-137
19229528-8	2009	CONCLUSIONS: Our results suggest that routine genotyping of renal transplant recipients for TPMT variants may be useful in reducing the risk of AZA-related myelotoxicity, but there is not enough evidence to introduce ITPA testing into clinical practice.	Azathioprine	144-147	thiopurine S-methyltransferase	Homo sapiens	92-96
19675376-1	2009	BACKGROUND &amp; OBJECTIVE: Mercaptopurine, azathioprine, and thioguanine, used as antineoplastic agents and immunosuppressants are catabolized by thiopurine methyltransferase (TPMT) enzyme, which exhibits genetic polymorphism.	Azathioprine	44-56	thiopurine S-methyltransferase	Homo sapiens	147-175
19675376-1	2009	BACKGROUND &amp; OBJECTIVE: Mercaptopurine, azathioprine, and thioguanine, used as antineoplastic agents and immunosuppressants are catabolized by thiopurine methyltransferase (TPMT) enzyme, which exhibits genetic polymorphism.	Azathioprine	44-56	thiopurine S-methyltransferase	Homo sapiens	177-181
19473575-2	2009	The aim of the present study was to evaluate the prevalence of TPMT genetic polymorphisms in a cohort of Italian Caucasian patients affected by rheumatic diseases and treated with AZA, and to establish correlations with the tolerability of AZA treatment.	Azathioprine	180-183	thiopurine S-methyltransferase	Homo sapiens	63-67
19013015-3	2009	Treatment with AZA followed by co-administration of TSA plus tamoxifen resulted in the greatest ER re-expression and tamoxifen sensitivity, although sensitivity was not increased as robustly as expected.	Azathioprine	15-18	estrogen receptor 1	Homo sapiens	96-98
19300195-8	2009	Discontinuation of AZA or MMF resulted in significant increased numbers of third-party (P=0.003) and tetanus toxoid-reactive (P=0.008) IL-10 producing cells, and a trend in higher numbers of donor-reactive IL-10 producing cells (P=0.06).	Azathioprine	19-22	interleukin 10	Homo sapiens	135-140
19300195-8	2009	Discontinuation of AZA or MMF resulted in significant increased numbers of third-party (P=0.003) and tetanus toxoid-reactive (P=0.008) IL-10 producing cells, and a trend in higher numbers of donor-reactive IL-10 producing cells (P=0.06).	Azathioprine	19-22	interleukin 10	Homo sapiens	206-211
19300195-10	2009	CONCLUSIONS: In HLA-identical LR renal transplant recipients, therapy with AZA and MMF suppress the IL-10 production and the maturation of DC.	Azathioprine	75-78	interleukin 10	Homo sapiens	100-105
19473575-2	2009	The aim of the present study was to evaluate the prevalence of TPMT genetic polymorphisms in a cohort of Italian Caucasian patients affected by rheumatic diseases and treated with AZA, and to establish correlations with the tolerability of AZA treatment.	Azathioprine	240-243	thiopurine S-methyltransferase	Homo sapiens	63-67
19028832-2	2009	OBJECTIVE: We wanted to test whether immunosuppression with cyclic methylprednisolone (MP) in combination with azathioprine (AZA) for 6 months accelerates recovery of IFN-beta bioactivity in patients with multiple sclerosis (MS) with abolished in-vivo myxovirus resistance protein A (MxA) mRNA response to IFN-beta.	Azathioprine	111-123	interferon beta 1	Homo sapiens	167-175
19048245-0	2009	Relationships between thiopurine S-methyltransferase polymorphism and azathioprine-related adverse drug reactions in Chinese renal transplant recipients.	Azathioprine	70-82	thiopurine S-methyltransferase	Homo sapiens	22-52
19048245-1	2009	OBJECTIVE: To systematically investigate the relationships between thiopurine S-methyltransferase (TPMT) polymorphisms and azathioprine-related adverse drug reactions in patients with kidney transplantation.	Azathioprine	123-135	thiopurine S-methyltransferase	Homo sapiens	67-97
19048245-1	2009	OBJECTIVE: To systematically investigate the relationships between thiopurine S-methyltransferase (TPMT) polymorphisms and azathioprine-related adverse drug reactions in patients with kidney transplantation.	Azathioprine	123-135	thiopurine S-methyltransferase	Homo sapiens	99-103
19048245-12	2009	AZA-induced hematotoxicity is related to the reduced TPMT activity.	Azathioprine	0-3	thiopurine S-methyltransferase	Homo sapiens	53-57
19028832-2	2009	OBJECTIVE: We wanted to test whether immunosuppression with cyclic methylprednisolone (MP) in combination with azathioprine (AZA) for 6 months accelerates recovery of IFN-beta bioactivity in patients with multiple sclerosis (MS) with abolished in-vivo myxovirus resistance protein A (MxA) mRNA response to IFN-beta.	Azathioprine	125-128	interferon beta 1	Homo sapiens	167-175
19026728-7	2009	In vivo, DNA demethylation experiments performed by treating human embryonic kidney (HEK293) cells with 5-Aza-2-deoxycytidine (Aza) revealed that endogenous yy2 expression is more than 3-fold enhanced whereas the mbtps2 level appears unaffected.	Azathioprine	106-109	YY2 transcription factor	Homo sapiens	157-160
19037090-3	2009	In studies of the mechanistic basis for the selective expression of FPR in more highly malignant gliomas, we found that the DNA methyltransferase inhibitor 5-Aza-2"-deoxycytidine (Aza), while promoting the differentiation of human glioblastoma cells, downregulated FPR expression.	Azathioprine	158-161	formyl peptide receptor 1	Homo sapiens	68-71
19037090-4	2009	Aza also reduced the global methylation levels in glioblastoma cells and activated the pathway of p53 tumor suppressor.	Azathioprine	0-3	tumor protein p53	Homo sapiens	98-101
19037090-5	2009	Methylation-specific polymerase chain reaction revealed that Aza treatment of tumor cells reduced the methylation of p53 promoter, which was accompanied by increased expression of p53 gene and protein.	Azathioprine	61-64	tumor protein p53	Homo sapiens	117-120
19037090-5	2009	Methylation-specific polymerase chain reaction revealed that Aza treatment of tumor cells reduced the methylation of p53 promoter, which was accompanied by increased expression of p53 gene and protein.	Azathioprine	61-64	tumor protein p53	Homo sapiens	180-183
19037090-6	2009	In addition, overexpression of p53 in glioblastoma cells mimicked the effect of Aza treatment as shown by increased cell differentiation but reduction in FPR expression, the capacity of tumor sphere formation in soft agar and tumorigenesis in nude mice.	Azathioprine	80-83	transformation related protein 53, pseudogene	Mus musculus	31-34
19037090-6	2009	In addition, overexpression of p53 in glioblastoma cells mimicked the effect of Aza treatment as shown by increased cell differentiation but reduction in FPR expression, the capacity of tumor sphere formation in soft agar and tumorigenesis in nude mice.	Azathioprine	80-83	formyl peptide receptor 1	Mus musculus	154-157
19037090-7	2009	Furthermore, Aza treatment or overexpression of the wild-type p53 in glioblastoma cells increased the binding of p53 to FPR promoter region shown by chromatin immunoprecipitation.	Azathioprine	13-16	tumor protein p53	Homo sapiens	113-116
19037090-7	2009	Furthermore, Aza treatment or overexpression of the wild-type p53 in glioblastoma cells increased the binding of p53 to FPR promoter region shown by chromatin immunoprecipitation.	Azathioprine	13-16	formyl peptide receptor 1	Homo sapiens	120-123
19363997-8	2009	Regarding the treatment of NMO, there are refractory patients which can be treated with interferon beta, so immunosuppressive agents such as low-dose oral prednisolone and/or azathioprine reduce the rate of relapse, while, unlike in MS, the therapeutic efficacy of interferon beta is unclear in NMO.	Azathioprine	175-187	interferon beta 1	Homo sapiens	88-103
19363997-8	2009	Regarding the treatment of NMO, there are refractory patients which can be treated with interferon beta, so immunosuppressive agents such as low-dose oral prednisolone and/or azathioprine reduce the rate of relapse, while, unlike in MS, the therapeutic efficacy of interferon beta is unclear in NMO.	Azathioprine	175-187	interferon beta 1	Homo sapiens	265-280
19217567-0	2009	[Optimising azathioprine treatment: determination of thiopurine methyltransferase activity and thiopurine metabolites].	Azathioprine	12-24	thiopurine S-methyltransferase	Homo sapiens	53-81
19217567-1	2009	INTRODUCTION: Individualised doses of azathioprine (AZA) may be prescribed by monitoring the levels of the enzyme thiopurine methyltransferase (TPMT).	Azathioprine	38-50	thiopurine S-methyltransferase	Homo sapiens	114-142
19217567-1	2009	INTRODUCTION: Individualised doses of azathioprine (AZA) may be prescribed by monitoring the levels of the enzyme thiopurine methyltransferase (TPMT).	Azathioprine	38-50	thiopurine S-methyltransferase	Homo sapiens	144-148
19217567-1	2009	INTRODUCTION: Individualised doses of azathioprine (AZA) may be prescribed by monitoring the levels of the enzyme thiopurine methyltransferase (TPMT).	Azathioprine	52-55	thiopurine S-methyltransferase	Homo sapiens	114-142
19217567-1	2009	INTRODUCTION: Individualised doses of azathioprine (AZA) may be prescribed by monitoring the levels of the enzyme thiopurine methyltransferase (TPMT).	Azathioprine	52-55	thiopurine S-methyltransferase	Homo sapiens	144-148
19217567-12	2009	CONCLUSIONS: Determination of TPMT and monitoring of thiopurine metabolites allows AZA treatment to be optimised, although further studies are necessary to establish therapeutic effectiveness and toxicity ranges.	Azathioprine	83-86	thiopurine S-methyltransferase	Homo sapiens	30-34
19252404-8	2009	Exons of the TPMT gene from patients who suffered from azathioprine-induced toxicity were amplified and sequenced to detect TPMT mutations.	Azathioprine	55-67	thiopurine S-methyltransferase	Homo sapiens	13-17
19543639-1	2009	BACKGROUND: Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that catalyzes the S-methylation of 6-mercaptopurine and azathioprine.	Azathioprine	129-141	thiopurine S-methyltransferase	Homo sapiens	12-42
19543639-1	2009	BACKGROUND: Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that catalyzes the S-methylation of 6-mercaptopurine and azathioprine.	Azathioprine	129-141	thiopurine S-methyltransferase	Homo sapiens	44-48
19117405-5	2009	Promoter methylation analysis was examined for those protein spots showing significant alterations, and our results revealed that specific genes, such as aldehyde dehydrogenase 1 (ALDH1), can be hypomethylated by HBx, and two calcium ion-binding proteins, S100A6 and S100A4, were hypermethylated by HBx and could be re-expressed by AZA (DNA methylase inhibitor) treatment.	Azathioprine	332-335	aldehyde dehydrogenase 1 family member A1	Homo sapiens	154-178
19117405-5	2009	Promoter methylation analysis was examined for those protein spots showing significant alterations, and our results revealed that specific genes, such as aldehyde dehydrogenase 1 (ALDH1), can be hypomethylated by HBx, and two calcium ion-binding proteins, S100A6 and S100A4, were hypermethylated by HBx and could be re-expressed by AZA (DNA methylase inhibitor) treatment.	Azathioprine	332-335	aldehyde dehydrogenase 1 family member A1	Homo sapiens	180-185
19117405-5	2009	Promoter methylation analysis was examined for those protein spots showing significant alterations, and our results revealed that specific genes, such as aldehyde dehydrogenase 1 (ALDH1), can be hypomethylated by HBx, and two calcium ion-binding proteins, S100A6 and S100A4, were hypermethylated by HBx and could be re-expressed by AZA (DNA methylase inhibitor) treatment.	Azathioprine	332-335	S100 calcium binding protein A6	Homo sapiens	256-262
19117405-5	2009	Promoter methylation analysis was examined for those protein spots showing significant alterations, and our results revealed that specific genes, such as aldehyde dehydrogenase 1 (ALDH1), can be hypomethylated by HBx, and two calcium ion-binding proteins, S100A6 and S100A4, were hypermethylated by HBx and could be re-expressed by AZA (DNA methylase inhibitor) treatment.	Azathioprine	332-335	S100 calcium binding protein A4	Homo sapiens	267-273
19117405-5	2009	Promoter methylation analysis was examined for those protein spots showing significant alterations, and our results revealed that specific genes, such as aldehyde dehydrogenase 1 (ALDH1), can be hypomethylated by HBx, and two calcium ion-binding proteins, S100A6 and S100A4, were hypermethylated by HBx and could be re-expressed by AZA (DNA methylase inhibitor) treatment.	Azathioprine	332-335	X protein	Hepatitis B virus	299-302
19236780-3	2009	FVIII inhibitor in the patient"s serum was at a level &gt;32.0 Bethesda units/ml after acquired hemophilia was diagnosed, the patient was admitted to hospital and given orally prednisone and azathioprine therapy.	Azathioprine	191-203	coagulation factor VIII	Homo sapiens	0-5
21475797-8	2009	We further checked the cytostatic effect of statins in combination with azathioprine, a compound that specifically blocks Rac1 activation.	Azathioprine	72-84	Rac family small GTPase 1	Mus musculus	122-126
19214663-3	2009	METHODS: Gene mutations of TPMT and ITPA, the major AZA/6-MP -metabolizing enzymes, were investigated retrospectively in 16 Japanese patients with inflammatory bowel disease (IBD) in whom AZA/6MP treatment induced adverse reactions.	Azathioprine	52-56	thiopurine S-methyltransferase	Homo sapiens	27-31
19214663-3	2009	METHODS: Gene mutations of TPMT and ITPA, the major AZA/6-MP -metabolizing enzymes, were investigated retrospectively in 16 Japanese patients with inflammatory bowel disease (IBD) in whom AZA/6MP treatment induced adverse reactions.	Azathioprine	52-56	inosine triphosphatase	Homo sapiens	36-40
19214663-3	2009	METHODS: Gene mutations of TPMT and ITPA, the major AZA/6-MP -metabolizing enzymes, were investigated retrospectively in 16 Japanese patients with inflammatory bowel disease (IBD) in whom AZA/6MP treatment induced adverse reactions.	Azathioprine	52-55	thiopurine S-methyltransferase	Homo sapiens	27-31
19214663-3	2009	METHODS: Gene mutations of TPMT and ITPA, the major AZA/6-MP -metabolizing enzymes, were investigated retrospectively in 16 Japanese patients with inflammatory bowel disease (IBD) in whom AZA/6MP treatment induced adverse reactions.	Azathioprine	52-55	inosine triphosphatase	Homo sapiens	36-40
19214663-8	2009	CONCLUSIONS: It is suggested that the ITPA gene mutation is closely related to the adverse reactions of AZA/6-MP in Japanese patients, and screening for the mutant allele is useful for predicting the most serious adverse reactions, agranulocytosis and acute bone marrow suppression.	Azathioprine	104-107	inosine triphosphatase	Homo sapiens	38-42
19214663-0	2009	Thiopurine S-methyltransferase and inosine triphosphate pyrophosphohydrolase genes in Japanese patients with inflammatory bowel disease in whom adverse drug reactions were induced by azathioprine/6-mercaptopurine treatment.	Azathioprine	183-195	thiopurine S-methyltransferase	Homo sapiens	0-30
19214663-0	2009	Thiopurine S-methyltransferase and inosine triphosphate pyrophosphohydrolase genes in Japanese patients with inflammatory bowel disease in whom adverse drug reactions were induced by azathioprine/6-mercaptopurine treatment.	Azathioprine	183-195	inosine triphosphatase	Homo sapiens	35-76
19214663-1	2009	BACKGROUND: The main cause of azathioprine (AZA)/6-mercaptopurine (6MP)-induced adverse reactions is a reduction in the activities of the metabolizing enzymes thiopurine S-methyltransferase (TPMT) and inosine triphosphate pyrophosphohydrolase (ITPA).	Azathioprine	30-42	thiopurine S-methyltransferase	Homo sapiens	159-189
19214663-1	2009	BACKGROUND: The main cause of azathioprine (AZA)/6-mercaptopurine (6MP)-induced adverse reactions is a reduction in the activities of the metabolizing enzymes thiopurine S-methyltransferase (TPMT) and inosine triphosphate pyrophosphohydrolase (ITPA).	Azathioprine	30-42	thiopurine S-methyltransferase	Homo sapiens	191-195
19214663-1	2009	BACKGROUND: The main cause of azathioprine (AZA)/6-mercaptopurine (6MP)-induced adverse reactions is a reduction in the activities of the metabolizing enzymes thiopurine S-methyltransferase (TPMT) and inosine triphosphate pyrophosphohydrolase (ITPA).	Azathioprine	30-42	inosine triphosphatase	Homo sapiens	201-242
19214663-1	2009	BACKGROUND: The main cause of azathioprine (AZA)/6-mercaptopurine (6MP)-induced adverse reactions is a reduction in the activities of the metabolizing enzymes thiopurine S-methyltransferase (TPMT) and inosine triphosphate pyrophosphohydrolase (ITPA).	Azathioprine	30-42	inosine triphosphatase	Homo sapiens	244-248
19214663-1	2009	BACKGROUND: The main cause of azathioprine (AZA)/6-mercaptopurine (6MP)-induced adverse reactions is a reduction in the activities of the metabolizing enzymes thiopurine S-methyltransferase (TPMT) and inosine triphosphate pyrophosphohydrolase (ITPA).	Azathioprine	44-47	thiopurine S-methyltransferase	Homo sapiens	159-189
19214663-1	2009	BACKGROUND: The main cause of azathioprine (AZA)/6-mercaptopurine (6MP)-induced adverse reactions is a reduction in the activities of the metabolizing enzymes thiopurine S-methyltransferase (TPMT) and inosine triphosphate pyrophosphohydrolase (ITPA).	Azathioprine	44-47	thiopurine S-methyltransferase	Homo sapiens	191-195
19214663-1	2009	BACKGROUND: The main cause of azathioprine (AZA)/6-mercaptopurine (6MP)-induced adverse reactions is a reduction in the activities of the metabolizing enzymes thiopurine S-methyltransferase (TPMT) and inosine triphosphate pyrophosphohydrolase (ITPA).	Azathioprine	44-47	inosine triphosphatase	Homo sapiens	201-242
