PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33970400-0	2021	The Role of p53 Expression in Patients with RAS/BRAF Wild-Type Metastatic Colorectal Cancer Receiving Irinotecan and Cetuximab as Later Line Treatment.	Irinotecan	102-112	tumor protein p53	Homo sapiens	12-15
33930649-11	2021	The green tea extract and EGCG also had a dose-dependent inhibitory effect on irinotecan-induced secretion of interleukin-6 and interleukin-8 by oral epithelial cells.	Irinotecan	78-88	interleukin 6	Homo sapiens	110-123
33930649-11	2021	The green tea extract and EGCG also had a dose-dependent inhibitory effect on irinotecan-induced secretion of interleukin-6 and interleukin-8 by oral epithelial cells.	Irinotecan	78-88	C-X-C motif chemokine ligand 8	Homo sapiens	128-141
34037277-0	2021	SENP1 participates in Irinotecan resistance in human colon cancer cells.	Irinotecan	22-32	SUMO specific peptidase 1	Homo sapiens	0-5
34037277-7	2021	Knockdown of SENP1 reduced the migration ability and trigged re-sensitivity of LoVoR-CPT-11 cells to CPT-11 treatment.	Irinotecan	85-91	SUMO specific peptidase 1	Homo sapiens	13-18
34037277-9	2021	In conclusion, SENP1 might play an important role in CPT-11 resistance in colorectal cancer.	Irinotecan	53-59	SUMO specific peptidase 1	Homo sapiens	15-20
32743640-0	2021	Irinotecan and vandetanib create synergies for treatment of pancreatic cancer patients with concomitant TP53 and KRAS mutations.	Irinotecan	0-10	tumor protein p53	Homo sapiens	104-108
32743640-0	2021	Irinotecan and vandetanib create synergies for treatment of pancreatic cancer patients with concomitant TP53 and KRAS mutations.	Irinotecan	0-10	KRAS proto-oncogene, GTPase	Homo sapiens	113-117
32743640-8	2021	Irinotecan and vandetanib are prospective drugs for PAAD patients with KRASG12Dmutation and TP53 mutation.	Irinotecan	0-10	tumor protein p53	Homo sapiens	92-96
33930649-12	2021	Lastly, the irinotecan-induced decrease in the secretion of MMP-2 and MMP-9 by oral epithelial cells was partially restored by the green tea extract and EGCG.	Irinotecan	12-22	matrix metallopeptidase 2	Homo sapiens	60-65
33930649-12	2021	Lastly, the irinotecan-induced decrease in the secretion of MMP-2 and MMP-9 by oral epithelial cells was partially restored by the green tea extract and EGCG.	Irinotecan	12-22	matrix metallopeptidase 9	Homo sapiens	70-75
33970400-3	2021	OBJECTIVE: In our study, we evaluated the role of p53 expression in patients with RAS/BRAF wild-type metastatic colorectal cancer (mCRC) receiving irinotecan/cetuximab in an exploratory and a validation cohort.	Irinotecan	147-157	tumor protein p53	Homo sapiens	50-53
33970400-4	2021	PATIENTS AND METHODS: p53 expression was analysed in patients with RAS/BRAF wild-type mCRC receiving second-line or third-line irinotecan/cetuximab.	Irinotecan	127-137	tumor protein p53	Homo sapiens	22-25
33922657-3	2021	In this study, we demonstrated that curcumin, a plant polyphenol, sensitizes BRCA2-deficient cells to CPT-11 by impairing RAD52 recombinase in MCF7 cells.	Irinotecan	102-108	BRCA2 DNA repair associated	Homo sapiens	77-82
34025639-6	2021	The elevated disease activity index and histological score of colon as well as the up-regulated mRNA and protein levels of TNF-alpha, IL-1beta, and IL-6 in the colonic tissue of CPT-11-treated mice were significantly decreased by TFGU.	Irinotecan	178-184	tumor necrosis factor	Mus musculus	123-132
34025639-6	2021	The elevated disease activity index and histological score of colon as well as the up-regulated mRNA and protein levels of TNF-alpha, IL-1beta, and IL-6 in the colonic tissue of CPT-11-treated mice were significantly decreased by TFGU.	Irinotecan	178-184	interleukin 1 alpha	Mus musculus	134-142
34025639-6	2021	The elevated disease activity index and histological score of colon as well as the up-regulated mRNA and protein levels of TNF-alpha, IL-1beta, and IL-6 in the colonic tissue of CPT-11-treated mice were significantly decreased by TFGU.	Irinotecan	178-184	interleukin 6	Mus musculus	148-152
34025639-10	2021	Since uric acid is a ligand of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, TFGU was further validated to inhibit the activation of NLRP3 inflammasome by CPT-11.	Irinotecan	186-192	NLR family, pyrin domain containing 3	Mus musculus	164-169
33677798-9	2021	Cerv54 had increased levels of CES1, which catalyzes the conversion of irinotecan to the active form, SN38, although in Cerv54 cells, SN38 was undetectable, CES1 expression and activity were markedly low compared to the liver, and a CES1 inhibitor had no effect on irinotecan sensitivity.	Irinotecan	71-81	carboxylesterase 1	Homo sapiens	31-35
33677798-9	2021	Cerv54 had increased levels of CES1, which catalyzes the conversion of irinotecan to the active form, SN38, although in Cerv54 cells, SN38 was undetectable, CES1 expression and activity were markedly low compared to the liver, and a CES1 inhibitor had no effect on irinotecan sensitivity.	Irinotecan	265-275	carboxylesterase 1	Homo sapiens	31-35
33907276-6	2021	We established that chemotherapy agents, particularly 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, stimulated the expression of stimulatory MHC class I alleles through stimulation the pathway of transporters associated with antigen processing 1 and 2 (TAP1 and TAP2) in cell line models.	Irinotecan	54-84	transporter 1, ATP binding cassette subfamily B member	Homo sapiens	284-288
33907276-6	2021	We established that chemotherapy agents, particularly 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, stimulated the expression of stimulatory MHC class I alleles through stimulation the pathway of transporters associated with antigen processing 1 and 2 (TAP1 and TAP2) in cell line models.	Irinotecan	54-84	transporter 2, ATP binding cassette subfamily B member	Homo sapiens	293-297
33907276-6	2021	We established that chemotherapy agents, particularly 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, stimulated the expression of stimulatory MHC class I alleles through stimulation the pathway of transporters associated with antigen processing 1 and 2 (TAP1 and TAP2) in cell line models.	Irinotecan	86-91	transporter 1, ATP binding cassette subfamily B member	Homo sapiens	284-288
33907276-6	2021	We established that chemotherapy agents, particularly 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, stimulated the expression of stimulatory MHC class I alleles through stimulation the pathway of transporters associated with antigen processing 1 and 2 (TAP1 and TAP2) in cell line models.	Irinotecan	86-91	transporter 2, ATP binding cassette subfamily B member	Homo sapiens	293-297
33907276-6	2021	We established that chemotherapy agents, particularly 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, stimulated the expression of stimulatory MHC class I alleles through stimulation the pathway of transporters associated with antigen processing 1 and 2 (TAP1 and TAP2) in cell line models.	Irinotecan	119-129	transporter 1, ATP binding cassette subfamily B member	Homo sapiens	284-288
33907276-6	2021	We established that chemotherapy agents, particularly 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, stimulated the expression of stimulatory MHC class I alleles through stimulation the pathway of transporters associated with antigen processing 1 and 2 (TAP1 and TAP2) in cell line models.	Irinotecan	119-129	transporter 2, ATP binding cassette subfamily B member	Homo sapiens	293-297
33995089-0	2021	Case Report: 7-Ethyl-10-Hydroxycamptothecin, a DNA Topoisomerase I Inhibitor, Performs BRD4 Inhibitory Activity and Inhibits Human Leukemic Cell Growth.	Irinotecan	13-43	bromodomain containing 4	Homo sapiens	87-91
33995089-2	2021	In our study, SN-38 was characterized as a potent and reversible BRD4 inhibitor [IC50 = 660.2 nM against BRD4 (BD1) and IC50 = 547.7 nM against BRD4 (BD2)] in biochemical assay using drug repurposing strategy.	Irinotecan	14-19	bromodomain containing 4	Homo sapiens	65-69
33995089-2	2021	In our study, SN-38 was characterized as a potent and reversible BRD4 inhibitor [IC50 = 660.2 nM against BRD4 (BD1) and IC50 = 547.7 nM against BRD4 (BD2)] in biochemical assay using drug repurposing strategy.	Irinotecan	14-19	bromodomain containing 4	Homo sapiens	105-109
33995089-2	2021	In our study, SN-38 was characterized as a potent and reversible BRD4 inhibitor [IC50 = 660.2 nM against BRD4 (BD1) and IC50 = 547.7 nM against BRD4 (BD2)] in biochemical assay using drug repurposing strategy.	Irinotecan	14-19	defensin beta 1	Homo sapiens	111-114
33995089-2	2021	In our study, SN-38 was characterized as a potent and reversible BRD4 inhibitor [IC50 = 660.2 nM against BRD4 (BD1) and IC50 = 547.7 nM against BRD4 (BD2)] in biochemical assay using drug repurposing strategy.	Irinotecan	14-19	bromodomain containing 4	Homo sapiens	105-109
33995089-2	2021	In our study, SN-38 was characterized as a potent and reversible BRD4 inhibitor [IC50 = 660.2 nM against BRD4 (BD1) and IC50 = 547.7 nM against BRD4 (BD2)] in biochemical assay using drug repurposing strategy.	Irinotecan	14-19	defensin beta 4A	Homo sapiens	150-153
33995089-3	2021	Additional cellular assay suggested that SN-38 can bind BRD4 in human leukemic cell K562 and inhibit cell growth with IC50 = 0.2798 muM in a BRD4 dependent manner partially.	Irinotecan	41-46	bromodomain containing 4	Homo sapiens	56-60
33995089-3	2021	Additional cellular assay suggested that SN-38 can bind BRD4 in human leukemic cell K562 and inhibit cell growth with IC50 = 0.2798 muM in a BRD4 dependent manner partially.	Irinotecan	41-46	bromodomain containing 4	Homo sapiens	141-145
33995089-4	2021	Additionally, mechanism study indicated that SN-38 can induce the accumulation of BRD4 substrate c-Myc and cleavage of caspase 3.	Irinotecan	45-50	bromodomain containing 4	Homo sapiens	82-86
33995089-4	2021	Additionally, mechanism study indicated that SN-38 can induce the accumulation of BRD4 substrate c-Myc and cleavage of caspase 3.	Irinotecan	45-50	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	97-102
33995089-4	2021	Additionally, mechanism study indicated that SN-38 can induce the accumulation of BRD4 substrate c-Myc and cleavage of caspase 3.	Irinotecan	45-50	caspase 3	Homo sapiens	119-128
33995089-5	2021	In sum, our findings identified BRD4 as a new target of SN-38 and reveals SN-38 as a modifier of histone acetylation reader for the first time, which may provide a new insight for further optimization of dual target inhibitor.	Irinotecan	56-61	bromodomain containing 4	Homo sapiens	32-36
33888518-12	2021	Conclusion AREG/EREG IHC identified patients who benefitted from the addition of panitumumab to irinotecan chemotherapy.	Irinotecan	96-106	amphiregulin	Homo sapiens	11-15
33888518-12	2021	Conclusion AREG/EREG IHC identified patients who benefitted from the addition of panitumumab to irinotecan chemotherapy.	Irinotecan	96-106	epiregulin	Homo sapiens	16-20
33922657-6	2021	In vivo, xenograft model studies showed that curcumin combined with CPT-11 reduced the growth of BRCA2-knockout MCF7 tumors but not MCF7 tumors.	Irinotecan	68-74	BRCA2 DNA repair associated	Homo sapiens	97-102
33837924-7	2021	Reports for UGT1A1-metabolized irinotecan and the CYP2C19-metabolized drugs voriconazole, escitalopram and clopidogrel were selected for comparison between the subgroups based upon known genetic polymorphisms with high prevalence in Japan.	Irinotecan	31-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
33882206-2	2021	Sacituzumab govitecan is an antibody-drug conjugate composed of an antibody targeting the human trophoblast cell-surface antigen 2 (Trop-2), which is expressed in the majority of breast cancers, coupled to SN-38 (topoisomerase I inhibitor) through a proprietary hydrolyzable linker.	Irinotecan	206-211	tumor associated calcium signal transducer 2	Homo sapiens	132-138
32981006-1	2021	Camptothecin (CPT) and its derivatives, irinotecan and topotecan are specific topoisomerase I (Top1) inhibitors and potent anticancer drugs.	Irinotecan	40-50	DNA topoisomerase I	Homo sapiens	95-99
33872865-6	2021	Pasta containing 20% lupin flour and 10% RS4 had higher gelatinization onset temperature values, and lower enthalpy than 100% semolina pasta.	Irinotecan	41-44	solute carrier family 45 member 1	Homo sapiens	0-5
33795652-7	2021	Lastly, we preliminary explored the translational effect of HOXC6 and found that silencing of HOXC6 made HCT116 and HT29 cells more sensitive to irinotecan.	Irinotecan	145-155	homeobox C6	Homo sapiens	94-99
33475937-7	2021	Further results revealed that the downregulation of the efflux transporter BCRP by long-term fractionated irradiation was an important factor contributing to the increased cytotoxicity of SN-38.	Irinotecan	188-193	BCR pseudogene 1	Homo sapiens	75-79
33462346-2	2021	DPYD and UGT1A1 variants are relevant predictors of fluoropyrimidine and irinotecan-associated adverse events (AEs).	Irinotecan	73-83	dihydropyrimidine dehydrogenase	Homo sapiens	0-4
33593942-1	2021	CF10 is a 2nd generation polymeric fluoropyrimidine (FP) that targets both thymidylate synthase (TS), the target of 5-fluorouracil (5-FU), and DNA topoisomerase 1 (Top1), the target of irinotecan, two drugs that are key components of FOLFIRNOX, a standard of care regimen for pancreatic ductal adenocarcinoma (PDAC).	Irinotecan	185-195	thymidylate synthetase	Homo sapiens	97-99
33593942-1	2021	CF10 is a 2nd generation polymeric fluoropyrimidine (FP) that targets both thymidylate synthase (TS), the target of 5-fluorouracil (5-FU), and DNA topoisomerase 1 (Top1), the target of irinotecan, two drugs that are key components of FOLFIRNOX, a standard of care regimen for pancreatic ductal adenocarcinoma (PDAC).	Irinotecan	185-195	DNA topoisomerase I	Homo sapiens	164-168
33733372-3	2021	METHODS: Two pharmacokinetic and one myelosuppression model were assembled to predict concentrations of irinotecan and its metabolite SN-38 given different UGT1A1 genotypes (poor metabolizers: CLSN-38: -36%) and neutropenia following conventional versus PGx-based dosing (350 versus 245 mg/m2 (-30%)).	Irinotecan	104-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	156-162
33462346-2	2021	DPYD and UGT1A1 variants are relevant predictors of fluoropyrimidine and irinotecan-associated adverse events (AEs).	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
33733372-3	2021	METHODS: Two pharmacokinetic and one myelosuppression model were assembled to predict concentrations of irinotecan and its metabolite SN-38 given different UGT1A1 genotypes (poor metabolizers: CLSN-38: -36%) and neutropenia following conventional versus PGx-based dosing (350 versus 245 mg/m2 (-30%)).	Irinotecan	134-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	156-162
33462346-9	2021	DPYD IVS14+1A allele is confirmed to be associated with fluoropyrimidine life-threatening toxicities, and UGT1A1*28 is related with a higher risk of hematologic AEs following irinotecan treatment.	Irinotecan	175-185	dihydropyrimidine dehydrogenase	Homo sapiens	0-4
33462346-9	2021	DPYD IVS14+1A allele is confirmed to be associated with fluoropyrimidine life-threatening toxicities, and UGT1A1*28 is related with a higher risk of hematologic AEs following irinotecan treatment.	Irinotecan	175-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
33869031-10	2021	In PDX models with mutated p53 status, there was significant tumor growth inhibition from the combination of AZD1775 with irinotecan or capecitabine (P <= 0.03), while PDX models with wild type p53 did not show anti-tumor synergy from the same combinations (P >= 0.08).	Irinotecan	122-132	tumor protein p53	Homo sapiens	27-30
33790625-0	2021	Influence of UGT1A1 *6/*28 Polymorphisms on Irinotecan-Related Toxicity and Survival in Pediatric Patients with Relapsed/Refractory Solid Tumors Treated with the VIT Regimen.	Irinotecan	44-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
33790625-0	2021	Influence of UGT1A1 *6/*28 Polymorphisms on Irinotecan-Related Toxicity and Survival in Pediatric Patients with Relapsed/Refractory Solid Tumors Treated with the VIT Regimen.	Irinotecan	44-54	vitrin	Homo sapiens	162-165
33790625-1	2021	Objective: The association between UGT1A1*6/*28 polymorphisms and treatment outcomes of irinotecan in children remains unknown.	Irinotecan	88-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
33790625-2	2021	This retrospective study investigated the influence of UGT1A1*6/*28 polymorphisms on irinotecan toxicity and survival of pediatric patients with relapsed/refractory solid tumors.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
33790625-8	2021	Moreover, patients with mutant UGT1A1*6 genotypes were more likely to develop grade I-IV irinotecan-related diarrhea (P = 0.043) and anemia (P = 0.002).	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
33790625-9	2021	Overall, the UGT1A1*28 polymorphism may play a protective role against irinotecan-related diarrhea and abdominal pain.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
33790625-10	2021	Conclusion: In relapsed/refractory pediatric solid tumors, the UGT1A1*6 polymorphism was a risk factor of irinotecan-related diarrhea and anemia.	Irinotecan	106-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
33790625-11	2021	The UGT1A1*28 polymorphism may serve a protective role in irinotecan-related abdominal pain and diarrhea.	Irinotecan	58-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
33664385-0	2021	Entropy-driven binding of gut bacterial beta-glucuronidase inhibitors ameliorates irinotecan-induced toxicity.	Irinotecan	82-92	glucuronidase beta	Homo sapiens	40-58
33630990-1	2021	Carboxylesterase 2 (CES 2) is a key enzyme in the activation of the prodrug irinotecan (CPT-11) in the treatment against colorectal cancer and also has some relationship with the side effect of CPT-11 in clinical applications.	Irinotecan	88-94	carboxylesterase 2	Homo sapiens	20-25
33630990-1	2021	Carboxylesterase 2 (CES 2) is a key enzyme in the activation of the prodrug irinotecan (CPT-11) in the treatment against colorectal cancer and also has some relationship with the side effect of CPT-11 in clinical applications.	Irinotecan	194-200	carboxylesterase 2	Homo sapiens	0-18
33630990-1	2021	Carboxylesterase 2 (CES 2) is a key enzyme in the activation of the prodrug irinotecan (CPT-11) in the treatment against colorectal cancer and also has some relationship with the side effect of CPT-11 in clinical applications.	Irinotecan	194-200	carboxylesterase 2	Homo sapiens	20-25
33728696-0	2021	UGT1A1 Gene Polymorphisms in Patients with Small Cell Lung Cancer Treated with Irinotecan-Platinum Doublet Chemotherapy and Their Association with Gastrointestinal Toxicity and Overall Survival.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
33728696-1	2021	BACKGROUND: Irinotecan (CPT11) is an important drug for small cell lung cancer (SCLC) chemotherapy (CTx).	Irinotecan	12-22	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	100-103
33728696-1	2021	BACKGROUND: Irinotecan (CPT11) is an important drug for small cell lung cancer (SCLC) chemotherapy (CTx).	Irinotecan	24-29	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	100-103
33728696-18	2021	IMPLICATIONS FOR PRACTICE: UGT1A1 gene polymorphisms are known to influence irinotecan-related toxicity.	Irinotecan	76-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
33728696-19	2021	In this prospective cohort study of patients with small cell lung cancer receiving first-line irinotecan-platinum chemotherapy, the prevalence of UGT1A1*6 polymorphisms was found to be 10.8% UGT1A1*6 and 58.8% UGT1A1*28 homo/heterozygous mutant, respectively.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
33728696-19	2021	In this prospective cohort study of patients with small cell lung cancer receiving first-line irinotecan-platinum chemotherapy, the prevalence of UGT1A1*6 polymorphisms was found to be 10.8% UGT1A1*6 and 58.8% UGT1A1*28 homo/heterozygous mutant, respectively.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
33728696-19	2021	In this prospective cohort study of patients with small cell lung cancer receiving first-line irinotecan-platinum chemotherapy, the prevalence of UGT1A1*6 polymorphisms was found to be 10.8% UGT1A1*6 and 58.8% UGT1A1*28 homo/heterozygous mutant, respectively.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
33630990-1	2021	Carboxylesterase 2 (CES 2) is a key enzyme in the activation of the prodrug irinotecan (CPT-11) in the treatment against colorectal cancer and also has some relationship with the side effect of CPT-11 in clinical applications.	Irinotecan	76-86	carboxylesterase 2	Homo sapiens	0-18
33630990-1	2021	Carboxylesterase 2 (CES 2) is a key enzyme in the activation of the prodrug irinotecan (CPT-11) in the treatment against colorectal cancer and also has some relationship with the side effect of CPT-11 in clinical applications.	Irinotecan	76-86	carboxylesterase 2	Homo sapiens	20-25
33630990-1	2021	Carboxylesterase 2 (CES 2) is a key enzyme in the activation of the prodrug irinotecan (CPT-11) in the treatment against colorectal cancer and also has some relationship with the side effect of CPT-11 in clinical applications.	Irinotecan	88-94	carboxylesterase 2	Homo sapiens	0-18
33662636-10	2021	In addition, ZFX expression was negatively correlated with the sensitivity of fresh ESCC tissues to chemotherapeutic drugs, including cisplatin, docetaxel, fluorouracil, and irinotecan.	Irinotecan	174-184	zinc finger protein X-linked	Homo sapiens	13-16
33569738-1	2021	INTRODUCTION: Recently the phase 3 BEACON trial showed that the combination of encorafenib, cetuximab, and binimetinib versus cetuximab and irinotecan/FOLFIRI improved overall survival in pre-treated patients with metastatic colorectal cancer (mCRC) with BRAF V600E mutation.	Irinotecan	140-150	ubiquitin like 5	Homo sapiens	35-41
33386925-9	2021	CONCLUSION: Based on our findings, we recommend that in Japanese advanced PC patients with UGT1A1- DV treated with FOLFIRINOX, irinotecan be administered at an initial dose of  <= 120 mg/m2.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
33323683-5	2021	MGMT expression also correlated significantly with resistance to TMZ+irinotecan (IRN) (in-vitro as the SN38 active metabolite).	Irinotecan	69-79	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-4
33386925-1	2021	BACKGROUND: UGT1A1 *28 and *6 polymorphism is associated with reduced enzyme activity and severe toxicities of irinotecan, especially in patients with homozygous or heterozygous for UGT1A1*28 or *6 polymorphism for both UGT1A1*28 and *6 (double-variant-type of UGT1A1 polymorphism, UGT1A1-DV).	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
33386925-1	2021	BACKGROUND: UGT1A1 *28 and *6 polymorphism is associated with reduced enzyme activity and severe toxicities of irinotecan, especially in patients with homozygous or heterozygous for UGT1A1*28 or *6 polymorphism for both UGT1A1*28 and *6 (double-variant-type of UGT1A1 polymorphism, UGT1A1-DV).	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
33386925-1	2021	BACKGROUND: UGT1A1 *28 and *6 polymorphism is associated with reduced enzyme activity and severe toxicities of irinotecan, especially in patients with homozygous or heterozygous for UGT1A1*28 or *6 polymorphism for both UGT1A1*28 and *6 (double-variant-type of UGT1A1 polymorphism, UGT1A1-DV).	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
33386925-1	2021	BACKGROUND: UGT1A1 *28 and *6 polymorphism is associated with reduced enzyme activity and severe toxicities of irinotecan, especially in patients with homozygous or heterozygous for UGT1A1*28 or *6 polymorphism for both UGT1A1*28 and *6 (double-variant-type of UGT1A1 polymorphism, UGT1A1-DV).	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
33386925-1	2021	BACKGROUND: UGT1A1 *28 and *6 polymorphism is associated with reduced enzyme activity and severe toxicities of irinotecan, especially in patients with homozygous or heterozygous for UGT1A1*28 or *6 polymorphism for both UGT1A1*28 and *6 (double-variant-type of UGT1A1 polymorphism, UGT1A1-DV).	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
33386925-3	2021	The optimal dose of irinotecan as a component of the FOLFIRINOX has not been established yet for patients with UGT1A1-DV.	Irinotecan	20-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
33386925-5	2021	We evaluated the patient characteristics, efficacy and safety of FOLFIRINOX and investigate the optimal initial dose of irinotecan in Japanese advanced PC patients with UGT1A1-DV.	Irinotecan	120-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	169-175
33531790-10	2021	The bioinformatic analysis revealed a higher binding efficiency of CPT and its derivatives, toptecan and irinotecan against Mpro and RdRp.	Irinotecan	105-115	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	124-128
33619631-0	2021	Effect of UGT1A1, CYP3A and CES Activities on the Pharmacokinetics of Irinotecan and its Metabolites in Patients with UGT1A1 Gene Polymorphisms.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
33619631-0	2021	Effect of UGT1A1, CYP3A and CES Activities on the Pharmacokinetics of Irinotecan and its Metabolites in Patients with UGT1A1 Gene Polymorphisms.	Irinotecan	70-80	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	18-23
33619631-0	2021	Effect of UGT1A1, CYP3A and CES Activities on the Pharmacokinetics of Irinotecan and its Metabolites in Patients with UGT1A1 Gene Polymorphisms.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-124
33619631-2	2021	SN-38 is then converted to the inactive metabolite SN-38 glucuronide (SN-38G) by glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
33619631-3	2021	Genetic polymorphisms in UGT1A1 have been associated with altered SN-38 pharmacokinetics, which increase the risk of toxicity in patients.	Irinotecan	66-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
33619631-4	2021	CPT-11 is also converted to 7-ethyl-10-[4-N-(5-aminopentanoic acid)-1-piperidino]carbonyloxycamptothecin (APC) and 7-ethyl-10-(4-amino-1-piperidino) carbonyloxycamptothecin (NPC) by cytochrome P450 3A (CYP3A), and this route also affects the plasma concentration of SN-38.	Irinotecan	0-6	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	182-200
33619631-4	2021	CPT-11 is also converted to 7-ethyl-10-[4-N-(5-aminopentanoic acid)-1-piperidino]carbonyloxycamptothecin (APC) and 7-ethyl-10-(4-amino-1-piperidino) carbonyloxycamptothecin (NPC) by cytochrome P450 3A (CYP3A), and this route also affects the plasma concentration of SN-38.	Irinotecan	0-6	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	202-207
33619631-5	2021	We evaluated the activities of UGT1A1, CYP3A, and CES and the factors affecting the pharmacokinetics of plasma SN-38 in patients with UGT1A1 gene polymorphisms.	Irinotecan	111-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-140
33619631-12	2021	Since UGT1A1 activity was low in patient 1 with a high AUC of SN-38, it can be said that the increase in plasma concentration was due to a decrease in UGT1A1 activity.	Irinotecan	62-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-12
33619631-14	2021	Patient 3 had the lowest AUC of SN-38, caused by a lower level of CES activity and increased CYP3A activity.	Irinotecan	32-37	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	93-98
33619631-15	2021	CONCLUSION: In this study, we indicated that the plasma AUC of SN-38 and AUC ratio of SN-38G/SN-38 may depend on changes in the activities of CYP3A, CES, and UGT1A1.	Irinotecan	63-68	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	142-147
33619631-15	2021	CONCLUSION: In this study, we indicated that the plasma AUC of SN-38 and AUC ratio of SN-38G/SN-38 may depend on changes in the activities of CYP3A, CES, and UGT1A1.	Irinotecan	63-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
33619631-15	2021	CONCLUSION: In this study, we indicated that the plasma AUC of SN-38 and AUC ratio of SN-38G/SN-38 may depend on changes in the activities of CYP3A, CES, and UGT1A1.	Irinotecan	86-91	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	142-147
33619631-15	2021	CONCLUSION: In this study, we indicated that the plasma AUC of SN-38 and AUC ratio of SN-38G/SN-38 may depend on changes in the activities of CYP3A, CES, and UGT1A1.	Irinotecan	86-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
33531790-10	2021	The bioinformatic analysis revealed a higher binding efficiency of CPT and its derivatives, toptecan and irinotecan against Mpro and RdRp.	Irinotecan	105-115	ORF1a polyprotein;ORF1ab polyprotein	Severe acute respiratory syndrome coronavirus 2	133-137
33912512-1	2021	Background: This study investigated the inhibition of tumor growth in castrate-resistant prostate cancer (CRPC)-bearing mice by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-overexpressing adipose-derived stem cells (ADSCs) (hTERT-ADSC.sTRAIL), which was enhanced by combined treatment with CPT-11.	Irinotecan	309-315	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	128-183
33574948-7	2021	AKT1/CTNNB1 mutations were also associated with oxaliplatin, irinotecan, SN-38 and 5-fluorouracil resistance.	Irinotecan	61-71	AKT serine/threonine kinase 1	Homo sapiens	0-4
33574948-7	2021	AKT1/CTNNB1 mutations were also associated with oxaliplatin, irinotecan, SN-38 and 5-fluorouracil resistance.	Irinotecan	61-71	catenin beta 1	Homo sapiens	5-11
33574948-7	2021	AKT1/CTNNB1 mutations were also associated with oxaliplatin, irinotecan, SN-38 and 5-fluorouracil resistance.	Irinotecan	73-78	AKT serine/threonine kinase 1	Homo sapiens	0-4
33574948-7	2021	AKT1/CTNNB1 mutations were also associated with oxaliplatin, irinotecan, SN-38 and 5-fluorouracil resistance.	Irinotecan	73-78	catenin beta 1	Homo sapiens	5-11
33912512-1	2021	Background: This study investigated the inhibition of tumor growth in castrate-resistant prostate cancer (CRPC)-bearing mice by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-overexpressing adipose-derived stem cells (ADSCs) (hTERT-ADSC.sTRAIL), which was enhanced by combined treatment with CPT-11.	Irinotecan	309-315	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	185-190
33912512-12	2021	In the in vivo study, the inhibition of tumor growth in CRPC-bearing mice by TRAIL-overexpressing adipose stem cells was enhanced by combined treatment with the chemotherapeutic agent CPT-11 compared with that in the treatment with cpt-11 alone.	Irinotecan	184-190	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	77-82
33912512-12	2021	In the in vivo study, the inhibition of tumor growth in CRPC-bearing mice by TRAIL-overexpressing adipose stem cells was enhanced by combined treatment with the chemotherapeutic agent CPT-11 compared with that in the treatment with cpt-11 alone.	Irinotecan	232-238	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	77-82
33291124-1	2021	Human carboxylesterase 2 (hCES2A) is a key target to ameliorate the intestinal toxicity triggered by irinotecan that causes severe diarrhea in 50%-80% of patients receiving this anticancer agent.	Irinotecan	101-111	carboxylesterase 2	Homo sapiens	6-24
33568030-11	2021	CONCLUSION: Clotrimazole displayed a strong inhibitory effect against hCE2, which might be used as a potential combined agent co-administrated with CPT-11 to alleviate the hCE2-mediated severe side effects.	Irinotecan	148-154	carboxylesterase 2	Homo sapiens	70-74
33568030-11	2021	CONCLUSION: Clotrimazole displayed a strong inhibitory effect against hCE2, which might be used as a potential combined agent co-administrated with CPT-11 to alleviate the hCE2-mediated severe side effects.	Irinotecan	148-154	carboxylesterase 2	Homo sapiens	172-176
33089597-2	2021	Here, we determined whether an inhibitor of EZH2 enhanced the effect of standard of care chemotherapeutic agents: irinotecan, vincristine, and cyclophosphamide.	Irinotecan	114-124	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	44-48
33615175-9	2021	Further, formation of glucuronides of raloxifene and 7-ethyl-10-hydroxycamptothecin were reduced in the cells expressing the UGT1A1 P152T mutant.	Irinotecan	53-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	125-131
33526988-5	2021	Thus, this study was aimed to examine whether MutS homolog (MSH) 2, one member of DNA repair system, plays a role to affect the cytotoxicity of CPT-11 to CRCs.	Irinotecan	144-150	mutS homolog 2	Homo sapiens	46-66
33526988-7	2021	It was shown that MSH2 gene and protein expression could be upregulated in DLD-1 cells under CPT-11 treatment and this upregulation subsequently attenuates the sensitivity of DLD-1 cells to CPT-11.	Irinotecan	93-99	mutS homolog 2	Homo sapiens	18-22
33526988-7	2021	It was shown that MSH2 gene and protein expression could be upregulated in DLD-1 cells under CPT-11 treatment and this upregulation subsequently attenuates the sensitivity of DLD-1 cells to CPT-11.	Irinotecan	190-196	mutS homolog 2	Homo sapiens	18-22
33526988-9	2021	These results elucidate the drug resistance role of MSH2 upregulation in the CPT-11-treated DLD-1 CRC cells.	Irinotecan	77-83	mutS homolog 2	Homo sapiens	52-56
33692943-4	2020	In the present study, we established a novel irinotecan-resistant human colon cell line to investigate the underlying mechanism(s) of irinotecan resistance, particularly the overexpression of ABC transporters.	Irinotecan	45-55	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	192-195
33692943-4	2020	In the present study, we established a novel irinotecan-resistant human colon cell line to investigate the underlying mechanism(s) of irinotecan resistance, particularly the overexpression of ABC transporters.	Irinotecan	134-144	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	192-195
33692943-10	2020	This finding was further confirmed by reversal studies that inhibiting efflux function of ABCG2 was able to completely abolish drug resistance to irinotecan as well as other ABCG2 substrates in S1-IR20 cells.	Irinotecan	146-156	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	90-95
33692943-11	2020	In conclusion, our work established an in vitro model of irinotecan resistance in CRC and suggested ABCG2 overexpression as one of the underlying mechanisms of acquired resistance to irinotecan.	Irinotecan	183-193	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	100-105
33611805-1	2021	BACKGROUND: Both protracted irinotecan and antiangiogenesis therapy have shown promising efficacy against Ewing sarcoma (EWS).	Irinotecan	28-38	EWS RNA binding protein 1	Homo sapiens	121-124
33611805-15	2021	CONCLUSION: The combination of vincristine, irinotecan, and anlotinib demonstrated an acceptable toxicity profile and promising clinical efficacy in patients with advanced EWS.	Irinotecan	44-54	EWS RNA binding protein 1	Homo sapiens	172-175
33611805-16	2021	IMPLICATIONS FOR PRACTICE: This is the first trial to evaluate an irinotecan-based regimen in combination with antiangiogenesis tyrosine kinase inhibitors in Ewing sarcoma (EWS).	Irinotecan	66-76	EWS RNA binding protein 1	Homo sapiens	173-176
33611805-21	2021	This study shows that the combination of vincristine, irinotecan, and anlotinib demonstrates an acceptable toxicity profile and promising clinical efficacy in patients with advanced EWS.	Irinotecan	54-64	EWS RNA binding protein 1	Homo sapiens	182-185
33568030-9	2021	Furthermore, the inhibitions of clotrimazole towards hCE2-mediated hydrolysis of FD, NCEN and CPT-11 were all in competitive mode with the Ki values of 0.483 muM, 8.63 muM and 29.0 muM, respectively.	Irinotecan	94-100	carboxylesterase 2	Homo sapiens	53-57
32840656-0	2021	The introduction of immunosuppressor (TDO inhibitor) significantly improved the efficacy of irinotecan in treating hepatocellular carcinoma.	Irinotecan	92-102	tryptophan 2,3-dioxygenase	Homo sapiens	38-41
32840656-1	2021	As TDO inhibitors can improve the efficacy of tumor chemotherapeutics, two TDO-targeted conjugates consisting of irinotecan (Ir) and a TDO inhibitor unit were designed and prepared to reverse tumor immune suppression, which could remarkably enhance antitumor activity of Ir by boosting cellular uptakes against TDO overexpressed HepG2 cancer cells.	Irinotecan	113-123	tryptophan 2,3-dioxygenase	Homo sapiens	3-6
32840656-1	2021	As TDO inhibitors can improve the efficacy of tumor chemotherapeutics, two TDO-targeted conjugates consisting of irinotecan (Ir) and a TDO inhibitor unit were designed and prepared to reverse tumor immune suppression, which could remarkably enhance antitumor activity of Ir by boosting cellular uptakes against TDO overexpressed HepG2 cancer cells.	Irinotecan	113-123	tryptophan 2,3-dioxygenase	Homo sapiens	75-78
32840656-1	2021	As TDO inhibitors can improve the efficacy of tumor chemotherapeutics, two TDO-targeted conjugates consisting of irinotecan (Ir) and a TDO inhibitor unit were designed and prepared to reverse tumor immune suppression, which could remarkably enhance antitumor activity of Ir by boosting cellular uptakes against TDO overexpressed HepG2 cancer cells.	Irinotecan	113-123	tryptophan 2,3-dioxygenase	Homo sapiens	75-78
32840656-1	2021	As TDO inhibitors can improve the efficacy of tumor chemotherapeutics, two TDO-targeted conjugates consisting of irinotecan (Ir) and a TDO inhibitor unit were designed and prepared to reverse tumor immune suppression, which could remarkably enhance antitumor activity of Ir by boosting cellular uptakes against TDO overexpressed HepG2 cancer cells.	Irinotecan	113-123	tryptophan 2,3-dioxygenase	Homo sapiens	75-78
32840656-7	2021	Conjugates obtained by combining an immune checkpoint TDO inhibitor with irinotecan via different linkers could improve tumor immune microenvironment by inhibiting the TDO enzyme expression to block kynurenine production and induce HepG2 cancer cell apoptosis via DNA damage through releasing a TDO inhibitor and irinotecan in cancer cells.	Irinotecan	73-83	tryptophan 2,3-dioxygenase	Homo sapiens	168-171
32840656-7	2021	Conjugates obtained by combining an immune checkpoint TDO inhibitor with irinotecan via different linkers could improve tumor immune microenvironment by inhibiting the TDO enzyme expression to block kynurenine production and induce HepG2 cancer cell apoptosis via DNA damage through releasing a TDO inhibitor and irinotecan in cancer cells.	Irinotecan	73-83	tryptophan 2,3-dioxygenase	Homo sapiens	168-171
32840656-7	2021	Conjugates obtained by combining an immune checkpoint TDO inhibitor with irinotecan via different linkers could improve tumor immune microenvironment by inhibiting the TDO enzyme expression to block kynurenine production and induce HepG2 cancer cell apoptosis via DNA damage through releasing a TDO inhibitor and irinotecan in cancer cells.	Irinotecan	313-323	tryptophan 2,3-dioxygenase	Homo sapiens	54-57
32840656-7	2021	Conjugates obtained by combining an immune checkpoint TDO inhibitor with irinotecan via different linkers could improve tumor immune microenvironment by inhibiting the TDO enzyme expression to block kynurenine production and induce HepG2 cancer cell apoptosis via DNA damage through releasing a TDO inhibitor and irinotecan in cancer cells.	Irinotecan	313-323	tryptophan 2,3-dioxygenase	Homo sapiens	168-171
32840656-7	2021	Conjugates obtained by combining an immune checkpoint TDO inhibitor with irinotecan via different linkers could improve tumor immune microenvironment by inhibiting the TDO enzyme expression to block kynurenine production and induce HepG2 cancer cell apoptosis via DNA damage through releasing a TDO inhibitor and irinotecan in cancer cells.	Irinotecan	313-323	tryptophan 2,3-dioxygenase	Homo sapiens	168-171
33039558-6	2021	STAG3 knockdown inhibited cell migration and increased drug sensitivity to oxaliplatin, 5-fluorouracil, irinotecan hydrochloride hydrate, and BRAF inhibitor in CRC cell lines.	Irinotecan	104-136	stromal antigen 3	Homo sapiens	0-5
33747719-2	2021	It is demonstrated that improved irinotecan delivery by a lipid bilayer coated mesoporous silica nanoparticle, also known as a silicasome, can improve PDAC survival through a chemo-immunotherapy response in an orthotopic Kras-dependent pancreatic cancer model.	Irinotecan	33-43	KRAS proto-oncogene, GTPase	Homo sapiens	221-225
33747719-6	2021	The improved delivery of irinotecan by the silicasome is accompanied by robust antitumor immunity, which can be synergistically enhanced by anti-PD-1 in the orthotopic model.	Irinotecan	25-35	programmed cell death 1	Homo sapiens	145-149
33367449-6	2021	We fully validated the assay for quality control of the irinotecan solution in the injection dosage form: the standard curve was linear over the concentration range of 0.90 to at least 37.00 mug ml-1.	Irinotecan	56-66	interleukin 17F	Homo sapiens	195-199
33500629-0	2021	Gastric Cancer Harboring an ERBB3 Mutation Treated with a Pyrotinib-Irinotecan Combo: A Case Study.	Irinotecan	68-78	erb-b2 receptor tyrosine kinase 3	Homo sapiens	28-33
33500629-6	2021	Therefore, the combined administration of irinotecan and pyrotinib may improve the clinical condition of patients with gastric cancer harboring an ERBB3 mutation.	Irinotecan	42-52	erb-b2 receptor tyrosine kinase 3	Homo sapiens	147-152
33407715-0	2021	Vulnerability to low-dose combination of irinotecan and niraparib in ATM-mutated colorectal cancer.	Irinotecan	41-51	ATM serine/threonine kinase	Homo sapiens	69-72
33407715-12	2021	CONCLUSIONS: This work demonstrates that a numerically relevant subset of CRCs carrying heterozygous ATM mutations may benefit from the combination treatment with low doses of niraparib and irinotecan, suggesting a new potential approach in the treatment of ATM-mutated CRC, that deserves to be prospectively validated in clinical trials.	Irinotecan	190-200	ATM serine/threonine kinase	Homo sapiens	101-104
33407715-12	2021	CONCLUSIONS: This work demonstrates that a numerically relevant subset of CRCs carrying heterozygous ATM mutations may benefit from the combination treatment with low doses of niraparib and irinotecan, suggesting a new potential approach in the treatment of ATM-mutated CRC, that deserves to be prospectively validated in clinical trials.	Irinotecan	190-200	ATM serine/threonine kinase	Homo sapiens	258-261
33249316-4	2021	Through in vitro screening among several DNA-targeting chemo agents, we identified 7-ethyl-10-hydroxycamptothecin (SN38) as the most potent drug for stimulating interferon (IFN)-beta secretion and proved that this process is mediated by the passage of DNA-containing exosomes from treated tumor cells to bone marrow-derived dendritic cells (BMDCs) and subsequent activation of the STING pathway.	Irinotecan	83-113	IFN1@	Homo sapiens	161-182
33569416-3	2021	Adenosine triphosphate (ATP)-binding cassette sub-family G member 2 (ABCG2) has been found highly expressed in CRC patients with poor responsiveness to folinic acid/5-FU/irinotecan.	Irinotecan	170-180	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-67
33569416-3	2021	Adenosine triphosphate (ATP)-binding cassette sub-family G member 2 (ABCG2) has been found highly expressed in CRC patients with poor responsiveness to folinic acid/5-FU/irinotecan.	Irinotecan	170-180	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	69-74
33249316-4	2021	Through in vitro screening among several DNA-targeting chemo agents, we identified 7-ethyl-10-hydroxycamptothecin (SN38) as the most potent drug for stimulating interferon (IFN)-beta secretion and proved that this process is mediated by the passage of DNA-containing exosomes from treated tumor cells to bone marrow-derived dendritic cells (BMDCs) and subsequent activation of the STING pathway.	Irinotecan	115-119	IFN1@	Homo sapiens	161-182
33390536-9	2021	BCRP mRNA and protein levels were both decreased in Snail-expressing cells, which showed an increase in the intracellular accumulation of 7-ethyl-10-hydroxycamptothecin (SN-38), a BCRP substrate, resulting in reduced viability.	Irinotecan	138-168	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-4
33468749-4	2021	NAC with FOLFOXIRI(5-fluorouracil/oxaliplatin/leucovorin/irinotecan)plus bevacizumab(BEV)was inisiated as NAC.	Irinotecan	57-67	synuclein alpha	Homo sapiens	0-3
33390536-9	2021	BCRP mRNA and protein levels were both decreased in Snail-expressing cells, which showed an increase in the intracellular accumulation of 7-ethyl-10-hydroxycamptothecin (SN-38), a BCRP substrate, resulting in reduced viability.	Irinotecan	138-168	snail family transcriptional repressor 1	Homo sapiens	52-57
33390536-9	2021	BCRP mRNA and protein levels were both decreased in Snail-expressing cells, which showed an increase in the intracellular accumulation of 7-ethyl-10-hydroxycamptothecin (SN-38), a BCRP substrate, resulting in reduced viability.	Irinotecan	138-168	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	180-184
33390536-9	2021	BCRP mRNA and protein levels were both decreased in Snail-expressing cells, which showed an increase in the intracellular accumulation of 7-ethyl-10-hydroxycamptothecin (SN-38), a BCRP substrate, resulting in reduced viability.	Irinotecan	170-175	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-4
33390536-9	2021	BCRP mRNA and protein levels were both decreased in Snail-expressing cells, which showed an increase in the intracellular accumulation of 7-ethyl-10-hydroxycamptothecin (SN-38), a BCRP substrate, resulting in reduced viability.	Irinotecan	170-175	snail family transcriptional repressor 1	Homo sapiens	52-57
33390536-9	2021	BCRP mRNA and protein levels were both decreased in Snail-expressing cells, which showed an increase in the intracellular accumulation of 7-ethyl-10-hydroxycamptothecin (SN-38), a BCRP substrate, resulting in reduced viability.	Irinotecan	170-175	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	180-184
33402591-4	2021	Uridine diphosphate glucuronosyltransferase (UGT) gene polymorphisms such as UGT1A1*28/*6, age, performance status, serum lactate dehydrogenase levels, and bilirubin levels could be important considerations for predicting outcomes and tolerability with irinotecan-based regimens.	Irinotecan	253-263	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	0-43
33377131-6	2020	Susceptible tumors are characterized by a stemness signature, an activated interferon pathway, and suppression of PD-1 ligands in response to 5-FU+irinotecan.	Irinotecan	147-157	programmed cell death 1	Homo sapiens	114-118
33490922-5	2021	Topoisomerase 1 (TOP1) inhibitors such as irinotecan enhance cisplatin-induced SASP, which depends on the TOP1 cleavage complex-regulated cGAS pathway.	Irinotecan	42-52	cyclic GMP-AMP synthase	Mus musculus	138-142
33119477-1	2020	PURPOSE: Differentiating the irinotecan dose on the basis of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) genotype improves the pathologic complete response (pCR) rate.	Irinotecan	29-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-112
33119477-1	2020	PURPOSE: Differentiating the irinotecan dose on the basis of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) genotype improves the pathologic complete response (pCR) rate.	Irinotecan	29-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
33119477-14	2020	CONCLUSION: Adding irinotecan guided by UGT1A1 genotype to capecitabine-based neoadjuvant chemoradiotherapy significantly increased complete tumor response in Chinese patients.	Irinotecan	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
32930615-6	2020	For example, graphene oxide incorporated with PEG and loaded with SN 38 for camptothecin analolgue as anticancer drug and revealed high cytotoxicity has an effect of 1000 times better effect than CPT in HCT-116 cells.	Irinotecan	66-71	choline phosphotransferase 1	Homo sapiens	196-199
33348673-0	2020	The Paradoxical Effect of PARP Inhibitor BGP-15 on Irinotecan-Induced Cachexia and Skeletal Muscle Dysfunction.	Irinotecan	51-61	poly (ADP-ribose) polymerase family, member 1	Mus musculus	26-30
33311600-0	2021	Anti-PD-L1 mediating tumor-targeted codelivery of liposomal irinotecan/JQ1 for chemo-immunotherapy.	Irinotecan	60-70	CD274 molecule	Homo sapiens	5-10
33311600-6	2021	Here, we develop a PD-L1-targeting immune liposome (P-Lipo) for co-delivering irinotecan (IRI) and JQ1, and this system can successfully elicit antitumor immunity in colorectal cancer through inducing ICD by IRI and interfering in the immunosuppressive PD-1/PD-L1 pathway by JQ1.	Irinotecan	78-88	CD274 molecule	Homo sapiens	19-24
33311600-6	2021	Here, we develop a PD-L1-targeting immune liposome (P-Lipo) for co-delivering irinotecan (IRI) and JQ1, and this system can successfully elicit antitumor immunity in colorectal cancer through inducing ICD by IRI and interfering in the immunosuppressive PD-1/PD-L1 pathway by JQ1.	Irinotecan	78-88	programmed cell death 1	Homo sapiens	253-257
33311600-6	2021	Here, we develop a PD-L1-targeting immune liposome (P-Lipo) for co-delivering irinotecan (IRI) and JQ1, and this system can successfully elicit antitumor immunity in colorectal cancer through inducing ICD by IRI and interfering in the immunosuppressive PD-1/PD-L1 pathway by JQ1.	Irinotecan	78-88	CD274 molecule	Homo sapiens	258-263
33336394-0	2020	Cetuximab plus irinotecan administered biweekly with reduced infusion time to heavily pretreated patients with metastatic colorectal cancer and related RAS and BRAF mutation status.	Irinotecan	15-25	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	160-164
33263997-1	2020	Tyrosyl-DNA phosphodiesterase 1 (TDP1) is a molecular target for the sensitization of cancer cells to the FDA-approved topoisomerase inhibitors topotecan and irinotecan.	Irinotecan	158-168	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	0-31
33263997-1	2020	Tyrosyl-DNA phosphodiesterase 1 (TDP1) is a molecular target for the sensitization of cancer cells to the FDA-approved topoisomerase inhibitors topotecan and irinotecan.	Irinotecan	158-168	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	33-37
33322698-6	2020	Chemosensitivity profiling of PDAC cell lines and patient-derived organoids found that CDKN2A inactivation was associated with the increased sensitivity to paclitaxel and SN-38 (the active metabolite of irinotecan).	Irinotecan	171-176	cyclin dependent kinase inhibitor 2A	Homo sapiens	87-93
33322698-6	2020	Chemosensitivity profiling of PDAC cell lines and patient-derived organoids found that CDKN2A inactivation was associated with the increased sensitivity to paclitaxel and SN-38 (the active metabolite of irinotecan).	Irinotecan	203-213	cyclin dependent kinase inhibitor 2A	Homo sapiens	87-93
33011217-11	2020	When combined with niclosamide or specific STAT3 inhibitor (C188-9), the cytotoxicity and DNA damage response from SN38 (the active metabolite from irinotecan) were significantly enhanced.	Irinotecan	115-119	signal transducer and activator of transcription 3	Homo sapiens	43-48
33125947-0	2020	Pre-therapeutic UGT1A1 genotyping to reduce the risk of irinotecan-induced severe toxicity: Ready for prime time.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
33125947-1	2020	BACKGROUND: Pre-therapeutic UGT1A1 genotyping is not yet routinely performed in most hospitals in patients starting irinotecan chemotherapy.	Irinotecan	116-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
33125947-5	2020	A high level of evidence (level I) was found for a higher incidence of irinotecan-induced severe toxicity in homozygous carriers of UGT1A1*28 or UGT1A1*6.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	132-138
33125947-5	2020	A high level of evidence (level I) was found for a higher incidence of irinotecan-induced severe toxicity in homozygous carriers of UGT1A1*28 or UGT1A1*6.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	145-151
33125947-9	2020	CONCLUSION: Pre-therapeutic genotyping of UGT1A1 in patients initiating treatment with irinotecan improves patient safety, is likely to be cost-saving, and should, therefore, become standard of care.	Irinotecan	87-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
33096057-4	2020	Moreover, the resistant cells suppressed formation of reactive 4-hydroxy-2-nonenal by CPT11 treatment, and the suppressive effect was almost completely abolished by addition of an AKR1C3 inhibitor.	Irinotecan	86-91	aldo-keto reductase family 1 member C3	Homo sapiens	180-186
33011217-11	2020	When combined with niclosamide or specific STAT3 inhibitor (C188-9), the cytotoxicity and DNA damage response from SN38 (the active metabolite from irinotecan) were significantly enhanced.	Irinotecan	148-158	signal transducer and activator of transcription 3	Homo sapiens	43-48
33152996-7	2020	Compared with the control condition, irinotecan diminished (p < 0.05) intestinal villus height, caused a loss of crypt integrity and intense inflammatory cell infiltration, increased myeloperoxidase (MPO), IL-6 and IL-1beta levels and decreased reduced glutathione (GSH) levels in duodenum segments and increased gastric retention and decreased liquid retention in the medial intestinal segment, resulting in increased intestinal transit, severe diarrhea and reduced survival (approximately 72%).	Irinotecan	37-47	myeloperoxidase	Mus musculus	183-198
33158067-6	2020	Mechanistic studies indicated that poziotinib increases the intracellular accumulation of the ABCB1 transporter substrates, paclitaxel and doxorubicin, and the ABCG2 transporter substrates, mitoxantrone and SN-38, by inhibiting their substrate efflux function.	Irinotecan	207-212	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	160-165
33152996-7	2020	Compared with the control condition, irinotecan diminished (p < 0.05) intestinal villus height, caused a loss of crypt integrity and intense inflammatory cell infiltration, increased myeloperoxidase (MPO), IL-6 and IL-1beta levels and decreased reduced glutathione (GSH) levels in duodenum segments and increased gastric retention and decreased liquid retention in the medial intestinal segment, resulting in increased intestinal transit, severe diarrhea and reduced survival (approximately 72%).	Irinotecan	37-47	myeloperoxidase	Mus musculus	200-203
33152996-7	2020	Compared with the control condition, irinotecan diminished (p < 0.05) intestinal villus height, caused a loss of crypt integrity and intense inflammatory cell infiltration, increased myeloperoxidase (MPO), IL-6 and IL-1beta levels and decreased reduced glutathione (GSH) levels in duodenum segments and increased gastric retention and decreased liquid retention in the medial intestinal segment, resulting in increased intestinal transit, severe diarrhea and reduced survival (approximately 72%).	Irinotecan	37-47	interleukin 6	Mus musculus	206-210
33152996-7	2020	Compared with the control condition, irinotecan diminished (p < 0.05) intestinal villus height, caused a loss of crypt integrity and intense inflammatory cell infiltration, increased myeloperoxidase (MPO), IL-6 and IL-1beta levels and decreased reduced glutathione (GSH) levels in duodenum segments and increased gastric retention and decreased liquid retention in the medial intestinal segment, resulting in increased intestinal transit, severe diarrhea and reduced survival (approximately 72%).	Irinotecan	37-47	interleukin 1 alpha	Mus musculus	215-223
33138058-13	2020	Both SN-38-incorporated micelles showed two-fold higher caspase-3/7 activation levels than irinotecan.	Irinotecan	5-10	caspase 3	Homo sapiens	56-67
32863385-2	2020	METHODS: This Phase 2 trial evaluated the efficacy and safety of irinotecan plus cetuximab rechallenge as third-line treatment in KRAS wild-type mCRC patients who achieved clinical benefit with first-line cetuximab-containing therapy.	Irinotecan	65-75	KRAS proto-oncogene, GTPase	Homo sapiens	130-134
32863385-10	2020	CONCLUSIONS: Irinotecan plus cetuximab rechallenge as third-line treatment for KRAS wild-type mCRC was safe and had promising activity, especially in those with a long CFI, warranting further investigation in a Phase 3 randomised trial.	Irinotecan	13-23	KRAS proto-oncogene, GTPase	Homo sapiens	79-83
32863385-10	2020	CONCLUSIONS: Irinotecan plus cetuximab rechallenge as third-line treatment for KRAS wild-type mCRC was safe and had promising activity, especially in those with a long CFI, warranting further investigation in a Phase 3 randomised trial.	Irinotecan	13-23	complement factor I	Homo sapiens	168-171
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	46-56	tumor protein p53	Homo sapiens	91-94
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	46-56	carboxylesterase 2	Homo sapiens	118-136
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	46-56	carboxylesterase 2	Homo sapiens	138-142
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	58-73	tumor protein p53	Homo sapiens	91-94
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	58-73	carboxylesterase 2	Homo sapiens	118-136
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	58-73	carboxylesterase 2	Homo sapiens	138-142
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	75-81	tumor protein p53	Homo sapiens	91-94
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	75-81	carboxylesterase 2	Homo sapiens	118-136
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	75-81	carboxylesterase 2	Homo sapiens	138-142
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	147-153	tumor protein p53	Homo sapiens	91-94
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	147-153	carboxylesterase 2	Homo sapiens	118-136
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	147-153	carboxylesterase 2	Homo sapiens	138-142
32961616-5	2020	Knocking down CES2 in MM cells reduced the effect of the drug combination, and its forced expression in MESO4 cells enhanced the growth inhibitory activity of CPT-11 in the absence of nutlin-3a.	Irinotecan	159-165	carboxylesterase 2	Homo sapiens	14-18
32737884-0	2020	Pharmacogenetic impact of UGT1A1 polymorphisms on pulmonary neuroendocrine tumours treated with metronomic irinotecan-based chemotherapy in Chinese populations.	Irinotecan	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
32737884-11	2020	CONCLUSIONS: The impact of UGT1A1 polymorphisms varies in different irinotecan-based chemotherapies.	Irinotecan	68-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
32737884-12	2020	UGT1A1*6 and UGTA1A*28 were useful for the prediction of irinotecan-related severe toxicity in Chinese PNT patients treated with metronomic IBC.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
32936306-0	2020	Association of UGT1A1*6 polymorphism with irinotecan-based chemotherapy reaction in colorectal cancer patients: a systematic review and a meta-analysis.	Irinotecan	42-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
32694423-11	2020	The biological function of anlotinib and irinotecan may be mediated through the AKT/ERK signaling pathway.	Irinotecan	41-51	AKT serine/threonine kinase 1	Homo sapiens	80-83
32694423-11	2020	The biological function of anlotinib and irinotecan may be mediated through the AKT/ERK signaling pathway.	Irinotecan	41-51	EPH receptor B2	Homo sapiens	84-87
32580836-7	2020	Moreover, the combined treatment of irinotecan with anti-hDLL4 or ABL001 showed synergistic antitumor activity.	Irinotecan	36-46	delta like canonical Notch ligand 4	Homo sapiens	57-62
32580836-10	2020	Collectively, DLL4 inhibition significantly decreased cell motility and stem-like phenotype and the combination treatment of DLL4/VEGF bispecific therapeutic antibody with irinotecan synergistically reduced the GC burden in mouse models.	Irinotecan	172-182	delta like canonical Notch ligand 4	Mus musculus	125-129
32580836-10	2020	Collectively, DLL4 inhibition significantly decreased cell motility and stem-like phenotype and the combination treatment of DLL4/VEGF bispecific therapeutic antibody with irinotecan synergistically reduced the GC burden in mouse models.	Irinotecan	172-182	vascular endothelial growth factor A	Mus musculus	130-134
33103961-6	2020	Conclusion: Therefore, the superparamagnetic iron oxide@poly(sodium styrene sulfonate)/irinotecan/human serum albumin-anti-CD133 nanoparticles are a powerful candidate for future antitumor strategies.	Irinotecan	87-97	albumin	Homo sapiens	104-117
33103961-6	2020	Conclusion: Therefore, the superparamagnetic iron oxide@poly(sodium styrene sulfonate)/irinotecan/human serum albumin-anti-CD133 nanoparticles are a powerful candidate for future antitumor strategies.	Irinotecan	87-97	prominin 1	Homo sapiens	123-128
32985005-5	2020	In this review, the PGx profiles of drug-gene pairs with potential impact in GI malignancy therapy - DPYD-5-fluorouracil/capecitabine and UGT1A1-irinotecan - and the available clinical evidence of their roles in reducing severe adverse events are discussed.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
33092063-2	2020	The activation of mechanistic Target Of Rapamycin (mTor)/hypoxia inducible factor (HIF)-1 pathway can be targeted by rapamycin and irinotecan, respectively.	Irinotecan	131-141	mechanistic target of rapamycin kinase	Homo sapiens	18-49
33120790-4	2020	PATIENT CONCERNS: A 72-year-old man diagnosed with stage IV rectal adenocarcinoma (KRAS mutation) with peritoneal carcinomatosis and liver metastases developed resistance to 2 lines of treatment (bevacizumab/irinotecan/S-1 and bevacizumab/oxaliplatin/HDFL [high-dose 24-hour infusion of 5-fluorouracil and leucovorin regimen]) within 5 months.	Irinotecan	208-218	KRAS proto-oncogene, GTPase	Homo sapiens	83-87
33092063-2	2020	The activation of mechanistic Target Of Rapamycin (mTor)/hypoxia inducible factor (HIF)-1 pathway can be targeted by rapamycin and irinotecan, respectively.	Irinotecan	131-141	mechanistic target of rapamycin kinase	Homo sapiens	51-55
33092063-2	2020	The activation of mechanistic Target Of Rapamycin (mTor)/hypoxia inducible factor (HIF)-1 pathway can be targeted by rapamycin and irinotecan, respectively.	Irinotecan	131-141	hypoxia inducible factor 1 subunit alpha	Homo sapiens	57-89
32829105-0	2020	Determination of the UGT1A1 polymorphism as guidance for irinotecan dose escalation in metastatic colorectal cancer treated with first-line bevacizumab and FOLFIRI (PURE FIST).	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
33069191-1	2021	OBJECTIVES: The aim of the present review is to discuss the potential link between RAS, BRAF and microsatellite instability (MSI) mutational patterns and chemotherapeutic agent efficacy [Irinotecan (IRI) vs. Oxaliplatin (OXA)], and how this can potentially influence the choice of the chemotherapy backbone.	Irinotecan	187-197	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	88-92
32816496-0	2020	Treatment of Lung Cancer by Peptide-Modified Liposomal Irinotecan Endowed with Tumor Penetration and NF-kappaB Inhibitory Activities.	Irinotecan	55-65	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	101-110
32816496-7	2020	These results strongly suggest that antitumor efficacy of the irinotecan liposomes can be enhanced by tumor-penetrating and NF-kappaB-inhibiting functions of CB5005.	Irinotecan	62-72	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	124-133
32829105-1	2020	AIM: Uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) polymorphism plays a crucial role in the increased susceptibility of patients to irinotecan and its toxicity.	Irinotecan	143-153	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-52
32829105-1	2020	AIM: Uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) polymorphism plays a crucial role in the increased susceptibility of patients to irinotecan and its toxicity.	Irinotecan	143-153	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
32829105-7	2020	Dose escalation of irinotecan, an independent factor of ORR (P < 0.001) and DCR (P = 0.006), improved PFS in mCRC patients with wild-type and mutant KRAS (P = 0.007 and P = 0.019, respectively).	Irinotecan	19-29	KRAS proto-oncogene, GTPase	Homo sapiens	149-153
32829105-8	2020	CONCLUSION: The current study revealed that mCRC patients, regardless of KRAS gene status, with UGT1A1 genotyping can tolerate escalated doses of irinotecan and potentially achieve a more favourable clinical outcome without significantly increased toxicities.	Irinotecan	146-156	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
32993166-0	2020	Injectable Thermo-Sensitive Chitosan Hydrogel Containing CPT-11-Loaded EGFR-Targeted Graphene Oxide and SLP2 shRNA for Localized Drug/Gene Delivery in Glioblastoma Therapy.	Irinotecan	57-63	epidermal growth factor receptor	Homo sapiens	71-75
32666389-0	2020	Impact of single-heterozygous UGT1A1 on the clinical outcomes of irinotecan monotherapy after fluoropyrimidine and platinum-based combination therapy for gastric cancer: a multicenter retrospective study.	Irinotecan	65-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
32666389-2	2020	We investigated the association between clinical outcomes (efficacy and safety) and UGT1A1 status in patients who received irinotecan monotherapy.	Irinotecan	123-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
32993166-2	2020	Toward this end, we load irinotecan (CPT-11) to cetuximab (CET)-conjugated GO (GO-CET/CPT11) for pH-responsive drug release after endocytosis by epidermal growth factor receptor (EGFR) over-expressed U87 human glioblastoma cells.	Irinotecan	25-35	epidermal growth factor receptor	Homo sapiens	145-177
32993166-2	2020	Toward this end, we load irinotecan (CPT-11) to cetuximab (CET)-conjugated GO (GO-CET/CPT11) for pH-responsive drug release after endocytosis by epidermal growth factor receptor (EGFR) over-expressed U87 human glioblastoma cells.	Irinotecan	25-35	epidermal growth factor receptor	Homo sapiens	179-183
32993166-2	2020	Toward this end, we load irinotecan (CPT-11) to cetuximab (CET)-conjugated GO (GO-CET/CPT11) for pH-responsive drug release after endocytosis by epidermal growth factor receptor (EGFR) over-expressed U87 human glioblastoma cells.	Irinotecan	37-43	epidermal growth factor receptor	Homo sapiens	145-177
32993166-2	2020	Toward this end, we load irinotecan (CPT-11) to cetuximab (CET)-conjugated GO (GO-CET/CPT11) for pH-responsive drug release after endocytosis by epidermal growth factor receptor (EGFR) over-expressed U87 human glioblastoma cells.	Irinotecan	37-43	epidermal growth factor receptor	Homo sapiens	179-183
32993166-6	2020	Confocal microscopy analysis confirmed the intracellular trafficking for the targeted delivery of CPT-11 through interactions of CET with EGFR on the U87 cell surface.	Irinotecan	98-104	epidermal growth factor receptor	Homo sapiens	138-142
33042471-4	2020	The biological significance of CD44 expression in the chemoresistance response to fluorouracil, oxaliplatin or irinotecan, three major anti-cancer agents for colon cancer in the clinical setting, was examined using colon cancer cell lines.	Irinotecan	111-121	CD44 molecule (Indian blood group)	Homo sapiens	31-35
33042265-5	2020	Methods: Using a microfluidic microbubble production platform, we generated thMBs comprising VEGFR2-targeted microbubbles with attached liposomal payloads for localised ultrasound-triggered delivery of irinotecan and SN38 in mouse models of colorectal cancer.	Irinotecan	202-212	kinase insert domain protein receptor	Mus musculus	93-99
32927892-2	2020	It is well-known that irinotecan as a chemotherapeutic drug against non-small-cell lung carcinoma (NSCLC) has limited anticancer effect due to NF-kappaB activation.	Irinotecan	22-32	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	143-152
32927892-12	2020	Collectively, irinotecan and GRA16 co-treatment promotes the anticancer effects of irinotecan via NF-kappaB inhibition and cell cycle arrest induced by GRA16, subsequently increasing the chemotherapeutic effect of irinotecan to NSCLC cells via NF-kappaB inhibition.	Irinotecan	14-24	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	98-107
32927892-12	2020	Collectively, irinotecan and GRA16 co-treatment promotes the anticancer effects of irinotecan via NF-kappaB inhibition and cell cycle arrest induced by GRA16, subsequently increasing the chemotherapeutic effect of irinotecan to NSCLC cells via NF-kappaB inhibition.	Irinotecan	14-24	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	244-253
32927892-12	2020	Collectively, irinotecan and GRA16 co-treatment promotes the anticancer effects of irinotecan via NF-kappaB inhibition and cell cycle arrest induced by GRA16, subsequently increasing the chemotherapeutic effect of irinotecan to NSCLC cells via NF-kappaB inhibition.	Irinotecan	83-93	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	98-107
32927892-12	2020	Collectively, irinotecan and GRA16 co-treatment promotes the anticancer effects of irinotecan via NF-kappaB inhibition and cell cycle arrest induced by GRA16, subsequently increasing the chemotherapeutic effect of irinotecan to NSCLC cells via NF-kappaB inhibition.	Irinotecan	83-93	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	244-253
32927892-12	2020	Collectively, irinotecan and GRA16 co-treatment promotes the anticancer effects of irinotecan via NF-kappaB inhibition and cell cycle arrest induced by GRA16, subsequently increasing the chemotherapeutic effect of irinotecan to NSCLC cells via NF-kappaB inhibition.	Irinotecan	83-93	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	98-107
32927892-12	2020	Collectively, irinotecan and GRA16 co-treatment promotes the anticancer effects of irinotecan via NF-kappaB inhibition and cell cycle arrest induced by GRA16, subsequently increasing the chemotherapeutic effect of irinotecan to NSCLC cells via NF-kappaB inhibition.	Irinotecan	83-93	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	244-253
32548889-1	2020	BACKGROUND AND PURPOSE: Irinotecan, a drug used in colorectal cancer therapy is metabolized by glucuronidation involving different UDP-glucuronosyltransferase (UGT)1A isoforms, which leads to facilitated elimination from the body.	Irinotecan	24-34	Ugt1a@	Mus musculus	160-166
32548889-2	2020	Individuals homozygous for the genetic variants UGT1A1*28 (Gilbert syndrome) and UGT1A7*3 are more susceptible to irinotecan drug side effects such as severe diarrhea and leukopenia.	Irinotecan	114-124	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	48-54
32548889-2	2020	Individuals homozygous for the genetic variants UGT1A1*28 (Gilbert syndrome) and UGT1A7*3 are more susceptible to irinotecan drug side effects such as severe diarrhea and leukopenia.	Irinotecan	114-124	UDP glucuronosyltransferase 1 family, polypeptide A6A	Mus musculus	81-87
32548889-6	2020	KEY RESULTS: Only the combination of the two coffee ingredients, CA and CAPE, mediates the protective effects of coffee in a model of irinotecan toxicity by activation of UGT1A genes.	Irinotecan	134-144	Ugt1a@	Mus musculus	171-176
32532788-0	2020	Plasma Interleukin-8 is a biomarker for TAK1 activation and predicts resistance to nanoliposomal irinotecan in patients with gemcitabine-refractory pancreatic cancer.	Irinotecan	97-107	C-X-C motif chemokine ligand 8	Homo sapiens	7-20
32846370-7	2020	ATRX mutant cells also showed selective sensitivity to the DNA damaging agents, sapacitabine and irinotecan.	Irinotecan	97-107	ATRX chromatin remodeler	Homo sapiens	0-4
32846370-8	2020	HRR deficiency was also seen in the ATRX deleted CHLA-90 cell line, and significant sensitivity demonstrated to olaparib/irinotecan combination therapy in all ATRX LoF models.	Irinotecan	121-131	ATRX chromatin remodeler	Homo sapiens	159-163
32846370-9	2020	In-vivo sensitivity to olaparib/irinotecan was seen in ATRX mutant but not wild-type xenografts.	Irinotecan	32-42	ATRX chromatin remodeler	Homo sapiens	55-59
32846370-10	2020	Finally, sustained responses to olaparib/irinotecan therapy were seen in an ATRX deleted neuroblastoma patient derived xenograft.	Irinotecan	41-51	ATRX chromatin remodeler	Homo sapiens	76-80
32846370-12	2020	In ATRX LoF models, preclinical sensitivity is demonstrated to olaparib and irinotecan, a combination that can be rapidly translated into the clinic.	Irinotecan	76-86	ATRX chromatin remodeler	Homo sapiens	3-7
32776374-6	2020	CPT-11 increased levels of tissue factor (TF) both in the blood and in intestines, and decreased the intestinal blood flow in mice.	Irinotecan	0-6	coagulation factor III	Mus musculus	27-40
32776374-6	2020	CPT-11 increased levels of tissue factor (TF) both in the blood and in intestines, and decreased the intestinal blood flow in mice.	Irinotecan	0-6	coagulation factor III	Mus musculus	42-44
32776374-10	2020	Ozone inhibited TF expression induced by CPT-11 via activating AMPK/SOCS3, and effectively ameliorated the intestinal mucosal injury in mice.	Irinotecan	41-47	coagulation factor III	Mus musculus	16-18
32776374-10	2020	Ozone inhibited TF expression induced by CPT-11 via activating AMPK/SOCS3, and effectively ameliorated the intestinal mucosal injury in mice.	Irinotecan	41-47	suppressor of cytokine signaling 3	Mus musculus	68-73
32502622-0	2020	P53 activation suppresses irinotecan metabolite SN-38-induced cell damage in non-malignant but not malignant epithelial colonic cells.	Irinotecan	26-36	tumor protein p53	Homo sapiens	0-3
32502622-0	2020	P53 activation suppresses irinotecan metabolite SN-38-induced cell damage in non-malignant but not malignant epithelial colonic cells.	Irinotecan	48-53	tumor protein p53	Homo sapiens	0-3
32502622-5	2020	SN-38 treatment induced significant apoptosis in all cell lines after 48 h. Nutlin-3a unexpectedly increased cell death in the p53 wild-type CRC cell line, HCT116+/+, while Nutlin-3a pre-treatment provided protection from SN-38 in the p53 wild-type normal cell line, FHS 74.	Irinotecan	0-5	tumor protein p53	Homo sapiens	127-130
32502622-5	2020	SN-38 treatment induced significant apoptosis in all cell lines after 48 h. Nutlin-3a unexpectedly increased cell death in the p53 wild-type CRC cell line, HCT116+/+, while Nutlin-3a pre-treatment provided protection from SN-38 in the p53 wild-type normal cell line, FHS 74.	Irinotecan	0-5	tumor protein p53	Homo sapiens	235-238
32778670-3	2020	Thus, the aim of this study was to assess the allele and genotype frequencies and the relationship between CYP3A4/5, DPYD, UGT1A1, ABCB1, and ABCC2 genetic variations and irinotecan-induced toxicity in Thai colorectal cancer patients.	Irinotecan	171-181	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	107-115
32778670-10	2020	This finding suggests that UGT1A1*28, *6, and ABCC2 c.3972C > T might be an important predictor for irinotecan-induced severe neutropenia.	Irinotecan	100-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
32778670-3	2020	Thus, the aim of this study was to assess the allele and genotype frequencies and the relationship between CYP3A4/5, DPYD, UGT1A1, ABCB1, and ABCC2 genetic variations and irinotecan-induced toxicity in Thai colorectal cancer patients.	Irinotecan	171-181	dihydropyrimidine dehydrogenase	Homo sapiens	117-121
32778670-10	2020	This finding suggests that UGT1A1*28, *6, and ABCC2 c.3972C > T might be an important predictor for irinotecan-induced severe neutropenia.	Irinotecan	100-110	ATP binding cassette subfamily C member 2	Homo sapiens	46-51
32778670-3	2020	Thus, the aim of this study was to assess the allele and genotype frequencies and the relationship between CYP3A4/5, DPYD, UGT1A1, ABCB1, and ABCC2 genetic variations and irinotecan-induced toxicity in Thai colorectal cancer patients.	Irinotecan	171-181	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
32821126-8	2020	Results: The expression of MCT1 and LDHB was high in the liver metastases of irinotecan-resistant patients, and the high level of IL-6 in the plasma of patients with CRLM was associated with poor response to irinotecan-based chemotherapy.	Irinotecan	77-87	solute carrier family 16 member 1	Homo sapiens	27-31
32764831-0	2020	CTDSP1 inhibitor rabeprazole regulates DNA-PKcs dependent topoisomerase I degradation and irinotecan drug resistance in colorectal cancer.	Irinotecan	90-100	CTD small phosphatase 1	Homo sapiens	0-6
32764831-3	2020	We have published that the deregulated DNA-PKcs kinase cascade ensures rapid degradation of topoI and is at the core of the drug resistance mechanism of topoI inhibitors, including irinotecan.	Irinotecan	181-191	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	39-47
32764831-7	2020	Using differentially expressing CTDSP1 cells, we demonstrated that CTDSP1 contributes to the irinotecan sensitivity by preventing topoI degradation.	Irinotecan	93-103	CTD small phosphatase 1	Homo sapiens	32-38
32764831-7	2020	Using differentially expressing CTDSP1 cells, we demonstrated that CTDSP1 contributes to the irinotecan sensitivity by preventing topoI degradation.	Irinotecan	93-103	CTD small phosphatase 1	Homo sapiens	67-73
32764831-8	2020	Retrospective analysis of patients receiving irinotecan with or without rabeprazole has shown the effects of CTDSP1 on irinotecan response.	Irinotecan	45-55	CTD small phosphatase 1	Homo sapiens	109-115
32764831-8	2020	Retrospective analysis of patients receiving irinotecan with or without rabeprazole has shown the effects of CTDSP1 on irinotecan response.	Irinotecan	119-129	CTD small phosphatase 1	Homo sapiens	109-115
32764831-9	2020	These results indicate that CTDSP1 promotes sensitivity to irinotecan and rabeprazole prevents this effect, resulting in drug resistance.	Irinotecan	59-69	CTD small phosphatase 1	Homo sapiens	28-34
32821126-8	2020	Results: The expression of MCT1 and LDHB was high in the liver metastases of irinotecan-resistant patients, and the high level of IL-6 in the plasma of patients with CRLM was associated with poor response to irinotecan-based chemotherapy.	Irinotecan	77-87	lactate dehydrogenase B	Homo sapiens	36-40
32821126-8	2020	Results: The expression of MCT1 and LDHB was high in the liver metastases of irinotecan-resistant patients, and the high level of IL-6 in the plasma of patients with CRLM was associated with poor response to irinotecan-based chemotherapy.	Irinotecan	208-218	solute carrier family 16 member 1	Homo sapiens	27-31
32821126-8	2020	Results: The expression of MCT1 and LDHB was high in the liver metastases of irinotecan-resistant patients, and the high level of IL-6 in the plasma of patients with CRLM was associated with poor response to irinotecan-based chemotherapy.	Irinotecan	208-218	interleukin 6	Homo sapiens	130-134
32529410-1	2020	Sacituzumab govitecan (sacituzumab govitecan-hziy; Trodelvy ) is a Trop-2-directed antibody conjugated to a topoisomerase I inhibitor (SN-38) that is being developed by Immunomedics for the treatment of solid tumours, including breast cancer.	Irinotecan	135-140	tumor associated calcium signal transducer 2	Homo sapiens	67-73
32758288-0	2020	UGT1A1 polymorphism has a prognostic effect in patients with stage IB or II uterine cervical cancer and one or no metastatic pelvic nodes receiving irinotecan chemotherapy: a retrospective study.	Irinotecan	148-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
32758288-1	2020	BACKGROUND: Uridine diphosphate glucuronosyltransferase 1 family polypeptide A1 (UGT1A1) is a predictive biomarker for the side-effects of irinotecan chemotherapy, which reduces the volume of tumors harboring UGT1A1 polymorphisms.	Irinotecan	139-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-79
32758288-1	2020	BACKGROUND: Uridine diphosphate glucuronosyltransferase 1 family polypeptide A1 (UGT1A1) is a predictive biomarker for the side-effects of irinotecan chemotherapy, which reduces the volume of tumors harboring UGT1A1 polymorphisms.	Irinotecan	139-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
32758288-1	2020	BACKGROUND: Uridine diphosphate glucuronosyltransferase 1 family polypeptide A1 (UGT1A1) is a predictive biomarker for the side-effects of irinotecan chemotherapy, which reduces the volume of tumors harboring UGT1A1 polymorphisms.	Irinotecan	139-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	209-215
32758288-2	2020	We aimed to determine whether UGT1A1 polymorphisms can predict progression-free survival in patients with local cervical cancer treated with irinotecan chemotherapy.	Irinotecan	141-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
32758288-10	2020	Among patients with <=1 metastatic lymph node, those with UGT1A1 polymorphisms benefited from irinotecan chemotherapy and demonstrated significantly longer progression-free survival (p = 0.020) than those with wild-type UGT1A1.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
32758288-11	2020	CONCLUSIONS: Irinotecan chemotherapy might be beneficial in patients with cervical cancer, UGT1A1 polymorphisms, and <= 1 metastatic lymph nodes.	Irinotecan	13-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
32850329-8	2020	Pharmacogenomic analyses revealed multiple alterations of fluoropyrimidine and irinotecan metabolism: severe deficiency of fluorouracil degradation rate (FUDR), single nucleotide polymorphisms of UGT1A1 *28 variable number of tandem repeats (VNTR) 7R/7R homozygote, ABCB1 c.C3435T, c.C1236T, MTHFR c.C667T homozygote, DPYD c.A166G, TSER 28bp VNTR 2R/3R heterozygote.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
32387453-10	2020	Patients with right-PTL and high EREG/AREG or HER3 expression, had IrPan PFS improvement (high EREG/AREG HR=0.20, p=0.04; high HER3 HR=0.33, p=0.10) compared with irinotecan.	Irinotecan	163-173	epiregulin	Homo sapiens	33-37
32387453-10	2020	Patients with right-PTL and high EREG/AREG or HER3 expression, had IrPan PFS improvement (high EREG/AREG HR=0.20, p=0.04; high HER3 HR=0.33, p=0.10) compared with irinotecan.	Irinotecan	163-173	amphiregulin	Homo sapiens	38-42
32487736-9	2020	Interestingly, irinotecan selectively inhibited hOCT1 whereas crizotinib potently inhibited hOCT3-mediated mIBG uptake.	Irinotecan	15-25	solute carrier family 22 member 1	Homo sapiens	48-53
34007623-0	2020	Dosage Adjustment of Irinotecan in Patients with UGT1A1 Polymorphisms: A Review of Current Literature.	Irinotecan	21-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
34007623-1	2020	Objective: To review available literature regarding pharmacogenomics (PGx) effects on the metabolism of irinotecan by the UGT1A1 gene and the resulting dose adjustments based on PGx genetic variant.	Irinotecan	104-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
34007623-3	2020	The extent of decreased function of UGT1A1 varies based on genotype so irinotecan dose adjustments may be needed.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
34007623-7	2020	Conclusion: These findings add to a growing body of literature that suggest patients with UGT1A1 *28 or *6 variant alleles benefit from lower doses of irinotecan.	Irinotecan	151-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
32708825-0	2020	ABCG2 Protein Levels and Association to Response to First-Line Irinotecan-Based Therapy for Patients with Metastatic Colorectal Cancer.	Irinotecan	63-73	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
32708825-1	2020	In this study we investigated the use of cancer cell protein expression of ABCG2 to predict efficacy of systemic first-line irinotecan containing therapy in patients with metastatic colorectal cancer (mCRC).	Irinotecan	124-134	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	75-80
32708825-10	2020	These results suggest that measurement of the ABCG2 drug efflux pump might be used to select patients with mCRC for irinotecan treatment.	Irinotecan	116-126	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	46-51
32708825-12	2020	Moreover, patients with high ABCG2 immunoreactivity could be candidates for specific ABCG2 inhibition treatment in combination with irinotecan.	Irinotecan	132-142	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	29-34
32503654-4	2020	Therefore, this trial was designed to observe whether irinotecan with a ketogenic diet can promote sensitivity to chemotherapy and remit target lesions in locally recurrent or metastatic Her-2-negative breast cancer patients.	Irinotecan	54-64	erb-b2 receptor tyrosine kinase 2	Homo sapiens	187-192
32387182-0	2020	Irinotecan-mediated diarrhea is mainly correlated with intestinal exposure to SN-38: Critical role of gut Ugt.	Irinotecan	0-10	solute carrier family 35 (UDP-galactose transporter), member A2	Mus musculus	106-109
32387182-13	2020	CONCLUSION AND IMPLICATIONS: Intestinal SN-38 exposure is mainly affected by intestinal Ugt activities and blood esterase activities, and strongly correlated with severity of IID.	Irinotecan	40-45	solute carrier family 35 (UDP-galactose transporter), member A2	Mus musculus	88-91
32695000-0	2020	ABCB1 Genetic Variants as Predictors of Irinotecan-Induced Severe Gastrointestinal Toxicity in Metastatic Colorectal Cancer Patients.	Irinotecan	40-50	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
32695000-5	2020	P-gp is involved in the biliary excretion of irinotecan and its active metabolite SN-38.	Irinotecan	45-55	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
32695000-5	2020	P-gp is involved in the biliary excretion of irinotecan and its active metabolite SN-38.	Irinotecan	82-87	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
32184294-9	2020	Pharmacodynamic markers induced by eribulin (phospho-histone H3) and irinotecan (gamma-H2A.X) were abrogated in combination treated tumors.	Irinotecan	69-79	H2A.X variant histone	Mus musculus	81-92
32184294-16	2020	Although a mechanism for in vivo synergy requires further study, it is possible that eribulin-induced inhibition of microtubule dynamics enhances irinotecan-induced nuclear accumulation of TP53, leading to rapid cell death.	Irinotecan	146-156	transformation related protein 53	Mus musculus	189-193
32343642-0	2020	Irinotecan, Temozolomide, and Dinutuximab With GM-CSF in Children With Refractory or Relapsed Neuroblastoma: A Report From the Children"s Oncology Group.	Irinotecan	0-10	colony stimulating factor 2	Homo sapiens	47-53
31479512-7	2020	Based on concurrent biomarker expression, combinations of immunotherapy with platinum (ERCC1 negativity) or with doxorubicin, epirubicin, or etoposide (TOP2A positivity), have a higher probability of response while combinations with irinotecan or topotecan (TOPO1 positivity), with gemcitabine (RRM1 negativity), and fluorouracil, pemetrexed, or capecitabine (TS negativity) may be of less benefit.	Irinotecan	233-243	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	87-92
32265117-12	2020	CONCLUSION: Our analysis suggested higher completion of concurrent irinotecan was associated with better tumor response for patients with locally advanced rectal cancer with UGT1A1*1*1 or UGT1A1*1*28 phenotypes in the neoadjuvant setting, and at least 4 cycles was recommended.	Irinotecan	67-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
32265117-12	2020	CONCLUSION: Our analysis suggested higher completion of concurrent irinotecan was associated with better tumor response for patients with locally advanced rectal cancer with UGT1A1*1*1 or UGT1A1*1*28 phenotypes in the neoadjuvant setting, and at least 4 cycles was recommended.	Irinotecan	67-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	188-194
31479512-7	2020	Based on concurrent biomarker expression, combinations of immunotherapy with platinum (ERCC1 negativity) or with doxorubicin, epirubicin, or etoposide (TOP2A positivity), have a higher probability of response while combinations with irinotecan or topotecan (TOPO1 positivity), with gemcitabine (RRM1 negativity), and fluorouracil, pemetrexed, or capecitabine (TS negativity) may be of less benefit.	Irinotecan	233-243	DNA topoisomerase II alpha	Homo sapiens	152-157
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	Irinotecan	50-55	tumor protein p53	Homo sapiens	15-18
32471996-0	2020	Soluble HLA-G expression levels and HLA-G/irinotecan association in metastatic colorectal cancer treated with irinotecan-based strategy.	Irinotecan	110-120	major histocompatibility complex, class I, G	Homo sapiens	8-13
32471996-3	2020	The results suggest a link between HLA-G levels and irinotecan (CPT-11) pharmacokinetic, leading to hypothesize a molecular interaction between sHLA-G and CPT-11.	Irinotecan	52-62	major histocompatibility complex, class I, G	Homo sapiens	35-40
32471996-3	2020	The results suggest a link between HLA-G levels and irinotecan (CPT-11) pharmacokinetic, leading to hypothesize a molecular interaction between sHLA-G and CPT-11.	Irinotecan	64-70	major histocompatibility complex, class I, G	Homo sapiens	35-40
32471996-3	2020	The results suggest a link between HLA-G levels and irinotecan (CPT-11) pharmacokinetic, leading to hypothesize a molecular interaction between sHLA-G and CPT-11.	Irinotecan	155-161	major histocompatibility complex, class I, G	Homo sapiens	35-40
32471996-6	2020	The interaction between HLA-G polymorphs and CPT-11 was explored by means of computational modelling, confirming the hypothesis that CPT-11 could actually target the peptide binding cleft of the most common HLA-G polymorphs.	Irinotecan	45-51	major histocompatibility complex, class I, G	Homo sapiens	24-29
32471996-6	2020	The interaction between HLA-G polymorphs and CPT-11 was explored by means of computational modelling, confirming the hypothesis that CPT-11 could actually target the peptide binding cleft of the most common HLA-G polymorphs.	Irinotecan	45-51	major histocompatibility complex, class I, G	Homo sapiens	207-212
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	Irinotecan	50-55	poly(ADP-ribose) polymerase 1	Homo sapiens	196-200
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	Irinotecan	272-277	tumor protein p53	Homo sapiens	15-18
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	Irinotecan	272-277	tumor protein p53	Homo sapiens	148-151
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	Irinotecan	272-277	poly(ADP-ribose) polymerase 1	Homo sapiens	196-200
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	Irinotecan	272-277	tumor protein p53	Homo sapiens	148-151
32393425-0	2020	Effects of cyclosporin A on the pharmacokinetics and toxicities of irinotecan mediated by UGT1A1 in vitro and in vivo.	Irinotecan	67-77	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	90-96
32393425-4	2020	At present, most studies focused on the inhibition of bile excretion by cyclosporin A through the transporters MRP2 and MDR1 and its effect the irinotecan treatment in vivo.	Irinotecan	144-154	ATP binding cassette subfamily C member 2	Rattus norvegicus	111-115
32393425-4	2020	At present, most studies focused on the inhibition of bile excretion by cyclosporin A through the transporters MRP2 and MDR1 and its effect the irinotecan treatment in vivo.	Irinotecan	144-154	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	120-124
32393425-5	2020	However, UDP glucuronyltransferase-1 polypeptide A1 (UGT1A1) was related to a significantly altered disposition of irinotecan and its metabolites, and was therefore associated with irinotecan-induced toxicity.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	9-51
32393425-5	2020	However, UDP glucuronyltransferase-1 polypeptide A1 (UGT1A1) was related to a significantly altered disposition of irinotecan and its metabolites, and was therefore associated with irinotecan-induced toxicity.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	53-59
32393425-5	2020	However, UDP glucuronyltransferase-1 polypeptide A1 (UGT1A1) was related to a significantly altered disposition of irinotecan and its metabolites, and was therefore associated with irinotecan-induced toxicity.	Irinotecan	181-191	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	9-51
32393425-5	2020	However, UDP glucuronyltransferase-1 polypeptide A1 (UGT1A1) was related to a significantly altered disposition of irinotecan and its metabolites, and was therefore associated with irinotecan-induced toxicity.	Irinotecan	181-191	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	53-59
32393425-6	2020	This study focused on UGT1A1-mediated conversion of SN-38 to SN-38G, and systematically investigated the CsA-irinotecan interactions in vitro and in vivo.	Irinotecan	52-57	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	22-28
32393425-6	2020	This study focused on UGT1A1-mediated conversion of SN-38 to SN-38G, and systematically investigated the CsA-irinotecan interactions in vitro and in vivo.	Irinotecan	61-66	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	22-28
32393425-11	2020	The present study indicated that CsA treatment could enhance the systemic exposure and toxicity of SN-38 by inhibiting the UGT1A1 enzyme.	Irinotecan	99-104	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	123-129
32393425-12	2020	The inhibition of UGT1A1 enzyme might be a critical factor in the failure of CsA improving irinotecan"s treatment index.	Irinotecan	91-101	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	18-24
32264830-0	2020	Correlation between UGT1A1 gene polymorphism and irinotecan chemotherapy in metastatic colorectal cancer: a study from Guangxi Zhuang.	Irinotecan	49-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
32349240-7	2020	Dual inhibition of P-gp/Bcrp, or Mrp showed a significant increase on SN-38 BBB transport: Cerebrum (8.3-fold and 3-fold, respectively), cerebellum (4.2-fold and 2.8-fold), and brainstem (2.6-fold and 2.2-fold).	Irinotecan	70-75	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	19-23
32349240-7	2020	Dual inhibition of P-gp/Bcrp, or Mrp showed a significant increase on SN-38 BBB transport: Cerebrum (8.3-fold and 3-fold, respectively), cerebellum (4.2-fold and 2.8-fold), and brainstem (2.6-fold and 2.2-fold).	Irinotecan	70-75	ATP binding cassette subfamily C member 1	Rattus norvegicus	33-36
32326511-2	2020	We tested ABCG2 and topoisomerase 1 (TOP1) mRNA expression as predictive biomarkers for irinotecan benefit in the PETACC-3 patient cohort.	Irinotecan	88-98	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	10-15
32264830-14	2020	The UGT1A1 gene polymorphism with irinotecan chemotherapy-associated diarrhea and neutropenia were closely related.	Irinotecan	34-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
32308415-0	2020	Irinotecan Induces Autophagy-Dependent Apoptosis and Positively Regulates ROS-Related JNK- and P38-MAPK Pathways in Gastric Cancer Cells.	Irinotecan	0-10	mitogen-activated protein kinase 8	Homo sapiens	86-89
32308415-0	2020	Irinotecan Induces Autophagy-Dependent Apoptosis and Positively Regulates ROS-Related JNK- and P38-MAPK Pathways in Gastric Cancer Cells.	Irinotecan	0-10	mitogen-activated protein kinase 14	Homo sapiens	95-103
32308415-9	2020	A mechanistic analysis showed that IRI-induced autophagy and apoptosis were related to increased reactive oxygen species (ROS) accumulation and activation of the JNK- and p38-MAPK pathways.	Irinotecan	35-38	mitogen-activated protein kinase 8	Homo sapiens	162-165
32308415-9	2020	A mechanistic analysis showed that IRI-induced autophagy and apoptosis were related to increased reactive oxygen species (ROS) accumulation and activation of the JNK- and p38-MAPK pathways.	Irinotecan	35-38	mitogen-activated protein kinase 14	Homo sapiens	171-179
30514181-4	2020	Irinotecan is bioactivated into its metabolite SN-38, which is subsequently detoxified by uridine diphosphate-glucuronosyl transferases (mainly UGT1A1).	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
31924737-12	2020	CONCLUSIONS: Tolerability and activity observed in this phase I trial support further investigation of the FTD/TPI-irinotecan-bevacizumab combination in previously treated mCRC.	Irinotecan	115-125	triosephosphate isomerase 1	Homo sapiens	111-114
31975441-4	2020	BCRP and P-gp functions were evaluated by means of efflux and uptake assays using 7-ethyl-10-hydroxycamptothecin (SN-38) and rhodamine123 (Rho123) as specific substrates, respectively, in non-small cell lung cancer HCC827 cells, intestinal cancer Caco-2 cells and renal cancer Caki-1 cells.	Irinotecan	82-112	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-4
31975441-4	2020	BCRP and P-gp functions were evaluated by means of efflux and uptake assays using 7-ethyl-10-hydroxycamptothecin (SN-38) and rhodamine123 (Rho123) as specific substrates, respectively, in non-small cell lung cancer HCC827 cells, intestinal cancer Caco-2 cells and renal cancer Caki-1 cells.	Irinotecan	82-112	phosphoglycolate phosphatase	Homo sapiens	9-13
31975441-4	2020	BCRP and P-gp functions were evaluated by means of efflux and uptake assays using 7-ethyl-10-hydroxycamptothecin (SN-38) and rhodamine123 (Rho123) as specific substrates, respectively, in non-small cell lung cancer HCC827 cells, intestinal cancer Caco-2 cells and renal cancer Caki-1 cells.	Irinotecan	114-119	phosphoglycolate phosphatase	Homo sapiens	9-13
31975441-5	2020	KEY FINDINGS: In HCC827 cells, the efflux rates of SN-38 and Rho123 were significantly decreased by knockdown of Ezr or Msn, but not Rdx.	Irinotecan	51-56	ezrin	Homo sapiens	113-116
31975441-5	2020	KEY FINDINGS: In HCC827 cells, the efflux rates of SN-38 and Rho123 were significantly decreased by knockdown of Ezr or Msn, but not Rdx.	Irinotecan	51-56	moesin	Homo sapiens	120-123
31975441-7	2020	In Caki-1 cells, Rdx knockdown increased the intracellular SN-38 concentration, while knockdown of Ezr or Msn had no effect.	Irinotecan	59-64	radixin	Homo sapiens	17-20
30514181-4	2020	Irinotecan is bioactivated into its metabolite SN-38, which is subsequently detoxified by uridine diphosphate-glucuronosyl transferases (mainly UGT1A1).	Irinotecan	47-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
32143347-7	2020	In silico interaction analyses supported the ATPase assay data and suggest that SCO-201 competes with SN-38 for the BCRP drug-binding site.	Irinotecan	102-107	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	116-120
32256654-11	2020	In addition, CPT-11 increased the productions of tumor necrosis factor-alpha (TNF-alpha), tumor necrosis factor-beta (TNF-beta), interleukin-6 (IL-6), and interleukin-1 (IL-1), but decreased interleukin-15 (IL-15), interleukin-7 (IL-7), and uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	13-19	tumor necrosis factor	Mus musculus	49-76
32256654-11	2020	In addition, CPT-11 increased the productions of tumor necrosis factor-alpha (TNF-alpha), tumor necrosis factor-beta (TNF-beta), interleukin-6 (IL-6), and interleukin-1 (IL-1), but decreased interleukin-15 (IL-15), interleukin-7 (IL-7), and uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	13-19	tumor necrosis factor	Mus musculus	78-87
32256654-11	2020	In addition, CPT-11 increased the productions of tumor necrosis factor-alpha (TNF-alpha), tumor necrosis factor-beta (TNF-beta), interleukin-6 (IL-6), and interleukin-1 (IL-1), but decreased interleukin-15 (IL-15), interleukin-7 (IL-7), and uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	13-19	tumor necrosis factor	Mus musculus	118-126
32256654-11	2020	In addition, CPT-11 increased the productions of tumor necrosis factor-alpha (TNF-alpha), tumor necrosis factor-beta (TNF-beta), interleukin-6 (IL-6), and interleukin-1 (IL-1), but decreased interleukin-15 (IL-15), interleukin-7 (IL-7), and uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	13-19	interleukin 6	Mus musculus	129-142
32256654-11	2020	In addition, CPT-11 increased the productions of tumor necrosis factor-alpha (TNF-alpha), tumor necrosis factor-beta (TNF-beta), interleukin-6 (IL-6), and interleukin-1 (IL-1), but decreased interleukin-15 (IL-15), interleukin-7 (IL-7), and uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	13-19	interleukin 6	Mus musculus	144-148
32256654-11	2020	In addition, CPT-11 increased the productions of tumor necrosis factor-alpha (TNF-alpha), tumor necrosis factor-beta (TNF-beta), interleukin-6 (IL-6), and interleukin-1 (IL-1), but decreased interleukin-15 (IL-15), interleukin-7 (IL-7), and uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	13-19	interleukin 15	Mus musculus	191-205
32256654-11	2020	In addition, CPT-11 increased the productions of tumor necrosis factor-alpha (TNF-alpha), tumor necrosis factor-beta (TNF-beta), interleukin-6 (IL-6), and interleukin-1 (IL-1), but decreased interleukin-15 (IL-15), interleukin-7 (IL-7), and uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	13-19	interleukin 15	Mus musculus	207-212
32256654-11	2020	In addition, CPT-11 increased the productions of tumor necrosis factor-alpha (TNF-alpha), tumor necrosis factor-beta (TNF-beta), interleukin-6 (IL-6), and interleukin-1 (IL-1), but decreased interleukin-15 (IL-15), interleukin-7 (IL-7), and uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	13-19	interleukin 7	Mus musculus	215-228
32256654-11	2020	In addition, CPT-11 increased the productions of tumor necrosis factor-alpha (TNF-alpha), tumor necrosis factor-beta (TNF-beta), interleukin-6 (IL-6), and interleukin-1 (IL-1), but decreased interleukin-15 (IL-15), interleukin-7 (IL-7), and uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	13-19	interleukin 7	Mus musculus	230-234
32256654-11	2020	In addition, CPT-11 increased the productions of tumor necrosis factor-alpha (TNF-alpha), tumor necrosis factor-beta (TNF-beta), interleukin-6 (IL-6), and interleukin-1 (IL-1), but decreased interleukin-15 (IL-15), interleukin-7 (IL-7), and uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	13-19	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	241-288
32256654-11	2020	In addition, CPT-11 increased the productions of tumor necrosis factor-alpha (TNF-alpha), tumor necrosis factor-beta (TNF-beta), interleukin-6 (IL-6), and interleukin-1 (IL-1), but decreased interleukin-15 (IL-15), interleukin-7 (IL-7), and uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	13-19	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	290-296
32170007-1	2020	Irinotecan treats a range of solid tumors, but its effectiveness is severely limited by gastrointestinal (GI) tract toxicity caused by gut bacterial beta-glucuronidase (GUS) enzymes.	Irinotecan	0-10	glucuronidase, beta	Mus musculus	169-172
32170007-2	2020	Targeted bacterial GUS inhibitors have been shown to partially alleviate irinotecan-induced GI tract damage and resultant diarrhea in mice.	Irinotecan	73-83	glucuronidase, beta	Mus musculus	19-22
32170007-5	2020	We demonstrate that a single dose of irinotecan increases GI bacterial GUS activity in 1 d and reduces intestinal epithelial cell proliferation in 5 d, both blocked by a single dose of a GUS inhibitor.	Irinotecan	37-47	glucuronidase, beta	Mus musculus	71-74
32170007-5	2020	We demonstrate that a single dose of irinotecan increases GI bacterial GUS activity in 1 d and reduces intestinal epithelial cell proliferation in 5 d, both blocked by a single dose of a GUS inhibitor.	Irinotecan	37-47	glucuronidase, beta	Mus musculus	187-190
32170007-6	2020	In a tumor xenograft model, GUS inhibition prevents intestinal toxicity and maintains the antitumor efficacy of irinotecan.	Irinotecan	112-122	glucuronidase, beta	Mus musculus	28-31
32170007-7	2020	Remarkably, GUS inhibitor also effectively blocks the striking irinotecan-induced bloom of Enterobacteriaceae in immune-deficient mice.	Irinotecan	63-73	glucuronidase, beta	Mus musculus	12-15
32170007-8	2020	In a genetically engineered mouse model of cancer, GUS inhibition alleviates gut damage, improves survival, and does not alter gut microbial composition; however, by allowing dose intensification, it dramatically improves irinotecan"s effectiveness, reducing tumors to a fraction of that achieved by irinotecan alone, while simultaneously promoting epithelial regeneration.	Irinotecan	300-310	glucuronidase, beta	Mus musculus	51-54
31857431-0	2020	Phase I Clinical Trial of the Wee1 Inhibitor Adavosertib (AZD1775) with Irinotecan in Children with Relapsed Solid Tumors: A COG Phase I Consortium Report (ADVL1312).	Irinotecan	72-82	WEE1 G2 checkpoint kinase	Homo sapiens	30-34
31857431-14	2020	CONCLUSIONS: Adavosertib (85 mg/m2) in combination with irinotecan (90 mg/m2) administered orally for 5 days was the MTD in children and adolescents with solid and CNS tumors.	Irinotecan	56-66	metallothionein 1E	Homo sapiens	117-120
32033066-4	2020	This study analyses the impact of CAPE on the cytotoxic (MTT assay), genotoxic (comet assay) and proapoptotic (caspase-3/7 activity) potential of irinotecan and its metabolite SN-38 in cultures of gastrointestinal neoplastic cells (HCT116, HT29, AGS).	Irinotecan	146-156	caspase 3	Homo sapiens	111-122
31769323-11	2020	Progression-free survival on first-line irinotecan chemotherapy was longer in high SATB2 cases (median 8 vs 4 months respectively, p = .019).	Irinotecan	40-50	SATB homeobox 2	Homo sapiens	83-88
31189762-5	2020	This linker is more stable in aqueous neutral buffer than a corresponding carbonate-type linker, and releases a payload anti-cancer drug, SN-38, through a two-step sequence upon cathepsin B treatment.	Irinotecan	138-143	cathepsin B	Homo sapiens	178-189
32269848-7	2020	AGS and NCI-N87 cells transfected with si-RNA-Bcl-3 (si-Bcl-3) showed significantly reduced migratory ability and increased chemosensitivity to oxaliplatin, 5-fluorouracil, and irinotecan.	Irinotecan	177-187	BCL3 transcription coactivator	Homo sapiens	46-51
31891442-2	2020	The antibody-drug conjugate (ADC) sacituzumab govitecan (SG) targets trophoblast cell-surface antigen-2 (Trop-2) - a cell-surface glycoprotein highly expressed in many epithelial tumors - and delivers the active metabolite of irinotecan SN-38 to Trop-2-positive tumor cells.	Irinotecan	226-236	tumor associated calcium signal transducer 2	Homo sapiens	105-111
31891442-2	2020	The antibody-drug conjugate (ADC) sacituzumab govitecan (SG) targets trophoblast cell-surface antigen-2 (Trop-2) - a cell-surface glycoprotein highly expressed in many epithelial tumors - and delivers the active metabolite of irinotecan SN-38 to Trop-2-positive tumor cells.	Irinotecan	237-242	tumor associated calcium signal transducer 2	Homo sapiens	105-111
32117765-0	2020	Preclinical Activity of Sacituzumab Govitecan, an Antibody-Drug Conjugate Targeting Trophoblast Cell-Surface Antigen 2 (Trop-2) Linked to the Active Metabolite of Irinotecan (SN-38), in Ovarian Cancer.	Irinotecan	163-173	tumor associated calcium signal transducer 2	Homo sapiens	120-126
32117765-0	2020	Preclinical Activity of Sacituzumab Govitecan, an Antibody-Drug Conjugate Targeting Trophoblast Cell-Surface Antigen 2 (Trop-2) Linked to the Active Metabolite of Irinotecan (SN-38), in Ovarian Cancer.	Irinotecan	175-180	tumor associated calcium signal transducer 2	Homo sapiens	120-126
32117765-2	2020	Sacituzumab govitecan (SG) is a novel antibody-drug-conjugate (ADC) targeting trophoblast-antigen-2 (Trop-2), a cell surface glycoprotein highly expressed in many epithelial tumors, to deliver SN-38, the active metabolite of irinotecan.	Irinotecan	193-198	tumor associated calcium signal transducer 2	Homo sapiens	101-107
32117765-2	2020	Sacituzumab govitecan (SG) is a novel antibody-drug-conjugate (ADC) targeting trophoblast-antigen-2 (Trop-2), a cell surface glycoprotein highly expressed in many epithelial tumors, to deliver SN-38, the active metabolite of irinotecan.	Irinotecan	225-235	tumor associated calcium signal transducer 2	Homo sapiens	101-107
32058557-2	2020	Evaluation of pharmacogenomically dosed perioperative gFOLFIRINOX (fluorouracil, leucovorin, oxaliplatin, and UGT1A1 genotype-directed irinotecan) to optimize efficacy while limiting toxic effects may have value.	Irinotecan	135-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
32082489-2	2020	Sacituzumab-govitecan (SG) is a new class of antibody-drug-conjugate (ADC) targeting the human-trophoblast-cell-surface marker (Trop-2) conjugated with the active metabolite of irinotecan (SN-38).	Irinotecan	177-187	tumor associated calcium signal transducer 2	Homo sapiens	128-134
32082489-2	2020	Sacituzumab-govitecan (SG) is a new class of antibody-drug-conjugate (ADC) targeting the human-trophoblast-cell-surface marker (Trop-2) conjugated with the active metabolite of irinotecan (SN-38).	Irinotecan	189-194	tumor associated calcium signal transducer 2	Homo sapiens	128-134
31604667-12	2019	An ARID1A-deficient case that was resistant to multiple cytotoxic drugs, including paclitaxel plus carboplatin in the adjuvant and etoposide plus irinotecan in the first-line treatment, exhibited a dramatic response to gemcitabine in the second-line treatment.	Irinotecan	146-156	AT-rich interaction domain 1A	Homo sapiens	3-9
31889589-0	2020	Cetuximab enhances the efficiency of irinotecan through simultaneously inhibiting the MAPK signaling and ABCG2 in colorectal cancer cells.	Irinotecan	37-47	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	105-110
31889589-3	2020	RESULTS: Cetuximab was found to increase intracellular concentrations of irinotecan as well as cytotoxicity by inhibiting the epidermal growth factor receptor and, by extension, the downstream RAS-RAF-MEK-ERK signaling pathway.	Irinotecan	73-83	epidermal growth factor receptor	Homo sapiens	126-158
31889589-6	2020	In combination with irinotecan, cetuximab can both significantly induce cell apoptosis by inhibiting the RAS-RAF-MEK-ERK signaling pathway and improve the effects of irinotecan by decreasing drug efflux through the inhibition of ABCG2.	Irinotecan	20-30	mitogen-activated protein kinase kinase 7	Homo sapiens	113-116
31889589-6	2020	In combination with irinotecan, cetuximab can both significantly induce cell apoptosis by inhibiting the RAS-RAF-MEK-ERK signaling pathway and improve the effects of irinotecan by decreasing drug efflux through the inhibition of ABCG2.	Irinotecan	20-30	mitogen-activated protein kinase 1	Homo sapiens	117-120
31889589-6	2020	In combination with irinotecan, cetuximab can both significantly induce cell apoptosis by inhibiting the RAS-RAF-MEK-ERK signaling pathway and improve the effects of irinotecan by decreasing drug efflux through the inhibition of ABCG2.	Irinotecan	20-30	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	229-234
31558477-2	2020	UDP Glucuronosyltransferase 1A1 (UGT1A1) clears SN-38, the active metabolite of irinotecan.	Irinotecan	48-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
31558477-2	2020	UDP Glucuronosyltransferase 1A1 (UGT1A1) clears SN-38, the active metabolite of irinotecan.	Irinotecan	48-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
31558477-2	2020	UDP Glucuronosyltransferase 1A1 (UGT1A1) clears SN-38, the active metabolite of irinotecan.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
31558477-2	2020	UDP Glucuronosyltransferase 1A1 (UGT1A1) clears SN-38, the active metabolite of irinotecan.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
31558477-4	2020	We performed a trial to assess the safety and tolerability of FOLFIRABRAX with UGT1A1 genotype-guided dosing of irinotecan.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
31558477-16	2020	CONCLUSIONS: FOLFIRABRAX with genotype-guided dosing of irinotecan is tolerable in patients with advanced gastrointestinal cancer and UGT1A1*1*1 or UGT1A1*1*28 genotypes.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-140
31558477-16	2020	CONCLUSIONS: FOLFIRABRAX with genotype-guided dosing of irinotecan is tolerable in patients with advanced gastrointestinal cancer and UGT1A1*1*1 or UGT1A1*1*28 genotypes.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	148-154
31856090-4	2020	We present the case of a 44-year-old woman with ATM-mutated PC who achieved stable disease as the best response to first-line fluorouracil, leucovorin, irinotecan, and oxaliplatin, followed by progression on a PARP inhibitor.	Irinotecan	152-162	ATM serine/threonine kinase	Homo sapiens	48-51
31878088-1	2019	Tyrosyl-DNA phosphodiesterase 1 (Tdp1) is an important DNA repair enzyme in humans, and a current and promising inhibition target for the development of new chemosensitizing agents due to its ability to remove DNA damage caused by topoisomerase 1 (Top1) poisons such as topotecan and irinotecan.	Irinotecan	284-294	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	0-31
31878088-1	2019	Tyrosyl-DNA phosphodiesterase 1 (Tdp1) is an important DNA repair enzyme in humans, and a current and promising inhibition target for the development of new chemosensitizing agents due to its ability to remove DNA damage caused by topoisomerase 1 (Top1) poisons such as topotecan and irinotecan.	Irinotecan	284-294	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	33-37
31878088-1	2019	Tyrosyl-DNA phosphodiesterase 1 (Tdp1) is an important DNA repair enzyme in humans, and a current and promising inhibition target for the development of new chemosensitizing agents due to its ability to remove DNA damage caused by topoisomerase 1 (Top1) poisons such as topotecan and irinotecan.	Irinotecan	284-294	DNA topoisomerase I	Homo sapiens	231-246
31402291-0	2019	Angiogenic and Antiangiogenic VEGFA Splice Variants in Colorectal Cancer: Prospective Retrospective Cohort Study in Patients Treated With Irinotecan-Based Chemotherapy and Bevacizumab.	Irinotecan	138-148	vascular endothelial growth factor A	Homo sapiens	30-35
31719636-3	2019	The study aimed to elucidate the effects of insulin (INS), an inexpensive drug with a convincing safety profile, on the susceptibility of colon cancer to chemotherapeutic agents: 5-fluorouracil (FU), oxaliplatin (OXA), irinotecan (IRI), cyclophosphamide (CPA) and docetaxel (DOC).	Irinotecan	219-229	insulin	Homo sapiens	44-51
31719636-3	2019	The study aimed to elucidate the effects of insulin (INS), an inexpensive drug with a convincing safety profile, on the susceptibility of colon cancer to chemotherapeutic agents: 5-fluorouracil (FU), oxaliplatin (OXA), irinotecan (IRI), cyclophosphamide (CPA) and docetaxel (DOC).	Irinotecan	231-234	insulin	Homo sapiens	44-51
31704837-8	2019	These results indicated that the simultaneous expression of APEX1 and Jagged-1 might be associated with chemoresistance toward 5-FU, oxaliplatin, and irinotecan.	Irinotecan	150-160	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	60-65
31704837-8	2019	These results indicated that the simultaneous expression of APEX1 and Jagged-1 might be associated with chemoresistance toward 5-FU, oxaliplatin, and irinotecan.	Irinotecan	150-160	jagged canonical Notch ligand 1	Homo sapiens	70-78
31432188-0	2019	The identification of CRNDE, H19, UCA1 and HOTAIR as the key lncRNAs involved in oxaliplatin or irinotecan resistance in the chemotherapy of colorectal cancer based on integrative bioinformatics analysis.	Irinotecan	96-106	colorectal neoplasia differentially expressed	Homo sapiens	22-27
31598748-0	2019	MiR-218 and miR-100 polymorphisms as markers of irinotecan-based chemotherapy response in metastatic colorectal cancer.	Irinotecan	48-58	microRNA 100	Homo sapiens	12-19
31598748-4	2019	METHODS: We investigated the correlation between rs11134527 miR-218 and rs1834306 miR-100 polymorphisms and irinotecan-based regimens with regard to drug efficacy and toxicity.	Irinotecan	108-118	microRNA 100	Homo sapiens	82-89
31598748-10	2019	Carriers of the A allele of the miR-218 rs11134527 and T allele of the miR-100 rs1834306 polymorphisms are more likely not to respond to irinotecan-based therapies.	Irinotecan	137-147	microRNA 100	Homo sapiens	71-78
31444231-6	2019	Here, we show that loss of LGR5 in colon cancer cells enhanced resistance to irinotecan and 5-fluorouracil and increased expression of adhesion G-protein-coupled receptor, GPR56.	Irinotecan	77-87	leucine rich repeat containing G protein-coupled receptor 5	Homo sapiens	27-31
30811654-11	2019	This study found significant changes in the pharmacokinetics of CPT-11 in rats after exposure to X-ray irradiation, and they might be due to significant increases in the expressions of CYP3A1 and CES1.	Irinotecan	64-70	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	185-191
30811654-11	2019	This study found significant changes in the pharmacokinetics of CPT-11 in rats after exposure to X-ray irradiation, and they might be due to significant increases in the expressions of CYP3A1 and CES1.	Irinotecan	64-70	carboxylesterase 1E	Rattus norvegicus	196-200
30612311-0	2019	Sensitization of colorectal cancer to irinotecan therapy by PARP inhibitor rucaparib.	Irinotecan	38-48	poly(ADP-ribose) polymerase 1	Homo sapiens	60-64
31432188-0	2019	The identification of CRNDE, H19, UCA1 and HOTAIR as the key lncRNAs involved in oxaliplatin or irinotecan resistance in the chemotherapy of colorectal cancer based on integrative bioinformatics analysis.	Irinotecan	96-106	H19 imprinted maternally expressed transcript	Homo sapiens	29-32
31432188-0	2019	The identification of CRNDE, H19, UCA1 and HOTAIR as the key lncRNAs involved in oxaliplatin or irinotecan resistance in the chemotherapy of colorectal cancer based on integrative bioinformatics analysis.	Irinotecan	96-106	urothelial cancer associated 1	Homo sapiens	34-38
31415918-3	2019	Moreover, medicinal TOP1 inhibitors TPT and SN-38 also augmented IL-10 production significantly, whereas knockdown of TOP1 prevented NC, TPT, and SN-38 from enhancing IL-10 expression.	Irinotecan	44-49	interleukin 10	Mus musculus	65-70
31432188-0	2019	The identification of CRNDE, H19, UCA1 and HOTAIR as the key lncRNAs involved in oxaliplatin or irinotecan resistance in the chemotherapy of colorectal cancer based on integrative bioinformatics analysis.	Irinotecan	96-106	HOX transcript antisense RNA	Homo sapiens	43-49
31222885-5	2019	One example of this type of combination is the addition of the WEE1 inhibitor AZD1775 to the conventional cytotoxic chemotherapeutics, vincristine and irinotecan.	Irinotecan	151-161	WEE1 G2 checkpoint kinase	Homo sapiens	63-67
31505885-5	2019	The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) cell viability assay found that miR-21 overexpression induced drug resistance to topoisomerase inhibitors (SN-38, doxorubicin, and etoposide/VP-16).	Irinotecan	179-184	microRNA 21	Homo sapiens	104-110
31402355-0	2019	Promoting antitumor efficacy by suppressing hypoxia via nano self-assembly of two irinotecan-based dual drug conjugates having a HIF-1alpha inhibitor.	Irinotecan	82-92	hypoxia inducible factor 1 subunit alpha	Homo sapiens	129-139
31402355-3	2019	To promote the antitumor efficacy of chemical drugs by suppressing hypoxia, we designed and conjugated a hydrophobic HIF-1alpha inhibitor (YC-1) to a hydrophilic anticancer drug, irinotecan (Ir), into one molecular entity via dicarboxylate and PEG3 linkages.	Irinotecan	179-189	hypoxia inducible factor 1 subunit alpha	Homo sapiens	117-127
31402355-3	2019	To promote the antitumor efficacy of chemical drugs by suppressing hypoxia, we designed and conjugated a hydrophobic HIF-1alpha inhibitor (YC-1) to a hydrophilic anticancer drug, irinotecan (Ir), into one molecular entity via dicarboxylate and PEG3 linkages.	Irinotecan	179-189	paternally expressed 3	Homo sapiens	244-248
31415918-3	2019	Moreover, medicinal TOP1 inhibitors TPT and SN-38 also augmented IL-10 production significantly, whereas knockdown of TOP1 prevented NC, TPT, and SN-38 from enhancing IL-10 expression.	Irinotecan	146-151	interleukin 10	Mus musculus	167-172
31363167-0	2019	A phase 2 study of panitumumab with irinotecan as salvage therapy in chemorefractory KRAS exon 2 wild-type metastatic colorectal cancer patients.	Irinotecan	36-46	KRAS proto-oncogene, GTPase	Homo sapiens	85-89
31444410-6	2019	In mechanistic studies, irinotecan not only induces apoptosis by eliciting a DNA damage response, but also acts synergistically with AZD2014 to potentiate the hypophosphorylation of 4E-BP1, a downstream target of mTORC1.	Irinotecan	24-34	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	182-188
31444410-6	2019	In mechanistic studies, irinotecan not only induces apoptosis by eliciting a DNA damage response, but also acts synergistically with AZD2014 to potentiate the hypophosphorylation of 4E-BP1, a downstream target of mTORC1.	Irinotecan	24-34	CREB regulated transcription coactivator 1	Mus musculus	213-219
31466383-9	2019	For example, Sorafenib was applicable for the basal subtype treatment, Irinotecan was optimum for Her2 subtype treatment, Vemurafenib was suitable for the LumA subtype treatment, and Vorinostat could apply to LumB subtype treatment.	Irinotecan	71-81	erb-b2 receptor tyrosine kinase 2	Homo sapiens	98-102
31302002-5	2019	Furthermore, IKKalpha or BRAF inhibition synergistically enhances the therapeutic potential of 5-FU and irinotecan to eradicate chemotherapy-resistant metastatic human tumors in vivo.	Irinotecan	104-114	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	13-21
31302002-5	2019	Furthermore, IKKalpha or BRAF inhibition synergistically enhances the therapeutic potential of 5-FU and irinotecan to eradicate chemotherapy-resistant metastatic human tumors in vivo.	Irinotecan	104-114	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	25-29
31289894-0	2019	Functional mismatch repair and inactive p53 drive sensitization of colorectal cancer cells to irinotecan via the IAP antagonist BV6.	Irinotecan	94-104	tumor protein p53	Homo sapiens	40-43
31289894-0	2019	Functional mismatch repair and inactive p53 drive sensitization of colorectal cancer cells to irinotecan via the IAP antagonist BV6.	Irinotecan	94-104	alkaline phosphatase, intestinal	Homo sapiens	113-116
31289894-2	2019	The purpose of this study was to analyze the cytostatic/cytotoxic response of colorectal carcinoma (CRC) cells to irinotecan, depending on the mismatch repair (MMR) and p53 status and to examine the impact of BV6, a bivalent antagonist of inhibitors of apoptosis c-IAP1/c-IAP2, alone or combined with irinotecan.	Irinotecan	114-124	tumor protein p53	Homo sapiens	169-172
31289894-2	2019	The purpose of this study was to analyze the cytostatic/cytotoxic response of colorectal carcinoma (CRC) cells to irinotecan, depending on the mismatch repair (MMR) and p53 status and to examine the impact of BV6, a bivalent antagonist of inhibitors of apoptosis c-IAP1/c-IAP2, alone or combined with irinotecan.	Irinotecan	114-124	baculoviral IAP repeat containing 2	Homo sapiens	263-269
31289894-2	2019	The purpose of this study was to analyze the cytostatic/cytotoxic response of colorectal carcinoma (CRC) cells to irinotecan, depending on the mismatch repair (MMR) and p53 status and to examine the impact of BV6, a bivalent antagonist of inhibitors of apoptosis c-IAP1/c-IAP2, alone or combined with irinotecan.	Irinotecan	114-124	baculoviral IAP repeat containing 3	Homo sapiens	270-276
31289894-4	2019	Upon irinotecan, MMR-deficient/p53-mutated lines repaired DNA double-strand breaks by homologous recombination less efficiently than MMR-proficient/p53-mutated lines and underwent elevated caspase-9-dependent apoptosis.	Irinotecan	5-15	tumor protein p53	Homo sapiens	31-34
31289894-4	2019	Upon irinotecan, MMR-deficient/p53-mutated lines repaired DNA double-strand breaks by homologous recombination less efficiently than MMR-proficient/p53-mutated lines and underwent elevated caspase-9-dependent apoptosis.	Irinotecan	5-15	caspase 9	Homo sapiens	189-198
31289894-8	2019	Therefore, the particular MMR+/p53mt signature, often found in non-metastasizing (stage II) CRC might be used as a prognostic factor for an adjuvant therapy using low-dose irinotecan combined with a bivalent IAP antagonist.	Irinotecan	172-182	tumor protein p53	Homo sapiens	31-34
31011814-0	2019	SN-38, the active metabolite of irinotecan, inhibits the acute inflammatory response by targeting toll-like receptor 4.	Irinotecan	0-5	toll-like receptor 4	Mus musculus	98-118
31011814-0	2019	SN-38, the active metabolite of irinotecan, inhibits the acute inflammatory response by targeting toll-like receptor 4.	Irinotecan	32-42	toll-like receptor 4	Mus musculus	98-118
31011814-5	2019	RESULTS: Non-cytotoxic concentrations of SN-38 attenuated LPS (a TLR4 agonist)-driven cell activation without affecting peptidoglycan (a TLR2 agonist)-activating response.	Irinotecan	41-46	toll-like receptor 4	Mus musculus	65-69
31011814-8	2019	In addition, SN-38 abrogated LPS-dependent neutrophil migration and reduced TNF-alpha, IL-6, and keratinocyte chemoattractant levels in the air-pouch model, but failed to inhibit zymosan (a TLR2 agonist)-induced cell migration.	Irinotecan	13-18	tumor necrosis factor	Mus musculus	76-85
31011814-8	2019	In addition, SN-38 abrogated LPS-dependent neutrophil migration and reduced TNF-alpha, IL-6, and keratinocyte chemoattractant levels in the air-pouch model, but failed to inhibit zymosan (a TLR2 agonist)-induced cell migration.	Irinotecan	13-18	interleukin 6	Mus musculus	87-91
31011814-8	2019	In addition, SN-38 abrogated LPS-dependent neutrophil migration and reduced TNF-alpha, IL-6, and keratinocyte chemoattractant levels in the air-pouch model, but failed to inhibit zymosan (a TLR2 agonist)-induced cell migration.	Irinotecan	13-18	toll-like receptor 2	Mus musculus	190-194
31011814-9	2019	A two-step molecular docking analysis indicated two potential binding sites for the SN-38 in the MD-2/TLR4 complex, the hydrophobic MD-2 pocket (binding energy of - 8.1 kcal/mol) and the rim of the same molecule (- 6.9 kcal/mol).	Irinotecan	84-89	toll-like receptor 4	Mus musculus	102-106
31011814-13	2019	CONCLUSIONS: Therefore, SN-38 inhibits acute inflammation by blocking LPS-driven TLR4 signaling.	Irinotecan	24-29	toll-like receptor 4	Mus musculus	81-85
31208270-0	2019	Antibody-drug conjugates targeting TROP-2 and incorporating SN-38: A case study of anti-TROP-2 sacituzumab govitecan.	Irinotecan	60-65	tumor associated calcium signal transducer 2	Homo sapiens	88-94
31208270-2	2019	SN-38 has been conjugated to a humanized antibody against trophoblast cell surface antigen 2 (TROP-2), which is involved in cancer signaling pathways and has increased expression by many cancer cell types, yielding the ADC sacituzumab govitecan.	Irinotecan	0-5	tumor associated calcium signal transducer 2	Homo sapiens	94-100
31141714-0	2019	Comments on: "Clinical utility of ABCB1 genotyping for preventing toxicity in treatment with irinotecan".	Irinotecan	93-103	ATP binding cassette subfamily B member 1	Homo sapiens	34-39
31270411-6	2019	The study identified novel off-target interactions by Dactinomycin, Temsirolimus, and Everolimus against NMDA, AMPA, PKA and ERK2, while Irinotecan, Bromocriptine and Dasatinib were top interacting drugs for CaMKII.	Irinotecan	137-147	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	208-214
30635626-7	2019	Treatment of mice with AML with irinotecan, known to inhibit topoisomerase I and FUBP1, significantly prolonged survival alone or in combination with cytarabine.	Irinotecan	32-42	far upstream element (FUSE) binding protein 1	Mus musculus	81-86
30831128-0	2019	Intestinal bacterial beta-glucuronidase as a possible predictive biomarker of irinotecan-induced diarrhea severity.	Irinotecan	78-88	glucuronidase beta	Homo sapiens	21-39
30831128-4	2019	Recent studies have highlighted the important role of the intestinal bacterial beta-glucuronidase (BGUS) in the onset of irinotecan-induced diarrhea.	Irinotecan	121-131	glucuronidase beta	Homo sapiens	79-97
30831128-4	2019	Recent studies have highlighted the important role of the intestinal bacterial beta-glucuronidase (BGUS) in the onset of irinotecan-induced diarrhea.	Irinotecan	121-131	glucuronidase beta	Homo sapiens	99-103
30831128-6	2019	BGUS selective inhibitors that are currently in development may alleviate irinotecan-induced diarrhea, and may help to reduce its morbidity and enhance its activity.	Irinotecan	74-84	glucuronidase beta	Homo sapiens	0-4
30831128-8	2019	In addition, we hypothesize that using BGUS activity as a predictive biomarker of irinotecan-induced diarrhea severity will help to select cancer patients for treatment with irinotecan chemotherapy (whether at full or adapted dose).	Irinotecan	82-92	glucuronidase beta	Homo sapiens	39-43
30831128-8	2019	In addition, we hypothesize that using BGUS activity as a predictive biomarker of irinotecan-induced diarrhea severity will help to select cancer patients for treatment with irinotecan chemotherapy (whether at full or adapted dose).	Irinotecan	174-184	glucuronidase beta	Homo sapiens	39-43
30603911-0	2019	Association between UGT1A1 gene polymorphism and safety and efficacy of irinotecan monotherapy as the third-line treatment for advanced gastric cancer.	Irinotecan	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
30603911-1	2019	BACKGROUND: While uridine diphosphate glucuronosyltransferase (UGT) 1A1 is a key enzyme in the metabolism of irinotecan, relationship between UGT1A1 genotype and safety and efficacy of irinotecan monotherapy in patients with advanced gastric cancer is not clarified.	Irinotecan	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-71
30603911-1	2019	BACKGROUND: While uridine diphosphate glucuronosyltransferase (UGT) 1A1 is a key enzyme in the metabolism of irinotecan, relationship between UGT1A1 genotype and safety and efficacy of irinotecan monotherapy in patients with advanced gastric cancer is not clarified.	Irinotecan	185-195	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
30603911-8	2019	CONCLUSIONS: The UGT1A1 polymorphism may be related to the clinical outcomes of irinotecan monotherapy as the third-line treatment for advanced gastric cancer.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
31141715-0	2019	Comments on: "Clinical utility of ABCB1 genotyping for preventing toxicity in treatment with irinotecan".	Irinotecan	93-103	ATP binding cassette subfamily B member 1	Homo sapiens	34-39
31217818-0	2019	An expansion study of genotype-driven weekly irinotecan and capecitabine in combination with neoadjuvant radiotherapy for locally advanced rectal cancer with UGT1A1 *1*1 genotype.	Irinotecan	45-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
31243264-6	2019	We found that the interaction between GRP78 and SPARC increased during exposure to 5-FU, CPT-11, and tunicamycin, resulting in an attenuation of GRP78"s inhibition of apoptosis.	Irinotecan	89-95	heat shock protein family A (Hsp70) member 5	Homo sapiens	38-43
31243264-6	2019	We found that the interaction between GRP78 and SPARC increased during exposure to 5-FU, CPT-11, and tunicamycin, resulting in an attenuation of GRP78"s inhibition of apoptosis.	Irinotecan	89-95	secreted protein acidic and cysteine rich	Homo sapiens	48-53
31243264-6	2019	We found that the interaction between GRP78 and SPARC increased during exposure to 5-FU, CPT-11, and tunicamycin, resulting in an attenuation of GRP78"s inhibition of apoptosis.	Irinotecan	89-95	heat shock protein family A (Hsp70) member 5	Homo sapiens	145-150
31056264-0	2019	A novel mechanism of irinotecan targeting MDM2 and Bcl-xL.	Irinotecan	21-31	MDM2 proto-oncogene	Homo sapiens	42-46
31056264-0	2019	A novel mechanism of irinotecan targeting MDM2 and Bcl-xL.	Irinotecan	21-31	BCL2 like 1	Homo sapiens	51-57
31056264-2	2019	In this study, we present a new mechanism of Irinotecan which inhibits the activities of MDM2, an E3 ligase of tumour suppressor p53, and Bcl-xL, an anti-apoptotic protein, through direct binding.	Irinotecan	45-55	MDM2 proto-oncogene	Homo sapiens	89-93
31056264-2	2019	In this study, we present a new mechanism of Irinotecan which inhibits the activities of MDM2, an E3 ligase of tumour suppressor p53, and Bcl-xL, an anti-apoptotic protein, through direct binding.	Irinotecan	45-55	tumor protein p53	Homo sapiens	129-132
31056264-2	2019	In this study, we present a new mechanism of Irinotecan which inhibits the activities of MDM2, an E3 ligase of tumour suppressor p53, and Bcl-xL, an anti-apoptotic protein, through direct binding.	Irinotecan	45-55	BCL2 like 1	Homo sapiens	138-144
31056264-3	2019	In our structure modelling study, Irinotecan could fit to the binding sites of MDM2 and Bcl-xL for their known drugs, Nutlin-3 and ABT-737, with a better binding affinity than to Topo I.	Irinotecan	34-44	MDM2 proto-oncogene	Homo sapiens	79-83
31056264-3	2019	In our structure modelling study, Irinotecan could fit to the binding sites of MDM2 and Bcl-xL for their known drugs, Nutlin-3 and ABT-737, with a better binding affinity than to Topo I.	Irinotecan	34-44	BCL2 like 1	Homo sapiens	88-94
31056264-5	2019	We further showed that Irinotecan increased the amount of p53 only in the presence of MDM2 and inhibited the physical interaction of Bcl-xL with Bim, a core pro-apoptotic protein.	Irinotecan	23-33	tumor protein p53	Homo sapiens	58-61
31056264-5	2019	We further showed that Irinotecan increased the amount of p53 only in the presence of MDM2 and inhibited the physical interaction of Bcl-xL with Bim, a core pro-apoptotic protein.	Irinotecan	23-33	MDM2 proto-oncogene	Homo sapiens	86-90
31056264-5	2019	We further showed that Irinotecan increased the amount of p53 only in the presence of MDM2 and inhibited the physical interaction of Bcl-xL with Bim, a core pro-apoptotic protein.	Irinotecan	23-33	BCL2 like 1	Homo sapiens	133-139
31056264-5	2019	We further showed that Irinotecan increased the amount of p53 only in the presence of MDM2 and inhibited the physical interaction of Bcl-xL with Bim, a core pro-apoptotic protein.	Irinotecan	23-33	BCL2 like 11	Homo sapiens	145-148
31056264-7	2019	Collectively, we suggest a new mechanism of action for Irinotecan as a dual target inhibitor of MDM2 and Bcl-xL facilitating the anticancer activities mediated by p53 and Bcl-xL interaction partners.	Irinotecan	55-65	MDM2 proto-oncogene	Homo sapiens	96-100
31056264-7	2019	Collectively, we suggest a new mechanism of action for Irinotecan as a dual target inhibitor of MDM2 and Bcl-xL facilitating the anticancer activities mediated by p53 and Bcl-xL interaction partners.	Irinotecan	55-65	BCL2 like 1	Homo sapiens	105-111
31056264-7	2019	Collectively, we suggest a new mechanism of action for Irinotecan as a dual target inhibitor of MDM2 and Bcl-xL facilitating the anticancer activities mediated by p53 and Bcl-xL interaction partners.	Irinotecan	55-65	tumor protein p53	Homo sapiens	163-166
31056264-7	2019	Collectively, we suggest a new mechanism of action for Irinotecan as a dual target inhibitor of MDM2 and Bcl-xL facilitating the anticancer activities mediated by p53 and Bcl-xL interaction partners.	Irinotecan	55-65	BCL2 like 1	Homo sapiens	171-177
31242600-2	2019	As torsional stress is generated during transcription by progression of RNA polymerase II through the transcribed gene, we tested the effects of camptothecin and of the approved TOP1 inhibitors Topotecan and SN-38 on TNFalpha-induced gene expression.	Irinotecan	208-213	tumor necrosis factor	Homo sapiens	217-225
31217818-1	2019	Background: In our previous dose-escalation study, we uncovered the maximum tolerated dose (MTD) of weekly irinotecan was escalated to 80 mg/m2 and 65 mg/m2 for UDP glucuronosyltransferase family 1 member A1 (UGT1A1) *1*1 and *1*28 rectal cancer patients in neoadjuvant chemoradiotherapy (nCRT).	Irinotecan	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	161-207
31217818-1	2019	Background: In our previous dose-escalation study, we uncovered the maximum tolerated dose (MTD) of weekly irinotecan was escalated to 80 mg/m2 and 65 mg/m2 for UDP glucuronosyltransferase family 1 member A1 (UGT1A1) *1*1 and *1*28 rectal cancer patients in neoadjuvant chemoradiotherapy (nCRT).	Irinotecan	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	209-215
30953637-8	2019	Moreover, the combination of SN-38 and sunitinib caused synergism on colon cancer cells, with significant inhibition of the ABCG2 gene expression and an increase of SN-38 intracellular concentrations.	Irinotecan	29-34	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	124-129
30968312-9	2019	For illustration purpose, the approaches were also applied to an irinotecan mixture model demonstrating 36% lower clearance of irinotecan metabolite (SN-38) in individuals with UGT1A1 homo/heterozygote versus wild-type genotype.	Irinotecan	65-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
31011934-0	2019	Cytotoxic synergy between alisertib and carboplatin versus alisertib and irinotecan are inversely dependent on MGMT levels in glioblastoma cells.	Irinotecan	73-83	O-6-methylguanine-DNA methyltransferase	Homo sapiens	111-115
31011934-7	2019	MGMT knockdown increased apoptosis caused by combined alisertib and irinotecan, while exogenous MGMT overexpression increased apoptosis from alisertib and carboplatin combination treatment.	Irinotecan	68-78	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-4
30968312-9	2019	For illustration purpose, the approaches were also applied to an irinotecan mixture model demonstrating 36% lower clearance of irinotecan metabolite (SN-38) in individuals with UGT1A1 homo/heterozygote versus wild-type genotype.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
30968312-9	2019	For illustration purpose, the approaches were also applied to an irinotecan mixture model demonstrating 36% lower clearance of irinotecan metabolite (SN-38) in individuals with UGT1A1 homo/heterozygote versus wild-type genotype.	Irinotecan	150-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	177-183
31126331-13	2019	CONCLUSIONS: Treatment with CMAB009 plus irinotecan was found to be a superior second-line regimen in comparison to irinotecan-only in KRAS wild-type mCRC patients.	Irinotecan	41-51	KRAS proto-oncogene, GTPase	Homo sapiens	135-139
31067275-5	2019	We now further demonstrate that high levels of HMGA2 also protected cancer cells against DNA breaks triggered by the clinically important TOP1 poison irinotecan.	Irinotecan	150-160	high mobility group AT-hook 2	Homo sapiens	47-52
30645764-2	2019	UGT1A1 (UDP glucuronosyltransferase 1A1) eliminates the active metabolite of irinotecan.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
30645764-2	2019	UGT1A1 (UDP glucuronosyltransferase 1A1) eliminates the active metabolite of irinotecan.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-39
30645764-6	2019	Irinotecan doses of 180, 135, and 90 mg/m2 were administered for UGT1A1 genotypes *1/*1, *1/*28, and *28/*28, respectively.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
30925062-5	2019	In addition, the thienopyrimidine could also sensitize ABCB1- as well as ABCG2-overexpressing cells toward daunorubicin and SN-38, respectively, in concentration ranges that qualified it as one of the ten best triple ABCC1/ABCB1/ABCG2 inhibitors in the literature.	Irinotecan	124-129	ATP binding cassette subfamily B member 1	Homo sapiens	55-60
30925062-5	2019	In addition, the thienopyrimidine could also sensitize ABCB1- as well as ABCG2-overexpressing cells toward daunorubicin and SN-38, respectively, in concentration ranges that qualified it as one of the ten best triple ABCC1/ABCB1/ABCG2 inhibitors in the literature.	Irinotecan	124-129	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	73-78
30925062-5	2019	In addition, the thienopyrimidine could also sensitize ABCB1- as well as ABCG2-overexpressing cells toward daunorubicin and SN-38, respectively, in concentration ranges that qualified it as one of the ten best triple ABCC1/ABCB1/ABCG2 inhibitors in the literature.	Irinotecan	124-129	ATP binding cassette subfamily C member 1	Homo sapiens	217-222
30925062-5	2019	In addition, the thienopyrimidine could also sensitize ABCB1- as well as ABCG2-overexpressing cells toward daunorubicin and SN-38, respectively, in concentration ranges that qualified it as one of the ten best triple ABCC1/ABCB1/ABCG2 inhibitors in the literature.	Irinotecan	124-129	ATP binding cassette subfamily B member 1	Homo sapiens	223-228
30925062-5	2019	In addition, the thienopyrimidine could also sensitize ABCB1- as well as ABCG2-overexpressing cells toward daunorubicin and SN-38, respectively, in concentration ranges that qualified it as one of the ten best triple ABCC1/ABCB1/ABCG2 inhibitors in the literature.	Irinotecan	124-129	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	229-234
31067275-7	2019	In contrast, low to moderate HMGA2 protein levels surprisingly potentiated the formation of irinotecan-induced genotoxic covalent TOP1-DNA cleavage complexes.	Irinotecan	92-102	high mobility group AT-hook 2	Homo sapiens	29-34
31067275-10	2019	These findings were corroborated by an increased irinotecan sensitivity of patient-derived xenografts of colorectal cancers exhibiting low to moderate HMGA2 levels.	Irinotecan	49-59	high mobility group AT-hook 2	Homo sapiens	151-156
30810774-6	2019	RESULTS: Concentration-dependent inhibition of SN-38 glucuronidation was observed in the HLMs and recombinant human UGT1A1 experiments: Pazopanib noncompetitively inhibited SN-38 glucuronidation by HLMs (Ki,u = 1.6 +- 0.05 microM) and recombinant human UGT1A1 (Ki,u = 0.69 +- 0.02 microM).	Irinotecan	47-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-122
30898612-6	2019	Interestingly, co-treatment with nutlin-3a and certain chemotherapeutic drug such as irinotecan and oxaliplatin resulted in antagonistic effects in cells both lacking and containing WT-TP53 activity.	Irinotecan	85-95	tumor protein p53	Homo sapiens	185-189
30840064-3	2019	PATIENTS AND METHODS: This was a single-arm phase II trial that analysed 38 KRAS, NRAS, BRAF and PIK3CA hotspots in tumour tissues of irinotecan-resistant metastatic colorectal cancer patients who received panitumumab plus FOLFIRI until disease progression or early withdrawal.	Irinotecan	134-144	KRAS proto-oncogene, GTPase	Homo sapiens	76-80
30840064-3	2019	PATIENTS AND METHODS: This was a single-arm phase II trial that analysed 38 KRAS, NRAS, BRAF and PIK3CA hotspots in tumour tissues of irinotecan-resistant metastatic colorectal cancer patients who received panitumumab plus FOLFIRI until disease progression or early withdrawal.	Irinotecan	134-144	NRAS proto-oncogene, GTPase	Homo sapiens	82-86
30840064-3	2019	PATIENTS AND METHODS: This was a single-arm phase II trial that analysed 38 KRAS, NRAS, BRAF and PIK3CA hotspots in tumour tissues of irinotecan-resistant metastatic colorectal cancer patients who received panitumumab plus FOLFIRI until disease progression or early withdrawal.	Irinotecan	134-144	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	88-92
30840064-3	2019	PATIENTS AND METHODS: This was a single-arm phase II trial that analysed 38 KRAS, NRAS, BRAF and PIK3CA hotspots in tumour tissues of irinotecan-resistant metastatic colorectal cancer patients who received panitumumab plus FOLFIRI until disease progression or early withdrawal.	Irinotecan	134-144	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	97-103
30810774-0	2019	Pazopanib interacts with irinotecan by inhibiting UGT1A1-mediated glucuronidation, but not OATP1B1-mediated hepatic uptake, of an active metabolite SN-38.	Irinotecan	25-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
30810774-6	2019	RESULTS: Concentration-dependent inhibition of SN-38 glucuronidation was observed in the HLMs and recombinant human UGT1A1 experiments: Pazopanib noncompetitively inhibited SN-38 glucuronidation by HLMs (Ki,u = 1.6 +- 0.05 microM) and recombinant human UGT1A1 (Ki,u = 0.69 +- 0.02 microM).	Irinotecan	47-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	253-259
30810774-10	2019	CONCLUSIONS: Results showed that pazopanib inhibits UGT1A1-mediated SN-38 glucuronidation, but not OATP1B1-mediated SN-38 uptake.	Irinotecan	68-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
30815720-0	2019	Irinotecan induces enterocyte cell death and changes to muc2 and muc4 composition during mucositis in a tumour-bearing DA rat model.	Irinotecan	0-10	mucin 2, oligomeric mucus/gel-forming	Rattus norvegicus	56-60
30815720-0	2019	Irinotecan induces enterocyte cell death and changes to muc2 and muc4 composition during mucositis in a tumour-bearing DA rat model.	Irinotecan	0-10	mucin 4, cell surface associated	Rattus norvegicus	65-69
30782852-2	2019	In the past decade, OATPs, primarily OATP1A2, OATP1B1, and OATP1B3, have emerged as potential mediators of chemotherapy disposition, including drugs such as methotrexate, doxorubicin, paclitaxel, docetaxel, irinotecan and its important metabolite 7-ethyl-10-hydroxycamptothecin, and certain tyrosine kinase inhibitors.	Irinotecan	207-217	solute carrier organic anion transporter family member 1A2	Homo sapiens	37-44
30782852-2	2019	In the past decade, OATPs, primarily OATP1A2, OATP1B1, and OATP1B3, have emerged as potential mediators of chemotherapy disposition, including drugs such as methotrexate, doxorubicin, paclitaxel, docetaxel, irinotecan and its important metabolite 7-ethyl-10-hydroxycamptothecin, and certain tyrosine kinase inhibitors.	Irinotecan	207-217	solute carrier organic anion transporter family member 1B3	Homo sapiens	59-66
30782852-2	2019	In the past decade, OATPs, primarily OATP1A2, OATP1B1, and OATP1B3, have emerged as potential mediators of chemotherapy disposition, including drugs such as methotrexate, doxorubicin, paclitaxel, docetaxel, irinotecan and its important metabolite 7-ethyl-10-hydroxycamptothecin, and certain tyrosine kinase inhibitors.	Irinotecan	247-277	solute carrier organic anion transporter family member 1A2	Homo sapiens	37-44
30782852-2	2019	In the past decade, OATPs, primarily OATP1A2, OATP1B1, and OATP1B3, have emerged as potential mediators of chemotherapy disposition, including drugs such as methotrexate, doxorubicin, paclitaxel, docetaxel, irinotecan and its important metabolite 7-ethyl-10-hydroxycamptothecin, and certain tyrosine kinase inhibitors.	Irinotecan	247-277	solute carrier organic anion transporter family member 1B3	Homo sapiens	59-66
32259055-6	2019	S phase arrest was induced with the topoisomerase I inhibitor SN38; the addition of CHK1i rapidly activated CDK2, inducing S phase progression that was inhibited by the CDK2 inhibitor CVT-313.	Irinotecan	62-66	checkpoint kinase 1	Homo sapiens	84-89
31105879-3	2019	Acute and chronic exposition of colon cancer cell lines to CT/CTE PEDF-derived peptides decreased drug-resistance to conventional colorectal cancer treatments, such as oxaliplatin or irinotecan.	Irinotecan	183-193	serpin family F member 1	Homo sapiens	66-70
32259055-6	2019	S phase arrest was induced with the topoisomerase I inhibitor SN38; the addition of CHK1i rapidly activated CDK2, inducing S phase progression that was inhibited by the CDK2 inhibitor CVT-313.	Irinotecan	62-66	cyclin dependent kinase 2	Homo sapiens	169-173