19214663-1	2009	BACKGROUND: The main cause of azathioprine (AZA)/6-mercaptopurine (6MP)-induced adverse reactions is a reduction in the activities of the metabolizing enzymes thiopurine S-methyltransferase (TPMT) and inosine triphosphate pyrophosphohydrolase (ITPA).	Azathioprine	44-47	inosine triphosphatase	Homo sapiens	244-248
18854826-0	2008	PTCH mutations in basal cell carcinomas from azathioprine-treated organ transplant recipients.	Azathioprine	45-57	patched 1	Homo sapiens	0-4
29783387-0	2009	TPMT testing in azathioprine: a "cost-effective use of healthcare resources"?	Azathioprine	16-28	thiopurine S-methyltransferase	Homo sapiens	0-4
29783387-1	2009	This study aimed to critically appraise the current level of economic evidence available for thiopurine S-methyltransferase (TPMT) testing of thiopurine drugs, such as azathioprine.	Azathioprine	168-180	thiopurine S-methyltransferase	Homo sapiens	93-123
29783387-1	2009	This study aimed to critically appraise the current level of economic evidence available for thiopurine S-methyltransferase (TPMT) testing of thiopurine drugs, such as azathioprine.	Azathioprine	168-180	thiopurine S-methyltransferase	Homo sapiens	125-129
18793759-4	2008	Using the hOGG1 comet assay, we herein demonstrate high levels of 8-oxodG and alkali-labile sites (ALS) in cells treated with biologically relevant doses of 6-TG, or Aza, plus UVA.	Azathioprine	166-169	8-oxoguanine DNA glycosylase	Homo sapiens	10-15
18703291-7	2008	An analogue of a metabolite of azathioprine (ESP) was evaluated for antiviral activity against these two viral strains.	Azathioprine	31-43	protein tyrosine phosphatase receptor type V, pseudogene	Homo sapiens	45-48
18703291-9	2008	Since ESP is an analogue of the active metabolite of azathioprine, which exhibits positive outcomes when administered to MS patients, we submit that this metabolite is acting on MSMV, in a similar fashion to the action of ESP on MV-H.	Azathioprine	53-65	protein tyrosine phosphatase receptor type V, pseudogene	Homo sapiens	6-9
18703291-9	2008	Since ESP is an analogue of the active metabolite of azathioprine, which exhibits positive outcomes when administered to MS patients, we submit that this metabolite is acting on MSMV, in a similar fashion to the action of ESP on MV-H.	Azathioprine	53-65	protein tyrosine phosphatase receptor type V, pseudogene	Homo sapiens	222-225
18854826-8	2008	This study of post-transplant BCC provides the first indication that azathioprine exposure may be associated with PTCH mutations, particularly in tumours from non-sun-exposed skin.	Azathioprine	69-81	patched 1	Homo sapiens	114-118
20027160-0	2009	Importance of thiopurine S-Methyltransferase gene polymorphisms for prediction of azathioprine toxicity.	Azathioprine	82-94	thiopurine S-methyltransferase	Homo sapiens	14-44
20027160-1	2009	OBJECTIVES: Our study aims to find the relationship between metabolic enzyme thiopurine S-methyltransferase (TPMT) gene polymorphisms and clinical output of the therapy with azathioprine.	Azathioprine	174-186	thiopurine S-methyltransferase	Homo sapiens	77-107
20027160-1	2009	OBJECTIVES: Our study aims to find the relationship between metabolic enzyme thiopurine S-methyltransferase (TPMT) gene polymorphisms and clinical output of the therapy with azathioprine.	Azathioprine	174-186	thiopurine S-methyltransferase	Homo sapiens	109-113
20027160-6	2009	RESULTS: We have found statistical association between the presence of non-standard TPMT alleles and adverse event associated with azathioprine treatment - leucopenia (p=0.0033).	Azathioprine	131-143	thiopurine S-methyltransferase	Homo sapiens	84-88
20027160-7	2009	CONCLUSION: Our results confirm that TPMT genotyping prior to the treatment with azathioprine could predict patients with genetic predisposition for serious leucopenia and seems to be a useful genetic marker for individualisation of the therapy.	Azathioprine	81-93	thiopurine S-methyltransferase	Homo sapiens	37-41
19048591-8	2008	In 2007 we presented the results of a study that compared corticosteroids alone vs corticosteroids and azathioprine in 253 IgAN patients.	Azathioprine	103-115	IGAN1	Homo sapiens	123-127
18557988-8	2008	The TPMT-deficient patient excreted 89% of daily AZA dose as 6TU, but excretion by TPMT carriers was essentially normal.	Azathioprine	49-52	thiopurine S-methyltransferase	Homo sapiens	4-8
18922390-5	2008	Immunosuppressive therapy with prednisolone and azathioprine improved her symptoms and left ventricular function accompanied by a striking decrease of cTnT levels.	Azathioprine	48-60	troponin T2, cardiac type	Homo sapiens	151-155
18729367-1	2008	The aza-MBH reaction of imines 1 and beta-naphthyl acrylate 2 in the presence of C-6" modified beta-isocupreidine derivative 1c (0.1 equiv) and beta-naphthol 5 (0.1 equiv) afforded the corresponding (3S)-aza-MBH adducts 4 in high yield and excellent enantiomeric excess.	Azathioprine	4-7	complement C6	Homo sapiens	81-84
18786444-0	2008	Acute erythroleukemia with der(1;7)(q10;p10) as a sole acquired abnormality after treatment with azathioprine.	Azathioprine	97-109	S100 calcium binding protein A10	Homo sapiens	40-43
18692056-8	2008	Multivariate Cox models showed that both structuring behavior at diagnosis (hazard ratio [HR], 2.54; 95% confidence interval [CI]: 1.58-4.01) and treatment with corticosteroids (HR, 2.98; 95% CI: 1.64-5.41) were associated with increased risk for surgery, whereas treatment with azathioprine (HR, 0.51; 95% CI: 0.33-0.78) was associated with decreased risk.	Azathioprine	279-291	cytochrome c oxidase subunit 8A	Homo sapiens	13-16
18600523-3	2008	We describe the case of a young patient with ulcerative colitis, homozygous for TPMT*3A alleles, who suffered fatal azathioprine-induced myelotoxicity after standard dosing with azathioprine.	Azathioprine	116-128	thiopurine S-methyltransferase	Homo sapiens	80-84
18794458-0	2008	Role of thiopurine methyltransferase activity in the safety and efficacy of azathioprine in the treatment of pemphigus vulgaris.	Azathioprine	76-88	thiopurine S-methyltransferase	Homo sapiens	8-36
18794458-1	2008	OBJECTIVE: To evaluate the relationship between thiopurine methyltransferase (TPMT) activity and the safety and efficacy of azathioprine sodium in the treatment of pemphigus vulgaris.	Azathioprine	124-143	thiopurine S-methyltransferase	Homo sapiens	48-76
18794458-1	2008	OBJECTIVE: To evaluate the relationship between thiopurine methyltransferase (TPMT) activity and the safety and efficacy of azathioprine sodium in the treatment of pemphigus vulgaris.	Azathioprine	124-143	thiopurine S-methyltransferase	Homo sapiens	78-82
18693152-1	2008	Thiopurine S-methyltransferase (TPMT) activity is inversely related to the risk of developing severe hematopoietic toxicity in patients treated with azathioprine.	Azathioprine	149-161	thiopurine S-methyltransferase	Homo sapiens	0-30
18693152-1	2008	Thiopurine S-methyltransferase (TPMT) activity is inversely related to the risk of developing severe hematopoietic toxicity in patients treated with azathioprine.	Azathioprine	149-161	thiopurine S-methyltransferase	Homo sapiens	32-36
18693152-2	2008	The aim of this study was to evaluate the usefulness of TPMT genotyping in severe cases of autoimmune bullous diseases treated with azathioprine.	Azathioprine	132-144	thiopurine S-methyltransferase	Homo sapiens	56-60
18693152-3	2008	A retrospective study of TPMT genotyping was performed in patients with autoimmune bullous diseases hospitalized in a single centre between 1999 and 2006 and susceptible of being treated by azathioprine.	Azathioprine	190-202	thiopurine S-methyltransferase	Homo sapiens	25-29
18693152-5	2008	TPMT genotyping was performed in 33/34 patients currently treated with azathioprine.	Azathioprine	71-83	thiopurine S-methyltransferase	Homo sapiens	0-4
18693152-8	2008	Although strongly recommended before azathioprine treatment, predicting TPMT activity appears only marginally helpful in patients with autoimmune bullous diseases, mainly for adjusting the azathioprine dosage.	Azathioprine	189-201	thiopurine S-methyltransferase	Homo sapiens	72-76
18633531-0	2008	The aza-analogues of 1,4-naphthoquinones are potent substrates and inhibitors of plasmodial thioredoxin and glutathione reductases and of human erythrocyte glutathione reductase.	Azathioprine	4-7	thioredoxin	Homo sapiens	92-103
18633531-0	2008	The aza-analogues of 1,4-naphthoquinones are potent substrates and inhibitors of plasmodial thioredoxin and glutathione reductases and of human erythrocyte glutathione reductase.	Azathioprine	4-7	glutathione-disulfide reductase	Homo sapiens	108-129
18633531-1	2008	Various aza-analogues of 1,4-naphthoquinone and menadione were prepared and tested as inhibitors and substrates of the plasmodial thioredoxin and glutathione reductases as well as the human glutathione reductase.	Azathioprine	8-11	thioredoxin	Homo sapiens	130-141
18512990-2	2008	The key step in the method is an aza-Wacker oxidative cyclization catalyzed by palladium(II)/Cu(OTf)2.	Azathioprine	33-36	POU class 2 homeobox 2	Homo sapiens	96-101
19145729-1	2008	BACKGROUND: Hepatotoxicity results in the withdrawal of thiopurines drugs, azathioprine (AZA) and mercaptopurine (MP), in up to 10% of patients with inflammatory bowel disease.	Azathioprine	75-87	azurocidin 1	Homo sapiens	89-92
18340638-5	2008	According to annexin V binding, erythrocytes from patients indeed showed a significant increase of PS exposure within 1 week of treatment with azathioprine.	Azathioprine	143-155	annexin A5	Homo sapiens	13-22
18340638-7	2008	RESULTS: Exposure to azathioprine (&gt; or =2 microg/mL) for 48 hours increased cytosolic Ca2+ activity and annexin V binding and decreased forward scatter.	Azathioprine	21-33	annexin A5	Homo sapiens	108-117
18340638-8	2008	The effect of azathioprine on both annexin V binding and forward scatter was significantly blunted in the nominal absence of extracellular Ca2+.	Azathioprine	14-26	annexin A5	Homo sapiens	35-44
18597652-2	2008	Many genetic variants have been studied in genes possibly involved in the metabolism or mechanism of action of therapeutic agents such as glucocorticosteroids, azathioprine/6-mercaptopurine, methotrexate, calcineurin inhibitors or anti-TNF agents.	Azathioprine	160-172	tumor necrosis factor	Homo sapiens	236-239
18477684-0	2008	Dosing azathioprine in thiopurine S-methyltransferase deficient inflammatory bowel disease patients.	Azathioprine	7-19	thiopurine S-methyltransferase	Homo sapiens	23-53
18338327-4	2008	It is shown that the (13)C resonances of C-6, C-7 and C-11 carbon atoms are suitable for distinguishing between the tautomeric forms of aza-derivatives of gossypol in the solid state.	Azathioprine	136-139	complement C6	Homo sapiens	41-44
18338327-4	2008	It is shown that the (13)C resonances of C-6, C-7 and C-11 carbon atoms are suitable for distinguishing between the tautomeric forms of aza-derivatives of gossypol in the solid state.	Azathioprine	136-139	complement C7	Homo sapiens	46-49
18600523-3	2008	We describe the case of a young patient with ulcerative colitis, homozygous for TPMT*3A alleles, who suffered fatal azathioprine-induced myelotoxicity after standard dosing with azathioprine.	Azathioprine	178-190	thiopurine S-methyltransferase	Homo sapiens	80-84
18600523-4	2008	Screening for decreased activity of TPMT in patients prior to azathioprine treatment is advised to minimize the risk of drug-induced toxicity.	Azathioprine	62-74	thiopurine S-methyltransferase	Homo sapiens	36-40
18528853-7	2008	The reactivity of the external amine groups is used to link covalently azobenzene chromophores (disperse Red 1 residues) through aza-Michael addition in aqueous suspension.	Azathioprine	129-132	adenosine deaminase RNA specific B1	Homo sapiens	105-110
18520612-0	2008	Paradoxical elevated thiopurine S-methyltransferase activity after pancytopenia during azathioprine therapy: potential influence of red blood cell age.	Azathioprine	87-99	thiopurine S-methyltransferase	Homo sapiens	21-51
18433093-6	2008	For the aza systems MgTAP and ZnTAP, the simulated MCD spectra in the Soret region are dominated by the two one-electron excitations 2a2u--&gt;2eg and 1a2u--&gt;2eg and has the appearance of a positive A term (with values between 1.33-1.55, depending on the MTAP system) made asymmetric by a negative B term, in good agreement with experiment.	Azathioprine	8-11	methylthioadenosine phosphorylase	Homo sapiens	258-262
18343842-8	2008	Either chemically bypassing or inhibiting TPMT modulates antiviral activity of AZA metabolites.	Azathioprine	79-82	thiopurine S-methyltransferase	Homo sapiens	42-46
29783500-3	2008	The importance of genetic variability in determining thiopurine toxicity was first recognized over 25 years ago with the discovery of the thiopurine S-methyltransferase (TPMT) polymorphism and the occurrence of azathioprine-induced myelosuppression in TPMT-deficient patients.	Azathioprine	211-223	thiopurine S-methyltransferase	Homo sapiens	170-174
18336531-0	2008	The haemotoxicity of azathioprine in repeat dose studies in the female CD-1 mouse.	Azathioprine	21-33	CD1 antigen complex	Mus musculus	71-75
18336531-3	2008	The present studies were to characterize the haemotoxicity of AZA in the female CD-1 mouse.	Azathioprine	62-65	CD1 antigen complex	Mus musculus	80-84
18336531-6	2008	At day 1 after the final dose, AZA induced a dose-related pancytopaenia, reduced femoral marrow cellularity, increases in serum levels of the cytokine fms-like tyrosine kinase 3 ligand, reduction in granulocyte-monocyte colony-forming units and erythroid colonies, and increased bone marrow apoptosis.	Azathioprine	31-34	FMS-like tyrosine kinase 3 ligand	Mus musculus	151-184
18336531-12	2008	We conclude that the CD-1 mouse provides an acceptable model for the haemotoxicity of AZA in man.	Azathioprine	86-89	CD1 antigen complex	Mus musculus	21-25
17979968-8	2008	P53 patches were more prevalent in RTR than in ICP in normal skin adjacent to carcinomas (P = 0.02), in spite of a lower mean age in the RTR (52 vs 63 years, P = 0.001), but we found no increase in UV-induced p53 patches in mice that were immunosuppressed by azathioprine.	Azathioprine	259-271	transformation related protein 53, pseudogene	Mus musculus	0-3
18343842-9	2008	TPMT exists in several variants with varying levels of activity and since 6MMPr is a potent antiviral, the antiviral activity of AZA may be modulated by host genetics.	Azathioprine	129-132	thiopurine S-methyltransferase	Homo sapiens	0-4
18303966-1	2008	UNLABELLED: The use of azathioprine (and its metabolite mercaptopurine) is limited by toxicity, especially myelosuppression, which is related to activity of the enzyme thiopurine S-methyltransferase (TPMT).	Azathioprine	23-35	thiopurine S-methyltransferase	Homo sapiens	168-198
18086528-3	2008	A series of aza-, oxa-, and thia-analogues of homoisocitrate was designed and synthesized as an inhibitor for homoisocitrate dehydrogenase.	Azathioprine	12-15	homoisocitrate dehydrogenase	Saccharomyces cerevisiae S288C	110-138
18303966-1	2008	UNLABELLED: The use of azathioprine (and its metabolite mercaptopurine) is limited by toxicity, especially myelosuppression, which is related to activity of the enzyme thiopurine S-methyltransferase (TPMT).	Azathioprine	23-35	thiopurine S-methyltransferase	Homo sapiens	200-204
18172295-5	2008	Ten Aza-dC and/or TSA up-regulated genes (CPEB1, CD9, GJA1, BCL7c, GADD45G, AKAP12, TFPI2, CCNA1, SPARC, and BNIP3) were selected for methylation analysis in six MM cell lines, 24 samples from patients with monoclonal gammopathy of undetermined significance (MGUS), and 111 samples from patients with MM.	Azathioprine	4-7	cytoplasmic polyadenylation element binding protein 1	Homo sapiens	42-47
18197679-1	2008	We have synthesized a series of C3-symmetric aza-beta3-cyclohexapeptides with functionally diverse side chains carrying a good functional diversity.	Azathioprine	45-48	eukaryotic translation elongation factor 1 beta 2 pseudogene 2	Homo sapiens	49-54
18172295-5	2008	Ten Aza-dC and/or TSA up-regulated genes (CPEB1, CD9, GJA1, BCL7c, GADD45G, AKAP12, TFPI2, CCNA1, SPARC, and BNIP3) were selected for methylation analysis in six MM cell lines, 24 samples from patients with monoclonal gammopathy of undetermined significance (MGUS), and 111 samples from patients with MM.	Azathioprine	4-7	tissue factor pathway inhibitor 2	Homo sapiens	84-89
18250137-0	2008	Azathioprine-induced fatal myelosuppression in systemic lupus erythematosus patient carrying TPMT*3C polymorphism.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	93-97
18250137-6	2008	We describe herein a case of AZA-induced severe myelosuppression associated with TPMT*3C heterozygous mutant allele in a SLE patient.	Azathioprine	29-32	thiopurine S-methyltransferase	Homo sapiens	81-85
18250137-9	2008	Measurement of TPMT activity and determination of TPMT variant allele may identify patients at risk for AZA-induced myelosuppression.	Azathioprine	104-107	thiopurine S-methyltransferase	Homo sapiens	50-54
18172295-5	2008	Ten Aza-dC and/or TSA up-regulated genes (CPEB1, CD9, GJA1, BCL7c, GADD45G, AKAP12, TFPI2, CCNA1, SPARC, and BNIP3) were selected for methylation analysis in six MM cell lines, 24 samples from patients with monoclonal gammopathy of undetermined significance (MGUS), and 111 samples from patients with MM.	Azathioprine	4-7	cyclin A1	Homo sapiens	91-96