30968152-1	2019	Irinotecan (CPT-11) is a DNA topoisomerase I inhibitor which is widely used in clinical chemotherapy, particularly for colorectal cancer treatment.	Irinotecan	0-10	DNA topoisomerase I	Rattus norvegicus	25-44
31164525-2	2019	Since both patients were revealed to harbor UGT1A1 polymorphisms, which were highly associated with irinotecan-induced toxicity(the former: UGT1A1 *6/*28, the latter: UGT1A1*6/*6), there was no alternative hopeful treatment other than FOLFIRINOX for them.	Irinotecan	100-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
31164525-2	2019	Since both patients were revealed to harbor UGT1A1 polymorphisms, which were highly associated with irinotecan-induced toxicity(the former: UGT1A1 *6/*28, the latter: UGT1A1*6/*6), there was no alternative hopeful treatment other than FOLFIRINOX for them.	Irinotecan	100-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
31164525-2	2019	Since both patients were revealed to harbor UGT1A1 polymorphisms, which were highly associated with irinotecan-induced toxicity(the former: UGT1A1 *6/*28, the latter: UGT1A1*6/*6), there was no alternative hopeful treatment other than FOLFIRINOX for them.	Irinotecan	100-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
30952738-0	2019	Cytoplasmic E-Cadherin Expression Is Associated With Higher Tumour Level of VEGFA, Lower Response Rate to Irinotecan-based Treatment and Poorer Prognosis in Patients With Metastatic Colorectal Cancer.	Irinotecan	106-116	cadherin 1	Homo sapiens	12-22
30952738-10	2019	In addition, among the patients with intense VEGFA expression (n=36), those who had positive cytoplasmic E-cadherin in their tumours had a lower response-rate to first-line therapy with irinotecan, fluorouracil and leucovorin regimen: 5 out of 36 (14%) were chemosensitive.	Irinotecan	186-196	cadherin 1	Homo sapiens	105-115
30339275-7	2019	In patients receiving fluoropyrimidine/irinotecan, the incremental cost between DPYD variant and UGT1A1*28/*28 carriers and noncarriers was $2,975.	Irinotecan	39-49	dihydropyrimidine dehydrogenase	Homo sapiens	80-84
30339275-7	2019	In patients receiving fluoropyrimidine/irinotecan, the incremental cost between DPYD variant and UGT1A1*28/*28 carriers and noncarriers was $2,975.	Irinotecan	39-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
30968152-1	2019	Irinotecan (CPT-11) is a DNA topoisomerase I inhibitor which is widely used in clinical chemotherapy, particularly for colorectal cancer treatment.	Irinotecan	12-18	DNA topoisomerase I	Rattus norvegicus	25-44
30415007-0	2019	Combined treatment of ABT199 and irinotecan suppresses KRAS-mutant lung cancer cells.	Irinotecan	33-43	KRAS proto-oncogene, GTPase	Homo sapiens	55-59
30881507-2	2019	Expression of CYP3A5, which is involved in the degradation of irinotecan, has also been reported in colorectal cancer (CRC).	Irinotecan	62-72	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	14-20
30881507-10	2019	A statistically significant inverse correlation was identified between CYP3A5 expression in CRC tissues and tumor response to irinotecan therapy.	Irinotecan	126-136	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	71-77
30881507-12	2019	As CYP3A5 is involved in the degradation of irinotecan, the significantly higher intratumoral expression of CYP3A5 in patients with CRC who do not respond to irinotecan-based chemotherapy may indicate a causal role of CYP3A5 in tumor resistance.	Irinotecan	44-54	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	3-9
30881507-12	2019	As CYP3A5 is involved in the degradation of irinotecan, the significantly higher intratumoral expression of CYP3A5 in patients with CRC who do not respond to irinotecan-based chemotherapy may indicate a causal role of CYP3A5 in tumor resistance.	Irinotecan	158-168	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	108-114
30881507-12	2019	As CYP3A5 is involved in the degradation of irinotecan, the significantly higher intratumoral expression of CYP3A5 in patients with CRC who do not respond to irinotecan-based chemotherapy may indicate a causal role of CYP3A5 in tumor resistance.	Irinotecan	158-168	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	108-114
30881507-0	2019	Tumor response to irinotecan is associated with CYP3A5 expression in colorectal cancer.	Irinotecan	18-28	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	48-54
30476968-16	2019	Conclusions and Relevance: This is the first prospective demonstration that a rechallenge strategy with cetuximab and irinotecan may be active in patients with RAS and BRAF wild-type mCRC with acquired resistance to first-line irinotecan- and cetuximab-based therapy.	Irinotecan	118-128	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	168-172
29884612-10	2019	Finally, EAC cell lines showed subtype-specific responses to topotecan, SN-38 and palbociclib treatment.	Irinotecan	72-77	CYLD lysine 63 deubiquitinase	Homo sapiens	9-12
30602616-4	2019	We present the case of a recurrent nasoethmoidal ITAC informed as RAS and BRAF wild-type by standard real-time polymerase chain reaction methods and treated with first-line cetuximab and irinotecan without response.	Irinotecan	187-197	C-X-C motif chemokine ligand 11	Homo sapiens	49-53
30602616-4	2019	We present the case of a recurrent nasoethmoidal ITAC informed as RAS and BRAF wild-type by standard real-time polymerase chain reaction methods and treated with first-line cetuximab and irinotecan without response.	Irinotecan	187-197	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	74-78
30820689-8	2019	In pharmacokinetics studies, for pro-drug IRT, the t1/2beta of IRT-PLGA-NPs was extended from 0.483 to 3.327 h compared with irinotecan solution (IRT-Sol), and for its active metabolite SN-38, the t1/2beta was extended from 1.889 to 4.811 h, which indicated that IRT-PLGA-NPs could prolong the retention times of both IRT and SN-38.	Irinotecan	186-191	interleukin 1 receptor like 1	Homo sapiens	51-59
30899442-7	2019	In vitro CD133 expression and its co-expression with CD44 were associated with primary-resistance to irinotecan and acquired-resistance to anti-EGFR inhibitors respectively.	Irinotecan	101-111	prominin 1	Homo sapiens	9-14
30899442-7	2019	In vitro CD133 expression and its co-expression with CD44 were associated with primary-resistance to irinotecan and acquired-resistance to anti-EGFR inhibitors respectively.	Irinotecan	101-111	CD44 molecule (Indian blood group)	Homo sapiens	53-57
30820689-8	2019	In pharmacokinetics studies, for pro-drug IRT, the t1/2beta of IRT-PLGA-NPs was extended from 0.483 to 3.327 h compared with irinotecan solution (IRT-Sol), and for its active metabolite SN-38, the t1/2beta was extended from 1.889 to 4.811 h, which indicated that IRT-PLGA-NPs could prolong the retention times of both IRT and SN-38.	Irinotecan	326-331	interleukin 1 receptor like 1	Homo sapiens	51-59
30315927-0	2019	A molecular basis for the synergy between 17-allylamino-17-demethoxy geldanamycin with Capecitabine and Irinotecan in human colorectal cancer cells through VEFG and MMP-9 gene expression.	Irinotecan	104-114	matrix metallopeptidase 9	Homo sapiens	165-170
30447099-1	2019	Studies have indicated an association between UDP-glucuronosyltransferase-1A1 (UGT1A1) genetic polymorphisms and irinotecan-induced toxicity.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
30447099-2	2019	We undertook this study to investigate the association between UGT1A1 genetic polymorphisms and toxicity in patients treated with the FOLFIRINOX (comprising oxaliplatin, irinotecan, fluorouracil, and leucovorin) chemotherapy regimen in the JASPAC 06 study.	Irinotecan	170-180	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
30447099-1	2019	Studies have indicated an association between UDP-glucuronosyltransferase-1A1 (UGT1A1) genetic polymorphisms and irinotecan-induced toxicity.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-77
30696915-8	2019	Knockdown of Crabp2 further inhibited the growth of cancer cells as compared with that by gemcitabine or irinotecan alone.	Irinotecan	105-115	cellular retinoic acid binding protein 2	Homo sapiens	13-19
30733972-0	2019	A Novel Anti-EGFR mAb Ame55 with Lower Toxicity and Better Efficacy than Cetuximab When Combined with Irinotecan.	Irinotecan	102-112	epidermal growth factor receptor	Homo sapiens	13-17
30634695-7	2019	These results indicate that the substitution of Gly at position 187 of ABCC4 to Trp resulted in reduced SN-38 resistance.	Irinotecan	104-109	ATP binding cassette subfamily C member 4	Homo sapiens	71-76
30551482-11	2019	Additionally, a potent inhibitory effect of GQT extract against hCE2 was observedin vitro, with its IC50 value of 0.187 mg/ml, suggesting alleviating activity on hCE2-mediated severe diarrhea in patients suffered from CPT-11.	Irinotecan	218-224	carboxylesterase 2	Homo sapiens	64-68
30662270-0	2019	Complete response with fluorouracil and irinotecan with a BRAFV600E and EGFR inhibitor in BRAF-mutated metastatic colorectal cancer: a case report.	Irinotecan	40-50	epidermal growth factor receptor	Homo sapiens	72-76
30662270-0	2019	Complete response with fluorouracil and irinotecan with a BRAFV600E and EGFR inhibitor in BRAF-mutated metastatic colorectal cancer: a case report.	Irinotecan	40-50	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	58-62
30662270-9	2019	Conclusion: The combination of fluorouracil and irinotecan with a BRAFV600E and EGFR inhibitor may have synergistic action, leading to recession of secondary metastases in patients with BRAFV600E-mutated colorectal cancer.	Irinotecan	48-58	epidermal growth factor receptor	Homo sapiens	80-84
30551482-11	2019	Additionally, a potent inhibitory effect of GQT extract against hCE2 was observedin vitro, with its IC50 value of 0.187 mg/ml, suggesting alleviating activity on hCE2-mediated severe diarrhea in patients suffered from CPT-11.	Irinotecan	218-224	carboxylesterase 2	Homo sapiens	162-166
30377777-11	2019	CONCLUSION: The present study demonstrated that dose reduction by 20% ensured safety and efficacy of irinotecan in mCRC patients with homozygous mutation in UGT1A1 genes.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	157-163
30585257-1	2019	BACKGROUND: Patients harbouring the UGT1A1*28/*28 genotype are at risk of severe toxicity with the standard irinotecan dose.	Irinotecan	108-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
30585257-6	2019	In the experimental group, the irinotecan dose was 300 mg/m2 for UGT1A1*1/*1 and 260 mg/m2 for *1/*28 patients.	Irinotecan	31-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
30585257-13	2019	CONCLUSIONS: Patients with the UGT1A1*1/*1 and *1/*28 genotypes can receive high doses of irinotecan to achieve a more favourable ORR without significant adverse events.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
30307354-2	2019	CASE PRESENTATION: Here we present a KRAS/NRAS/BRAF wild-type mCRC patient who has been previously treated with FOLFIRI (fluorouracil, leucovorin, and irinotecan), XELOX (capecitabine and oxaliplatin), cetuximab and bevacizumab, and then received the next generation sequencing (NGS) and whose metastatic subcutaneous nodule was resected to generate patient-derived xenograft (PDX) models.	Irinotecan	151-161	KRAS proto-oncogene, GTPase	Homo sapiens	37-41
30377777-0	2019	Dose adjustment of irinotecan based on UGT1A1 polymorphisms in patients with colorectal cancer.	Irinotecan	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
31045514-4	2019	OBJECTIVE: Investigation of the association between rs4759314 HOTAIR and rs3200401 MALAT1 polymorphisms and irinotecan-based chemotherapy in terms of drug efficacy and toxicity.	Irinotecan	108-118	HOX transcript antisense RNA	Homo sapiens	62-68
30377777-2	2019	SN-38 is an active metabolite of irinotecan, which is formed by carboxylesterase and inactivated by UDP-glucuronyltransferase (UGT) 1A1.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-135
30377777-2	2019	SN-38 is an active metabolite of irinotecan, which is formed by carboxylesterase and inactivated by UDP-glucuronyltransferase (UGT) 1A1.	Irinotecan	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-135
30377777-3	2019	The UGT enzyme activity is reduced in patients with homozygous mutation in UGT1A1 genes (*6/*6, *28/*28 and *6/*28); thus dose reduction is required for prevention of severe adverse events associated with irinotecan.	Irinotecan	205-215	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	4-7
30377777-3	2019	The UGT enzyme activity is reduced in patients with homozygous mutation in UGT1A1 genes (*6/*6, *28/*28 and *6/*28); thus dose reduction is required for prevention of severe adverse events associated with irinotecan.	Irinotecan	205-215	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
30377777-4	2019	The present study was designed to investigate the relationship between UGT1A1 polymorphisms and the incidence of adverse events or the therapeutic effect in mCRC patients who received irinotecan.	Irinotecan	184-194	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
30307354-2	2019	CASE PRESENTATION: Here we present a KRAS/NRAS/BRAF wild-type mCRC patient who has been previously treated with FOLFIRI (fluorouracil, leucovorin, and irinotecan), XELOX (capecitabine and oxaliplatin), cetuximab and bevacizumab, and then received the next generation sequencing (NGS) and whose metastatic subcutaneous nodule was resected to generate patient-derived xenograft (PDX) models.	Irinotecan	151-161	NRAS proto-oncogene, GTPase	Homo sapiens	42-46
30307354-2	2019	CASE PRESENTATION: Here we present a KRAS/NRAS/BRAF wild-type mCRC patient who has been previously treated with FOLFIRI (fluorouracil, leucovorin, and irinotecan), XELOX (capecitabine and oxaliplatin), cetuximab and bevacizumab, and then received the next generation sequencing (NGS) and whose metastatic subcutaneous nodule was resected to generate patient-derived xenograft (PDX) models.	Irinotecan	151-161	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	47-51
31045514-4	2019	OBJECTIVE: Investigation of the association between rs4759314 HOTAIR and rs3200401 MALAT1 polymorphisms and irinotecan-based chemotherapy in terms of drug efficacy and toxicity.	Irinotecan	108-118	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	83-89
30396915-5	2019	Under these suppression conditions, cER values for irinotecan and topotecan (dual substrates of ABCB1 and ABCG2) were elevated by more than 4-fold and 2-fold, respectively, compared with cER values without the suppression.	Irinotecan	51-61	ATP binding cassette subfamily B member 1	Canis lupus familiaris	96-101
29932028-4	2019	SN-38 is detoxified by the formation of SN-38 glucuronide, through UGT1A1.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
29932028-5	2019	Genetic polymorphisms in the UGT1A1 gene are associated to higher exposures to SN-38 and severe toxicity.	Irinotecan	79-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
30396915-5	2019	Under these suppression conditions, cER values for irinotecan and topotecan (dual substrates of ABCB1 and ABCG2) were elevated by more than 4-fold and 2-fold, respectively, compared with cER values without the suppression.	Irinotecan	51-61	ATP binding cassette subfamily G member 2	Canis lupus familiaris	106-111
30595211-0	2019	Cytoprotective and genotoxic effects of vitamins K1 and B1 on irinotecan in vitro.	Irinotecan	62-72	keratin 1	Homo sapiens	49-58
30372160-5	2019	The results showed that 5 mug/ml of OED combined with 40 muM of irinotecan possessed significant synergetic inhibition on SW-480 cells with a combination index (CI) of 0.56.	Irinotecan	64-74	Oregon eye disease	Homo sapiens	36-39
30372160-6	2019	Besides, the percentage of apoptotic cells was significantly increased from 69.57% (40 muM of irinotecan) or 72.7% (5 mug/ml of OED) to 95.6% after treatment of OED combined with irinotecan (OCI), suggesting OED and irinotecan possess the synergistic apoptotic effect (P &lt; 0.01).	Irinotecan	94-104	Oregon eye disease	Homo sapiens	161-164
30372160-6	2019	Besides, the percentage of apoptotic cells was significantly increased from 69.57% (40 muM of irinotecan) or 72.7% (5 mug/ml of OED) to 95.6% after treatment of OED combined with irinotecan (OCI), suggesting OED and irinotecan possess the synergistic apoptotic effect (P &lt; 0.01).	Irinotecan	94-104	Oregon eye disease	Homo sapiens	161-164
30372160-6	2019	Besides, the percentage of apoptotic cells was significantly increased from 69.57% (40 muM of irinotecan) or 72.7% (5 mug/ml of OED) to 95.6% after treatment of OED combined with irinotecan (OCI), suggesting OED and irinotecan possess the synergistic apoptotic effect (P &lt; 0.01).	Irinotecan	179-189	Oregon eye disease	Homo sapiens	128-131
30372160-6	2019	Besides, the percentage of apoptotic cells was significantly increased from 69.57% (40 muM of irinotecan) or 72.7% (5 mug/ml of OED) to 95.6% after treatment of OED combined with irinotecan (OCI), suggesting OED and irinotecan possess the synergistic apoptotic effect (P &lt; 0.01).	Irinotecan	179-189	Oregon eye disease	Homo sapiens	128-131
30372160-9	2019	These data indicated that OED could enhance antiproliferative effects of irinotecan on colorectal cancer cells, which was related with induction of apoptosis and regulations of activity of caspase-3.	Irinotecan	73-83	Oregon eye disease	Homo sapiens	26-29
28963609-6	2019	TIMP-1 overexpressing U87MG cells were significantly more resistant than low TIMP-1 expressing clones and parental cells when exposed to SN-38 (TOP1 inhibitor) or epirubicin (TOP2 inhibitor).	Irinotecan	137-142	TIMP metallopeptidase inhibitor 1	Homo sapiens	0-6
30527657-1	2019	Differences in drug metabolism associated with UGT1A1 polymorphism could result in individualized local response to hepatic chemoembolization with irinotecan-eluting beads (DEBIRI) or predictable toxicities.	Irinotecan	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
30009852-4	2018	Herein we evidenced, for the first time, that PTHrP induces resistance to CPT-11 in Caco-2 and HCT116 cells; although both cell lines responded to the drug through different molecular mechanisms, the chemoresistance by PTHrP in these models is mediated through ERK, which in turn is activated by PCK, Src and Akt.	Irinotecan	74-80	parathyroid hormone like hormone	Homo sapiens	46-51
28963609-11	2019	Whether TIMP-1 plays a role in irinotecan resistance and has a predictive potential in glioblastoma patients remains to be elucidated.	Irinotecan	31-41	TIMP metallopeptidase inhibitor 1	Homo sapiens	8-14
30391354-0	2019	Pharmacological inhibition of bacterial beta-glucuronidase prevents irinotecan-induced diarrhea without impairing its antitumor efficacy in vivo.	Irinotecan	68-78	glucuronidase, beta	Mus musculus	40-58
30391354-2	2019	The underlying mechanism has been shown that the active metabolite of CPT-11, SN-38, is metabolized to the inactive metabolite SN-38 glucuronide (SN-38 G) during hepatic glucuronidation, and subsequently is exported into the intestine, where SN-38 G is hydrolyzed by bacterial beta-glucuronidase (betaG) to be SN-38, thus leading to intestinal toxicity.	Irinotecan	70-76	glucuronidase, beta	Mus musculus	277-295
30391354-2	2019	The underlying mechanism has been shown that the active metabolite of CPT-11, SN-38, is metabolized to the inactive metabolite SN-38 glucuronide (SN-38 G) during hepatic glucuronidation, and subsequently is exported into the intestine, where SN-38 G is hydrolyzed by bacterial beta-glucuronidase (betaG) to be SN-38, thus leading to intestinal toxicity.	Irinotecan	78-83	glucuronidase, beta	Mus musculus	277-295
30391354-2	2019	The underlying mechanism has been shown that the active metabolite of CPT-11, SN-38, is metabolized to the inactive metabolite SN-38 glucuronide (SN-38 G) during hepatic glucuronidation, and subsequently is exported into the intestine, where SN-38 G is hydrolyzed by bacterial beta-glucuronidase (betaG) to be SN-38, thus leading to intestinal toxicity.	Irinotecan	127-132	glucuronidase, beta	Mus musculus	277-295
30391354-2	2019	The underlying mechanism has been shown that the active metabolite of CPT-11, SN-38, is metabolized to the inactive metabolite SN-38 glucuronide (SN-38 G) during hepatic glucuronidation, and subsequently is exported into the intestine, where SN-38 G is hydrolyzed by bacterial beta-glucuronidase (betaG) to be SN-38, thus leading to intestinal toxicity.	Irinotecan	127-132	glucuronidase, beta	Mus musculus	277-295
30391354-2	2019	The underlying mechanism has been shown that the active metabolite of CPT-11, SN-38, is metabolized to the inactive metabolite SN-38 glucuronide (SN-38 G) during hepatic glucuronidation, and subsequently is exported into the intestine, where SN-38 G is hydrolyzed by bacterial beta-glucuronidase (betaG) to be SN-38, thus leading to intestinal toxicity.	Irinotecan	127-132	glucuronidase, beta	Mus musculus	277-295
30246377-0	2018	UGT1A1 polymorphisms in rectal cancer associated with the efficacy and toxicity of preoperative chemoradiotherapy using irinotecan.	Irinotecan	120-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
29499902-9	2018	Furthermore, it was observed that those patients with wild-type in UGT family genes analysed have lower rates of toxicity associated with irinotecan treatment than those with certain mutated allele (P=.010).	Irinotecan	138-148	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	67-70
29499902-10	2018	CONCLUSIONS: These results suggest that the presence of certain polymorphisms in the UGT1A family of genes is related to the development of toxicity during treatment with irinotecan.	Irinotecan	171-181	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	85-90
30246377-11	2018	Our results indicate that UGT1A1 polymorphism is a predictive factor to determine the clinical efficacy of preoperative chemoradiotherapy and hematological toxicity induced by chemoradiotherapy using irinotecan in locally advanced rectal cancer patients.	Irinotecan	200-210	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
29499902-0	2018	Effect of UGT, SLCO, ABCB and ABCC polymorphisms on irinotecan toxicity.	Irinotecan	52-62	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	10-13
29499902-0	2018	Effect of UGT, SLCO, ABCB and ABCC polymorphisms on irinotecan toxicity.	Irinotecan	52-62	ATP binding cassette subfamily C member 1	Homo sapiens	30-34
29499902-1	2018	BACKGROUND AND OBJECTIVES: Evaluate the relationship between the presence of polymorphisms in genes involved in the pharmacodynamics of irinotecan (UGT1A, SLCO1B1, ABCB1 and ABCC2) and the safety of irinotecan in the treatment of metastatic colorectal cancer (mCRC).	Irinotecan	136-146	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	148-153
29499902-1	2018	BACKGROUND AND OBJECTIVES: Evaluate the relationship between the presence of polymorphisms in genes involved in the pharmacodynamics of irinotecan (UGT1A, SLCO1B1, ABCB1 and ABCC2) and the safety of irinotecan in the treatment of metastatic colorectal cancer (mCRC).	Irinotecan	136-146	solute carrier organic anion transporter family member 1B1	Homo sapiens	155-162
29499902-1	2018	BACKGROUND AND OBJECTIVES: Evaluate the relationship between the presence of polymorphisms in genes involved in the pharmacodynamics of irinotecan (UGT1A, SLCO1B1, ABCB1 and ABCC2) and the safety of irinotecan in the treatment of metastatic colorectal cancer (mCRC).	Irinotecan	136-146	ATP binding cassette subfamily B member 1	Homo sapiens	164-169
29499902-1	2018	BACKGROUND AND OBJECTIVES: Evaluate the relationship between the presence of polymorphisms in genes involved in the pharmacodynamics of irinotecan (UGT1A, SLCO1B1, ABCB1 and ABCC2) and the safety of irinotecan in the treatment of metastatic colorectal cancer (mCRC).	Irinotecan	136-146	ATP binding cassette subfamily C member 2	Homo sapiens	174-179
30246377-1	2018	The purpose of the present study was to assess the efficacy and toxicity of preoperative chemoradiotherapy using irinotecan against locally advanced lower rectal cancer according to UDP-glucuronosyltransferase 1A1 (UGT1A1) polymorphisms.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-213
30246377-1	2018	The purpose of the present study was to assess the efficacy and toxicity of preoperative chemoradiotherapy using irinotecan against locally advanced lower rectal cancer according to UDP-glucuronosyltransferase 1A1 (UGT1A1) polymorphisms.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	215-221
30527181-2	2018	Uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1) is thought to be largely responsible for the glucuronidation of etoposide as well as that of irinotecan, suggesting that polymorphisms of UGT1A1 might be predictive of etoposide toxicity.	Irinotecan	156-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-53
30367935-0	2018	beta-Casein micelles for oral delivery of SN-38 and elacridar to overcome BCRP-mediated multidrug resistance in gastric cancer.	Irinotecan	42-47	casein beta	Homo sapiens	0-11
30367935-5	2018	The chemotherapeutic drug SN-38, a BCRP transport substrate, and the BCRP efflux transport inhibitor, elacridar, exhibited high binding affinity to beta-CN, as demonstrated by spectrophotometry and spectrofluorometry.	Irinotecan	26-31	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	35-39
30367935-5	2018	The chemotherapeutic drug SN-38, a BCRP transport substrate, and the BCRP efflux transport inhibitor, elacridar, exhibited high binding affinity to beta-CN, as demonstrated by spectrophotometry and spectrofluorometry.	Irinotecan	26-31	casein beta	Homo sapiens	148-155
30191738-2	2018	TDP1 plays an essential role in the resistance of cancer cells to currently used antitumour drugs based on Top1 inhibitors such as topotecan and irinotecan.	Irinotecan	145-155	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	0-4
30692298-10	2018	Chemotherapy containing cisplatin(CDDP)and irinotecan(CPT-11)was initiated; although the blood hCG level was temporally lowered, the patient died of liver failure 8 months after the surgery.	Irinotecan	43-53	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
30692298-10	2018	Chemotherapy containing cisplatin(CDDP)and irinotecan(CPT-11)was initiated; although the blood hCG level was temporally lowered, the patient died of liver failure 8 months after the surgery.	Irinotecan	54-60	hypertrichosis 2 (generalised, congenital)	Homo sapiens	95-98
30527181-2	2018	Uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1) is thought to be largely responsible for the glucuronidation of etoposide as well as that of irinotecan, suggesting that polymorphisms of UGT1A1 might be predictive of etoposide toxicity.	Irinotecan	156-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
30527181-2	2018	Uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1) is thought to be largely responsible for the glucuronidation of etoposide as well as that of irinotecan, suggesting that polymorphisms of UGT1A1 might be predictive of etoposide toxicity.	Irinotecan	156-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	201-207
30139840-1	2018	LESSONS LEARNED: The maximum tolerated dose of the combination of linsitinib and irinotecan is linsitinib 450 mg daily on days 1-3 every 7 days and irinotecan 125 mg/m2 days 1 and 8 of a 21-day cycle.The adverse effects associated with the combination are not significantly increased beyond what is expected of each drug as a single agent.Multiple negative trials of insulin-like growth factor-1 receptor inhibitors performed in unselected patient populations led to the early discontinuation of linistinib development and this trial.Earlier integration of assessment of potential predictive biomarkers into clinical trials, as was planned in this study, is vital to the development of targeted therapies in oncology.	Irinotecan	81-91	insulin like growth factor 1 receptor	Homo sapiens	367-404
30538568-0	2018	Value of plasma SN-38 levels and DPD activity in irinotecan-based individualized chemotherapy for advanced colorectal cancer with heterozygous type UGT1A1*6 or UGT1A1*28.	Irinotecan	49-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	148-154
30538568-0	2018	Value of plasma SN-38 levels and DPD activity in irinotecan-based individualized chemotherapy for advanced colorectal cancer with heterozygous type UGT1A1*6 or UGT1A1*28.	Irinotecan	49-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
30498448-4	2018	Genetic variants resulting in decreased enzymatic activity of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) are known to increase irinotecan and 5-fluorouracil-related toxicity, respectively.	Irinotecan	183-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-109
30498448-4	2018	Genetic variants resulting in decreased enzymatic activity of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) are known to increase irinotecan and 5-fluorouracil-related toxicity, respectively.	Irinotecan	183-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
30498448-4	2018	Genetic variants resulting in decreased enzymatic activity of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) are known to increase irinotecan and 5-fluorouracil-related toxicity, respectively.	Irinotecan	183-193	dihydropyrimidine dehydrogenase	Homo sapiens	123-154
30498448-4	2018	Genetic variants resulting in decreased enzymatic activity of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) are known to increase irinotecan and 5-fluorouracil-related toxicity, respectively.	Irinotecan	183-193	dihydropyrimidine dehydrogenase	Homo sapiens	156-159
30385821-6	2018	Similar inhibition of pRAD50 (68%) was observed following ATM inhibitor treatment post irinotecan in a colorectal cancer xenograft model.	Irinotecan	87-97	ATM serine/threonine kinase	Homo sapiens	58-61
30396964-0	2018	Patients with hMLH1 or/and hMSH2-deficient Metastatic Colorectal Cancer Are Associated with Reduced Levels of Vascular Endothelial Growth Factor-1 Expression and Higher Response Rate to Irinotecan-based Regimen.	Irinotecan	186-196	mutL homolog 1	Homo sapiens	14-19
30519050-0	2018	Association of MLH1 single nucleotide polymorphisms with clinical outcomes of first-line irinotecan-based chemotherapy in colorectal cancer.	Irinotecan	89-99	mutL homolog 1	Homo sapiens	15-19
30519050-2	2018	The aim of this study explored the influence of MLH1 SNPs on clinical outcomes of first-line irinotecan-based chemotherapy in CRC.	Irinotecan	93-103	mutL homolog 1	Homo sapiens	48-52
30519050-11	2018	Conclusion: The AA variant of MLH1 rs1800734 SNPs has a longer PFS in first-line irinotecan-based chemotherapy for mCRC patients, and the result needs to be further confirmed by prospective studies in the future.	Irinotecan	81-91	mutL homolog 1	Homo sapiens	30-34
30257334-3	2018	The MTT assay was used to detect growth inhibition of differentially-expressed KDM5c colon cancer cells, for which L-OHP or CPT-11 were added.	Irinotecan	124-130	lysine demethylase 5C	Homo sapiens	79-84
30135242-3	2018	The hiPSC-IECs showed the transport activities of P-glycoprotein (P-gp), breast cancer resistance protein (BCRP), and peptide transporter 1 (PEPT1), revealed by using their probe substrates ([3H]digoxin, sulfasalazine, and [14C]glycylsarcosine), and the metabolic activities of CYP3A4, CES2, and CES1, which were clarified using their probe substrates (midazolam, irinotecan, and temocapril).	Irinotecan	364-374	ATP binding cassette subfamily B member 1	Homo sapiens	50-64
30135242-3	2018	The hiPSC-IECs showed the transport activities of P-glycoprotein (P-gp), breast cancer resistance protein (BCRP), and peptide transporter 1 (PEPT1), revealed by using their probe substrates ([3H]digoxin, sulfasalazine, and [14C]glycylsarcosine), and the metabolic activities of CYP3A4, CES2, and CES1, which were clarified using their probe substrates (midazolam, irinotecan, and temocapril).	Irinotecan	364-374	ATP binding cassette subfamily B member 1	Homo sapiens	66-70
30166404-0	2018	Gene-by-Environment Interaction of Bcrp-/- and Methionine- and Choline-Deficient Diet-Induced Nonalcoholic Steatohepatitis Alters SN-38 Disposition.	Irinotecan	130-135	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	35-39
30166404-4	2018	SN-38, the active irinotecan metabolite, is reported to be a substrate for Bcrp, whereas SN-38 glucuronide (SN-38G) is a Mrp2 substrate.	Irinotecan	0-5	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	75-79
30135242-3	2018	The hiPSC-IECs showed the transport activities of P-glycoprotein (P-gp), breast cancer resistance protein (BCRP), and peptide transporter 1 (PEPT1), revealed by using their probe substrates ([3H]digoxin, sulfasalazine, and [14C]glycylsarcosine), and the metabolic activities of CYP3A4, CES2, and CES1, which were clarified using their probe substrates (midazolam, irinotecan, and temocapril).	Irinotecan	364-374	solute carrier family 15 member 1	Homo sapiens	118-139
30166404-4	2018	SN-38, the active irinotecan metabolite, is reported to be a substrate for Bcrp, whereas SN-38 glucuronide (SN-38G) is a Mrp2 substrate.	Irinotecan	18-28	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	75-79
30166404-4	2018	SN-38, the active irinotecan metabolite, is reported to be a substrate for Bcrp, whereas SN-38 glucuronide (SN-38G) is a Mrp2 substrate.	Irinotecan	89-94	ATP binding cassette subfamily C member 2	Rattus norvegicus	121-125
30166404-5	2018	The purpose of this study was to determine the function of Bcrp in NASH through alterations in the disposition of SN-38 and SN-38G in a Bcrp knockout (Bcrp-/- KO) and methionine- and choline-deficient (MCD) model of NASH.	Irinotecan	114-119	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	59-63
30135242-3	2018	The hiPSC-IECs showed the transport activities of P-glycoprotein (P-gp), breast cancer resistance protein (BCRP), and peptide transporter 1 (PEPT1), revealed by using their probe substrates ([3H]digoxin, sulfasalazine, and [14C]glycylsarcosine), and the metabolic activities of CYP3A4, CES2, and CES1, which were clarified using their probe substrates (midazolam, irinotecan, and temocapril).	Irinotecan	364-374	solute carrier family 15 member 1	Homo sapiens	141-146
30166404-9	2018	These data indicate that Bcrp is not solely responsible for SN-38 biliary efflux, but rather implicate a combined role for BCRP and MRP2.	Irinotecan	60-65	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	25-29
30166404-10	2018	Furthermore, the disposition of SN-38 and SN-38G is altered by Bcrp-/- and NASH in a gene-by-environment interaction and may result in variable drug response to irinotecan therapy in polymorphic patients.	Irinotecan	32-37	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	63-67
30361780-0	2018	Irinotecan Alters the Disposition of Morphine Via Inhibition of Organic Cation Transporter 1 (OCT1) and 2 (OCT2).	Irinotecan	0-10	solute carrier family 22 member 1	Homo sapiens	64-92
30166404-10	2018	Furthermore, the disposition of SN-38 and SN-38G is altered by Bcrp-/- and NASH in a gene-by-environment interaction and may result in variable drug response to irinotecan therapy in polymorphic patients.	Irinotecan	42-47	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	63-67
30166404-10	2018	Furthermore, the disposition of SN-38 and SN-38G is altered by Bcrp-/- and NASH in a gene-by-environment interaction and may result in variable drug response to irinotecan therapy in polymorphic patients.	Irinotecan	161-171	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	63-67
30360603-0	2018	Effects of ABCC2 and SLCO1B1 Polymorphisms on Treatment Responses in Thai Metastatic Colorectal Cancer Patients Treated with Irinotecan-Based Chemotherapy Purpose: Irinotecan is an anticancer medicine which is used mostly in metastatic colorectal cancer (mCRC) treatmentas second or third line chemotherapy.	Irinotecan	164-174	ATP binding cassette subfamily C member 2	Homo sapiens	11-16
30360603-0	2018	Effects of ABCC2 and SLCO1B1 Polymorphisms on Treatment Responses in Thai Metastatic Colorectal Cancer Patients Treated with Irinotecan-Based Chemotherapy Purpose: Irinotecan is an anticancer medicine which is used mostly in metastatic colorectal cancer (mCRC) treatmentas second or third line chemotherapy.	Irinotecan	164-174	solute carrier organic anion transporter family member 1B1	Homo sapiens	21-28
30361780-0	2018	Irinotecan Alters the Disposition of Morphine Via Inhibition of Organic Cation Transporter 1 (OCT1) and 2 (OCT2).	Irinotecan	0-10	solute carrier family 22 member 1	Homo sapiens	94-98
30361780-0	2018	Irinotecan Alters the Disposition of Morphine Via Inhibition of Organic Cation Transporter 1 (OCT1) and 2 (OCT2).	Irinotecan	0-10	POU class 2 homeobox 2	Homo sapiens	107-111
30120489-0	2018	Replica to the Opinion Letter regarding the article "Sensitization of colorectal cancer cells to irinotecan by the Survivin inhibitor LLP3 depends on XAF1 proficiency in the context of mutated p53" (Arch Toxicol https://doi.org/10.1007/s00204-018-240-x).	Irinotecan	97-107	XIAP associated factor 1	Homo sapiens	150-154
30361780-7	2018	All of the six drugs examined, including amitriptyline, fluoxetine, imipramine, irinotecan, ondansetron, and verapamil, were inhibitors of OCT1/2-mediated morphine uptake.	Irinotecan	80-90	solute carrier family 22 member 1	Homo sapiens	139-143
30361780-10	2018	Clinician should be aware that the disposition of and thus the response to morphine may be altered by co-administration of an OCT1/2 inhibitor, such as irinotecan.	Irinotecan	152-162	solute carrier family 22 member 1	Homo sapiens	126-132
32913994-0	2018	Temporal Dynamics of Genomic Alterations in a BRCA1 Germline-Mutated Pancreatic Cancer With Low Genomic Instability Burden but Exceptional Response to Fluorouracil, Oxaliplatin, Leucovorin, and Irinotecan.	Irinotecan	194-204	BRCA1 DNA repair associated	Homo sapiens	46-51
29753314-5	2018	In contrast, both types of mGluR8 activators significantly enhanced toxic effects of doxorubicin and irinotecan in RA-SH-SY5Y cells.	Irinotecan	101-111	glutamate receptor, metabotropic 8	Mus musculus	27-33
30120489-0	2018	Replica to the Opinion Letter regarding the article "Sensitization of colorectal cancer cells to irinotecan by the Survivin inhibitor LLP3 depends on XAF1 proficiency in the context of mutated p53" (Arch Toxicol https://doi.org/10.1007/s00204-018-240-x).	Irinotecan	97-107	tumor protein p53	Homo sapiens	193-196
30213564-0	2018	Clinical utility of ABCB1 genotyping for preventing toxicity in treatment with irinotecan.	Irinotecan	79-89	ATP binding cassette subfamily B member 1	Homo sapiens	20-25
29932297-0	2018	UGT1A1*6 and UGT1A1*28 polymorphisms are correlated with irinotecan-induced toxicity: A meta-analysis.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
29932297-0	2018	UGT1A1*6 and UGT1A1*28 polymorphisms are correlated with irinotecan-induced toxicity: A meta-analysis.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
29932297-1	2018	BACKGROUND: Previous articles explored the role of UGT1A1 polymorphism on predicting irinotecan-induced toxicity, but the conclusions were still inconsistent and not comprehensive.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
29932297-2	2018	We performed this meta-analysis to investigate the association between UGT1A1 polymorphism and irinotecan-induced toxicity.	Irinotecan	95-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
29932297-8	2018	Both UGT1A1*6 and UGT1A1*28 polymorphism are significantly associated with severe irinotecan-induced toxicity.	Irinotecan	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-11
29932297-8	2018	Both UGT1A1*6 and UGT1A1*28 polymorphism are significantly associated with severe irinotecan-induced toxicity.	Irinotecan	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
29932297-12	2018	Subgroup analysis exhibited that for UGT1A1*6 polymorphism, patients treated with low-dose irinotecan were at a notable risk of toxicity.	Irinotecan	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
29932297-13	2018	Moreover, the association between UGT1A1*6 polymorphism and irinotecan-induced toxicity was found in patients suffering from respiratory system cancers.	Irinotecan	60-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
29932297-14	2018	CONCLUSIONS: Both UGT1A1*6 and UGT1A1*28 polymorphisms can be considered as predictors of irinotecan-induced toxicity, with effect varying by race, cancer type and irinotecan dose.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
29932297-14	2018	CONCLUSIONS: Both UGT1A1*6 and UGT1A1*28 polymorphisms can be considered as predictors of irinotecan-induced toxicity, with effect varying by race, cancer type and irinotecan dose.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
30069943-13	2018	CONCLUSIONS: A novel ADAM17 inhibitor ZLDI-8 may be a potential chemosensitizer which sensitized CRC cells to 5-fluorouracil or irinotecan by reversing Notch and EMT pathways.	Irinotecan	128-138	ADAM metallopeptidase domain 17	Homo sapiens	21-27
30130528-7	2018	Irinotecan treatment induced elevation of aspartate aminotransferase (AST) in rats without diarrheal symptoms and without an increase in circulating pro-inflammatory mediators.	Irinotecan	0-10	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	42-68
30130528-7	2018	Irinotecan treatment induced elevation of aspartate aminotransferase (AST) in rats without diarrheal symptoms and without an increase in circulating pro-inflammatory mediators.	Irinotecan	0-10	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	70-73
30085332-0	2018	Radiosensitization by irinotecan is attributed to G2/M phase arrest, followed by enhanced apoptosis, probably through the ATM/Chk/Cdc25C/Cdc2 pathway in p53-mutant colorectal cancer cells.	Irinotecan	22-32	ATM serine/threonine kinase	Homo sapiens	122-125
30085332-0	2018	Radiosensitization by irinotecan is attributed to G2/M phase arrest, followed by enhanced apoptosis, probably through the ATM/Chk/Cdc25C/Cdc2 pathway in p53-mutant colorectal cancer cells.	Irinotecan	22-32	choline kinase alpha	Homo sapiens	126-129
30085332-0	2018	Radiosensitization by irinotecan is attributed to G2/M phase arrest, followed by enhanced apoptosis, probably through the ATM/Chk/Cdc25C/Cdc2 pathway in p53-mutant colorectal cancer cells.	Irinotecan	22-32	cell division cycle 25C	Homo sapiens	130-136
30085332-0	2018	Radiosensitization by irinotecan is attributed to G2/M phase arrest, followed by enhanced apoptosis, probably through the ATM/Chk/Cdc25C/Cdc2 pathway in p53-mutant colorectal cancer cells.	Irinotecan	22-32	cyclin dependent kinase 1	Homo sapiens	130-134
30085332-0	2018	Radiosensitization by irinotecan is attributed to G2/M phase arrest, followed by enhanced apoptosis, probably through the ATM/Chk/Cdc25C/Cdc2 pathway in p53-mutant colorectal cancer cells.	Irinotecan	22-32	tumor protein p53	Homo sapiens	153-156
30085332-4	2018	In the present study, we examined the radiosensitizing effects of irinotecan on the p53-mutant colorectal cancer cell lines, HT29 and SW620, and explored the potential underlying mechanisms.	Irinotecan	66-76	tumor protein p53	Homo sapiens	84-87
30085332-11	2018	In addition, the expression of Ser216p-Cdc25C was also increased in the combined group, indicating that irinotecan likely radiosensitized the p53-mutant HT29 and SW620 cells through the ATM/Chk/Cdc25C/Cdc2 pathway.	Irinotecan	104-114	cell division cycle 25C	Homo sapiens	39-45
30085332-11	2018	In addition, the expression of Ser216p-Cdc25C was also increased in the combined group, indicating that irinotecan likely radiosensitized the p53-mutant HT29 and SW620 cells through the ATM/Chk/Cdc25C/Cdc2 pathway.	Irinotecan	104-114	tumor protein p53	Homo sapiens	142-145
30085332-11	2018	In addition, the expression of Ser216p-Cdc25C was also increased in the combined group, indicating that irinotecan likely radiosensitized the p53-mutant HT29 and SW620 cells through the ATM/Chk/Cdc25C/Cdc2 pathway.	Irinotecan	104-114	ATM serine/threonine kinase	Homo sapiens	186-189
30085332-11	2018	In addition, the expression of Ser216p-Cdc25C was also increased in the combined group, indicating that irinotecan likely radiosensitized the p53-mutant HT29 and SW620 cells through the ATM/Chk/Cdc25C/Cdc2 pathway.	Irinotecan	104-114	choline kinase alpha	Homo sapiens	190-193
30085332-11	2018	In addition, the expression of Ser216p-Cdc25C was also increased in the combined group, indicating that irinotecan likely radiosensitized the p53-mutant HT29 and SW620 cells through the ATM/Chk/Cdc25C/Cdc2 pathway.	Irinotecan	104-114	cell division cycle 25C	Homo sapiens	194-200
30085332-11	2018	In addition, the expression of Ser216p-Cdc25C was also increased in the combined group, indicating that irinotecan likely radiosensitized the p53-mutant HT29 and SW620 cells through the ATM/Chk/Cdc25C/Cdc2 pathway.	Irinotecan	104-114	cyclin dependent kinase 1	Homo sapiens	39-43
28747102-1	2018	We report the case of a 50-year-old human immunodeficiency virus-positive patient with stage IV KRAS-mutated colorectal cancer who experienced visible muscle twitching in the right lateral triceps brachii from irinotecan administration for which typical supportive care measures were unsuccessful, including the administration of atropine and slowing down the infusion rate.	Irinotecan	210-220	KRAS proto-oncogene, GTPase	Homo sapiens	96-100
29273261-1	2018	PURPOSE: We aimed to identify the maximum tolerated dose (MTD) of weekly irinotecan in combination with capecitabine-based neoadjuvant chemoradiation according to the UGT1A1*28 genotype in patients with locally advanced rectal cancer.	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-173
29273261-11	2018	CONCLUSION: A higher dose of weekly irinotecan in combination with capecitabine-based CRT is feasible under the guidance of the UGT1A1*28 genotype.	Irinotecan	36-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-134
30213564-9	2018	Genotyping of ABCB1 variants can help to prevent severe adverse reactions to irinotecan-based treatments in colorectal cancer.	Irinotecan	77-87	ATP binding cassette subfamily B member 1	Homo sapiens	14-19
29034773-10	2018	In contrast, afatinib stimulated OATP1B1-mediated uptake of FL and SN-38, ceritinib stimulated that of valsartan, and nintedanib stimulated that of FL and valsartan.	Irinotecan	67-72	solute carrier organic anion transporter family member 1B1	Homo sapiens	33-40
29034773-6	2018	We used OATP1B1-transfected cells to compare the effects of molecular-targeted agents on OATP1B1-mediated uptake of fluorescein (FL), 2",7"-dichlorofluorescein (DCF), atorvastatin, SN-38 and valsartan.	Irinotecan	181-186	solute carrier organic anion transporter family member 1B1	Homo sapiens	89-96
28229371-5	2018	RESULTS: In patients whose tumors expressed the KRAS wild type, the longest median OS was observed with irinotecan-based chemotherapy combined with bevacizumab (38 months), or with cetuximab (41 months).	Irinotecan	104-114	KRAS proto-oncogene, GTPase	Homo sapiens	48-52
29980022-3	2018	The intrinsic fluorescence of SN-38 allowed its quantification in the range 10-500 ng mL-1 with a LOQ of 5.0 ng mL-1 and a LOD of 1.5 ng mL-1.	Irinotecan	30-35	L1 cell adhesion molecule	Mus musculus	86-90
29980022-3	2018	The intrinsic fluorescence of SN-38 allowed its quantification in the range 10-500 ng mL-1 with a LOQ of 5.0 ng mL-1 and a LOD of 1.5 ng mL-1.	Irinotecan	30-35	L1 cell adhesion molecule	Mus musculus	112-116
29980022-3	2018	The intrinsic fluorescence of SN-38 allowed its quantification in the range 10-500 ng mL-1 with a LOQ of 5.0 ng mL-1 and a LOD of 1.5 ng mL-1.	Irinotecan	30-35	L1 cell adhesion molecule	Mus musculus	112-116
29885518-4	2018	The mGluR8-downregulated SH-SY5Y clones proliferated faster and were more resistant to cytotoxic action of staurosporine, doxorubicin, irinotecan and cisplatin when compared to control cells.	Irinotecan	135-145	glutamate receptor, metabotropic 8	Mus musculus	4-10
29885518-6	2018	The mGluR8-downregulated LN229 clones migrated faster and were less prone to cell-damaging effect of staurosporine and irinotecan when compared with relevant control cells.	Irinotecan	119-129	glutamate receptor, metabotropic 8	Mus musculus	4-10
30075623-5	2018	Introduction of a 6-nitro function led to extraordinarily potent compounds that were highly selective for ABCG2 and also able to reverse the MDR toward the chemotherapeutic drugs SN-38 and mitoxantrone.	Irinotecan	179-184	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	106-111
29860358-0	2018	Temozolomide and irinotecan (TEMIRI regimen) as salvage treatment of irinotecan-sensitive advanced colorectal cancer patients bearing MGMT methylation.	Irinotecan	17-27	O-6-methylguanine-DNA methyltransferase	Homo sapiens	134-138
30103709-6	2018	RESULTS: Irinotecan induced in vivo the activation of AKT and MEK1 phosphorylation.	Irinotecan	9-19	thymoma viral proto-oncogene 1	Mus musculus	54-57
30103709-6	2018	RESULTS: Irinotecan induced in vivo the activation of AKT and MEK1 phosphorylation.	Irinotecan	9-19	mitogen-activated protein kinase kinase 1	Mus musculus	62-66
30103709-7	2018	The dose matrix approach showed that BKM120 (PI3K inhibitor) and MEK162 (MEK inhibitor) are synergistic in vitro and in vivo with a cytostatic and cytotoxic effect, while combination of BKM120 and irinotecan or MEK162 and irinotecan are only additive or even antagonistic.	Irinotecan	197-207	midkine	Mus musculus	65-68
30103709-7	2018	The dose matrix approach showed that BKM120 (PI3K inhibitor) and MEK162 (MEK inhibitor) are synergistic in vitro and in vivo with a cytostatic and cytotoxic effect, while combination of BKM120 and irinotecan or MEK162 and irinotecan are only additive or even antagonistic.	Irinotecan	222-232	midkine	Mus musculus	65-68
29925895-0	2018	Potential role of PIN1 genotypes in predicting benefit from oxaliplatin-based and irinotecan-based treatment in patients with metastatic colorectal cancer.	Irinotecan	82-92	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	18-22
29925895-2	2018	We hypothesized that genetic polymorphisms in PIN1-related pathways may affect tumor sensitivity to oxaliplatin or irinotecan in metastatic colorectal cancer (mCRC) patients.	Irinotecan	115-125	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	46-50
29925895-9	2018	Germline PIN1 polymorphisms may predict clinical outcomes in mCRC patients receiving oxaliplatin-based or irinotecan-based therapy, and identify specific populations favorable to oxaliplatin plus irinotecan combination therapy.	Irinotecan	106-116	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	9-13
29925895-9	2018	Germline PIN1 polymorphisms may predict clinical outcomes in mCRC patients receiving oxaliplatin-based or irinotecan-based therapy, and identify specific populations favorable to oxaliplatin plus irinotecan combination therapy.	Irinotecan	196-206	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	9-13
30139029-0	2018	[Relationship between UGT1A1 gene polymorphisms and irinotecan-induced severe adverse events].	Irinotecan	52-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
30139029-1	2018	Objective: To investigate the relationship between UGT1A1*6, UGT1A1*28, UGT1A1*60 and UGT1A1*93 polymorphisms and irinotecan-induced severe adverse reactions(grade 3-4 delayed diarrhea and neutropenia) in Chinese cancer patients.	Irinotecan	114-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
30139029-16	2018	Conclusion: The cancer patients who carried UGT1A1*6, UGT1A1*28 and UGT1A1*60 gene polymorphisms have high risk of severe adverse events caused by irinotecan-based chemotherapy.	Irinotecan	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
30139029-16	2018	Conclusion: The cancer patients who carried UGT1A1*6, UGT1A1*28 and UGT1A1*60 gene polymorphisms have high risk of severe adverse events caused by irinotecan-based chemotherapy.	Irinotecan	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
30139029-16	2018	Conclusion: The cancer patients who carried UGT1A1*6, UGT1A1*28 and UGT1A1*60 gene polymorphisms have high risk of severe adverse events caused by irinotecan-based chemotherapy.	Irinotecan	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
30117422-1	2018	The adverse reaction to irinotecan is related to the single nucleotide polymorphism (SNP) of UGT1A1*6 genotype.	Irinotecan	24-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
30111719-1	2018	As part of our initial efforts into developing a tumor-targeting therapy, C-10 substituted derivatives of a camptothecin analog (SN-38) have been synthesized (2-, 3- and 4-nitrobenzyl) for use as potential hypoxia-activated prodrugs and evaluated for their cytotoxicity, topoisomerase I inhibition and electrochemical (reductive) properties.	Irinotecan	129-134	homeobox C10	Homo sapiens	74-78
30111719-7	2018	Chemical reduction of the 4-nitrobenzyl analog led to the formation/release of SN-38 and validated the prodrug ability of the C-10 substituted derivative.	Irinotecan	79-84	homeobox C10	Homo sapiens	126-130
30016861-2	2018	Abnormal CE2 levels are associated with various cancers, and CE2 is a key mediator of anticancer prodrugs, including irinotecan.	Irinotecan	117-127	carboxylesterase 2H	Mus musculus	61-64
30016861-6	2018	In CE2 overexpression studies, cancer cells had a markedly enhanced sensitivity to the cytotoxic effect of irinotecan, corresponding well with the TPM ratio of the probe.	Irinotecan	107-117	carboxylesterase 2H	Mus musculus	3-6
29980405-5	2018	Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisplatin, irinotecan, oxaliplatin, and paclitaxel increased significantly.	Irinotecan	203-213	tumor protein p53	Homo sapiens	28-32
29947891-0	2018	Sensitization of colorectal cancer cells to irinotecan by the Survivin inhibitor LLP3 depends on XAF1 proficiency in the context of mutated p53.	Irinotecan	44-54	XIAP associated factor 1	Homo sapiens	97-101
29947891-0	2018	Sensitization of colorectal cancer cells to irinotecan by the Survivin inhibitor LLP3 depends on XAF1 proficiency in the context of mutated p53.	Irinotecan	44-54	tumor protein p53	Homo sapiens	140-143
29947891-7	2018	When combined with irinotecan, expression of the tumor suppressor X-linked inhibitor of apoptosis factor 1 (XAF1) plays a decisive role for sensitization of CRC cells to this first-line drug, however, only in the p53-mutated background.	Irinotecan	19-29	XIAP associated factor 1	Homo sapiens	108-112
29860358-0	2018	Temozolomide and irinotecan (TEMIRI regimen) as salvage treatment of irinotecan-sensitive advanced colorectal cancer patients bearing MGMT methylation.	Irinotecan	69-79	O-6-methylguanine-DNA methyltransferase	Homo sapiens	134-138
29860358-2	2018	In this phase II trial, irinotecan and temozolomide (TEMIRI) combination regimen was assessed in irinotecan-sensitive, MGMT methylated/microsatellite stable (MSS) pretreated mCRC patients.	Irinotecan	24-34	O-6-methylguanine-DNA methyltransferase	Homo sapiens	119-123
29860358-14	2018	Conclusions: TEMIRI regimen is a safe and active option in pre-treated, irinotecan-sensitive mCRC patients with MGMT methylation.	Irinotecan	72-82	O-6-methylguanine-DNA methyltransferase	Homo sapiens	112-116
29721577-6	2018	Results showed that CPT-11 caused dramatic changes in heart tissue for oxidative stress parameters (TBARS, SOD, CAT, GSH, and GPx levels), histological tissue damage, and cytokine levels (TNF and IL-4).	Irinotecan	20-26	tumor necrosis factor	Rattus norvegicus	188-191
28679068-0	2018	Berberine hydrochloride counteracts enhanced IL-8 expression induced by SN 38 in AGS cells.	Irinotecan	72-77	C-X-C motif chemokine ligand 8	Homo sapiens	45-49
28679068-3	2018	BER could down-regulate the enhanced IL-8 expression through down-regulating ERK1/2 and p38 MAPK over-activation induced by SN 38.	Irinotecan	124-129	C-X-C motif chemokine ligand 8	Homo sapiens	37-41
28679068-3	2018	BER could down-regulate the enhanced IL-8 expression through down-regulating ERK1/2 and p38 MAPK over-activation induced by SN 38.	Irinotecan	124-129	mitogen-activated protein kinase 3	Homo sapiens	77-83
28679068-4	2018	The increased IL-8 mediated adhesive ability of AGS cells to HUVECs induced by SN 38, could be reduced by BER.	Irinotecan	79-84	C-X-C motif chemokine ligand 8	Homo sapiens	14-18
29908105-0	2018	Phase II trial of biweekly cetuximab and irinotecan as third-line therapy for pretreated KRAS exon 2 wild-type colorectal cancer.	Irinotecan	41-51	KRAS proto-oncogene, GTPase	Homo sapiens	89-93
29909091-2	2018	We assessed potential clinical variables that may predict toxicity and more specifically the role of UGT1A1 polymorphisms associated with irinotecan toxicity.	Irinotecan	138-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
29721577-6	2018	Results showed that CPT-11 caused dramatic changes in heart tissue for oxidative stress parameters (TBARS, SOD, CAT, GSH, and GPx levels), histological tissue damage, and cytokine levels (TNF and IL-4).	Irinotecan	20-26	interleukin 4	Rattus norvegicus	196-200
30013661-1	2018	Transarterial chemoembolization with irinotecan loaded beads (DEBIRI-TACE) represents an investigative treatment option for patients with metastatic colorectal cancer (mCRC).	Irinotecan	37-47	ADAM metallopeptidase domain 17	Homo sapiens	69-73
29533113-1	2018	BACKGROUND: Data on temozolomide (TEM) and irinotecan (IRI) activity in recurrent Ewing sarcoma (EWS), especially in adult patients, are limited.	Irinotecan	43-53	EWS RNA binding protein 1	Homo sapiens	97-100
30140379-0	2018	Topoisomerase I inhibitor, irinotecan, depletes regulatory T cells and up-regulates MHC class I and PD-L1 expression, resulting in a supra-additive antitumor effect when combined with anti-PD-L1 antibodies.	Irinotecan	27-37	CD274 antigen	Mus musculus	100-105
30140379-0	2018	Topoisomerase I inhibitor, irinotecan, depletes regulatory T cells and up-regulates MHC class I and PD-L1 expression, resulting in a supra-additive antitumor effect when combined with anti-PD-L1 antibodies.	Irinotecan	27-37	CD274 antigen	Mus musculus	189-194
30140379-4	2018	Despite a transient decrease in lymphocytes in the peripheral blood after irinotecan treatment, the antitumor activity of anti-PD-L1 antibody plus irinotecan was significantly greater than each agent alone.	Irinotecan	74-84	CD274 antigen	Mus musculus	127-132
30140379-7	2018	In addition, irinotecan augmented MHC class I expression on tumor cells and concurrently increased PD-L1 expression on tumor cells and tumor-infiltrating immune cells.	Irinotecan	13-23	CD274 antigen	Mus musculus	99-104
30140379-8	2018	These results indicate that irinotecan may enhance the effect of T cell activation caused by anti-PD-L1 treatment by reducing Tregs and augmenting MHC class I-mediated tumor antigen presentation, and concurrent upregulation of PD-L1 expression can be blocked by the anti-PD-L1 antibody.	Irinotecan	28-38	CD274 antigen	Mus musculus	98-103
30140379-8	2018	These results indicate that irinotecan may enhance the effect of T cell activation caused by anti-PD-L1 treatment by reducing Tregs and augmenting MHC class I-mediated tumor antigen presentation, and concurrent upregulation of PD-L1 expression can be blocked by the anti-PD-L1 antibody.	Irinotecan	28-38	CD274 antigen	Mus musculus	227-232
30140379-8	2018	These results indicate that irinotecan may enhance the effect of T cell activation caused by anti-PD-L1 treatment by reducing Tregs and augmenting MHC class I-mediated tumor antigen presentation, and concurrent upregulation of PD-L1 expression can be blocked by the anti-PD-L1 antibody.	Irinotecan	28-38	CD274 antigen	Mus musculus	227-232
30131854-8	2018	Moreover, FSTL1 knockdown made CRC cells more susceptible to oxaliplatin and irinotecan-induced death.	Irinotecan	77-87	follistatin like 1	Homo sapiens	10-15
29728798-0	2018	UGT1A polymorphisms associated with worse outcome in colorectal cancer patients treated with irinotecan-based chemotherapy.	Irinotecan	93-103	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	0-5
29728798-1	2018	PURPOSE: To investigate the association between UDP-glucuronosyltransferase (UGT)1A polymorphisms and irinotecan-treatment efficacy in a Chinese population with metastatic colorectal cancer (mCRC).	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	77-83
29728798-9	2018	CONCLUSIONS: UGT1A polymorphisms are predictive of survival outcome of irinotecan-treated Chinese mCRC patients.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	13-18
29842993-1	2018	INTRODUCTION: The coexpression of pIGF-1R and MMP-7 (double-positive phenotype, DP) correlates with poor overall survival (OS) in KRAS wild-type (WT) (exon 2) metastatic colorectal cancer (mCRC) patients treated with irinotecan-cetuximab in second/third line.	Irinotecan	217-227	matrix metallopeptidase 7	Homo sapiens	46-51
30075835-8	2018	Pharmacogenomics guidelines have been published by some international scientific consortia such as the Clinical Pharmacogenomics Implementation Consortium (CPIC) and the Dutch Pharmacogenetics Working Group (DPWG) strongly suggesting a pre-treatment dose adjustment of irinotecan based on UGT1A1*28 genotype and of fluoropyrimidines based on some DPYD genetic variants, to increase treatment safety.	Irinotecan	269-279	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	289-295
30075835-8	2018	Pharmacogenomics guidelines have been published by some international scientific consortia such as the Clinical Pharmacogenomics Implementation Consortium (CPIC) and the Dutch Pharmacogenetics Working Group (DPWG) strongly suggesting a pre-treatment dose adjustment of irinotecan based on UGT1A1*28 genotype and of fluoropyrimidines based on some DPYD genetic variants, to increase treatment safety.	Irinotecan	269-279	dihydropyrimidine dehydrogenase	Homo sapiens	347-351
29977740-6	2018	Results: The GE11/HA/TATp-irinotecan liposomes evidently increased the uptake of irinotecan and showed significant antitumor efficacy in the xenografted A549 cancer cells in nude mice by intravenous administration.	Irinotecan	26-36	tyrosine aminotransferase	Mus musculus	21-25
29989029-4	2018	When the irinotecan metabolite, SN-38, is conjugated to a humanized anti-TROP-2 antibody (sacituzumab govitecan), it shows potent broad anticancer activity in human cancer xenografts and in patients with advanced triple-negative breast, non-small cell and small-cell lung, as well as urothelial cancers.	Irinotecan	9-19	tumor associated calcium signal transducer 2	Homo sapiens	73-79
29989029-4	2018	When the irinotecan metabolite, SN-38, is conjugated to a humanized anti-TROP-2 antibody (sacituzumab govitecan), it shows potent broad anticancer activity in human cancer xenografts and in patients with advanced triple-negative breast, non-small cell and small-cell lung, as well as urothelial cancers.	Irinotecan	32-37	tumor associated calcium signal transducer 2	Homo sapiens	73-79
29468758-3	2018	In this study, the inhibitory effects of shikonin on the activity of hCE2 in human liver microsomes are investigated by using fluorescein diacetate (FD), N-(2-butyl-1,3-dioxo-2,3-dihydro-1H-phenalen-6-yl)-2-chloroacetamide (NCEN), and CPT-11 as substrates of hCE2.	Irinotecan	235-241	carboxylesterase 2	Homo sapiens	69-73
29468758-4	2018	The results demonstrate that shikonin significantly inhibits the activity of hCE2 when FD and NCEN are used as substrates, whereas the half inhibition concentration value of shikonin increased by 5-30 times when CPT-11 was used as the substrate.	Irinotecan	212-218	carboxylesterase 2	Homo sapiens	77-81
29518481-3	2018	The efficacy of SN-38, topotecan, and mitoxantrone (MX) were significantly increased by PD153035, PD153035 significantly reversed ABCG2-mediated MDR by attenuating the efflux activity of this transporter.	Irinotecan	16-21	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	130-135
29977740-6	2018	Results: The GE11/HA/TATp-irinotecan liposomes evidently increased the uptake of irinotecan and showed significant antitumor efficacy in the xenografted A549 cancer cells in nude mice by intravenous administration.	Irinotecan	81-91	tyrosine aminotransferase	Mus musculus	21-25
29930754-1	2018	Nrf2 is a transcription factor that regulates cellular stress response and irinotecan-metabolising pathways.	Irinotecan	75-85	nuclear factor, erythroid derived 2, like 2	Mus musculus	0-4
29121274-1	2018	Background: The GLARIUS trial, which investigated the efficacy of bevacizumab (BEV)/irinotecan (IRI) compared with standard temozolomide in the first-line therapy of O6-methylguanine-DNA methyltransferase (MGMT)-nonmethylated glioblastoma, showed that progression-free survival was significantly prolonged by BEV/IRI, while overall survival was similar in both arms.	Irinotecan	84-94	O-6-methylguanine-DNA methyltransferase	Homo sapiens	166-204
29963241-3	2018	Here we demonstrate that CPT-11 stalls such cells in the G2/M phase of the cell cycle, induces an accumulation of the tumor suppressor p53, the replicative stress/DNA damage marker gammaH2AX, phosphorylation of the checkpoint kinases ATM and ATR, and an ATR-dependent accumulation of the pro-survival molecule survivin.	Irinotecan	25-31	tumor protein p53	Homo sapiens	135-138
29963241-3	2018	Here we demonstrate that CPT-11 stalls such cells in the G2/M phase of the cell cycle, induces an accumulation of the tumor suppressor p53, the replicative stress/DNA damage marker gammaH2AX, phosphorylation of the checkpoint kinases ATM and ATR, and an ATR-dependent accumulation of the pro-survival molecule survivin.	Irinotecan	25-31	ATM serine/threonine kinase	Homo sapiens	234-237
29963241-3	2018	Here we demonstrate that CPT-11 stalls such cells in the G2/M phase of the cell cycle, induces an accumulation of the tumor suppressor p53, the replicative stress/DNA damage marker gammaH2AX, phosphorylation of the checkpoint kinases ATM and ATR, and an ATR-dependent accumulation of the pro-survival molecule survivin.	Irinotecan	25-31	ATR serine/threonine kinase	Homo sapiens	242-245
29963241-3	2018	Here we demonstrate that CPT-11 stalls such cells in the G2/M phase of the cell cycle, induces an accumulation of the tumor suppressor p53, the replicative stress/DNA damage marker gammaH2AX, phosphorylation of the checkpoint kinases ATM and ATR, and an ATR-dependent accumulation of the pro-survival molecule survivin.	Irinotecan	25-31	ATR serine/threonine kinase	Homo sapiens	254-257
29738245-8	2018	In an intraperitoneal tumor xenograft model mimicking late-stage metastatic cervical cancer, the LPQDEA/DNA vector with TRAIL suicide gene exerted strong tumor inhibition as effective as paclitaxel, the first-line anticancer drug, but gave much less tumor relapse and much longer survival than the clinical chemotherapy drugs, irinotecan and paclitaxel.	Irinotecan	327-337	TNF superfamily member 10	Homo sapiens	120-125
29930754-5	2018	In vitro experiments in CRC cell lines revealed that Nrf2 siRNA and brusatol, which is known to inhibit Nrf2, decreased viability and sensitised cells to irinotecan toxicity.	Irinotecan	154-164	nuclear factor, erythroid derived 2, like 2	Mus musculus	53-57
29653076-8	2018	E4bp4-/- mice also showed reduced Ces-mediated metabolism and elevated systemic exposure of CPT-11, a well-known Ces substrate.	Irinotecan	92-98	nuclear factor, interleukin 3, regulated	Mus musculus	0-5
29688721-0	2018	Nanoencapsulation of Novel Inhibitors of PNKP for Selective Sensitization to Ionizing Radiation and Irinotecan and Induction of Synthetic Lethality.	Irinotecan	100-110	polynucleotide kinase 3'-phosphatase	Homo sapiens	41-45
29848680-0	2018	SN-38 Acts as a Radiosensitizer for Colorectal Cancer by Inhibiting the Radiation-induced Up-regulation of HIF-1alpha.	Irinotecan	0-5	hypoxia inducible factor 1 subunit alpha	Homo sapiens	107-117
29848680-2	2018	The aim of the study was to investigate whether SN-38, the active metabolite of irinotecan, acts as a radiosensitizer through inhibition of hypoxia-inducible factor (HIF)-1alpha in the human colorectal cancer (CRC) cells.	Irinotecan	48-53	hypoxia inducible factor 1 subunit alpha	Homo sapiens	140-177
29848680-2	2018	The aim of the study was to investigate whether SN-38, the active metabolite of irinotecan, acts as a radiosensitizer through inhibition of hypoxia-inducible factor (HIF)-1alpha in the human colorectal cancer (CRC) cells.	Irinotecan	80-90	hypoxia inducible factor 1 subunit alpha	Homo sapiens	140-177
29848680-3	2018	MATERIALS AND METHODS: HT29 and SW480 cells were cultured with SN-38 (0-4 muM) immediately after irradiation (0-8 Gy).	Irinotecan	63-68	latexin	Homo sapiens	74-77
29848680-7	2018	RESULTS: Radiation up-regulated HIF-1alpha, and SN-38 inhibited the radiation-induced HIF-1alpha.	Irinotecan	48-53	hypoxia inducible factor 1 subunit alpha	Homo sapiens	86-96
29848680-8	2018	The combination of radiation and SN-38 inhibited cell proliferation more than radiation alone; treatment with SN-38 after radiation exposure did not increase the number of apoptotic cells, whereas, it enhanced the S and G2/M cell-cycle arrest and decreased the population of cells in G1 Conclusion: SN-38 inhibits the radiation-induced up-regulation of HIF-1alpha and acts as a radiosensitizer by inducing cell-cycle arrest in CRC cells.	Irinotecan	33-38	hypoxia inducible factor 1 subunit alpha	Homo sapiens	353-363
29848680-8	2018	The combination of radiation and SN-38 inhibited cell proliferation more than radiation alone; treatment with SN-38 after radiation exposure did not increase the number of apoptotic cells, whereas, it enhanced the S and G2/M cell-cycle arrest and decreased the population of cells in G1 Conclusion: SN-38 inhibits the radiation-induced up-regulation of HIF-1alpha and acts as a radiosensitizer by inducing cell-cycle arrest in CRC cells.	Irinotecan	110-115	hypoxia inducible factor 1 subunit alpha	Homo sapiens	353-363
29848680-8	2018	The combination of radiation and SN-38 inhibited cell proliferation more than radiation alone; treatment with SN-38 after radiation exposure did not increase the number of apoptotic cells, whereas, it enhanced the S and G2/M cell-cycle arrest and decreased the population of cells in G1 Conclusion: SN-38 inhibits the radiation-induced up-regulation of HIF-1alpha and acts as a radiosensitizer by inducing cell-cycle arrest in CRC cells.	Irinotecan	110-115	hypoxia inducible factor 1 subunit alpha	Homo sapiens	353-363
29504153-0	2018	Relevance of CYP3A4*20, UGT1A1*37 and UGT1A1*28 variants in irinotecan-induced severe toxicity.	Irinotecan	60-70	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	13-19
29653076-2	2018	Here, we investigate a potential role of E4 promoter-binding protein 4 (E4bp4) in regulation of Ces and CPT-11 (irinotecan, a first-line drug for treating colorectal cancer) pharmacokinetics in mice.	Irinotecan	104-110	nuclear factor, interleukin 3, regulated	Mus musculus	41-70
29653076-2	2018	Here, we investigate a potential role of E4 promoter-binding protein 4 (E4bp4) in regulation of Ces and CPT-11 (irinotecan, a first-line drug for treating colorectal cancer) pharmacokinetics in mice.	Irinotecan	104-110	nuclear factor, interleukin 3, regulated	Mus musculus	72-77
29653076-2	2018	Here, we investigate a potential role of E4 promoter-binding protein 4 (E4bp4) in regulation of Ces and CPT-11 (irinotecan, a first-line drug for treating colorectal cancer) pharmacokinetics in mice.	Irinotecan	112-122	nuclear factor, interleukin 3, regulated	Mus musculus	41-70
29653076-2	2018	Here, we investigate a potential role of E4 promoter-binding protein 4 (E4bp4) in regulation of Ces and CPT-11 (irinotecan, a first-line drug for treating colorectal cancer) pharmacokinetics in mice.	Irinotecan	112-122	nuclear factor, interleukin 3, regulated	Mus musculus	72-77
29504153-0	2018	Relevance of CYP3A4*20, UGT1A1*37 and UGT1A1*28 variants in irinotecan-induced severe toxicity.	Irinotecan	60-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
29504153-0	2018	Relevance of CYP3A4*20, UGT1A1*37 and UGT1A1*28 variants in irinotecan-induced severe toxicity.	Irinotecan	60-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
29873288-1	2018	BACKGROUND: Irinotecan (IRN) (CPT-11) is a camptothecin derivative with low oral bioavailability due to active efflux by intestinal P-glycoprotein (p-gp) receptors.	Irinotecan	12-22	ATP binding cassette subfamily B member 1	Homo sapiens	132-146
29504153-1	2018	Severe irinotecan-induced toxicity is associated with UGT1A1 polymorphisms.	Irinotecan	7-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
29504153-3	2018	As CYP3A4 is also an irinotecan-metabolizing enzyme, our study aimed to elucidate the influence of the CYP3A4*20 loss-of-function allele in the toxicity profile of these patients.	Irinotecan	21-31	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	3-9
29504153-3	2018	As CYP3A4 is also an irinotecan-metabolizing enzyme, our study aimed to elucidate the influence of the CYP3A4*20 loss-of-function allele in the toxicity profile of these patients.	Irinotecan	21-31	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	103-109
29873288-1	2018	BACKGROUND: Irinotecan (IRN) (CPT-11) is a camptothecin derivative with low oral bioavailability due to active efflux by intestinal P-glycoprotein (p-gp) receptors.	Irinotecan	24-27	ATP binding cassette subfamily B member 1	Homo sapiens	132-146
29873288-1	2018	BACKGROUND: Irinotecan (IRN) (CPT-11) is a camptothecin derivative with low oral bioavailability due to active efflux by intestinal P-glycoprotein (p-gp) receptors.	Irinotecan	30-36	ATP binding cassette subfamily B member 1	Homo sapiens	132-146
29706892-6	2018	VDR rs11574077 polymorphism was demonstrated to affect both irinotecan biliary index (BI) and glucuronidation ratio (GR) by a pharmacokinetic analysis.	Irinotecan	60-70	vitamin D receptor	Homo sapiens	0-3
29899822-6	2018	Furthermore, treatment of aRMS cells with clinically relevant CPT derivative irinotecan restores MyoD function, and myogenic differentiation in vitro and in a xenograft model.	Irinotecan	77-87	myogenic differentiation 1	Homo sapiens	97-101
29861877-5	2018	Contrasting results, however, have been reported on the capability of variants of other genes as MTHFR, TYMS, ERCC1, XRCC1, GSTP1, CYP3A4/3A5 and ABCB1, in predicting either therapy efficacy or toxicity in patients undergoing treatment with pyrimidine antimetabolites, platinum derivatives, irinotecan and taxanes.	Irinotecan	291-301	methylenetetrahydrofolate reductase	Homo sapiens	97-102
29861877-5	2018	Contrasting results, however, have been reported on the capability of variants of other genes as MTHFR, TYMS, ERCC1, XRCC1, GSTP1, CYP3A4/3A5 and ABCB1, in predicting either therapy efficacy or toxicity in patients undergoing treatment with pyrimidine antimetabolites, platinum derivatives, irinotecan and taxanes.	Irinotecan	291-301	thymidylate synthetase	Homo sapiens	104-108
29861877-5	2018	Contrasting results, however, have been reported on the capability of variants of other genes as MTHFR, TYMS, ERCC1, XRCC1, GSTP1, CYP3A4/3A5 and ABCB1, in predicting either therapy efficacy or toxicity in patients undergoing treatment with pyrimidine antimetabolites, platinum derivatives, irinotecan and taxanes.	Irinotecan	291-301	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	110-115
29861877-5	2018	Contrasting results, however, have been reported on the capability of variants of other genes as MTHFR, TYMS, ERCC1, XRCC1, GSTP1, CYP3A4/3A5 and ABCB1, in predicting either therapy efficacy or toxicity in patients undergoing treatment with pyrimidine antimetabolites, platinum derivatives, irinotecan and taxanes.	Irinotecan	291-301	ATP binding cassette subfamily B member 1	Homo sapiens	146-151
29649683-9	2018	This effect contradicted irinotecan mediated UGT inhibition.	Irinotecan	25-35	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	45-48
29861877-4	2018	Among the examined germline polymorphic variants, several SNPs of dihydropyrimidine dehydrogenase (DPYD) and uridine diphosphate glucuronosyltransferases (UGT) have shown a robust role as predictors of toxicity following fluoropyrimidine- and/or irinotecan-based treatments respectively, and a few guidelines are mandatory in their detection before therapy initiation.	Irinotecan	246-256	dihydropyrimidine dehydrogenase	Homo sapiens	66-97
29861877-4	2018	Among the examined germline polymorphic variants, several SNPs of dihydropyrimidine dehydrogenase (DPYD) and uridine diphosphate glucuronosyltransferases (UGT) have shown a robust role as predictors of toxicity following fluoropyrimidine- and/or irinotecan-based treatments respectively, and a few guidelines are mandatory in their detection before therapy initiation.	Irinotecan	246-256	dihydropyrimidine dehydrogenase	Homo sapiens	99-103
29861877-4	2018	Among the examined germline polymorphic variants, several SNPs of dihydropyrimidine dehydrogenase (DPYD) and uridine diphosphate glucuronosyltransferases (UGT) have shown a robust role as predictors of toxicity following fluoropyrimidine- and/or irinotecan-based treatments respectively, and a few guidelines are mandatory in their detection before therapy initiation.	Irinotecan	246-256	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	109-153
29861877-4	2018	Among the examined germline polymorphic variants, several SNPs of dihydropyrimidine dehydrogenase (DPYD) and uridine diphosphate glucuronosyltransferases (UGT) have shown a robust role as predictors of toxicity following fluoropyrimidine- and/or irinotecan-based treatments respectively, and a few guidelines are mandatory in their detection before therapy initiation.	Irinotecan	246-256	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	155-158
29760556-4	2018	Patients treated by anti-epidermal growth factor receptor (EGFR) antibodies with irinotecan were included in the control arm.	Irinotecan	81-91	epidermal growth factor receptor	Homo sapiens	20-57
29760556-4	2018	Patients treated by anti-epidermal growth factor receptor (EGFR) antibodies with irinotecan were included in the control arm.	Irinotecan	81-91	epidermal growth factor receptor	Homo sapiens	59-63
29760556-12	2018	The present study found that rechallenge of oxaliplatin-containing regimens produced equivalent tumor control and survival benefit to that of anti-EGFR antibodies with irinotecan in mCRC.	Irinotecan	168-178	epidermal growth factor receptor	Homo sapiens	147-151
29713498-1	2018	Background: In the RAISE trial, ramucirumab+leucovorin/fluorouracil/irinotecan (FOLFIRI) improved the median overall survival (mOS) of patients with previously treated metastatic colorectal cancer versus patients treated with placebo+FOLFIRI but had a higher incidence of neutropaenia, leading to more chemotherapy dose modifications and discontinuations.	Irinotecan	68-78	Moloney sarcoma oncogene	Mus musculus	127-130
29076612-0	2018	New Insights into SN-38 Glucuronidation: Evidence for the Important Role of UDP Glucuronosyltransferase 1A9.	Irinotecan	18-23	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	76-107
29420338-9	2018	After curcumin treatment, drug-resistant cell proliferation was significantly inhibited; in the curcumin+irinotecan treatment group, E-cadherin expression was upregulated, whereas vimentin and N-cadherin expressions were downregulated.	Irinotecan	105-115	cadherin 1	Homo sapiens	133-143
29420338-9	2018	After curcumin treatment, drug-resistant cell proliferation was significantly inhibited; in the curcumin+irinotecan treatment group, E-cadherin expression was upregulated, whereas vimentin and N-cadherin expressions were downregulated.	Irinotecan	105-115	cadherin 2	Homo sapiens	193-203
29599307-10	2018	Irinotecan, 5-FU and 50 mg/kg EEG significantly decreased the protein expression of beta-catenin and MMP-7.	Irinotecan	0-10	catenin beta 1	Homo sapiens	84-96
29599307-10	2018	Irinotecan, 5-FU and 50 mg/kg EEG significantly decreased the protein expression of beta-catenin and MMP-7.	Irinotecan	0-10	matrix metallopeptidase 7	Homo sapiens	101-106
29599307-11	2018	Cyclin D1 expression was decreased and E-cadherin expression was increased by irinotecan, 5-FU and all three doses of EEG.	Irinotecan	78-88	cadherin 1	Homo sapiens	39-49
28520360-0	2012	Irinotecan Therapy and UGT1A1 Genotype Irinotecan is a topoisomerase inhibitor that is widely used in the treatment of cancer.	Irinotecan	39-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
28520360-3	2012	Irinotecan is metabolized and inactivated by an UDP-glucuronosyltransferase enzyme encoded by the gene UGT1A1.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
28520360-5	2012	Variants of this gene, such as UGT1A1*28, are associated with reduced enzyme activity and an increased risk of irinotecan toxicity.	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
28520360-6	2012	Approximately 10% of North Americans are homozygous for the UGT1A1*28 allele and are more likely to develop neutropenia following irinotecan therapy (3).	Irinotecan	130-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
28520360-7	2012	The FDA-approved drug label for irinotecan states that "when administered as a single-agent, a reduction in the starting dose by at least one level of irinotecan hydrochloride injection should be considered for patients known to be homozygous for the UGT1A1*28 allele.	Irinotecan	32-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	251-257
28520360-7	2012	The FDA-approved drug label for irinotecan states that "when administered as a single-agent, a reduction in the starting dose by at least one level of irinotecan hydrochloride injection should be considered for patients known to be homozygous for the UGT1A1*28 allele.	Irinotecan	151-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	251-257
28520360-9	2012	A guideline from the Dutch Pharmacogenetics Working Group (KNMP) mentions "although results are not consistent, there is sufficient evidence that a reduction in the initial dose by 30% is required for regimens containing &gt;250 mg/m(2) of irinotecan prescribed to homozygous carriers of the UGT1A1*28 allele.	Irinotecan	240-250	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	292-298
29076612-6	2018	For UGT1A9 and HLM, BSA can significantly accelerate SN-38 glucuronidation activities and similar effects are further observed on kinetic patterns.	Irinotecan	53-58	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	4-10
29076612-9	2018	To get the true contribution of UGT1A9 in SN-38 glucuronidation, a relative activity factor (RAF) approach was additionally used.	Irinotecan	42-47	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	32-38
29076612-12	2018	Results together conclude that UGT1A9 serves as an additional important contributor to hepatic SN-38 glucuronidation.	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	31-37
29421708-2	2018	Among all identified hCEs, human carboxylesterase 2 (hCE2) plays crucial roles in the metabolic activation of ester drugs including irinotecan and flutamide.	Irinotecan	132-142	carboxylesterase 2	Homo sapiens	33-51
29421708-2	2018	Among all identified hCEs, human carboxylesterase 2 (hCE2) plays crucial roles in the metabolic activation of ester drugs including irinotecan and flutamide.	Irinotecan	132-142	carboxylesterase 2	Homo sapiens	53-57
29541236-3	2018	DAC potentiated the antitumor activity of CPT-11 additively, and that of SN-38 synergistically, as measured by colony formation in the human colorectal cancer HCT116 cell line.	Irinotecan	42-48	arylacetamide deacetylase	Homo sapiens	0-3
28053052-12	2018	CONCLUSIONS: Irinotecan induces hepatic steatosis via autophagy impairment and inflammation via ERK activation.	Irinotecan	13-23	mitogen-activated protein kinase 1	Homo sapiens	96-99
29075780-10	2018	Higher HER3 was predictive, being associated with prolonged PFS on irinotecan plus panitumumab (IrPan) (HR, 0.71; 95% CI, 0.61-0.82; P &lt; .001), but not irinotecan (HR, 0.96; 95% CI, 0.82-1.13; P = .65) in patients with RAS wt, with significant interaction between biomarker and treatment (P = .001).	Irinotecan	67-77	erb-b2 receptor tyrosine kinase 3	Homo sapiens	7-11
29075780-10	2018	Higher HER3 was predictive, being associated with prolonged PFS on irinotecan plus panitumumab (IrPan) (HR, 0.71; 95% CI, 0.61-0.82; P &lt; .001), but not irinotecan (HR, 0.96; 95% CI, 0.82-1.13; P = .65) in patients with RAS wt, with significant interaction between biomarker and treatment (P = .001).	Irinotecan	155-165	erb-b2 receptor tyrosine kinase 3	Homo sapiens	7-11
29075780-12	2018	In an exploratory binary model, dividing the population at the 66th percentile, HER3 was predictive of panitumumab benefit: in patients with high HER3 expression, median PFS was 8.2 months (IrPan) vs 4.4 months (irinotecan) (HR, 0.33; 95% CI, 0.19-0.58; P &lt; .001).	Irinotecan	212-222	erb-b2 receptor tyrosine kinase 3	Homo sapiens	80-84
29541236-5	2018	Anti-apoptotic B-cell lymphoma-2 (Bcl-2) protein expression was reduced to 50-67% of the control following a single treatment with CPT-11, SN-38, or DAC, and was markedly reduced to 7-8% following the combination of CPT-11/SN-38 with DAC.	Irinotecan	131-137	arylacetamide deacetylase	Homo sapiens	234-237
29541236-5	2018	Anti-apoptotic B-cell lymphoma-2 (Bcl-2) protein expression was reduced to 50-67% of the control following a single treatment with CPT-11, SN-38, or DAC, and was markedly reduced to 7-8% following the combination of CPT-11/SN-38 with DAC.	Irinotecan	139-144	BCL2 apoptosis regulator	Homo sapiens	34-39
29541236-5	2018	Anti-apoptotic B-cell lymphoma-2 (Bcl-2) protein expression was reduced to 50-67% of the control following a single treatment with CPT-11, SN-38, or DAC, and was markedly reduced to 7-8% following the combination of CPT-11/SN-38 with DAC.	Irinotecan	216-222	BCL2 apoptosis regulator	Homo sapiens	34-39
29541236-5	2018	Anti-apoptotic B-cell lymphoma-2 (Bcl-2) protein expression was reduced to 50-67% of the control following a single treatment with CPT-11, SN-38, or DAC, and was markedly reduced to 7-8% following the combination of CPT-11/SN-38 with DAC.	Irinotecan	223-228	BCL2 apoptosis regulator	Homo sapiens	34-39
29541236-7	2018	Wilms" tumor protein (WT1), which has been shown to be a positive regulator of Bcl-2 in HCT116 cells through WT1-kncokdown experiments, was downregulated in HCT116 and HT29 cells when treated with CPT-11/SN-38 combined with DAC, with decreases greater than any single administration of CPT-11, SN-38, or DAC.	Irinotecan	197-203	WT1 transcription factor	Homo sapiens	0-20
29541236-7	2018	Wilms" tumor protein (WT1), which has been shown to be a positive regulator of Bcl-2 in HCT116 cells through WT1-kncokdown experiments, was downregulated in HCT116 and HT29 cells when treated with CPT-11/SN-38 combined with DAC, with decreases greater than any single administration of CPT-11, SN-38, or DAC.	Irinotecan	197-203	WT1 transcription factor	Homo sapiens	22-25
29541236-7	2018	Wilms" tumor protein (WT1), which has been shown to be a positive regulator of Bcl-2 in HCT116 cells through WT1-kncokdown experiments, was downregulated in HCT116 and HT29 cells when treated with CPT-11/SN-38 combined with DAC, with decreases greater than any single administration of CPT-11, SN-38, or DAC.	Irinotecan	197-203	BCL2 apoptosis regulator	Homo sapiens	79-84
29541236-7	2018	Wilms" tumor protein (WT1), which has been shown to be a positive regulator of Bcl-2 in HCT116 cells through WT1-kncokdown experiments, was downregulated in HCT116 and HT29 cells when treated with CPT-11/SN-38 combined with DAC, with decreases greater than any single administration of CPT-11, SN-38, or DAC.	Irinotecan	204-209	WT1 transcription factor	Homo sapiens	0-20
29541236-7	2018	Wilms" tumor protein (WT1), which has been shown to be a positive regulator of Bcl-2 in HCT116 cells through WT1-kncokdown experiments, was downregulated in HCT116 and HT29 cells when treated with CPT-11/SN-38 combined with DAC, with decreases greater than any single administration of CPT-11, SN-38, or DAC.	Irinotecan	204-209	WT1 transcription factor	Homo sapiens	22-25
29541236-7	2018	Wilms" tumor protein (WT1), which has been shown to be a positive regulator of Bcl-2 in HCT116 cells through WT1-kncokdown experiments, was downregulated in HCT116 and HT29 cells when treated with CPT-11/SN-38 combined with DAC, with decreases greater than any single administration of CPT-11, SN-38, or DAC.	Irinotecan	204-209	BCL2 apoptosis regulator	Homo sapiens	79-84
29541236-7	2018	Wilms" tumor protein (WT1), which has been shown to be a positive regulator of Bcl-2 in HCT116 cells through WT1-kncokdown experiments, was downregulated in HCT116 and HT29 cells when treated with CPT-11/SN-38 combined with DAC, with decreases greater than any single administration of CPT-11, SN-38, or DAC.	Irinotecan	286-292	WT1 transcription factor	Homo sapiens	0-20
29541236-7	2018	Wilms" tumor protein (WT1), which has been shown to be a positive regulator of Bcl-2 in HCT116 cells through WT1-kncokdown experiments, was downregulated in HCT116 and HT29 cells when treated with CPT-11/SN-38 combined with DAC, with decreases greater than any single administration of CPT-11, SN-38, or DAC.	Irinotecan	286-292	WT1 transcription factor	Homo sapiens	22-25
28053052-0	2018	ERK activation and autophagy impairment are central mediators of irinotecan-induced steatohepatitis.	Irinotecan	65-75	mitogen-activated protein kinase 1	Homo sapiens	0-3
28053052-6	2018	ERK inhibition prevented irinotecan-induced pro-inflammatory gene expression but had only a slight effect on lipid accumulation.	Irinotecan	25-35	mitogen-activated protein kinase 1	Homo sapiens	0-3
28053052-9	2018	Also in mice, irinotecan treatment induced hepatic ACOX1 expression, ERK phosphorylation and inflammation, as well as impairment of autophagy and significant steatosis.	Irinotecan	14-24	acyl-Coenzyme A oxidase 1, palmitoyl	Mus musculus	51-56
28053052-9	2018	Also in mice, irinotecan treatment induced hepatic ACOX1 expression, ERK phosphorylation and inflammation, as well as impairment of autophagy and significant steatosis.	Irinotecan	14-24	mitogen-activated protein kinase 1	Mus musculus	69-72
28053052-10	2018	Furthermore, irinotecan-treated patients revealed higher hepatic ERK activity, expression of pro-inflammatory genes and markers indicative for a shift to peroxisomal fatty acid oxidation and an impaired autophagic flux.	Irinotecan	13-23	mitogen-activated protein kinase 1	Homo sapiens	65-68
28053052-11	2018	Pretreatment with the multityrosine kinase inhibitor sorafenib did not affect autophagy impairment and steatosis but significantly reduced ERK phosphorylation and inflammatory response in irinotecan-treated hepatocytes and murine livers.	Irinotecan	188-198	mitogen-activated protein kinase 1	Mus musculus	139-142
29541236-7	2018	Wilms" tumor protein (WT1), which has been shown to be a positive regulator of Bcl-2 in HCT116 cells through WT1-kncokdown experiments, was downregulated in HCT116 and HT29 cells when treated with CPT-11/SN-38 combined with DAC, with decreases greater than any single administration of CPT-11, SN-38, or DAC.	Irinotecan	286-292	BCL2 apoptosis regulator	Homo sapiens	79-84
29541236-7	2018	Wilms" tumor protein (WT1), which has been shown to be a positive regulator of Bcl-2 in HCT116 cells through WT1-kncokdown experiments, was downregulated in HCT116 and HT29 cells when treated with CPT-11/SN-38 combined with DAC, with decreases greater than any single administration of CPT-11, SN-38, or DAC.	Irinotecan	294-299	WT1 transcription factor	Homo sapiens	0-20
29541236-7	2018	Wilms" tumor protein (WT1), which has been shown to be a positive regulator of Bcl-2 in HCT116 cells through WT1-kncokdown experiments, was downregulated in HCT116 and HT29 cells when treated with CPT-11/SN-38 combined with DAC, with decreases greater than any single administration of CPT-11, SN-38, or DAC.	Irinotecan	294-299	WT1 transcription factor	Homo sapiens	22-25
29541236-5	2018	Anti-apoptotic B-cell lymphoma-2 (Bcl-2) protein expression was reduced to 50-67% of the control following a single treatment with CPT-11, SN-38, or DAC, and was markedly reduced to 7-8% following the combination of CPT-11/SN-38 with DAC.	Irinotecan	131-137	BCL2 apoptosis regulator	Homo sapiens	34-39
29541236-7	2018	Wilms" tumor protein (WT1), which has been shown to be a positive regulator of Bcl-2 in HCT116 cells through WT1-kncokdown experiments, was downregulated in HCT116 and HT29 cells when treated with CPT-11/SN-38 combined with DAC, with decreases greater than any single administration of CPT-11, SN-38, or DAC.	Irinotecan	294-299	BCL2 apoptosis regulator	Homo sapiens	79-84
29541236-8	2018	The extent of CPT-11/SN-38 potentiation by DAC may depend on Bcl-2 expression levels in human colorectal cancer cells.	Irinotecan	14-20	arylacetamide deacetylase	Homo sapiens	43-46
29541236-8	2018	The extent of CPT-11/SN-38 potentiation by DAC may depend on Bcl-2 expression levels in human colorectal cancer cells.	Irinotecan	14-20	BCL2 apoptosis regulator	Homo sapiens	61-66
29541236-8	2018	The extent of CPT-11/SN-38 potentiation by DAC may depend on Bcl-2 expression levels in human colorectal cancer cells.	Irinotecan	21-26	arylacetamide deacetylase	Homo sapiens	43-46
29541236-8	2018	The extent of CPT-11/SN-38 potentiation by DAC may depend on Bcl-2 expression levels in human colorectal cancer cells.	Irinotecan	21-26	BCL2 apoptosis regulator	Homo sapiens	61-66
29261002-0	2018	Expression of Topoisomerase 1 and carboxylesterase 2 correlates with irinotecan treatment response in metastatic colorectal cancer.	Irinotecan	69-79	carboxylesterase 2	Homo sapiens	34-52
29261002-13	2018	In summary, our findings suggest that TOPO-1 and CES-2 may play important roles irinotecan sensitivity in mCRC patients.	Irinotecan	80-90	carboxylesterase 2	Homo sapiens	49-54
29261002-14	2018	Evaluation of expression of TOPO-1 and CES-2 may provide preliminary clinical evidence for the management of irinotecan-based therapy in mCRC patients.	Irinotecan	109-119	carboxylesterase 2	Homo sapiens	39-44
31352923-3	2018	In this study, to improve water dispersity and the anti-tumor efficiency of SN-38, a prodrug, SN-38-BOC, that could efficiently transform to active SN-38 in the acidic tumor microenvironment was synthesized and encapsulated into MPEG-P(CL-ran-TMC) micelles (SN-38-BOC micelles).	Irinotecan	94-99	BOC cell adhesion associated, oncogene regulated	Homo sapiens	100-103
29228087-1	2018	Background: The phase III RAISE trial (NCT01183780) demonstrated that the vascular endothelial growth factor (VEGF) receptor (VEGFR)-2 binding monoclonal antibody ramucirumab plus 5-fluororuracil, leucovorin, and irinotecan (FOLFIRI) significantly improved overall survival (OS) and progression-free survival (PFS) compared with placebo + FOLFIRI as second-line metastatic colorectal cancer (mCRC) treatment.	Irinotecan	213-223	kinase insert domain receptor	Homo sapiens	126-131
29246888-5	2018	The EC50 of 7-ethyl-10-hydroxycamptothecin (SN-38), topotecan, and mitoxantrone decreased in the presence of a BCRP inhibitor in PANC-1 and AsPC-1 cells, which exhibit high BCRP expression.	Irinotecan	12-42	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	111-115
29246888-5	2018	The EC50 of 7-ethyl-10-hydroxycamptothecin (SN-38), topotecan, and mitoxantrone decreased in the presence of a BCRP inhibitor in PANC-1 and AsPC-1 cells, which exhibit high BCRP expression.	Irinotecan	12-42	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	173-177
29246888-5	2018	The EC50 of 7-ethyl-10-hydroxycamptothecin (SN-38), topotecan, and mitoxantrone decreased in the presence of a BCRP inhibitor in PANC-1 and AsPC-1 cells, which exhibit high BCRP expression.	Irinotecan	44-49	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	111-115
29519997-0	2018	Overexpression of Nitrogen Permease Regulator Like-2 (NPRL2) Enhances Sensitivity to Irinotecan (CPT-11) in Colon Cancer Cells by Activating the DNA Damage Checkpoint Pathway.	Irinotecan	85-95	NPR2 like, GATOR1 complex subunit	Homo sapiens	18-52
29519997-0	2018	Overexpression of Nitrogen Permease Regulator Like-2 (NPRL2) Enhances Sensitivity to Irinotecan (CPT-11) in Colon Cancer Cells by Activating the DNA Damage Checkpoint Pathway.	Irinotecan	85-95	NPR2 like, GATOR1 complex subunit	Homo sapiens	54-59
29519997-0	2018	Overexpression of Nitrogen Permease Regulator Like-2 (NPRL2) Enhances Sensitivity to Irinotecan (CPT-11) in Colon Cancer Cells by Activating the DNA Damage Checkpoint Pathway.	Irinotecan	97-103	NPR2 like, GATOR1 complex subunit	Homo sapiens	18-52
29519997-0	2018	Overexpression of Nitrogen Permease Regulator Like-2 (NPRL2) Enhances Sensitivity to Irinotecan (CPT-11) in Colon Cancer Cells by Activating the DNA Damage Checkpoint Pathway.	Irinotecan	97-103	NPR2 like, GATOR1 complex subunit	Homo sapiens	54-59
29519997-3	2018	The aim of this study was to investigate the role of NPRL2 in improving sensitivity to CPT-11 in colon cancer cells.	Irinotecan	87-93	NPR2 like, GATOR1 complex subunit	Homo sapiens	53-58
29519997-10	2018	RESULTS A CCK8 assay revealed that the overexpression of NPRL2 improved the sensitivity of CPT-11 in HCT116 cells (P&lt;0.05).	Irinotecan	91-97	NPR2 like, GATOR1 complex subunit	Homo sapiens	57-62
29519997-11	2018	Functionally, NPRL2 overexpression elevated the sensitivity of CPT-11 by preventing colon cancer cell proliferation, cell movement, and invasion, and promoting cell apoptosis and G2/M cell cycle arrest.	Irinotecan	63-69	NPR2 like, GATOR1 complex subunit	Homo sapiens	14-19
29519997-12	2018	Mechanistically, NPRL2 overexpression enhanced CPT-11 sensitivity by activating the DNA damage checkpoint pathway.	Irinotecan	47-53	NPR2 like, GATOR1 complex subunit	Homo sapiens	17-22
29169974-0	2018	A Prospective, Multicenter Phase II Study of the Efficacy and Feasibility of 15-minute Panitumumab Infusion Plus Irinotecan for Oxaliplatin- and Irinotecan-refractory, KRAS Wild-type Metastatic Colorectal Cancer (Short Infusion of Panitumumab Trial).	Irinotecan	113-123	KRAS proto-oncogene, GTPase	Homo sapiens	168-172
29328485-12	2018	hnRNP A2/B1 knock-down significantly induced the suppression of proliferation, migration, invasion and also enhancement of apoptosis and reduced the IC50 of lobaplatin and irinotecan.	Irinotecan	172-182	heterogeneous nuclear ribonucleoprotein A2/B1	Homo sapiens	0-11
29328485-17	2018	In addition, after silencing hnRNP A2/B1 can increase the sensitivity of cervical cancer cells to lobaplatin and irinotecan.	Irinotecan	113-123	heterogeneous nuclear ribonucleoprotein A2/B1	Homo sapiens	29-40
29963254-3	2018	In the animal model for irinotecan (CPT-11) induced CID, Hst could selectively inhibit intestinal carboxylesterase (CES2) and thus reduce the local conversion of CPT-11 to cytotoxic SN-38 which causes intestinal toxicity.	Irinotecan	24-34	carboxylesterase 2	Homo sapiens	116-120
29963254-3	2018	In the animal model for irinotecan (CPT-11) induced CID, Hst could selectively inhibit intestinal carboxylesterase (CES2) and thus reduce the local conversion of CPT-11 to cytotoxic SN-38 which causes intestinal toxicity.	Irinotecan	36-42	carboxylesterase 2	Homo sapiens	116-120
29963254-6	2018	Moreover, Hst was found to work synergistically with CPT-11 in tumor inhibition by suppressing the tumor"s STAT3 activity and recruiting tumoricidal macrophages into the tumor microenvironment.	Irinotecan	53-59	signal transducer and activator of transcription 3	Homo sapiens	107-112
31352923-3	2018	In this study, to improve water dispersity and the anti-tumor efficiency of SN-38, a prodrug, SN-38-BOC, that could efficiently transform to active SN-38 in the acidic tumor microenvironment was synthesized and encapsulated into MPEG-P(CL-ran-TMC) micelles (SN-38-BOC micelles).	Irinotecan	76-81	BOC cell adhesion associated, oncogene regulated	Homo sapiens	100-103
31352923-3	2018	In this study, to improve water dispersity and the anti-tumor efficiency of SN-38, a prodrug, SN-38-BOC, that could efficiently transform to active SN-38 in the acidic tumor microenvironment was synthesized and encapsulated into MPEG-P(CL-ran-TMC) micelles (SN-38-BOC micelles).	Irinotecan	76-81	BOC cell adhesion associated, oncogene regulated	Homo sapiens	264-267
31352923-3	2018	In this study, to improve water dispersity and the anti-tumor efficiency of SN-38, a prodrug, SN-38-BOC, that could efficiently transform to active SN-38 in the acidic tumor microenvironment was synthesized and encapsulated into MPEG-P(CL-ran-TMC) micelles (SN-38-BOC micelles).	Irinotecan	94-99	BOC cell adhesion associated, oncogene regulated	Homo sapiens	264-267
31352923-3	2018	In this study, to improve water dispersity and the anti-tumor efficiency of SN-38, a prodrug, SN-38-BOC, that could efficiently transform to active SN-38 in the acidic tumor microenvironment was synthesized and encapsulated into MPEG-P(CL-ran-TMC) micelles (SN-38-BOC micelles).	Irinotecan	94-99	BOC cell adhesion associated, oncogene regulated	Homo sapiens	100-103
31352923-3	2018	In this study, to improve water dispersity and the anti-tumor efficiency of SN-38, a prodrug, SN-38-BOC, that could efficiently transform to active SN-38 in the acidic tumor microenvironment was synthesized and encapsulated into MPEG-P(CL-ran-TMC) micelles (SN-38-BOC micelles).	Irinotecan	94-99	BOC cell adhesion associated, oncogene regulated	Homo sapiens	264-267
31352923-4	2018	SN-38-BOC micelles could accumulate in tumors due to the EPR effect and exhibit a sustained release behavior, which was rapidly transformed to active SN-38 by the acidic environment of tumor tissues (pH 5.5-6.8), thus achieving efficient anti-tumor activity.	Irinotecan	0-5	BOC cell adhesion associated, oncogene regulated	Homo sapiens	6-9
31352923-4	2018	SN-38-BOC micelles could accumulate in tumors due to the EPR effect and exhibit a sustained release behavior, which was rapidly transformed to active SN-38 by the acidic environment of tumor tissues (pH 5.5-6.8), thus achieving efficient anti-tumor activity.	Irinotecan	150-155	BOC cell adhesion associated, oncogene regulated	Homo sapiens	6-9
31352923-5	2018	Compared with the free SN-38-BOC group, enhanced cytotoxicity and apoptotic induction were obtained from the SN-38-BOC micelle-treated group in both HCT116 and CT26 cells.	Irinotecan	23-28	BOC cell adhesion associated, oncogene regulated	Homo sapiens	29-32
29167313-2	2018	We show that the antibiotic minocycline, by its ability to minimize DNA repair via reduced expression of tyrosyl-DNA phosphodiesterase-1 (Tdp1), removes a key process attenuating the efficacy of irinotecan, a frequently used chemotherapeutic against metastatic disease.	Irinotecan	195-205	tyrosyl-DNA phosphodiesterase 1	Mus musculus	105-136
29167313-2	2018	We show that the antibiotic minocycline, by its ability to minimize DNA repair via reduced expression of tyrosyl-DNA phosphodiesterase-1 (Tdp1), removes a key process attenuating the efficacy of irinotecan, a frequently used chemotherapeutic against metastatic disease.	Irinotecan	195-205	tyrosyl-DNA phosphodiesterase 1	Mus musculus	138-142
29167313-3	2018	Moreover, minocycline and irinotecan cooperatively mitigate each other"s undesired cytokine inductions of VEGF and IL8, respectively, thereby reinforcing the benefits of each modality.	Irinotecan	26-36	vascular endothelial growth factor A	Mus musculus	106-110
29167313-3	2018	Moreover, minocycline and irinotecan cooperatively mitigate each other"s undesired cytokine inductions of VEGF and IL8, respectively, thereby reinforcing the benefits of each modality.	Irinotecan	26-36	chemokine (C-X-C motif) ligand 15	Mus musculus	115-118
29257266-0	2018	Wee1 inhibition can suppress tumor proliferation and sensitize p53 mutant colonic cancer cells to the anticancer effect of irinotecan.	Irinotecan	123-133	WEE1 G2 checkpoint kinase	Homo sapiens	0-4
29257266-0	2018	Wee1 inhibition can suppress tumor proliferation and sensitize p53 mutant colonic cancer cells to the anticancer effect of irinotecan.	Irinotecan	123-133	tumor protein p53	Homo sapiens	63-66
30166915-0	2018	Simvastatin enhances irinotecan-induced apoptosis in prostate cancer via inhibition of MCL-1.	Irinotecan	21-31	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	87-92
30166915-6	2018	PC3 cells were treated with simvastatin, irinotecan or combination.	Irinotecan	41-51	proprotein convertase subtilisin/kexin type 1	Homo sapiens	0-3
30166915-11	2018	Combined treatment of simvastatin with irinotecan exhibited a significant inhibition of PC3 cell growth compared to each treatment alone.	Irinotecan	39-49	proprotein convertase subtilisin/kexin type 1	Homo sapiens	88-91
30166915-12	2018	Flow cytometry analysis showed that PC3 cell treatment with simvastatin and irinotecan combination demonstrated a remarkable increase in the percentage of apoptotic cells and those accumulated at G0/G1 phase when compared to each treatment alone.	Irinotecan	76-86	proprotein convertase subtilisin/kexin type 1	Homo sapiens	36-39
29651325-1	2018	Irinotecan (CPT-11) is an anticancer prodrug that is activated by the carboxylesterase CES2 and has been approved for the treatment of many types of solid tumors, including colorectal cancer.	Irinotecan	0-10	carboxylesterase 2	Homo sapiens	70-86
29124328-1	2018	PURPOSE: We aimed to retrospectively evaluate the efficacy and toxicity of an irinotecan hydrochloride (CPT) and nedaplatin (N) combination therapy for recurrent and refractory endometrial carcinoma, administered based on UGT1A1 genotype.	Irinotecan	78-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	222-228
29124328-9	2018	Patients with a wild-type UGT1A1 status received higher doses of CPT-11 (p = 0.048) and had similar RR and CBR compared to those with a UGT1A1*6 and *28 status.	Irinotecan	65-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
29486476-8	2018	RESULTS: Voruciclib significantly potentiated the effect of paclitaxel and doxorubicin in ABCB1-overexpressing cells, as well as mitoxantrone and SN-38 in ABCG2-overexpressing cells.	Irinotecan	146-151	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	155-160
29651325-1	2018	Irinotecan (CPT-11) is an anticancer prodrug that is activated by the carboxylesterase CES2 and has been approved for the treatment of many types of solid tumors, including colorectal cancer.	Irinotecan	0-10	carboxylesterase 2	Homo sapiens	87-91
29651325-1	2018	Irinotecan (CPT-11) is an anticancer prodrug that is activated by the carboxylesterase CES2 and has been approved for the treatment of many types of solid tumors, including colorectal cancer.	Irinotecan	12-18	carboxylesterase 2	Homo sapiens	70-86
29651325-1	2018	Irinotecan (CPT-11) is an anticancer prodrug that is activated by the carboxylesterase CES2 and has been approved for the treatment of many types of solid tumors, including colorectal cancer.	Irinotecan	12-18	carboxylesterase 2	Homo sapiens	87-91
29316651-0	2018	CPT-11-Induced Delayed Diarrhea Develops via Reduced Aquaporin-3 Expression in the Colon.	Irinotecan	0-6	aquaporin 3 (Gill blood group)	Rattus norvegicus	53-64
29316651-2	2018	In this study, we analyzed the pathogenic mechanism of CPT-11-induced delayed diarrhea by focusing on water channel aquaporin-3 (AQP3) in the colon.	Irinotecan	55-61	aquaporin 3 (Gill blood group)	Rattus norvegicus	116-127
29316651-2	2018	In this study, we analyzed the pathogenic mechanism of CPT-11-induced delayed diarrhea by focusing on water channel aquaporin-3 (AQP3) in the colon.	Irinotecan	55-61	aquaporin 3 (Gill blood group)	Rattus norvegicus	129-133
29316651-3	2018	When rats received CPT-11, the expression level of AQP3 was reduced during severe diarrhea.	Irinotecan	19-25	aquaporin 3 (Gill blood group)	Rattus norvegicus	51-55
29316651-5	2018	When celecoxib, an anti-inflammatory drug, was concomitantly administered, both the diarrhea and the reduced expression of AQP3 induced by CPT-11 were suppressed.	Irinotecan	139-145	aquaporin 3 (Gill blood group)	Rattus norvegicus	123-127
29316651-7	2018	These results showed that when CPT-11 is administered, the expression level of AQP3 in the colon is reduced, resulting in delayed diarrhea by preventing water transport from the intestinal tract.	Irinotecan	31-37	aquaporin 3 (Gill blood group)	Rattus norvegicus	79-83
29316651-8	2018	It was also suggested that the reduced expression of AQP3 might be due to the inflammation that occurs following the loss of colonic crypt cells and to the damage caused by the direct activation of macrophages by CPT-11.	Irinotecan	213-219	aquaporin 3 (Gill blood group)	Rattus norvegicus	53-57
29316651-9	2018	Therefore, it was considered that anti-inflammatory drugs that suppress the reduction of AQP3 expression could prevent CPT-11-induced delayed diarrhea.	Irinotecan	119-125	aquaporin 3 (Gill blood group)	Rattus norvegicus	89-93
30504681-7	2018	Vitamin C and/or irinotecan administration decreased the plasma level of ROS and IL-6 and increased the expression of collagen type I and caspase-1.	Irinotecan	17-27	interleukin 6	Mus musculus	81-85
30504681-7	2018	Vitamin C and/or irinotecan administration decreased the plasma level of ROS and IL-6 and increased the expression of collagen type I and caspase-1.	Irinotecan	17-27	caspase 1	Mus musculus	138-147
29210644-4	2018	CES2 plays crucial roles in the metabolic activation of many prodrugs including anticancer agents capecitabine and CPT-11.	Irinotecan	115-121	carboxylesterase 2	Homo sapiens	0-4
29210644-5	2018	Co-administration with CES2 inhibitors may ameliorate CPT-11 associated lifethreatening diarrhea or improve the half-lives of CES2-substrate drugs.	Irinotecan	54-60	carboxylesterase 2	Homo sapiens	23-27
31352923-5	2018	Compared with the free SN-38-BOC group, enhanced cytotoxicity and apoptotic induction were obtained from the SN-38-BOC micelle-treated group in both HCT116 and CT26 cells.	Irinotecan	23-28	BOC cell adhesion associated, oncogene regulated	Homo sapiens	115-118
31352923-7	2018	Furthermore, SN-38-BOC micelles exhibited stronger inhibition of tumor growth in both HCT116 and CT26 subcutaneous xenograft tumor models.	Irinotecan	13-18	BOC cell adhesion associated, oncogene regulated	Homo sapiens	19-22
31352923-8	2018	Histological analysis revealed that SN-38-BOC micelles showed a more effective anti-tumor activity than the free drug by inducing more apoptosis, inhibiting angiogenesis, and suppressing proliferation.	Irinotecan	36-41	BOC cell adhesion associated, oncogene regulated	Homo sapiens	42-45
31352923-9	2018	Thus, the pH-activatable SN-38-BOC micelle could serve as a promising candidate in colorectal tumor therapy.	Irinotecan	25-30	BOC cell adhesion associated, oncogene regulated	Homo sapiens	31-34
29125991-4	2018	The in vitro study evaluated the efficacy of high-dose SN-38 and quercetin combined with low-dose SN-38 on cell viability, apoptosis, and beta-catenin expression.	Irinotecan	55-60	catenin beta 1	Homo sapiens	138-150
29125991-6	2018	AGS cells treated with a high dose of SN-38 exhibited up-regulation of beta-catenin protein expression, whereas quercetin-treated cells (either quercetin alone or combined with low-dose SN-38) exhibited lower protein levels of beta-catenin.	Irinotecan	38-43	catenin beta 1	Homo sapiens	71-83
29125991-6	2018	AGS cells treated with a high dose of SN-38 exhibited up-regulation of beta-catenin protein expression, whereas quercetin-treated cells (either quercetin alone or combined with low-dose SN-38) exhibited lower protein levels of beta-catenin.	Irinotecan	38-43	catenin beta 1	Homo sapiens	227-239
29125991-6	2018	AGS cells treated with a high dose of SN-38 exhibited up-regulation of beta-catenin protein expression, whereas quercetin-treated cells (either quercetin alone or combined with low-dose SN-38) exhibited lower protein levels of beta-catenin.	Irinotecan	186-191	catenin beta 1	Homo sapiens	227-239
29125991-7	2018	In the AGS xenograft mouse model, gene expression of cyclooxygenase-2 and epithelial-mesenchymal transition-related markers, such as Twist1 and ITGbeta6, were lower in combined treatments with quercetin and low-dose irinotecan than high-dose irinotecan alone.	Irinotecan	216-226	prostaglandin-endoperoxide synthase 2	Mus musculus	53-69
29125991-7	2018	In the AGS xenograft mouse model, gene expression of cyclooxygenase-2 and epithelial-mesenchymal transition-related markers, such as Twist1 and ITGbeta6, were lower in combined treatments with quercetin and low-dose irinotecan than high-dose irinotecan alone.	Irinotecan	242-252	prostaglandin-endoperoxide synthase 2	Mus musculus	53-69
29125991-8	2018	Furthermore, the concentration of angiogenesis-associated factors (vascular endothelial growth factor (VEGF)-A and VEGF-receptor 2) and percentage of Tie2-expressing monocytes was significantly down-regulated in combined treatments with quercetin and irinotecan.	Irinotecan	251-261	vascular endothelial growth factor A	Homo sapiens	67-101
29125991-8	2018	Furthermore, the concentration of angiogenesis-associated factors (vascular endothelial growth factor (VEGF)-A and VEGF-receptor 2) and percentage of Tie2-expressing monocytes was significantly down-regulated in combined treatments with quercetin and irinotecan.	Irinotecan	251-261	vascular endothelial growth factor A	Homo sapiens	103-107
29125991-8	2018	Furthermore, the concentration of angiogenesis-associated factors (vascular endothelial growth factor (VEGF)-A and VEGF-receptor 2) and percentage of Tie2-expressing monocytes was significantly down-regulated in combined treatments with quercetin and irinotecan.	Irinotecan	251-261	vascular endothelial growth factor A	Homo sapiens	115-119
29125991-8	2018	Furthermore, the concentration of angiogenesis-associated factors (vascular endothelial growth factor (VEGF)-A and VEGF-receptor 2) and percentage of Tie2-expressing monocytes was significantly down-regulated in combined treatments with quercetin and irinotecan.	Irinotecan	251-261	TEK receptor tyrosine kinase	Homo sapiens	150-154
28834127-4	2018	Replacement of vincristine, irinotecan, and temozolomide (VIT) for VAC induced a marked tumor reduction and normalization of the miR-206 levels.	Irinotecan	28-38	microRNA 206	Homo sapiens	129-136
29589315-7	2018	It has been established that UGT1A1*28 polymorphism is associated with irinotecan toxicity, but this test is rarely performed as the management strategy has not been identified.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
29079710-0	2018	Selective and Concentrated Accretion of SN-38 with a CEACAM5-Targeting Antibody-Drug Conjugate (ADC), Labetuzumab Govitecan (IMMU-130).	Irinotecan	40-45	CEA cell adhesion molecule 5	Homo sapiens	53-60
29138869-3	2018	Mutated p53 in CRC was reported to be associated with resistance to commonly used chemotherapeutic agents including, 5-fluorouracil, oxaliplatin and irinotecan.	Irinotecan	149-159	tumor protein p53	Homo sapiens	8-11
29192320-0	2018	Combined SN-38 and gefitinib treatment promotes CD44 degradation in head and neck squamous cell carcinoma cells.	Irinotecan	9-14	CD44 molecule (Indian blood group)	Homo sapiens	48-52
29192320-2	2018	Among the tested drugs, we focused on combined SN-38, which is the active metabolite produced from irinotecan hydrochloride - a type I DNA topoisomerase inhibitor - after it is metabolized by carboxylesterase in the liver and gefitinib, an EGFR tyrosine kinase inhibitor treatment, based on the ability of this combination to inhibit HNSCC cell growth.	Irinotecan	47-52	DNA topoisomerase I	Homo sapiens	128-152
29192320-2	2018	Among the tested drugs, we focused on combined SN-38, which is the active metabolite produced from irinotecan hydrochloride - a type I DNA topoisomerase inhibitor - after it is metabolized by carboxylesterase in the liver and gefitinib, an EGFR tyrosine kinase inhibitor treatment, based on the ability of this combination to inhibit HNSCC cell growth.	Irinotecan	99-123	DNA topoisomerase I	Homo sapiens	128-152
29192320-6	2018	Next, we investigated the mechanism whereby SN-38 and gefitinib inhibited CD44 expression in vitro.	Irinotecan	44-49	CD44 molecule (Indian blood group)	Homo sapiens	74-78
29192320-8	2018	The present study revealed that combined gefitinib and SN-38 treatment inhibits CD44 expression by promoting its lysosomal degradation in HNSCC cells.	Irinotecan	55-60	CD44 molecule (Indian blood group)	Homo sapiens	80-84
29891024-10	2018	Previous reports, studies of recombinant UGT isoforms indicated that SN-38 glucuronidation was mainly catalyzed by UGT1A1.	Irinotecan	69-74	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	41-44
29891024-10	2018	Previous reports, studies of recombinant UGT isoforms indicated that SN-38 glucuronidation was mainly catalyzed by UGT1A1.	Irinotecan	69-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
30673201-4	2018	On the other hand, carriers of various genotypes of UGT1A1 differ significantly in metabolism characteristics of a number of common medications (irinotecan, belinostat, etc.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
27845419-0	2018	ABC transporter polymorphisms are associated with irinotecan pharmacokinetics and neutropenia.	Irinotecan	50-60	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-15
27845419-4	2018	rs6498588 (ABCC1) and rs12720066 (ABCB1) were associated with increased SN-38 exposure, and rs17501331 (ABCC1) and rs12720066 were associated with lower absolute neutrophil count nadir.	Irinotecan	72-77	ATP binding cassette subfamily C member 1	Homo sapiens	11-16
27845419-4	2018	rs6498588 (ABCC1) and rs12720066 (ABCB1) were associated with increased SN-38 exposure, and rs17501331 (ABCC1) and rs12720066 were associated with lower absolute neutrophil count nadir.	Irinotecan	72-77	ATP binding cassette subfamily B member 1	Homo sapiens	34-39
27845419-7	2018	These results suggest that genetic variation in ABCC1 and ABCB1 may contribute to irinotecan-induced neutropenia by altering expression of transporters involved in irinotecan metabolite disposition.	Irinotecan	82-92	ATP binding cassette subfamily C member 1	Homo sapiens	48-53
27845419-7	2018	These results suggest that genetic variation in ABCC1 and ABCB1 may contribute to irinotecan-induced neutropenia by altering expression of transporters involved in irinotecan metabolite disposition.	Irinotecan	82-92	ATP binding cassette subfamily B member 1	Homo sapiens	58-63
27845419-7	2018	These results suggest that genetic variation in ABCC1 and ABCB1 may contribute to irinotecan-induced neutropenia by altering expression of transporters involved in irinotecan metabolite disposition.	Irinotecan	164-174	ATP binding cassette subfamily C member 1	Homo sapiens	48-53
29199543-4	2018	NR1I2 and NR1I3 genetic polymorphisms can affect the pharmacokinetics and therapeutic response to many drugs, such as irinotecan, tacrolimus and atazanavir.	Irinotecan	118-128	nuclear receptor subfamily 1 group I member 2	Homo sapiens	0-5
27845419-7	2018	These results suggest that genetic variation in ABCC1 and ABCB1 may contribute to irinotecan-induced neutropenia by altering expression of transporters involved in irinotecan metabolite disposition.	Irinotecan	164-174	ATP binding cassette subfamily B member 1	Homo sapiens	58-63
29019266-2	2018	The purpose of this study was to develop a thermo-sensitive hydrogel system with acidic SN-38 liposomes (SN-38-Lip-Gel) for local chemotherapy to solve these problems and to evaluate its antitumor activity and tissue distribution in tumor-bearing mice.	Irinotecan	88-93	CCAAT/enhancer binding protein (C/EBP), beta	Mus musculus	111-114
29019266-7	2018	SN-38-Lip-Gel suggested pH-dependent stability, the percentage of SN-38 A remaining decreased along with the increasing pH.	Irinotecan	0-5	CCAAT/enhancer binding protein (C/EBP), beta	Mus musculus	6-9
29019266-9	2018	In conclusion, SN-38-Lip-Gel could improve the effective use of SN-38 by stabilizing the lactone form, extending the drug release, providing a high local drug concentration, and reducing systemic toxicity.	Irinotecan	15-20	CCAAT/enhancer binding protein (C/EBP), beta	Mus musculus	21-24
29019266-9	2018	In conclusion, SN-38-Lip-Gel could improve the effective use of SN-38 by stabilizing the lactone form, extending the drug release, providing a high local drug concentration, and reducing systemic toxicity.	Irinotecan	64-69	CCAAT/enhancer binding protein (C/EBP), beta	Mus musculus	21-24
29199543-4	2018	NR1I2 and NR1I3 genetic polymorphisms can affect the pharmacokinetics and therapeutic response to many drugs, such as irinotecan, tacrolimus and atazanavir.	Irinotecan	118-128	nuclear receptor subfamily 1 group I member 3	Homo sapiens	10-15
29052349-0	2018	Relationship between UGT1A1*27 and UGT1A1*7 polymorphisms and irinotecan-related toxicities in patients with lung cancer.	Irinotecan	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
29052349-0	2018	Relationship between UGT1A1*27 and UGT1A1*7 polymorphisms and irinotecan-related toxicities in patients with lung cancer.	Irinotecan	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
29052349-1	2018	BACKGROUND: The objective of this study was to evaluate the effects of gene polymorphisms, including UGT1A1*7, *27, and *29, on the safety of irinotecan therapy.	Irinotecan	142-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
29052349-8	2018	SN-38 tended to remain in the blood for a prolonged period after the infusion of irinotecan in patients with UGT1A1*27 or UGT1A1*28 polymorphisms.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
29052349-8	2018	SN-38 tended to remain in the blood for a prolonged period after the infusion of irinotecan in patients with UGT1A1*27 or UGT1A1*28 polymorphisms.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
29052349-8	2018	SN-38 tended to remain in the blood for a prolonged period after the infusion of irinotecan in patients with UGT1A1*27 or UGT1A1*28 polymorphisms.	Irinotecan	81-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
29052349-10	2018	CONCLUSION: UGT1A1*27 can occur separately from UGT1A1*28 and is related to leukopenia during irinotecan treatment.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
29052349-10	2018	CONCLUSION: UGT1A1*27 can occur separately from UGT1A1*28 and is related to leukopenia during irinotecan treatment.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
29052349-11	2018	UGT1A1*7 is less relevant to irinotecan-induced toxicities, and UGT1A1*29 seems to have little clinical impact.	Irinotecan	29-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
29487697-1	2018	Our study addresses the issue of the clinical reliability of three candidate DPYD and one UGT single nucleotide polymorphisms in predicting 5-fluorouracil- and irinotecan-related adverse events.	Irinotecan	160-170	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	90-93
29487697-5	2018	Present results support the preemptive screening of mentioned DPYD and UGT1A1 variants to identify patients at risk of clinically relevant 5-fluoruracil- and irinotecan-related AEs, in order to improve treatments" safety through a "genotype-guided" approach.	Irinotecan	158-168	dihydropyrimidine dehydrogenase	Homo sapiens	62-66
29487697-5	2018	Present results support the preemptive screening of mentioned DPYD and UGT1A1 variants to identify patients at risk of clinically relevant 5-fluoruracil- and irinotecan-related AEs, in order to improve treatments" safety through a "genotype-guided" approach.	Irinotecan	158-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
29031818-0	2017	Camptothecin and its analog SN-38, the active metabolite of irinotecan, inhibit binding of the transcriptional regulator and oncoprotein FUBP1 to its DNA target sequence FUSE.	Irinotecan	28-33	far upstream element binding protein 1	Homo sapiens	137-142
29277179-1	2017	BACKGROUND: Uridine-diphosphoglucuronosyl transferase 1A1 (UGT1A1), UGT1A1*28 polymorphism can reduce UGT1A1 enzymatic activity, which may lead to severe toxicities in patients who receive irinotecan.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-57
29277179-1	2017	BACKGROUND: Uridine-diphosphoglucuronosyl transferase 1A1 (UGT1A1), UGT1A1*28 polymorphism can reduce UGT1A1 enzymatic activity, which may lead to severe toxicities in patients who receive irinotecan.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
29277179-1	2017	BACKGROUND: Uridine-diphosphoglucuronosyl transferase 1A1 (UGT1A1), UGT1A1*28 polymorphism can reduce UGT1A1 enzymatic activity, which may lead to severe toxicities in patients who receive irinotecan.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
29277179-1	2017	BACKGROUND: Uridine-diphosphoglucuronosyl transferase 1A1 (UGT1A1), UGT1A1*28 polymorphism can reduce UGT1A1 enzymatic activity, which may lead to severe toxicities in patients who receive irinotecan.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
29031818-0	2017	Camptothecin and its analog SN-38, the active metabolite of irinotecan, inhibit binding of the transcriptional regulator and oncoprotein FUBP1 to its DNA target sequence FUSE.	Irinotecan	28-33	Polykaryocytosis inducer	Homo sapiens	170-174
29031818-0	2017	Camptothecin and its analog SN-38, the active metabolite of irinotecan, inhibit binding of the transcriptional regulator and oncoprotein FUBP1 to its DNA target sequence FUSE.	Irinotecan	60-70	far upstream element binding protein 1	Homo sapiens	137-142
29031818-0	2017	Camptothecin and its analog SN-38, the active metabolite of irinotecan, inhibit binding of the transcriptional regulator and oncoprotein FUBP1 to its DNA target sequence FUSE.	Irinotecan	60-70	Polykaryocytosis inducer	Homo sapiens	170-174
29031818-3	2017	In this study, we screened an FDA-approved drug library and discovered that the Topoisomerase I (TOP1) inhibitor camptothecin (CPT) and its derivative 7-ethyl-10-hydroxycamptothecin (SN-38), the active irinotecan metabolite that is used in the clinics in combination with other chemotherapeutics to treat carcinoma, inhibit FUBP1 activity.	Irinotecan	151-181	far upstream element binding protein 1	Homo sapiens	324-329
29031818-3	2017	In this study, we screened an FDA-approved drug library and discovered that the Topoisomerase I (TOP1) inhibitor camptothecin (CPT) and its derivative 7-ethyl-10-hydroxycamptothecin (SN-38), the active irinotecan metabolite that is used in the clinics in combination with other chemotherapeutics to treat carcinoma, inhibit FUBP1 activity.	Irinotecan	183-188	far upstream element binding protein 1	Homo sapiens	324-329
29031818-5	2017	Our results suggest the interference with the FUBP1/FUSE interaction as a further molecular mechanism that, in addition to the inactivation of TOP1, may contribute to the therapeutic potential of CPT/SN-38.	Irinotecan	200-205	far upstream element binding protein 1	Homo sapiens	46-51
29031818-5	2017	Our results suggest the interference with the FUBP1/FUSE interaction as a further molecular mechanism that, in addition to the inactivation of TOP1, may contribute to the therapeutic potential of CPT/SN-38.	Irinotecan	200-205	Polykaryocytosis inducer	Homo sapiens	52-56
29031818-6	2017	Targeting of FUBP1 in HCC therapy with SN-38/irinotecan could be a particularly interesting option because of the high FUBP1 levels in HCC cells and their dependency on FUBP1 expression.	Irinotecan	39-44	far upstream element binding protein 1	Homo sapiens	13-18
29031818-6	2017	Targeting of FUBP1 in HCC therapy with SN-38/irinotecan could be a particularly interesting option because of the high FUBP1 levels in HCC cells and their dependency on FUBP1 expression.	Irinotecan	39-44	far upstream element binding protein 1	Homo sapiens	119-124
29031818-6	2017	Targeting of FUBP1 in HCC therapy with SN-38/irinotecan could be a particularly interesting option because of the high FUBP1 levels in HCC cells and their dependency on FUBP1 expression.	Irinotecan	39-44	far upstream element binding protein 1	Homo sapiens	119-124
29031818-6	2017	Targeting of FUBP1 in HCC therapy with SN-38/irinotecan could be a particularly interesting option because of the high FUBP1 levels in HCC cells and their dependency on FUBP1 expression.	Irinotecan	45-55	far upstream element binding protein 1	Homo sapiens	13-18
29031818-6	2017	Targeting of FUBP1 in HCC therapy with SN-38/irinotecan could be a particularly interesting option because of the high FUBP1 levels in HCC cells and their dependency on FUBP1 expression.	Irinotecan	45-55	far upstream element binding protein 1	Homo sapiens	119-124
29031818-6	2017	Targeting of FUBP1 in HCC therapy with SN-38/irinotecan could be a particularly interesting option because of the high FUBP1 levels in HCC cells and their dependency on FUBP1 expression.	Irinotecan	45-55	far upstream element binding protein 1	Homo sapiens	119-124
29340025-0	2017	The novel ATM inhibitor (AZ31) enhances antitumor activity in patient derived xenografts that are resistant to irinotecan monotherapy.	Irinotecan	111-121	ATM serine/threonine kinase	Homo sapiens	10-13
28940490-6	2017	KEY FINDINGS: Eight amino acids residues in TRPA1 established stable interactions with carvacryl acetate, which led to pharmacological efficacy against CPT-11-induced intestinal mucositis via reduction of both neutropenia and bacteremia, increase in villi height and crypt depth, decrease in pro-inflammatory cytokines (interleukin-1beta, keratinocyte chemoattractant and tumour necrosis factor-alpha) and decrease in malondialdehyde and nitric oxide metabolite levels in the jejunum.	Irinotecan	152-158	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	44-49
29312810-8	2017	Thus, the sequential treatment with SN-38 followed by FTD may be useful for the combination therapy of FTD/TPI and CPT-11 against relapsed colorectal cancer after 5-FU-based chemotherapy.	Irinotecan	36-41	triosephosphate isomerase 1	Homo sapiens	107-110
29340025-3	2017	The objective of this preclinical study was to determine whether ATM inhibition would enhance sensitivity to irinotecan treatment.	Irinotecan	109-119	ATM serine/threonine kinase	Homo sapiens	65-68
29340025-8	2017	Treatment with irinotecan significantly elevated the ATM pathway evident by an increase in the activation of H2AX and RAD50.	Irinotecan	15-25	ATM serine/threonine kinase	Homo sapiens	53-56
29340025-8	2017	Treatment with irinotecan significantly elevated the ATM pathway evident by an increase in the activation of H2AX and RAD50.	Irinotecan	15-25	H2A.X variant histone	Homo sapiens	109-113
29340025-8	2017	Treatment with irinotecan significantly elevated the ATM pathway evident by an increase in the activation of H2AX and RAD50.	Irinotecan	15-25	RAD50 double strand break repair protein	Homo sapiens	118-123
29340025-9	2017	Combinational therapy reduced the activation of H2AX and RAD50 when compared to irinotecan alone in the combination sensitive CRC098.	Irinotecan	80-90	H2A.X variant histone	Homo sapiens	48-52
29174536-3	2017	Irinotecan and etoposide inhibited the uptake of [3H]-uridine and [3H]-DAC at 10 s and 5 min, while cytarabine and gemcitabine only inhibited that of [3H]-DAC at 5 min.	Irinotecan	0-10	arylacetamide deacetylase	Homo sapiens	71-74
29174536-3	2017	Irinotecan and etoposide inhibited the uptake of [3H]-uridine and [3H]-DAC at 10 s and 5 min, while cytarabine and gemcitabine only inhibited that of [3H]-DAC at 5 min.	Irinotecan	0-10	arylacetamide deacetylase	Homo sapiens	155-158
29174536-4	2017	Irinotecan and etoposide inhibited [3H]-DAC uptake in negative control small interfering RNA (siRNA)- or dCK siRNA-transfected cells at 10 s, whereas cytarabine and gemcitabine did not.	Irinotecan	0-10	arylacetamide deacetylase	Homo sapiens	40-43
29174536-4	2017	Irinotecan and etoposide inhibited [3H]-DAC uptake in negative control small interfering RNA (siRNA)- or dCK siRNA-transfected cells at 10 s, whereas cytarabine and gemcitabine did not.	Irinotecan	0-10	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	105-108
28940490-6	2017	KEY FINDINGS: Eight amino acids residues in TRPA1 established stable interactions with carvacryl acetate, which led to pharmacological efficacy against CPT-11-induced intestinal mucositis via reduction of both neutropenia and bacteremia, increase in villi height and crypt depth, decrease in pro-inflammatory cytokines (interleukin-1beta, keratinocyte chemoattractant and tumour necrosis factor-alpha) and decrease in malondialdehyde and nitric oxide metabolite levels in the jejunum.	Irinotecan	152-158	interleukin 1 beta	Mus musculus	320-337
28940490-7	2017	CONCLUSIONS: Carvacryl acetate is a promising anti-inflammatory and antioxidant agent, a fact confirmed through observations of its interactions with TRPA1 in CPT-11-induced intestinal mucositis in mice.	Irinotecan	159-165	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	150-155
28948511-4	2017	The involvement of ABCG2 transporter in irinotecan resistance has been established.	Irinotecan	40-50	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	19-24
28801072-9	2017	Oxidative stress parameters and intracellular mediators as well as the MPO activity were determined in intestinal mucosa by colorimetric methods Our result indicated that irinotecan produces an intestinal fluid accumulation and electrolyte transport disorders.	Irinotecan	171-181	myeloperoxidase	Rattus norvegicus	71-74
29344244-6	2017	Furthermore, PSAT1 overexpression was associated with response to irinotecan, 5-fluorouracil and leucovorin chemotherapy, and with shorter survival time, and retained significance as an independent prognostic factor for CRC when subjected to the multivariate analysis with a Cox"s proportional hazards model.	Irinotecan	66-76	phosphoserine aminotransferase 1	Homo sapiens	13-18
28948511-5	2017	The current study was designed to characterize SN38-loaded pegylated (polyethylene glycol) PLGA [poly(lactic-co-glycolic acid)]-verapamil nanoparticles (NPs), and to distinguish the cytotoxic effect of SN38-PEG-PLGA-Ver NPs and the ability of SN38-PEG-PLGA-Ver NPs to inhibit drug resistance through the inhibition of ABCG2 expression.	Irinotecan	47-51	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	318-323
29184868-1	2017	We describe an extremely rare case of advanced pure primary ovarian squamous cell carcinoma (SCC), treated by adjuvant chemotherapy with dose-dense paclitaxel combined with carboplatin (dd-TC) plus the combination chemotherapy with irinotecan and cisplatin (CPT-P), with long-term recurrence-free survival.	Irinotecan	232-242	serpin family B member 3	Homo sapiens	93-96
29067643-5	2017	The MTD for the combination of gedatolisib with irinotecan 180 mg/m2 was estimated to be 110 mg weekly and for the combination with PD-0325901 was not reached at the highest dose evaluated (gedatolisib 154 mg weekly).	Irinotecan	48-58	metallothionein 1E	Homo sapiens	4-7
29180337-3	2017	Western blotting was performed to analyze the effect of bFGF-mAb combined with irinotecan on AKT and ERK1/2 phosphorylation in the cells.	Irinotecan	79-89	AKT serine/threonine kinase 1	Homo sapiens	93-96
29180337-3	2017	Western blotting was performed to analyze the effect of bFGF-mAb combined with irinotecan on AKT and ERK1/2 phosphorylation in the cells.	Irinotecan	79-89	mitogen-activated protein kinase 3	Homo sapiens	101-107
29180337-5	2017	The inhibitory rate was significantly higher in H223 cells treated with bFGF mAb + irinotecan (54.30%) than in cell treated with bFGF mAb (18.73%) or irinotecan (21.96%) alone (P&lt;0.05).	Irinotecan	83-93	fibroblast growth factor 2	Homo sapiens	72-76
29180337-6	2017	Both bFGF mAb and irinotecan induced H223 cell apoptosis in a dose-dependent manner (P&lt;0.05), and the combined treatment resulted in a significantly higher early apoptosis rates (6.5%) than treatment with bFGF mAb (2.7%) or irinotecan (4.3%) alone (P&lt;0.05).	Irinotecan	18-28	fibroblast growth factor 2	Homo sapiens	208-212
29180337-6	2017	Both bFGF mAb and irinotecan induced H223 cell apoptosis in a dose-dependent manner (P&lt;0.05), and the combined treatment resulted in a significantly higher early apoptosis rates (6.5%) than treatment with bFGF mAb (2.7%) or irinotecan (4.3%) alone (P&lt;0.05).	Irinotecan	227-237	fibroblast growth factor 2	Homo sapiens	5-9
29180337-7	2017	bFGF mAb and irinotecan, either alone or in combination, significantly inhibited the levels of p-AKT protein and p-ERK1/2 protein without obviously affecting AKT and ERK1/2 protein levels.	Irinotecan	13-23	AKT serine/threonine kinase 1	Homo sapiens	97-100
29180337-7	2017	bFGF mAb and irinotecan, either alone or in combination, significantly inhibited the levels of p-AKT protein and p-ERK1/2 protein without obviously affecting AKT and ERK1/2 protein levels.	Irinotecan	13-23	mitogen-activated protein kinase 3	Homo sapiens	115-121
29180337-7	2017	bFGF mAb and irinotecan, either alone or in combination, significantly inhibited the levels of p-AKT protein and p-ERK1/2 protein without obviously affecting AKT and ERK1/2 protein levels.	Irinotecan	13-23	AKT serine/threonine kinase 1	Homo sapiens	158-161
29180337-7	2017	bFGF mAb and irinotecan, either alone or in combination, significantly inhibited the levels of p-AKT protein and p-ERK1/2 protein without obviously affecting AKT and ERK1/2 protein levels.	Irinotecan	13-23	mitogen-activated protein kinase 3	Homo sapiens	166-172
29180337-8	2017	CONCLUSION: bFGF mAb and irinotecan produce synergistic inhibitory effects on small cell lung cancer H223 cells by suppressing proliferation and promoting apoptosis of the cells, and can effectively block the MAPK/ERK and PI3K/AKT signaling pathways associated with bFGF.	Irinotecan	25-35	mitogen-activated protein kinase 3	Homo sapiens	209-213
29180337-8	2017	CONCLUSION: bFGF mAb and irinotecan produce synergistic inhibitory effects on small cell lung cancer H223 cells by suppressing proliferation and promoting apoptosis of the cells, and can effectively block the MAPK/ERK and PI3K/AKT signaling pathways associated with bFGF.	Irinotecan	25-35	mitogen-activated protein kinase 1	Homo sapiens	214-217
29180337-8	2017	CONCLUSION: bFGF mAb and irinotecan produce synergistic inhibitory effects on small cell lung cancer H223 cells by suppressing proliferation and promoting apoptosis of the cells, and can effectively block the MAPK/ERK and PI3K/AKT signaling pathways associated with bFGF.	Irinotecan	25-35	AKT serine/threonine kinase 1	Homo sapiens	227-230
29180337-8	2017	CONCLUSION: bFGF mAb and irinotecan produce synergistic inhibitory effects on small cell lung cancer H223 cells by suppressing proliferation and promoting apoptosis of the cells, and can effectively block the MAPK/ERK and PI3K/AKT signaling pathways associated with bFGF.	Irinotecan	25-35	fibroblast growth factor 2	Homo sapiens	266-270
29016119-5	2017	The best compound was active in a very low micromolar concentration range against all three transporters and restored sensitivity toward daunorubicin (P-gp and MRP1) and SN-38 (BCRP) in A2780/ADR (P-gp), H69AR (MRP1), and MDCK II BCRP (BCRP) cells.	Irinotecan	170-175	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	177-181
29016119-5	2017	The best compound was active in a very low micromolar concentration range against all three transporters and restored sensitivity toward daunorubicin (P-gp and MRP1) and SN-38 (BCRP) in A2780/ADR (P-gp), H69AR (MRP1), and MDCK II BCRP (BCRP) cells.	Irinotecan	170-175	ATP binding cassette subfamily B member 1	Homo sapiens	197-201
29016119-5	2017	The best compound was active in a very low micromolar concentration range against all three transporters and restored sensitivity toward daunorubicin (P-gp and MRP1) and SN-38 (BCRP) in A2780/ADR (P-gp), H69AR (MRP1), and MDCK II BCRP (BCRP) cells.	Irinotecan	170-175	ATP binding cassette subfamily C member 1	Homo sapiens	211-215
29016119-5	2017	The best compound was active in a very low micromolar concentration range against all three transporters and restored sensitivity toward daunorubicin (P-gp and MRP1) and SN-38 (BCRP) in A2780/ADR (P-gp), H69AR (MRP1), and MDCK II BCRP (BCRP) cells.	Irinotecan	170-175	ATP binding cassette subfamily G member 2	Canis lupus familiaris	222-234
29016119-5	2017	The best compound was active in a very low micromolar concentration range against all three transporters and restored sensitivity toward daunorubicin (P-gp and MRP1) and SN-38 (BCRP) in A2780/ADR (P-gp), H69AR (MRP1), and MDCK II BCRP (BCRP) cells.	Irinotecan	170-175	ATP binding cassette subfamily G member 2	Canis lupus familiaris	230-234
28904007-7	2017	In addition, when used in cytotoxicity assays, GO-Y030 and GO-Y078 were found to improve the sensitivity of the anticancer drug, SN-38, in K562/BCRP cells.	Irinotecan	129-134	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	144-148
29113203-1	2017	Uridine diphosphate glucuronosyltransferase 1A (UGT1A1), which affects irinotecan metabolism, has been associated with severe adverse reactions in patients with cancer treated with irinotecan.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
29113203-1	2017	Uridine diphosphate glucuronosyltransferase 1A (UGT1A1), which affects irinotecan metabolism, has been associated with severe adverse reactions in patients with cancer treated with irinotecan.	Irinotecan	181-191	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
29113203-9	2017	These findings suggested that the UGT1A1*28 and UGT1A1*6 genotypes may be associated with irinotecan-induced severe toxicity, and clarified the clinical importance of UGT1A1 polymorphisms, particularly UGT1A1*6, regarding irinotecan therapy in Chinese patients.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
29113203-9	2017	These findings suggested that the UGT1A1*28 and UGT1A1*6 genotypes may be associated with irinotecan-induced severe toxicity, and clarified the clinical importance of UGT1A1 polymorphisms, particularly UGT1A1*6, regarding irinotecan therapy in Chinese patients.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
29113203-9	2017	These findings suggested that the UGT1A1*28 and UGT1A1*6 genotypes may be associated with irinotecan-induced severe toxicity, and clarified the clinical importance of UGT1A1 polymorphisms, particularly UGT1A1*6, regarding irinotecan therapy in Chinese patients.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
29113203-9	2017	These findings suggested that the UGT1A1*28 and UGT1A1*6 genotypes may be associated with irinotecan-induced severe toxicity, and clarified the clinical importance of UGT1A1 polymorphisms, particularly UGT1A1*6, regarding irinotecan therapy in Chinese patients.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
29113203-9	2017	These findings suggested that the UGT1A1*28 and UGT1A1*6 genotypes may be associated with irinotecan-induced severe toxicity, and clarified the clinical importance of UGT1A1 polymorphisms, particularly UGT1A1*6, regarding irinotecan therapy in Chinese patients.	Irinotecan	222-232	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
29163158-11	2017	And the underlying mechanism of drug interaction between CPT-11 and SXD involves decreasing hepatic Mrp-2 and P-gp expression and altering the activities of CES and UGT.	Irinotecan	57-63	ATP binding cassette subfamily C member 2	Rattus norvegicus	100-105
29163158-11	2017	And the underlying mechanism of drug interaction between CPT-11 and SXD involves decreasing hepatic Mrp-2 and P-gp expression and altering the activities of CES and UGT.	Irinotecan	57-63	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	110-114
29066969-0	2017	Improved Progression-Free Survival in Irinotecan-Treated Metastatic Colorectal Cancer Patients Carrying the HNF1A Coding Variant p.I27L.	Irinotecan	38-48	HNF1 homeobox A	Homo sapiens	108-113
29072417-1	2017	Irinotecan life threatening toxicity is partly related to cytotoxic drugmetabolite which is primarily inactivated by the UGT1A1 enzyme.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	121-127
29072417-2	2017	The primary aim of the present research was tofind the correlation between UGT1A1-genotype and clinical toxicity of irinotecan.	Irinotecan	116-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
29072417-13	2017	Conclusions: UGT1A1 28*/28* is strongly associatedwith drug"s life-threatening toxicity even in a moderate dose of Irinotecan.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
28881286-6	2017	Moreover, via its effects on NF-kappaB, S06 effectively enhanced the sensitivity of the gastric cancer cells to irinotecan.	Irinotecan	112-122	nuclear factor kappa B subunit 1	Homo sapiens	29-38
28817371-1	2017	Purpose The objectives were to evaluate dosing schedules of labetuzumab govitecan, an antibody-drug conjugate targeting carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) for tumor delivery of 7-ethyl-10-hydroxycamptothecin (SN-38), in an expanded phase II trial of patients with relapsed or refractory metastatic colorectal cancer.	Irinotecan	210-240	CEA cell adhesion molecule 5	Homo sapiens	179-186
29066969-9	2017	Our findings suggest that the HNF1A rs2244608, or the tightly linked functional coding variant p.I27L, might be a potential prognostic marker with irinotecan-based regimens.	Irinotecan	147-157	HNF1 homeobox A	Homo sapiens	30-35
28679770-1	2017	Purpose: We evaluated a Trop-2-targeting antibody conjugated with SN-38 in metastatic small cell lung cancer (mSCLC) patients.Experimental Design: Sacituzumab govitecan was studied in patients with pretreated (median, 2; range, 1-7) mSCLC who received either 8 or 10 mg/kg i.v.	Irinotecan	66-71	tumor associated calcium signal transducer 2	Homo sapiens	24-30
28878234-4	2017	Here, we identified a novel relationship between IL-7R signaling and steroid-resistance, and showed that an anti-IL-7R antibody conjugated with SN-38 (A7R-ADC-SN-38) has strong anti-tumor effects against both parental and steroid-resistant malignant cells.	Irinotecan	144-149	interleukin 7 receptor	Mus musculus	49-54
28421347-11	2017	CPT-11 caused a significant increase in the expression of TLR4, IL-6, TNF-alpha, IL-1beta and caspase-3 mRNAs in the large intestine.	Irinotecan	0-6	toll-like receptor 4	Rattus norvegicus	58-62
28421347-11	2017	CPT-11 caused a significant increase in the expression of TLR4, IL-6, TNF-alpha, IL-1beta and caspase-3 mRNAs in the large intestine.	Irinotecan	0-6	interleukin 6	Rattus norvegicus	64-68
28421347-11	2017	CPT-11 caused a significant increase in the expression of TLR4, IL-6, TNF-alpha, IL-1beta and caspase-3 mRNAs in the large intestine.	Irinotecan	0-6	tumor necrosis factor	Rattus norvegicus	70-79