18172295-5	2008	Ten Aza-dC and/or TSA up-regulated genes (CPEB1, CD9, GJA1, BCL7c, GADD45G, AKAP12, TFPI2, CCNA1, SPARC, and BNIP3) were selected for methylation analysis in six MM cell lines, 24 samples from patients with monoclonal gammopathy of undetermined significance (MGUS), and 111 samples from patients with MM.	Azathioprine	4-7	secreted protein acidic and cysteine rich	Homo sapiens	98-103
18172295-5	2008	Ten Aza-dC and/or TSA up-regulated genes (CPEB1, CD9, GJA1, BCL7c, GADD45G, AKAP12, TFPI2, CCNA1, SPARC, and BNIP3) were selected for methylation analysis in six MM cell lines, 24 samples from patients with monoclonal gammopathy of undetermined significance (MGUS), and 111 samples from patients with MM.	Azathioprine	4-7	CD9 molecule	Homo sapiens	49-52
18172295-5	2008	Ten Aza-dC and/or TSA up-regulated genes (CPEB1, CD9, GJA1, BCL7c, GADD45G, AKAP12, TFPI2, CCNA1, SPARC, and BNIP3) were selected for methylation analysis in six MM cell lines, 24 samples from patients with monoclonal gammopathy of undetermined significance (MGUS), and 111 samples from patients with MM.	Azathioprine	4-7	gap junction protein alpha 1	Homo sapiens	54-58
18172295-5	2008	Ten Aza-dC and/or TSA up-regulated genes (CPEB1, CD9, GJA1, BCL7c, GADD45G, AKAP12, TFPI2, CCNA1, SPARC, and BNIP3) were selected for methylation analysis in six MM cell lines, 24 samples from patients with monoclonal gammopathy of undetermined significance (MGUS), and 111 samples from patients with MM.	Azathioprine	4-7	BAF chromatin remodeling complex subunit BCL7C	Homo sapiens	60-65
18172295-5	2008	Ten Aza-dC and/or TSA up-regulated genes (CPEB1, CD9, GJA1, BCL7c, GADD45G, AKAP12, TFPI2, CCNA1, SPARC, and BNIP3) were selected for methylation analysis in six MM cell lines, 24 samples from patients with monoclonal gammopathy of undetermined significance (MGUS), and 111 samples from patients with MM.	Azathioprine	4-7	BCL2 interacting protein 3	Homo sapiens	109-114
18172295-5	2008	Ten Aza-dC and/or TSA up-regulated genes (CPEB1, CD9, GJA1, BCL7c, GADD45G, AKAP12, TFPI2, CCNA1, SPARC, and BNIP3) were selected for methylation analysis in six MM cell lines, 24 samples from patients with monoclonal gammopathy of undetermined significance (MGUS), and 111 samples from patients with MM.	Azathioprine	4-7	growth arrest and DNA damage inducible gamma	Homo sapiens	67-74
18172295-5	2008	Ten Aza-dC and/or TSA up-regulated genes (CPEB1, CD9, GJA1, BCL7c, GADD45G, AKAP12, TFPI2, CCNA1, SPARC, and BNIP3) were selected for methylation analysis in six MM cell lines, 24 samples from patients with monoclonal gammopathy of undetermined significance (MGUS), and 111 samples from patients with MM.	Azathioprine	4-7	A-kinase anchoring protein 12	Homo sapiens	76-82
18008354-0	2007	Effect of chronic azathioprine treatment on germ-line transmission of Hprt mutation in mice.	Azathioprine	18-30	hypoxanthine guanine phosphoribosyl transferase	Mus musculus	70-74
18090994-0	2008	Thiopurine-methyltransferase and inosine triphosphate pyrophosphatase polymorphism in a liver transplant recipient developing nodular regenerative hyperplasia on low-dose azathioprine.	Azathioprine	171-183	thiopurine S-methyltransferase	Homo sapiens	0-28
18090994-0	2008	Thiopurine-methyltransferase and inosine triphosphate pyrophosphatase polymorphism in a liver transplant recipient developing nodular regenerative hyperplasia on low-dose azathioprine.	Azathioprine	171-183	inosine triphosphatase	Homo sapiens	33-69
18827410-1	2008	BACKGROUND AND AIMS: Myelosuppression observed in patients with inflammatory bowel disease (IBD) treated with azathioprine (AZA) has been attributed to low thiopurine S-methyltransferase (TPMT) activity.	Azathioprine	110-122	thiopurine S-methyltransferase	Homo sapiens	156-186
18827410-1	2008	BACKGROUND AND AIMS: Myelosuppression observed in patients with inflammatory bowel disease (IBD) treated with azathioprine (AZA) has been attributed to low thiopurine S-methyltransferase (TPMT) activity.	Azathioprine	110-122	thiopurine S-methyltransferase	Homo sapiens	188-192
18827410-1	2008	BACKGROUND AND AIMS: Myelosuppression observed in patients with inflammatory bowel disease (IBD) treated with azathioprine (AZA) has been attributed to low thiopurine S-methyltransferase (TPMT) activity.	Azathioprine	124-127	thiopurine S-methyltransferase	Homo sapiens	156-186
18827410-1	2008	BACKGROUND AND AIMS: Myelosuppression observed in patients with inflammatory bowel disease (IBD) treated with azathioprine (AZA) has been attributed to low thiopurine S-methyltransferase (TPMT) activity.	Azathioprine	124-127	thiopurine S-methyltransferase	Homo sapiens	188-192
20020851-7	2008	AZA administered rats displayed declined levels of endogenous antioxidants [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH)], along with elevated levels of malondialdehyde (MDA).	Azathioprine	0-3	catalase	Rattus norvegicus	104-112
20020851-7	2008	AZA administered rats displayed declined levels of endogenous antioxidants [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH)], along with elevated levels of malondialdehyde (MDA).	Azathioprine	0-3	catalase	Rattus norvegicus	114-117
20020851-7	2008	AZA administered rats displayed declined levels of endogenous antioxidants [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH)], along with elevated levels of malondialdehyde (MDA).	Azathioprine	0-3	glutathione-disulfide reductase	Rattus norvegicus	150-171
20020851-7	2008	AZA administered rats displayed declined levels of endogenous antioxidants [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH)], along with elevated levels of malondialdehyde (MDA).	Azathioprine	0-3	glutathione-disulfide reductase	Rattus norvegicus	173-175
18008354-2	2007	Extremely high HPRT lymphocyte mutant frequencies (MFs) are found in humans and mice chronically treated with Aza, and these elevated MFs appear to be caused by selection and amplification of pre-existing HPRT mutant lymphocytes.	Azathioprine	110-113	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	15-19
18008354-2	2007	Extremely high HPRT lymphocyte mutant frequencies (MFs) are found in humans and mice chronically treated with Aza, and these elevated MFs appear to be caused by selection and amplification of pre-existing HPRT mutant lymphocytes.	Azathioprine	110-113	hypoxanthine guanine phosphoribosyl transferase	Mus musculus	205-209
18008354-3	2007	In the present study, we investigated if in vivo selection by Aza also promotes the germ-line transmission of Hprt mutants.	Azathioprine	62-65	hypoxanthine guanine phosphoribosyl transferase	Mus musculus	110-114
18008354-6	2007	Analysis of the Aza-treated males after the breeding period indicated that 12 had highly elevated Hprt lymphocyte MFs (1 x 10(-4)-2.5 x 10(-1) vs. normal MFs of &lt;1 x 10(-5)), indicating that the Aza treatment successfully selected somatic cell mutants.	Azathioprine	16-19	hypoxanthine guanine phosphoribosyl transferase	Mus musculus	98-102
18008354-8	2007	Most of the 364 female offspring (332 from Aza-treated fathers) had Hprt MFs of 0-6 x 10(-6), but seven of the offspring had moderately elevated MFs of 16 x 10(-6)-55 x 10(-6).	Azathioprine	43-46	hypoxanthine guanine phosphoribosyl transferase	Mus musculus	68-72
17978158-0	2007	Azathioprine and diffuse alveolar haemorrhage: the pharmacogenetics of thiopurine methyltransferase.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	71-99
17900274-7	2007	In milder cases of ligneous conjunctivitis, topical application of plg-containing eye drops, fresh frozen plasma, heparin, corticosteroids or certain immunosuppressive agents (such as azathioprine) may be more or less effective.	Azathioprine	184-196	plasminogen	Homo sapiens	67-70
17978158-2	2007	However, some patients with genetic polymorphisms of thiopurine methyltransferase (TPMT) are at risk of severe azathioprine myelotoxicity.	Azathioprine	111-123	thiopurine S-methyltransferase	Homo sapiens	53-81
17978158-2	2007	However, some patients with genetic polymorphisms of thiopurine methyltransferase (TPMT) are at risk of severe azathioprine myelotoxicity.	Azathioprine	111-123	thiopurine S-methyltransferase	Homo sapiens	83-87
17978158-4	2007	Leukocyte genetic TPMT testing revealed that the patient had homozygous polymorphisms associated with the absence of TPMT activity and severe azathioprine-induced myelotoxicity.	Azathioprine	142-154	thiopurine S-methyltransferase	Homo sapiens	18-22
17574424-0	2007	Aza analogues of equol: novel ligands for estrogen receptor beta.	Azathioprine	0-3	estrogen receptor 2	Homo sapiens	42-64
17001353-0	2007	IMPDH1 promoter mutations in a patient exhibiting azathioprine resistance.	Azathioprine	50-62	inosine monophosphate dehydrogenase 1	Homo sapiens	0-6
17001353-3	2007	To test this hypothesis, we screened 20 azathioprine-resistant patients for variations in the two IMPDH genes (IMPDH1 and IMPDH2) using dHPLC and DNA sequencing.	Azathioprine	40-52	inosine monophosphate dehydrogenase 1	Homo sapiens	111-117
17001353-3	2007	To test this hypothesis, we screened 20 azathioprine-resistant patients for variations in the two IMPDH genes (IMPDH1 and IMPDH2) using dHPLC and DNA sequencing.	Azathioprine	40-52	inosine monophosphate dehydrogenase 2	Homo sapiens	122-128
17001353-4	2007	A 9 bp insertion within the IMPDH1 P3 promoter was found in a patient exhibiting severe azathioprine resistance.	Azathioprine	88-100	inosine monophosphate dehydrogenase 1 pseudogene 3	Homo sapiens	28-37
17713889-8	2007	More recent anti TNF-alpha antibodies can be applied without an azathioprine comedication.	Azathioprine	64-76	tumor necrosis factor	Homo sapiens	17-26
17713436-11	2007	After adjusting for donor age and azathioprine use, homozygous TLR2 mutation (RR 5.20 [1.65-13.9]; P=0.007) remained associated with the primary outcome.	Azathioprine	34-46	toll like receptor 2	Homo sapiens	63-67
17493759-1	2007	Glutathione transferases (GSTs) catalyze the bioactivation of the thiopurine prodrugs azathioprine, cis-6-(2-acetylvinylthio)purine (cAVTP) and trans-6-(2-acetylvinylthio)guanine (tAVTG), thereby releasing the antimetabolites 6-mercaptopurine and 6-thioguanine.	Azathioprine	86-98	glutathione S-transferase kappa 1	Homo sapiens	26-30
17924837-4	2007	In recent years, evidence has started to accumulate that polymorphisms in the gene encoding ITPase are associated with potentially severe adverse drug reactions towards the thiopurine drugs azathioprine and 6-mercaptopurine.	Azathioprine	190-202	inosine triphosphatase	Homo sapiens	92-98
17613395-3	2007	This prospective study aims to assess: (1) the possible role of IL-17 as a link between LTx clinical outcomes (such as infection, acute rejection and BOS) and airway immunopathologic measures from endobronchial biopsy (EBB) and bronchoalveolar lavage (BAL); and (2) any differences in IL-17 production between ERL and azathioprine (AZA)-based immunosuppression.	Azathioprine	318-330	interleukin 17A	Homo sapiens	64-69
17654066-1	2007	Thiopurine methyltransferase (TPMT) is the main enzyme responsible for inactivating toxic products of azathioprine (AZA) metabolism.	Azathioprine	102-114	thiopurine S-methyltransferase	Homo sapiens	0-28
17654066-1	2007	Thiopurine methyltransferase (TPMT) is the main enzyme responsible for inactivating toxic products of azathioprine (AZA) metabolism.	Azathioprine	102-114	thiopurine S-methyltransferase	Homo sapiens	30-34
17654066-1	2007	Thiopurine methyltransferase (TPMT) is the main enzyme responsible for inactivating toxic products of azathioprine (AZA) metabolism.	Azathioprine	116-119	thiopurine S-methyltransferase	Homo sapiens	0-28
17654066-1	2007	Thiopurine methyltransferase (TPMT) is the main enzyme responsible for inactivating toxic products of azathioprine (AZA) metabolism.	Azathioprine	116-119	thiopurine S-methyltransferase	Homo sapiens	30-34
17654066-4	2007	We describe a patient with homozygous deficiency of TPMT who developed life threatening neutropenic sepsis, and advocate that all patients should be tested for TPMT activity prior to starting AZA therapy.	Azathioprine	192-195	thiopurine S-methyltransferase	Homo sapiens	52-56
17593067-1	2007	BACKGROUND: High frequency of incomplete or non-response to azathioprine (AZA) and/or mercaptopurine (MP) limit their use in Crohn"s disease (CD).	Azathioprine	60-72	azurocidin 1	Homo sapiens	74-77
17888219-6	2007	RESULTS: The improvement from a year of CYC therapy was maintained by AZA treatment.	Azathioprine	70-73	cytochrome c, somatic	Homo sapiens	40-43
17888219-8	2007	CONCLUSION: This study suggests a role of AZA in maintaining the improvement induced by low dose pulse CYC in early dcSSc, making it possible a short duration of treatment at a low cumulative dose of the drug.	Azathioprine	42-45	cytochrome c, somatic	Homo sapiens	103-106
17919375-1	2007	OBJECTIVE: To discuss the relationship between the genotype of thiopurine methyltransferase (TPMT) and azathioprine tolerance in the patients with rheumatic diseases.	Azathioprine	103-115	thiopurine S-methyltransferase	Homo sapiens	63-91
17919375-1	2007	OBJECTIVE: To discuss the relationship between the genotype of thiopurine methyltransferase (TPMT) and azathioprine tolerance in the patients with rheumatic diseases.	Azathioprine	103-115	thiopurine S-methyltransferase	Homo sapiens	93-97
17919375-10	2007	CONCLUSION: Patients with mutation alleles of TPMT are intolerant to azathioprine, and likely to have severe crisis of hematopoietic system.	Azathioprine	69-81	thiopurine S-methyltransferase	Homo sapiens	46-50
17919375-11	2007	To detect the TPMT genotype before using azathioprine is significant to improve the therapeutic safety.	Azathioprine	41-53	thiopurine S-methyltransferase	Homo sapiens	14-18
17613395-3	2007	This prospective study aims to assess: (1) the possible role of IL-17 as a link between LTx clinical outcomes (such as infection, acute rejection and BOS) and airway immunopathologic measures from endobronchial biopsy (EBB) and bronchoalveolar lavage (BAL); and (2) any differences in IL-17 production between ERL and azathioprine (AZA)-based immunosuppression.	Azathioprine	332-335	interleukin 17A	Homo sapiens	64-69
17584603-3	2007	It has been demonstrated that 6-thio-GTP, a metabolite of azathioprine, specifically inhibits Vav1-Rac activity in T lymphocytes.	Azathioprine	58-70	vav 1 oncogene	Mus musculus	94-98
17517340-1	2007	In silico docking analysis reported here suggests that insect cellular cytoskeletal beta-actin could be the target of Azadirachtin A (Aza-the principle bioactive compound of neem seeds).	Azathioprine	118-121	POTE ankyrin domain family member F	Homo sapiens	84-94
17230494-10	2007	Mucosal Foxp3 mRNA levels and Foxp3+CD3+ cells were significantly reduced in transplant recipients using prednisone/azathioprine/tacrolimus compared with controls but no direct relationship between Foxp3 expression and 1 specific drug was detected.	Azathioprine	116-128	forkhead box P3	Homo sapiens	8-13
17517340-4	2007	Our results show that few scattered amino acid changes have caused significant steric hindrance in the binding pocket for mammalian beta-actin, causing a reverse orientation of Aza.	Azathioprine	177-180	POTE ankyrin domain family member F	Homo sapiens	132-142
17824492-0	2007	Ref: Role of azathioprine in preventing recurrence of ENL in a patient--article by K K Verma et al.	Azathioprine	13-25	MLLT1 super elongation complex subunit	Homo sapiens	54-57
17334911-1	2007	We sought to assess the activity of thiopurine methyltransferase (TPMT) in 14,545 Spanish patients with different diseases amenable to treatment with azathioprine/6-mercaptopurine (6-MP), and to evaluate the proportion of patients with low TPMT activity and therefore a higher risk of myelotoxicity with these drugs.	Azathioprine	150-162	thiopurine S-methyltransferase	Homo sapiens	66-70
17439508-0	2007	Assessment of thiopurine methyltransferase enzyme activity is superior to genotype in predicting myelosuppression following azathioprine therapy in patients with inflammatory bowel disease.	Azathioprine	124-136	thiopurine S-methyltransferase	Homo sapiens	14-42
17334911-8	2007	In the multivariate analysis, gender, hematocrit, and treatment with 5-aminosalicylates/steroids/azathioprine/6-MP statistically influenced TPMT activity, although, probably, in a clinically irrelevant manner.	Azathioprine	97-109	thiopurine S-methyltransferase	Homo sapiens	140-144
17334911-9	2007	This study shows, in a large sample of 14,545 patients, that 0.5% had low TPMT activity, indicating a higher risk of myelotoxicity with azathioprine/6-MP, a figure similar or slightly higher than that reported in other areas.	Azathioprine	136-148	thiopurine S-methyltransferase	Homo sapiens	74-78
17334911-11	2007	The drugs prescribed for the treatment of autoimmune diseases, including azathioprine/6-MP, modified TPMT activity, but the magnitude of this effect was very small and the differences found are probably irrelevant from the clinical point of view.	Azathioprine	73-85	thiopurine S-methyltransferase	Homo sapiens	101-105
17304143-0	2007	Monitoring of thiopurine methyltransferase activity in postsurgical patients with Crohn"s disease during 1 year of treatment with azathioprine or mesalazine.	Azathioprine	130-142	thiopurine S-methyltransferase	Homo sapiens	14-42
17262810-0	2007	MDR1 polymorphisms and response to azathioprine therapy in patients with Crohn"s disease.	Azathioprine	35-47	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
17262810-1	2007	BACKGROUND: To investigate the contribution of multidrug resistance 1 (MDR1) gene pharmacogenetics (G2677T/A and C3435T) to the efficacy of azathioprine in inducing remission in patients with Crohn"s disease (CD).	Azathioprine	140-152	ATP binding cassette subfamily B member 1	Homo sapiens	47-69
17262810-1	2007	BACKGROUND: To investigate the contribution of multidrug resistance 1 (MDR1) gene pharmacogenetics (G2677T/A and C3435T) to the efficacy of azathioprine in inducing remission in patients with Crohn"s disease (CD).	Azathioprine	140-152	ATP binding cassette subfamily B member 1	Homo sapiens	71-75
17381669-3	2007	Thiopurine methyltransferase (TPMT) is a genetically moderated key enzyme involved in the metabolism of AZA that can be used to stratify individuals into different levels of risk of developing neutropaenia.	Azathioprine	104-107	thiopurine S-methyltransferase	Homo sapiens	0-28
17381669-3	2007	Thiopurine methyltransferase (TPMT) is a genetically moderated key enzyme involved in the metabolism of AZA that can be used to stratify individuals into different levels of risk of developing neutropaenia.	Azathioprine	104-107	thiopurine S-methyltransferase	Homo sapiens	30-34
17381669-17	2007	High uptake of TPMT enzyme-level testing by dermatologists, compared with gastroenterologists and rheumatologists, may reflect national guidelines advocating its use prior to AZA.	Azathioprine	175-178	thiopurine S-methyltransferase	Homo sapiens	15-19
17178220-1	2007	Carbonic anhydrase inhibitors AZA, EZA, and 4-acetamidobenzsulfonamide were found to inhibit human AQP4-M23 mediated water transport by 80%, 68%, and 23%, respectively, at 20 microM in an in vitro functional assay.	Azathioprine	30-33	aquaporin 4	Homo sapiens	99-103
17178220-2	2007	AZA was found to have an IC50 against AQP4 of 0.9 microM.	Azathioprine	0-3	aquaporin 4	Homo sapiens	38-42
17241387-1	2007	BACKGROUND AND AIM: Thiopurine S-methyltransferase (TPMT) genotypes or phenotypes may be a predictive factor for azathioprine-induced toxicities.	Azathioprine	113-125	thiopurine S-methyltransferase	Homo sapiens	20-50
17241387-1	2007	BACKGROUND AND AIM: Thiopurine S-methyltransferase (TPMT) genotypes or phenotypes may be a predictive factor for azathioprine-induced toxicities.	Azathioprine	113-125	thiopurine S-methyltransferase	Homo sapiens	52-56
17241387-2	2007	We investigated the genotypic status of TPMT to evaluate the risk of azathioprine-related adverse effects in Japanese patients with different liver diseases, including autoimmune hepatitis (AIH).	Azathioprine	69-81	thiopurine S-methyltransferase	Homo sapiens	40-44
17241387-7	2007	Severe myelosuppression occurred in two of nine patients with AIH who received azathioprine, one of whom was homozygous for TPMT*3C.	Azathioprine	79-91	thiopurine S-methyltransferase	Homo sapiens	124-128
17304144-1	2007	Mutations in the inosine triphosphate pyrophosphohydrolase (ITPA) gene causing enzyme deficiency were shown to have pharmacogenetic implications in azathioprine-induced adverse drug reactions.	Azathioprine	148-160	inosine triphosphatase	Homo sapiens	17-58
17304144-1	2007	Mutations in the inosine triphosphate pyrophosphohydrolase (ITPA) gene causing enzyme deficiency were shown to have pharmacogenetic implications in azathioprine-induced adverse drug reactions.	Azathioprine	148-160	inosine triphosphatase	Homo sapiens	60-64
17304143-1	2007	Thiopurine methyltransferase (TPMT) activity determines biotransformation of azathioprine and, thereby, drug efficacy and safety.	Azathioprine	77-89	thiopurine S-methyltransferase	Homo sapiens	0-28
17304143-1	2007	Thiopurine methyltransferase (TPMT) activity determines biotransformation of azathioprine and, thereby, drug efficacy and safety.	Azathioprine	77-89	thiopurine S-methyltransferase	Homo sapiens	30-34
17304143-2	2007	Evaluation of a possible long-term effect of mesalazine or azathioprine on TPMT activity is of particular clinical importance because both drugs can to be given for several years in inflammatory bowel disease.	Azathioprine	59-71	thiopurine S-methyltransferase	Homo sapiens	75-79
17360301-10	2007	CONCLUSION: Immunosuppressive therapy with azathioprine seems to be responsible for our patient"s remission of type B insulin resistance, although the possibility of the occurrence of a spontaneous remission cannot be completely excluded.	Azathioprine	43-55	insulin	Homo sapiens	118-125
18093457-5	2007	There is an enzyme in the metabolism of azathioprine called thiopurine s-methyltransferase (TPMT).	Azathioprine	40-52	thiopurine S-methyltransferase	Homo sapiens	60-90
18093457-5	2007	There is an enzyme in the metabolism of azathioprine called thiopurine s-methyltransferase (TPMT).	Azathioprine	40-52	thiopurine S-methyltransferase	Homo sapiens	92-96
18093457-6	2007	It is very important to measure the TPMT activity before initiating therapy so that proper dosing of azathioprine can be achieved.	Azathioprine	101-113	thiopurine S-methyltransferase	Homo sapiens	36-40
17113761-3	2007	The ITPA c.94C&gt;A [P32T] sequence variant is associated with an increased risk of adverse drug reactions in patients treated with the thiopurine drug azathioprine.	Azathioprine	152-164	inosine triphosphatase	Homo sapiens	4-8
17265738-3	2007	For example, the analysis of thiopurine S-methyltransferase genotypes enables the prediction of toxicity in patients to be treated with either 6-mercaptopurine or azathioprine, while the uridine 5"-diphosphoglucuronosyl-transferase 1A1 genotype may predict irinotecan toxicity.	Azathioprine	163-175	thiopurine S-methyltransferase	Homo sapiens	29-59
17206640-1	2007	BACKGROUND: Adverse drug reactions to azathioprine, the prodrug of 6-mercaptopurine, occur in 15%-38% of patients and the majority are not explained by thiopurine-S-methyltransferase (TPMT) deficiency.	Azathioprine	38-50	thiopurine S-methyltransferase	Homo sapiens	184-188
17206640-2	2007	Azathioprine is known to induce glutathione depletion and consumption of glutathione is greater in cells with high glutathione-S-transferase (GST) activity compared with those with low activity; moreover, some reports indicate that GST might play a direct role in the reaction of glutathione with azathioprine.	Azathioprine	0-12	glutathione S-transferase kappa 1	Homo sapiens	115-140
17206640-2	2007	Azathioprine is known to induce glutathione depletion and consumption of glutathione is greater in cells with high glutathione-S-transferase (GST) activity compared with those with low activity; moreover, some reports indicate that GST might play a direct role in the reaction of glutathione with azathioprine.	Azathioprine	0-12	glutathione S-transferase kappa 1	Homo sapiens	142-145
17206640-2	2007	Azathioprine is known to induce glutathione depletion and consumption of glutathione is greater in cells with high glutathione-S-transferase (GST) activity compared with those with low activity; moreover, some reports indicate that GST might play a direct role in the reaction of glutathione with azathioprine.	Azathioprine	0-12	glutathione S-transferase kappa 1	Homo sapiens	232-235
17206640-2	2007	Azathioprine is known to induce glutathione depletion and consumption of glutathione is greater in cells with high glutathione-S-transferase (GST) activity compared with those with low activity; moreover, some reports indicate that GST might play a direct role in the reaction of glutathione with azathioprine.	Azathioprine	297-309	glutathione S-transferase kappa 1	Homo sapiens	115-140
17206640-2	2007	Azathioprine is known to induce glutathione depletion and consumption of glutathione is greater in cells with high glutathione-S-transferase (GST) activity compared with those with low activity; moreover, some reports indicate that GST might play a direct role in the reaction of glutathione with azathioprine.	Azathioprine	297-309	glutathione S-transferase kappa 1	Homo sapiens	142-145
17206640-2	2007	Azathioprine is known to induce glutathione depletion and consumption of glutathione is greater in cells with high glutathione-S-transferase (GST) activity compared with those with low activity; moreover, some reports indicate that GST might play a direct role in the reaction of glutathione with azathioprine.	Azathioprine	297-309	glutathione S-transferase kappa 1	Homo sapiens	232-235
17206640-3	2007	The association between polymorphisms of GST-M1, GST-P1, GST-T1, and TPMT genes and the adverse effects of azathioprine was therefore investigated.	Azathioprine	107-119	glutathione S-transferase kappa 1	Homo sapiens	41-44
17206640-3	2007	The association between polymorphisms of GST-M1, GST-P1, GST-T1, and TPMT genes and the adverse effects of azathioprine was therefore investigated.	Azathioprine	107-119	thiopurine S-methyltransferase	Homo sapiens	69-73
17176368-0	2006	TPMT genotype and its clinical implication in renal transplant recipients with azathioprine treatment.	Azathioprine	79-91	thiopurine S-methyltransferase	Homo sapiens	0-4
17206640-6	2007	RESULTS: Fifteen patients developed adverse effects (21.4%); there was a significant underrepresentation of the GST-M1 null genotype among patients developing adverse drug reactions to azathioprine (odds ratio [OR] = 0.18, 95% confidence interval [CI] = 0.037-0.72, P = 0.0072) compared with patients who did not develop adverse effects.	Azathioprine	185-197	glutathione S-transferase kappa 1	Homo sapiens	112-115
17206640-8	2007	Moreover, among the 55 patients who did not develop adverse effects, there was a significant underrepresentation of the GST-M1 null genotype among patients who displayed lymphopenia as compared with those that did not display this effect of azathioprine (OR = 0.15, 95% CI = 0.013-1.08, P = 0.032).	Azathioprine	241-253	glutathione S-transferase kappa 1	Homo sapiens	120-123
17206640-9	2007	CONCLUSION: Patients with IBD with a wildtype GST-M1 genotype present increased probability of developing adverse effects and increased incidence of lymphopenia during azathioprine treatment.	Azathioprine	168-180	glutathione S-transferase kappa 1	Homo sapiens	46-49
17454960-1	2007	Immunosuppressive therapy with azathioprine has been documented to cause squamous cell carcinoma (SCC) at various sites.	Azathioprine	31-43	serpin family B member 3	Homo sapiens	98-101
17454960-2	2007	We report possibly the first case of SCC of the kidney in a young male who received azathioprine for a long time.	Azathioprine	84-96	serpin family B member 3	Homo sapiens	37-40
17026564-2	2006	METHODS: TPMT activity in red blood cells (RBC) was measured by a radiochemical method in 394 consecutive patients with Crohn"s disease (238) or ulcerative colitis (156) starting treatment with azathioprine.	Azathioprine	194-206	thiopurine S-methyltransferase	Homo sapiens	9-13
17026564-11	2006	CONCLUSIONS: The strategy of determining TPMT activity in all patients prior to initiating treatment with azathioprine could help to minimize the risk of myelotoxicity, as patients with intermediate TPMT activity had fourfold more risk than high TPMT activity patients.	Azathioprine	106-118	thiopurine S-methyltransferase	Homo sapiens	41-45
17176368-11	2006	CONCLUSION: Our results, together with those of others pointing in the same direction, suggest that genotyping the major TPMT variant alleles may be a valuable tool in preventing AZA toxicity and optimization of immunosuppressive therapy.	Azathioprine	179-182	thiopurine S-methyltransferase	Homo sapiens	121-125
17143995-0	2006	Azathioprine and tubulointerstitial nephritis in HSP.	Azathioprine	0-12	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	49-52
17149058-6	2006	Tumor necrosis factor (TNF) inhibitors such as infliximab or etanercept should be considered as the next step in the treatment if azathioprine or methotrexate fails.	Azathioprine	130-142	tumor necrosis factor	Homo sapiens	0-21
17149058-6	2006	Tumor necrosis factor (TNF) inhibitors such as infliximab or etanercept should be considered as the next step in the treatment if azathioprine or methotrexate fails.	Azathioprine	130-142	tumor necrosis factor	Homo sapiens	23-26
17533736-2	2006	METHODS: MDA-MB-435 cells were treated with HDAC inhibitor trichostatin A(TSA)and DNMT1 inhibitor 5-AZA-CdR (AZA).	Azathioprine	100-103	DNA methyltransferase 1	Homo sapiens	82-87
17175307-12	2006	At last follow-up; GFR (MDRD method) for SRL: MMF: AZA were 39 +/- 13: 35 +/- 21: 40 +/- 24 mL/min; GFR (C-G method) 46 +/- 17, 37 +/- 18, 46 +/- 25 mL/min; BP 128 +/- 11/79 +/- 7: 131 +/- 22/80 +/- 14: 132 +/- 20/82 +/- 11 mm Hg; and CsA level 52 +/- 25: 122 +/- 41: 155 +/- 49.	Azathioprine	51-54	Rap guanine nucleotide exchange factor 5	Homo sapiens	19-22
17175307-16	2006	Delta GFR (C-G method) was also significantly improved in the SRL group (-0.02 +/- 0.47; P = .05) but not in the MMF (-0.13 +/- 0.51; P = .53) or AZA (-0.54 +/- 1.78; P = .44).	Azathioprine	146-149	Rap guanine nucleotide exchange factor 5	Homo sapiens	6-9
17533736-6	2006	RESULTS: After treatment with AZA and TSA, mRNA expression of ER alpha, PR and pS2 was up-regulated in MDA-MB-435 cells.	Azathioprine	30-33	estrogen receptor 1	Homo sapiens	62-70
17533736-6	2006	RESULTS: After treatment with AZA and TSA, mRNA expression of ER alpha, PR and pS2 was up-regulated in MDA-MB-435 cells.	Azathioprine	30-33	taste 2 receptor member 64 pseudogene	Homo sapiens	79-82
17533736-7	2006	The mRNA level of ER alpha was the hightest when MDA-MB-435 cells were treated with 2.5 micromol/L AZA and 100 ng/ml TSA.	Azathioprine	99-102	estrogen receptor 1	Homo sapiens	18-26
17533736-13	2006	CONCLUSION: After treatment with TSA and AZA, ER alpha-negative MDA-MB-435 cells can express functional ER alpha and regain responsiveness to estrogen both in vitro and in vivo.	Azathioprine	41-44	estrogen receptor 1	Homo sapiens	46-54
17533736-13	2006	CONCLUSION: After treatment with TSA and AZA, ER alpha-negative MDA-MB-435 cells can express functional ER alpha and regain responsiveness to estrogen both in vitro and in vivo.	Azathioprine	41-44	estrogen receptor 1	Homo sapiens	104-112
17030779-0	2006	Improvement with corticosteroids and azathioprine in GAD65-associated cerebellar ataxia.	Azathioprine	37-49	glutamate decarboxylase 2	Homo sapiens	53-58
17129552-0	2006	[Monitoring of thiopurine methyltransferase and thiopurine metabolites to optimize azathioprine therapy in inflammatory bowel disease].	Azathioprine	83-95	thiopurine S-methyltransferase	Homo sapiens	15-43
17129552-1	2006	Determination of the activity of thiopurine methyltransferase (TPMT) and of thiopurine metabolites (6-thioguanine and 6-methylmercaptopurine nucleotides) could be useful for individualized monitoring of azathioprine (AZA) and 6-mercaptopurine (6-MP) doses.	Azathioprine	203-215	thiopurine S-methyltransferase	Homo sapiens	33-61
17129552-1	2006	Determination of the activity of thiopurine methyltransferase (TPMT) and of thiopurine metabolites (6-thioguanine and 6-methylmercaptopurine nucleotides) could be useful for individualized monitoring of azathioprine (AZA) and 6-mercaptopurine (6-MP) doses.	Azathioprine	203-215	thiopurine S-methyltransferase	Homo sapiens	63-67
17129552-1	2006	Determination of the activity of thiopurine methyltransferase (TPMT) and of thiopurine metabolites (6-thioguanine and 6-methylmercaptopurine nucleotides) could be useful for individualized monitoring of azathioprine (AZA) and 6-mercaptopurine (6-MP) doses.	Azathioprine	217-220	thiopurine S-methyltransferase	Homo sapiens	33-61
17129552-1	2006	Determination of the activity of thiopurine methyltransferase (TPMT) and of thiopurine metabolites (6-thioguanine and 6-methylmercaptopurine nucleotides) could be useful for individualized monitoring of azathioprine (AZA) and 6-mercaptopurine (6-MP) doses.	Azathioprine	217-220	thiopurine S-methyltransferase	Homo sapiens	63-67
17112853-0	2006	Conversion from azathioprine to mycophenolate mofetil followed by calcineurin inhibitor minimization or elimination in patients with chronic allograft dysfunction.	Azathioprine	16-28	calcineurin binding protein 1	Homo sapiens	66-87
17064038-1	2006	cis-2-Methyl-6-substituted piperidin-3-ol alkaloids of the Cassia and Prosopis species are readily prepared by a combination of an aza-Achmatowicz oxidative rearrangement and dihydropyridone reduction followed by a stereoselective allylsilane addition to a N-sulfonyliminium ion.	Azathioprine	131-134	suppressor of cytokine signaling 2	Homo sapiens	0-5
17110316-5	2006	Immunosuppressive and cytotoxic drugs used in antirheumatic therapy, such as methotrexate, cyclophosphamide, azathioprine or anti-TNF biologicals may also lead to the development of such tumors.	Azathioprine	109-121	tumor necrosis factor	Homo sapiens	130-133
16980004-11	2006	Although the mean plasma erythropoietin levels in AZA-treated patients were higher than those of MMF-treated patients, the trend did not reach statistical significance (P = .066).	Azathioprine	50-53	erythropoietin	Homo sapiens	25-39
17015970-9	2006	This aza-Michael reaction was successfully applied to asymmetric synthesis of the CETP inhibitor torcetrapib.	Azathioprine	5-8	cholesteryl ester transfer protein	Homo sapiens	82-86
16876902-1	2006	BACKGROUND/AIMS: Azathioprine is a key drug in the management of autoimmune hepatitis (AIH), with effects mediated via conversion to 6-thioguanine (6-TG) and 6-methylmercaptopurine (6-MMP), the latter controlled by thiopurine methyltransferase (TPMT).	Azathioprine	17-29	thiopurine S-methyltransferase	Homo sapiens	215-243