28421347-11	2017	CPT-11 caused a significant increase in the expression of TLR4, IL-6, TNF-alpha, IL-1beta and caspase-3 mRNAs in the large intestine.	Irinotecan	0-6	interleukin 1 beta	Rattus norvegicus	81-89
28421347-11	2017	CPT-11 caused a significant increase in the expression of TLR4, IL-6, TNF-alpha, IL-1beta and caspase-3 mRNAs in the large intestine.	Irinotecan	0-6	caspase 3	Rattus norvegicus	94-103
29262551-0	2017	The combination of temozolomide-irinotecan regresses a doxorubicin-resistant patient-derived orthotopic xenograft (PDOX) nude-mouse model of recurrent Ewing"s sarcoma with a FUS-ERG fusion and CDKN2A deletion: Direction for third-line patient therapy.	Irinotecan	32-42	fused in sarcoma	Mus musculus	174-177
29262551-0	2017	The combination of temozolomide-irinotecan regresses a doxorubicin-resistant patient-derived orthotopic xenograft (PDOX) nude-mouse model of recurrent Ewing"s sarcoma with a FUS-ERG fusion and CDKN2A deletion: Direction for third-line patient therapy.	Irinotecan	32-42	cyclin dependent kinase inhibitor 2A	Mus musculus	193-199
29066704-1	2017	We report 2 unusual cases of Stage IV rectal cancer for which pathological complete response was achieved with neoadjuvant chemotherapy(NAC)consisting of a combination of 5-fluorouracil(5-FU), oxaliplatin, Leucovorin(mFOLFOX6)or irinotecan(FOLFIRI), and bevacizumab, without radiotherapy.	Irinotecan	229-239	X-linked Kx blood group	Homo sapiens	136-139
28880238-0	2017	Implications of ABCG2 Expression on Irinotecan Treatment of Colorectal Cancer Patients: A Review.	Irinotecan	36-46	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	16-21
28880238-3	2017	The ATP-binding cassette (ABC) transporter ABCG2/breast cancer resistance protein (BRCP) through its function in xenobiotic clearance might play an important role in irinotecan resistance.	Irinotecan	166-176	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	43-48
28880238-3	2017	The ATP-binding cassette (ABC) transporter ABCG2/breast cancer resistance protein (BRCP) through its function in xenobiotic clearance might play an important role in irinotecan resistance.	Irinotecan	166-176	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	49-81
28880238-4	2017	With a goal to evaluate the clinical significance of ABCG2 measurements, we here review the current literature on ABCG2 in relation to irinotecan treatment in CRC patients.	Irinotecan	135-145	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	114-119
28880238-11	2017	In contrast, our recent exploratory study of ABCG2 mRNA expression in 580 patients with stage III primary CRC (subgroup from the randomized PETACC-3 study) indicated that high ABCG2 tumor tissue mRNA expression might be predictive for lack of efficacy of irinotecan.	Irinotecan	255-265	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	176-181
28880238-12	2017	CONCLUSION: The biological role of ABCG2 in predicting clinical irinotecan sensitivity/resistance in CRC is uncertain.	Irinotecan	64-74	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	35-40
28878234-4	2017	Here, we identified a novel relationship between IL-7R signaling and steroid-resistance, and showed that an anti-IL-7R antibody conjugated with SN-38 (A7R-ADC-SN-38) has strong anti-tumor effects against both parental and steroid-resistant malignant cells.	Irinotecan	144-149	interleukin 7 receptor	Mus musculus	113-118
28878234-4	2017	Here, we identified a novel relationship between IL-7R signaling and steroid-resistance, and showed that an anti-IL-7R antibody conjugated with SN-38 (A7R-ADC-SN-38) has strong anti-tumor effects against both parental and steroid-resistant malignant cells.	Irinotecan	159-164	interleukin 7 receptor	Mus musculus	49-54
28878234-4	2017	Here, we identified a novel relationship between IL-7R signaling and steroid-resistance, and showed that an anti-IL-7R antibody conjugated with SN-38 (A7R-ADC-SN-38) has strong anti-tumor effects against both parental and steroid-resistant malignant cells.	Irinotecan	159-164	interleukin 7 receptor	Mus musculus	113-118
28735070-0	2017	Suppression of the ATP-binding cassette transporter ABCC4 impairs neuroblastoma tumour growth and sensitises to irinotecan in vivo.	Irinotecan	112-122	ATP binding cassette subfamily C member 4	Homo sapiens	52-57
28711984-3	2017	Recently, the efficacy of combining CPT-11 and anti-epidermal growth factor receptor (EGFR) agents was confirmed in patients with KRAS wild-type metastatic colorectal cancer.	Irinotecan	36-42	KRAS proto-oncogene, GTPase	Homo sapiens	130-134
28735070-5	2017	Loss of Abcc4 in the Th-MYCN transgenic neuroblastoma mouse model did not impact tumour formation; however, Abcc4-null neuroblastomas were strongly sensitised to the ABCC4 substrate drug irinotecan.	Irinotecan	187-197	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	108-113
28735070-5	2017	Loss of Abcc4 in the Th-MYCN transgenic neuroblastoma mouse model did not impact tumour formation; however, Abcc4-null neuroblastomas were strongly sensitised to the ABCC4 substrate drug irinotecan.	Irinotecan	187-197	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	166-171
28894577-3	2017	The aim of the present study was to assess the feasibility and efficacy of irinotecan and cisplatin in the management of patients with vaginal squamous cell cancer (SCC).	Irinotecan	75-85	serpin family B member 3	Homo sapiens	165-168
28894577-11	2017	Thus, neoadjuvant chemotherapy with irinotecan combined with cisplatin is a feasible treatment for patients with early-stage vaginal SCC.	Irinotecan	36-46	serpin family B member 3	Homo sapiens	133-136
28850174-24	2017	For HER-2 negative people, all different two-and three-drug combinations including irinotecan, docetaxel, oxaliplatin or oral 5-FU prodrugs are valid treatment options for advanced gastric cancer, and consideration of the side effects of each regimen is essential in the treatment decision.	Irinotecan	83-93	erb-b2 receptor tyrosine kinase 2	Homo sapiens	4-9
28627611-0	2017	Epithelial-mesenchymal transition and cancer stem cell-like phenotype induced by Twist1 contribute to acquired resistance to irinotecan in colon cancer.	Irinotecan	125-135	twist family bHLH transcription factor 1	Homo sapiens	81-87
28548889-0	2017	Therapy of Advanced Non-Small-Cell Lung Cancer With an SN-38-Anti-Trop-2 Drug Conjugate, Sacituzumab Govitecan.	Irinotecan	55-60	tumor associated calcium signal transducer 2	Homo sapiens	66-72
28548889-2	2017	We studied sacituzumab govitecan (IMMU-132), a Trop-2 ADC, for the targeting of SN-38.	Irinotecan	80-85	tumor associated calcium signal transducer 2	Homo sapiens	47-53
28627611-5	2017	In the present study, we further investigated how Twist1 contribute to acquired resistance to irinotecan in colon cancer.	Irinotecan	94-104	twist family bHLH transcription factor 1	Homo sapiens	50-56
28627611-10	2017	Results showed that the LoVo/Twist1 cells perform a distinctly decreased sensitivity to irinotecan, downregulated expression of E-cadherin, upregulated expression of cluster of differentiation 44 (CD44), and a significant enhancement of invasion and migration potential by regulation of MMP2 compared with control cells.	Irinotecan	88-98	twist family bHLH transcription factor 1	Homo sapiens	29-35
28627611-11	2017	In contrast, the inhibition of Twist1 transfected with siRNA could enhance the irinotecan sensitivity in LoVo/CPT-11R cells and downregulate the expression of vimentin and CD44.	Irinotecan	79-89	twist family bHLH transcription factor 1	Homo sapiens	31-37
28627611-12	2017	Our data provide evidence that EMT and CSC-like phenotype induced by Twist1 contribute to acquire resistance to irinotecan and enhanced migration and invasion in colon cancer.	Irinotecan	112-122	twist family bHLH transcription factor 1	Homo sapiens	69-75
28120346-6	2017	Cytotoxicity studies show that compound 7d sensitizes the ABCG2-overexpressing cells to chemotherapeutic drugs mitoxantrone and SN-38, which are well-established substrates of the ABCG2 transporter.	Irinotecan	128-133	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	58-63
28120346-6	2017	Cytotoxicity studies show that compound 7d sensitizes the ABCG2-overexpressing cells to chemotherapeutic drugs mitoxantrone and SN-38, which are well-established substrates of the ABCG2 transporter.	Irinotecan	128-133	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	180-185
28397089-5	2017	Of these, 19 sets gave relatively good description of the effect of UGT1A1 *28 and SLCO1B1 c.521T&gt;C polymorphism on the SN-38 plasma concentration, neutropenia, and diarrhea observed in clinical studies reported mainly by Teft et al.	Irinotecan	123-128	solute carrier organic anion transporter family member 1B1	Homo sapiens	83-90
28542923-0	2017	The polysialic acid mimetics idarubicin and irinotecan stimulate neuronal survival and neurite outgrowth and signal via protein kinase C. Polysialic acid (PSA) is a large, negatively charged, linear homopolymer of alpha2-8-linked sialic acid residues.	Irinotecan	44-54	immunoglobulin binding protein 1	Homo sapiens	214-222
28542923-6	2017	Idarubicin and irinotecan stimulate neurite outgrowth and survival of cultured cerebellar neurons after oxidative stress via protein kinase C and Erk1/2 in a similar manner as colominic acid, whereas Fyn, casein kinase II and the phosphatase and tensin homolog are only involved in idarubicin and irinotecan-stimulated neurite outgrowth.	Irinotecan	15-25	mitogen-activated protein kinase 3	Homo sapiens	146-152
28542923-6	2017	Idarubicin and irinotecan stimulate neurite outgrowth and survival of cultured cerebellar neurons after oxidative stress via protein kinase C and Erk1/2 in a similar manner as colominic acid, whereas Fyn, casein kinase II and the phosphatase and tensin homolog are only involved in idarubicin and irinotecan-stimulated neurite outgrowth.	Irinotecan	15-25	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	200-203
28397089-9	2017	CONCLUSION: The VCS confirmed the importance of genetic polymorphisms of UGT1A1 *28 and SLCO1B1 c.521T&gt;C in the irinotecan induced side effects.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
28397089-9	2017	CONCLUSION: The VCS confirmed the importance of genetic polymorphisms of UGT1A1 *28 and SLCO1B1 c.521T&gt;C in the irinotecan induced side effects.	Irinotecan	115-125	solute carrier organic anion transporter family member 1B1	Homo sapiens	88-95
28749961-13	2017	In addition, FGF9 was also associated with irinotecan resistance and poor disease free survival.	Irinotecan	43-53	fibroblast growth factor 9	Homo sapiens	13-17
28749961-15	2017	CONCLUSION: Targeting the MAPK signal transduction pathway through the targeting of the FGF2, FGF9, MECOM, PLA2G4C and PRKACB might increase tumor responsiveness to irinotecan treatment.	Irinotecan	165-175	fibroblast growth factor 2	Homo sapiens	88-92
28749961-15	2017	CONCLUSION: Targeting the MAPK signal transduction pathway through the targeting of the FGF2, FGF9, MECOM, PLA2G4C and PRKACB might increase tumor responsiveness to irinotecan treatment.	Irinotecan	165-175	fibroblast growth factor 9	Homo sapiens	94-98
28749961-15	2017	CONCLUSION: Targeting the MAPK signal transduction pathway through the targeting of the FGF2, FGF9, MECOM, PLA2G4C and PRKACB might increase tumor responsiveness to irinotecan treatment.	Irinotecan	165-175	MDS1 and EVI1 complex locus	Homo sapiens	100-105
28749961-15	2017	CONCLUSION: Targeting the MAPK signal transduction pathway through the targeting of the FGF2, FGF9, MECOM, PLA2G4C and PRKACB might increase tumor responsiveness to irinotecan treatment.	Irinotecan	165-175	phospholipase A2 group IVC	Homo sapiens	107-114
28749961-15	2017	CONCLUSION: Targeting the MAPK signal transduction pathway through the targeting of the FGF2, FGF9, MECOM, PLA2G4C and PRKACB might increase tumor responsiveness to irinotecan treatment.	Irinotecan	165-175	protein kinase cAMP-activated catalytic subunit beta	Homo sapiens	119-125
28526406-4	2017	However, irinotecan-resistant SCLC cells, such as SBC-3/SN-38, were refractory to trastuzumab despite high HER2 expression.	Irinotecan	9-19	erb-b2 receptor tyrosine kinase 2	Homo sapiens	107-111
28207160-0	2017	Pharmacokinetic interactions in mice between irinotecan and MBL-II-141, an ABCG2 inhibitor.	Irinotecan	45-55	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	75-80
28526406-6	2017	Treatment with T-DM1 significantly suppressed the growth of SBC-3/SN-38 xenografts in mice compared with trastuzumab (P &lt; 0.05).	Irinotecan	66-71	immunoglobulin heavy diversity 1-7	Homo sapiens	17-20
27737534-0	2017	ERCC1 Expression-Based Randomized Phase II Study of Gemcitabine/Cisplatin Versus Irinotecan/Cisplatin in Patients with Advanced Non-small Cell Lung Cancer.	Irinotecan	81-91	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	0-5
28585035-0	2017	UGT1A1*6 polymorphisms are correlated with irinotecan-induced neutropenia: a systematic review and meta-analysis.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
28474802-0	2017	Rapid and sensitive detection of UGT1A1 polymorphisms associated with irinotecan toxicity by a novel DNA microarray.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
28474802-4	2017	It is established that the polymorphisms of UGT1A1*28 and UGT1A1*6 are significantly associated with severe toxicity induced by the anti-cancer drug irinotecan.	Irinotecan	149-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
28474802-4	2017	It is established that the polymorphisms of UGT1A1*28 and UGT1A1*6 are significantly associated with severe toxicity induced by the anti-cancer drug irinotecan.	Irinotecan	149-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
28074472-0	2017	Cost Evaluation of Irinotecan-Related Toxicities Associated With the UGT1A1*28 Patient Genotype.	Irinotecan	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
28677646-5	2017	EC50 values of 6-mercaptopurine or 7-Ethyl-10-hydroxy-camptothecin (SN-38) against cells expressing ABCC4 (WT) were also 1.4-2.0- or 1.9-fold higher than those against cells expressing the SNP variants of ABCC4 (K304N or E757K) or (K304N; P403L or E757K); respectively.	Irinotecan	68-73	ATP binding cassette subfamily C member 4	Homo sapiens	100-105
28677646-5	2017	EC50 values of 6-mercaptopurine or 7-Ethyl-10-hydroxy-camptothecin (SN-38) against cells expressing ABCC4 (WT) were also 1.4-2.0- or 1.9-fold higher than those against cells expressing the SNP variants of ABCC4 (K304N or E757K) or (K304N; P403L or E757K); respectively.	Irinotecan	68-73	ATP binding cassette subfamily C member 4	Homo sapiens	205-210
28074472-1	2017	The adoption of a preemptive UGT1A1*28 genotyping to increase irinotecan safety in clinical practice is still limited.	Irinotecan	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
28637434-1	2017	BACKGROUND: To evaluate a new UGT1A and DPYD polymorphism panel to better predict irinotecan-induced toxicity and the clinical response in Chinese patients with metastatic colorectal cancer (mCRC).	Irinotecan	82-92	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	30-35
28685075-3	2017	The aim of the present study was to evaluate the efficacy and adverse events (AE) of combination therapy with irinotecan and platinum (CPT-Pt) for ROC.	Irinotecan	110-120	choline phosphotransferase 1	Homo sapiens	135-138
28025786-1	2017	Genetic variability in KRAS and EGFR predicts response to cetuximab in irinotecan refractory colorectal cancer.	Irinotecan	71-81	KRAS proto-oncogene, GTPase	Homo sapiens	23-27
28025786-1	2017	Genetic variability in KRAS and EGFR predicts response to cetuximab in irinotecan refractory colorectal cancer.	Irinotecan	71-81	epidermal growth factor receptor	Homo sapiens	32-36
28069724-0	2017	Synthetic Lethality Exploitation by an Anti-Trop-2-SN-38 Antibody-Drug Conjugate, IMMU-132, Plus PARP Inhibitors in BRCA1/2-wild-type Triple-Negative Breast Cancer.	Irinotecan	51-56	tropomyosin 2, beta	Mus musculus	44-50
28291390-2	2017	Sacituzumab govitecan, an antibody-drug conjugate, targets Trop-2 for the selective delivery of SN-38, the active metabolite of irinotecan.	Irinotecan	96-101	tumor associated calcium signal transducer 2	Homo sapiens	59-65
28291390-2	2017	Sacituzumab govitecan, an antibody-drug conjugate, targets Trop-2 for the selective delivery of SN-38, the active metabolite of irinotecan.	Irinotecan	128-138	tumor associated calcium signal transducer 2	Homo sapiens	59-65
28804517-8	2017	It is imperative to check UGT1A1 gene status in all patients being considered for treatment with nanoliposomal irinotecan.	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
28968978-0	2017	Decoy receptor 1 (DCR1) promoter hypermethylation and response to irinotecan in metastatic colorectal cancer.	Irinotecan	66-76	TNF receptor superfamily member 10c	Homo sapiens	0-16
28968978-0	2017	Decoy receptor 1 (DCR1) promoter hypermethylation and response to irinotecan in metastatic colorectal cancer.	Irinotecan	66-76	TNF receptor superfamily member 10c	Homo sapiens	18-22
28968978-7	2017	In conclusion, DCR1 promoter hypermethylation status is a potential predictive biomarker for response to treatment with irinotecan, when combined with capecitabine.	Irinotecan	120-130	TNF receptor superfamily member 10c	Homo sapiens	15-19
28157715-0	2017	Combined use of irinotecan with histone deacetylase inhibitor belinostat could cause severe toxicity by inhibiting SN-38 glucuronidation via UGT1A1.	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
28157715-3	2017	This inhibitory effect was determined by measuring the formation rate of SN-38 glucuronide after SN-38 incubation with human recombinant UGT1A isoforms (1A1, 1A6, 1A7 and 1A9) and pooled human liver microsomes (HLM, wild type, UGT1A1*1*28 and UGT1A1*28*28 allelic variants), with and without HDACis.	Irinotecan	73-78	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	137-142
28157715-4	2017	The data showed that belinostat at 100 and 200 micromol/L inhibited SN-38 glucuronidation via UGT1A1 in a dose-dependent manner, causing significant decrease in Vmax and CLint (p &lt; 0.05) from 12.60 to 1.95 pmol/min/mg and 21.59 to 4.20 muL/min/mg protein respectively.	Irinotecan	68-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
28637434-1	2017	BACKGROUND: To evaluate a new UGT1A and DPYD polymorphism panel to better predict irinotecan-induced toxicity and the clinical response in Chinese patients with metastatic colorectal cancer (mCRC).	Irinotecan	82-92	dihydropyrimidine dehydrogenase	Homo sapiens	40-44
28637434-11	2017	In the first-line irinotecan-based treatment, UGT1A1*28 and DPYD*5 contributed to higher response rates (P = 0.043 and P = 0.019, respectively), while DPYD*5 was found to associate with better progression-free survival (P = 0.015).	Irinotecan	18-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
28637434-11	2017	In the first-line irinotecan-based treatment, UGT1A1*28 and DPYD*5 contributed to higher response rates (P = 0.043 and P = 0.019, respectively), while DPYD*5 was found to associate with better progression-free survival (P = 0.015).	Irinotecan	18-28	dihydropyrimidine dehydrogenase	Homo sapiens	60-66
28637434-11	2017	In the first-line irinotecan-based treatment, UGT1A1*28 and DPYD*5 contributed to higher response rates (P = 0.043 and P = 0.019, respectively), while DPYD*5 was found to associate with better progression-free survival (P = 0.015).	Irinotecan	18-28	dihydropyrimidine dehydrogenase	Homo sapiens	151-157
28637434-13	2017	CONCLUSION: Results still showed UGT1A1*6 and UGT1A1*28 to be partially associated with irinotecan-induced toxicity and clinical response.	Irinotecan	88-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
28637434-13	2017	CONCLUSION: Results still showed UGT1A1*6 and UGT1A1*28 to be partially associated with irinotecan-induced toxicity and clinical response.	Irinotecan	88-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
28502040-0	2017	UGT1A1 polymorphisms with irinotecan-induced toxicities and treatment outcome in Asians with Lung Cancer: a meta-analysis.	Irinotecan	26-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
28790841-0	2017	Relationship between UGT1A1*6/*28 gene polymorphisms and the efficacy and toxicity of irinotecan-based chemotherapy.	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
28790841-1	2017	PURPOSE: A retrospective study was performed to analyze the relationship between uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) *6/*28 gene polymorphisms and adverse reactions associated with irinotecan (CPT-11)-based chemotherapy.	Irinotecan	202-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-128
28790841-1	2017	PURPOSE: A retrospective study was performed to analyze the relationship between uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) *6/*28 gene polymorphisms and adverse reactions associated with irinotecan (CPT-11)-based chemotherapy.	Irinotecan	202-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
28790841-1	2017	PURPOSE: A retrospective study was performed to analyze the relationship between uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) *6/*28 gene polymorphisms and adverse reactions associated with irinotecan (CPT-11)-based chemotherapy.	Irinotecan	214-220	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-128
28790841-2	2017	The correlation between UGT1A1 polymorphisms and the clinical efficacy of CPT-11 was also analyzed, along with the influence of age and tumor type.	Irinotecan	74-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
28790841-5	2017	RESULTS: Colorectal cancer patients with the UGT1A1*6 mutant genotype had a significantly higher risk of severe delayed diarrhea than that of wild-type individuals when administered a CPT-11 dose &gt;=130 mg/m2 (P=0.042); the same phenomenon was observed when the UGT1A1*6 and UGT1A1*28 mutant genotypes were considered together (P=0.028).	Irinotecan	184-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
28790841-5	2017	RESULTS: Colorectal cancer patients with the UGT1A1*6 mutant genotype had a significantly higher risk of severe delayed diarrhea than that of wild-type individuals when administered a CPT-11 dose &gt;=130 mg/m2 (P=0.042); the same phenomenon was observed when the UGT1A1*6 and UGT1A1*28 mutant genotypes were considered together (P=0.028).	Irinotecan	184-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	264-270
28790841-5	2017	RESULTS: Colorectal cancer patients with the UGT1A1*6 mutant genotype had a significantly higher risk of severe delayed diarrhea than that of wild-type individuals when administered a CPT-11 dose &gt;=130 mg/m2 (P=0.042); the same phenomenon was observed when the UGT1A1*6 and UGT1A1*28 mutant genotypes were considered together (P=0.028).	Irinotecan	184-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	264-270
28790841-6	2017	However, in lung cancer patients administered a low dose of CPT-11, UGT1A1*6/*28 variants were not significantly associated with severe neutropenia or delayed diarrhea.	Irinotecan	60-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
28586388-10	2017	Two had partial responses by RECIST 1.1 on a clinical trial involving a PD-1 inhibitor + irinotecan (indicated by MLH1 alteration).	Irinotecan	89-99	mutL homolog 1	Homo sapiens	114-118
28502040-1	2017	Previous studies of irinotecan pharmacogenetics have shown that the UGT1A1*28 polymorphism has an effect on irinotecan (IRI)-induced toxicities in Caucasians.	Irinotecan	20-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
28502040-1	2017	Previous studies of irinotecan pharmacogenetics have shown that the UGT1A1*28 polymorphism has an effect on irinotecan (IRI)-induced toxicities in Caucasians.	Irinotecan	108-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
28502040-1	2017	Previous studies of irinotecan pharmacogenetics have shown that the UGT1A1*28 polymorphism has an effect on irinotecan (IRI)-induced toxicities in Caucasians.	Irinotecan	120-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
28695301-7	2017	The influence of the chemotherapy backbone on anti-EGFR mAb efficacy, evaluated with meta-regression, indicated a higher ORR with irinotecan-based versus oxaliplatin-based regimens, but comparable PFS and OS.	Irinotecan	130-140	epidermal growth factor receptor	Homo sapiens	51-55
28439659-3	2017	This report demonstrated the outcomes of adjuvant nimotuzumab, an EGFR inhibitor, with irinotecan in pediatric HGGs.	Irinotecan	87-97	epidermal growth factor receptor	Homo sapiens	66-70
28081962-1	2017	BACKGROUND: Adding cetuximab to FOLFIRI (5-fluorouracil, leucovorin, irinotecan) significantly improved progression-free survival (PFS), overall survival (OS), and objective response rate (ORR) in patients with KRAS or RAS (KRAS/NRAS, exons 2-4) wild-type (wt) metastatic colorectal cancer (mCRC) in the first-line CRYSTAL study.	Irinotecan	69-79	KRAS proto-oncogene, GTPase	Homo sapiens	211-215
28081962-1	2017	BACKGROUND: Adding cetuximab to FOLFIRI (5-fluorouracil, leucovorin, irinotecan) significantly improved progression-free survival (PFS), overall survival (OS), and objective response rate (ORR) in patients with KRAS or RAS (KRAS/NRAS, exons 2-4) wild-type (wt) metastatic colorectal cancer (mCRC) in the first-line CRYSTAL study.	Irinotecan	69-79	KRAS proto-oncogene, GTPase	Homo sapiens	224-228
28081962-1	2017	BACKGROUND: Adding cetuximab to FOLFIRI (5-fluorouracil, leucovorin, irinotecan) significantly improved progression-free survival (PFS), overall survival (OS), and objective response rate (ORR) in patients with KRAS or RAS (KRAS/NRAS, exons 2-4) wild-type (wt) metastatic colorectal cancer (mCRC) in the first-line CRYSTAL study.	Irinotecan	69-79	NRAS proto-oncogene, GTPase	Homo sapiens	229-233
28242239-0	2017	Role of Toll-like receptor 4 in drug-drug interaction between paclitaxel and irinotecan in vitro.	Irinotecan	77-87	toll like receptor 4	Homo sapiens	8-28
28242239-8	2017	Paclitaxel treatment increased the levels of irinotecan metabolites, SN-38 and SN-38 glucuronide (SN-38G) in TLR4-dependent manner.	Irinotecan	45-55	toll like receptor 4	Homo sapiens	109-113
28242239-9	2017	Paclitaxel-mediated induction of genes involved in irinotecan metabolism such as Cyp3a11 and Ugt1a1 was TLR4-dependent, while induction of the transporter Mrp2 was TLR4-independent.	Irinotecan	51-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
28242239-9	2017	Paclitaxel-mediated induction of genes involved in irinotecan metabolism such as Cyp3a11 and Ugt1a1 was TLR4-dependent, while induction of the transporter Mrp2 was TLR4-independent.	Irinotecan	51-61	toll like receptor 4	Homo sapiens	104-108
28340475-0	2017	Irinotecan Upregulates Fibroblast Growth Factor Receptor 3 Expression in Colorectal Cancer Cells, Which Mitigates Irinotecan-Induced Apoptosis.	Irinotecan	0-10	fibroblast growth factor receptor 3	Homo sapiens	23-58
28242239-8	2017	Paclitaxel treatment increased the levels of irinotecan metabolites, SN-38 and SN-38 glucuronide (SN-38G) in TLR4-dependent manner.	Irinotecan	79-84	toll like receptor 4	Homo sapiens	109-113
28242239-10	2017	These novel findings demonstrate that paclitaxel can affect irinotecan metabolism by a TLR4-dependent mechanism.	Irinotecan	60-70	toll like receptor 4	Homo sapiens	87-91
27938508-0	2017	Regorafenib Plus FOLFIRI With Irinotecan Dose Escalated According to Uridine Diphosphate Glucuronosyltransferase 1A1 Genotyping in Patients With Metastatic Colorectal Cancer.	Irinotecan	30-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-116
28279925-0	2017	Irinotecan binds to the internal cavity of beta-lactoglobulin: A multi-spectroscopic and computational investigation.	Irinotecan	0-10	beta-lactoglobulin	Bos taurus	43-61
28279925-3	2017	Molecular docking results were in full agreement with the results obtained from thermodynamic analysis of the fluorescence data indicating the existence of one binding site for irinotecan in beta-LG structure and revealed the hydrophobic nature of the interaction between irinotecan and the protein.	Irinotecan	177-187	beta-lactoglobulin	Bos taurus	191-198
28279925-3	2017	Molecular docking results were in full agreement with the results obtained from thermodynamic analysis of the fluorescence data indicating the existence of one binding site for irinotecan in beta-LG structure and revealed the hydrophobic nature of the interaction between irinotecan and the protein.	Irinotecan	272-282	beta-lactoglobulin	Bos taurus	191-198
28279925-4	2017	The binding distance between beta-LG and irinotecan, r, was estimated to be 5.74nm based on the Forster"s theory of non-radiative energy transfer.	Irinotecan	41-51	beta-lactoglobulin	Bos taurus	29-36
28279925-6	2017	Based on the experimental data and the possible binding mode revealed by molecular docking study, we concluded that irinotecan binds to the hydrophobic calyx of beta-LG with induction of some alterations in the secondary and tertiary structure of the protein.	Irinotecan	116-126	beta-lactoglobulin	Bos taurus	161-168
27938508-8	2017	Our findings indicate that regorafenib plus FOLFIRI with irinotecan dose escalation based on UGT1A1 genotyping in previously treated patients with mCRC and with UGT1A1*1/*1 and UGT1A1*1/*28 genotypes is clinically effective and yields improved oncological outcomes.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
28442401-9	2017	In sum, our findings indicate that TRIB3 plays an anti-apoptotic role in doxorubicin-treated gastric cancer cell lines, perhaps indicating that the status of TRIB3 expression in response to anticancer drugs, such as doxorubicin, irinotecan or oxaliplatin, may reflect the efficiency for cancer therapy.	Irinotecan	229-239	tribbles pseudokinase 3	Homo sapiens	35-40
28596680-12	2017	AXL silencing showed a subtle trend to restore colon cancer cell sensitivity to 5FU or irinotecan.	Irinotecan	87-97	AXL receptor tyrosine kinase	Homo sapiens	0-3
28442401-9	2017	In sum, our findings indicate that TRIB3 plays an anti-apoptotic role in doxorubicin-treated gastric cancer cell lines, perhaps indicating that the status of TRIB3 expression in response to anticancer drugs, such as doxorubicin, irinotecan or oxaliplatin, may reflect the efficiency for cancer therapy.	Irinotecan	229-239	tribbles pseudokinase 3	Homo sapiens	158-163
27641154-7	2017	Polymorphisms in DPYD, TPMT, and UGT1A1 have been described that have a major impact on the pharmacokinetics of 5-fluorouracil, mercaptopurine, and irinotecan, respectively.	Irinotecan	148-158	dihydropyrimidine dehydrogenase	Homo sapiens	17-21
28468698-8	2017	The proposed method was successfully applied to the determination of irinotecan in tap water, river water, and urine samples spiked with 10.20 mg/L for the water samples and 8.32 mg/L for the urine sample.	Irinotecan	69-79	nuclear RNA export factor 1	Homo sapiens	83-86
28468698-9	2017	The average recovery values of irinotecan determined were 99.1% for tap water, 109.4% for river water, and 96.1% for urine.	Irinotecan	31-41	nuclear RNA export factor 1	Homo sapiens	68-71
28414297-4	2017	In a KRAS-induced orthotopic PDAC model, coadministration of iRGD enhanced the uptake of an irinotecan-loaded silicasome carrier that comprises lipid bilayer-coated mesoporous silica nanoparticles (MSNPs); this uptake resulted in enhanced survival and markedly reduced metastasis.	Irinotecan	92-102	KRAS proto-oncogene, GTPase	Homo sapiens	5-9
28265824-0	2017	Relationship between magnetic resonance imaging characteristics and plasmatic levels of MMP2 and MMP9 in patients with recurrent high-grade gliomas treated by Bevacizumab and Irinotecan.	Irinotecan	175-185	matrix metallopeptidase 2	Homo sapiens	88-92
28265824-0	2017	Relationship between magnetic resonance imaging characteristics and plasmatic levels of MMP2 and MMP9 in patients with recurrent high-grade gliomas treated by Bevacizumab and Irinotecan.	Irinotecan	175-185	matrix metallopeptidase 9	Homo sapiens	97-101
28267710-0	2017	Dasatinib synergises with irinotecan to suppress hepatocellular carcinoma via inhibiting the protein synthesis of PLK1.	Irinotecan	26-36	polo like kinase 1	Homo sapiens	114-118
28267710-14	2017	CONCLUSIONS: Dasatinib is able to reinforce the anti-HCC efficacy of irinotecan/SN38 by downregulation of PLK1 synthesis.	Irinotecan	69-79	polo like kinase 1	Homo sapiens	106-110
28388962-9	2017	Concomitantly, CPT-11 enhanced tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels and inducible nitric oxide synthase (iNOS) gene expression, associated with an increase in the total number macrophages (positive cells for ionized calcium-binding adapter molecule, Iba-1) and degranulated mast cells in the small intestine segments and caused significant weight loss.	Irinotecan	15-21	tumor necrosis factor	Mus musculus	60-69
28388962-9	2017	Concomitantly, CPT-11 enhanced tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels and inducible nitric oxide synthase (iNOS) gene expression, associated with an increase in the total number macrophages (positive cells for ionized calcium-binding adapter molecule, Iba-1) and degranulated mast cells in the small intestine segments and caused significant weight loss.	Irinotecan	15-21	interleukin 6	Mus musculus	75-88
26245851-0	2017	Phase II study of cetuximab with irinotecan for KRAS wild-type colorectal cancer in Japanese patients.	Irinotecan	33-43	KRAS proto-oncogene, GTPase	Homo sapiens	48-52
28288854-0	2017	Irinotecan-induced bile acid malabsorption is associated with down-regulation of ileal Asbt (Slc10a2) in mice.	Irinotecan	0-10	solute carrier family 10, member 2	Mus musculus	93-100
28220486-1	2017	The addition of irinotecan to an epidermal growth factor receptor (EGFR) antibody has previously been shown to improve tumor response rate and time to progression but not overall survival (OS) for refractory metastatic colorectal cancer (mCRC).	Irinotecan	16-26	epidermal growth factor receptor	Homo sapiens	33-65
28220486-1	2017	The addition of irinotecan to an epidermal growth factor receptor (EGFR) antibody has previously been shown to improve tumor response rate and time to progression but not overall survival (OS) for refractory metastatic colorectal cancer (mCRC).	Irinotecan	16-26	epidermal growth factor receptor	Homo sapiens	67-71
28131876-5	2017	Cabozantinib, at non-toxic concentrations (3 or 5muM), sensitized the ABCG2-overexpressing cells to mitoxantrone, SN-38, and topotecan.	Irinotecan	114-119	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	70-75
28388962-9	2017	Concomitantly, CPT-11 enhanced tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels and inducible nitric oxide synthase (iNOS) gene expression, associated with an increase in the total number macrophages (positive cells for ionized calcium-binding adapter molecule, Iba-1) and degranulated mast cells in the small intestine segments and caused significant weight loss.	Irinotecan	15-21	interleukin 6	Mus musculus	90-94
28388962-9	2017	Concomitantly, CPT-11 enhanced tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels and inducible nitric oxide synthase (iNOS) gene expression, associated with an increase in the total number macrophages (positive cells for ionized calcium-binding adapter molecule, Iba-1) and degranulated mast cells in the small intestine segments and caused significant weight loss.	Irinotecan	15-21	nitric oxide synthase 2, inducible	Mus musculus	107-138
28388962-9	2017	Concomitantly, CPT-11 enhanced tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels and inducible nitric oxide synthase (iNOS) gene expression, associated with an increase in the total number macrophages (positive cells for ionized calcium-binding adapter molecule, Iba-1) and degranulated mast cells in the small intestine segments and caused significant weight loss.	Irinotecan	15-21	nitric oxide synthase 2, inducible	Mus musculus	140-144
28388962-9	2017	Concomitantly, CPT-11 enhanced tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels and inducible nitric oxide synthase (iNOS) gene expression, associated with an increase in the total number macrophages (positive cells for ionized calcium-binding adapter molecule, Iba-1) and degranulated mast cells in the small intestine segments and caused significant weight loss.	Irinotecan	15-21	induction of brown adipocytes 1	Mus musculus	285-290
27834032-9	2017	CD107a+/ROSlow cells were enriched in HT29 and DLD1 cultures after treatments with oxaliplatin, 5-fluorouracil, and the irinotecan metabolite SN38.	Irinotecan	120-130	lysosomal associated membrane protein 1	Homo sapiens	0-6
28314987-0	2017	Cooperative inhibitory effects of uremic toxins and other serum components on OATP1B1-mediated transport of SN-38.	Irinotecan	108-113	solute carrier organic anion transporter family member 1B1	Homo sapiens	78-85
28314987-2	2017	Uremic toxins (UTs), which accumulate in the serum of ESKD patients, were reported to inhibit organic anion-transporting polypeptide (OATP) 1B1-mediated uptake of SN-38; however, the relevance of this finding in a clinical setting is unknown.	Irinotecan	163-168	solute carrier organic anion transporter family member 1B1	Homo sapiens	94-143
28314987-3	2017	This study focused on cooperative effects of serum components and UTs on OATP1B1-mediated transport of SN-38.	Irinotecan	103-108	solute carrier organic anion transporter family member 1B1	Homo sapiens	73-80
28314987-4	2017	METHODS: Uptake of SN-38 by OATP1B1 was evaluated using cells stably expressing OATP1B1.	Irinotecan	19-24	solute carrier organic anion transporter family member 1B1	Homo sapiens	28-35
28314987-4	2017	METHODS: Uptake of SN-38 by OATP1B1 was evaluated using cells stably expressing OATP1B1.	Irinotecan	19-24	solute carrier organic anion transporter family member 1B1	Homo sapiens	80-87
28314987-7	2017	RESULTS: Uptake clearance of SN-38 in OATP1B1 cells decreased by 40% in the presence of uremic serum residue with albumin compared to that in the presence of normal serum residue.	Irinotecan	29-34	solute carrier organic anion transporter family member 1B1	Homo sapiens	38-45
28314987-10	2017	CONCLUSIONS: Hepatic uptake of SN-38 via OATP1B1 decreases in ESKD patients through cooperative inhibitory effects of UTs and serum components.	Irinotecan	31-36	solute carrier organic anion transporter family member 1B1	Homo sapiens	41-48
27641154-7	2017	Polymorphisms in DPYD, TPMT, and UGT1A1 have been described that have a major impact on the pharmacokinetics of 5-fluorouracil, mercaptopurine, and irinotecan, respectively.	Irinotecan	148-158	thiopurine S-methyltransferase	Homo sapiens	23-27
27641154-7	2017	Polymorphisms in DPYD, TPMT, and UGT1A1 have been described that have a major impact on the pharmacokinetics of 5-fluorouracil, mercaptopurine, and irinotecan, respectively.	Irinotecan	148-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
28443467-3	2017	In this study, the effect of irinotecan on high-mobility group protein B1 and MMP9 content, gene expression, cell cycle, and cell growth in human breast cancer cells (MCF-7) was investigated.	Irinotecan	29-39	high mobility group box 1	Homo sapiens	43-73
28087739-6	2017	Downregulation of RIP1 in a xenograft model impaired tumor growth inhibition from SN38 treatment, suggesting the potential of RIP1 to determine the clinical outcome of irinotecan treatment.	Irinotecan	168-178	receptor interacting serine/threonine kinase 1	Homo sapiens	18-22
28262261-3	2017	This review presents the usefulness of pharmacogenetic tests for some key applications: dihydropyrimidine dehydrogenase (DPYD) genotyping for fluoropyrimidine (5-fluorouracil, capecitabine), UDP glucuronosylstransferase (UGT1A1) for irinotecan and thiopurine S-methyltransferase (TPMT) for thiopurine drugs.	Irinotecan	233-243	dihydropyrimidine dehydrogenase	Homo sapiens	88-119
28262261-3	2017	This review presents the usefulness of pharmacogenetic tests for some key applications: dihydropyrimidine dehydrogenase (DPYD) genotyping for fluoropyrimidine (5-fluorouracil, capecitabine), UDP glucuronosylstransferase (UGT1A1) for irinotecan and thiopurine S-methyltransferase (TPMT) for thiopurine drugs.	Irinotecan	233-243	dihydropyrimidine dehydrogenase	Homo sapiens	121-125
28443467-3	2017	In this study, the effect of irinotecan on high-mobility group protein B1 and MMP9 content, gene expression, cell cycle, and cell growth in human breast cancer cells (MCF-7) was investigated.	Irinotecan	29-39	matrix metallopeptidase 9	Homo sapiens	78-82
28443467-9	2017	Irinotecan decreased H3K9 acetylation and increased poly ADP-ribose polymerase fragmentation to 89 kDa and anion superoxide production suggesting induction of apoptosis in these cells.	Irinotecan	0-10	poly(ADP-ribose) polymerase 1	Homo sapiens	52-78
28443467-11	2017	From the results, it is concluded that overexpression of high-mobility group protein B1 in the presence of irinotecan precedes breast cancer cells into apoptosis and in this response the binding of irinotecan to chromatin or high-mobility group protein B1 may condense/aggregate chromatin, preventing high-mobility group protein B1 release from chromatin.	Irinotecan	107-117	high mobility group box 1	Homo sapiens	57-87
28443467-11	2017	From the results, it is concluded that overexpression of high-mobility group protein B1 in the presence of irinotecan precedes breast cancer cells into apoptosis and in this response the binding of irinotecan to chromatin or high-mobility group protein B1 may condense/aggregate chromatin, preventing high-mobility group protein B1 release from chromatin.	Irinotecan	198-208	high mobility group box 1	Homo sapiens	57-87
28278081-0	2017	Correlative analysis of plasma SN-38 levels and DPD activity with outcomes of FOLFIRI regimen for metastatic colorectal cancer with UGT1A1 *28 and *6 wild type and its implication for individualized chemotherapy.	Irinotecan	31-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	132-138
29069732-5	2017	Secondly, based on the concept of a bi-therapy targeting in pHGGs mTORC1 (rapamycin) and HIF-1alpha (irinotecan), we hypothesized that the balanced expressions between RAS/ERK, PI3K/AKT and HIF-1alpha/HIF-2alpha/MYC proteins or genes may provide a modulation of the cell response to this double targeting.	Irinotecan	101-111	hypoxia inducible factor 1 subunit alpha	Homo sapiens	89-99
28278081-1	2017	It remains uncertain whether there is an correlation between clinical pharmacokinetic parameters and outcomes for metastatic colorectal cancer especially with UGT1A1 *28 and *6 wild type (*1/*1-*1/*1) for serious events associated with Irinotecan are largely excluded.	Irinotecan	236-246	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
28278081-2	2017	This study retrospectively analyzed the relationship between Irinotecan metabolite levels and outcomes of UGT1A1 *1/*1-*1/*1 genotype arrangement.	Irinotecan	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
28278081-8	2017	Therefore, plasma SN-38 levels is related to outcomes for UGT1A1 *1/*1-*1/*1 genotype, to improve efficacy, patients with CSN-38 1.5 h lower than 50.24 ng/ml, CPT-11 dosage could be added in next chemmotherapy on SN-38 plasma level monitoring.	Irinotecan	18-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
28255900-9	2017	The differences between HSPC1 inhibitors were also reflected in combination treatment-17-DMAG was more effective compared with NVP-AUY922 in potentiating the cytotoxic effects of 5-fluorouracil, oxaliplatin and irinotecan.	Irinotecan	211-221	heat shock protein 90 alpha family class A member 1	Homo sapiens	24-29
28000054-11	2017	Furthermore, 5-FU retains its ability to cause nuclear accumulation of p53 in the presence of irinotecan or topotecan.	Irinotecan	94-104	tumor protein p53	Homo sapiens	71-74
28280378-0	2017	UGT1A1 polymorphisms in cancer: impact on irinotecan treatment.	Irinotecan	42-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
28126414-3	2017	hCE1 is known to play crucial roles in the metabolism of a wide variety of endogenous esters, clinical drugs and insecticides, while hCE2 plays a key role in the metabolic activation of anticancer agents including irinotecan and capecitabine.	Irinotecan	214-224	carboxylesterase 2	Homo sapiens	133-137
28131902-0	2017	CQ synergistically sensitizes human colorectal cancer cells to SN-38/CPT-11 through lysosomal and mitochondrial apoptotic pathway via p53-ROS cross-talk.	Irinotecan	63-68	tumor protein p53	Homo sapiens	134-137
28131902-0	2017	CQ synergistically sensitizes human colorectal cancer cells to SN-38/CPT-11 through lysosomal and mitochondrial apoptotic pathway via p53-ROS cross-talk.	Irinotecan	69-75	tumor protein p53	Homo sapiens	134-137
28131902-4	2017	Notably, another autophagy inhibitor chloroquine (CQ) synergistically enhanced the anti-tumor activity of SN-38 in CRC cells with wild type (WT) p53.	Irinotecan	106-111	tumor protein p53	Homo sapiens	145-148
28131902-5	2017	Subsequently, we identified a potential mechanism of this cooperative interaction by showing that CQ and SN-38 acted together to trigger reactive oxygen species (ROS) burst, upregulate p53 expression, elicit the loss of lysosomal membrane potential (LMP) and mitochondrial membrane potential ( psim).	Irinotecan	105-110	tumor protein p53	Homo sapiens	185-188
28131902-6	2017	In addition, ROS induced by CQ plus SN-38 upregulated p53 levels by activating p38, conversely, p53 stimulated ROS.	Irinotecan	36-41	tumor protein p53	Homo sapiens	54-57
28131902-6	2017	In addition, ROS induced by CQ plus SN-38 upregulated p53 levels by activating p38, conversely, p53 stimulated ROS.	Irinotecan	36-41	mitogen-activated protein kinase 14	Homo sapiens	79-82
28131902-9	2017	Altogether, all results suggested that CQ synergistically sensitized human CRC cells with WT p53 to SN-38 through lysosomal and mitochondrial apoptotic pathway via p53-ROS cross-talk.	Irinotecan	100-105	tumor protein p53	Homo sapiens	93-96
27169843-7	2017	In tumor specimens, cytoplasmic accumulation of BLM correlates with DNA damage and gammaH2AX and phosphorylated ATM foci and predicts long-term progression-free survival in metastatic patients treated with irinotecan.	Irinotecan	206-216	BLM RecQ like helicase	Homo sapiens	48-51
27169843-7	2017	In tumor specimens, cytoplasmic accumulation of BLM correlates with DNA damage and gammaH2AX and phosphorylated ATM foci and predicts long-term progression-free survival in metastatic patients treated with irinotecan.	Irinotecan	206-216	ATM serine/threonine kinase	Homo sapiens	112-115
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	175-180	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	175-180	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	182-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	182-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	233-243	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
28280378-3	2017	Among them, UGT1A1*28 and UGT1A1*6 have been reported to be associated with severe toxicities in patients treated with irinotecan-based chemotherapy by increasing the dose of SN-38 (7-ethyl-10-hydroxycamptothecin), an active form of irinotecan.	Irinotecan	233-243	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
28280378-4	2017	Many association studies and meta-analyses have demonstrated the contribution of UGT1A1*28 and UGT1A1*6 polymorphisms to the toxicities caused by irinotecan-based therapy.	Irinotecan	146-156	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
28367249-0	2017	Predictive Value of UGT1A1*28 Polymorphism In Irinotecan-based Chemotherapy.	Irinotecan	46-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
28367249-1	2017	The UGT1A1*28 polymorphism was suggested to be significantly connected with irinotecan-induced toxicity and response to chemotherapy.	Irinotecan	76-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
28280378-4	2017	Many association studies and meta-analyses have demonstrated the contribution of UGT1A1*28 and UGT1A1*6 polymorphisms to the toxicities caused by irinotecan-based therapy.	Irinotecan	146-156	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
28367249-3	2017	Hence we carried out a meta-analysis to investigate the effect of UGT1A1*28 polymorphism on severe diarrhea, neutropenia, and response of patients who had undergone irinotecan-based chemotherapy.	Irinotecan	165-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
28173214-0	2017	UGT1A1 polymorphism as a prognostic indicator of stage I ovarian clear cell carcinoma patients treated with irinotecan.	Irinotecan	108-118	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
28367249-10	2017	Our data showed that the UGT1A1*28 polymorphism had a significant relationship with toxicity and response to irinotecan-based chemotherapy.	Irinotecan	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
28112927-1	2017	Carboxylesterases (CEs) are ubiquitous enzymes that are responsible for the metabolism of xenobiotics, including drugs such as irinotecan and oseltamivir.	Irinotecan	127-137	carboxylesterase 1	Homo sapiens	0-17
28180300-5	2017	Subsequent treatment of irinotecan-resistant, but not parental, CRC cells with histone deacetylase (HDAC) inhibitors can effectively overcome resistance.	Irinotecan	24-34	histone deacetylase 9	Homo sapiens	79-98
28180300-5	2017	Subsequent treatment of irinotecan-resistant, but not parental, CRC cells with histone deacetylase (HDAC) inhibitors can effectively overcome resistance.	Irinotecan	24-34	histone deacetylase 9	Homo sapiens	100-104
28180300-8	2017	These findings identify perturbed chromatin acetylation in irinotecan resistance and establish HDAC inhibitors as potential therapeutic means to overcome resistance.	Irinotecan	59-69	histone deacetylase 9	Homo sapiens	95-99
27507617-1	2017	Purpose:UGT1A1*28 confers a higher risk of toxicity in patients treated with irinotecan.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
27507617-3	2017	We aimed to identify the MTD of irinotecan in patients with metastatic colorectal cancer (mCRC) with *1/*1 and *1/*28 genotypes treated with FOLFIRI plus bevacizumab, and to determine whether bevacizumab alters irinotecan pharmacokinetics.Experimental Design: Previously untreated patients with mCRC (25 *1/*1; 23 *1/*28) were given FOLFIRI plus bevacizumab every 2 weeks.	Irinotecan	32-42	metallothionein 1E	Homo sapiens	25-28
27507617-3	2017	We aimed to identify the MTD of irinotecan in patients with metastatic colorectal cancer (mCRC) with *1/*1 and *1/*28 genotypes treated with FOLFIRI plus bevacizumab, and to determine whether bevacizumab alters irinotecan pharmacokinetics.Experimental Design: Previously untreated patients with mCRC (25 *1/*1; 23 *1/*28) were given FOLFIRI plus bevacizumab every 2 weeks.	Irinotecan	211-221	metallothionein 1E	Homo sapiens	25-28
27507617-4	2017	The irinotecan dose was escalated using a 3 + 3 design in each genotype group as follows: 260, 310, and 370 mg/m2 The MTD was the highest dose at which &lt;4/10 patients had a dose-limiting toxicity (DLT).	Irinotecan	4-14	metallothionein 1E	Homo sapiens	118-121
27507617-8	2017	Changes in the AUCs of irinotecan and SN-38 associated with bevacizumab treatment were marginal.Conclusions: The MTD of irinotecan in FOLFIRI plus bevacizumab is 310 mg/m2 for UGT1A1 *1/*1 patients and 260 mg/m2 for *1/*28 patients.	Irinotecan	120-130	metallothionein 1E	Homo sapiens	113-116
27507617-8	2017	Changes in the AUCs of irinotecan and SN-38 associated with bevacizumab treatment were marginal.Conclusions: The MTD of irinotecan in FOLFIRI plus bevacizumab is 310 mg/m2 for UGT1A1 *1/*1 patients and 260 mg/m2 for *1/*28 patients.	Irinotecan	120-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	176-182
28052029-8	2017	Moreover, RLYE showed a synergistic effect of the cytotoxic agent irinotecan on tumor cell apoptosis and tumor progression via tumor vessel normalization due to stabilization of VE-cadherin-mediated adherens junction, improvement of pericyte coverage, and inhibition of vascular leakage in tumors.	Irinotecan	66-76	cadherin 5	Mus musculus	178-189
28173214-1	2017	We investigated whether UGT1A1 polymorphisms are associated with the prognosis of ovarian cancer patients treated with irinotecan.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
28173214-7	2017	We conclude that UGT1A1 polymorphisms have the potential to be a prognostic marker of irinotecan treatment.	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
27060453-0	2017	Inhibition of NF-kappaB and metastasis in irinotecan (CPT-11)-resistant LoVo colon cancer cells by thymoquinone via JNK and p38.	Irinotecan	42-52	mitogen-activated protein kinase 1	Homo sapiens	124-127
28011980-0	2017	Potential safety concerns of TLR4 antagonism with irinotecan: a preclinical observational report.	Irinotecan	50-60	toll-like receptor 4	Rattus norvegicus	29-33
28011980-1	2017	PURPOSE: Irinotecan-induced gut toxicity is mediated in part by Toll-Like receptor 4 (TLR4) signalling.	Irinotecan	9-19	toll-like receptor 4	Rattus norvegicus	64-84
28011980-1	2017	PURPOSE: Irinotecan-induced gut toxicity is mediated in part by Toll-Like receptor 4 (TLR4) signalling.	Irinotecan	9-19	toll-like receptor 4	Rattus norvegicus	86-90
28011980-2	2017	The primary purpose of this preclinical study was to determine whether blocking TLR4 signalling by administering (-)-naloxone, a TLR4 antagonist, would improve irinotecan-induced gut toxicity.	Irinotecan	160-170	toll-like receptor 4	Rattus norvegicus	80-84
27770239-0	2017	Irinotecan-induced mucositis: the interactions and potential role of GLP-2 analogues.	Irinotecan	0-10	glucagon	Homo sapiens	69-74
27060453-0	2017	Inhibition of NF-kappaB and metastasis in irinotecan (CPT-11)-resistant LoVo colon cancer cells by thymoquinone via JNK and p38.	Irinotecan	54-60	mitogen-activated protein kinase 1	Homo sapiens	124-127
27060453-5	2017	Irinotecan resistant (CPT-11-R) LoVo colon cancer cell line was previous constructed by step-wise CPT-11 challenges to un-treated parental LoVo cells and expresses EGFR/IKKalpha/beta/NF-kappaB pathway.	Irinotecan	0-10	epidermal growth factor receptor	Homo sapiens	164-168
27060453-5	2017	Irinotecan resistant (CPT-11-R) LoVo colon cancer cell line was previous constructed by step-wise CPT-11 challenges to un-treated parental LoVo cells and expresses EGFR/IKKalpha/beta/NF-kappaB pathway.	Irinotecan	0-10	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	169-182
27060453-5	2017	Irinotecan resistant (CPT-11-R) LoVo colon cancer cell line was previous constructed by step-wise CPT-11 challenges to un-treated parental LoVo cells and expresses EGFR/IKKalpha/beta/NF-kappaB pathway.	Irinotecan	22-28	epidermal growth factor receptor	Homo sapiens	164-168
27060453-5	2017	Irinotecan resistant (CPT-11-R) LoVo colon cancer cell line was previous constructed by step-wise CPT-11 challenges to un-treated parental LoVo cells and expresses EGFR/IKKalpha/beta/NF-kappaB pathway.	Irinotecan	22-28	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	169-182
29956901-11	2017	CONCLUSION: SXD could significantly reduce irinotecan-induced hematological and gastrointestinaltoxicities in UGT1A1*28 or *6 variant patients (high risk group), while this treatment didn"t affect clinicalresponse of chemotherapy.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
27324368-7	2017	In vivo data were in agreement with Ki67 staining, showing a significantly lower percentage of Ki67-positive cells in the irinotecan group as compared with other groups (p &lt;= 0.0001).	Irinotecan	122-132	antigen identified by monoclonal antibody Ki 67	Mus musculus	36-40
27324368-7	2017	In vivo data were in agreement with Ki67 staining, showing a significantly lower percentage of Ki67-positive cells in the irinotecan group as compared with other groups (p &lt;= 0.0001).	Irinotecan	122-132	antigen identified by monoclonal antibody Ki 67	Mus musculus	95-99
27324368-8	2017	Tumor expression of thymidine kinase 1 phosphorylated on serine 13, thymidylate synthase, and thymidine phosphorylase remained unaffected, while thymidine kinase 1 expression was, surprisingly, significantly higher in irinotecan-treated animals (p &lt;= 0.01).	Irinotecan	218-228	thymidine kinase 1	Mus musculus	145-163
28395759-2	2017	Patients were stratified by their pharmacogenetic/phenotypic status: the irinotecan dose was adjusted according to the number of TA tandem repeats in the UGT1A1 promoter, while the 5-fluorouracil (5-FU) dose was initially adjusted according to dihydropyrimidine dehydrogenase (DPD) activity at initial screening (5-FUODPM Tox) followed by PK-guided dose optimization (5-FUODPM Protocol).	Irinotecan	73-83	dihydropyrimidine dehydrogenase	Homo sapiens	244-275
28395759-2	2017	Patients were stratified by their pharmacogenetic/phenotypic status: the irinotecan dose was adjusted according to the number of TA tandem repeats in the UGT1A1 promoter, while the 5-fluorouracil (5-FU) dose was initially adjusted according to dihydropyrimidine dehydrogenase (DPD) activity at initial screening (5-FUODPM Tox) followed by PK-guided dose optimization (5-FUODPM Protocol).	Irinotecan	73-83	dihydropyrimidine dehydrogenase	Homo sapiens	277-280
28395759-2	2017	Patients were stratified by their pharmacogenetic/phenotypic status: the irinotecan dose was adjusted according to the number of TA tandem repeats in the UGT1A1 promoter, while the 5-fluorouracil (5-FU) dose was initially adjusted according to dihydropyrimidine dehydrogenase (DPD) activity at initial screening (5-FUODPM Tox) followed by PK-guided dose optimization (5-FUODPM Protocol).	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
28395759-2	2017	Patients were stratified by their pharmacogenetic/phenotypic status: the irinotecan dose was adjusted according to the number of TA tandem repeats in the UGT1A1 promoter, while the 5-fluorouracil (5-FU) dose was initially adjusted according to dihydropyrimidine dehydrogenase (DPD) activity at initial screening (5-FUODPM Tox) followed by PK-guided dose optimization (5-FUODPM Protocol).	Irinotecan	73-83	thymocyte selection associated high mobility group box	Homo sapiens	322-325
28011495-8	2017	Granulocyte colony-stimulating factor (G-CSF) in serum was elevated at 5.6 pg/ml, which further raised to 43 pg/ml one week after FOLFIRINOX chemotherapy (oxaliplatin, irinotecan, 5-fluorouracil), while WBC decreased from 103.3 G/l to 59.3 G/l.	Irinotecan	168-178	colony stimulating factor 3	Homo sapiens	0-37
27650103-7	2017	P-selectin expression decreased significantly in the jejunum following irinotecan.	Irinotecan	71-81	selectin P	Rattus norvegicus	0-10
27650103-10	2017	CONCLUSIONS: Irinotecan induced a significant alteration in CAM expression in the jejunum and colon.	Irinotecan	13-23	calmodulin 1	Rattus norvegicus	60-63
27959571-9	2017	These RDT-coated nanoparticles (RDT-NP) were further used for preferential delivery of Irinotecan, a chemotherapeutic agent, to cells overexpressing HB-EGF.	Irinotecan	87-97	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1	Homo sapiens	6-9
27959571-9	2017	These RDT-coated nanoparticles (RDT-NP) were further used for preferential delivery of Irinotecan, a chemotherapeutic agent, to cells overexpressing HB-EGF.	Irinotecan	87-97	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1	Homo sapiens	32-35
27959571-10	2017	We show that receptor-mediated enhanced uptake of RDT-NPs increases the potency of irinotecan in these cells.	Irinotecan	83-93	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1	Homo sapiens	50-53
28011495-8	2017	Granulocyte colony-stimulating factor (G-CSF) in serum was elevated at 5.6 pg/ml, which further raised to 43 pg/ml one week after FOLFIRINOX chemotherapy (oxaliplatin, irinotecan, 5-fluorouracil), while WBC decreased from 103.3 G/l to 59.3 G/l.	Irinotecan	168-178	colony stimulating factor 3	Homo sapiens	39-44
29098099-0	2017	Life-Threatening Irinotecan-Induced Toxicity in an Adult Patient with Alveolar Rhabdomyosarcoma: The Role of a UGT1A1 Polymorphism.	Irinotecan	17-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
29098099-7	2017	The analysis of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene revealed homozygous UGT1A1 *28 polymorphism with an associated homozygous mutation c.-3275T&gt;G; the latter is associated with a decrease of about 80% of UGT1A1 transcription explaining this irinotecan induced toxicity.	Irinotecan	274-284	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-67
29098099-7	2017	The analysis of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene revealed homozygous UGT1A1 *28 polymorphism with an associated homozygous mutation c.-3275T&gt;G; the latter is associated with a decrease of about 80% of UGT1A1 transcription explaining this irinotecan induced toxicity.	Irinotecan	274-284	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
29098099-7	2017	The analysis of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene revealed homozygous UGT1A1 *28 polymorphism with an associated homozygous mutation c.-3275T&gt;G; the latter is associated with a decrease of about 80% of UGT1A1 transcription explaining this irinotecan induced toxicity.	Irinotecan	274-284	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
29098099-7	2017	The analysis of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene revealed homozygous UGT1A1 *28 polymorphism with an associated homozygous mutation c.-3275T&gt;G; the latter is associated with a decrease of about 80% of UGT1A1 transcription explaining this irinotecan induced toxicity.	Irinotecan	274-284	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
29098099-8	2017	Physician must be aware of the potential hematological (mainly neutropenia and infectious disease) and digestive (mainly diarrhea) toxicities caused by irinotecan and especially when the patient presents a UGT1A1 *28 homozygous allele.	Irinotecan	152-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	206-212
29098099-9	2017	UGT1A genotyping performed before initiating treatment is useful to anticipate severe toxic reaction to irinotecan and improve the benefit/risk ratio of its use.	Irinotecan	104-114	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	0-5
27503581-5	2017	Both UGT1A1*6 and *28 were reliably demonstrated to be risk factors for irinotecan-induced neutropenia, with tests for both polymorphisms potentially being particularly useful in Asian cancer patients.	Irinotecan	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-11
28167974-11	2017	Additionally, SXD decreased the activity of beta-glucuronidase after irinotecan administration.	Irinotecan	69-79	glucuronidase, beta	Rattus norvegicus	44-62
28881354-1	2017	OBJECTIVES: This phase II trial was aimed at assessing the safety and activity of capecitabine, oxaliplatin, and irinotecan (COI regimen) as a preoperative treatment for resectable gastric cancer (GC) or gastroesophageal junction (GEJ) cancer.	Irinotecan	113-123	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	125-128
27654129-3	2017	Dose escalation of irinotecan was performed according to the results of UGT1A1 genotyping in all patients.	Irinotecan	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
27878250-7	2017	Thus, the potential benefit of the use of a combination of camptothecin-11 with other chemical drugs with inhibitory effects on IL-8 expression, should be paid more attention in treating colon cancer.	Irinotecan	59-74	C-X-C motif chemokine ligand 8	Homo sapiens	128-132
27883280-0	2017	Phase I study of irinotecan for previously treated lung cancer patients with the UGT1A1*28 or *6 polymorphism: Results of the Lung Oncology Group in Kyushu (LOGIK1004A).	Irinotecan	17-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	186-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-90
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	186-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-98
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	186-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	186-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	126-132
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	238-248	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-90
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	238-248	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-98
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	238-248	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
27883280-1	2017	BACKGROUND: Various polymorphisms have been detected in the UDP-glucuronosyltransferase 1A ( UGT1A ) gene, and UGT1A1 *28 and UGT1A1 *6 have important effects on the pharmacokinetics of irinotecan and the risk of severe toxicities during irinotecan therapy.	Irinotecan	238-248	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	126-132
27883280-2	2017	This study was conducted to determine the maximum tolerated dose (MTD) of irinotecan chemotherapy according to the UGT1A1 genotype in previously treated lung cancer patients with the UGT1A1 *28 or UGT1A1 *6 polymorphism.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
27883280-2	2017	This study was conducted to determine the maximum tolerated dose (MTD) of irinotecan chemotherapy according to the UGT1A1 genotype in previously treated lung cancer patients with the UGT1A1 *28 or UGT1A1 *6 polymorphism.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	183-189
27883280-2	2017	This study was conducted to determine the maximum tolerated dose (MTD) of irinotecan chemotherapy according to the UGT1A1 genotype in previously treated lung cancer patients with the UGT1A1 *28 or UGT1A1 *6 polymorphism.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	183-189
27883280-10	2017	CONCLUSIONS: The MTD of irinotecan for previously treated lung cancer patients that are heterozygous for the UGT1A1 * 28 or UGT1A1 * 6 gene polymorphism is 60 mg/m2 .	Irinotecan	24-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
27883280-10	2017	CONCLUSIONS: The MTD of irinotecan for previously treated lung cancer patients that are heterozygous for the UGT1A1 * 28 or UGT1A1 * 6 gene polymorphism is 60 mg/m2 .	Irinotecan	24-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
27638859-0	2016	ATM Expression Predicts Veliparib and Irinotecan Sensitivity in Gastric Cancer by Mediating P53-Independent Regulation of Cell Cycle and Apoptosis.	Irinotecan	38-48	ATM serine/threonine kinase	Homo sapiens	0-3
27838229-0	2016	Carvacrol reduces irinotecan-induced intestinal mucositis through inhibition of inflammation and oxidative damage via TRPA1 receptor activation.	Irinotecan	18-28	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	118-123
27838229-4	2016	Thus, the aim of the present study was to verify the supposed anti-inflammatory and protective action of carvacrol via TRPA1 activation against intestinal mucositis induced by CPT-11 in mice.	Irinotecan	176-182	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	119-124
27838229-10	2016	Carvacrol was found to exert an anti-inflammatory action against CPT-11-induced intestinal mucositis through strong interactions with TRPA1 receptors; reduction in the production or release or both of pro-inflammatory cytokines (TNF-alpha, IL-1beta, and KC); and decrease in other indicators of inflammation (MPO, NF-kappaB, COX-2) and oxidative stress (GSH, MDA, and NOx levels).	Irinotecan	65-71	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	134-139
27838229-10	2016	Carvacrol was found to exert an anti-inflammatory action against CPT-11-induced intestinal mucositis through strong interactions with TRPA1 receptors; reduction in the production or release or both of pro-inflammatory cytokines (TNF-alpha, IL-1beta, and KC); and decrease in other indicators of inflammation (MPO, NF-kappaB, COX-2) and oxidative stress (GSH, MDA, and NOx levels).	Irinotecan	65-71	interleukin 1 beta	Mus musculus	240-248
27838229-10	2016	Carvacrol was found to exert an anti-inflammatory action against CPT-11-induced intestinal mucositis through strong interactions with TRPA1 receptors; reduction in the production or release or both of pro-inflammatory cytokines (TNF-alpha, IL-1beta, and KC); and decrease in other indicators of inflammation (MPO, NF-kappaB, COX-2) and oxidative stress (GSH, MDA, and NOx levels).	Irinotecan	65-71	myeloperoxidase	Mus musculus	309-312
27838229-10	2016	Carvacrol was found to exert an anti-inflammatory action against CPT-11-induced intestinal mucositis through strong interactions with TRPA1 receptors; reduction in the production or release or both of pro-inflammatory cytokines (TNF-alpha, IL-1beta, and KC); and decrease in other indicators of inflammation (MPO, NF-kappaB, COX-2) and oxidative stress (GSH, MDA, and NOx levels).	Irinotecan	65-71	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	314-323
27838229-10	2016	Carvacrol was found to exert an anti-inflammatory action against CPT-11-induced intestinal mucositis through strong interactions with TRPA1 receptors; reduction in the production or release or both of pro-inflammatory cytokines (TNF-alpha, IL-1beta, and KC); and decrease in other indicators of inflammation (MPO, NF-kappaB, COX-2) and oxidative stress (GSH, MDA, and NOx levels).	Irinotecan	65-71	cytochrome c oxidase II, mitochondrial	Mus musculus	325-330
28118131-8	2016	The proposed method was successfully applied to the determination of irinotecan in tap water, river water, and urine samples spiked with 10.20 mg/L for the water samples and 8.32 mg/L for the urine sample.	Irinotecan	69-79	nuclear RNA export factor 1	Homo sapiens	83-86
28118131-9	2016	The average recovery values of irinotecan determined were 99.1% for tap water, 109.4% for river water, and 96.1% for urine.	Irinotecan	31-41	nuclear RNA export factor 1	Homo sapiens	68-71
27587582-7	2016	This is demonstrated with the discovery that HMGA2 potentiates the clinically important topoisomerase I inhibitor irinotecan/SN-38 in trapping the enzyme in covalent DNA-complexes, thereby attenuating transcription.	Irinotecan	114-124	high mobility group AT-hook 2	Homo sapiens	45-50
27587582-7	2016	This is demonstrated with the discovery that HMGA2 potentiates the clinically important topoisomerase I inhibitor irinotecan/SN-38 in trapping the enzyme in covalent DNA-complexes, thereby attenuating transcription.	Irinotecan	125-130	high mobility group AT-hook 2	Homo sapiens	45-50
28345025-4	2017	Human-derived NB cell lines were significantly more sensitive to treatment with hCE1m6-NSCs and irinotecan as compared with drug alone.	Irinotecan	96-106	carboxylesterase 1	Homo sapiens	80-84
27729313-1	2016	In vitro, EGFR inhibition, combined with the BRAF inhibitor vemurafenib, causes synergistic cytotoxicity for BRAFV600E metastatic colorectal cancer, further augmented by irinotecan.	Irinotecan	170-180	epidermal growth factor receptor	Homo sapiens	10-14
27888624-0	2016	RhoA regulates resistance to irinotecan by regulating membrane transporter and apoptosis signaling in colorectal cancer.	Irinotecan	29-39	ras homolog family member A	Homo sapiens	0-4
27888624-4	2016	In this study, we show that, compared with parental cells, RhoA is up-regulated in irinotecan (CPT-11)-resistant CRC cells.	Irinotecan	83-93	ras homolog family member A	Homo sapiens	59-63
27888624-4	2016	In this study, we show that, compared with parental cells, RhoA is up-regulated in irinotecan (CPT-11)-resistant CRC cells.	Irinotecan	95-101	ras homolog family member A	Homo sapiens	59-63
27888624-5	2016	Furthermore, inhibition of RhoA in drug resistant cells, at least partially, rescues the resistance against irinotecan and increases the sensitivity to other chemotherapeutic drug by inhibiting expression of MDR1, MRP1and GSTP1, promotes apoptosis by suppressing the expression of BCL-XL and Bcl-2 and increasing Bax expression, and significantly decreases side population cells.	Irinotecan	108-118	ras homolog family member A	Homo sapiens	27-31
27960424-2	2016	TP1, consisting of the antineoplastic camptothecin analogue SN-38, and the fluorescent dye rhodol green have been covalently conjugated through a disulfide bond.	Irinotecan	60-65	transition protein 1	Homo sapiens	0-3
26687137-0	2016	Complete Clinical Response of BRAF-Mutated Cholangiocarcinoma to Vemurafenib, Panitumumab, and Irinotecan.	Irinotecan	95-105	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	30-34
27638859-4	2016	The present study evaluated ATM-induced synthetic lethality and its role in sensitization of gastric cancer cells to PARP and TOP1 inhibitors, veliparib (ABT-888) and irinotecan (CPT-11), respectively.	Irinotecan	167-177	ATM serine/threonine kinase	Homo sapiens	28-31
27638859-4	2016	The present study evaluated ATM-induced synthetic lethality and its role in sensitization of gastric cancer cells to PARP and TOP1 inhibitors, veliparib (ABT-888) and irinotecan (CPT-11), respectively.	Irinotecan	179-185	ATM serine/threonine kinase	Homo sapiens	28-31
27638859-6	2016	The combinatorial effect of ABT-888 and CPT-11 in gastric cancer cells was also determined both in vitro and in vivo ATM deficiency was found to be associated with enhanced sensitivity to ABT-888 and CPT-11 monotherapy, hence suggesting a mechanism of synthetic lethality.	Irinotecan	40-46	ATM serine/threonine kinase	Homo sapiens	117-120