16876902-1	2006	BACKGROUND/AIMS: Azathioprine is a key drug in the management of autoimmune hepatitis (AIH), with effects mediated via conversion to 6-thioguanine (6-TG) and 6-methylmercaptopurine (6-MMP), the latter controlled by thiopurine methyltransferase (TPMT).	Azathioprine	17-29	thiopurine S-methyltransferase	Homo sapiens	245-249
17097956-7	2006	The target range levels between 5 and 10 ng/mL seemed to be sufficient for complete CNI elimination, especially in patients also receiving antiproliferative drugs (such as mycophenolate mofetil or azathioprine) in whom levels near the lower end of the range might be adequate.	Azathioprine	197-209	calcineurin binding protein 1	Homo sapiens	84-87
16995866-7	2006	CONCLUSIONS: The data suggest that azathioprine may be "safe" during breastfeeding in patients with the wild-type TPMT genotype ( approximately 90% of caucasian patients) taking "normal" doses.	Azathioprine	35-47	thiopurine S-methyltransferase	Homo sapiens	114-118
16995868-0	2006	Two cases of thiopurine methyltransferase (TPMT) deficiency--a lucky save and a near miss with azathioprine.	Azathioprine	95-107	thiopurine S-methyltransferase	Homo sapiens	13-41
16995868-0	2006	Two cases of thiopurine methyltransferase (TPMT) deficiency--a lucky save and a near miss with azathioprine.	Azathioprine	95-107	thiopurine S-methyltransferase	Homo sapiens	43-47
16995868-1	2006	BACKGROUND: The association between thiopurine methyltransferase (TPMT) deficiency and myelosuppression with azathioprine is well recognized.	Azathioprine	109-121	thiopurine S-methyltransferase	Homo sapiens	36-64
16995868-1	2006	BACKGROUND: The association between thiopurine methyltransferase (TPMT) deficiency and myelosuppression with azathioprine is well recognized.	Azathioprine	109-121	thiopurine S-methyltransferase	Homo sapiens	66-70
17086913-4	2006	Combined therapy with Avonex, prednisone and AZA was associated with a significant increase in the serum level of interleukin (IL)10 (P &lt;0.001).	Azathioprine	45-48	interleukin 10	Homo sapiens	114-132
16970398-0	2006	Design, synthesis, and evaluation of aza-peptide Michael acceptors as selective and potent inhibitors of caspases-2, -3, -6, -7, -8, -9, and -10.	Azathioprine	37-40	caspase 2	Homo sapiens	105-144
16970398-6	2006	High-resolution crystal structures of caspase-3 and caspase-8 in complex with aza-peptide Michael acceptor inhibitors demonstrate the nucleophilic attack on C2 and provide insight into the selectivity and potency of the inhibitors with respect to the P1" moiety.	Azathioprine	78-81	caspase 3	Homo sapiens	38-47
16970398-6	2006	High-resolution crystal structures of caspase-3 and caspase-8 in complex with aza-peptide Michael acceptor inhibitors demonstrate the nucleophilic attack on C2 and provide insight into the selectivity and potency of the inhibitors with respect to the P1" moiety.	Azathioprine	78-81	caspase 8	Homo sapiens	52-61
16954954-7	2006	RESULTS: Patients with normal TPMT level received a higher starting dose of AZA than in patients who were heterozygous for TPMT deficiency (1.7 vs 0.9 mg/[kg x d], P &lt; 0.0001).	Azathioprine	76-79	thiopurine S-methyltransferase	Homo sapiens	30-34
17144099-12	2006	The tubular expressions of mRNA for IL-6 and TGF-gamma 1 in biopsies with acute rejection obtained from patients treated with MMF were significantly lower than in biopsies obtained from patients treated with azathioprine.	Azathioprine	208-220	interleukin 6	Homo sapiens	36-40
17971736-0	2006	Formal synthesis of the ACE inhibitor benazepril x HCl via an asymmetric aza-Michael reaction.	Azathioprine	73-76	angiotensin I converting enzyme	Homo sapiens	24-27
24678102-0	2006	Correlation of thiopurine methyltransferase activity and 6-thioguanine nucleotide concentration in Han Chinese patients treated with azathioprine 25 to 100 mg: A 1-year, single-center, prospective study.	Azathioprine	133-145	thiopurine S-methyltransferase	Homo sapiens	15-43
24678102-1	2006	BACKGROUND: Of the enzymes involved in the metabolism of azathioprine, thiopurine methyltransferase (TPMT) is the one characterized by genetic polymorphisms and ethnic variations.	Azathioprine	57-69	thiopurine S-methyltransferase	Homo sapiens	71-99
24678102-1	2006	BACKGROUND: Of the enzymes involved in the metabolism of azathioprine, thiopurine methyltransferase (TPMT) is the one characterized by genetic polymorphisms and ethnic variations.	Azathioprine	57-69	thiopurine S-methyltransferase	Homo sapiens	101-105
24678102-3	2006	OBJECTIVE: The aim of this study was to examine the relationship between TPMT activity and the steady-state concentration (Css) of 6-TGN, the primary active metabolite of azathioprine, in red blood cells (RBCs) in Han Chinese patients treated with azathioprine.	Azathioprine	171-183	thiopurine S-methyltransferase	Homo sapiens	73-77
24678102-3	2006	OBJECTIVE: The aim of this study was to examine the relationship between TPMT activity and the steady-state concentration (Css) of 6-TGN, the primary active metabolite of azathioprine, in red blood cells (RBCs) in Han Chinese patients treated with azathioprine.	Azathioprine	248-260	thiopurine S-methyltransferase	Homo sapiens	73-77
16473374-3	2006	During our study, we investigated the effects of azathioprine on the inducible nitric oxide synthase (iNOS) in lipopolysaccharide stimulated murine macrophages (RAW 264.7) by measurement of iNOS protein (immunoblotting), iNOS mRNA (semiquantitative competitive RT-PCR), and NO production (nitrite levels).	Azathioprine	49-61	nitric oxide synthase 2, inducible	Mus musculus	69-100
16766757-0	2006	Do ITPA and TPMT genotypes predict the development of side effects to AZA?	Azathioprine	70-73	thiopurine S-methyltransferase	Homo sapiens	12-16
17074104-1	2006	OBJECTIVE: To detect the activity of thiopurine methyltransferase (TPMT) and its relationship with azathioprine (AZA) tolerance.	Azathioprine	99-111	thiopurine S-methyltransferase	Homo sapiens	37-65
17074104-1	2006	OBJECTIVE: To detect the activity of thiopurine methyltransferase (TPMT) and its relationship with azathioprine (AZA) tolerance.	Azathioprine	99-111	thiopurine S-methyltransferase	Homo sapiens	67-71
17074104-1	2006	OBJECTIVE: To detect the activity of thiopurine methyltransferase (TPMT) and its relationship with azathioprine (AZA) tolerance.	Azathioprine	113-116	thiopurine S-methyltransferase	Homo sapiens	37-65
17074104-1	2006	OBJECTIVE: To detect the activity of thiopurine methyltransferase (TPMT) and its relationship with azathioprine (AZA) tolerance.	Azathioprine	113-116	thiopurine S-methyltransferase	Homo sapiens	67-71
17074104-12	2006	CONCLUSIONS: Hematological side effects were highly associated with TPMT activity in AZA usage.	Azathioprine	85-88	thiopurine S-methyltransferase	Homo sapiens	68-72
17074104-13	2006	Patients with low TPMT activity should use low dose of AZA routinely, even though, toxicity may occur.	Azathioprine	55-58	thiopurine S-methyltransferase	Homo sapiens	18-22
16473374-11	2006	iNOS inhibition by azathioprine was associated with a decreased expression of IRF-1 (interferon regulatory factor 1) and IFN-beta (beta-interferon) mRNA.	Azathioprine	19-31	nitric oxide synthase 2, inducible	Mus musculus	0-4
16473374-3	2006	During our study, we investigated the effects of azathioprine on the inducible nitric oxide synthase (iNOS) in lipopolysaccharide stimulated murine macrophages (RAW 264.7) by measurement of iNOS protein (immunoblotting), iNOS mRNA (semiquantitative competitive RT-PCR), and NO production (nitrite levels).	Azathioprine	49-61	nitric oxide synthase 2, inducible	Mus musculus	102-106
16473374-11	2006	iNOS inhibition by azathioprine was associated with a decreased expression of IRF-1 (interferon regulatory factor 1) and IFN-beta (beta-interferon) mRNA.	Azathioprine	19-31	interferon regulatory factor 1	Mus musculus	78-83
16473374-11	2006	iNOS inhibition by azathioprine was associated with a decreased expression of IRF-1 (interferon regulatory factor 1) and IFN-beta (beta-interferon) mRNA.	Azathioprine	19-31	interferon regulatory factor 1	Mus musculus	85-115
16473374-5	2006	iNOS protein expression showed a concentration dependent reduction as revealed by immunoblotting when cells were incubated with increasing amounts of azathioprine.	Azathioprine	150-162	nitric oxide synthase 2, inducible	Mus musculus	0-4
16473374-11	2006	iNOS inhibition by azathioprine was associated with a decreased expression of IRF-1 (interferon regulatory factor 1) and IFN-beta (beta-interferon) mRNA.	Azathioprine	19-31	interferon beta 1, fibroblast	Mus musculus	121-129
16473374-6	2006	Azathioprine decreases iNOS mRNA levels as shown by semiquantitative competitive RT-PCR.	Azathioprine	0-12	nitric oxide synthase 2, inducible	Mus musculus	23-27
16473374-12	2006	Azathioprine induced iNOS inhibition seems to be associated with an action of the methylnitroimidazolyl substituent.	Azathioprine	0-12	nitric oxide synthase 2, inducible	Mus musculus	21-25
18666383-1	2006	Thiopurine methyltransferase (TPMT) catalyzes the S-methylation of thiopurine drugs such as 6-mercaptopurine (6-MP), thioguanine and azathioprine (AZA).	Azathioprine	147-150	thiopurine S-methyltransferase	Homo sapiens	30-34
16855176-1	2006	As azathioprine is one of the standard immunosuppressive drugs used for treatment of patients with different chronic inflammatory diseases, the effect of the azathioprine metabolizing enzyme thiopurine methyltransferase (TPMT) activity on incidence of adverse events (AE) was examined.	Azathioprine	3-15	thiopurine S-methyltransferase	Homo sapiens	221-225
16855176-1	2006	As azathioprine is one of the standard immunosuppressive drugs used for treatment of patients with different chronic inflammatory diseases, the effect of the azathioprine metabolizing enzyme thiopurine methyltransferase (TPMT) activity on incidence of adverse events (AE) was examined.	Azathioprine	158-170	thiopurine S-methyltransferase	Homo sapiens	221-225
16855176-9	2006	Reduced activity of TPMT in patients with chronic inflammatory diseases requiring immunosuppressive therapy with azathioprine, especially below a distinct cutoff, appears to inherit a substantial risk for development of AE.	Azathioprine	113-125	thiopurine S-methyltransferase	Homo sapiens	20-24
16704656-0	2006	The frequency and significance of thiopurine S-methyltransferase gene polymorphisms in azathioprine-treated renal transplant recipients.	Azathioprine	87-99	thiopurine S-methyltransferase	Homo sapiens	34-64
16716758-9	2006	Also, 88% of patients already on azathioprine and requiring colectomy underwent surgery within the first year of receiving CSA.	Azathioprine	33-45	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	123-126
16929618-5	2006	We report a patient with HPS which was complicated by granulomatous colitis with perineal and rectovaginal fistulas refractory to antibiotics and azathioprine but dramatically responded to repeated infusions of infliximab.	Azathioprine	146-158	HPS1 biogenesis of lysosomal organelles complex 3 subunit 1	Homo sapiens	25-28
16643135-2	2006	Patients with an impaired thiopurine S-methyltransferase (TPMT) activity are at risk of developing severe myelo-suppression upon treatment with thiopurines such as azathioprine.	Azathioprine	164-176	thiopurine S-methyltransferase	Homo sapiens	26-56
16643135-2	2006	Patients with an impaired thiopurine S-methyltransferase (TPMT) activity are at risk of developing severe myelo-suppression upon treatment with thiopurines such as azathioprine.	Azathioprine	164-176	thiopurine S-methyltransferase	Homo sapiens	58-62
29783434-0	2006	Typing TPMT and ITPase to detect azathioprine toxicity.	Azathioprine	33-45	inosine triphosphatase	Homo sapiens	16-22
29783434-1	2006	Genetic variation in thiopurine methyltransferase (TPMT) enzyme activity strongly predicts adverse effects in patients treated with the thiopurine drugs, azathioprine and 6-mercaptopurine, and is one of the classic examples of pharmacogenetics in clinical practice.	Azathioprine	154-166	thiopurine S-methyltransferase	Homo sapiens	21-49
29783434-1	2006	Genetic variation in thiopurine methyltransferase (TPMT) enzyme activity strongly predicts adverse effects in patients treated with the thiopurine drugs, azathioprine and 6-mercaptopurine, and is one of the classic examples of pharmacogenetics in clinical practice.	Azathioprine	154-166	thiopurine S-methyltransferase	Homo sapiens	51-55
16409140-3	2006	Loss of function of thiopurine S-methyltransferase (TPMT) results in severe and life-threatening hematopoietic toxicity if patients receive standard doses of mercaptopurine and azathioprine.	Azathioprine	177-189	thiopurine S-methyltransferase	Homo sapiens	20-50
16409140-3	2006	Loss of function of thiopurine S-methyltransferase (TPMT) results in severe and life-threatening hematopoietic toxicity if patients receive standard doses of mercaptopurine and azathioprine.	Azathioprine	177-189	thiopurine S-methyltransferase	Homo sapiens	52-56
18666383-1	2006	Thiopurine methyltransferase (TPMT) catalyzes the S-methylation of thiopurine drugs such as 6-mercaptopurine (6-MP), thioguanine and azathioprine (AZA).	Azathioprine	133-145	thiopurine S-methyltransferase	Homo sapiens	0-28
18666383-1	2006	Thiopurine methyltransferase (TPMT) catalyzes the S-methylation of thiopurine drugs such as 6-mercaptopurine (6-MP), thioguanine and azathioprine (AZA).	Azathioprine	133-145	thiopurine S-methyltransferase	Homo sapiens	30-34
18666383-1	2006	Thiopurine methyltransferase (TPMT) catalyzes the S-methylation of thiopurine drugs such as 6-mercaptopurine (6-MP), thioguanine and azathioprine (AZA).	Azathioprine	147-150	thiopurine S-methyltransferase	Homo sapiens	0-28
16399845-10	2006	In the azathioprine group, a positive c-ANCA titre at the time of switching to azathioprine (RR 2.2; 95% CI 1.0-5.4) was associated with relapse.	Azathioprine	7-19	proteinase 3	Homo sapiens	38-44
16399845-10	2006	In the azathioprine group, a positive c-ANCA titre at the time of switching to azathioprine (RR 2.2; 95% CI 1.0-5.4) was associated with relapse.	Azathioprine	79-91	proteinase 3	Homo sapiens	38-44
17699253-1	2006	A previous trial showed that treatment of children with severe IgA nephropathy (IgAN) using prednisolone, azathioprine, heparin-warfarin, and dipyridamole for 2 yr early in the course of disease reduced the severity of immunologic renal injury and prevented any increase in the percentage of sclerosed glomeruli.	Azathioprine	106-118	IGAN1	Homo sapiens	63-78
17699253-1	2006	A previous trial showed that treatment of children with severe IgA nephropathy (IgAN) using prednisolone, azathioprine, heparin-warfarin, and dipyridamole for 2 yr early in the course of disease reduced the severity of immunologic renal injury and prevented any increase in the percentage of sclerosed glomeruli.	Azathioprine	106-118	IGAN1	Homo sapiens	80-84
16795981-8	2006	In patients with Crohn"s disease, mean TPMT activity significantly decreased after AZA/6-MP therapy, while in patients with ulcerative colitis this activity did not change.	Azathioprine	83-86	thiopurine S-methyltransferase	Homo sapiens	39-43
16611274-2	2006	The occurrence and type of adverse events to azathioprine may be related to thiopurine S-methyltransferase (TPMT) enzyme activity and to inosine triphophate pyrophosphatase (ITPase) deficiency.	Azathioprine	45-57	thiopurine S-methyltransferase	Homo sapiens	76-106
16611274-2	2006	The occurrence and type of adverse events to azathioprine may be related to thiopurine S-methyltransferase (TPMT) enzyme activity and to inosine triphophate pyrophosphatase (ITPase) deficiency.	Azathioprine	45-57	thiopurine S-methyltransferase	Homo sapiens	108-112
16611274-2	2006	The occurrence and type of adverse events to azathioprine may be related to thiopurine S-methyltransferase (TPMT) enzyme activity and to inosine triphophate pyrophosphatase (ITPase) deficiency.	Azathioprine	45-57	inosine triphosphatase	Homo sapiens	137-172
16611274-2	2006	The occurrence and type of adverse events to azathioprine may be related to thiopurine S-methyltransferase (TPMT) enzyme activity and to inosine triphophate pyrophosphatase (ITPase) deficiency.	Azathioprine	45-57	inosine triphosphatase	Homo sapiens	174-180
16611274-3	2006	AIM: Investigate frequencies of functional TPMT polymorphisms and ITPA polymorphisms and their association with the occurrence of adverse events during azathioprine therapy in a paediatric inflammatory bowel disease population.	Azathioprine	152-164	thiopurine S-methyltransferase	Homo sapiens	43-47
16530578-0	2006	Azathioprine dosed by thiopurine methyltransferase activity for moderate-to-severe atopic eczema: a double-blind, randomised controlled trial.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	22-50
16530578-5	2006	As maintenance treatment, patients with heterozygous range TPMT activity received azathioprine 1.0 mg/kg daily, compared with 2.5 mg/kg daily in patients with normal TPMT activity.	Azathioprine	82-94	thiopurine S-methyltransferase	Homo sapiens	59-63
16530578-15	2006	Participants with heterozygous range TPMT activity responded to azathioprine in similar proportions to other participants, but none developed bone-marrow toxicity.	Azathioprine	64-76	thiopurine S-methyltransferase	Homo sapiens	37-41
16614955-3	2006	The objective of this study was to verify, in a population of young patients with IBD, the presence of an association among mutations in the MTHFR gene, the incidence of IBD, and the risk of adverse events during the treatment with thiopurines azathioprine (AZA) or 6-mercaptopurine (6MP).	Azathioprine	258-261	methylenetetrahydrofolate reductase	Homo sapiens	141-146
16431304-0	2006	Inosine triphosphate pyrophosphatase and thiopurine s-methyltransferase genotypes relationship to azathioprine-induced myelosuppression.	Azathioprine	98-110	inosine triphosphatase	Homo sapiens	0-36
16431304-0	2006	Inosine triphosphate pyrophosphatase and thiopurine s-methyltransferase genotypes relationship to azathioprine-induced myelosuppression.	Azathioprine	98-110	thiopurine S-methyltransferase	Homo sapiens	41-71
16431304-2	2006	Mutations in the thiopurine S-methyltransferase (TPMT) and inosine triphosphate pyrophosphatase (ITPA) genes have been associated with the occurrence of AZA-related toxicity.	Azathioprine	153-156	thiopurine S-methyltransferase	Homo sapiens	17-47
16431304-2	2006	Mutations in the thiopurine S-methyltransferase (TPMT) and inosine triphosphate pyrophosphatase (ITPA) genes have been associated with the occurrence of AZA-related toxicity.	Azathioprine	153-156	thiopurine S-methyltransferase	Homo sapiens	49-53
16431304-2	2006	Mutations in the thiopurine S-methyltransferase (TPMT) and inosine triphosphate pyrophosphatase (ITPA) genes have been associated with the occurrence of AZA-related toxicity.	Azathioprine	153-156	inosine triphosphatase	Homo sapiens	59-95
16431304-2	2006	Mutations in the thiopurine S-methyltransferase (TPMT) and inosine triphosphate pyrophosphatase (ITPA) genes have been associated with the occurrence of AZA-related toxicity.	Azathioprine	153-156	inosine triphosphatase	Homo sapiens	97-101
16431304-3	2006	The aim of our study was to determine the relative contribution of ITPA and TPMT mutations to the development of toxicity induced by AZA treatment in IBD patients.	Azathioprine	133-136	inosine triphosphatase	Homo sapiens	67-71
16431304-3	2006	The aim of our study was to determine the relative contribution of ITPA and TPMT mutations to the development of toxicity induced by AZA treatment in IBD patients.	Azathioprine	133-136	thiopurine S-methyltransferase	Homo sapiens	76-80
16431304-9	2006	CONCLUSIONS: ITPA 94C&gt;A and TPMT polymorphisms are associated with AZA-related leukopenia in IBD patients.	Azathioprine	70-73	inosine triphosphatase	Homo sapiens	13-17
16431304-9	2006	CONCLUSIONS: ITPA 94C&gt;A and TPMT polymorphisms are associated with AZA-related leukopenia in IBD patients.	Azathioprine	70-73	thiopurine S-methyltransferase	Homo sapiens	31-35
28210198-3	2006	Indeed, tailoring the dose of AZA based on TPMT activity has been proposed as a useful clinical tool to improve overall clinical response and to avoid untoward side effects.	Azathioprine	30-33	thiopurine S-methyltransferase	Homo sapiens	43-47
28210198-4	2006	Recent studies have shown that patients with intermediate TPMT activity should be initiated on a low (1 mg/kg) dosage of AZA and carefully monitored in order to minimize the risk of bone marrow suppression.	Azathioprine	121-124	thiopurine S-methyltransferase	Homo sapiens	58-62
28210198-5	2006	Patients with very high TPMT enzyme activity levels (&gt;15 U/mL) may very well respond to a higher (&gt;2 mg/kg) dosage of AZA.	Azathioprine	124-127	thiopurine S-methyltransferase	Homo sapiens	24-28
28210198-7	2006	Individualized AZA dosing based on TPMT enzyme activity is based on the notion of achieving therapeutic erythrocyte 6-TGn metabolite levels between 235-260 pmol/8x108 red blood cells.	Azathioprine	15-18	thiopurine S-methyltransferase	Homo sapiens	35-39
16365460-6	2006	Azathioprine-generated 6-Thio-GTP thus prevents the development of an effective immune response via blockade of Vav activity on Rac proteins.	Azathioprine	0-12	vav guanine nucleotide exchange factor 1	Homo sapiens	112-115
16365460-0	2006	Azathioprine suppresses ezrin-radixin-moesin-dependent T cell-APC conjugation through inhibition of Vav guanosine exchange activity on Rac proteins.	Azathioprine	0-12	vav guanine nucleotide exchange factor 1	Homo sapiens	100-103
16365460-0	2006	Azathioprine suppresses ezrin-radixin-moesin-dependent T cell-APC conjugation through inhibition of Vav guanosine exchange activity on Rac proteins.	Azathioprine	0-12	Rac family small GTPase 1	Homo sapiens	135-138
16365460-6	2006	Azathioprine-generated 6-Thio-GTP thus prevents the development of an effective immune response via blockade of Vav activity on Rac proteins.	Azathioprine	0-12	Rac family small GTPase 1	Homo sapiens	128-131
16365460-7	2006	These findings provide novel insights into the immunosuppressive effects of azathioprine and suggest that antagonists of the Vav-Rac signaling pathway may be useful for suppression of T cell-dependent pathogenic immune responses.	Azathioprine	76-88	vav guanine nucleotide exchange factor 1	Homo sapiens	125-128
16365460-7	2006	These findings provide novel insights into the immunosuppressive effects of azathioprine and suggest that antagonists of the Vav-Rac signaling pathway may be useful for suppression of T cell-dependent pathogenic immune responses.	Azathioprine	76-88	Rac family small GTPase 1	Homo sapiens	129-132
17065099-1	2006	The efficiency of Mycophenolate mofetil (MMF) and Azathioprine (AZA) as immunosuppressive agents depends on the activity of 2 enzymes, inosine monophosphate dehydrogenase (IMPDH) and thiopurine methyltransferase (TPMT) respectively.	Azathioprine	50-62	thiopurine S-methyltransferase	Homo sapiens	183-211
16438485-5	2006	Genetic factors are also important in the treatment of RA because the activity of enzymes relevant in the metabolism of drugs such as methotrexate and azathioprine, including methylenetetrahydrofolate reductase and thiopurine methyltransferase, are in part genetically determined.	Azathioprine	151-163	methylenetetrahydrofolate reductase	Homo sapiens	175-210
17065099-1	2006	The efficiency of Mycophenolate mofetil (MMF) and Azathioprine (AZA) as immunosuppressive agents depends on the activity of 2 enzymes, inosine monophosphate dehydrogenase (IMPDH) and thiopurine methyltransferase (TPMT) respectively.	Azathioprine	50-62	thiopurine S-methyltransferase	Homo sapiens	213-217
17065099-1	2006	The efficiency of Mycophenolate mofetil (MMF) and Azathioprine (AZA) as immunosuppressive agents depends on the activity of 2 enzymes, inosine monophosphate dehydrogenase (IMPDH) and thiopurine methyltransferase (TPMT) respectively.	Azathioprine	64-67	thiopurine S-methyltransferase	Homo sapiens	183-211
17065099-1	2006	The efficiency of Mycophenolate mofetil (MMF) and Azathioprine (AZA) as immunosuppressive agents depends on the activity of 2 enzymes, inosine monophosphate dehydrogenase (IMPDH) and thiopurine methyltransferase (TPMT) respectively.	Azathioprine	64-67	thiopurine S-methyltransferase	Homo sapiens	213-217
16272700-1	2005	We investigated the genotypic status of thiopurine methyltransferase (TPMT) polymorphism to evaluate the possible risk of the toxicity of azathioprine (AZA) in 68 patients with systemic lupus erythematosus (SLE).	Azathioprine	138-150	thiopurine S-methyltransferase	Homo sapiens	70-74
16355988-1	2005	[structure: see text] A solid-phase fluorenylmethyloxycarbonyl (Fmoc)-based synthesis strategy is described for "mixed" aza-beta3-peptides as well as a convenient general approach for their required building blocks, the aza-beta3-amino acid residues (aza-beta3-aa).	Azathioprine	120-123	eukaryotic translation elongation factor 1 beta 2 pseudogene 2	Homo sapiens	124-129
16214825-0	2005	Association of inosine triphosphatase 94C&gt;A and thiopurine S-methyltransferase deficiency with adverse events and study drop-outs under azathioprine therapy in a prospective Crohn disease study.	Azathioprine	139-151	inosine triphosphatase	Homo sapiens	15-37
16187368-1	2005	Bifunctional thiourea 1a catalyzes aza-Henry reaction of nitroalkanes with N-Boc-imines to give syn-beta-nitroamines with good to high diastereo- and enantioselectivity.	Azathioprine	35-38	synemin	Homo sapiens	96-99
16214825-6	2005	RESULTS: Early drop-out (within 2 weeks) from aza therapy was associated with ITPA 94C &gt; A [P = 0.020; odds ratio (OR), 4.6; 95% confidence interval (95% CI), 1.2-17.4] and low TPMT activity [&lt;10 nmol/(mL erythrocytes .	Azathioprine	46-49	inosine triphosphatase	Homo sapiens	78-82
16214825-6	2005	RESULTS: Early drop-out (within 2 weeks) from aza therapy was associated with ITPA 94C &gt; A [P = 0.020; odds ratio (OR), 4.6; 95% confidence interval (95% CI), 1.2-17.4] and low TPMT activity [&lt;10 nmol/(mL erythrocytes .	Azathioprine	46-49	thiopurine S-methyltransferase	Homo sapiens	180-184
16214825-10	2005	For only drop-outs attributable to aza-related side effects (n = 16), there was a significant association with ITPA 94C &gt; A (P = 0.002; OR = 7.8; 95% CI, 2.1-29.1).	Azathioprine	35-38	inosine triphosphatase	Homo sapiens	111-115
16214825-12	2005	CONCLUSIONS: Patients with ITPA 94C &gt; A mutations or low TPMT activity constitute a pharmacogenetic high-risk group for drop-out from aza therapy.	Azathioprine	137-140	inosine triphosphatase	Homo sapiens	27-31
16214825-12	2005	CONCLUSIONS: Patients with ITPA 94C &gt; A mutations or low TPMT activity constitute a pharmacogenetic high-risk group for drop-out from aza therapy.	Azathioprine	137-140	thiopurine S-methyltransferase	Homo sapiens	60-64
16214825-13	2005	ITPA 94C&gt;A appears to be a promising marker indicating predisposition to aza intolerance.	Azathioprine	76-79	inosine triphosphatase	Homo sapiens	0-4
16306775-0	2005	TPMT genotype screening for patients about to begin azathioprine treatment--a look at costs and potential benefits.	Azathioprine	52-64	thiopurine S-methyltransferase	Homo sapiens	0-4
16272700-4	2005	Two out of 4 SLE patients with TPMT*1/*3C had been treated with AZA, and one patient showed a leucopenia.	Azathioprine	64-67	thiopurine S-methyltransferase	Homo sapiens	31-35
16272700-5	2005	The TPMT genotyping before AZA treatment is recommended for Japanese SLE patient group to avoid the AZA-induced adverse events, although detection of the patient with low TPMT activity by genotyping is still imperfect.	Azathioprine	100-103	thiopurine S-methyltransferase	Homo sapiens	4-8
16107271-0	2005	Lymphocyte Hprt mutant frequency and sperm toxicity in C57BL/6 mice treated chronically with Azathioprine.	Azathioprine	93-105	hypoxanthine guanine phosphoribosyl transferase	Mus musculus	11-15
16396707-0	2005	Thiopurine S-methyltransferase polymorphisms and the relationship between the mutant alleles and the adverse effects in systemic lupus erythematosus patients taking azathioprine.	Azathioprine	165-177	thiopurine S-methyltransferase	Homo sapiens	0-30
16396707-1	2005	OBJECTIVE: The present study sought to elucidate the genetic basis of thiopurine methyltransferase (TPMT) polymorphism and subsequently to investigate the relationship between mutant TPMT and an adverse response observed in Korean patients with systemic lupus erythematosus (SLE) taking azathioprine (AZA).	Azathioprine	287-299	thiopurine S-methyltransferase	Homo sapiens	100-104
16396707-1	2005	OBJECTIVE: The present study sought to elucidate the genetic basis of thiopurine methyltransferase (TPMT) polymorphism and subsequently to investigate the relationship between mutant TPMT and an adverse response observed in Korean patients with systemic lupus erythematosus (SLE) taking azathioprine (AZA).	Azathioprine	287-299	thiopurine S-methyltransferase	Homo sapiens	183-187
16396707-1	2005	OBJECTIVE: The present study sought to elucidate the genetic basis of thiopurine methyltransferase (TPMT) polymorphism and subsequently to investigate the relationship between mutant TPMT and an adverse response observed in Korean patients with systemic lupus erythematosus (SLE) taking azathioprine (AZA).	Azathioprine	301-304	thiopurine S-methyltransferase	Homo sapiens	100-104
16396707-1	2005	OBJECTIVE: The present study sought to elucidate the genetic basis of thiopurine methyltransferase (TPMT) polymorphism and subsequently to investigate the relationship between mutant TPMT and an adverse response observed in Korean patients with systemic lupus erythematosus (SLE) taking azathioprine (AZA).	Azathioprine	301-304	thiopurine S-methyltransferase	Homo sapiens	183-187
16396707-2	2005	METHODS: The TPMT genotype of 342 patients with SLE was determined by MALDI-TOF mass spectrometry and correlated with the effects of clinical exposure to AZA.	Azathioprine	154-157	thiopurine S-methyltransferase	Homo sapiens	13-17
16107271-1	2005	Many patients undergoing chronic therapy with the purine analogue Azathioprine (Aza) have highly elevated HPRT lymphocyte mutant frequencies (MFs), and it is likely that these increases are due to selection of pre-existing HPRT mutant lymphocytes.	Azathioprine	66-78	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	106-110
16107271-1	2005	Many patients undergoing chronic therapy with the purine analogue Azathioprine (Aza) have highly elevated HPRT lymphocyte mutant frequencies (MFs), and it is likely that these increases are due to selection of pre-existing HPRT mutant lymphocytes.	Azathioprine	66-78	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	223-227
16107271-1	2005	Many patients undergoing chronic therapy with the purine analogue Azathioprine (Aza) have highly elevated HPRT lymphocyte mutant frequencies (MFs), and it is likely that these increases are due to selection of pre-existing HPRT mutant lymphocytes.	Azathioprine	66-69	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	106-110
16107271-1	2005	Many patients undergoing chronic therapy with the purine analogue Azathioprine (Aza) have highly elevated HPRT lymphocyte mutant frequencies (MFs), and it is likely that these increases are due to selection of pre-existing HPRT mutant lymphocytes.	Azathioprine	66-69	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	223-227
16107271-11	2005	The data suggest that mice chronically treated with 5 and 10mg/kg Aza (doses similar to those used in humans) have elevated Hprt MFs due to clonal amplification of selected Hprt mutants.	Azathioprine	66-69	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	124-128
16107271-11	2005	The data suggest that mice chronically treated with 5 and 10mg/kg Aza (doses similar to those used in humans) have elevated Hprt MFs due to clonal amplification of selected Hprt mutants.	Azathioprine	66-69	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	173-177
16107271-12	2005	The results also suggest that mice treated with these doses of Aza retain reasonable fertility, and will be useful for breeding experiments to examine the possibility of increasing the germ-line transmission of Hprt mutations.	Azathioprine	63-66	hypoxanthine guanine phosphoribosyl transferase	Mus musculus	211-215
16181376-3	2005	AZA dose selection based on pharmacogenetic testing of TPMT and metabolite monitoring (MM) may offer a safety and efficacy advantage over traditional dosing strategies.	Azathioprine	0-3	thiopurine S-methyltransferase	Homo sapiens	55-59
16175140-1	2005	Metabolism of thiopurine drugs--azathioprine, 6-mercaptopurine, and 6-thioguanine--has provided a powerful pharmacogenetic model incorporating polymorphism of the enzyme thiopurine methyltransferase (TPMT) and the primary active metabolite, thioguanine nucleotide (TGN).	Azathioprine	32-44	thiopurine S-methyltransferase	Homo sapiens	170-198
16181301-10	2005	In the fistulizing Crohn"s disease cohort, the same Fas ligand -843 CC/CT genotype was the only predictor of response (P = 0.002; OR = 1.66; 95% CI: 1.21-2.29), interacting with caspase-9 93 polymorphism but not with azathioprine/mercaptopurine.	Azathioprine	217-229	Fas ligand	Homo sapiens	52-62
16181376-2	2005	Thiopurine methyltransferase (TPMT) is important for the metabolism of AZA and influences the production of active AZA metabolites.	Azathioprine	71-74	thiopurine S-methyltransferase	Homo sapiens	0-28
16181376-2	2005	Thiopurine methyltransferase (TPMT) is important for the metabolism of AZA and influences the production of active AZA metabolites.	Azathioprine	71-74	thiopurine S-methyltransferase	Homo sapiens	30-34
16181376-2	2005	Thiopurine methyltransferase (TPMT) is important for the metabolism of AZA and influences the production of active AZA metabolites.	Azathioprine	115-118	thiopurine S-methyltransferase	Homo sapiens	0-28
16181376-2	2005	Thiopurine methyltransferase (TPMT) is important for the metabolism of AZA and influences the production of active AZA metabolites.	Azathioprine	115-118	thiopurine S-methyltransferase	Homo sapiens	30-34
16175140-1	2005	Metabolism of thiopurine drugs--azathioprine, 6-mercaptopurine, and 6-thioguanine--has provided a powerful pharmacogenetic model incorporating polymorphism of the enzyme thiopurine methyltransferase (TPMT) and the primary active metabolite, thioguanine nucleotide (TGN).	Azathioprine	32-44	thiopurine S-methyltransferase	Homo sapiens	200-204
16245692-2	2005	The conformational models of the active site of adenosine deaminase (ADA) and its complexes in the basic state with adenosine and 13 isosteric analogues of the aza, deaza, and azadeaza series were constructed.	Azathioprine	160-163	adenosine deaminase	Homo sapiens	48-67