27638859-6	2016	The combinatorial effect of ABT-888 and CPT-11 in gastric cancer cells was also determined both in vitro and in vivo ATM deficiency was found to be associated with enhanced sensitivity to ABT-888 and CPT-11 monotherapy, hence suggesting a mechanism of synthetic lethality.	Irinotecan	200-206	ATM serine/threonine kinase	Homo sapiens	117-120
27638859-7	2016	Cells with high ATM expression showed reduced sensitivity to monotherapy; however, they showed a higher therapeutic effect with ABT-888 and CPT-11 combinatorial therapy.	Irinotecan	140-146	ATM serine/threonine kinase	Homo sapiens	16-19
27550942-0	2016	TLR4-Dependent Claudin-1 Internalization and Secretagogue-Mediated Chloride Secretion Regulate Irinotecan-Induced Diarrhea.	Irinotecan	95-105	toll-like receptor 4	Mus musculus	0-4
27697767-9	2016	The net result of combined lurbinectedin and irinotecan treatment was a complete reversal of EWS-FLI1 activity and elimination of established tumors in 30% to 70% of mice after only 11 days of therapy.	Irinotecan	45-55	Ewing sarcoma breakpoint region 1	Mus musculus	93-96
27697767-9	2016	The net result of combined lurbinectedin and irinotecan treatment was a complete reversal of EWS-FLI1 activity and elimination of established tumors in 30% to 70% of mice after only 11 days of therapy.	Irinotecan	45-55	Friend leukemia integration 1	Mus musculus	97-101
27546072-8	2016	This review aims to summarize and evaluate the implications of pharmacogenetic variants in the ABC and SLC transporters genes on the pharmacokinetics and clinical outcomes of three anti-cancer agents: irinotecan, docetaxel and doxorubicin in Caucasian and Asian patients.	Irinotecan	201-211	C-C motif chemokine ligand 21	Homo sapiens	103-106
28133330-5	2016	S-1/irinotecan combination chemotherapy was administered as second-line chemotherapy, but he developed grade 3 diarrhea, and the S-1/irinotecan combination chemotherapy was immediately stopped.Weekly paclitaxel chemother- apy was administered as third-line chemotherapy, and S-1/docetaxel combination chemotherapy was administered as fourth-line chemotherapy.	Irinotecan	133-143	proteasome 26S subunit, non-ATPase 1	Homo sapiens	0-3
27550942-0	2016	TLR4-Dependent Claudin-1 Internalization and Secretagogue-Mediated Chloride Secretion Regulate Irinotecan-Induced Diarrhea.	Irinotecan	95-105	claudin 1	Mus musculus	15-24
27550942-8	2016	Irinotecan caused internalization of claudin-1 with focal lesions of ZO-1 and occludin proteolysis in the ileum and colon of wild-type mice.	Irinotecan	0-10	claudin 1	Mus musculus	37-46
27550942-8	2016	Irinotecan caused internalization of claudin-1 with focal lesions of ZO-1 and occludin proteolysis in the ileum and colon of wild-type mice.	Irinotecan	0-10	tight junction protein 1	Mus musculus	69-73
27550942-12	2016	Increased carbachol-induced chloride secretion was seen in irinotecan-treated wild-type and Tlr4-/- mice at 24 hours (wild-type: 100.35 +- 18.37 muA/cm2; P = 0.022; Tlr4-/-: 102.72 +- 18.80 muA/cm2; P = 0.023).	Irinotecan	59-69	toll-like receptor 4	Mus musculus	92-96
27550942-12	2016	Increased carbachol-induced chloride secretion was seen in irinotecan-treated wild-type and Tlr4-/- mice at 24 hours (wild-type: 100.35 +- 18.37 muA/cm2; P = 0.022; Tlr4-/-: 102.72 +- 18.80 muA/cm2; P = 0.023).	Irinotecan	59-69	toll-like receptor 4	Mus musculus	165-169
27748862-0	2016	Gap junction composed of connexin43 modulates 5-fluorouracil, oxaliplatin and irinotecan resistance on colorectal cancers.	Irinotecan	78-88	gap junction protein alpha 1	Homo sapiens	25-35
27550942-13	2016	Results suggest that TLR4-dependent claudin-1 internalization and secondary anion secretion contribute to irinotecan-induced diarrhea.	Irinotecan	106-116	toll-like receptor 4	Mus musculus	21-25
27748862-4	2016	The current study investigated the effects of connexin43 (Cx43) gap junctions on 5-fluorouracil (5-FU), oxaliplatin and irinotecan in colon cancer cells.	Irinotecan	120-130	gap junction protein alpha 1	Homo sapiens	58-62
27550942-13	2016	Results suggest that TLR4-dependent claudin-1 internalization and secondary anion secretion contribute to irinotecan-induced diarrhea.	Irinotecan	106-116	claudin 1	Mus musculus	36-45
27748862-7	2016	Downregulation of Cx43 gap junction functioning attenuated 5-FU, oxaliplatin and irinotecan toxicity in colon cancer cells, which was increased in cells treated with a Cx43 gap junction function enhancer.	Irinotecan	81-91	gap junction protein alpha 1	Homo sapiens	18-22
27748862-7	2016	Downregulation of Cx43 gap junction functioning attenuated 5-FU, oxaliplatin and irinotecan toxicity in colon cancer cells, which was increased in cells treated with a Cx43 gap junction function enhancer.	Irinotecan	81-91	gap junction protein alpha 1	Homo sapiens	168-172
30550693-3	2016	Recent pharmacogenetic studies on irinotecan have revealed the impact of UGT1A1 polymorphisms on severe adverse effects.	Irinotecan	34-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
27895797-4	2016	The promoter (-1000 bp) and exon 1 regions of UDP glucuronosyltransferase family 1 member A complex locus (UGT1A1) gene family members UGT1A1, UGT1A7 and UGT1A9 were sequenced, and comprehensive analysis of their genetic polymorphisms was performed to determine the association between inherited genetic variations and irinotecan-induced toxicity.	Irinotecan	319-329	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
27895797-6	2016	The results of the present study revealed that UGT1A1*6 and UGT1A7*3 are risk factors for irinotecan-induced severe neutropenia, and UGT1A9*1b is associated with severe diarrhea.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
27895797-6	2016	The results of the present study revealed that UGT1A1*6 and UGT1A7*3 are risk factors for irinotecan-induced severe neutropenia, and UGT1A9*1b is associated with severe diarrhea.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	60-66
27895797-0	2016	UGT1A1*6, UGT1A7*3 and UGT1A9*1b polymorphisms are predictive markers for severe toxicity in patients with metastatic gastrointestinal cancer treated with irinotecan-based regimens.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
27895797-0	2016	UGT1A1*6, UGT1A7*3 and UGT1A9*1b polymorphisms are predictive markers for severe toxicity in patients with metastatic gastrointestinal cancer treated with irinotecan-based regimens.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	23-29
27895797-4	2016	The promoter (-1000 bp) and exon 1 regions of UDP glucuronosyltransferase family 1 member A complex locus (UGT1A1) gene family members UGT1A1, UGT1A7 and UGT1A9 were sequenced, and comprehensive analysis of their genetic polymorphisms was performed to determine the association between inherited genetic variations and irinotecan-induced toxicity.	Irinotecan	319-329	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
30550693-4	2016	The concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, markedly alters the disposition of irinotecan, potentially increasing toxicity.	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
30550693-4	2016	The concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, markedly alters the disposition of irinotecan, potentially increasing toxicity.	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
30550693-5	2016	For patients showing homozygosity for UGT1A1*28, *6 or compound heterozygosity for UGT1A1*6 and *28, dose reduction of irinotecan is strongly recommended.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
30550693-5	2016	For patients showing homozygosity for UGT1A1*28, *6 or compound heterozygosity for UGT1A1*6 and *28, dose reduction of irinotecan is strongly recommended.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
27770825-0	2016	Suppression of lupus nephritis and skin lesions in MRL/lpr mice by administration of the topoisomerase I inhibitor irinotecan.	Irinotecan	115-125	Fas (TNF receptor superfamily member 6)	Mus musculus	55-58
27770825-8	2016	RESULTS: Administration of both high- and low-dose irinotecan prevented proteinuria and prolonged survival in MRL/lpr mice.	Irinotecan	51-61	Fas (TNF receptor superfamily member 6)	Mus musculus	114-117
27115099-9	2016	Among these, the irinotecan/temozolomide combination induced strong tumor regression in the TCLT and in a model derived from an AFP-negative relapsing HB.	Irinotecan	17-27	alpha fetoprotein	Mus musculus	128-131
27267850-5	2016	EXPERIMENTAL DESIGN: To avoid DLT for useful cytotoxic agents, the recently developed drug STA-8666 combines a chemical moiety targeting active HSP90 (concentrated in tumors) fused via cleavable linker to SN38, the active metabolite of irinotecan.	Irinotecan	236-246	GCY	Homo sapiens	91-94
27267850-6	2016	We compare potency and mechanism of action of STA-8666 and irinotecan in vitro and in vivo RESULTS: In two SCLC xenograft and patient-derived xenograft models, STA-8666 was tolerated without side effects up to 150 mg/kg.	Irinotecan	59-69	GCY	Homo sapiens	160-163
27510985-0	2016	Effect of hesperidin on the pharmacokinetics of CPT-11 and its active metabolite SN-38 by regulating hepatic Mrp2 in rats.	Irinotecan	48-54	ATP binding cassette subfamily C member 2	Rattus norvegicus	109-113
27510985-0	2016	Effect of hesperidin on the pharmacokinetics of CPT-11 and its active metabolite SN-38 by regulating hepatic Mrp2 in rats.	Irinotecan	81-86	ATP binding cassette subfamily C member 2	Rattus norvegicus	109-113
27510985-3	2016	Accumulated evidence showed that the regulatory effect of hesperidin on the expression of Mrp2 in the liver may be one of the critical factors controlling the biliary excretion of SN-38.	Irinotecan	180-185	ATP binding cassette subfamily C member 2	Rattus norvegicus	90-94
27399284-4	2016	FANCJ interacts with HP1gamma in a BARD1-dependent manner, and this interaction was enhanced by ionizing radiation or irinotecan hydrochloride treatment.	Irinotecan	118-142	BRCA1 interacting helicase 1	Homo sapiens	0-5
27399284-4	2016	FANCJ interacts with HP1gamma in a BARD1-dependent manner, and this interaction was enhanced by ionizing radiation or irinotecan hydrochloride treatment.	Irinotecan	118-142	chromobox 3	Homo sapiens	21-29
27399284-4	2016	FANCJ interacts with HP1gamma in a BARD1-dependent manner, and this interaction was enhanced by ionizing radiation or irinotecan hydrochloride treatment.	Irinotecan	118-142	BRCA1 associated RING domain 1	Homo sapiens	35-40
27716027-6	2016	Both Irinotecan/HAS2 (Hyaluronan synthase 2) and Bevacizumab/PGAM1 (Phosphoglycerate mutase 1) are interactions found in this study with independent confirmation.	Irinotecan	5-15	hyaluronan synthase 2	Homo sapiens	16-20
27716027-6	2016	Both Irinotecan/HAS2 (Hyaluronan synthase 2) and Bevacizumab/PGAM1 (Phosphoglycerate mutase 1) are interactions found in this study with independent confirmation.	Irinotecan	5-15	hyaluronan synthase 2	Homo sapiens	22-43
27716027-6	2016	Both Irinotecan/HAS2 (Hyaluronan synthase 2) and Bevacizumab/PGAM1 (Phosphoglycerate mutase 1) are interactions found in this study with independent confirmation.	Irinotecan	5-15	phosphoglycerate mutase 1	Homo sapiens	61-66
27716027-6	2016	Both Irinotecan/HAS2 (Hyaluronan synthase 2) and Bevacizumab/PGAM1 (Phosphoglycerate mutase 1) are interactions found in this study with independent confirmation.	Irinotecan	5-15	phosphoglycerate mutase 1	Homo sapiens	68-93
27608846-0	2016	STA-8666, a novel HSP90 inhibitor/SN-38 drug conjugate, causes complete tumor regression in preclinical mouse models of pediatric sarcoma.	Irinotecan	34-39	autosomal striping	Mus musculus	0-3
27608846-3	2016	In this study we have evaluated the efficacy and toxicity of STA-8666, a novel drug conjugate which uses an HSP90 inhibitor to facilitate intracellular, tumor-targeted delivery of the topoisomerase 1 inhibitor SN-38, thus preferentially delivering and concentrating SN-38 within tumor tissue.	Irinotecan	210-215	autosomal striping	Mus musculus	61-64
27608846-3	2016	In this study we have evaluated the efficacy and toxicity of STA-8666, a novel drug conjugate which uses an HSP90 inhibitor to facilitate intracellular, tumor-targeted delivery of the topoisomerase 1 inhibitor SN-38, thus preferentially delivering and concentrating SN-38 within tumor tissue.	Irinotecan	210-215	heat shock protein 86, pseudogene 1	Mus musculus	108-113
27608846-3	2016	In this study we have evaluated the efficacy and toxicity of STA-8666, a novel drug conjugate which uses an HSP90 inhibitor to facilitate intracellular, tumor-targeted delivery of the topoisomerase 1 inhibitor SN-38, thus preferentially delivering and concentrating SN-38 within tumor tissue.	Irinotecan	266-271	autosomal striping	Mus musculus	61-64
27608846-6	2016	Gene expression analysis performed on xenograft tumors treated with either irinotecan or STA-8666 showed that STA-8666 affected expression of DNA damage and repair genes more robustly than irinotecan.	Irinotecan	75-85	autosomal striping	Mus musculus	110-113
27608846-6	2016	Gene expression analysis performed on xenograft tumors treated with either irinotecan or STA-8666 showed that STA-8666 affected expression of DNA damage and repair genes more robustly than irinotecan.	Irinotecan	189-199	autosomal striping	Mus musculus	89-92
27116457-0	2016	Effect of Single Nucleotide Polymorphisms in the Xenobiotic-sensing Receptors NR1I2 and NR1I3 on the Pharmacokinetics and Toxicity of Irinotecan in Colorectal Cancer Patients.	Irinotecan	134-144	nuclear receptor subfamily 1 group I member 2	Homo sapiens	78-83
27698852-0	2016	ABCG2 expression in colorectal adenocarcinomas may predict resistance to irinotecan.	Irinotecan	73-83	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
27698852-3	2016	The aim of the present study was to evaluate whether the expression levels of adenosine triphosphate-binding cassette sub-family G (WHITE) member 2 (Junior blood group) (ABCG2) in primary colorectal tumors predict chemoresistance to irinotecan.	Irinotecan	233-243	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	170-175
27698852-4	2016	Using the resected primary tumor specimens of 189 patients with colorectal cancer, the association between the immunohistochemical expression of ABCG2 protein and the results of the collagen gel droplet embedded culture drug sensitivity test, performed to evaluate the chemosensitivity to SN-38 (an active metabolite of irinotecan), was investigated.	Irinotecan	289-294	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	145-150
27698852-4	2016	Using the resected primary tumor specimens of 189 patients with colorectal cancer, the association between the immunohistochemical expression of ABCG2 protein and the results of the collagen gel droplet embedded culture drug sensitivity test, performed to evaluate the chemosensitivity to SN-38 (an active metabolite of irinotecan), was investigated.	Irinotecan	320-330	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	145-150
27698852-6	2016	The tumors of patients with increased ABCG2 expression accounted for 60% of the tumors examined, and were significantly more resistant to SN-38, compared with patients with low ABCG2 expression (P&lt;0.001).	Irinotecan	138-143	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	38-43
27698852-7	2016	In a multivariate logistic regression analysis, increased expression of ABCG2 protein was an independent and significant predictor of resistance to SN-38, increasing the risk of resistance by 12-fold.	Irinotecan	148-153	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	72-77
27698852-8	2016	Increased expression of ABCG2 and a low sensitivity to SN-38 was significantly associated with resistance to irinotecan-based chemotherapy (P=0.01 and 0.028, respectively).	Irinotecan	109-119	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	24-29
27698852-10	2016	The increased immunohistochemical expression of ABCG2 in primary tumors may be a useful predictive biomarker of resistance to irinotecan-based chemotherapy for patients with recurrent or metastatic colorectal cancer.	Irinotecan	126-136	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	48-53
27121793-1	2016	PURPOSE: WRN promoter CpG island hypermethylation in colorectal cancer has been reported to increase sensitivity to irinotecan-based therapies.	Irinotecan	116-126	WRN RecQ like helicase	Homo sapiens	9-12
27468920-1	2016	PURPOSE: Anti-epidermal growth factor receptor antibody therapy alone or in combination with irinotecan is recognized as a standard third-line treatment for KRAS wild-type unresectable metastatic colorectal cancer.	Irinotecan	93-103	KRAS proto-oncogene, GTPase	Homo sapiens	157-161
27468920-13	2016	CONCLUSIONS: Combination therapy with cetuximab and S-1 was effective and well tolerated in patients with irinotecan-, oxaliplatin-, and fluoropyrimidine-refractory metastatic colorectal cancer.	Irinotecan	106-116	proteasome 26S subunit, non-ATPase 1	Homo sapiens	52-55
27116457-0	2016	Effect of Single Nucleotide Polymorphisms in the Xenobiotic-sensing Receptors NR1I2 and NR1I3 on the Pharmacokinetics and Toxicity of Irinotecan in Colorectal Cancer Patients.	Irinotecan	134-144	nuclear receptor subfamily 1 group I member 3	Homo sapiens	88-93
27116457-1	2016	BACKGROUND AND OBJECTIVES: Nuclear receptors PXR (pregnane X receptor, NR1I2) and CAR (constitutive androstane receptor, NR1I3) are key regulators of irinotecan metabolism, and ligand-dependent modulation of their activity leads to significant drug-drug interactions.	Irinotecan	150-160	nuclear receptor subfamily 1 group I member 2	Homo sapiens	45-48
27116457-1	2016	BACKGROUND AND OBJECTIVES: Nuclear receptors PXR (pregnane X receptor, NR1I2) and CAR (constitutive androstane receptor, NR1I3) are key regulators of irinotecan metabolism, and ligand-dependent modulation of their activity leads to significant drug-drug interactions.	Irinotecan	150-160	nuclear receptor subfamily 1 group I member 2	Homo sapiens	50-69
27116457-1	2016	BACKGROUND AND OBJECTIVES: Nuclear receptors PXR (pregnane X receptor, NR1I2) and CAR (constitutive androstane receptor, NR1I3) are key regulators of irinotecan metabolism, and ligand-dependent modulation of their activity leads to significant drug-drug interactions.	Irinotecan	150-160	nuclear receptor subfamily 1 group I member 2	Homo sapiens	71-76
27116457-1	2016	BACKGROUND AND OBJECTIVES: Nuclear receptors PXR (pregnane X receptor, NR1I2) and CAR (constitutive androstane receptor, NR1I3) are key regulators of irinotecan metabolism, and ligand-dependent modulation of their activity leads to significant drug-drug interactions.	Irinotecan	150-160	nuclear receptor subfamily 1 group I member 3	Homo sapiens	82-126
27116457-4	2016	RESULTS: After adjustment of the tests by the UGT1A1*28 genotype and correction for multiple testing, the A allele of NR1I2-rs10934498 was associated with a decreased exposition and an increased degradation of SN-38, the active metabolite (p = 0.009 and p = 0.017, respectively).	Irinotecan	210-215	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
27116457-4	2016	RESULTS: After adjustment of the tests by the UGT1A1*28 genotype and correction for multiple testing, the A allele of NR1I2-rs10934498 was associated with a decreased exposition and an increased degradation of SN-38, the active metabolite (p = 0.009 and p = 0.017, respectively).	Irinotecan	210-215	nuclear receptor subfamily 1 group I member 2	Homo sapiens	118-123
27116457-6	2016	CONCLUSION: Our results reveal for the first time the involvement of NR1I2 in the pharmacogenetics of irinotecan and suggest that it may help to predict the toxicity of low-dose irinotecan.	Irinotecan	102-112	nuclear receptor subfamily 1 group I member 2	Homo sapiens	69-74
27116457-6	2016	CONCLUSION: Our results reveal for the first time the involvement of NR1I2 in the pharmacogenetics of irinotecan and suggest that it may help to predict the toxicity of low-dose irinotecan.	Irinotecan	178-188	nuclear receptor subfamily 1 group I member 2	Homo sapiens	69-74
26750665-7	2016	Moreover, the GA-mediated repression of CES2 attenuated CPT-11-induced apoptosis.	Irinotecan	56-62	carboxylesterase 2	Homo sapiens	40-44
27338835-7	2016	NDRG1 was a favorable prognostic factor of mCRC, although might be responsible for CPT-11 resistance in vitro.	Irinotecan	83-89	N-myc downstream regulated 1	Homo sapiens	0-5
26744836-12	2016	The substrate uptakes of OAT1, OCTN1 and OCTN2 were significantly decreased in the presence of CZ112, while CPT-11 potently down-regulated the transport activity of OCT1 and OCT3.	Irinotecan	108-114	solute carrier family 22 member 1	Homo sapiens	165-169
27207776-0	2016	Combining ABCG2 Inhibitors with IMMU-132, an Anti-Trop-2 Antibody Conjugate of SN-38, Overcomes Resistance to SN-38 in Breast and Gastric Cancers.	Irinotecan	79-84	tumor associated calcium signal transducer 2	Homo sapiens	50-56
27380166-0	2016	Erratum to: UDP-glucuronosyltransferase 1A1*6 and *28 polymorphisms as indicators of initial dose level of irinotecan to reduce risk of neutropenia in patients receiving FOLFIRI for colorectal cancer.	Irinotecan	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-43
26950035-0	2016	MRP1 expression in CTCs confers resistance to irinotecan-based chemotherapy in metastatic colorectal cancer.	Irinotecan	46-56	ATP binding cassette subfamily C member 1	Homo sapiens	0-4
26950035-3	2016	Multidrug resistance-associated protein 1 (MRP1) and Multidrug resistance-associated protein 4 (MRP4) play a role in irinotecan-resistance, and Excision Repair Cross-Complementation group 1 (ERCC1) expression can confer resistance to platinum compounds.	Irinotecan	117-127	ATP binding cassette subfamily C member 1	Homo sapiens	0-41
26950035-3	2016	Multidrug resistance-associated protein 1 (MRP1) and Multidrug resistance-associated protein 4 (MRP4) play a role in irinotecan-resistance, and Excision Repair Cross-Complementation group 1 (ERCC1) expression can confer resistance to platinum compounds.	Irinotecan	117-127	ATP binding cassette subfamily C member 1	Homo sapiens	43-47
26950035-3	2016	Multidrug resistance-associated protein 1 (MRP1) and Multidrug resistance-associated protein 4 (MRP4) play a role in irinotecan-resistance, and Excision Repair Cross-Complementation group 1 (ERCC1) expression can confer resistance to platinum compounds.	Irinotecan	117-127	ATP binding cassette subfamily C member 4	Homo sapiens	53-94
26950035-3	2016	Multidrug resistance-associated protein 1 (MRP1) and Multidrug resistance-associated protein 4 (MRP4) play a role in irinotecan-resistance, and Excision Repair Cross-Complementation group 1 (ERCC1) expression can confer resistance to platinum compounds.	Irinotecan	117-127	ATP binding cassette subfamily C member 4	Homo sapiens	96-100
26950035-3	2016	Multidrug resistance-associated protein 1 (MRP1) and Multidrug resistance-associated protein 4 (MRP4) play a role in irinotecan-resistance, and Excision Repair Cross-Complementation group 1 (ERCC1) expression can confer resistance to platinum compounds.	Irinotecan	117-127	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	191-196
26950035-7	2016	Among patients treated with irinotecan-based chemotherapy, 4 out of 19 cases with MRP1 positive CTCs showed a worse progression free survival (PFS) in comparison to those with MRP1 negative CTCs (2.1 months vs. 9.1 months; p = 0.003).	Irinotecan	28-38	ATP binding cassette subfamily C member 1	Homo sapiens	82-86
26950035-7	2016	Among patients treated with irinotecan-based chemotherapy, 4 out of 19 cases with MRP1 positive CTCs showed a worse progression free survival (PFS) in comparison to those with MRP1 negative CTCs (2.1 months vs. 9.1 months; p = 0.003).	Irinotecan	28-38	ATP binding cassette subfamily C member 1	Homo sapiens	176-180
26950035-10	2016	Our results show MRP1 as a potential biomarker of resistance to treatment with irinotecan when found in CTCs from mCRC patients.	Irinotecan	79-89	ATP binding cassette subfamily C member 1	Homo sapiens	17-21
26710796-0	2016	UDP-glucuronosyltransferase 1A1*6 and *28 polymorphisms as indicators of initial dose level of irinotecan to reduce risk of neutropenia in patients receiving FOLFIRI for colorectal cancer.	Irinotecan	95-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
27207776-0	2016	Combining ABCG2 Inhibitors with IMMU-132, an Anti-Trop-2 Antibody Conjugate of SN-38, Overcomes Resistance to SN-38 in Breast and Gastric Cancers.	Irinotecan	110-115	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	10-15
27207776-0	2016	Combining ABCG2 Inhibitors with IMMU-132, an Anti-Trop-2 Antibody Conjugate of SN-38, Overcomes Resistance to SN-38 in Breast and Gastric Cancers.	Irinotecan	110-115	tumor associated calcium signal transducer 2	Homo sapiens	50-56
27207776-6	2016	Importantly, treatment of both S120 sublines with known ABCG2 inhibitors (fumitremorgin C, Ko143, and YHO-13351) restored toxicity of SN-38, and the combination of YHO-13351 with IMMU-132 increased the median survival of mice bearing NCI-N87-S120 xenografts.	Irinotecan	134-139	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	56-61
27006309-10	2016	The median progression-free survival was significantly different between groups with low or high MGMT expression for the irinotecan-based regimen (p = 0.025), but MGMT protein expression was not observed to be a prognostic factor.	Irinotecan	121-131	O-6-methylguanine-DNA methyltransferase	Homo sapiens	97-101
26739304-0	2016	High Resectability Rate of Initially Unresectable Colorectal Liver Metastases After UGT1A1-Adapted High-Dose Irinotecan Combined with LV5FU2 and Cetuximab: A Multicenter Phase II Study (ERBIFORT).	Irinotecan	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
27348241-0	2016	Targeting Colorectal Cancer Stem-Like Cells with Anti-CD133 Antibody-Conjugated SN-38 Nanoparticles.	Irinotecan	80-85	prominin 1	Homo sapiens	54-59
27348241-5	2016	To resolve the problem of chemotherapy failure, SN-38-loaded nanoparticles were conjugated with anti-CD133 antibody to target CD133-positive (CD133(+)) cells.	Irinotecan	48-53	prominin 1	Homo sapiens	101-106
27348241-5	2016	To resolve the problem of chemotherapy failure, SN-38-loaded nanoparticles were conjugated with anti-CD133 antibody to target CD133-positive (CD133(+)) cells.	Irinotecan	48-53	prominin 1	Homo sapiens	126-131
27348241-5	2016	To resolve the problem of chemotherapy failure, SN-38-loaded nanoparticles were conjugated with anti-CD133 antibody to target CD133-positive (CD133(+)) cells.	Irinotecan	48-53	prominin 1	Homo sapiens	126-131
27348241-6	2016	In this study, anti-CD133 antibody-conjugated SN-38-loaded nanoparticles (CD133Ab-NPs-SN-38) efficiently bound to HCT116 cells, which overexpress CD133 glycoprotein.	Irinotecan	46-51	prominin 1	Homo sapiens	20-25
27348241-6	2016	In this study, anti-CD133 antibody-conjugated SN-38-loaded nanoparticles (CD133Ab-NPs-SN-38) efficiently bound to HCT116 cells, which overexpress CD133 glycoprotein.	Irinotecan	46-51	prominin 1	Homo sapiens	74-79
27348241-6	2016	In this study, anti-CD133 antibody-conjugated SN-38-loaded nanoparticles (CD133Ab-NPs-SN-38) efficiently bound to HCT116 cells, which overexpress CD133 glycoprotein.	Irinotecan	86-91	prominin 1	Homo sapiens	20-25
27348241-6	2016	In this study, anti-CD133 antibody-conjugated SN-38-loaded nanoparticles (CD133Ab-NPs-SN-38) efficiently bound to HCT116 cells, which overexpress CD133 glycoprotein.	Irinotecan	86-91	prominin 1	Homo sapiens	74-79
27348241-8	2016	Furthermore, CD133Ab-NPs-SN-38 could target CD133(+) cells and inhibit colony formation compared with NPs-SN-38.	Irinotecan	25-30	prominin 1	Homo sapiens	13-18
27348241-10	2016	A reduction in CD133 expression in HCT116 cells treated with CD133Ab-NPs-SN-38 was also observed in immunohistochemistry results.	Irinotecan	73-78	prominin 1	Homo sapiens	15-20
27280693-8	2016	Furthermore, they are able to reverse the ABCG2-mediated resistance toward SN-38 and inhibit the ATPase activity.	Irinotecan	75-80	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	42-47
27354601-0	2016	Early Experience with 70-150 mum Irinotecan Drug-eluting Beads (M1-DEBIRI) for the Treatment of Unresectable Hepatic Colorectal Metastases.	Irinotecan	33-43	myoregulin	Homo sapiens	64-73
27354601-1	2016	AIM: To report our early experience on the feasibility and safety of 70-150 mum drug-eluting beads loaded with irinotecan (M1-DEBIRI) for treating unresectable hepatic colorectal metastases.	Irinotecan	111-121	myoregulin	Homo sapiens	123-132
27286453-0	2016	UCN-01 enhances cytotoxicity of irinotecan in colorectal cancer stem-like cells by impairing DNA damage response.	Irinotecan	32-42	urocortin	Homo sapiens	0-3
27286453-5	2016	Nonetheless, broad-spectrum inhibition by the staurosporin derivative UCN-01 blocks CRC-SC growth and potentiates the activity of irinotecan in vitro and in vivo CRC-SC-derived models.	Irinotecan	130-140	urocortin	Homo sapiens	70-73
27286453-7	2016	Combination of LY2603618, a specific Chk1/2 inhibitor, with irinotecan resulted in a significant reduction of CRC-SC growth in vivo, confirming that irinotecan treatment coupled to inhibition of Chk1 represents a potentially effective therapeutic approach for CRC treatment.	Irinotecan	149-159	checkpoint kinase 1	Homo sapiens	37-43
27286453-7	2016	Combination of LY2603618, a specific Chk1/2 inhibitor, with irinotecan resulted in a significant reduction of CRC-SC growth in vivo, confirming that irinotecan treatment coupled to inhibition of Chk1 represents a potentially effective therapeutic approach for CRC treatment.	Irinotecan	149-159	checkpoint kinase 1	Homo sapiens	37-41
27354619-0	2016	Comparison of Panitumumab Plus Irinotecan and Cetuximab Plus Irinotecan for KRAS Wild-type Metastatic Colorectal Cancer.	Irinotecan	61-71	KRAS proto-oncogene, GTPase	Homo sapiens	76-80
26739304-14	2016	It seemed to be well-tolerated among healthy selected patients thanks to irinotecan dose adaptation according to UGT1A1 pharmacogenomics status.	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
27220761-0	2016	UGT1A1 gene polymorphism is associated with toxicity and clinical efficacy of irinotecan-based chemotherapy in patients with advanced colorectal cancer.	Irinotecan	78-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
27220761-1	2016	OBJECTIVES: To investigate the relationship between uridine diphosphate glucoronosyltransferase 1A1 (UGT1A1)*28/*6 and toxicity and clinical efficacy of irinotecan-based chemotherapy in patients with advanced colorectal cancer (CRC) in Xinjiang Uygur and Han population.	Irinotecan	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-99
27220761-1	2016	OBJECTIVES: To investigate the relationship between uridine diphosphate glucoronosyltransferase 1A1 (UGT1A1)*28/*6 and toxicity and clinical efficacy of irinotecan-based chemotherapy in patients with advanced colorectal cancer (CRC) in Xinjiang Uygur and Han population.	Irinotecan	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
27220761-11	2016	CONCLUSION: UGT1A1 gene polymorphism predicts irinotecan-related adverse reactions in advanced CRC patients of Xinjiang Uygur and Han nationality; UGT1A1 gene polymorphism is correlated with efficacy and prognosis in Uygur nationality, but only related to prognosis in Han nationality in irinotecan-based chemotherapy.	Irinotecan	46-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
27220761-11	2016	CONCLUSION: UGT1A1 gene polymorphism predicts irinotecan-related adverse reactions in advanced CRC patients of Xinjiang Uygur and Han nationality; UGT1A1 gene polymorphism is correlated with efficacy and prognosis in Uygur nationality, but only related to prognosis in Han nationality in irinotecan-based chemotherapy.	Irinotecan	288-298	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
27220761-11	2016	CONCLUSION: UGT1A1 gene polymorphism predicts irinotecan-related adverse reactions in advanced CRC patients of Xinjiang Uygur and Han nationality; UGT1A1 gene polymorphism is correlated with efficacy and prognosis in Uygur nationality, but only related to prognosis in Han nationality in irinotecan-based chemotherapy.	Irinotecan	288-298	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	147-153
27160286-0	2016	A novel genetic score model of UGT1A1 and TGFB pathway as predictor of severe irinotecan-related diarrhea in metastatic colorectal cancer patients.	Irinotecan	78-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
26842236-15	2016	CONCLUSIONS: Veliparib can be safely combined with irinotecan at doses that inhibit PARP catalytic activity.	Irinotecan	51-61	poly(ADP-ribose) polymerase 1	Homo sapiens	84-88
27101738-9	2016	D5D knockdown along with DGLA treatment also enhanced the cytotoxicities of various chemotherapeutic drugs, including 5-fluorouracil, regorafenib, and irinotecan, potentially through the activation of pro-apoptotic proteins, e.g. p53 and caspase 9.	Irinotecan	151-161	fatty acid desaturase 1	Homo sapiens	0-3
26891420-1	2016	Cetuximab in combination with an irinotecan-containing regimen is a standard treatment in patients with KRAS wild-type (KRAS WT), metastatic colorectal cancer (mCRC).	Irinotecan	33-43	KRAS proto-oncogene, GTPase	Homo sapiens	104-108
27160286-0	2016	A novel genetic score model of UGT1A1 and TGFB pathway as predictor of severe irinotecan-related diarrhea in metastatic colorectal cancer patients.	Irinotecan	78-88	transforming growth factor beta 1	Homo sapiens	42-46
26309154-0	2016	Biophysical and molecular docking insight into interaction mechanism and thermal stability of human serum albumin isoforms with a semi-synthetic water-soluble camptothecin analog irinotecan hydrochloride.	Irinotecan	179-203	albumin	Homo sapiens	100-113
26309154-1	2016	In the present work, we have examined the binding parameters, thermodynamics, and stability of human serum albumin (HSA) isoforms at pH 7.4 and 9.0, using spectroscopic, calorimetric, and molecular docking methods in the presence of water-soluble camptothecin analog irinotecan hydrochloride (CPT-11).	Irinotecan	267-291	albumin	Homo sapiens	101-114
26309154-1	2016	In the present work, we have examined the binding parameters, thermodynamics, and stability of human serum albumin (HSA) isoforms at pH 7.4 and 9.0, using spectroscopic, calorimetric, and molecular docking methods in the presence of water-soluble camptothecin analog irinotecan hydrochloride (CPT-11).	Irinotecan	293-299	albumin	Homo sapiens	101-114
27160286-1	2016	PURPOSE: UGT1A1*28/*6 as predictors of severe irinotecan-related diarrhea (SIRD) were duplicated by many studies.	Irinotecan	46-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
27246726-1	2016	BACKGROUND: Patients with metastatic colorectal cancer whose disease has progressed on oxaliplatin- and irinotecan-containing regimens may benefit from EGFR-inhibiting monoclonal antibodies if they do not contain mutations in the KRAS gene (are "wild type").	Irinotecan	104-114	epidermal growth factor receptor	Homo sapiens	152-156
26862009-0	2016	Impact of UGT1A1 genotype upon toxicities of combination with low-dose irinotecan plus platinum.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
26862009-1	2016	AIM: Irinotecan-induced severe toxicities are possibly related to UGT1A1*6 and *28 genotypes.	Irinotecan	5-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
26862009-2	2016	However, the correlation between UGT1A1 polymorphisms and the risk of toxicities induced by low-dose irinotecan plus platinum combination therapy still remains controversial.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
26862009-3	2016	This prospective observational study aimed to examine the correlation between UGT1A1 genotypes and clinical outcomes of low-dose irinotecan (median 60 mg/m(2) , range 25-115 mg/m(2) ) plus platinum in Japanese patients with solid tumors.	Irinotecan	129-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
26862009-10	2016	CONCLUSION: UGT1A1 genotype has a major impact on the increased risk of severe hematological toxicities, even in low-dose irinotecan regimens.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
26862009-11	2016	UGT1A1 genotypes are useful biomarkers for predicting severe hematological toxicities in patients treated with irinotecan plus platinum analog.	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
27143148-1	2016	PURPOSE: Patients with unresectable wild-type KRAS metastatic colorectal cancer benefit from fluoropyrimidines (FP), oxaliplatin (O), irinotecan (I), bevacizumab (Bev), and epithelial growth factor receptor inhibitors (EGFRI).	Irinotecan	134-144	KRAS proto-oncogene, GTPase	Homo sapiens	46-50
27197307-0	2016	Irinotecan-Induced Gastrointestinal Dysfunction and Pain Are Mediated by Common TLR4-Dependent Mechanisms.	Irinotecan	0-10	toll-like receptor 4	Mus musculus	80-84
27197307-9	2016	TLR4 deletion attenuated irinotecan-induced gut toxicity, with improvements in weight loss (P = 0.0003) and diarrhea (P &lt; 0.0001).	Irinotecan	25-35	toll-like receptor 4	Mus musculus	0-4
27197307-13	2016	These data indicate that TLR4 is uniquely positioned to mediate irinotecan-induced gut toxicity and pain, highlighting the possibility of a targetable gut/CNS axis for improved toxicity outcomes.	Irinotecan	64-74	toll-like receptor 4	Mus musculus	25-29
27313739-16	2016	In conclusion, panitumumab and irinotecan as salvage therapy for mCRC KRAS wild-type patients with skin toxicity prevention exhibits limited efficacy.	Irinotecan	31-41	KRAS proto-oncogene, GTPase	Homo sapiens	70-74
27246726-1	2016	BACKGROUND: Patients with metastatic colorectal cancer whose disease has progressed on oxaliplatin- and irinotecan-containing regimens may benefit from EGFR-inhibiting monoclonal antibodies if they do not contain mutations in the KRAS gene (are "wild type").	Irinotecan	104-114	KRAS proto-oncogene, GTPase	Homo sapiens	230-234
27380948-4	2016	RESULTS: Meta-analysis showed east-Asian patients expressing SLCO1B1 521T&gt;C or 1118G&gt;A to have a two- to fourfold increased risk of irinotecan-induced neutropenia but not diarrhea.	Irinotecan	138-148	solute carrier organic anion transporter family member 1B1	Homo sapiens	61-68
27385990-0	2016	Prospective study of the UGT1A1*27 gene polymorphism during irinotecan therapy in patients with lung cancer: Results of Lung Oncology Group in Kyusyu (LOGIK1004B).	Irinotecan	60-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
27385990-2	2016	To evaluate the effect of the UGT1A1*27 polymorphism in irinotecan therapy, we conducted a prospective study.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
27385990-10	2016	In an evaluation of the side effects of irinotecan, patients with UGT1A1*28 and UGT1A1*6 polymorphisms had a higher tendency to experience febrile neutropenia than wild type (25% and 32% vs. 14%).	Irinotecan	40-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
27385990-10	2016	In an evaluation of the side effects of irinotecan, patients with UGT1A1*28 and UGT1A1*6 polymorphisms had a higher tendency to experience febrile neutropenia than wild type (25% and 32% vs. 14%).	Irinotecan	40-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
27340349-2	2016	In addition, the combined strategies of administering EGFR mAbs and traditional cytotoxic agents, such as 5-fluorouracil, oxaliplatin and irinotecan, have resulted in a more complicated management of CRC treatment-related side effects compared with EGFR mAb monotherapy.	Irinotecan	138-148	epidermal growth factor receptor	Homo sapiens	54-58
27340349-2	2016	In addition, the combined strategies of administering EGFR mAbs and traditional cytotoxic agents, such as 5-fluorouracil, oxaliplatin and irinotecan, have resulted in a more complicated management of CRC treatment-related side effects compared with EGFR mAb monotherapy.	Irinotecan	138-148	epidermal growth factor receptor	Homo sapiens	249-253
27009215-8	2016	In immunodeficient mice, systemically transplanted HB1.F3.CE stem cells migrated toward the tumor implanted by the TCCSUP bladder cancer cell line, and, in combination with CPT-11, the volume of tumors was significantly reduced.	Irinotecan	173-179	paternally expressed 10	Mus musculus	51-54
27269636-7	2016	Meta-analysis showed an decreased risk of irinotecan-induced neutropenia in patients expressing ABCB1 2677G&gt;T/G (odds ratio [OR]: 0.24; 95% CI: 0.1-0.59; p = 0.002) but increased risk for ABCC2 3972T&gt;T (OR: 1.67; 95% CI: 1.01-2.74; p = 0.04).	Irinotecan	42-52	ATP binding cassette subfamily B member 1	Homo sapiens	96-101
27269636-7	2016	Meta-analysis showed an decreased risk of irinotecan-induced neutropenia in patients expressing ABCB1 2677G&gt;T/G (odds ratio [OR]: 0.24; 95% CI: 0.1-0.59; p = 0.002) but increased risk for ABCC2 3972T&gt;T (OR: 1.67; 95% CI: 1.01-2.74; p = 0.04).	Irinotecan	42-52	ATP binding cassette subfamily C member 2	Homo sapiens	191-196
27269636-8	2016	ABCG2 34G&gt;A was associated with a threefold increased risk of irinotecan-induced diarrhea (95% CI: 1.00-6.24; p = 0.05).	Irinotecan	65-75	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
26518357-11	2016	These findings suggest that the reduction in the serum SN-38 concentration following co-administration of ciprofloxacin during irinotecan treatment is due, at least partly, to the decreased enterohepatic circulation of SN-38 through the non-competitive inhibition of intestinal beta-glucuronidase-mediated SN-38-G deconjugation.	Irinotecan	219-224	glucuronidase beta	Homo sapiens	278-296
27070848-6	2016	The release of therapeutic drug SN-38 in the presence of CTB was confirmed by HPLC and prodrug 1a showed potent in vitro cytotoxicity against all tested cell lines.	Irinotecan	32-37	cathepsin B	Homo sapiens	57-60
27135737-5	2016	Upon preferential cancer cell delivery and uptake, aided by biotin, the enzyme-triggered theranostic prodrug 1 is cleaved by NQO1, with the subsequent release of SN-38, inhibiting topoisomerase I, leading to apoptosis.	Irinotecan	162-167	NAD(P)H quinone dehydrogenase 1	Homo sapiens	125-129
27135737-6	2016	The drug release and induced apoptosis of cancer cells expressing both biotin receptors and high levels of NQO1 was simultaneously monitored via the innate fluorescence of the released SN-38 by confocal microscopy.	Irinotecan	185-190	NAD(P)H quinone dehydrogenase 1	Homo sapiens	107-111
27070088-0	2016	The novel tankyrase inhibitor (AZ1366) enhances irinotecan activity in tumors that exhibit elevated tankyrase and irinotecan resistance.	Irinotecan	48-58	tankyrase	Homo sapiens	10-19
27070088-0	2016	The novel tankyrase inhibitor (AZ1366) enhances irinotecan activity in tumors that exhibit elevated tankyrase and irinotecan resistance.	Irinotecan	48-58	tankyrase	Homo sapiens	100-109
27070088-0	2016	The novel tankyrase inhibitor (AZ1366) enhances irinotecan activity in tumors that exhibit elevated tankyrase and irinotecan resistance.	Irinotecan	114-124	tankyrase	Homo sapiens	10-19
26518357-0	2016	The Inhibitory Effect of Ciprofloxacin on the beta-Glucuronidase-mediated Deconjugation of the Irinotecan Metabolite SN-38-G.	Irinotecan	95-105	glucuronidase beta	Homo sapiens	46-64
26518357-4	2016	In this study, we established an in vitro system to evaluate the beta-glucuronidase-mediated deconjugation of the irinotecan metabolite SN-38-G to its active SN-38 form and the effect of ciprofloxacin thereon.	Irinotecan	114-124	glucuronidase beta	Homo sapiens	65-83
26518357-4	2016	In this study, we established an in vitro system to evaluate the beta-glucuronidase-mediated deconjugation of the irinotecan metabolite SN-38-G to its active SN-38 form and the effect of ciprofloxacin thereon.	Irinotecan	136-141	glucuronidase beta	Homo sapiens	65-83
26518357-4	2016	In this study, we established an in vitro system to evaluate the beta-glucuronidase-mediated deconjugation of the irinotecan metabolite SN-38-G to its active SN-38 form and the effect of ciprofloxacin thereon.	Irinotecan	158-163	glucuronidase beta	Homo sapiens	65-83
26518357-7	2016	Ciprofloxacin and phenolphthalein-beta-D-glucuronide (PhePG), a typical beta-glucuronidase substrate, significantly decreased SN-38-G deconjugation and, hence SN-38 formation.	Irinotecan	126-131	glucuronidase beta	Homo sapiens	72-90
26518357-9	2016	Ciprofloxacin showed a dose-dependent inhibitory effect on the beta-glucuronidase-mediated conversion of SN-38-G to SN-38 with a half-maximal inhibitory concentration (IC50 ) value of 83.8 muM.	Irinotecan	105-110	glucuronidase beta	Homo sapiens	63-81
26518357-11	2016	These findings suggest that the reduction in the serum SN-38 concentration following co-administration of ciprofloxacin during irinotecan treatment is due, at least partly, to the decreased enterohepatic circulation of SN-38 through the non-competitive inhibition of intestinal beta-glucuronidase-mediated SN-38-G deconjugation.	Irinotecan	55-60	glucuronidase beta	Homo sapiens	278-296
26518357-11	2016	These findings suggest that the reduction in the serum SN-38 concentration following co-administration of ciprofloxacin during irinotecan treatment is due, at least partly, to the decreased enterohepatic circulation of SN-38 through the non-competitive inhibition of intestinal beta-glucuronidase-mediated SN-38-G deconjugation.	Irinotecan	219-224	glucuronidase beta	Homo sapiens	278-296
26115978-1	2016	OBJECTIVE: This study sought to evaluate the toxicity and curative effect of irinotecan plus cisplatin neoadjuvant chemotherapy (NACT) for stage Ib2, IIa2, and IIb cervical cancer patients.	Irinotecan	77-87	mitogen-activated protein kinase 8 interacting protein 2	Homo sapiens	145-148
27037412-9	2016	In combination with irinotecan or doxorubicin, FAP-DR5 treatment resulted in substantial tumor regression in patient-derived xenograft models.	Irinotecan	20-30	fibroblast activation protein alpha	Homo sapiens	47-50
25917796-8	2016	UbcH10 suppression decreased CRC cell growth rate (at least in part through deregulation of Cyclin B and ERK1) and sensitized them to pharmacological treatments with irinotecan, SN-38 and cetuximab (at least in part through a down-regulation of AKT).	Irinotecan	166-176	ubiquitin conjugating enzyme E2 C	Homo sapiens	0-6
25917796-8	2016	UbcH10 suppression decreased CRC cell growth rate (at least in part through deregulation of Cyclin B and ERK1) and sensitized them to pharmacological treatments with irinotecan, SN-38 and cetuximab (at least in part through a down-regulation of AKT).	Irinotecan	178-183	ubiquitin conjugating enzyme E2 C	Homo sapiens	0-6
26826119-8	2016	Treatment of the Gb3-expressing gastric carcinoma cell line St3051 with STxB coupled to SN38, the active metabolite of the topoisomerase type I inhibitor irinotecan, resulted in &gt;100-fold increased cytotoxicity, as compared with irinotecan alone.	Irinotecan	154-164	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	17-20
26826119-8	2016	Treatment of the Gb3-expressing gastric carcinoma cell line St3051 with STxB coupled to SN38, the active metabolite of the topoisomerase type I inhibitor irinotecan, resulted in &gt;100-fold increased cytotoxicity, as compared with irinotecan alone.	Irinotecan	232-242	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	17-20
27037412-9	2016	In combination with irinotecan or doxorubicin, FAP-DR5 treatment resulted in substantial tumor regression in patient-derived xenograft models.	Irinotecan	20-30	TNF receptor superfamily member 10b	Homo sapiens	51-54
26988911-1	2016	We previously reported that ATP7B is involved in cisplatin resistance and ATP7A confers multidrug resistance (MDR) in cancer cells.In this study, we show that ATP7B expressing cells also are resistant to doxorubicin, SN-38, etoposide, and paclitaxel as well as cisplatin.In ATP7B expressing cells, doxorubicin relocated from the nuclei to the late-endosome at 4 hours after doxorubicin exposure.	Irinotecan	217-222	ATPase, Cu++ transporting, alpha polypeptide	Gallus gallus	74-79
26987941-11	2016	Irinotecan also induced increased ROS production in enterocytes, oxidative stress, IL-1beta production, neutrophil and eosinophil influx in the ileum.	Irinotecan	0-10	interleukin 1 beta	Mus musculus	83-91
26581898-6	2016	Irinotecan also caused a decrease in TLR4 and 5, and an increase in GFAP expression in jejuna crypt at 96 and 120 h (all P &lt; 0.05); with lower TLR4 expression associated with lower pain (P = 0.012).	Irinotecan	0-10	toll-like receptor 4	Rattus norvegicus	37-47
26581898-6	2016	Irinotecan also caused a decrease in TLR4 and 5, and an increase in GFAP expression in jejuna crypt at 96 and 120 h (all P &lt; 0.05); with lower TLR4 expression associated with lower pain (P = 0.012).	Irinotecan	0-10	glial fibrillary acidic protein	Rattus norvegicus	68-72
26581898-6	2016	Irinotecan also caused a decrease in TLR4 and 5, and an increase in GFAP expression in jejuna crypt at 96 and 120 h (all P &lt; 0.05); with lower TLR4 expression associated with lower pain (P = 0.012).	Irinotecan	0-10	toll-like receptor 4	Rattus norvegicus	37-41
27122675-1	2016	AIM: To examine the predictive effects of baseline serum bilirubin levels and UDP-glucuronosyltransferase (UGT) 1A1*28 polymorphism on response of colorectal cancer to irinotecan-based chemotherapy.	Irinotecan	168-178	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-115
27122675-16	2016	CONCLUSION: CoBil and UGT1A1*28 are both independent biomarkers for predicting the treatment response of mCRC patients to irinotecan-based chemotherapy.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
26988911-1	2016	We previously reported that ATP7B is involved in cisplatin resistance and ATP7A confers multidrug resistance (MDR) in cancer cells.In this study, we show that ATP7B expressing cells also are resistant to doxorubicin, SN-38, etoposide, and paclitaxel as well as cisplatin.In ATP7B expressing cells, doxorubicin relocated from the nuclei to the late-endosome at 4 hours after doxorubicin exposure.	Irinotecan	217-222	ATPase copper transporting beta	Gallus gallus	159-164
26988911-1	2016	We previously reported that ATP7B is involved in cisplatin resistance and ATP7A confers multidrug resistance (MDR) in cancer cells.In this study, we show that ATP7B expressing cells also are resistant to doxorubicin, SN-38, etoposide, and paclitaxel as well as cisplatin.In ATP7B expressing cells, doxorubicin relocated from the nuclei to the late-endosome at 4 hours after doxorubicin exposure.	Irinotecan	217-222	ATPase copper transporting beta	Gallus gallus	159-164
27091477-0	2016	Epidermal growth factor receptor inhibitor with fluorouracil, leucovorin, and irinotecan as an alternative treatment for advanced upper tract urothelial carcinoma: a case report.	Irinotecan	78-88	epidermal growth factor receptor	Homo sapiens	0-32
26900660-1	2016	Human carboxylesterase 2 (hCE2), one of the major carboxylesterases in the human intestine and various tumour tissues, plays important roles in the oral bioavailability and treatment outcomes of ester- or amide-containing drugs or prodrugs, such as anticancer agents CPT-11 (irinotecan) and LY2334737 (gemcitabine).	Irinotecan	267-273	carboxylesterase 2	Homo sapiens	6-24
26900660-1	2016	Human carboxylesterase 2 (hCE2), one of the major carboxylesterases in the human intestine and various tumour tissues, plays important roles in the oral bioavailability and treatment outcomes of ester- or amide-containing drugs or prodrugs, such as anticancer agents CPT-11 (irinotecan) and LY2334737 (gemcitabine).	Irinotecan	267-273	carboxylesterase 2	Homo sapiens	26-30
26900660-1	2016	Human carboxylesterase 2 (hCE2), one of the major carboxylesterases in the human intestine and various tumour tissues, plays important roles in the oral bioavailability and treatment outcomes of ester- or amide-containing drugs or prodrugs, such as anticancer agents CPT-11 (irinotecan) and LY2334737 (gemcitabine).	Irinotecan	267-273	carboxylesterase 1	Homo sapiens	50-67
26900660-1	2016	Human carboxylesterase 2 (hCE2), one of the major carboxylesterases in the human intestine and various tumour tissues, plays important roles in the oral bioavailability and treatment outcomes of ester- or amide-containing drugs or prodrugs, such as anticancer agents CPT-11 (irinotecan) and LY2334737 (gemcitabine).	Irinotecan	275-285	carboxylesterase 2	Homo sapiens	6-24
26900660-1	2016	Human carboxylesterase 2 (hCE2), one of the major carboxylesterases in the human intestine and various tumour tissues, plays important roles in the oral bioavailability and treatment outcomes of ester- or amide-containing drugs or prodrugs, such as anticancer agents CPT-11 (irinotecan) and LY2334737 (gemcitabine).	Irinotecan	275-285	carboxylesterase 2	Homo sapiens	26-30
26900660-1	2016	Human carboxylesterase 2 (hCE2), one of the major carboxylesterases in the human intestine and various tumour tissues, plays important roles in the oral bioavailability and treatment outcomes of ester- or amide-containing drugs or prodrugs, such as anticancer agents CPT-11 (irinotecan) and LY2334737 (gemcitabine).	Irinotecan	275-285	carboxylesterase 1	Homo sapiens	50-67
27461651-2	2016	DPYD*2A/*5A/*9A and UGT1A1 * 6/*28 polymorphisms are related to the toxicity of fluorouracil drugs and irinotecan, respectively.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
26896610-5	2016	The SN-38/USPIO-loaded siRNA-PEG mixed micelleplexes passively targeted to tumor regions and synergistically facilitated VEGF silencing and chemotherapy, thus efficiently suppressing tumor growth via a multi-dose therapy regimen.	Irinotecan	4-9	vascular endothelial growth factor A	Homo sapiens	121-125
26857987-3	2016	Etirinotecan pegol, comprising irinotecan bound to polyethylene glycol by a biodegradable linker, is a new cytotoxic agent for patients with MBC that has achieved encouraging response rates in phase II studies; it has been further evaluated in the phase III BEACON trial.	Irinotecan	2-12	ubiquitin like 5	Homo sapiens	258-264
27034809-6	2016	The presence of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) *28 polymorphism is associated with toxicity from irinotecan, although it has not been universally applied.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-67
27034809-6	2016	The presence of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) *28 polymorphism is associated with toxicity from irinotecan, although it has not been universally applied.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	69-75
26719532-4	2016	However, the full potential of irinotecan treatment is hindered by several cancer cell survival mechanisms, including ATP-binding cassette G2 (ABCG2) transporter-mediated irinotecan efflux from cells.	Irinotecan	31-41	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	118-141
27080842-6	2016	Other tests are also commonly performed to address the toxicity of certain anticancer drugs (DPYD-capecitabine, UGT1A1-irinotecan, TPMT 6-mercaptopurine).	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	112-118
26872382-3	2016	We found that adenovirus prevents Chk1-mediated checkpoint activation through inactivation of Mre11 and downregulation of the pChk1 adaptor-protein, Claspin, in cells with high levels of DNA-damage induced by the cytotoxic drugs gemcitabine and irinotecan.	Irinotecan	245-255	checkpoint kinase 1	Homo sapiens	34-38
26872382-3	2016	We found that adenovirus prevents Chk1-mediated checkpoint activation through inactivation of Mre11 and downregulation of the pChk1 adaptor-protein, Claspin, in cells with high levels of DNA-damage induced by the cytotoxic drugs gemcitabine and irinotecan.	Irinotecan	245-255	claspin	Homo sapiens	149-156
26719532-4	2016	However, the full potential of irinotecan treatment is hindered by several cancer cell survival mechanisms, including ATP-binding cassette G2 (ABCG2) transporter-mediated irinotecan efflux from cells.	Irinotecan	31-41	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	143-148
26719532-4	2016	However, the full potential of irinotecan treatment is hindered by several cancer cell survival mechanisms, including ATP-binding cassette G2 (ABCG2) transporter-mediated irinotecan efflux from cells.	Irinotecan	171-181	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	118-141
26719532-4	2016	However, the full potential of irinotecan treatment is hindered by several cancer cell survival mechanisms, including ATP-binding cassette G2 (ABCG2) transporter-mediated irinotecan efflux from cells.	Irinotecan	171-181	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	143-148
26719532-5	2016	Here, we demonstrate that benzoporphyrin derivative-based photodynamic therapy (PDT), a photochemical cytotoxic modality that activates the apoptotic pathway, reduced ABCG2 expression to increase intracellular irinotecan levels in pancreatic cancer.	Irinotecan	210-220	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	167-172
26719532-7	2016	Although PDT potentiated irinotecan treatment, we also demonstrate that irinotecan reduced the tumoral expression of monocarboxylate transporter 4, which was upregulated by PDT.	Irinotecan	72-82	solute carrier family 16 member 3	Homo sapiens	117-146
26857783-4	2016	RESULTS AND CONCLUSION: UGT1A1*6 and UGT1A1*28 polymorphisms were associated with severe neutropenia (p = 0.025, p = 0.022, respectively) but not diarrhea (p = 0.343, p = 0.185, respectively), and ABCB1- 3435C&gt;T polymorphism was not associated with irinotecan induced severe toxicities (p = 0.457, p = 0.161, respectively).	Irinotecan	252-262	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
26857783-4	2016	RESULTS AND CONCLUSION: UGT1A1*6 and UGT1A1*28 polymorphisms were associated with severe neutropenia (p = 0.025, p = 0.022, respectively) but not diarrhea (p = 0.343, p = 0.185, respectively), and ABCB1- 3435C&gt;T polymorphism was not associated with irinotecan induced severe toxicities (p = 0.457, p = 0.161, respectively).	Irinotecan	252-262	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
26773202-1	2016	Certain genetic polymorphisms of UDP glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) can reduce gene expression (*28, *60, *93) or activity (*6), thereby altering the pharmacokinetics, pharmacodynamics, and the risk of toxicities of UGT1A1 substrates, of which irinotecan is a widely-described example.	Irinotecan	271-281	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-85
26773202-1	2016	Certain genetic polymorphisms of UDP glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) can reduce gene expression (*28, *60, *93) or activity (*6), thereby altering the pharmacokinetics, pharmacodynamics, and the risk of toxicities of UGT1A1 substrates, of which irinotecan is a widely-described example.	Irinotecan	271-281	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	87-93
26773202-1	2016	Certain genetic polymorphisms of UDP glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) can reduce gene expression (*28, *60, *93) or activity (*6), thereby altering the pharmacokinetics, pharmacodynamics, and the risk of toxicities of UGT1A1 substrates, of which irinotecan is a widely-described example.	Irinotecan	271-281	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	243-249
26541586-4	2016	This antibody-drug conjugate comprises the active metabolite of irinotecan, SN-38, conjugated to an anti-Trop-2 antibody.	Irinotecan	64-74	tumor associated calcium signal transducer 2	Homo sapiens	105-111
26531131-9	2016	As GATA6 is a transcription factor that controls expression of multiple genes regulating peritoneal B-1 cell development and translocation, elimination of GATA6(+) LPMs led to a great reduction in B-1 cells in the peritoneal cavity after CPT-11 treatment.	Irinotecan	238-244	GATA binding protein 6	Mus musculus	3-8
26531131-9	2016	As GATA6 is a transcription factor that controls expression of multiple genes regulating peritoneal B-1 cell development and translocation, elimination of GATA6(+) LPMs led to a great reduction in B-1 cells in the peritoneal cavity after CPT-11 treatment.	Irinotecan	238-244	GATA binding protein 6	Mus musculus	155-160
26381420-3	2016	Cetuximab is a monoclonal antibody against EGFR with additive preclinical activity with irinotecan.	Irinotecan	88-98	epidermal growth factor receptor	Homo sapiens	43-47
26531131-7	2016	Consistent with this, the transcription factor GATA6 specifically expressed in LPMs was barely detectable in the macrophages from CPT-11-treated mice, indicative of elimination of LPMs.	Irinotecan	130-136	GATA binding protein 6	Mus musculus	47-52
26541586-4	2016	This antibody-drug conjugate comprises the active metabolite of irinotecan, SN-38, conjugated to an anti-Trop-2 antibody.	Irinotecan	76-81	tumor associated calcium signal transducer 2	Homo sapiens	105-111
26284333-9	2016	EREG expression appears as an independent prognostic marker in patients with mCRC receiving first-line irinotecan-based chemotherapy.	Irinotecan	103-113	epiregulin	Homo sapiens	0-4
27057810-5	2016	This changed markedly over the last decade with the approval of irinotecan, oxaliplatin, capecitabine, humanized monoclonal antibodies that target either vascular endothelial growth factor (bevacizumab, aflibercept, and ramucirumab) or the epidermal growth factor receptor (cetuximab and panitumumab), and, most recently, regorafenib and trifluridine/tipiracil.	Irinotecan	64-74	vascular endothelial growth factor A	Homo sapiens	154-188
26830078-0	2016	Correlation of UGT1A1(*)28 and (*)6 polymorphisms with irinotecan-induced neutropenia in Thai colorectal cancer patients.	Irinotecan	55-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
26830078-1	2016	UDP-glucuronosyltransferase1A1 (UGT1A1) polymorphisms have been related with irinotecan toxicity.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-30
26830078-1	2016	UDP-glucuronosyltransferase1A1 (UGT1A1) polymorphisms have been related with irinotecan toxicity.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
26830078-2	2016	The purpose of this study was to determine the associations between UGT1A1(*)28 and (*)6 polymorphisms and irinotecan toxicity in Thai patients with metastatic colorectal cancer.	Irinotecan	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
26830078-10	2016	Both UGT1A1(*)28 and (*)6 polymorphisms may have an increased risk of irinotecan-induced neutropenia in Thai colorectal cancer patients.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-11
25869015-5	2016	For irinotecan area under the concentration-time curve (AUC0-24), we replicated ABCC2 -24C&gt;T; however, ABCC2 -24C&gt;T only predicted a small fraction of the variance.	Irinotecan	4-14	ATP binding cassette subfamily C member 2	Homo sapiens	80-85
25869015-6	2016	For SN-38 AUC0-24 and the glucuronidation ratio, we replicated UGT1A1*28 and UGT1A1*93.	Irinotecan	4-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
25869015-6	2016	For SN-38 AUC0-24 and the glucuronidation ratio, we replicated UGT1A1*28 and UGT1A1*93.	Irinotecan	4-9	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
25869015-7	2016	In addition to UGT1A1*28, this study independently validated UGT1A1*93 and SLCO1B1*1b as new predictors of irinotecan neutropenia.	Irinotecan	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
25869015-7	2016	In addition to UGT1A1*28, this study independently validated UGT1A1*93 and SLCO1B1*1b as new predictors of irinotecan neutropenia.	Irinotecan	107-117	solute carrier organic anion transporter family member 1B1	Homo sapiens	75-82
26551156-9	2016	Finally, cetuximab (moAb) and irinotecan (chemotherapy) drugs are analyzed as first-line treatment of colorectal cancer with few KRAS mutated cells.	Irinotecan	30-40	KRAS proto-oncogene, GTPase	Homo sapiens	129-133
26820647-0	2016	Molecular Genetics External Quality Assessment Pilot Scheme for Irinotecan-Related UGT1A1 Genotyping in China.	Irinotecan	64-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
26820647-2	2016	Molecular testing for UGT1A1 genotyping is increasingly required in China for optimum irinotecan administration.	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
26811156-0	2016	Prospective analysis of UGT1A1 promoter polymorphism for irinotecan dose escalation in metastatic colorectal cancer patients treated with bevacizumab plus FOLFIRI as the first-line setting: study protocol for a randomized controlled trial.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
26811156-3	2016	Therefore, we plan to explore the effect of the genetic polymorphism of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) for irinotecan detoxification in mCRC patients.	Irinotecan	133-143	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-119
26811156-3	2016	Therefore, we plan to explore the effect of the genetic polymorphism of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) for irinotecan detoxification in mCRC patients.	Irinotecan	133-143	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	121-127
26811156-6	2016	METHODS/DESIGN: This trial is a prospective, multicenter, randomized clinical trial comparing UGT1A1 promoter polymorphism for irinotecan dose escalation in mCRC patients administered with bevacizumab plus FOLFIRI as the first-line setting.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
26811156-8	2016	The study group receive a biweekly FOLFIRI regimen, with irinotecan dose escalation based on UGT1A1 genotyping; whereas the control group receive the conventional biweekly FOLFIRI regimen without UGT1A1 genotyping.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
26811156-10	2016	DISCUSSION: Patients with mCRC undergoing UGT1A1 genotyping may receive escalated doses of irinotecan for a potentially more favorable clinical response and outcome, in addition to comparable toxicities.	Irinotecan	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
26808671-0	2016	Phenotyping of UGT1A1 Activity Using Raltegravir Predicts Pharmacokinetics and Toxicity of Irinotecan in FOLFIRI.	Irinotecan	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
26808671-1	2016	BACKGROUND: Irinotecan toxicity correlates with UGT1A1 activity.	Irinotecan	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
26801902-8	2016	The gene and protein expression of ABCG2/BCRP was up-regulated in the resistant sub-lines and functional assays revealed BCRP as a key mediator of SN-38 resistance.	Irinotecan	147-152	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	35-40
26801902-8	2016	The gene and protein expression of ABCG2/BCRP was up-regulated in the resistant sub-lines and functional assays revealed BCRP as a key mediator of SN-38 resistance.	Irinotecan	147-152	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	41-45
26801902-8	2016	The gene and protein expression of ABCG2/BCRP was up-regulated in the resistant sub-lines and functional assays revealed BCRP as a key mediator of SN-38 resistance.	Irinotecan	147-152	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	121-125
26801902-9	2016	CONCLUSIONS: Based on our preclinical results, we suggest analyzing the predictive value of the BCRP in breast cancer patients scheduled for irinotecan treatment.	Irinotecan	141-151	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	96-100
26752698-7	2016	Taken together, our data demonstrated for the first time that the combination of irinotecan and gefitinib showed potential benefit in HCC, which suggests that Rad51 is a promising target and provides a rationale for clinical trials investigating the efficacy of the combination of topoisomerase I inhibitors and gefitinib in HCC.	Irinotecan	81-91	RAD51 recombinase	Homo sapiens	159-164
26706406-0	2016	Irinotecan (CPT-11)-induced elevation of bile acids potentiates suppression of IL-10 expression.	Irinotecan	0-10	interleukin 10	Mus musculus	79-84
26706406-0	2016	Irinotecan (CPT-11)-induced elevation of bile acids potentiates suppression of IL-10 expression.	Irinotecan	12-18	interleukin 10	Mus musculus	79-84
26706406-5	2016	Analysis of immune cell populations further showed that CPT-11 treatment significantly decreased the IL-10-producing CD4 T cell frequency in intestinal lamina propria lymphocytes, but not in spleen or mesenteric lymph nodes.	Irinotecan	56-62	interleukin 10	Mus musculus	101-106
26706406-6	2016	In vitro cell culture studies showed that the addition of bile acids deoxycholic acid and taurodeoxycholic acid accelerated the CPT-11-induced suppression of IL-10 secretion by activated CD4(+) naive T cells isolated from mouse splenocytes.	Irinotecan	128-134	interleukin 10	Mus musculus	158-163
26706406-7	2016	These results showed that CPT-11 treatment caused metabolic changes in the composition of bile acids that altered CPT-11-induced suppression of IL-10 expression.	Irinotecan	26-32	interleukin 10	Mus musculus	144-149
26706406-7	2016	These results showed that CPT-11 treatment caused metabolic changes in the composition of bile acids that altered CPT-11-induced suppression of IL-10 expression.	Irinotecan	114-120	interleukin 10	Mus musculus	144-149
26098842-2	2016	This study evaluates the cost-effectiveness of UGT1A1 genotyping in patients with metastatic colorectal cancer undergoing irinotecan-based chemotherapy compared to no testing from the perspective of the German statutory health insurance.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
26872008-0	2016	Phase II and UGT1A1 Polymorphism Study of Two Different Irinotecan Dosages Combined with Cisplatin as First-Line Therapy for Advanced Gastric Cancer.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
26577300-1	2016	A phase II study indicates that sacituzumab govitecan (IMMU-132), a Trop-2-specific antibody linked to the irinotecan metabolite SN-38, prolongs the progression-free survival of patients with advanced triple-negative breast cancer.	Irinotecan	107-117	tumor associated calcium signal transducer 2	Homo sapiens	68-74
26577300-1	2016	A phase II study indicates that sacituzumab govitecan (IMMU-132), a Trop-2-specific antibody linked to the irinotecan metabolite SN-38, prolongs the progression-free survival of patients with advanced triple-negative breast cancer.	Irinotecan	129-134	tumor associated calcium signal transducer 2	Homo sapiens	68-74
29787016-8	2016	Postoperatively, the patient received six courses of combined therapy with irinotecan and cisplatin (CPT-P therapy), and the patient has survived disease- free for over two years.	Irinotecan	75-85	ceramide-1-phosphate transfer protein	Homo sapiens	101-106
26728136-0	2016	PEO-PPO-PEO/Poly(DL-lactide-co-caprolactone) Nanoparticles as Carriers for SN-38: Design, Optimization and Nano-Bio Interface Interactions.	Irinotecan	75-80	protoporphyrinogen oxidase	Homo sapiens	4-7
26728136-4	2016	In this article we defined the optimal region for manufacturing of SN-38 loaded PEO-PPO-PEO/P(DL)LCL nanoparticles (NPs) with high efficacy of encapsulation, suitable particle size and different surface properties, using D-optimal design and nanoprecipitation as production method.	Irinotecan	67-72	protoporphyrinogen oxidase	Homo sapiens	84-87
26526067-4	2016	Based on the fact that liver-specific organic anion transporting polypeptide (OATP)1B1, a member of the same family as OATP2B1, is known to be involved in hepatic transport of SN-38, we hypothesized that intestinal transporter OATP2B1 contributes to the accumulation of SN-38 in gastrointestinal tissues, and its inhibition would help prevent associated toxicity.	Irinotecan	176-181	solute carrier organic anion transporter family member 2B1 L homeolog	Xenopus laevis	119-126
26526067-4	2016	Based on the fact that liver-specific organic anion transporting polypeptide (OATP)1B1, a member of the same family as OATP2B1, is known to be involved in hepatic transport of SN-38, we hypothesized that intestinal transporter OATP2B1 contributes to the accumulation of SN-38 in gastrointestinal tissues, and its inhibition would help prevent associated toxicity.	Irinotecan	176-181	solute carrier organic anion transporter family member 2B1 L homeolog	Xenopus laevis	227-234
26526067-4	2016	Based on the fact that liver-specific organic anion transporting polypeptide (OATP)1B1, a member of the same family as OATP2B1, is known to be involved in hepatic transport of SN-38, we hypothesized that intestinal transporter OATP2B1 contributes to the accumulation of SN-38 in gastrointestinal tissues, and its inhibition would help prevent associated toxicity.	Irinotecan	270-275	solute carrier organic anion transporter family member 2B1 L homeolog	Xenopus laevis	119-126
26526067-5	2016	We found that uptake of SN-38 by OATP2B1-expressing Xenopus oocytes was significantly higher than that by control oocytes.	Irinotecan	24-29	solute carrier organic anion transporter family member 2B1 L homeolog	Xenopus laevis	33-40
26526067-6	2016	OATP2B1-mediated uptake of SN-38 was saturable, pH dependent, and decreased in the presence of baicalin, cefixime, or fruit juices such as apple juice.	Irinotecan	27-32	solute carrier organic anion transporter family member 2B1 L homeolog	Xenopus laevis	0-7
26526067-8	2016	Thus, OATP2B1 contributes to the uptake of SN-38 by intestinal tissues, triggering gastrointestinal toxicity.	Irinotecan	43-48	solute carrier organic anion transporter family member 2B1 L homeolog	Xenopus laevis	6-13