16159550-2	2005	BACKGROUND AND OBJECTIVE: Our objective was to assess the activity of thiopurine methyltransferase (TPMT) in a very large number of Spanish patients with inflammatory bowel disease (IBD), to evaluate the influence of several variables (including azathioprine or 6-mercaptopurine) on that activity, and to know the proportion of patients with low TPMT activity and therefore high risk of myelotoxicity when treated with these drugs.	Azathioprine	246-258	thiopurine S-methyltransferase	Homo sapiens	100-104
16159550-9	2005	In the univariate study, statistically significant differences (p &lt; 0.001), yet of doubtly clinical significance because its minimal magnitude, were demonstrated in TPMT values depending on age, sex, type of disease, and treatment with azathioprine/6-mercaptopurine.	Azathioprine	239-251	thiopurine S-methyltransferase	Homo sapiens	168-172
16159550-10	2005	In the multivariate study, the variables associated with TPMT activity were: sex, treatment with 5-aminosalicylates, steroids and azathioprine/6-mercaptopurine.	Azathioprine	130-142	thiopurine S-methyltransferase	Homo sapiens	57-61
16159550-11	2005	CONCLUSIONS: This study shows that 0.5% of the Spanish patients with IBD have low TPMT activity (&lt; 5 U/ml RBCs), a figure similar to that reported in other countries, these patients being at higher risk of myelotoxicity when treated with azathioprine or 6-mercaptopurine.	Azathioprine	241-253	thiopurine S-methyltransferase	Homo sapiens	82-86
16245692-2	2005	The conformational models of the active site of adenosine deaminase (ADA) and its complexes in the basic state with adenosine and 13 isosteric analogues of the aza, deaza, and azadeaza series were constructed.	Azathioprine	160-163	adenosine deaminase	Homo sapiens	69-72
15687239-5	2005	Major risk factors for the development of SCC were long duration of chronic GVHD therapy (P &lt; .001); use of azathioprine, particularly when combined with cyclosporine and steroids (P &lt; .001); and severe chronic GVHD (P = .004).	Azathioprine	111-123	serpin family B member 3	Homo sapiens	42-45
16175949-6	2005	After switching Aza to methotrexate (Mtx) treatment, his symptoms disappeared and CRP concentration returned to normal.	Azathioprine	16-19	C-reactive protein	Homo sapiens	82-85
15973722-3	2005	There is evidence that polymorphisms in the genes encoding thiopurine methyltransferase (TPMT) and inosine triphosphate pyrophosphatase (ITPase) predict adverse drug reactions to AZA therapy.	Azathioprine	179-182	thiopurine S-methyltransferase	Homo sapiens	59-87
15973722-3	2005	There is evidence that polymorphisms in the genes encoding thiopurine methyltransferase (TPMT) and inosine triphosphate pyrophosphatase (ITPase) predict adverse drug reactions to AZA therapy.	Azathioprine	179-182	thiopurine S-methyltransferase	Homo sapiens	89-93
15973722-7	2005	Clinical response to AZA was retrospectively correlated against TPMT activity, TPMT*2, *3A, and *3A genotypes, inosine triphosphatase (ITPA) 94C&gt;A and IVS2+21A&gt;C genotypes, and MTHFR 677C&gt;T and 1298A&gt;C genotypes.	Azathioprine	21-24	thiopurine S-methyltransferase	Homo sapiens	64-68
15973722-7	2005	Clinical response to AZA was retrospectively correlated against TPMT activity, TPMT*2, *3A, and *3A genotypes, inosine triphosphatase (ITPA) 94C&gt;A and IVS2+21A&gt;C genotypes, and MTHFR 677C&gt;T and 1298A&gt;C genotypes.	Azathioprine	21-24	thiopurine S-methyltransferase	Homo sapiens	79-83
15973722-7	2005	Clinical response to AZA was retrospectively correlated against TPMT activity, TPMT*2, *3A, and *3A genotypes, inosine triphosphatase (ITPA) 94C&gt;A and IVS2+21A&gt;C genotypes, and MTHFR 677C&gt;T and 1298A&gt;C genotypes.	Azathioprine	21-24	methylenetetrahydrofolate reductase	Homo sapiens	183-188
15829415-8	2005	It is worth noting that TNFR-Ig or prednisolone, which is effective for treatment of patients with severe-fulminant Crohn"s disease, markedly attenuated pathological clinical indices in this colitis model, whereas the immunosuppressive agents, azathioprine, tacrolimus, and cyclosporine A produced no significant effect.	Azathioprine	244-256	TNF receptor superfamily member 1A	Homo sapiens	24-28
15797890-2	2005	However, IgAN frequently recurs in allografts treated with azathioprine.	Azathioprine	59-71	IGAN1	Homo sapiens	9-13
15797890-9	2005	By 3 years post-transplant, IgAN developed in six of 60 (10.0%) azathioprine-treated allografts and five of 62 (8.1%) mycophenolate mofetil-treated allografts (P = 0.76).	Azathioprine	64-76	IGAN1	Homo sapiens	28-32
16044099-0	2005	The impact of thiopurine s-methyltransferase polymorphism on azathioprine-induced myelotoxicity in renal transplant recipients.	Azathioprine	61-73	thiopurine S-methyltransferase	Homo sapiens	14-44
16044099-1	2005	Thiopurine S-methyltransferase (TPMT) is an enzyme that catalyzes the S-methylation of thiopurine drugs such as 6-mercaptopurine, 6-thioguanine, and azathioprine.	Azathioprine	149-161	thiopurine S-methyltransferase	Homo sapiens	0-30
16044099-1	2005	Thiopurine S-methyltransferase (TPMT) is an enzyme that catalyzes the S-methylation of thiopurine drugs such as 6-mercaptopurine, 6-thioguanine, and azathioprine.	Azathioprine	149-161	thiopurine S-methyltransferase	Homo sapiens	32-36
16044099-10	2005	Our results suggest that polymorphisms in TPMT gene may be responsible for approximately 12.5% of all leukopenia episodes in renal transplant recipients treated with azathioprine.	Azathioprine	166-178	thiopurine S-methyltransferase	Homo sapiens	42-46
16044099-11	2005	Genotyping for the major TPMT variant alleles may be a valuable tool in preventing AZA toxicity and optimization of immunosuppressive therapy.	Azathioprine	83-86	thiopurine S-methyltransferase	Homo sapiens	25-29
15912111-13	2005	CONCLUSION: The reduction of calcineurin inhibitor dosage and replacement of azathioprine by mycophenolate mofetil is a safe way to improve renal function in children with heart transplants and calcineurin inhibitor induced nephrotoxicity.	Azathioprine	77-89	calcineurin binding protein 1	Homo sapiens	194-215
15687239-7	2005	Additional analyses determined that prolonged immunosuppressive therapy and azathioprine use were also significant risk factors for SCC of the skin and of the oral mucosa.	Azathioprine	76-88	serpin family B member 3	Homo sapiens	132-135
15819814-0	2005	Severe azathioprine-induced myelotoxicity in a kidney transplant patient with thiopurine S-methyltransferase-deficient genotype (TPMT*3A/*3C).	Azathioprine	7-19	thiopurine S-methyltransferase	Homo sapiens	78-108
15854172-2	2005	Thus, during treatment with azathioprine or mercaptopurine, both metabolized by thiopurine S-methyltransferase, sulfasalazine or 5-aminosalicylate could modify the action of azathioprine/mercaptopurine.	Azathioprine	28-40	thiopurine S-methyltransferase	Homo sapiens	80-110
15854172-2	2005	Thus, during treatment with azathioprine or mercaptopurine, both metabolized by thiopurine S-methyltransferase, sulfasalazine or 5-aminosalicylate could modify the action of azathioprine/mercaptopurine.	Azathioprine	174-186	thiopurine S-methyltransferase	Homo sapiens	80-110
15888259-5	2005	The combination of IFNbeta-1b with AZA resulted in a significant negative effect on the production of IL-2 (P=0.006), whereas TNF-alpha (P=0.02), IFN-gamma (P=0.03), IL-4 (P=0.2), and IL-10 (P=0.3) were not statistically impacted.	Azathioprine	35-38	interleukin 2	Homo sapiens	102-106
15792824-1	2005	Thiopurine methyltransferase (TPMT) is a key enzyme in azathioprine metabolism mediating both immunosuppression and cytotoxicity.	Azathioprine	55-67	thiopurine S-methyltransferase	Homo sapiens	0-28
15792824-1	2005	Thiopurine methyltransferase (TPMT) is a key enzyme in azathioprine metabolism mediating both immunosuppression and cytotoxicity.	Azathioprine	55-67	thiopurine S-methyltransferase	Homo sapiens	30-34
15792824-2	2005	TPMT activity may be influenced by a mutation in the TPMT gene resulting in individual differences in azathioprine metabolism.	Azathioprine	102-114	thiopurine S-methyltransferase	Homo sapiens	0-4
15792824-2	2005	TPMT activity may be influenced by a mutation in the TPMT gene resulting in individual differences in azathioprine metabolism.	Azathioprine	102-114	thiopurine S-methyltransferase	Homo sapiens	53-57
15792824-3	2005	Individuals heterozygous for TPMT mutations or with low TPMT activity may be susceptible to azathioprine toxicity.	Azathioprine	92-104	thiopurine S-methyltransferase	Homo sapiens	29-33
15792824-3	2005	Individuals heterozygous for TPMT mutations or with low TPMT activity may be susceptible to azathioprine toxicity.	Azathioprine	92-104	thiopurine S-methyltransferase	Homo sapiens	56-60
15792824-4	2005	We evaluate TPMT genotyping and TPMT enzyme activity as predictive tests for developing azathioprine-related adverse events.	Azathioprine	88-100	thiopurine S-methyltransferase	Homo sapiens	12-16
15792824-4	2005	We evaluate TPMT genotyping and TPMT enzyme activity as predictive tests for developing azathioprine-related adverse events.	Azathioprine	88-100	thiopurine S-methyltransferase	Homo sapiens	32-36
15788214-3	2005	Diminished activity of this enzyme decreases the methylation of thiopurines, theoretically resulting in potential overdosing, while high thiopurine (S)-methyltransferase status leads to overproduction of toxic metabolites and ineffectiveness of azathioprine and 6-mercaptopurine.	Azathioprine	245-257	thiopurine S-methyltransferase	Homo sapiens	137-169
15792824-0	2005	Thiopurine methyltransferase (TPMT) heterozygosity and enzyme activity as predictive tests for the development of azathioprine-related adverse events.	Azathioprine	114-126	thiopurine S-methyltransferase	Homo sapiens	0-28
15792824-0	2005	Thiopurine methyltransferase (TPMT) heterozygosity and enzyme activity as predictive tests for the development of azathioprine-related adverse events.	Azathioprine	114-126	thiopurine S-methyltransferase	Homo sapiens	30-34
15888259-5	2005	The combination of IFNbeta-1b with AZA resulted in a significant negative effect on the production of IL-2 (P=0.006), whereas TNF-alpha (P=0.02), IFN-gamma (P=0.03), IL-4 (P=0.2), and IL-10 (P=0.3) were not statistically impacted.	Azathioprine	35-38	interleukin 4	Homo sapiens	166-170
15888259-5	2005	The combination of IFNbeta-1b with AZA resulted in a significant negative effect on the production of IL-2 (P=0.006), whereas TNF-alpha (P=0.02), IFN-gamma (P=0.03), IL-4 (P=0.2), and IL-10 (P=0.3) were not statistically impacted.	Azathioprine	35-38	interleukin 10	Homo sapiens	184-189
15848526-5	2005	The tubular expression of mRNA for IL-6 and TGF-beta1 was significantly lower in biopsies with AR (n = 34) obtained from patients treated with MMF (n = 12) than in biopsies obtained from patients treated with azathioprine (n = 22) (P &lt; .02).	Azathioprine	209-221	interleukin 6	Homo sapiens	35-39
15864171-16	2005	CSA may act as a "bridge" until the therapeutic action of azathioprine is achieved for maintenance treatment.	Azathioprine	58-70	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	0-3
15776134-1	2005	BACKGROUND: Azathioprine (AZA), used to treat inflammatory bowel disease (IBD), is metabolized by thiopurine methyltransferase (TPMT).	Azathioprine	12-24	thiopurine S-methyltransferase	Homo sapiens	98-126
15776134-1	2005	BACKGROUND: Azathioprine (AZA), used to treat inflammatory bowel disease (IBD), is metabolized by thiopurine methyltransferase (TPMT).	Azathioprine	12-24	thiopurine S-methyltransferase	Homo sapiens	128-132
15776134-1	2005	BACKGROUND: Azathioprine (AZA), used to treat inflammatory bowel disease (IBD), is metabolized by thiopurine methyltransferase (TPMT).	Azathioprine	26-29	thiopurine S-methyltransferase	Homo sapiens	98-126
15776134-1	2005	BACKGROUND: Azathioprine (AZA), used to treat inflammatory bowel disease (IBD), is metabolized by thiopurine methyltransferase (TPMT).	Azathioprine	26-29	thiopurine S-methyltransferase	Homo sapiens	128-132
15776134-5	2005	OBJECTIVE: To determine whether assessment of TPMT activity before the administration of AZA would predict acute toxicity and, thus, allow for reductions in health care costs related to biochemical screening for, and management of, AZA-induced adverse events.	Azathioprine	232-235	thiopurine S-methyltransferase	Homo sapiens	46-50
15848526-5	2005	The tubular expression of mRNA for IL-6 and TGF-beta1 was significantly lower in biopsies with AR (n = 34) obtained from patients treated with MMF (n = 12) than in biopsies obtained from patients treated with azathioprine (n = 22) (P &lt; .02).	Azathioprine	209-221	transforming growth factor beta 1	Homo sapiens	44-53
15527680-5	2004	Azathioprine and 6-mercaptopurine remain efficient beyond 4 years in patients with relapses and elevated C-reactive protein in spite of this therapy.	Azathioprine	0-12	C-reactive protein	Homo sapiens	105-123
15776100-0	2005	Measurement of thiopurine methyl transferase activity guides dose-initiation and prevents toxicity from azathioprine.	Azathioprine	104-116	thiopurine S-methyltransferase	Homo sapiens	15-44
15776100-9	2005	The measurement of TPMT activity helps to guide dose initiation and may prevent toxicity from azathioprine.	Azathioprine	94-106	thiopurine S-methyltransferase	Homo sapiens	19-23
16078858-8	2005	The pharmacogenetic basis of toxicity is well known for azathioprine: several thiopurine methyltransferase (TPMT) polymorphisms that are associated with reduced activity of this thiopurine drug metabolizing enzyme result in cytotoxic and immunosuppressive adverse effects of azathioprine.	Azathioprine	56-68	thiopurine S-methyltransferase	Homo sapiens	78-106
16078858-8	2005	The pharmacogenetic basis of toxicity is well known for azathioprine: several thiopurine methyltransferase (TPMT) polymorphisms that are associated with reduced activity of this thiopurine drug metabolizing enzyme result in cytotoxic and immunosuppressive adverse effects of azathioprine.	Azathioprine	56-68	thiopurine S-methyltransferase	Homo sapiens	108-112
16078858-8	2005	The pharmacogenetic basis of toxicity is well known for azathioprine: several thiopurine methyltransferase (TPMT) polymorphisms that are associated with reduced activity of this thiopurine drug metabolizing enzyme result in cytotoxic and immunosuppressive adverse effects of azathioprine.	Azathioprine	275-287	thiopurine S-methyltransferase	Homo sapiens	78-106
16078858-8	2005	The pharmacogenetic basis of toxicity is well known for azathioprine: several thiopurine methyltransferase (TPMT) polymorphisms that are associated with reduced activity of this thiopurine drug metabolizing enzyme result in cytotoxic and immunosuppressive adverse effects of azathioprine.	Azathioprine	275-287	thiopurine S-methyltransferase	Homo sapiens	108-112
15564886-1	2004	A 94C&gt;A missense mutation in the ITPA gene which encodes inosine triphosphate pyrophosphatase has been associated with adverse effects from azathioprine, specifically flu-like symptoms, pancreatitis and rash.	Azathioprine	143-155	inosine triphosphatase	Homo sapiens	36-40
15476481-0	2004	Thiopurine S-methyltransferase genotype predicts azathioprine-induced myelotoxicity in kidney transplant recipients.	Azathioprine	49-61	thiopurine S-methyltransferase	Homo sapiens	0-30
15476481-1	2004	Azathioprine (AZA) is an immunosuppressive prodrug that undergoes metabolism by thiopurine S-methyltransferase (TPMT).	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	80-110
15476481-1	2004	Azathioprine (AZA) is an immunosuppressive prodrug that undergoes metabolism by thiopurine S-methyltransferase (TPMT).	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	112-116
15476481-1	2004	Azathioprine (AZA) is an immunosuppressive prodrug that undergoes metabolism by thiopurine S-methyltransferase (TPMT).	Azathioprine	14-17	thiopurine S-methyltransferase	Homo sapiens	80-110
15476481-1	2004	Azathioprine (AZA) is an immunosuppressive prodrug that undergoes metabolism by thiopurine S-methyltransferase (TPMT).	Azathioprine	14-17	thiopurine S-methyltransferase	Homo sapiens	112-116
15588444-1	2004	Determination of thiopurine S-methyltransferase (TPMT) activity prior to starting azathioprine therapy is used to identify individuals with low or deficient TPMT activities who are at risk of severe complications and even death This case describes a patient treated with azathioprine without prior knowledge of TPMT status.	Azathioprine	82-94	thiopurine S-methyltransferase	Homo sapiens	157-161
15588444-1	2004	Determination of thiopurine S-methyltransferase (TPMT) activity prior to starting azathioprine therapy is used to identify individuals with low or deficient TPMT activities who are at risk of severe complications and even death This case describes a patient treated with azathioprine without prior knowledge of TPMT status.	Azathioprine	82-94	thiopurine S-methyltransferase	Homo sapiens	157-161
15588444-1	2004	Determination of thiopurine S-methyltransferase (TPMT) activity prior to starting azathioprine therapy is used to identify individuals with low or deficient TPMT activities who are at risk of severe complications and even death This case describes a patient treated with azathioprine without prior knowledge of TPMT status.	Azathioprine	271-283	thiopurine S-methyltransferase	Homo sapiens	17-47
15588444-1	2004	Determination of thiopurine S-methyltransferase (TPMT) activity prior to starting azathioprine therapy is used to identify individuals with low or deficient TPMT activities who are at risk of severe complications and even death This case describes a patient treated with azathioprine without prior knowledge of TPMT status.	Azathioprine	271-283	thiopurine S-methyltransferase	Homo sapiens	49-53