25545261-1	2016	BACKGROUND: UGT1A1 is a polymorphic enzyme that has been associated with irinotecan drug metabolisms.	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
26966430-6	2016	The IC50 values of simvastatin alone and irinotecan alone were 115.4 +- 0.14 muM (r = 0.98) and 62.5 +- 0.18 muM (r = 0.98) in HT-29 cells without resistance to irinotecan.	Irinotecan	41-51	latexin	Homo sapiens	77-80
26966430-6	2016	The IC50 values of simvastatin alone and irinotecan alone were 115.4 +- 0.14 muM (r = 0.98) and 62.5 +- 0.18 muM (r = 0.98) in HT-29 cells without resistance to irinotecan.	Irinotecan	41-51	latexin	Homo sapiens	109-112
27072236-14	2016	Furthermore, as 5.FU and irinotecan metabolism is complex, numerous genes in addition to DPD and UGT1A1 should be investigated.	Irinotecan	25-35	dihydropyrimidine dehydrogenase	Homo sapiens	89-92
27072236-14	2016	Furthermore, as 5.FU and irinotecan metabolism is complex, numerous genes in addition to DPD and UGT1A1 should be investigated.	Irinotecan	25-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
27229742-3	2016	METHODS: Subjects were mCRC patients with mutated KRAS who showed disease aggravation even after two regimens with oxaliplatin and irinotecan.	Irinotecan	131-141	KRAS proto-oncogene, GTPase	Homo sapiens	50-54
27229742-12	2016	CONCLUSIONS: The results suggest that third-line chemotherapy with combined bevacizumab and S-1 is safe and may delay the progression of mCRC resistant to oxaliplatin and irinotecan with mutated KRAS.	Irinotecan	171-181	proteasome 26S subunit, non-ATPase 1	Homo sapiens	92-95
27843533-9	2016	Accordingly, NPOA could be a candidate chemosensitizer of CPT derivative agents such as irinotecan or topotecan in the future.	Irinotecan	88-98	choline phosphotransferase 1	Homo sapiens	58-61
27803477-5	2016	1) In 2005, information regarding the genetic polymorphism of UGT1A1*28 was described in the package insert of the drug irinotecan in the United States.	Irinotecan	120-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
27803477-7	2016	Through clinical research, we demonstrated that UGT1A1*6 was a significant factor for neutropenia, as induced by irinotecan.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
26439663-3	2015	In this study, three kinds of linkers were designed to connect SN-38, the bioactive metabolite of the anticancer drug irinotecan (CPT-11), which is 100-1000 times more potent than CPT-11, with the anti-HER2 antibody trastuzumab to prepare three different ADC conjugates (T-SN38 A, B and C).	Irinotecan	63-68	erb-b2 receptor tyrosine kinase 2	Homo sapiens	202-206
26439663-3	2015	In this study, three kinds of linkers were designed to connect SN-38, the bioactive metabolite of the anticancer drug irinotecan (CPT-11), which is 100-1000 times more potent than CPT-11, with the anti-HER2 antibody trastuzumab to prepare three different ADC conjugates (T-SN38 A, B and C).	Irinotecan	118-128	erb-b2 receptor tyrosine kinase 2	Homo sapiens	202-206
26439663-3	2015	In this study, three kinds of linkers were designed to connect SN-38, the bioactive metabolite of the anticancer drug irinotecan (CPT-11), which is 100-1000 times more potent than CPT-11, with the anti-HER2 antibody trastuzumab to prepare three different ADC conjugates (T-SN38 A, B and C).	Irinotecan	130-136	erb-b2 receptor tyrosine kinase 2	Homo sapiens	202-206
26664141-0	2015	The relationship between UGT1A1 gene polymorphism and irinotecan effect on extensive-stage small-cell lung cancer.	Irinotecan	54-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
26485768-0	2015	Akt inhibition improves irinotecan treatment and prevents cell emergence by switching the senescence response to apoptosis.	Irinotecan	24-34	AKT serine/threonine kinase 1	Homo sapiens	0-3
25915850-7	2015	Moreover, administration of DSB-inducing chemicals, camptothecin (CPT) or irinotecan, to Myc-ELAS1-expressing U2OS cells also induced efficient apoptosis with only 1/100th (CPT) or 1/5th (irinotecan) of the amounts of drugs required for this effect in Myc-vector-expressing cells.	Irinotecan	74-84	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	89-92
25915850-7	2015	Moreover, administration of DSB-inducing chemicals, camptothecin (CPT) or irinotecan, to Myc-ELAS1-expressing U2OS cells also induced efficient apoptosis with only 1/100th (CPT) or 1/5th (irinotecan) of the amounts of drugs required for this effect in Myc-vector-expressing cells.	Irinotecan	74-84	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	252-255
25915850-7	2015	Moreover, administration of DSB-inducing chemicals, camptothecin (CPT) or irinotecan, to Myc-ELAS1-expressing U2OS cells also induced efficient apoptosis with only 1/100th (CPT) or 1/5th (irinotecan) of the amounts of drugs required for this effect in Myc-vector-expressing cells.	Irinotecan	188-198	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	89-92
26664141-11	2015	CONCLUSION: For irinotecan-based regimens in E-SCLC, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for severe adverse events.	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
26664141-11	2015	CONCLUSION: For irinotecan-based regimens in E-SCLC, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for severe adverse events.	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
25799948-3	2015	TACE with 100 mg of Irinotecan loaded into 2-ml of 70-150 microm drug-eluting beads was administrated every 4 weeks in patients with unilobar disease (2 treatments) and every 2 weeks in patients with bilobar disease (4 treatments).	Irinotecan	20-30	ADAM metallopeptidase domain 17	Homo sapiens	0-4
27551256-4	2015	The decoy vascular endothelial growth factor receptor aflibercept has been approved in combination with 5-fluorouracil, leucovorin and irinotecan-based chemotherapy in metastatic colorectal cancer patients whose disease has progressed on a prior oxaliplatin-based chemotherapy regimen.	Irinotecan	135-145	vascular endothelial growth factor A	Homo sapiens	10-44
25216634-2	2015	Irinotecan-induced diarrhea is closely related with the UDP-glucuronosyltransferase 1A1-catalyzed glucuronidation of SN-38 which has been widely regarded to be the toxic substance basis of irinotecan.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-87
25216634-2	2015	Irinotecan-induced diarrhea is closely related with the UDP-glucuronosyltransferase 1A1-catalyzed glucuronidation of SN-38 which has been widely regarded to be the toxic substance basis of irinotecan.	Irinotecan	117-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-87
25216634-2	2015	Irinotecan-induced diarrhea is closely related with the UDP-glucuronosyltransferase 1A1-catalyzed glucuronidation of SN-38 which has been widely regarded to be the toxic substance basis of irinotecan.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-87
26494856-2	2015	UDP-glucuronosyltransferase: (UGT1A1) polymorphism may be predictive of toxicity and efficacy of irinotecan.	Irinotecan	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
26438158-3	2015	Here, we report that PARP inhibitors synergize with temozolomide (TMZ) or SN-38 to induce apoptosis and also somewhat enhance the cytotoxicity of doxorubicin, etoposide, or ifosfamide, whereas actinomycin D and vincristine show little synergism.	Irinotecan	74-79	poly(ADP-ribose) polymerase 1	Homo sapiens	21-25
26637886-2	2015	We conducted a multicenter phase II study of nedaplatin (NP) and irinotecan (CPT) for SCC of the lung.	Irinotecan	65-75	serpin family B member 3	Homo sapiens	86-89
26692528-0	2015	Clinical Implication of UGT1A1 Promoter Polymorphism for Irinotecan Dose Escalation in Metastatic Colorectal Cancer Patients Treated with Bevacizumab Combined with FOLFIRI in the First-line Setting.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
26352872-0	2015	ABCC5 and ABCG1 polymorphisms predict irinotecan-induced severe toxicity in metastatic colorectal cancer patients.	Irinotecan	38-48	ATP binding cassette subfamily C member 5	Homo sapiens	0-5
26352872-0	2015	ABCC5 and ABCG1 polymorphisms predict irinotecan-induced severe toxicity in metastatic colorectal cancer patients.	Irinotecan	38-48	ATP binding cassette subfamily G member 1	Homo sapiens	10-15
26352872-4	2015	MATERIALS AND METHODS: In this study, we aimed to discover toxicity-associated markers in seven transporter genes participating in irinotecan pharmacokinetics involving the ABC transporter genes ABCB1, ABCC1, ABCC2, ABCC5, ABCG1, and ABCG2 and the solute carrier organic anion transporter gene SLCO1B1 and using a haplotype-tagging single-nucleotide polymorphisms (n=210 htSNPs) strategy.	Irinotecan	131-141	ATP binding cassette subfamily B member 1	Homo sapiens	195-200
26352872-4	2015	MATERIALS AND METHODS: In this study, we aimed to discover toxicity-associated markers in seven transporter genes participating in irinotecan pharmacokinetics involving the ABC transporter genes ABCB1, ABCC1, ABCC2, ABCC5, ABCG1, and ABCG2 and the solute carrier organic anion transporter gene SLCO1B1 and using a haplotype-tagging single-nucleotide polymorphisms (n=210 htSNPs) strategy.	Irinotecan	131-141	ATP binding cassette subfamily C member 1	Homo sapiens	202-207
26352872-4	2015	MATERIALS AND METHODS: In this study, we aimed to discover toxicity-associated markers in seven transporter genes participating in irinotecan pharmacokinetics involving the ABC transporter genes ABCB1, ABCC1, ABCC2, ABCC5, ABCG1, and ABCG2 and the solute carrier organic anion transporter gene SLCO1B1 and using a haplotype-tagging single-nucleotide polymorphisms (n=210 htSNPs) strategy.	Irinotecan	131-141	ATP binding cassette subfamily C member 2	Homo sapiens	209-214
26352872-4	2015	MATERIALS AND METHODS: In this study, we aimed to discover toxicity-associated markers in seven transporter genes participating in irinotecan pharmacokinetics involving the ABC transporter genes ABCB1, ABCC1, ABCC2, ABCC5, ABCG1, and ABCG2 and the solute carrier organic anion transporter gene SLCO1B1 and using a haplotype-tagging single-nucleotide polymorphisms (n=210 htSNPs) strategy.	Irinotecan	131-141	ATP binding cassette subfamily C member 5	Homo sapiens	216-221
26352872-4	2015	MATERIALS AND METHODS: In this study, we aimed to discover toxicity-associated markers in seven transporter genes participating in irinotecan pharmacokinetics involving the ABC transporter genes ABCB1, ABCC1, ABCC2, ABCC5, ABCG1, and ABCG2 and the solute carrier organic anion transporter gene SLCO1B1 and using a haplotype-tagging single-nucleotide polymorphisms (n=210 htSNPs) strategy.	Irinotecan	131-141	ATP binding cassette subfamily G member 1	Homo sapiens	223-228
26352872-4	2015	MATERIALS AND METHODS: In this study, we aimed to discover toxicity-associated markers in seven transporter genes participating in irinotecan pharmacokinetics involving the ABC transporter genes ABCB1, ABCC1, ABCC2, ABCC5, ABCG1, and ABCG2 and the solute carrier organic anion transporter gene SLCO1B1 and using a haplotype-tagging single-nucleotide polymorphisms (n=210 htSNPs) strategy.	Irinotecan	131-141	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	234-239
26352872-4	2015	MATERIALS AND METHODS: In this study, we aimed to discover toxicity-associated markers in seven transporter genes participating in irinotecan pharmacokinetics involving the ABC transporter genes ABCB1, ABCC1, ABCC2, ABCC5, ABCG1, and ABCG2 and the solute carrier organic anion transporter gene SLCO1B1 and using a haplotype-tagging single-nucleotide polymorphisms (n=210 htSNPs) strategy.	Irinotecan	131-141	solute carrier organic anion transporter family member 1B1	Homo sapiens	294-301
26431797-0	2015	CPT-11 activates NLRP3 inflammasome through JNK and NF-kappaB signalings.	Irinotecan	0-6	NLR family pyrin domain containing 3	Homo sapiens	17-22
26431797-0	2015	CPT-11 activates NLRP3 inflammasome through JNK and NF-kappaB signalings.	Irinotecan	0-6	mitogen-activated protein kinase 8	Homo sapiens	44-47
26431797-0	2015	CPT-11 activates NLRP3 inflammasome through JNK and NF-kappaB signalings.	Irinotecan	0-6	nuclear factor kappa B subunit 1	Homo sapiens	52-61
26431797-5	2015	In this study, we have discovered that CPT-11 promotes macrophage infiltration into intestinal tissues and activates the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome, resulting in a robust IL-1beta response and colonic inflammation similar to DSS (dextran sodium sulfate) induced experimental colitis.	Irinotecan	39-45	NLR family pyrin domain containing 3	Homo sapiens	174-179
26431797-5	2015	In this study, we have discovered that CPT-11 promotes macrophage infiltration into intestinal tissues and activates the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome, resulting in a robust IL-1beta response and colonic inflammation similar to DSS (dextran sodium sulfate) induced experimental colitis.	Irinotecan	39-45	interleukin 1 beta	Homo sapiens	217-225
25778466-0	2015	A novel UGT1 marker associated with better tolerance against irinotecan-induced severe neutropenia in metastatic colorectal cancer patients.	Irinotecan	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-12
25778466-1	2015	The risk of severe irinotecan-induced neutropenia has been shown to be related to the UGT1 variant UGT1A1*28, which increases exposure to the potent metabolite SN-38.	Irinotecan	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-90
25778466-1	2015	The risk of severe irinotecan-induced neutropenia has been shown to be related to the UGT1 variant UGT1A1*28, which increases exposure to the potent metabolite SN-38.	Irinotecan	19-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
25778466-1	2015	The risk of severe irinotecan-induced neutropenia has been shown to be related to the UGT1 variant UGT1A1*28, which increases exposure to the potent metabolite SN-38.	Irinotecan	160-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-90
25778466-1	2015	The risk of severe irinotecan-induced neutropenia has been shown to be related to the UGT1 variant UGT1A1*28, which increases exposure to the potent metabolite SN-38.	Irinotecan	160-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
26692528-10	2015	CONCLUSIONS: Our study showed that mCRC patients with UGT1A1 *1/*1 and *1/*28 genotypes could receive escalated doses of irinotecan to obtain a more favorable clinical outcome without significant AEs.	Irinotecan	121-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
26692528-1	2015	PURPOSE: This study aimed to identify the efficacy and toxicity of the FOLFIRI regimen (fluorouracil, leucovorin, and irinotecan) with irinotecan dose escalation plus bevacizumab as first-line chemotherapy for metastatic colorectal cancer (mCRC) via UGT1A1 genotyping.	Irinotecan	135-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	250-256
26552750-7	2015	Orthotopic HT-29 xenografts treated with standard CRC chemotherapeutics 5-fluorouracil, irinotecan, or oxaliplatin showed dramatic increases in CD26 compared to untreated tumors.	Irinotecan	88-98	dipeptidyl peptidase 4	Homo sapiens	144-148
26142736-3	2015	As a target of 5-FU, thymidylate synthase (TS) expression level might be influenced by irinotecan.	Irinotecan	87-97	thymidylate synthetase	Homo sapiens	21-41
26142736-3	2015	As a target of 5-FU, thymidylate synthase (TS) expression level might be influenced by irinotecan.	Irinotecan	87-97	thymidylate synthetase	Homo sapiens	43-45
26142736-4	2015	Understanding whether this influence of TS is related with MMR status is helpful to the further exploration of the mechanism of irinotecan sensitivity in metastatic colon cancer with different MMR status.	Irinotecan	128-138	thymidylate synthetase	Homo sapiens	40-42
26142736-9	2015	Regulation of TS by irinotecan was evaluated by western blotting and quantitative real-time PCR assay.	Irinotecan	20-30	thymidylate synthetase	Homo sapiens	14-16
26142736-12	2015	TS expression level was reduced more in dMMR cells after irinotecan treatment (p &lt; 0.05).	Irinotecan	57-67	thymidylate synthetase	Homo sapiens	0-2
26452027-10	2015	Another patient had a newly emerged PIK3CA H1047R mutation on cfDNA analysis at progression during cetuximab/irinotecan chemotherapy with gradual increase in allele frequency from 0.8 to 2.1%.	Irinotecan	109-119	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	36-42
26599335-7	2015	Enhanced effects were observed when regorafenib was combined with irradiation and irinotecan against PDGFRA amplified IGRG93 glioma and IGRM57 medulloblastoma respectively, resulting in 100% tumor regressions.	Irinotecan	82-92	platelet derived growth factor receptor alpha	Homo sapiens	101-107
26504021-1	2015	BACKGROUND: The combination of irinotecan, a topoisomerase I inhibitor with cetuximab, an antibody against epidermal growth factor receptor, produces synergistic and beneficial effects in patients with irinotecan-refractory colorectal cancer.	Irinotecan	31-41	epidermal growth factor receptor	Homo sapiens	107-139
26461062-10	2015	In our exploratory analysis anti-angiogenic/oxaliplatin-based regimens and anti-EGFR/irinotecan-based regimens were associated with the highest pR.	Irinotecan	85-95	epidermal growth factor receptor	Homo sapiens	80-84
26529243-0	2015	Human Lipocalin-Type Prostaglandin D Synthase-Based Drug Delivery System for Poorly Water-Soluble Anti-Cancer Drug SN-38.	Irinotecan	115-120	prostaglandin D2 synthase	Homo sapiens	6-45
26529243-3	2015	In this study, we show the development of a drug delivery system using L-PGDS, one that enables the direct clinical use of 7-ethyl-10-hydroxy-camptothecin (SN-38), a poorly water-soluble anti-cancer drug.	Irinotecan	156-161	prostaglandin D2 synthase	Homo sapiens	71-77
26529243-4	2015	In the presence of 2 mM L-PGDS, the concentration of SN-38 in PBS increased 1,130-fold as compared with that in PBS.	Irinotecan	53-58	prostaglandin D2 synthase	Homo sapiens	24-30
26529243-5	2015	Calorimetric experiments revealed that L-PGDS bound SN-38 at a molecular ratio of 1:3 with a dissociation constant value of 60 muM.	Irinotecan	52-57	prostaglandin D2 synthase	Homo sapiens	39-45
26529243-6	2015	The results of an in vitro growth inhibition assay revealed that the SN-38/L-PGDS complexes showed high anti-tumor activity against 3 human cancer cell lines, i.e., Colo201, MDA-MB-231, and PC-3 with a potency similar to that of SN-38 used alone.	Irinotecan	69-74	prostaglandin D2 synthase	Homo sapiens	75-81
26529243-6	2015	The results of an in vitro growth inhibition assay revealed that the SN-38/L-PGDS complexes showed high anti-tumor activity against 3 human cancer cell lines, i.e., Colo201, MDA-MB-231, and PC-3 with a potency similar to that of SN-38 used alone.	Irinotecan	229-234	prostaglandin D2 synthase	Homo sapiens	75-81
26529243-7	2015	The intravenous administration of SN-38/L-PGDS complexes to mice bearing Colo201 tumors showed a pronounced anti-tumor effect.	Irinotecan	34-39	prostaglandin D2 synthase (brain)	Mus musculus	40-46
26529243-9	2015	Taken together, L-PGDS enables the direct usage of SN-38 with reduced side effects.	Irinotecan	51-56	prostaglandin D2 synthase	Homo sapiens	16-22
26504021-1	2015	BACKGROUND: The combination of irinotecan, a topoisomerase I inhibitor with cetuximab, an antibody against epidermal growth factor receptor, produces synergistic and beneficial effects in patients with irinotecan-refractory colorectal cancer.	Irinotecan	202-212	epidermal growth factor receptor	Homo sapiens	107-139
26504021-9	2015	CONCLUSION: SN-38/cetuximab combination has synergistic anti-angiogenesis and anti-invasion activities mediated by down-regulation of phosphatidylinositol-3-kinases/AKT and mitogen-activated protein kinase/ERK pathways.	Irinotecan	12-17	AKT serine/threonine kinase 1	Homo sapiens	165-168
26504021-9	2015	CONCLUSION: SN-38/cetuximab combination has synergistic anti-angiogenesis and anti-invasion activities mediated by down-regulation of phosphatidylinositol-3-kinases/AKT and mitogen-activated protein kinase/ERK pathways.	Irinotecan	12-17	mitogen-activated protein kinase 3	Homo sapiens	206-209
26692923-6	2015	Lastly, in contrast to both SN-38 (active metabolite of irinotecan) and topotecan are substrates of the efflux pump proteins P-gp/MDR1 and ABCG2/BCRP, FL118 is not a substrate of P-gp and ABCG2.	Irinotecan	28-33	phosphoglycolate phosphatase	Homo sapiens	125-129
26271675-0	2015	HSP90 Inhibitor-SN-38 Conjugate Strategy for Targeted Delivery of Topoisomerase I Inhibitor to Tumors.	Irinotecan	16-21	heat shock protein 90 alpha family class A member 1	Homo sapiens	0-5
26271675-6	2015	In vivo modeling showed that the HSP90 inhibitor moiety was required for selective retention of STA-12-8666, and this enrichment promoted extended release of active SN-38 within the tumor compartment.	Irinotecan	165-170	heat shock protein 90 alpha family class A member 1	Homo sapiens	33-38
26216446-0	2015	Restoration of CBX7 expression increases the susceptibility of human lung carcinoma cells to irinotecan treatment.	Irinotecan	93-103	chromobox 7	Homo sapiens	15-19
26216446-6	2015	Taken together, these results suggest that the retention of CBX7 expression may play a role in the modulation of chemosensitivity of lung cancer patients to the treatment with irinotecan and etoposide.	Irinotecan	176-186	chromobox 7	Homo sapiens	60-64
26429709-7	2015	The study was amended to exclude 4 UGT1A1*28 7/7 homozygous patients due to frequent irinotecan-related grade 3/grade 4 diarrhea and/or febrile neutropenia.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
26509550-0	2015	Effect of Cellular Location of Human Carboxylesterase 2 on CPT-11 Hydrolysis and Anticancer Activity.	Irinotecan	59-65	carboxylesterase 2	Homo sapiens	37-55
26509550-2	2015	Hydrolysis of CPT-11 by human carboxylesterase 2 (CE2) generates SN-38, a topoisomerase I inhibitor that is the active anti-tumor agent.	Irinotecan	14-20	carboxylesterase 2	Homo sapiens	30-48
26509550-2	2015	Hydrolysis of CPT-11 by human carboxylesterase 2 (CE2) generates SN-38, a topoisomerase I inhibitor that is the active anti-tumor agent.	Irinotecan	14-20	carboxylesterase 2	Homo sapiens	50-53
26509550-2	2015	Hydrolysis of CPT-11 by human carboxylesterase 2 (CE2) generates SN-38, a topoisomerase I inhibitor that is the active anti-tumor agent.	Irinotecan	65-70	carboxylesterase 2	Homo sapiens	30-48
26509550-2	2015	Hydrolysis of CPT-11 by human carboxylesterase 2 (CE2) generates SN-38, a topoisomerase I inhibitor that is the active anti-tumor agent.	Irinotecan	65-70	carboxylesterase 2	Homo sapiens	50-53
26509550-9	2015	Cancer cells that expressed all three forms of CE2 were more sensitive to CPT-11 as compared to unmodified cancer cells, but the membrane-anchored and ER-retained forms of CE2 were consistently more effective than secreted CE2.	Irinotecan	74-80	carboxylesterase 2	Homo sapiens	47-50
26509550-10	2015	We conclude that expression of CE2 in the ER or on the membrane of cancer cells is suitable for enhancing CPT-11 anticancer activity.	Irinotecan	106-112	carboxylesterase 2	Homo sapiens	31-34
26692923-6	2015	Lastly, in contrast to both SN-38 (active metabolite of irinotecan) and topotecan are substrates of the efflux pump proteins P-gp/MDR1 and ABCG2/BCRP, FL118 is not a substrate of P-gp and ABCG2.	Irinotecan	28-33	ATP binding cassette subfamily B member 1	Homo sapiens	130-134
26692923-6	2015	Lastly, in contrast to both SN-38 (active metabolite of irinotecan) and topotecan are substrates of the efflux pump proteins P-gp/MDR1 and ABCG2/BCRP, FL118 is not a substrate of P-gp and ABCG2.	Irinotecan	28-33	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	139-144
26692923-6	2015	Lastly, in contrast to both SN-38 (active metabolite of irinotecan) and topotecan are substrates of the efflux pump proteins P-gp/MDR1 and ABCG2/BCRP, FL118 is not a substrate of P-gp and ABCG2.	Irinotecan	28-33	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	145-149
26692923-6	2015	Lastly, in contrast to both SN-38 (active metabolite of irinotecan) and topotecan are substrates of the efflux pump proteins P-gp/MDR1 and ABCG2/BCRP, FL118 is not a substrate of P-gp and ABCG2.	Irinotecan	56-66	phosphoglycolate phosphatase	Homo sapiens	125-129
26692923-6	2015	Lastly, in contrast to both SN-38 (active metabolite of irinotecan) and topotecan are substrates of the efflux pump proteins P-gp/MDR1 and ABCG2/BCRP, FL118 is not a substrate of P-gp and ABCG2.	Irinotecan	56-66	ATP binding cassette subfamily B member 1	Homo sapiens	130-134
26692923-6	2015	Lastly, in contrast to both SN-38 (active metabolite of irinotecan) and topotecan are substrates of the efflux pump proteins P-gp/MDR1 and ABCG2/BCRP, FL118 is not a substrate of P-gp and ABCG2.	Irinotecan	56-66	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	139-144
26315125-0	2015	Protein corona hampers targeting potential of MUC1 aptamer functionalized SN-38 core-shell nanoparticles.	Irinotecan	74-79	mucin 1, cell surface associated	Homo sapiens	46-50
26315125-3	2015	SN-38, an active metabolite of camptothecin, conjugated to hyaluronic acid (HA) was used as the shell of chitosan nanoparticles decorated with MUC1 aptamer.	Irinotecan	0-5	mucin 1, cell surface associated	Homo sapiens	143-147
26463521-3	2015	Conventional irinotecan distributes poorly to brain metastases; therefore, NKTR-102, a PEGylated irinotecan conjugate should enhance irinotecan and its active metabolite SN38 exposure in brain metastases leading to brain tumor cytotoxicity.	Irinotecan	97-107	natural killer tumor recognition sequence	Mus musculus	75-79
26334566-4	2015	SN-38G formation by Ugt1a1 enzyme was analyzed in liver S9 fractions.	Irinotecan	0-5	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	20-26
26334566-10	2015	Conversion of SN-38 to SN-38G by Ugt1a1 enzyme was reduced by ~2-fold in liver S9 fractions in DIO mice.	Irinotecan	14-19	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	33-39
26334566-10	2015	Conversion of SN-38 to SN-38G by Ugt1a1 enzyme was reduced by ~2-fold in liver S9 fractions in DIO mice.	Irinotecan	23-28	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	33-39
26334566-13	2015	SIGNIFICANCE: Our study demonstrates that reduced hepatic Ugt1a activity during obesity likely contributes to reduced glucuronidation, and results in higher levels of the toxic metabolite, SN-38.	Irinotecan	189-194	Ugt1a@	Mus musculus	58-63
26600773-2	2015	Bevacizumab, a monoclonal antibody to VEGF, in common use as an adjunct to standard chemotherapy like irinotecan in advanced colorectal cancer, also affects the normal (nontumor) vasculature.	Irinotecan	102-112	vascular endothelial growth factor A	Homo sapiens	38-42
26463521-3	2015	Conventional irinotecan distributes poorly to brain metastases; therefore, NKTR-102, a PEGylated irinotecan conjugate should enhance irinotecan and its active metabolite SN38 exposure in brain metastases leading to brain tumor cytotoxicity.	Irinotecan	97-107	natural killer tumor recognition sequence	Mus musculus	75-79
26440613-12	2015	This study shows a critical role of the MyD88-mediated TLR2 and TLR9 signaling in the pathogenesis of irinotecan-induced intestinal mucositis.	Irinotecan	102-112	toll-like receptor 9	Mus musculus	64-68
25891902-3	2015	RS1 is in the catalytic loop, RS2 is the Phe in the DFG motif, RS3 is at the C-terminus of the alphaC-Helix, and RS4 is at the beginning of beta4.	Irinotecan	113-116	tubulin beta 3 class III	Homo sapiens	140-145
26440613-0	2015	The Adaptor Protein Myd88 Is a Key Signaling Molecule in the Pathogenesis of Irinotecan-Induced Intestinal Mucositis.	Irinotecan	77-87	myeloid differentiation primary response gene 88	Mus musculus	20-25
26440613-4	2015	Then, we evaluated the involvement of TLRs and MyD88 in the pathogenesis of irinotecan-induced intestinal mucositis.	Irinotecan	76-86	myeloid differentiation primary response gene 88	Mus musculus	47-52
26440613-9	2015	Genetic deletion of MyD88, TLR2 or TLR9 effectively controlled the signs of intestinal injury when compared with irinotecan-administered WT controls (P&lt;0.05).	Irinotecan	113-123	myeloid differentiation primary response gene 88	Mus musculus	20-25
26440613-10	2015	In contrast to the MyD88-/- and TLR2-/- mice, the irinotecan-injected TLR9-/- mice showed a reduced survival, a marked diarrhea and an enhanced expression of IL-18 versus irinotecan-injected WT controls.	Irinotecan	50-60	toll-like receptor 9	Mus musculus	70-74
26440613-10	2015	In contrast to the MyD88-/- and TLR2-/- mice, the irinotecan-injected TLR9-/- mice showed a reduced survival, a marked diarrhea and an enhanced expression of IL-18 versus irinotecan-injected WT controls.	Irinotecan	50-60	interleukin 18	Mus musculus	158-163
26440613-10	2015	In contrast to the MyD88-/- and TLR2-/- mice, the irinotecan-injected TLR9-/- mice showed a reduced survival, a marked diarrhea and an enhanced expression of IL-18 versus irinotecan-injected WT controls.	Irinotecan	171-181	toll-like receptor 9	Mus musculus	70-74
26440613-12	2015	This study shows a critical role of the MyD88-mediated TLR2 and TLR9 signaling in the pathogenesis of irinotecan-induced intestinal mucositis.	Irinotecan	102-112	myeloid differentiation primary response gene 88	Mus musculus	40-45
26440613-12	2015	This study shows a critical role of the MyD88-mediated TLR2 and TLR9 signaling in the pathogenesis of irinotecan-induced intestinal mucositis.	Irinotecan	102-112	toll-like receptor 2	Mus musculus	55-59
26196680-8	2015	SW480 CRC cells that naturally express Lgr5 are those that are floating, and they are more sensitive to the chemotherapeutic compounds irinotecan (maximum difference approximately two times, 0.0001&lt;P&lt;0.0052) and oxaliplatin (maximum difference ~1.5 times, 0.0001&lt;P&lt;0.0024) than Lgr5-negative (attached) SW480 cells.	Irinotecan	135-145	leucine rich repeat containing G protein-coupled receptor 5	Homo sapiens	39-43
26196680-8	2015	SW480 CRC cells that naturally express Lgr5 are those that are floating, and they are more sensitive to the chemotherapeutic compounds irinotecan (maximum difference approximately two times, 0.0001&lt;P&lt;0.0052) and oxaliplatin (maximum difference ~1.5 times, 0.0001&lt;P&lt;0.0024) than Lgr5-negative (attached) SW480 cells.	Irinotecan	135-145	leucine rich repeat containing G protein-coupled receptor 5	Homo sapiens	290-294
26196680-11	2015	Transfected Lgr5-overexpressing attached cells showed similar results with irinotecan and oxaliplatin, confirming that the detected differences in sensitivity to these drugs were Lgr5 driven.	Irinotecan	75-85	leucine rich repeat containing G protein-coupled receptor 5	Homo sapiens	12-16
24724613-0	2015	Interleukin-18 as a target for modulation of irinotecan-induced intestinal toxicity: a step towards a better therapeutic index?	Irinotecan	45-55	interleukin 18	Homo sapiens	0-14
26316041-6	2015	Knockdown of E-cadherin by lentiviral delivery of shRNA significantly reduced chemosensitivity to 5-fluorouracil and irinotecan, increased beta-catenin protein level in HCT116 3D cultures.	Irinotecan	117-127	cadherin 1	Homo sapiens	13-23
26090722-7	2015	These results suggest that HGF produced by fibroblast induce CPT-11 resistance, and that anti-HGF antibody abrogate such resistance in vivo.	Irinotecan	61-67	hepatocyte growth factor	Homo sapiens	27-30
26316041-8	2015	Knockdown of beta-catenin significantly increased chemosensitivity to 5-fluorouracil and irinotecan in HCT116 3D cultures and LoVo 3D cultures.	Irinotecan	89-99	catenin beta 1	Homo sapiens	13-25
26224606-2	2015	Therefore, the aim of our study was to evaluate the differences in phenotype between germ-free (GF) and conventional (CV) mice, and the role of beta-glucuronidase-producing bacteria in the development of irinotecan treatment in a murine model.	Irinotecan	204-214	glucuronidase, beta	Mus musculus	144-162
26486455-0	2015	Exploratory biomarker analysis for treatment response in KRAS wild type metastatic colorectal cancer patients who received cetuximab plus irinotecan.	Irinotecan	138-148	KRAS proto-oncogene, GTPase	Homo sapiens	57-61
26090722-0	2015	Humanized anti-hepatocyte growth factor (HGF) antibody suppresses innate irinotecan (CPT-11) resistance induced by fibroblast-derived HGF.	Irinotecan	73-83	hepatocyte growth factor	Homo sapiens	10-39
26090722-0	2015	Humanized anti-hepatocyte growth factor (HGF) antibody suppresses innate irinotecan (CPT-11) resistance induced by fibroblast-derived HGF.	Irinotecan	73-83	hepatocyte growth factor	Homo sapiens	41-44
26090722-0	2015	Humanized anti-hepatocyte growth factor (HGF) antibody suppresses innate irinotecan (CPT-11) resistance induced by fibroblast-derived HGF.	Irinotecan	73-83	hepatocyte growth factor	Homo sapiens	134-137
26090722-0	2015	Humanized anti-hepatocyte growth factor (HGF) antibody suppresses innate irinotecan (CPT-11) resistance induced by fibroblast-derived HGF.	Irinotecan	85-91	hepatocyte growth factor	Homo sapiens	10-39
26090722-0	2015	Humanized anti-hepatocyte growth factor (HGF) antibody suppresses innate irinotecan (CPT-11) resistance induced by fibroblast-derived HGF.	Irinotecan	85-91	hepatocyte growth factor	Homo sapiens	41-44
26090722-0	2015	Humanized anti-hepatocyte growth factor (HGF) antibody suppresses innate irinotecan (CPT-11) resistance induced by fibroblast-derived HGF.	Irinotecan	85-91	hepatocyte growth factor	Homo sapiens	134-137
26090722-4	2015	Combination treatment of anti-HGF antibody and irinotecan (CPT-11) directly enhanced CPT-11 sensitivity in CRC.	Irinotecan	85-91	hepatocyte growth factor	Homo sapiens	30-33
26206183-6	2015	Under hypoxic growth condition, ABCG2 and ABCB1-overexpressing cells sorted out by FACS technique as side population (SP) were found to be significantly more responsive to SN-38 (ABCG2 and ABCB1 substrate anticancer drug) in the presence of vatalanib.	Irinotecan	172-177	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	32-37
26109630-2	2015	Patients with no response to first-line treatment with S-1 often receive a taxane-alone or irinotecan-alone as second-line treatment.	Irinotecan	91-101	proteasome 26S subunit, non-ATPase 1	Homo sapiens	55-58
26109630-3	2015	However, second-line treatment with S-1 plus irinotecan is widely used in patients with AGC resistant to first-line S-1-based chemotherapy.	Irinotecan	45-55	proteasome 26S subunit, non-ATPase 1	Homo sapiens	116-119
26206183-6	2015	Under hypoxic growth condition, ABCG2 and ABCB1-overexpressing cells sorted out by FACS technique as side population (SP) were found to be significantly more responsive to SN-38 (ABCG2 and ABCB1 substrate anticancer drug) in the presence of vatalanib.	Irinotecan	172-177	ATP binding cassette subfamily B member 1	Homo sapiens	42-47
26101915-2	2015	The rational development of IMMU-132 represents a paradigm shift as an ADC that binds a well-known moderately-cytotoxic drug, SN-38, to the anti-Trop-2 antibody.	Irinotecan	126-131	tumor associated calcium signal transducer 2	Homo sapiens	145-151
26516354-1	2015	BACKGROUND: Active efflux of irinotecan by ATP-binding cassette (ABC)-transporters, in particular ABCB1 and ABCG2, is a well-established drug resistance mechanism in vitro and in pre-clinical mouse models, but its relevance in colorectal cancer (CRC) patients is unknown.	Irinotecan	29-39	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	98-103
26516354-1	2015	BACKGROUND: Active efflux of irinotecan by ATP-binding cassette (ABC)-transporters, in particular ABCB1 and ABCG2, is a well-established drug resistance mechanism in vitro and in pre-clinical mouse models, but its relevance in colorectal cancer (CRC) patients is unknown.	Irinotecan	29-39	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	108-113
26516354-2	2015	Therefore, we assessed the association between ABC-transporter expression and tumour response to irinotecan in patients with metastatic CRC.	Irinotecan	97-107	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	47-62
26516354-4	2015	Kaplan-Meier and Cox proportional hazard regression analyses were performed to assess the association of ABC transporter expression with irinotecan response.	Irinotecan	137-147	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	105-120
26206183-6	2015	Under hypoxic growth condition, ABCG2 and ABCB1-overexpressing cells sorted out by FACS technique as side population (SP) were found to be significantly more responsive to SN-38 (ABCG2 and ABCB1 substrate anticancer drug) in the presence of vatalanib.	Irinotecan	172-177	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	179-184
26206183-6	2015	Under hypoxic growth condition, ABCG2 and ABCB1-overexpressing cells sorted out by FACS technique as side population (SP) were found to be significantly more responsive to SN-38 (ABCG2 and ABCB1 substrate anticancer drug) in the presence of vatalanib.	Irinotecan	172-177	ATP binding cassette subfamily B member 1	Homo sapiens	189-194
25934339-1	2015	The purpose of this study is to evaluate the influence of germline polymorphisms of cytochrome P450 (CYP450) on objective response, progression-free survival (PFS) and overall suruvival (OS) in metastatic colorectal cancer (mCRC) receiving the combination chemotherapy of irinotecan, 5-fluorouracil, and leucovorin (FOLFIRI).	Irinotecan	272-282	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	84-99
25782327-0	2015	DPD and UGT1A1 deficiency in colorectal cancer patients receiving triplet chemotherapy with fluoropyrimidines, oxaliplatin and irinotecan.	Irinotecan	127-137	dihydropyrimidine dehydrogenase	Homo sapiens	0-3
25782327-0	2015	DPD and UGT1A1 deficiency in colorectal cancer patients receiving triplet chemotherapy with fluoropyrimidines, oxaliplatin and irinotecan.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
25782327-2	2015	Single nucleotide polymorphisms (SNPs) in DPYD and UGT1A1 influence fluoropyrimdines and irinotecan adverse events (AEs).	Irinotecan	89-99	dihydropyrimidine dehydrogenase	Homo sapiens	42-46
25782327-2	2015	Single nucleotide polymorphisms (SNPs) in DPYD and UGT1A1 influence fluoropyrimdines and irinotecan adverse events (AEs).	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
26141947-8	2015	Irinotecan cytotoxicity was directly linked to clock gene BMAL1 expression: The least apoptosis resulted from drug exposure near BMAL1 mRNA nadir (P &lt; 0.001), whereas clock silencing through siBMAL1 exposure ablated all the chronopharmacology mechanisms.	Irinotecan	0-10	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	58-63
26141947-8	2015	Irinotecan cytotoxicity was directly linked to clock gene BMAL1 expression: The least apoptosis resulted from drug exposure near BMAL1 mRNA nadir (P &lt; 0.001), whereas clock silencing through siBMAL1 exposure ablated all the chronopharmacology mechanisms.	Irinotecan	0-10	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	129-134
25944802-0	2015	First-in-Human Trial of a Novel Anti-Trop-2 Antibody-SN-38 Conjugate, Sacituzumab Govitecan, for the Treatment of Diverse Metastatic Solid Tumors.	Irinotecan	53-58	tumor associated calcium signal transducer 2	Homo sapiens	37-43
25944802-1	2015	PURPOSE: Sacituzumab govitecan (IMMU-132) is an antibody-drug conjugate (ADC) targeting Trop-2, a surface glycoprotein expressed on many epithelial tumors, for delivery of SN-38, the active metabolite of irinotecan.	Irinotecan	172-177	tumor associated calcium signal transducer 2	Homo sapiens	88-94
25944802-1	2015	PURPOSE: Sacituzumab govitecan (IMMU-132) is an antibody-drug conjugate (ADC) targeting Trop-2, a surface glycoprotein expressed on many epithelial tumors, for delivery of SN-38, the active metabolite of irinotecan.	Irinotecan	204-214	tumor associated calcium signal transducer 2	Homo sapiens	88-94
26713521-2	2015	METHODS: SRB colorimetry was employed to measure the viability of HepG-2 and BEL-7402 cells after the treatment of SN-38 with sorafenib.	Irinotecan	115-120	chaperonin containing TCP1 subunit 4	Homo sapiens	9-12
25934339-1	2015	The purpose of this study is to evaluate the influence of germline polymorphisms of cytochrome P450 (CYP450) on objective response, progression-free survival (PFS) and overall suruvival (OS) in metastatic colorectal cancer (mCRC) receiving the combination chemotherapy of irinotecan, 5-fluorouracil, and leucovorin (FOLFIRI).	Irinotecan	272-282	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	101-107
26713521-5	2015	RESULTS: SRB colorimetry showed the synergistic anticancer activities of SN-38 combined with sorafenib, with a combination index of &lt;0.9.	Irinotecan	73-78	chaperonin containing TCP1 subunit 4	Homo sapiens	9-12
26229432-0	2015	Relationship between UGT1A1*6/*28 polymorphisms and severe toxicities in Chinese patients with pancreatic or biliary tract cancer treated with irinotecan-containing regimens.	Irinotecan	143-153	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
26275292-16	2015	CONCLUSION AND RELEVANCE: The addition of EGFR-I to irinotecan-based chemotherapy has consistent efficacy, regardless of FP regimen, whereas EGFR-I and oxaliplatin-based regimens were most active with infusional 5FU.	Irinotecan	52-62	epidermal growth factor receptor	Homo sapiens	42-46
26257651-0	2015	Simultaneous inhibition of ATR and PARP sensitizes colon cancer cell lines to irinotecan.	Irinotecan	78-88	ATR serine/threonine kinase	Homo sapiens	27-30
26257651-0	2015	Simultaneous inhibition of ATR and PARP sensitizes colon cancer cell lines to irinotecan.	Irinotecan	78-88	poly(ADP-ribose) polymerase 1	Homo sapiens	35-39
26229432-1	2015	PURPOSE: The aim of this retrospective study was to investigate the relationship between UGT1A1 polymorphisms and toxicities in Chinese patients with pancreatic or biliary tract cancer receiving irinotecan-containing regimens as the second- or third-line chemotherapy.	Irinotecan	195-205	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
26229432-12	2015	CONCLUSION: In Chinese patients with pancreatic or biliary tract cancer administered irinotecan-containing regimens, those with UGT1A1*6 variant may have a high risk of severe neutropenia.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-134
26125934-0	2015	Correlation of UGT1A1 and ERCC1 gene polymorphisms with the outcome of combined irinotecan plus cisplatin treatment in recurrent ovarian cancer.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
25870101-5	2015	OTS167 glucuronidation in HLM was highly correlated with thyroxine glucuronidation (r = 0.91, P &lt; 0.0001), SN-38 glucuronidation (r = 0.79, P &lt; 0.0001), and UGT1A1 mRNA (r = 0.72, P &lt; 0.0001).	Irinotecan	110-115	oxysterol binding protein 2	Homo sapiens	26-29
25213123-0	2015	Involvement of matrix metalloproteinases (MMP-3 and MMP-9) in the pathogenesis of irinotecan-induced oral mucositis.	Irinotecan	82-92	matrix metallopeptidase 3	Rattus norvegicus	42-47
25213123-0	2015	Involvement of matrix metalloproteinases (MMP-3 and MMP-9) in the pathogenesis of irinotecan-induced oral mucositis.	Irinotecan	82-92	matrix metallopeptidase 9	Rattus norvegicus	52-57
25213123-3	2015	We investigated tissue expression of MMP-3 and MMP-9 over time in a pre-clinical model of irinotecan-induced oral mucositis (OM).	Irinotecan	90-100	matrix metallopeptidase 3	Rattus norvegicus	37-42
25779651-3	2015	While irinotecan is known to stabilize the complex of topo I and DNA, the enzyme tyrosyl-DNA phosphodiesterase 1 (TDP-1) functions in an opposing manner by releasing topo I from DNA.	Irinotecan	6-16	tyrosyl-DNA phosphodiesterase 1	Mus musculus	81-112
25779651-3	2015	While irinotecan is known to stabilize the complex of topo I and DNA, the enzyme tyrosyl-DNA phosphodiesterase 1 (TDP-1) functions in an opposing manner by releasing topo I from DNA.	Irinotecan	6-16	tyrosyl-DNA phosphodiesterase 1	Mus musculus	114-119
24474168-5	2015	CPT-11 promoted the release of AIF from mitochondria and its translocation to the nucleus.	Irinotecan	0-6	apoptosis inducing factor mitochondria associated 1	Homo sapiens	31-34
24474168-7	2015	Induction of cell-cycle arrest by CPT-11 was associated with changes in expression of key cell-cycle regulators such as CDK2, Chk2, and cyclin D in HL-60 cells.	Irinotecan	34-40	cyclin dependent kinase 2	Homo sapiens	120-124
24474168-7	2015	Induction of cell-cycle arrest by CPT-11 was associated with changes in expression of key cell-cycle regulators such as CDK2, Chk2, and cyclin D in HL-60 cells.	Irinotecan	34-40	checkpoint kinase 2	Homo sapiens	126-130
26591441-0	2015	[UGT1A1 Genotyping for Proper Use of Irinotecan].	Irinotecan	37-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	1-7
26591441-3	2015	Irinotecan is metabolized to form active SN-38, which is further conjugated and detoxified by the UDP-glucuronosyltransferase (UGT) 1A1 enzyme.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-135
26591441-3	2015	Irinotecan is metabolized to form active SN-38, which is further conjugated and detoxified by the UDP-glucuronosyltransferase (UGT) 1A1 enzyme.	Irinotecan	41-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-135
26591441-4	2015	Recent pharmacogenetic studies on irinotecan have revealed the impact of UGT1A1 polymorphisms on severe adverse effects.	Irinotecan	34-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
26591441-5	2015	A variant in the promoter of the UGT1A1 gene, the UGT1A1 *28 allele, has been extensively studied, and pharmacogenetic relationships between the variant and severe toxicities of irinotecan have been reported.	Irinotecan	178-188	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
26591441-5	2015	A variant in the promoter of the UGT1A1 gene, the UGT1A1 *28 allele, has been extensively studied, and pharmacogenetic relationships between the variant and severe toxicities of irinotecan have been reported.	Irinotecan	178-188	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
26591441-8	2015	The concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, markedly alters the disposition of irinotecan, potentially increasing toxicity, which is now written on the label of irinotecan in Japan.	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
26591441-8	2015	The concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, markedly alters the disposition of irinotecan, potentially increasing toxicity, which is now written on the label of irinotecan in Japan.	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
26591441-8	2015	The concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, markedly alters the disposition of irinotecan, potentially increasing toxicity, which is now written on the label of irinotecan in Japan.	Irinotecan	184-194	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
26591441-8	2015	The concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, markedly alters the disposition of irinotecan, potentially increasing toxicity, which is now written on the label of irinotecan in Japan.	Irinotecan	184-194	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
26591441-9	2015	For patients showing homozygosity for UGT1A1*28, *6, or compound heterozygosity for UGT1A1*6 and *28, dose reduction of irinotecan is strongly recommended.	Irinotecan	120-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
26591441-9	2015	For patients showing homozygosity for UGT1A1*28, *6, or compound heterozygosity for UGT1A1*6 and *28, dose reduction of irinotecan is strongly recommended.	Irinotecan	120-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
26591441-12	2015	At present, irinotecan chemotherapy based on a patient"s UGT1A1 genetic status is scientifically reasonable.	Irinotecan	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
26125934-0	2015	Correlation of UGT1A1 and ERCC1 gene polymorphisms with the outcome of combined irinotecan plus cisplatin treatment in recurrent ovarian cancer.	Irinotecan	80-90	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	26-31
26125934-1	2015	The aim of this study was to define the genotypes of UGT1A1 and ERCC1 and to examine their relationship with the efficacy and toxicity of a combination therapy of irinotecan and cisplatin in patients with advanced ovarian cancer.	Irinotecan	163-173	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
26125934-1	2015	The aim of this study was to define the genotypes of UGT1A1 and ERCC1 and to examine their relationship with the efficacy and toxicity of a combination therapy of irinotecan and cisplatin in patients with advanced ovarian cancer.	Irinotecan	163-173	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	64-69
26125934-7	2015	Together, the results from this study suggest that UGT1A1 is a target gene for tardive diarrhea, and that the UGT1A1*28 gene mutation might increase the risk of diarrhea with irinotecan-based chemotherapy.	Irinotecan	175-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
26125934-7	2015	Together, the results from this study suggest that UGT1A1 is a target gene for tardive diarrhea, and that the UGT1A1*28 gene mutation might increase the risk of diarrhea with irinotecan-based chemotherapy.	Irinotecan	175-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
26125934-8	2015	Furthermore, the results suggest that ERCC1 WW carriers might obtain a better rate of clinical response from a combined irinotecan and cisplatin regimen than ERCC1 WM+MM carriers.	Irinotecan	120-130	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	38-43
25917289-4	2015	Our data indicated that both gefitinib and DMG are potent inhibitors of SN-38 glucuronidation via UGT1A1 inhibition.	Irinotecan	72-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
25996449-3	2015	The nanoshells having surface environment modified by hexanethiol SAMs provided high capacity both for hydrophilic DNAzyme (Dz) to induce gene silencing and for hydrophobic SN38 (7-ethyl-10-hydroxycamptothecin), anticancer drug.	Irinotecan	179-209	methionine adenosyltransferase 1A	Homo sapiens	66-70
25777966-1	2015	INTRODUCTION: Topoisomerase 1 (TOP1) and 2A (TOP2A) are potential predictive biomarkers for irinotecan and anthracycline treatment, respectively, in colorectal cancer (CRC), and we have recently reported a high frequency of gene gain of the TOP1 and TOP2A genes in CRC.	Irinotecan	92-102	DNA topoisomerase II alpha	Homo sapiens	45-50
25817555-4	2015	The present review on the impact of the deficient UGT1A1*28 variant on irinotecan efficacy and toxicity was produced by a French joint workgroup comprising the Group of Clinical Onco-pharmacology (GPCO-Unicancer) and the National Pharmacogenetics Network (RNPGx).	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
25817555-5	2015	It clearly emerges that for irinotecan doses at least equal to 180 mg/m(2) , patients homozygous for the UGT1A1*28 allele are at increased risk of developing hematological and/or digestive toxicities.	Irinotecan	28-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
25777966-1	2015	INTRODUCTION: Topoisomerase 1 (TOP1) and 2A (TOP2A) are potential predictive biomarkers for irinotecan and anthracycline treatment, respectively, in colorectal cancer (CRC), and we have recently reported a high frequency of gene gain of the TOP1 and TOP2A genes in CRC.	Irinotecan	92-102	DNA topoisomerase II alpha	Homo sapiens	250-255
25855895-10	2015	It was shown that they have a low cytotoxicity and the ability to reverse the BCRP-mediated SN-38 resistance.	Irinotecan	92-97	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	78-82
25608838-0	2015	TIMP-1 and CEA as biomarkers in third-line treatment with irinotecan and cetuximab for metastatic colorectal cancer.	Irinotecan	58-68	TIMP metallopeptidase inhibitor 1	Homo sapiens	0-6
25608838-0	2015	TIMP-1 and CEA as biomarkers in third-line treatment with irinotecan and cetuximab for metastatic colorectal cancer.	Irinotecan	58-68	CEA cell adhesion molecule 3	Homo sapiens	11-14
25608838-5	2015	The aim of the present study was to investigate the clinical value of TIMP-1 in patients with metastatic colorectal cancer (mCRC) treated with cetuximab and irinotecan.	Irinotecan	157-167	TIMP metallopeptidase inhibitor 1	Homo sapiens	70-76
26025324-0	2015	Carboxylesterase 2 as a Determinant of Response to Irinotecan and Neoadjuvant FOLFIRINOX Therapy in Pancreatic Ductal Adenocarcinoma.	Irinotecan	51-61	carboxylesterase 2	Homo sapiens	0-18
26025324-2	2015	We have undertaken a comprehensive proteomic analysis to assess the differential expression and cellular localization of SHs, which uncovered distinctive expression of Carboxylesterase 2 (CES2), the most efficient carboxyl esterase in activating the prodrug irinotecan into SN-38, in pancreatic ductal adenocarcinoma (PDAC).	Irinotecan	258-268	carboxylesterase 2	Homo sapiens	168-186
26025324-2	2015	We have undertaken a comprehensive proteomic analysis to assess the differential expression and cellular localization of SHs, which uncovered distinctive expression of Carboxylesterase 2 (CES2), the most efficient carboxyl esterase in activating the prodrug irinotecan into SN-38, in pancreatic ductal adenocarcinoma (PDAC).	Irinotecan	258-268	carboxylesterase 2	Homo sapiens	188-192
26025324-2	2015	We have undertaken a comprehensive proteomic analysis to assess the differential expression and cellular localization of SHs, which uncovered distinctive expression of Carboxylesterase 2 (CES2), the most efficient carboxyl esterase in activating the prodrug irinotecan into SN-38, in pancreatic ductal adenocarcinoma (PDAC).	Irinotecan	274-279	carboxylesterase 2	Homo sapiens	168-186
26025324-2	2015	We have undertaken a comprehensive proteomic analysis to assess the differential expression and cellular localization of SHs, which uncovered distinctive expression of Carboxylesterase 2 (CES2), the most efficient carboxyl esterase in activating the prodrug irinotecan into SN-38, in pancreatic ductal adenocarcinoma (PDAC).	Irinotecan	274-279	carboxylesterase 2	Homo sapiens	188-192
26025324-5	2015	CES2 activity was assessed by monitoring the hydrolysis of the substrate p-NPA and correlated with irinotecan IC50 values by means of Pearson"s correlation.	Irinotecan	99-109	carboxylesterase 2	Homo sapiens	0-4
26025324-9	2015	CES2 activity in 11 PDAC cell lines was inversely correlated with irinotecan IC50 values (R = -0.68, P = .02).	Irinotecan	66-76	carboxylesterase 2	Homo sapiens	0-4
26025324-11	2015	CONCLUSION: Our findings suggest that CES2 expression and activity, by mediating the intratumoral activation of irinotecan, is a contributor to FOLFIRINOX sensitivity in pancreatic cancer and CES2 assessment may define a subset of patients likely to respond to irinotecan based therapy.	Irinotecan	112-122	carboxylesterase 2	Homo sapiens	38-42
26025324-11	2015	CONCLUSION: Our findings suggest that CES2 expression and activity, by mediating the intratumoral activation of irinotecan, is a contributor to FOLFIRINOX sensitivity in pancreatic cancer and CES2 assessment may define a subset of patients likely to respond to irinotecan based therapy.	Irinotecan	261-271	carboxylesterase 2	Homo sapiens	38-42
25880011-1	2015	BACKGROUND: In Asians, the risk of irinotecan-induced severe toxicities is related in part to UGT1A1*6 (UGT, UDP glucuronosyltransferase) and UGT1A1*28, variant alleles that reduce the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	35-45	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	94-102
25915780-7	2015	Exposure of tumor cells to either free SN-38 or IMMU-132 demonstrated the same signaling pathways, with pJNK1/2 and p21(WAF1/Cip1) upregulation followed by cleavage of caspases 9, 7, and 3, ultimately leading to poly-ADP-ribose polymerase cleavage and double-stranded DNA breaks.	Irinotecan	39-44	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	116-119
25915780-7	2015	Exposure of tumor cells to either free SN-38 or IMMU-132 demonstrated the same signaling pathways, with pJNK1/2 and p21(WAF1/Cip1) upregulation followed by cleavage of caspases 9, 7, and 3, ultimately leading to poly-ADP-ribose polymerase cleavage and double-stranded DNA breaks.	Irinotecan	39-44	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	120-124
25915780-7	2015	Exposure of tumor cells to either free SN-38 or IMMU-132 demonstrated the same signaling pathways, with pJNK1/2 and p21(WAF1/Cip1) upregulation followed by cleavage of caspases 9, 7, and 3, ultimately leading to poly-ADP-ribose polymerase cleavage and double-stranded DNA breaks.	Irinotecan	39-44	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	125-129
25915780-7	2015	Exposure of tumor cells to either free SN-38 or IMMU-132 demonstrated the same signaling pathways, with pJNK1/2 and p21(WAF1/Cip1) upregulation followed by cleavage of caspases 9, 7, and 3, ultimately leading to poly-ADP-ribose polymerase cleavage and double-stranded DNA breaks.	Irinotecan	39-44	caspase 9	Mus musculus	168-188
25973791-0	2015	Identification of Sestrin3 Involved in the In vitro Resistance of Colorectal Cancer Cells to Irinotecan.	Irinotecan	93-103	sestrin 3	Homo sapiens	18-26
25973791-5	2015	After gene ontology (GO) and KEGG pathway analysis of the microarray data, we specifically investigated whether Sestrin3 could decrease irinotecan resistance.	Irinotecan	136-146	sestrin 3	Homo sapiens	112-120
25973791-6	2015	Our results revealed that Sestrin3 enhanced the anticancer effect of irinotecan in vitro in LoVo cells that had acquired resistance to irinotecan.	Irinotecan	69-79	sestrin 3	Homo sapiens	26-34
25973791-6	2015	Our results revealed that Sestrin3 enhanced the anticancer effect of irinotecan in vitro in LoVo cells that had acquired resistance to irinotecan.	Irinotecan	135-145	sestrin 3	Homo sapiens	26-34
25973791-8	2015	ROS production was increased by Sestrin3 knockdown in irinotecan-resistant LoVo cells.	Irinotecan	54-64	sestrin 3	Homo sapiens	32-40
25973791-9	2015	Our results indicate that Sestrin3 might be a good target to develop therapeutics that can help to overcome resistance to irinotecan.	Irinotecan	122-132	sestrin 3	Homo sapiens	26-34
25880011-1	2015	BACKGROUND: In Asians, the risk of irinotecan-induced severe toxicities is related in part to UGT1A1*6 (UGT, UDP glucuronosyltransferase) and UGT1A1*28, variant alleles that reduce the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	35-45	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	94-97
25880011-1	2015	BACKGROUND: In Asians, the risk of irinotecan-induced severe toxicities is related in part to UGT1A1*6 (UGT, UDP glucuronosyltransferase) and UGT1A1*28, variant alleles that reduce the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	35-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
25880011-1	2015	BACKGROUND: In Asians, the risk of irinotecan-induced severe toxicities is related in part to UGT1A1*6 (UGT, UDP glucuronosyltransferase) and UGT1A1*28, variant alleles that reduce the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	200-205	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	94-97
25880011-1	2015	BACKGROUND: In Asians, the risk of irinotecan-induced severe toxicities is related in part to UGT1A1*6 (UGT, UDP glucuronosyltransferase) and UGT1A1*28, variant alleles that reduce the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	200-205	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
25890497-0	2015	The oncogenic receptor ErbB2 modulates gemcitabine and irinotecan/SN-38 chemoresistance of human pancreatic cancer cells via hCNT1 transporter and multidrug-resistance associated protein MRP-2.	Irinotecan	55-65	erb-b2 receptor tyrosine kinase 2	Homo sapiens	23-28
25880011-1	2015	BACKGROUND: In Asians, the risk of irinotecan-induced severe toxicities is related in part to UGT1A1*6 (UGT, UDP glucuronosyltransferase) and UGT1A1*28, variant alleles that reduce the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	232-242	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	94-97
25880011-1	2015	BACKGROUND: In Asians, the risk of irinotecan-induced severe toxicities is related in part to UGT1A1*6 (UGT, UDP glucuronosyltransferase) and UGT1A1*28, variant alleles that reduce the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	232-242	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
25880011-2	2015	We prospectively studied the relation between the UGT1A1 genotype and the safety of irinotecan-based regimens in Japanese patients with advanced colorectal cancer, and then constructed a nomogram for predicting the risk of severe neutropenia in the first treatment cycle.	Irinotecan	84-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
25880011-6	2015	RESULTS: The UGT1A1 genotype was confirmed to be associated with increased risks of irinotecan-induced grade 3 or 4 neutropenia and diarrhoea.	Irinotecan	84-94	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
25890497-0	2015	The oncogenic receptor ErbB2 modulates gemcitabine and irinotecan/SN-38 chemoresistance of human pancreatic cancer cells via hCNT1 transporter and multidrug-resistance associated protein MRP-2.	Irinotecan	55-65	solute carrier family 28 member 1	Homo sapiens	125-130
25890497-0	2015	The oncogenic receptor ErbB2 modulates gemcitabine and irinotecan/SN-38 chemoresistance of human pancreatic cancer cells via hCNT1 transporter and multidrug-resistance associated protein MRP-2.	Irinotecan	66-71	erb-b2 receptor tyrosine kinase 2	Homo sapiens	23-28
26027741-8	2015	Heritable genetic variants in the ABC and SLC transport pathways; in the CYP450, GST, and UGT-mediated phase I and II metabolism; in the folate metabolic pathway; as well as in the EGF and VEGF signaling pathways, have been associated with a distinct tumor sensitivity phenotype in CRC patients treated with fluoropyrimidines combined with either irinotecan, oxaliplatin or targeted biological agents.	Irinotecan	347-357	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	34-37
26027741-8	2015	Heritable genetic variants in the ABC and SLC transport pathways; in the CYP450, GST, and UGT-mediated phase I and II metabolism; in the folate metabolic pathway; as well as in the EGF and VEGF signaling pathways, have been associated with a distinct tumor sensitivity phenotype in CRC patients treated with fluoropyrimidines combined with either irinotecan, oxaliplatin or targeted biological agents.	Irinotecan	347-357	C-C motif chemokine ligand 21	Homo sapiens	42-45
26027741-8	2015	Heritable genetic variants in the ABC and SLC transport pathways; in the CYP450, GST, and UGT-mediated phase I and II metabolism; in the folate metabolic pathway; as well as in the EGF and VEGF signaling pathways, have been associated with a distinct tumor sensitivity phenotype in CRC patients treated with fluoropyrimidines combined with either irinotecan, oxaliplatin or targeted biological agents.	Irinotecan	347-357	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	90-93
26027741-8	2015	Heritable genetic variants in the ABC and SLC transport pathways; in the CYP450, GST, and UGT-mediated phase I and II metabolism; in the folate metabolic pathway; as well as in the EGF and VEGF signaling pathways, have been associated with a distinct tumor sensitivity phenotype in CRC patients treated with fluoropyrimidines combined with either irinotecan, oxaliplatin or targeted biological agents.	Irinotecan	347-357	vascular endothelial growth factor A	Homo sapiens	189-193
25981652-2	2015	However, there are reports of an association between certain UGT1A1 genetic polymorphisms and the development of adverse reactions(such as neutropenia)related to irinotecan metabolism.	Irinotecan	162-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
25981652-7	2015	These results suggest that a dose reduction of irinotecan should be considered for patients who fall into the homozygous group upon analysis of their UGT1A1 genetic polymorphisms, as such patients might be susceptible to grade 4 neutropenia.	Irinotecan	47-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	150-156
25762723-3	2015	Several drugs are either substrates or inhibitors of multidrug resistance protein 4 (MRP4), such as the anti-colon cancer drug irinotecan and an anti-retroviral used to treat HIV infection, 3"-azido-3"-deoxythymidine (AZT).	Irinotecan	127-137	ATP binding cassette subfamily C member 4	Homo sapiens	53-83
25762723-3	2015	Several drugs are either substrates or inhibitors of multidrug resistance protein 4 (MRP4), such as the anti-colon cancer drug irinotecan and an anti-retroviral used to treat HIV infection, 3"-azido-3"-deoxythymidine (AZT).	Irinotecan	127-137	ATP binding cassette subfamily C member 4	Homo sapiens	85-89
26634139-0	2015	CPT-11/bevacizumab for the treatment of refractory brain metastases in patients with HER2-neu-positive breast cancer.	Irinotecan	0-6	erb-b2 receptor tyrosine kinase 2	Homo sapiens	85-89
25708528-0	2015	Fatty acid synthase-positive hepatocytes and subsequent steatosis in rat livers by irinotecan.	Irinotecan	83-93	fatty acid synthase	Rattus norvegicus	0-19
25708528-8	2015	Thus, irinotecan-induced liver steatosis was preceded by Fasn-strongly-positive hepatocytes and liver progenitor cell activation.	Irinotecan	6-16	fatty acid synthase	Rattus norvegicus	57-61
26634139-3	2015	We evaluated CPT-11 and bevacizumab, which can both cross the blood-brain barrier, as combination therapy to treat HER2-neu-positive breast cancer with brain metastases.	Irinotecan	13-19	erb-b2 receptor tyrosine kinase 2	Homo sapiens	115-119
25744244-2	2015	This work aimed to investigate the alterations in chemosensitivity of A549 lung cancer cells for 5-Fluorouracil (5-FU) and irinotecan by silencing ABCE1 using specific small interfering RNAs (siRNA).	Irinotecan	123-133	ATP binding cassette subfamily E member 1	Homo sapiens	147-152
26097871-4	2015	In vitro, the bioconjugate selectively interacted with ovarian cancer cells through the CD44 receptor, disclosed a dose-dependent tumor growth inhibition efficacy comparable to that of free SN-38 drug, and inhibited Topoisomerase I function leading to apoptosis by a mechanism involving caspase-3 and -7 activation and PARP cleavage.	Irinotecan	190-195	CD44 antigen	Mus musculus	88-92
25774912-9	2015	In vivo, the BRCA mutant cell line MX-1 treated with CPT-11 alone demonstrated significant decreased tumor growth; this decrease was enhanced further with the addition of ABT-888.	Irinotecan	53-59	BRCA1 DNA repair associated	Homo sapiens	13-17
25611302-0	2015	OATP1B1 and tumour OATP1B3 modulate exposure, toxicity, and survival after irinotecan-based chemotherapy.	Irinotecan	75-85	solute carrier organic anion transporter family member 1B1	Homo sapiens	0-7
25611302-2	2015	The active metabolite of irinotecan, SN-38, is a known substrate of drug-metabolising enzymes, including UGT1A1, as well as OATP and ABC drug transporters.	Irinotecan	37-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
25611302-0	2015	OATP1B1 and tumour OATP1B3 modulate exposure, toxicity, and survival after irinotecan-based chemotherapy.	Irinotecan	75-85	solute carrier organic anion transporter family member 1B3	Homo sapiens	19-26
25611302-5	2015	RESULTS: SLCO1B1 521C was significantly associated with increased SN-38 exposure (P&lt;0.001), which was additive with UGT1A1*28.	Irinotecan	66-71	solute carrier organic anion transporter family member 1B1	Homo sapiens	9-16
25611302-5	2015	RESULTS: SLCO1B1 521C was significantly associated with increased SN-38 exposure (P&lt;0.001), which was additive with UGT1A1*28.	Irinotecan	66-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
25611302-2	2015	The active metabolite of irinotecan, SN-38, is a known substrate of drug-metabolising enzymes, including UGT1A1, as well as OATP and ABC drug transporters.	Irinotecan	25-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
25611302-10	2015	CONCLUSIONS: Clarifying the association of host genetic variation in OATP and ABC transporters to SN-38 exposure, toxicity and PFS provides rationale for personalising irinotecan-based chemotherapy.	Irinotecan	98-103	solute carrier organic anion transporter family member 1A2	Homo sapiens	69-73
25645751-0	2015	Surface-enhanced Raman spectroscopy of the anti-cancer drug irinotecan in presence of human serum albumin.	Irinotecan	60-70	albumin	Homo sapiens	92-105
25611302-10	2015	CONCLUSIONS: Clarifying the association of host genetic variation in OATP and ABC transporters to SN-38 exposure, toxicity and PFS provides rationale for personalising irinotecan-based chemotherapy.	Irinotecan	168-178	solute carrier organic anion transporter family member 1A2	Homo sapiens	69-73
25433165-10	2015	The expression of OATP2A1 increased the sensitivity of AGS cells against irinotecan which led to reduced cell viability.	Irinotecan	73-83	solute carrier organic anion transporter family member 2A1	Homo sapiens	18-25
25733708-0	2015	Activity of MM-398, nanoliposomal irinotecan (nal-IRI), in Ewing"s family tumor xenografts is associated with high exposure of tumor to drug and high SLFN11 expression.	Irinotecan	34-44	schlafen family member 11	Homo sapiens	150-156
25733708-9	2015	Cytotoxicity of SN-38 inversely correlated with SLFN11 mRNA expression in 20 EFT cell lines.	Irinotecan	16-21	schlafen family member 11	Homo sapiens	48-54
25605843-1	2015	PURPOSE: The phase III CRYSTAL study demonstrated that addition of cetuximab to fluorouracil, leucovorin, and irinotecan (FOLFIRI) significantly improved overall survival, progression-free survival, and objective response in the first-line treatment of patients with KRAS codon 12/13 (exon 2) wild-type metastatic colorectal cancer (mCRC).	Irinotecan	110-120	KRAS proto-oncogene, GTPase	Homo sapiens	267-271
25554586-2	2015	Substrates transported by ABCC2 include antiepileptics, statins, tenofovir, cisplatin, irinotecan, and carbamazepine.	Irinotecan	87-97	ATP binding cassette subfamily C member 2	Homo sapiens	26-31
25783977-5	2015	The evidence to support broad utilization of uridine 5"-diphospho-glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) testing to guide irinotecan and fluorouracil dosing remains limited.	Irinotecan	162-172	dihydropyrimidine dehydrogenase	Homo sapiens	140-143
25601188-0	2015	Favorable response to trastuzumab plus irinotecan combination therapy in two patients with HER2-positive relapsed small-cell lung cancer.	Irinotecan	39-49	erb-b2 receptor tyrosine kinase 2	Homo sapiens	91-95
25601188-5	2015	Based on these preclinical data, we treated two patients with HER2-positive SCLC by combination of trastuzumab (6 mg/kg, day 1) and irinotecan (80 mg/m(2), days 1 and 8) every 21 days as the third-line chemotherapy following two prior regimens, first-line carboplatin plus etoposide and second-line amrubicin.	Irinotecan	132-142	erb-b2 receptor tyrosine kinase 2	Homo sapiens	62-66
25601188-9	2015	In conclusion, trastuzumab plus irinotecan chemotherapy is promising and feasible against HER2-positive relapsed SCLC.	Irinotecan	32-42	erb-b2 receptor tyrosine kinase 2	Homo sapiens	90-94
25644220-1	2015	In this study, we successfully synthesized d-alpha-tocopheryl polyethylene glycol 2000 succinate (TPGS2k) and prepared TPGS2k-modified poly(lactic-co-glycolic acid) nanoparticles (TPGS2k/PLGA NPs) loaded with 7-ethyl-10-hydroxycamptothecin (SN-38), designated TPGS2k/PLGA/SN-38 NPs.	Irinotecan	209-239	tubulin polyglutamylase complex subunit 2	Homo sapiens	119-124
25644220-1	2015	In this study, we successfully synthesized d-alpha-tocopheryl polyethylene glycol 2000 succinate (TPGS2k) and prepared TPGS2k-modified poly(lactic-co-glycolic acid) nanoparticles (TPGS2k/PLGA NPs) loaded with 7-ethyl-10-hydroxycamptothecin (SN-38), designated TPGS2k/PLGA/SN-38 NPs.	Irinotecan	241-246	tubulin polyglutamylase complex subunit 2	Homo sapiens	119-124
25644220-1	2015	In this study, we successfully synthesized d-alpha-tocopheryl polyethylene glycol 2000 succinate (TPGS2k) and prepared TPGS2k-modified poly(lactic-co-glycolic acid) nanoparticles (TPGS2k/PLGA NPs) loaded with 7-ethyl-10-hydroxycamptothecin (SN-38), designated TPGS2k/PLGA/SN-38 NPs.	Irinotecan	272-277	tubulin polyglutamylase complex subunit 2	Homo sapiens	119-124
25644220-3	2015	SN-38 was encapsulated in TPGS2k emulsified PLGA NPs with the entrapment efficiency and loading rates of SN-38 83.6 and 7.85%, respectively.	Irinotecan	0-5	tubulin polyglutamylase complex subunit 2	Homo sapiens	26-31
25644220-3	2015	SN-38 was encapsulated in TPGS2k emulsified PLGA NPs with the entrapment efficiency and loading rates of SN-38 83.6 and 7.85%, respectively.	Irinotecan	105-110	tubulin polyglutamylase complex subunit 2	Homo sapiens	26-31
25644220-4	2015	SN-38 could release constantly from TPGS2k/PLGA/SN-38 NPs in vitro.	Irinotecan	0-5	tubulin polyglutamylase complex subunit 2	Homo sapiens	36-41
25644220-4	2015	SN-38 could release constantly from TPGS2k/PLGA/SN-38 NPs in vitro.	Irinotecan	48-53	tubulin polyglutamylase complex subunit 2	Homo sapiens	36-41
25644220-5	2015	TPGS2k/PLGA/SN-38 NPs induced significantly higher cytotoxicity on A549 cells and the multidrug resistance (MDR) cell line (A549/DDP cells and A549/Taxol cells) compared with free SN-38.	Irinotecan	12-17	tubulin polyglutamylase complex subunit 2	Homo sapiens	0-5
25644220-5	2015	TPGS2k/PLGA/SN-38 NPs induced significantly higher cytotoxicity on A549 cells and the multidrug resistance (MDR) cell line (A549/DDP cells and A549/Taxol cells) compared with free SN-38.	Irinotecan	180-185	tubulin polyglutamylase complex subunit 2	Homo sapiens	0-5