15588444-1	2004	Determination of thiopurine S-methyltransferase (TPMT) activity prior to starting azathioprine therapy is used to identify individuals with low or deficient TPMT activities who are at risk of severe complications and even death This case describes a patient treated with azathioprine without prior knowledge of TPMT status.	Azathioprine	271-283	thiopurine S-methyltransferase	Homo sapiens	157-161
15588444-1	2004	Determination of thiopurine S-methyltransferase (TPMT) activity prior to starting azathioprine therapy is used to identify individuals with low or deficient TPMT activities who are at risk of severe complications and even death This case describes a patient treated with azathioprine without prior knowledge of TPMT status.	Azathioprine	271-283	thiopurine S-methyltransferase	Homo sapiens	157-161
15571265-0	2004	Mutation in the ITPA gene predicts intolerance to azathioprine.	Azathioprine	50-62	inosine triphosphatase	Homo sapiens	16-20
15571265-2	2004	In 62 patients treated with azathioprine for inflammatory bowel disease, the ITPA 94C&gt;A deficiency-associated allele was significantly associated with adverse drug reactions (OR 4.2, 95% CI 1.6-11.5, p = 0.0034).	Azathioprine	28-40	inosine triphosphatase	Homo sapiens	77-81
15571265-4	2004	Polymorphism in the ITPA gene thus predicts AZA intolerance.	Azathioprine	44-47	inosine triphosphatase	Homo sapiens	20-24
15571266-3	2004	A deficiency of ITPase may predict adverse reactions to therapy with the thiopurine drug 6-mercaptopurine and its prodrug azathioprine.	Azathioprine	122-134	inosine triphosphatase	Homo sapiens	16-22
15571267-2	2004	The aim of this study was to correlate Variable Number Tandem Repeat (VNTR) in the promoter region of the TPMT gene with induction of red cell TPMT activity in patients treated with azathioprine (AZA).	Azathioprine	182-194	thiopurine S-methyltransferase	Homo sapiens	106-110
15571267-2	2004	The aim of this study was to correlate Variable Number Tandem Repeat (VNTR) in the promoter region of the TPMT gene with induction of red cell TPMT activity in patients treated with azathioprine (AZA).	Azathioprine	182-194	thiopurine S-methyltransferase	Homo sapiens	143-147
15571267-2	2004	The aim of this study was to correlate Variable Number Tandem Repeat (VNTR) in the promoter region of the TPMT gene with induction of red cell TPMT activity in patients treated with azathioprine (AZA).	Azathioprine	196-199	thiopurine S-methyltransferase	Homo sapiens	106-110
15571267-2	2004	The aim of this study was to correlate Variable Number Tandem Repeat (VNTR) in the promoter region of the TPMT gene with induction of red cell TPMT activity in patients treated with azathioprine (AZA).	Azathioprine	196-199	thiopurine S-methyltransferase	Homo sapiens	143-147
15316356-3	2004	The first pharmacogenetic trait identified was monogenic, and concerned the prototypic example of thiopurine methyltransferase (TPMT) implicated in azathioprine metabolism.	Azathioprine	148-160	thiopurine S-methyltransferase	Homo sapiens	98-126
15385838-1	2004	Thiopurine S-methyltransferase (TPMT) is an enzyme that catalyzes the S-methylation of thiopurine drugs such as 6-mercaptopurine, 6-thioguanine, and azathioprine.	Azathioprine	149-161	thiopurine S-methyltransferase	Homo sapiens	0-30
15385838-1	2004	Thiopurine S-methyltransferase (TPMT) is an enzyme that catalyzes the S-methylation of thiopurine drugs such as 6-mercaptopurine, 6-thioguanine, and azathioprine.	Azathioprine	149-161	thiopurine S-methyltransferase	Homo sapiens	32-36
15381547-6	2004	RESULTS: The cumulative immunosuppressive drug dose 3 years after transplantation (calculated by a weighted linear combination of azathioprine, cyclosporine, and corticosteroid cumulative doses [WLC]) was independently associated with an increased risk of developing SCC but not BCC.	Azathioprine	130-142	serpin family B member 3	Homo sapiens	267-270
15518736-13	2004	Patients who received cyclosporine (CSA), prednisone (Pred), and mycophenolate mofetil (MMF) showed better graft survival than ones on CSA, Pred, and azathioprine (Aza) (P = .18).	Azathioprine	164-167	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	36-39
15349717-0	2004	The impact of thiopurine S-methyltransferase polymorphisms on azathioprine dose 1 year after renal transplantation.	Azathioprine	62-74	thiopurine S-methyltransferase	Homo sapiens	14-44
15349717-1	2004	Azathioprine metabolism is influenced by activity of the enzyme thiopurine S-methyltransferase (TPMT), which varies markedly between individuals.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	64-94
15349717-1	2004	Azathioprine metabolism is influenced by activity of the enzyme thiopurine S-methyltransferase (TPMT), which varies markedly between individuals.	Azathioprine	0-12	thiopurine S-methyltransferase	Homo sapiens	96-100
15349717-2	2004	In this study we examined the influence of TPMT gene polymorphisms on azathioprine dose 1 year after renal transplantation.	Azathioprine	70-82	thiopurine S-methyltransferase	Homo sapiens	43-47
15349717-8	2004	A significant correlation between the presence of &gt;/=11 variable number tandem repeats (VNTRs) in the TPMT promoter and reduction in azathioprine dose was also identified ( P=0.001).	Azathioprine	136-148	thiopurine S-methyltransferase	Homo sapiens	105-109
15349717-9	2004	We concluded that when azathioprine is administered at an initial dose of 1.5 mg/kg per day, both coding and promoter TPMT polymorphisms influence the dose tolerated.	Azathioprine	23-35	thiopurine S-methyltransferase	Homo sapiens	118-122
15316356-3	2004	The first pharmacogenetic trait identified was monogenic, and concerned the prototypic example of thiopurine methyltransferase (TPMT) implicated in azathioprine metabolism.	Azathioprine	148-160	thiopurine S-methyltransferase	Homo sapiens	128-132
15167635-1	2004	Thiopurine S-methyltransferase (TPMT), which exhibits a genetic polymorphism, plays an important role in the metabolism of thiopurine drugs such as mercaptopurine, thioguanine, and azathioprine.	Azathioprine	181-193	thiopurine S-methyltransferase	Homo sapiens	0-30
15298741-9	2004	Prior knowledge of TPMT status avoids exposure of individuals with zero TPMT to potentially fatal treatment with AZA or 6-MP and provides one of the best examples of predictive pharmacogenetics in therapeutics.	Azathioprine	113-116	thiopurine S-methyltransferase	Homo sapiens	19-23
15157830-5	2004	The hematopoietic toxicity of azathioprine is due to single nucleotide polymorphisms in the thiopurine S-methyltransferase enzyme.	Azathioprine	30-42	thiopurine S-methyltransferase	Homo sapiens	92-122
15167635-1	2004	Thiopurine S-methyltransferase (TPMT), which exhibits a genetic polymorphism, plays an important role in the metabolism of thiopurine drugs such as mercaptopurine, thioguanine, and azathioprine.	Azathioprine	181-193	thiopurine S-methyltransferase	Homo sapiens	32-36
12923290-0	2004	Pharmacoeconomic analysis of thiopurine methyltransferase polymorphism screening by polymerase chain reaction for treatment with azathioprine in Korea.	Azathioprine	129-141	thiopurine S-methyltransferase	Homo sapiens	29-57
15097439-0	2004	Discordant erythrocyte sedimentation rate and C-reactive protein in children with inflammatory bowel disease taking azathioprine or 6-mercaptopurine.	Azathioprine	116-128	C-reactive protein	Homo sapiens	46-64
15097439-5	2004	The authors observed an unexplained discordance between ESR and CRP in children with asymptomatic IBD who were being treated with AZA or 6-MP.	Azathioprine	130-133	C-reactive protein	Homo sapiens	64-67
15097439-6	2004	OBJECTIVE: To characterize children with IBD in remission treated with 6-MP or AZA who have persistently elevated ESR but normal CRP.	Azathioprine	79-82	C-reactive protein	Homo sapiens	129-132
15097439-12	2004	Duration of AZA or 6-MP therapy was greater in the 11 children with asymptomatic disease and discordant ESR and CRP than in those with or without symptoms and with concordant ESR and CRP (58.1 +/- 16.4 months v 36.6 +/- 24.1 months, P = 0.0043).	Azathioprine	12-15	C-reactive protein	Homo sapiens	112-115
15097439-12	2004	Duration of AZA or 6-MP therapy was greater in the 11 children with asymptomatic disease and discordant ESR and CRP than in those with or without symptoms and with concordant ESR and CRP (58.1 +/- 16.4 months v 36.6 +/- 24.1 months, P = 0.0043).	Azathioprine	12-15	C-reactive protein	Homo sapiens	183-186
15097439-16	2004	CONCLUSIONS: The results suggest that among children treated with AZA or 6-MP, CRP may be a more reliable indirect indicator of inflammation than ESR.	Azathioprine	66-69	C-reactive protein	Homo sapiens	79-82
15097439-17	2004	This report alerts clinicians that some children taking AZA or 6-MP may have persistent elevation of the ESR with a normal CRP and have no clinical evidence of active disease.	Azathioprine	56-59	C-reactive protein	Homo sapiens	123-126
15188821-0	2004	Relationship between red blood cell thiopurine methyltransferase activity and myelotoxicity in dogs receiving azathioprine.	Azathioprine	110-122	thiopurine S-methyltransferase	Canis lupus familiaris	36-64
15188821-1	2004	Thiopurine methyltransferase (TPMT) produces inactive metabolites of azathioprine and, in humans, has a variable amount of activity.	Azathioprine	69-81	thiopurine S-methyltransferase	Homo sapiens	0-28
15188821-1	2004	Thiopurine methyltransferase (TPMT) produces inactive metabolites of azathioprine and, in humans, has a variable amount of activity.	Azathioprine	69-81	thiopurine S-methyltransferase	Homo sapiens	30-34
15188821-2	2004	Humans with low TPMT activity commonly develop myelotoxicity when receiving azathioprine.	Azathioprine	76-88	thiopurine S-methyltransferase	Homo sapiens	16-20
15077271-0	2004	Positive classic antineutrophil cytoplasmic antibody (C-ANCA) titer at switch to azathioprine therapy associated with relapse in proteinase 3-related vasculitis.	Azathioprine	81-93	proteinase 3	Homo sapiens	54-60
15077271-0	2004	Positive classic antineutrophil cytoplasmic antibody (C-ANCA) titer at switch to azathioprine therapy associated with relapse in proteinase 3-related vasculitis.	Azathioprine	81-93	proteinase 3	Homo sapiens	129-141
15077271-11	2004	CONCLUSION: Switching cyclophosphamide to azathioprine after induction of remission in patients with PR3-ANCA-associated vasculitis who are still ANCA-positive at the time of treatment switch is associated with a high risk of relapse.	Azathioprine	42-54	proteinase 3	Homo sapiens	101-104
15167706-0	2004	Adverse drug reactions to azathioprine therapy are associated with polymorphism in the gene encoding inosine triphosphate pyrophosphatase (ITPase).	Azathioprine	26-38	inosine triphosphatase	Homo sapiens	101-137
15167706-0	2004	Adverse drug reactions to azathioprine therapy are associated with polymorphism in the gene encoding inosine triphosphate pyrophosphatase (ITPase).	Azathioprine	26-38	inosine triphosphatase	Homo sapiens	139-145
15167706-1	2004	Adverse drug reactions to azathioprine (AZA), the pro-drug of 6-mercaptopurine (6-MP), occur in 15% to 28% of patients and the majority are not explained by thiopurine methyltransferase (TPMT) deficiency.	Azathioprine	26-38	thiopurine S-methyltransferase	Homo sapiens	187-191
15167706-1	2004	Adverse drug reactions to azathioprine (AZA), the pro-drug of 6-mercaptopurine (6-MP), occur in 15% to 28% of patients and the majority are not explained by thiopurine methyltransferase (TPMT) deficiency.	Azathioprine	40-43	thiopurine S-methyltransferase	Homo sapiens	187-191
15167706-4	2004	The association between polymorphism in the ITPA gene and adverse drug reactions to AZA therapy was studied in patients treated for inflammatory bowel disease.	Azathioprine	84-87	inosine triphosphatase	Homo sapiens	44-48
15167706-9	2004	Overall, heterozygous TPMT genotypes did not predict adverse drug reactions but were significantly associated with a subgroup of patients experiencing nausea and vomiting as the predominant adverse reaction to AZA therapy (OR 5.5, 95% CI 1.4-21.3, P = 0.0206).	Azathioprine	210-213	thiopurine S-methyltransferase	Homo sapiens	22-26
15167706-10	2004	Polymorphism in the ITPA gene predicts AZA intolerance.	Azathioprine	39-42	inosine triphosphatase	Homo sapiens	20-24
14634722-11	2004	The plasma levels of big ET-1 are dependent on CyA plasma levels 1 year after successful OHTx in patients treated with the immunosuppressive combination of cyclosporine, azathioprine, and prednisone.	Azathioprine	170-182	endothelin 1	Homo sapiens	25-29
15118980-0	2004	Thiopurine methyltransferase activity influences clinical response to azathioprine in inflammatory bowel disease.	Azathioprine	70-82	thiopurine S-methyltransferase	Homo sapiens	0-28
15118980-1	2004	BACKGROUND &amp; AIMS: Genetic polymorphism in thiopurine methyltransferase (TPMT) activity may influence clinical responsiveness to azathioprine (AZA) therapy.	Azathioprine	133-145	thiopurine S-methyltransferase	Homo sapiens	47-75
15118980-1	2004	BACKGROUND &amp; AIMS: Genetic polymorphism in thiopurine methyltransferase (TPMT) activity may influence clinical responsiveness to azathioprine (AZA) therapy.	Azathioprine	133-145	thiopurine S-methyltransferase	Homo sapiens	77-81
15118980-1	2004	BACKGROUND &amp; AIMS: Genetic polymorphism in thiopurine methyltransferase (TPMT) activity may influence clinical responsiveness to azathioprine (AZA) therapy.	Azathioprine	147-150	thiopurine S-methyltransferase	Homo sapiens	47-75
15118980-1	2004	BACKGROUND &amp; AIMS: Genetic polymorphism in thiopurine methyltransferase (TPMT) activity may influence clinical responsiveness to azathioprine (AZA) therapy.	Azathioprine	147-150	thiopurine S-methyltransferase	Homo sapiens	77-81
15118980-2	2004	Our aim was to determine if the measurement of erythrocyte TPMT enzyme activity could be used to optimize clinical responsiveness to AZA therapy in patients with inflammatory bowel disease (IBD).	Azathioprine	133-136	thiopurine S-methyltransferase	Homo sapiens	59-63
15118980-6	2004	RESULTS: The response rate after 4 months of continuous AZA therapy was 69% (9/13) in those patients with below-average (&lt;/=12 U/mL blood) TPMT activity, and 29% (8/27) in patients with enzyme activity levels &gt;12 U/mL blood (P &lt; 0.001).	Azathioprine	56-59	thiopurine S-methyltransferase	Homo sapiens	142-146
15118980-7	2004	Patients with TPMT activity &lt;/=12 achieved a mean (SEM) erythrocyte 6-thioguanine ribonucleotide (6-TGn) level of 394 +/- 29 pmol/8 x 10(8) red blood cells (RBCs); higher than in patients with TPMT activity &gt;12 (218 +/- 28), despite similar mean (1.6 mg/kg/day) dosages of AZA (P &lt; 0.001).	Azathioprine	279-282	thiopurine S-methyltransferase	Homo sapiens	14-18
15118980-8	2004	By multivariate logistic regression analysis, patients with a TPMT level &lt;15.3 U/mL blood were 6.2 times more likely to respond to AZA therapy.	Azathioprine	134-137	thiopurine S-methyltransferase	Homo sapiens	62-66
15118980-10	2004	CONCLUSIONS: Patients with higher than average TPMT activity (&gt;12) may remain refractory to conventional dosages of AZA, and may require high (&gt;292) 6-TGn levels.	Azathioprine	119-122	thiopurine S-methyltransferase	Homo sapiens	47-51
15118980-11	2004	Prospective, randomized, controlled trials are needed to determine whether prior TPMT phenotype testing can be used to adjust the dose of AZA effectively to improve clinical response time and rate.	Azathioprine	138-141	thiopurine S-methyltransferase	Homo sapiens	81-85
15058773-1	2004	Thiopurine methyltransferase (TPMT) is an important enzyme in the metabolism of thiopurine medications such as azathioprine.	Azathioprine	111-123	thiopurine S-methyltransferase	Canis lupus familiaris	0-28
15058773-1	2004	Thiopurine methyltransferase (TPMT) is an important enzyme in the metabolism of thiopurine medications such as azathioprine.	Azathioprine	111-123	thiopurine S-methyltransferase	Canis lupus familiaris	30-34
15058773-3	2004	Low TPMT activity increases the risk of myelosuppression from azathioprine and 6-mercaptopurine, whereas high TPMT activity is associated with poor drug efficacy.	Azathioprine	62-74	thiopurine S-methyltransferase	Canis lupus familiaris	4-8
14987117-1	2004	Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that plays a major role in the metabolism of thiopurine drugs such as mercaptopurine and azathioprine.	Azathioprine	149-161	thiopurine S-methyltransferase	Homo sapiens	0-30
14987117-1	2004	Thiopurine S-methyltransferase (TPMT) is a cytosolic enzyme that plays a major role in the metabolism of thiopurine drugs such as mercaptopurine and azathioprine.	Azathioprine	149-161	thiopurine S-methyltransferase	Homo sapiens	32-36
14725455-0	2004	Highly efficient aza-Baylis-Hillman reaction of N-tosylated imines with MVK, acrolein, and phenyl acrylate or alpha-naphthyl acrylate: Lewis base effects and a convenient method to synthesize alpha,beta-unsaturated beta-amino carbonyl compounds.	Azathioprine	17-20	mevalonate kinase	Homo sapiens	72-75
14725455-1	2004	This paper describes several highly efficient aza-Baylis-Hillman reactions of N-tosylated imines with MVK, acrolein, and phenyl acrylate or alpha-naphthyl acrylate in the presence of a Lewis base.	Azathioprine	46-49	mevalonate kinase	Homo sapiens	102-105