25644220-6	2015	Further studies on the mechanism of the NPs in increasing the death of MDR cells showed that following the SN-38 releasing into cytoplasm the remaining TPGS2k/PLGA NPs could reverse the P-gp mediated MDR via interfering with the structure and function of mitochondria and rather than directly inhibiting the enzymatic activity of P-gp ATPase.	Irinotecan	107-112	tubulin polyglutamylase complex subunit 2	Homo sapiens	152-157
25644220-6	2015	Further studies on the mechanism of the NPs in increasing the death of MDR cells showed that following the SN-38 releasing into cytoplasm the remaining TPGS2k/PLGA NPs could reverse the P-gp mediated MDR via interfering with the structure and function of mitochondria and rather than directly inhibiting the enzymatic activity of P-gp ATPase.	Irinotecan	107-112	phosphoglycolate phosphatase	Homo sapiens	186-190
25644220-6	2015	Further studies on the mechanism of the NPs in increasing the death of MDR cells showed that following the SN-38 releasing into cytoplasm the remaining TPGS2k/PLGA NPs could reverse the P-gp mediated MDR via interfering with the structure and function of mitochondria and rather than directly inhibiting the enzymatic activity of P-gp ATPase.	Irinotecan	107-112	phosphoglycolate phosphatase	Homo sapiens	330-334
25885574-0	2015	A phase II study of weekly irinotecan in patients with locally advanced or metastatic HER2- negative breast cancer and increased copy numbers of the topoisomerase 1 (TOP1) gene: a study protocol.	Irinotecan	27-37	erb-b2 receptor tyrosine kinase 2	Homo sapiens	86-90
25462817-6	2015	Selected compounds were tested for their ability to sensitize MRP4-overexpressing cell lines to the MRP4 substrate drugs 6-mercaptopurine and SN-38, with sensitization up to 6.5-fold with the ryanodine receptor antagonist dantrolene.	Irinotecan	142-147	ATP binding cassette subfamily C member 4	Homo sapiens	62-66
25689738-4	2015	In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities.	Irinotecan	110-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
25611974-0	2015	Thymoquinone induces caspase-independent, autophagic cell death in CPT-11-resistant lovo colon cancer via mitochondrial dysfunction and activation of JNK and p38.	Irinotecan	67-73	mitogen-activated protein kinase 14	Homo sapiens	158-161
25713534-3	2015	Hangeshashinto improves irinotecan-induced diarrhea and chemotherapy-induced mucositis by inhibiting the activity of beta-glucuronidase as well as the synthesis of prostaglandin E2.	Irinotecan	24-34	glucuronidase beta	Homo sapiens	117-135
25685067-0	2015	Treatment with the PARP inhibitor, niraparib, sensitizes colorectal cancer cell lines to irinotecan regardless of MSI/MSS status.	Irinotecan	89-99	poly(ADP-ribose) polymerase 1	Homo sapiens	19-23
25689738-4	2015	In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities.	Irinotecan	110-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
25689738-4	2015	In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
25689738-4	2015	In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
25689738-4	2015	In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities.	Irinotecan	150-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
25689738-4	2015	In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities.	Irinotecan	150-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
25971303-1	2015	INTRODUCTION: Pegylated irinotecan NKTR-102 is a topoisomerase I inhibitor-polymer conjugate.	Irinotecan	24-34	natural killer cell triggering receptor	Homo sapiens	35-39
25971303-3	2015	To the best of our knowledge, this is the first case report of an impressive iterative response to pegylated irinotecan NKTR-102 in metastatic breast cancer.	Irinotecan	109-119	natural killer cell triggering receptor	Homo sapiens	120-124
25971303-5	2015	She showed no major response to conventional treatment, whereas, the tumor shrinkage under pegylated irinotecan NKTR-102 was impressive, durable and iterative.	Irinotecan	101-111	natural killer cell triggering receptor	Homo sapiens	112-116
25462817-6	2015	Selected compounds were tested for their ability to sensitize MRP4-overexpressing cell lines to the MRP4 substrate drugs 6-mercaptopurine and SN-38, with sensitization up to 6.5-fold with the ryanodine receptor antagonist dantrolene.	Irinotecan	142-147	ATP binding cassette subfamily C member 4	Homo sapiens	100-104
25522766-0	2015	Clinical and cellular roles for TDP1 and TOP1 in modulating colorectal cancer response to irinotecan.	Irinotecan	90-100	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	32-36
25445689-1	2015	The binding of irinotecan to serum proteins (hemoglobin, globulin and human serum albumin) was studied on the surface of epoxide modified superparamagnetic iron oxide nanoparticles (GPTS-SPIONs), which were synthesized by the coprecipitation of ferrous and ferric salts with NH4OH and then modified with [3-(2,3-epoxypropoxy)propyl] trimethoxy silane (GPTS) to obtain functional epoxide groups on the SPIONs" surface.	Irinotecan	15-25	albumin	Homo sapiens	76-89
25522766-8	2015	Conversely, TDP1 depletion increases DNA-strand breakage and hypersensitivity to irinotecan in a TOP1-dependent manner, presenting a potential therapeutic opportunity in colorectal cancer.	Irinotecan	81-91	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	12-16
25055799-0	2015	UGT1A1 *6 polymorphism predicts outcome in elderly patients with relapsed or refractory diffuse large B-cell lymphoma treated with carboplatin, dexamethasone, etoposide and irinotecan.	Irinotecan	173-183	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25055799-1	2015	The uridine diphosphate glucuronosyltransferase (UGT) gene 1A1*6 polymorphism, which affects irinotecan metabolism, has been associated with improved survival in lymphoma patients treated with of carboplatin, dexamethasone, etoposide and irinotecan (CDE-11).	Irinotecan	93-103	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	4-47
25055799-1	2015	The uridine diphosphate glucuronosyltransferase (UGT) gene 1A1*6 polymorphism, which affects irinotecan metabolism, has been associated with improved survival in lymphoma patients treated with of carboplatin, dexamethasone, etoposide and irinotecan (CDE-11).	Irinotecan	93-103	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	49-52
25055799-1	2015	The uridine diphosphate glucuronosyltransferase (UGT) gene 1A1*6 polymorphism, which affects irinotecan metabolism, has been associated with improved survival in lymphoma patients treated with of carboplatin, dexamethasone, etoposide and irinotecan (CDE-11).	Irinotecan	238-248	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	4-47
25055799-1	2015	The uridine diphosphate glucuronosyltransferase (UGT) gene 1A1*6 polymorphism, which affects irinotecan metabolism, has been associated with improved survival in lymphoma patients treated with of carboplatin, dexamethasone, etoposide and irinotecan (CDE-11).	Irinotecan	238-248	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	49-52
25466509-2	2015	PATIENTS AND METHODS: The results for efficacy and safety over the time course of the VEGF Trap (aflibercept) with irinotecan in colorectal cancer after failure of oxaliplatin regimen trial were analysed based on data from 1226 patients randomised to receive FOLFIRI plus either aflibercept (n=612) or placebo (n=614).	Irinotecan	115-125	vascular endothelial growth factor A	Homo sapiens	86-90
25648497-13	2015	In HT-29, HCT-116 and HCT-15 colorectal cancer lines, GHRH antagonist treatment caused cellular arrest in S-phase of cell cycle, potentiated inhibition of in vitro proliferation and in vivo growth produced by S-phase specific cytotoxic agents, 5-FU, irinotecan and cisplatin.	Irinotecan	250-260	growth hormone releasing hormone	Homo sapiens	54-58
25786458-0	2015	Therapy-related leukemia with Inv(16)(p13.1q22) and type D CBFB/MYH11 developing after exposure to irinotecan-containing chemoradiotherapy.	Irinotecan	99-109	inversin	Homo sapiens	30-33
25767314-0	2015	Liquid Chromatographic Method for Irinotecan Estimation: Screening of P-gp Modulators.	Irinotecan	34-44	phosphoglycolate phosphatase	Homo sapiens	70-74
25767314-1	2015	The present work is aimed to develop a simple, sensitive, robust and reliable HPLC method for the estimation of irinotecan in the physiological media in order to assess the permeability profile of irinotecan, using the everted gut sac, in the presence of various P-gp modulators.	Irinotecan	112-122	phosphoglycolate phosphatase	Homo sapiens	263-267
25767314-7	2015	The developed method was found to be precise (RSD &lt; 1.5%, for repeatability and &lt;2.55% for intermediate precision, acceptable ranges of precision), accurate (The recovered content of irinotecan in the presence of various P-gp modulators varied from 96.11-101.51%, within acceptable range, 80-120%), specific and robust (% RSD &lt; 2).	Irinotecan	189-199	phosphoglycolate phosphatase	Homo sapiens	227-231
25786458-0	2015	Therapy-related leukemia with Inv(16)(p13.1q22) and type D CBFB/MYH11 developing after exposure to irinotecan-containing chemoradiotherapy.	Irinotecan	99-109	core-binding factor subunit beta	Homo sapiens	59-63
25786458-0	2015	Therapy-related leukemia with Inv(16)(p13.1q22) and type D CBFB/MYH11 developing after exposure to irinotecan-containing chemoradiotherapy.	Irinotecan	99-109	myosin heavy chain 11	Homo sapiens	64-69
25352209-0	2015	Knockdown of Merm1/Wbscr22 attenuates sensitivity of H460 non-small cell lung cancer cells to SN-38 and 5-FU without alteration to p53 expression levels.	Irinotecan	94-99	BUD23 rRNA methyltransferase and ribosome maturation factor	Homo sapiens	13-18
25236593-0	2015	Erratum to: Effect of simvastatin plus cetuximab/irinotecan for KRAS mutant colorectal cancer and predictive value of the RAS signature for treatment response to cetuximab.	Irinotecan	49-59	KRAS proto-oncogene, GTPase	Homo sapiens	64-68
25352209-0	2015	Knockdown of Merm1/Wbscr22 attenuates sensitivity of H460 non-small cell lung cancer cells to SN-38 and 5-FU without alteration to p53 expression levels.	Irinotecan	94-99	BUD23 rRNA methyltransferase and ribosome maturation factor	Homo sapiens	19-26
25352209-7	2015	Downregulation of Merm1/Wbscr22 did not affect H1299 sensitivity to any of the six antitumor agents, whereas attenuated H460 sensitivity to SN-38 and 5-FU, without significant alteration in p53 at both mRNA and protein levels, was identified.	Irinotecan	140-145	BUD23 rRNA methyltransferase and ribosome maturation factor	Homo sapiens	18-23
25352209-11	2015	In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells.	Irinotecan	88-93	BUD23 rRNA methyltransferase and ribosome maturation factor	Homo sapiens	43-48
25352209-11	2015	In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells.	Irinotecan	88-93	BUD23 rRNA methyltransferase and ribosome maturation factor	Homo sapiens	49-56
25352209-11	2015	In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells.	Irinotecan	88-93	BUD23 rRNA methyltransferase and ribosome maturation factor	Homo sapiens	115-120
25352209-11	2015	In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells.	Irinotecan	88-93	BUD23 rRNA methyltransferase and ribosome maturation factor	Homo sapiens	121-128
25352209-11	2015	In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells.	Irinotecan	164-169	BUD23 rRNA methyltransferase and ribosome maturation factor	Homo sapiens	43-48
25352209-11	2015	In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells.	Irinotecan	164-169	BUD23 rRNA methyltransferase and ribosome maturation factor	Homo sapiens	49-56
25352209-11	2015	In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells.	Irinotecan	164-169	BUD23 rRNA methyltransferase and ribosome maturation factor	Homo sapiens	115-120
25352209-11	2015	In conclusion, shRNA-mediated knockdown of Merm1/Wbscr22 attenuates H460 sensitivity to SN-38 and 5-FU, suggesting Merm1/Wbscr22 is involved in chemosensitivity to SN-38 and 5-FU in H460 cells.	Irinotecan	164-169	BUD23 rRNA methyltransferase and ribosome maturation factor	Homo sapiens	121-128
25738310-11	2015	Sorafenib and irinotecan sequential treatment significantly increased the levels of cleaved caspase-8, -3, and PARP in HepG2 cells.	Irinotecan	14-24	caspase 8	Homo sapiens	92-101
25539916-7	2015	Finally, we provide cellular evidence that LIG3 and not PARP1 acts as the sensor for DNA damage caused by the topoisomerase I inhibitor, irinotecan.	Irinotecan	137-147	DNA ligase 3	Homo sapiens	43-47
25738310-11	2015	Sorafenib and irinotecan sequential treatment significantly increased the levels of cleaved caspase-8, -3, and PARP in HepG2 cells.	Irinotecan	14-24	collagen type XI alpha 2 chain	Homo sapiens	111-115
25738310-12	2015	Sorafenib suppressed p53 expression at both mRNA and protein levels, which might contribute to cell cycle arrest and sensitize tumor cells to irinotecan.	Irinotecan	142-152	tumor protein p53	Homo sapiens	21-24
25427841-0	2015	A phase I study of UGT1A1 *28/*6 genotype-directed dosing of irinotecan (CPT-11) in Korean patients with metastatic colorectal cancer receiving FOLFIRI.	Irinotecan	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
25427841-0	2015	A phase I study of UGT1A1 *28/*6 genotype-directed dosing of irinotecan (CPT-11) in Korean patients with metastatic colorectal cancer receiving FOLFIRI.	Irinotecan	73-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
25427841-1	2015	PURPOSE: A UGT1A1 genotype-directed dose escalation of irinotecan (CPT-11) was performed in patients with metastatic colorectal cancer receiving first-line FOLFIRI chemotherapy.	Irinotecan	55-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
25565667-0	2015	Irinotecan treatment and senescence failure promote the emergence of more transformed and invasive cells that depend on anti-apoptotic Mcl-1.	Irinotecan	0-10	myeloid cell leukemia sequence 1	Mus musculus	135-140
25427841-1	2015	PURPOSE: A UGT1A1 genotype-directed dose escalation of irinotecan (CPT-11) was performed in patients with metastatic colorectal cancer receiving first-line FOLFIRI chemotherapy.	Irinotecan	67-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
25565667-9	2015	Depletion of Mcl-1 increased irinotecan efficiency, induced the death of polyploid cells, prevented cell emergence and inhibited growth in low-adhesion conditions.	Irinotecan	29-39	myeloid cell leukemia sequence 1	Mus musculus	13-18
25565667-10	2015	We therefore propose that Mcl-1 targeting should be considered in the future to reduce senescence escape and to improve the treatment of irinotecan-refractory colorectal cancers.	Irinotecan	137-147	myeloid cell leukemia sequence 1	Mus musculus	26-31
25427841-8	2015	CONCLUSIONS: The MTD of irinotecan differed according to the UGT1A1 genotype, and higher doses of irinotecan are feasible with sLV5FU2 compared to the present regulatory approved doses.	Irinotecan	24-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
25427841-8	2015	CONCLUSIONS: The MTD of irinotecan differed according to the UGT1A1 genotype, and higher doses of irinotecan are feasible with sLV5FU2 compared to the present regulatory approved doses.	Irinotecan	98-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
25481222-5	2015	Whereas NTCP did not show any strong interactions with the cytostatics tested, we observed a very strong inhibition of OAT2 mediated [(3)H] cGMP uptake in the presence of bendamustine, irinotecan and paclitaxel.	Irinotecan	185-195	solute carrier family 22 member 7	Homo sapiens	119-123
25481222-6	2015	The Ki values of OAT2 for bendamustine, irinotecan and paclitaxel were determined to be 43.3+-4.33muM, 26.4+-2.34muM and 10.4+-0.45muM, respectively.	Irinotecan	40-50	solute carrier family 22 member 7	Homo sapiens	17-21
25481222-8	2015	A higher accumulation of irinotecan was observed in OAT2 expressing cells compared to control pcDNA cells by HPLC analysis of cell lysates.	Irinotecan	25-35	solute carrier family 22 member 7	Homo sapiens	52-56
25481222-9	2015	The accumulation was diminished in the presence of cGMP, the substrate we used to functionally characterize OAT2, suggesting specificity of this uptake and the fact that OAT2 mediates uptake of irinotecan.	Irinotecan	194-204	solute carrier family 22 member 7	Homo sapiens	108-112
25481222-9	2015	The accumulation was diminished in the presence of cGMP, the substrate we used to functionally characterize OAT2, suggesting specificity of this uptake and the fact that OAT2 mediates uptake of irinotecan.	Irinotecan	194-204	solute carrier family 22 member 7	Homo sapiens	170-174
25833236-2	2015	The present study investigated the anticancer effect of irinotecan on p53-negative Caco-2 and p53-positive CW2 human colorectal cancer cell lines.	Irinotecan	56-66	tumor protein p53	Homo sapiens	70-73
26068529-2	2015	UDP-glucuronosyltransferase 1A1 (UGT1A1) plays an irreplaceable role in detoxification of bilirubin and many drugs (e.g., SN-38).	Irinotecan	122-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
26087609-0	2015	[The role of assessing UGT1A1 gene polymorphism in the prediction of irinotecan-induced toxicity in the course of chemotherapy for colorectal cancer].	Irinotecan	69-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
26068529-2	2015	UDP-glucuronosyltransferase 1A1 (UGT1A1) plays an irreplaceable role in detoxification of bilirubin and many drugs (e.g., SN-38).	Irinotecan	122-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
25877315-0	2015	[Association of UGT1A1 (*28, *60 and * 93) polymorphism with the adverse reactions of irinotecan chemotherapy in extensive stage small cell lung cancer].	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
25877315-1	2015	OBJECTIVE: To explore the correlation between UGT1A1 (*28, *60 and * 93) polymorphism and the adverse reactions in small cell lung cancer patients after irinotecan chemotherapy.	Irinotecan	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
25877315-9	2015	Further prospective study in a larger number of patients is needed to clarify the association between UGT1A1*28, UGT1A1* 93 and UGT1A1*60 polymorphism and adverse reactions of irinotecan, and to help clinicians in choosing a better therapeutic modality for personalized chemotherapy to improve curative effect and reduce adverse reactions.	Irinotecan	176-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
24588516-4	2014	As irinotecan is a P-gp substrate, we tested here whether cetuximab could modify irinotecan concentration in mice.	Irinotecan	3-13	phosphoglycolate phosphatase	Mus musculus	19-23
25474134-0	2014	MBL-II-141, a chromone derivative, enhances irinotecan (CPT-11) anticancer efficiency in ABCG2-positive xenografts.	Irinotecan	44-54	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	89-94
25474134-0	2014	MBL-II-141, a chromone derivative, enhances irinotecan (CPT-11) anticancer efficiency in ABCG2-positive xenografts.	Irinotecan	56-62	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	89-94
25474134-4	2014	Combination of 10 mg/kg MBL-II-141 with the anticancer agent CPT-11 completely blocked the growth of 90% freshly implanted ABCG2-positive tumors.	Irinotecan	61-67	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	123-128
25474134-9	2014	MBL-II-141 induced a potent sensitization of ABCG2-positive xenografts to CPT-11 through in vivo ABCG2 inhibition.	Irinotecan	74-80	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	45-50
25474134-9	2014	MBL-II-141 induced a potent sensitization of ABCG2-positive xenografts to CPT-11 through in vivo ABCG2 inhibition.	Irinotecan	74-80	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	97-102
25544747-7	2014	In the primary lung cancer mouse models, tumor mass was 80% lower in response to HB1.F3.CE in conjunction with CPT-11, while it was only reduced by 40% in the group treated with CPT-11 alone.	Irinotecan	111-117	paternally expressed 10	Mus musculus	81-84
25544747-7	2014	In the primary lung cancer mouse models, tumor mass was 80% lower in response to HB1.F3.CE in conjunction with CPT-11, while it was only reduced by 40% in the group treated with CPT-11 alone.	Irinotecan	178-184	paternally expressed 10	Mus musculus	81-84
25515240-0	2014	DEK is a potential marker for aggressive phenotype and irinotecan-based therapy response in metastatic colorectal cancer.	Irinotecan	55-65	DEK proto-oncogene	Homo sapiens	0-3
25515240-8	2014	DEK expression was determined by immunohistochemistry in 67 formalin-fixed paraffin-embedded tumour samples from metastatic colorectal cancer patients treated with irinotecan-based therapy as first-line treatment.	Irinotecan	164-174	DEK proto-oncogene	Homo sapiens	0-3
25515240-10	2014	Knock-down of DEK on DLD1 and SW620 cell lines decreased cell migration and increased irinotecan-induced apoptosis.	Irinotecan	86-96	DEK proto-oncogene	Homo sapiens	14-17
25515240-11	2014	In addition, low DEK expression level predicted irinotecan-based chemotherapy response in metastatic colorectal cancer patients with KRAS wild-type.	Irinotecan	48-58	DEK proto-oncogene	Homo sapiens	17-20
25515240-11	2014	In addition, low DEK expression level predicted irinotecan-based chemotherapy response in metastatic colorectal cancer patients with KRAS wild-type.	Irinotecan	48-58	KRAS proto-oncogene, GTPase	Homo sapiens	133-137
25515240-12	2014	CONCLUSIONS: These data suggest DEK overexpression as a crucial event for the emergence of an aggressive phenotype in colorectal cancer and its potential role as biomarker for irinotecan response in those patients with KRAS wild-type status.	Irinotecan	176-186	DEK proto-oncogene	Homo sapiens	32-35
25515240-12	2014	CONCLUSIONS: These data suggest DEK overexpression as a crucial event for the emergence of an aggressive phenotype in colorectal cancer and its potential role as biomarker for irinotecan response in those patients with KRAS wild-type status.	Irinotecan	176-186	KRAS proto-oncogene, GTPase	Homo sapiens	219-223
24619075-0	2014	Comment on "KRAS-mutated plasma DNA as predictor of outcome from irinotecan monotherapy in metastatic colorectal cancer".	Irinotecan	65-75	KRAS proto-oncogene, GTPase	Homo sapiens	12-16
24619079-0	2014	Response to comment on "KRAS-mutated plasma DNA as predictor of outcome from irinotecan monotherapy in metastatic colorectal cancer".	Irinotecan	77-87	KRAS proto-oncogene, GTPase	Homo sapiens	24-28
25202035-1	2014	OBJECTIVE: To report a case of systemic irinotecan toxicity following regional transarterial chemoembolization with drug-eluting beads loaded with irinotecan (DEBIRI-TACE) in a patient later found to have a homozygous mutation for UGT1A1*28.	Irinotecan	40-50	ADAM metallopeptidase domain 17	Homo sapiens	166-170
25202035-1	2014	OBJECTIVE: To report a case of systemic irinotecan toxicity following regional transarterial chemoembolization with drug-eluting beads loaded with irinotecan (DEBIRI-TACE) in a patient later found to have a homozygous mutation for UGT1A1*28.	Irinotecan	40-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	231-237
25202035-1	2014	OBJECTIVE: To report a case of systemic irinotecan toxicity following regional transarterial chemoembolization with drug-eluting beads loaded with irinotecan (DEBIRI-TACE) in a patient later found to have a homozygous mutation for UGT1A1*28.	Irinotecan	147-157	ADAM metallopeptidase domain 17	Homo sapiens	166-170
25202035-1	2014	OBJECTIVE: To report a case of systemic irinotecan toxicity following regional transarterial chemoembolization with drug-eluting beads loaded with irinotecan (DEBIRI-TACE) in a patient later found to have a homozygous mutation for UGT1A1*28.	Irinotecan	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	231-237
25202035-7	2014	Patients with genetic polymorphisms of the genes encoding for the enzyme UGT1A1 may have increased incidence of irinotecan-associated toxicities because of decreased clearance of the active metabolite SN38 via the glucuronidation pathway.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
24588516-7	2014	Those results suggest that cetuximab influence irinotecan distribution into tissues probably due to inhibition of P-gp.	Irinotecan	47-57	ATP binding cassette subfamily B member 1	Homo sapiens	114-118
24588516-9	2014	Inhibiting SN-38 efflux by P-gp drug transporters in biliary system and tumour can lead to pharmacokinetic modification and a higher anticancer efficacy.	Irinotecan	11-16	ATP binding cassette subfamily B member 1	Homo sapiens	27-31
25473295-0	2014	FOLFIRI and regorafenib combination therapy with dose escalation of irinotecan as fourth-line treatment for patients with metastatic colon cancer according to UGT1A1 genotyping.	Irinotecan	68-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
25474278-9	2014	The post-progression survival (PPS) of p53-positive patients undergoing 2nd and/or 3rd line chemotherapy with irinotecan and/or cetuximab was significantly longer compared to p53-negative patients.	Irinotecan	110-120	tumor protein p53	Homo sapiens	39-42
25474278-11	2014	mCRC patients with p53 overexpression undergoing an irinotecan containing second- or third-line chemotherapy after oxaliplatin failure have a significantly longer post-progression survival compared to patients without p53 overexpression.	Irinotecan	52-62	tumor protein p53	Homo sapiens	19-22
25474278-12	2014	To validate the clinical impact of p53 in patients with mCRC treated with irinotecan- and/or cetuximab further studies are needed.	Irinotecan	74-84	tumor protein p53	Homo sapiens	35-38
25473295-1	2014	Here we report a case of metastatic colon cancer treated with 5-fluorouracil, leucovorin, and escalated doses of irinotecan (FOLFIRI) combined with regorafenib in the fourth-line setting after uridine diphosphate glucuronosyltransferase (UGT)1A1 genotyping analysis.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	238-245
25473295-9	2014	FOLFIRI, with dose escalation of irinotecan according to UGT1A1 genotyping plus regorafenib appears to be a promising salvage therapy for patients with refractory metastatic colorectal cancer.	Irinotecan	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
25520880-1	2014	We have previous found a positive correlation between post-therapy TCR repertoire normalization and remission of colorectal cancer (CRC) patients following fluorouracil, leucovorin, and irinotecan (FOLFIRI) plus bevacizumab or Rh-endostatin therapy.	Irinotecan	186-196	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	67-70
25089570-0	2014	Schlafen-11 sensitizes colorectal carcinoma cells to irinotecan.	Irinotecan	53-63	schlafen family member 11	Homo sapiens	0-11
25437539-4	2014	PARPi-induced cytotoxicity in EWS cells was 10- to 1,000-fold higher after administration of the DNA-damaging agents irinotecan or temozolomide.	Irinotecan	117-127	EWS RNA binding protein 1	Homo sapiens	30-33
25369798-12	2014	Additionally, the use of anti-EGFR MoAbs significantly increased the risk of severe infections when used in conjunction with cisplatin (RR 1.48, 95%CI 1.22 to 1.79, P&lt;0.001) or irinotecan (RR 1.53, 95%CI 1.12 to 2.10, P=0.008).	Irinotecan	180-190	epidermal growth factor receptor	Homo sapiens	30-34
25089570-4	2014	The present study aimed to investigate the mechanism of SLFN11 in the response of CRC cell lines to SN-38 (an active CPT-11 metabolite) treatment.	Irinotecan	100-105	schlafen family member 11	Homo sapiens	56-62
25089570-4	2014	The present study aimed to investigate the mechanism of SLFN11 in the response of CRC cell lines to SN-38 (an active CPT-11 metabolite) treatment.	Irinotecan	117-123	schlafen family member 11	Homo sapiens	56-62
25089570-7	2014	The effects of SN-38 treatment on CRC cells with different SLFN11 expression levels were detected, including inhibition of cell growth, induction of apoptosis, and cell cycle arrest.	Irinotecan	15-20	schlafen family member 11	Homo sapiens	59-65
25089570-8	2014	This study showed that SLFN11 expression varied between the CRC cell lines and high-level SLFN11 expression promoted SN-38-induced antiproliferative activity, apoptosis, and cell cycle arrest.	Irinotecan	117-122	schlafen family member 11	Homo sapiens	23-29
25368234-0	2014	Transcriptional targeting of human liver carboxylesterase (hCE1m6) and simultaneous expression of anti-BCRP shRNA enhances sensitivity of breast cancer cells to CPT-11.	Irinotecan	161-167	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	103-107
25089570-8	2014	This study showed that SLFN11 expression varied between the CRC cell lines and high-level SLFN11 expression promoted SN-38-induced antiproliferative activity, apoptosis, and cell cycle arrest.	Irinotecan	117-122	schlafen family member 11	Homo sapiens	90-96
25368234-2	2014	We hypothesized that conversion of camptothecin-11 (CPT-11) to its highly cytotoxic metabolite SN-38 by a mutant human carboxyl esterase (hCE1m6) specifically in cancer cells and inhibition of ABCG2 by anti-ABCG2 short hairpin RNA, leads to accumulation of a higher concentration of SN-38, resulting in higher therapeutic efficacy and less toxicity to normal cells.	Irinotecan	35-50	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	193-198
25368234-2	2014	We hypothesized that conversion of camptothecin-11 (CPT-11) to its highly cytotoxic metabolite SN-38 by a mutant human carboxyl esterase (hCE1m6) specifically in cancer cells and inhibition of ABCG2 by anti-ABCG2 short hairpin RNA, leads to accumulation of a higher concentration of SN-38, resulting in higher therapeutic efficacy and less toxicity to normal cells.	Irinotecan	35-50	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	207-212
25089570-9	2014	Our results suggest that SLFN11 plays a key role in cell cycle arrest and/or induction of apoptosis in response to exogenous SN-38-induced DNA damage and might be used as a new predictive biomarker for CRC treatment.	Irinotecan	125-130	schlafen family member 11	Homo sapiens	25-31
25368234-2	2014	We hypothesized that conversion of camptothecin-11 (CPT-11) to its highly cytotoxic metabolite SN-38 by a mutant human carboxyl esterase (hCE1m6) specifically in cancer cells and inhibition of ABCG2 by anti-ABCG2 short hairpin RNA, leads to accumulation of a higher concentration of SN-38, resulting in higher therapeutic efficacy and less toxicity to normal cells.	Irinotecan	52-58	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	193-198
25368234-2	2014	We hypothesized that conversion of camptothecin-11 (CPT-11) to its highly cytotoxic metabolite SN-38 by a mutant human carboxyl esterase (hCE1m6) specifically in cancer cells and inhibition of ABCG2 by anti-ABCG2 short hairpin RNA, leads to accumulation of a higher concentration of SN-38, resulting in higher therapeutic efficacy and less toxicity to normal cells.	Irinotecan	52-58	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	207-212
25285015-0	2014	Clinical significance of UGT1A1 gene polymorphisms on irinotecan-based regimens as the treatment in metastatic colorectal cancer.	Irinotecan	54-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
25368234-2	2014	We hypothesized that conversion of camptothecin-11 (CPT-11) to its highly cytotoxic metabolite SN-38 by a mutant human carboxyl esterase (hCE1m6) specifically in cancer cells and inhibition of ABCG2 by anti-ABCG2 short hairpin RNA, leads to accumulation of a higher concentration of SN-38, resulting in higher therapeutic efficacy and less toxicity to normal cells.	Irinotecan	95-100	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	193-198
25368234-2	2014	We hypothesized that conversion of camptothecin-11 (CPT-11) to its highly cytotoxic metabolite SN-38 by a mutant human carboxyl esterase (hCE1m6) specifically in cancer cells and inhibition of ABCG2 by anti-ABCG2 short hairpin RNA, leads to accumulation of a higher concentration of SN-38, resulting in higher therapeutic efficacy and less toxicity to normal cells.	Irinotecan	95-100	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	207-212
25450281-1	2014	OBJECTIVE: The aim was to investigate the association between uridine diphosphate glucuronide transferase 1A1 (UGT1A1) gene promoter region polymorphism and irinotecan-related adverse effects and efficacy on recurrent and refractory small cell lung cancer (SCLC).	Irinotecan	157-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-109
25450281-1	2014	OBJECTIVE: The aim was to investigate the association between uridine diphosphate glucuronide transferase 1A1 (UGT1A1) gene promoter region polymorphism and irinotecan-related adverse effects and efficacy on recurrent and refractory small cell lung cancer (SCLC).	Irinotecan	157-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
25450281-4	2014	DNA was extracted from peripheral blood and direct sequencing method was employed to test UGT1A1FNx0128 polymorphism, thus analyzing the correlation between UGT1A1FNx0128 polymorphism and irinotecan-related side-effects and efficacy.	Irinotecan	188-198	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	157-163
25285015-14	2014	CONCLUSION: For irinotecan-based regimens in metastatic colorectal cancer, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for irinotecan-associated severe delayed diarrhea, whereas no association between UGT1A1 gene polymorphisms and severe neutropenia was observed.	Irinotecan	152-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
25454761-5	2014	Compritol ATO 888 and capmule MCM C8 hybrid lipid mix was employed to prepare irinotecan containing nanostructured lipid carrier (NLC) by using functional excipients with P-gp inhibition activity.	Irinotecan	78-88	ATP binding cassette subfamily B member 1	Homo sapiens	171-175
25731272-8	2014	Treatment was changed to LV, 5-fluorouracil, and irinotecan (FOLFIRI), but after 4 courses, the patient"s carcinoembryonic antigen (CEA) levels rose.	Irinotecan	49-59	CEA cell adhesion molecule 3	Homo sapiens	106-130
25195021-10	2014	In addition, the method has been successfully applied to determine the intracellular accumulation of SN-38 investigating the transport through ABCB1 (P-gp) and ABCG2 (BCRP) efflux pumps in colorectal cancer cell lines.	Irinotecan	101-106	ATP binding cassette subfamily B member 1	Homo sapiens	143-148
25195021-10	2014	In addition, the method has been successfully applied to determine the intracellular accumulation of SN-38 investigating the transport through ABCB1 (P-gp) and ABCG2 (BCRP) efflux pumps in colorectal cancer cell lines.	Irinotecan	101-106	phosphoglycolate phosphatase	Homo sapiens	150-154
25195021-10	2014	In addition, the method has been successfully applied to determine the intracellular accumulation of SN-38 investigating the transport through ABCB1 (P-gp) and ABCG2 (BCRP) efflux pumps in colorectal cancer cell lines.	Irinotecan	101-106	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	160-165
25195021-10	2014	In addition, the method has been successfully applied to determine the intracellular accumulation of SN-38 investigating the transport through ABCB1 (P-gp) and ABCG2 (BCRP) efflux pumps in colorectal cancer cell lines.	Irinotecan	101-106	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	167-171
25310185-11	2014	In subgroup analyses, dMRE11 patients treated with irinotecan exhibited unexplained short-term mortality.	Irinotecan	51-61	meiotic recombination 11	Drosophila melanogaster	22-28
25272957-6	2014	The benefit on DFS in AREG-/EREG- patients was even stronger in the group that received 5-FU/FA/irinotecan as adjuvant treatment (p=0.002).	Irinotecan	96-106	amphiregulin	Homo sapiens	22-26
25272957-6	2014	The benefit on DFS in AREG-/EREG- patients was even stronger in the group that received 5-FU/FA/irinotecan as adjuvant treatment (p=0.002).	Irinotecan	96-106	epiregulin	Homo sapiens	28-32
25272957-7	2014	Patients with strong expression of PTEN profited more in terms of OS under adjuvant treatment containing irinotecan (p&lt; 0.05).	Irinotecan	105-115	phosphatase and tensin homolog	Homo sapiens	35-39
25272957-14	2014	Nevertheless, AREG/EREG negative, PTEN positive and Hif-1 alpha negative patients might profit significantly in terms of DFS from a treatment containing fluoropyrimidines and irinotecan.	Irinotecan	175-185	amphiregulin	Homo sapiens	14-18
25272957-14	2014	Nevertheless, AREG/EREG negative, PTEN positive and Hif-1 alpha negative patients might profit significantly in terms of DFS from a treatment containing fluoropyrimidines and irinotecan.	Irinotecan	175-185	epiregulin	Homo sapiens	19-23
25272957-14	2014	Nevertheless, AREG/EREG negative, PTEN positive and Hif-1 alpha negative patients might profit significantly in terms of DFS from a treatment containing fluoropyrimidines and irinotecan.	Irinotecan	175-185	phosphatase and tensin homolog	Homo sapiens	34-38
25272957-14	2014	Nevertheless, AREG/EREG negative, PTEN positive and Hif-1 alpha negative patients might profit significantly in terms of DFS from a treatment containing fluoropyrimidines and irinotecan.	Irinotecan	175-185	hypoxia inducible factor 1 subunit alpha	Homo sapiens	52-63
25064805-5	2014	The combination of Nano Se and irinotecan showed increased cytotoxic effect with HCT-8 tumor cells likely by p53 mediated apoptosis.	Irinotecan	31-41	tumor protein p53	Homo sapiens	109-112
25060396-0	2014	Contribution of transcription factor, SP1, to the promotion of HB-EGF expression in defense mechanism against the treatment of irinotecan in ovarian clear cell carcinoma.	Irinotecan	127-137	heparin binding EGF like growth factor	Homo sapiens	63-69
25175642-0	2014	A novel system for predicting the toxicity of irinotecan based on statistical pattern recognition with UGT1A genotypes.	Irinotecan	46-56	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	103-108
24709690-0	2014	The effect of the UGT1A1*28 allele on survival after irinotecan-based chemotherapy: a collaborative meta-analysis.	Irinotecan	53-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
24709690-1	2014	To date, studies of irinotecan pharmacogenetics have mostly focused on the effect of the UGT1A1*28 allele on irinotecan-related toxicity.	Irinotecan	20-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
24709690-1	2014	To date, studies of irinotecan pharmacogenetics have mostly focused on the effect of the UGT1A1*28 allele on irinotecan-related toxicity.	Irinotecan	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
24709690-2	2014	However, the clinical utility of routine UGT1A1*28 genotyping to pre-emptively adjust irinotecan dosage is dependent upon whether UGT1A1*28 also affects patient survival following irinotecan therapy.	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
24709690-2	2014	However, the clinical utility of routine UGT1A1*28 genotyping to pre-emptively adjust irinotecan dosage is dependent upon whether UGT1A1*28 also affects patient survival following irinotecan therapy.	Irinotecan	180-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
24709690-4	2014	A systematic review and meta-analysis of both published and unpublished data were performed to summarize the available evidence of the relationship between the UGT1A1*28 allele and patient survival related to irinotecan therapy.	Irinotecan	209-219	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
25172788-9	2014	Moreover, both cryptotanshinone and dihydrotanshinone could potentiate the cytotoxicity of doxorubicin and irinotecan in P-gp overexpressing SW620 Ad300 colon cancer cells.	Irinotecan	107-117	phosphoglycolate phosphatase	Homo sapiens	121-125
25285015-1	2014	PURPOSE: The primary aim of this research was to investigate the association between uridine diphosphate glucuronosyltransferase (UGT)1A1 gene polymorphisms and the toxicities of irinotecan-based regimens in Chinese patients with metastatic colorectal cancer.	Irinotecan	179-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-137
25285015-14	2014	CONCLUSION: For irinotecan-based regimens in metastatic colorectal cancer, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for irinotecan-associated severe delayed diarrhea, whereas no association between UGT1A1 gene polymorphisms and severe neutropenia was observed.	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
25285015-14	2014	CONCLUSION: For irinotecan-based regimens in metastatic colorectal cancer, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for irinotecan-associated severe delayed diarrhea, whereas no association between UGT1A1 gene polymorphisms and severe neutropenia was observed.	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
25285015-14	2014	CONCLUSION: For irinotecan-based regimens in metastatic colorectal cancer, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for irinotecan-associated severe delayed diarrhea, whereas no association between UGT1A1 gene polymorphisms and severe neutropenia was observed.	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
25285015-14	2014	CONCLUSION: For irinotecan-based regimens in metastatic colorectal cancer, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for irinotecan-associated severe delayed diarrhea, whereas no association between UGT1A1 gene polymorphisms and severe neutropenia was observed.	Irinotecan	152-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
25285015-14	2014	CONCLUSION: For irinotecan-based regimens in metastatic colorectal cancer, the UGT1A1*28 and UGT1A1*6 locus mutations can be regarded as predictors for irinotecan-associated severe delayed diarrhea, whereas no association between UGT1A1 gene polymorphisms and severe neutropenia was observed.	Irinotecan	152-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
24934408-4	2014	Whole-genome sequencing revealed a clonal hemizygous mutation in the Mre11 complex gene RAD50 that attenuated ATM signaling which in the context of CHK1 inhibition contributed, via synthetic lethality, to extreme sensitivity to irinotecan.	Irinotecan	228-238	MRE11 homolog, double strand break repair nuclease	Homo sapiens	69-74
25202056-0	2014	Expression of ABCB6 is related to resistance to 5-FU, SN-38 and vincristine.	Irinotecan	54-59	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	14-19
25202056-5	2014	ABCB6 expression enhanced resistance to 5-fluorouracil (5-FU), SN-38 and vincristine (Vcr) but not to arsenite.	Irinotecan	63-68	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	0-5
25202056-6	2014	Conversely, down-regulation of ABCB6 in KAS cells increased the sensitivity of KAS cells to 5-FU, SN-38 and Vcr, but not to arsenite.	Irinotecan	98-103	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	31-36
25202056-7	2014	Our findings suggest that ABCB6 is involved in 5-FU, SN-38 and Vcr resistance.	Irinotecan	53-58	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	26-31
25260839-0	2014	Influence of UGT1A1 gene methylation level in colorectal cancer cells on the sensitivity of the chemotherapy drug CPT-11.	Irinotecan	114-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
25260839-1	2014	OBJECTIVE: To study the influence of the methylation level of UGT1A1 gene related to CPT-11 metabolic enzymes in colorectal cancer cells on the sensitivity of chemotherapy drugs.	Irinotecan	85-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
25260839-6	2014	CONCLUSIONS: The cytotoxicity of CPT-11 to colorectal cancer cells has a negative correlation with UGT1A1 expression, and positive correlation with CES2 and GUSB.	Irinotecan	33-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
25260839-6	2014	CONCLUSIONS: The cytotoxicity of CPT-11 to colorectal cancer cells has a negative correlation with UGT1A1 expression, and positive correlation with CES2 and GUSB.	Irinotecan	33-39	carboxylesterase 2	Homo sapiens	148-152
25260839-6	2014	CONCLUSIONS: The cytotoxicity of CPT-11 to colorectal cancer cells has a negative correlation with UGT1A1 expression, and positive correlation with CES2 and GUSB.	Irinotecan	33-39	glucuronidase beta	Homo sapiens	157-161
25260839-7	2014	The specific silencing UGT1A1 gene of siRNA could significantly increase the sensitivity of CPT-11 to the chemotherapy of colorectal cancer cells.	Irinotecan	92-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
25260839-8	2014	UGT1A1 methylation was an important factor affecting the chemosensitivity of CPT-11.	Irinotecan	77-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
25185187-1	2014	SUMMARY: In this issue of Cancer Discovery, AI-Ahmadie and colleagues identify a somatic mutation in the RAD50 gene as a likely contributing factor to an unusual curative response to systemic combination therapy employing the DNA-damaging agent irinotecan and a checkpoint kinase 1 inhibitor in a patient with recurrent, metastatic small-cell cancer.	Irinotecan	245-255	RAD50 double strand break repair protein	Homo sapiens	105-110
24934408-4	2014	Whole-genome sequencing revealed a clonal hemizygous mutation in the Mre11 complex gene RAD50 that attenuated ATM signaling which in the context of CHK1 inhibition contributed, via synthetic lethality, to extreme sensitivity to irinotecan.	Irinotecan	228-238	RAD50 double strand break repair protein	Homo sapiens	88-93
24934408-4	2014	Whole-genome sequencing revealed a clonal hemizygous mutation in the Mre11 complex gene RAD50 that attenuated ATM signaling which in the context of CHK1 inhibition contributed, via synthetic lethality, to extreme sensitivity to irinotecan.	Irinotecan	228-238	ATM serine/threonine kinase	Homo sapiens	110-113
24934408-4	2014	Whole-genome sequencing revealed a clonal hemizygous mutation in the Mre11 complex gene RAD50 that attenuated ATM signaling which in the context of CHK1 inhibition contributed, via synthetic lethality, to extreme sensitivity to irinotecan.	Irinotecan	228-238	checkpoint kinase 1	Homo sapiens	148-152
24513691-7	2014	This prospective study did not confirm any previous retrospective finding, reporting a predictive or prognostic effect of EGFR (CA)n repeats allelic variants in chemo-refractory mCRC patients receiving cetuximab and irinotecan.	Irinotecan	216-226	epidermal growth factor receptor	Homo sapiens	122-126
24424522-2	2014	Here we show that interleukin-33 (IL-33) mediates the severe intestinal mucositis in mice treated with irinotecan (CPT-11), a commonly used cancer chemotherapeutic agent.	Irinotecan	103-113	interleukin 33	Mus musculus	34-39
24424522-2	2014	Here we show that interleukin-33 (IL-33) mediates the severe intestinal mucositis in mice treated with irinotecan (CPT-11), a commonly used cancer chemotherapeutic agent.	Irinotecan	115-121	interleukin 33	Mus musculus	18-32
24424522-2	2014	Here we show that interleukin-33 (IL-33) mediates the severe intestinal mucositis in mice treated with irinotecan (CPT-11), a commonly used cancer chemotherapeutic agent.	Irinotecan	115-121	interleukin 33	Mus musculus	34-39
24424522-3	2014	Systemic CPT-11 administration led to severe mucosal damage, diarrhea, and body weight loss concomitant with the induction of IL-33 in the small intestine (SI).	Irinotecan	9-15	interleukin 33	Mus musculus	126-131
24424522-5	2014	Moreover, recombinant IL-33 exacerbated the CPT-11-induced mucositis, whereas IL-33 blockade with anti-IL-33 antibody or soluble ST2 markedly attenuated the disease.	Irinotecan	44-50	interleukin 33	Mus musculus	22-27
24424522-7	2014	Supernatants from SI explants treated with CPT-11 enhanced transmigration of neutrophils in vitro in an IL-33-, CXCL1/2-, and CXCR2-dependent manner.	Irinotecan	43-49	interleukin 33	Mus musculus	104-109
24424522-7	2014	Supernatants from SI explants treated with CPT-11 enhanced transmigration of neutrophils in vitro in an IL-33-, CXCL1/2-, and CXCR2-dependent manner.	Irinotecan	43-49	chemokine (C-X-C motif) ligand 1	Mus musculus	112-117
24424522-7	2014	Supernatants from SI explants treated with CPT-11 enhanced transmigration of neutrophils in vitro in an IL-33-, CXCL1/2-, and CXCR2-dependent manner.	Irinotecan	43-49	chemokine (C-X-C motif) receptor 2	Mus musculus	126-131
24424522-8	2014	Importantly, IL-33 blockade reduced mucositis and enabled prolonged CPT-11 treatment of ectopic CT26 colon carcinoma, leading to a beneficial outcome of the chemotherapy.	Irinotecan	68-74	interleukin 33	Mus musculus	13-18
25127363-6	2014	We identified the SNP rs9351963 in potassium voltage-gated channel subfamily KQT member 5 (KCNQ5) as a candidate factor related to incidence of irinotecan-induced diarrhea.	Irinotecan	144-154	potassium voltage-gated channel subfamily Q member 5	Homo sapiens	35-89
25127363-6	2014	We identified the SNP rs9351963 in potassium voltage-gated channel subfamily KQT member 5 (KCNQ5) as a candidate factor related to incidence of irinotecan-induced diarrhea.	Irinotecan	144-154	potassium voltage-gated channel subfamily Q member 5	Homo sapiens	91-96
25127363-10	2014	These results suggest that rs9351963 in KCNQ5 is a possible predictive factor of incidence of diarrhea in cancer patients treated with irinotecan chemotherapy and for selecting chemotherapy regimens, such as irinotecan alone or a combination of irinotecan with a KCNQ5 opener.	Irinotecan	135-145	potassium voltage-gated channel subfamily Q member 5	Homo sapiens	40-45
25127363-10	2014	These results suggest that rs9351963 in KCNQ5 is a possible predictive factor of incidence of diarrhea in cancer patients treated with irinotecan chemotherapy and for selecting chemotherapy regimens, such as irinotecan alone or a combination of irinotecan with a KCNQ5 opener.	Irinotecan	135-145	potassium voltage-gated channel subfamily Q member 5	Homo sapiens	263-268
25127363-10	2014	These results suggest that rs9351963 in KCNQ5 is a possible predictive factor of incidence of diarrhea in cancer patients treated with irinotecan chemotherapy and for selecting chemotherapy regimens, such as irinotecan alone or a combination of irinotecan with a KCNQ5 opener.	Irinotecan	208-218	potassium voltage-gated channel subfamily Q member 5	Homo sapiens	40-45
25127363-10	2014	These results suggest that rs9351963 in KCNQ5 is a possible predictive factor of incidence of diarrhea in cancer patients treated with irinotecan chemotherapy and for selecting chemotherapy regimens, such as irinotecan alone or a combination of irinotecan with a KCNQ5 opener.	Irinotecan	208-218	potassium voltage-gated channel subfamily Q member 5	Homo sapiens	40-45
25110412-3	2014	Resistance to cisplatin, irinotecan and 5-fluorouracil chemotherapy has been shown to involve mitogen-activated protein kinase (MAPK) signaling and recent studies identified p38alpha MAPK as a mediator of resistance to various agents in CRC patients.	Irinotecan	25-35	mitogen-activated protein kinase 14	Homo sapiens	174-182
24958824-0	2014	Dose-finding and pharmacokinetic study to optimize the dosing of irinotecan according to the UGT1A1 genotype of patients with cancer.	Irinotecan	65-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
24958824-1	2014	PURPOSE: The risk of severe neutropenia from treatment with irinotecan is related in part to UGT1A1*28, a variant that reduces the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	60-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
24958824-1	2014	PURPOSE: The risk of severe neutropenia from treatment with irinotecan is related in part to UGT1A1*28, a variant that reduces the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	146-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
24958824-1	2014	PURPOSE: The risk of severe neutropenia from treatment with irinotecan is related in part to UGT1A1*28, a variant that reduces the elimination of SN-38, the active metabolite of irinotecan.	Irinotecan	178-188	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
24958824-14	2014	CONCLUSION: The UGT1A1*28 genotype can be used to individualize dosing of irinotecan.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
24968890-12	2014	CFZ significantly inhibited the growth of SW620 cells, and had synergistic inhibitory effects with CPT-11 on survival and colony formation; possibly by inhibition of NF-kappaB activation, MEK/ERK and PI3K/AKT pathway factor dephosphorylation and survivin downregulation.	Irinotecan	99-105	AKT serine/threonine kinase 1	Homo sapiens	205-208
24968890-13	2014	Co-administration of CFZ and CPT-11 induced G2/M arrest, increased p21WAF1/CIP, and decreased mutant p53 and cdc25c expression.	Irinotecan	29-35	tumor protein p53	Homo sapiens	101-104
24968890-13	2014	Co-administration of CFZ and CPT-11 induced G2/M arrest, increased p21WAF1/CIP, and decreased mutant p53 and cdc25c expression.	Irinotecan	29-35	cell division cycle 25C	Homo sapiens	109-115
24424522-2	2014	Here we show that interleukin-33 (IL-33) mediates the severe intestinal mucositis in mice treated with irinotecan (CPT-11), a commonly used cancer chemotherapeutic agent.	Irinotecan	103-113	interleukin 33	Mus musculus	18-32
25054039-0	2014	Clinical usefulness of testing for UDP glucuronosyltransferase 1 family, polypeptide A1 polymorphism prior to the inititation of irinotecan-based chemotherapy.	Irinotecan	129-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-87
25054039-1	2014	An association between UDP glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) polymorphisms and irinotecan-induced neutropenia has been previously reported.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-75
25054039-1	2014	An association between UDP glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) polymorphisms and irinotecan-induced neutropenia has been previously reported.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
23821377-0	2014	EGFR ligands as pharmacodynamic biomarkers in metastatic colorectal cancer patients treated with cetuximab and irinotecan.	Irinotecan	111-121	epidermal growth factor receptor	Homo sapiens	0-4
23821377-1	2014	This study was conducted to describe the modulation of plasma epidermal growth factor receptor (EGFR) ligands in EGFR-positive metastatic colorectal cancer (mCRC) patients during treatment with cetuximab and irinotecan and to explore the clinical implication of plasma levels" variations as potential biomarkers of benefit.	Irinotecan	208-218	epidermal growth factor receptor	Homo sapiens	62-94
23821377-1	2014	This study was conducted to describe the modulation of plasma epidermal growth factor receptor (EGFR) ligands in EGFR-positive metastatic colorectal cancer (mCRC) patients during treatment with cetuximab and irinotecan and to explore the clinical implication of plasma levels" variations as potential biomarkers of benefit.	Irinotecan	208-218	epidermal growth factor receptor	Homo sapiens	96-100
23821377-1	2014	This study was conducted to describe the modulation of plasma epidermal growth factor receptor (EGFR) ligands in EGFR-positive metastatic colorectal cancer (mCRC) patients during treatment with cetuximab and irinotecan and to explore the clinical implication of plasma levels" variations as potential biomarkers of benefit.	Irinotecan	208-218	epidermal growth factor receptor	Homo sapiens	113-117
23821377-8	2014	This hypothesis-generating study shows that EGFR ligands are significantly modulated by cetuximab plus irinotecan according to KRAS and BRAF mutational status, and they warrant further investigation as pharmacodynamic markers of resistance to anti-EGFRs.	Irinotecan	103-113	epidermal growth factor receptor	Homo sapiens	44-48
23821377-8	2014	This hypothesis-generating study shows that EGFR ligands are significantly modulated by cetuximab plus irinotecan according to KRAS and BRAF mutational status, and they warrant further investigation as pharmacodynamic markers of resistance to anti-EGFRs.	Irinotecan	103-113	KRAS proto-oncogene, GTPase	Homo sapiens	127-131
23821377-8	2014	This hypothesis-generating study shows that EGFR ligands are significantly modulated by cetuximab plus irinotecan according to KRAS and BRAF mutational status, and they warrant further investigation as pharmacodynamic markers of resistance to anti-EGFRs.	Irinotecan	103-113	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	136-140
25083297-0	2014	Breast cancer resistance protein (BCRP) and excision repair cross complement-1 (ERCC1) expression in esophageal cancers and response to cisplatin and irinotecan based chemotherapy.	Irinotecan	150-160	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
25083297-0	2014	Breast cancer resistance protein (BCRP) and excision repair cross complement-1 (ERCC1) expression in esophageal cancers and response to cisplatin and irinotecan based chemotherapy.	Irinotecan	150-160	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
25083297-0	2014	Breast cancer resistance protein (BCRP) and excision repair cross complement-1 (ERCC1) expression in esophageal cancers and response to cisplatin and irinotecan based chemotherapy.	Irinotecan	150-160	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	44-78
25083297-0	2014	Breast cancer resistance protein (BCRP) and excision repair cross complement-1 (ERCC1) expression in esophageal cancers and response to cisplatin and irinotecan based chemotherapy.	Irinotecan	150-160	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	80-85
25083297-5	2014	We examined the expression of BCRP and ERCC1 in patients with esophageal cancer and correlated it with survival in patients receiving irinotecan and cisplatin based chemotherapy.	Irinotecan	134-144	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	30-34
24513691-0	2014	Prospective study of EGFR intron 1 (CA)n repeats variants as predictors of benefit from cetuximab and irinotecan in chemo-refractory metastatic colorectal cancer (mCRC) patients.	Irinotecan	102-112	epidermal growth factor receptor	Homo sapiens	21-25
24824514-9	2014	Moreover, the ability of doxorubicin, SN-38 and CDDP to induce proapoptotic signals was weaker in Rho cells, as evidenced by survivin upregulation and reductions in Bax/Bcl-2 expression ratios.	Irinotecan	38-43	BCL2 associated X, apoptosis regulator	Homo sapiens	165-168
24952429-0	2014	Inflammasome activation is reactive oxygen species dependent and mediates irinotecan-induced mucositis through IL-1beta and IL-18 in mice.	Irinotecan	74-84	interleukin 1 beta	Mus musculus	111-119
24952429-0	2014	Inflammasome activation is reactive oxygen species dependent and mediates irinotecan-induced mucositis through IL-1beta and IL-18 in mice.	Irinotecan	74-84	interleukin 18	Mus musculus	124-129
24952429-8	2014	Irinotecan treatment resulted in increased IL-1beta and IL-18 production in ileum and NOX-2-dependent oxidative stress.	Irinotecan	0-10	interleukin 1 beta	Mus musculus	43-51
24952429-8	2014	Irinotecan treatment resulted in increased IL-1beta and IL-18 production in ileum and NOX-2-dependent oxidative stress.	Irinotecan	0-10	interleukin 18	Mus musculus	56-61
24952429-8	2014	Irinotecan treatment resulted in increased IL-1beta and IL-18 production in ileum and NOX-2-dependent oxidative stress.	Irinotecan	0-10	cytochrome b-245, beta polypeptide	Mus musculus	86-91
24952429-13	2014	NOX-2-derived oxidative stress mediates inflammasome activation and inflammasome-dependent production of IL-1beta and IL-18, which mediate tissue injury during irinotecan-induced mucositis in mice.	Irinotecan	160-170	cytochrome b-245, beta polypeptide	Mus musculus	0-5
24952429-13	2014	NOX-2-derived oxidative stress mediates inflammasome activation and inflammasome-dependent production of IL-1beta and IL-18, which mediate tissue injury during irinotecan-induced mucositis in mice.	Irinotecan	160-170	interleukin 1 beta	Mus musculus	105-113
24952429-13	2014	NOX-2-derived oxidative stress mediates inflammasome activation and inflammasome-dependent production of IL-1beta and IL-18, which mediate tissue injury during irinotecan-induced mucositis in mice.	Irinotecan	160-170	interleukin 18	Mus musculus	118-123
24780296-2	2014	Bacteria beta-glucuronidase (GUS) enzymes in intestines convert the nontoxic metabolite of CPT-11, SN-38G, to toxic SN-38, and finally lead to damage of intestinal epithelial cells and diarrhea.	Irinotecan	91-97	glucuronidase, beta	Mus musculus	9-27
24780296-2	2014	Bacteria beta-glucuronidase (GUS) enzymes in intestines convert the nontoxic metabolite of CPT-11, SN-38G, to toxic SN-38, and finally lead to damage of intestinal epithelial cells and diarrhea.	Irinotecan	91-97	glucuronidase, beta	Mus musculus	29-32
24780296-2	2014	Bacteria beta-glucuronidase (GUS) enzymes in intestines convert the nontoxic metabolite of CPT-11, SN-38G, to toxic SN-38, and finally lead to damage of intestinal epithelial cells and diarrhea.	Irinotecan	99-104	glucuronidase, beta	Mus musculus	9-27
24780296-2	2014	Bacteria beta-glucuronidase (GUS) enzymes in intestines convert the nontoxic metabolite of CPT-11, SN-38G, to toxic SN-38, and finally lead to damage of intestinal epithelial cells and diarrhea.	Irinotecan	99-104	glucuronidase, beta	Mus musculus	29-32
24780296-2	2014	Bacteria beta-glucuronidase (GUS) enzymes in intestines convert the nontoxic metabolite of CPT-11, SN-38G, to toxic SN-38, and finally lead to damage of intestinal epithelial cells and diarrhea.	Irinotecan	116-121	glucuronidase, beta	Mus musculus	9-27
24780296-2	2014	Bacteria beta-glucuronidase (GUS) enzymes in intestines convert the nontoxic metabolite of CPT-11, SN-38G, to toxic SN-38, and finally lead to damage of intestinal epithelial cells and diarrhea.	Irinotecan	116-121	glucuronidase, beta	Mus musculus	29-32
24940606-0	2014	miR-345 in metastatic colorectal cancer: a non-invasive biomarker for clinical outcome in non-KRAS mutant patients treated with 3rd line cetuximab and irinotecan.	Irinotecan	151-161	microRNA 345	Homo sapiens	0-7
24940606-9	2014	In addition, high miR-345 expression was associated with lack of response to treatment with cetuximab and irinotecan.	Irinotecan	106-116	microRNA 345	Homo sapiens	18-25
24462762-3	2014	The study group received irinotecan dose escalation based on UGT1A1 genotyping whereas the control group did not.	Irinotecan	25-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
24462762-8	2014	Patients with mCRC undergoing UGT1A1 genotyping may receive escalated doses of irinotecan to obtain a better clinical response/outcome with comparable toxicities.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
25056111-0	2014	Reprogramming ovarian and breast cancer cells into non-cancerous cells by low-dose metformin or SN-38 through FOXO3 activation.	Irinotecan	96-101	forkhead box O3	Homo sapiens	110-115
25056111-5	2014	Low-dose metformin or SN-38 increases FOXO3 nuclear localization as well as the amount of DNA damage markers and downregulates the expression of a cancer-stemness marker CD44 and other stemness markers, including Nanog, Oct-4, and c-Myc, in these cancer cells.	Irinotecan	22-27	forkhead box O3	Homo sapiens	38-43
25056111-5	2014	Low-dose metformin or SN-38 increases FOXO3 nuclear localization as well as the amount of DNA damage markers and downregulates the expression of a cancer-stemness marker CD44 and other stemness markers, including Nanog, Oct-4, and c-Myc, in these cancer cells.	Irinotecan	22-27	CD44 molecule (Indian blood group)	Homo sapiens	170-174
25056111-5	2014	Low-dose metformin or SN-38 increases FOXO3 nuclear localization as well as the amount of DNA damage markers and downregulates the expression of a cancer-stemness marker CD44 and other stemness markers, including Nanog, Oct-4, and c-Myc, in these cancer cells.	Irinotecan	22-27	Nanog homeobox	Homo sapiens	213-218
25056111-5	2014	Low-dose metformin or SN-38 increases FOXO3 nuclear localization as well as the amount of DNA damage markers and downregulates the expression of a cancer-stemness marker CD44 and other stemness markers, including Nanog, Oct-4, and c-Myc, in these cancer cells.	Irinotecan	22-27	POU class 5 homeobox 1	Homo sapiens	220-225
25056111-5	2014	Low-dose metformin or SN-38 increases FOXO3 nuclear localization as well as the amount of DNA damage markers and downregulates the expression of a cancer-stemness marker CD44 and other stemness markers, including Nanog, Oct-4, and c-Myc, in these cancer cells.	Irinotecan	22-27	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	231-236
25056111-8	2014	These results suggest that low-dose metformin or SN-38 may reprogram these cancer cells into non-cancerous cells in a FOXO3-dependent manner, and may allow patients to overcome these cancers with minimal side effects.	Irinotecan	49-54	forkhead box O3	Homo sapiens	118-123
24867782-0	2014	Irinotecan and temozolomide brain distribution: a focus on ABCB1.	Irinotecan	0-10	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	59-64
24867782-6	2014	Our results show that TMZ, CPT-11 and SN-38 are transported by ABCB1 at the BBB level with brain/plasma ratios of 1.1, 2.1 and 2.3, respectively.	Irinotecan	27-33	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	63-68
24867782-6	2014	Our results show that TMZ, CPT-11 and SN-38 are transported by ABCB1 at the BBB level with brain/plasma ratios of 1.1, 2.1 and 2.3, respectively.	Irinotecan	38-43	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	63-68
24727322-9	2014	Everolimus also markedly inhibited the hydrolysis of irinotecan and p-nitrophenyl acetate by mouse plasma carboxylesterase and recombinant human CES2, respectively.	Irinotecan	53-63	carboxylesterase 2	Homo sapiens	145-149
24824514-9	2014	Moreover, the ability of doxorubicin, SN-38 and CDDP to induce proapoptotic signals was weaker in Rho cells, as evidenced by survivin upregulation and reductions in Bax/Bcl-2 expression ratios.	Irinotecan	38-43	BCL2 apoptosis regulator	Homo sapiens	169-174
24726739-2	2014	Our results indicate for the first time that linsitinib significantly potentiate the effect of anti-neoplastic drugs mitoxantrone (MX) and SN-38 in ABCG2-overexpressing cells; paclitaxel, docetaxel and vinblastine in ABCC10-overexpressing cells.	Irinotecan	139-144	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	148-153
24977443-0	2014	[Interest of UGT1A1 genotyping within digestive cancers treatment by irinotecan].	Irinotecan	69-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
24977443-2	2014	Its anticancer activity results from its bioactivation into SN-38 metabolite, which is cleared through glucuronidation by the hepatic enzyme uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	60-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-188
24977443-2	2014	Its anticancer activity results from its bioactivation into SN-38 metabolite, which is cleared through glucuronidation by the hepatic enzyme uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	60-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	190-196
24977443-9	2014	The existence of a French laboratories network performing this test in clinical routine makes it possible to generalize UGT1A1 deficiency screening, so as to guarantee equal access to safe treatment and optimized irinorecan-based therapy for the many patients receiving irinotecan-based therapy in advanced colorectal cancer.	Irinotecan	270-280	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	120-126
24478107-5	2014	RS4 consumption compared with CF resulted in 7.2% (p = 0.002) lower mean total cholesterol, 5.5% (p = 0.04) lower non-HDL, and a 12.8% (p &lt; 0.001) lower HDL cholesterol in the With-MetS group.	Irinotecan	0-3	ETS variant transcription factor 3	Homo sapiens	179-188
24468885-2	2014	Therefore, we designed a study using simvastatin/cetuximab/irinotecan for KRAS mutant CRC patients who are refractory to irinotecan and oxaliplatin-based chemotherapy.	Irinotecan	59-69	KRAS proto-oncogene, GTPase	Homo sapiens	74-78
24468885-2	2014	Therefore, we designed a study using simvastatin/cetuximab/irinotecan for KRAS mutant CRC patients who are refractory to irinotecan and oxaliplatin-based chemotherapy.	Irinotecan	121-131	KRAS proto-oncogene, GTPase	Homo sapiens	74-78
24468885-13	2014	CONCLUSION: The simvastatin/cetuximab/irinotecan regimen showed promising efficacy and safety in KRAS mutant CRC patients who failed irinotecan and oxaliplatin-based chemotherapy.	Irinotecan	38-48	KRAS proto-oncogene, GTPase	Homo sapiens	97-101
24627085-9	2014	The veliparib and CPT-11 combination can be further explored as a treatment of metastatic castration-resistant prostate cancers that have frequent p53 mutations and enriched genomic instability.	Irinotecan	18-24	tumor protein p53 L homeolog	Xenopus laevis	147-150
24453052-1	2014	BACKGROUND AND OBJECTIVES: Uridine-diphosphate glucuronosyltransferase 1A (UGT1A) is a key enzyme involved in irinotecan metabolism, and polymorphisms in the UGT1A gene are associated with irinotecan-induced toxicity.	Irinotecan	110-120	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	27-73
24453052-1	2014	BACKGROUND AND OBJECTIVES: Uridine-diphosphate glucuronosyltransferase 1A (UGT1A) is a key enzyme involved in irinotecan metabolism, and polymorphisms in the UGT1A gene are associated with irinotecan-induced toxicity.	Irinotecan	110-120	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	75-80
24453052-1	2014	BACKGROUND AND OBJECTIVES: Uridine-diphosphate glucuronosyltransferase 1A (UGT1A) is a key enzyme involved in irinotecan metabolism, and polymorphisms in the UGT1A gene are associated with irinotecan-induced toxicity.	Irinotecan	110-120	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	158-163
24453052-1	2014	BACKGROUND AND OBJECTIVES: Uridine-diphosphate glucuronosyltransferase 1A (UGT1A) is a key enzyme involved in irinotecan metabolism, and polymorphisms in the UGT1A gene are associated with irinotecan-induced toxicity.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	27-73
24453052-1	2014	BACKGROUND AND OBJECTIVES: Uridine-diphosphate glucuronosyltransferase 1A (UGT1A) is a key enzyme involved in irinotecan metabolism, and polymorphisms in the UGT1A gene are associated with irinotecan-induced toxicity.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	75-80
24453052-1	2014	BACKGROUND AND OBJECTIVES: Uridine-diphosphate glucuronosyltransferase 1A (UGT1A) is a key enzyme involved in irinotecan metabolism, and polymorphisms in the UGT1A gene are associated with irinotecan-induced toxicity.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	158-163
24453052-10	2014	A comprehensive study of the influence of UGT1A1 polymorphisms on the risk of irinotecan-induced toxicity is necessary for optimal use of irinotecan treatment.	Irinotecan	78-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
24453052-10	2014	A comprehensive study of the influence of UGT1A1 polymorphisms on the risk of irinotecan-induced toxicity is necessary for optimal use of irinotecan treatment.	Irinotecan	138-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
23959273-0	2014	Intergenic polymorphisms in the amphiregulin gene region as biomarkers in metastatic colorectal cancer patients treated with anti-EGFR plus irinotecan.	Irinotecan	140-150	amphiregulin	Homo sapiens	32-44
24932285-0	2014	Association between the low-dose irinotecan regimen-induced occurrence of grade 4 neutropenia and genetic variants of UGT1A1 in patients with gynecological cancers.	Irinotecan	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-124
24932285-1	2014	The occurrence of severe neutropenia during treatment with irinotecan (CPT-11) is associated with the *6 and *28 alleles of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	59-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-171
24932285-1	2014	The occurrence of severe neutropenia during treatment with irinotecan (CPT-11) is associated with the *6 and *28 alleles of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	59-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	173-179
24932285-1	2014	The occurrence of severe neutropenia during treatment with irinotecan (CPT-11) is associated with the *6 and *28 alleles of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	71-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-171
24932285-1	2014	The occurrence of severe neutropenia during treatment with irinotecan (CPT-11) is associated with the *6 and *28 alleles of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	71-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	173-179
24932285-3	2014	There are also no studies regarding the association between the 421C&gt;A mutation in ATP-binding cassette sub-family G member 2 (ABCG2) and the occurrence of severe neutropenia in CPT-11-treated patients with gynecological cancers.	Irinotecan	181-187	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	86-128
24932285-3	2014	There are also no studies regarding the association between the 421C&gt;A mutation in ATP-binding cassette sub-family G member 2 (ABCG2) and the occurrence of severe neutropenia in CPT-11-treated patients with gynecological cancers.	Irinotecan	181-187	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	130-135
24932285-6	2014	The association between the absolute neutrophil count (ANC) nadir values, the total dose of CPT-11 and the genotypes of UGT1A1 or ABCG2 was studied.	Irinotecan	92-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	120-126
24932285-12	2014	In conclusion, the UGT1A1*6/*28 and *6/*6 genotypes were found to be associated with the occurrence of severe neutropenia in the low-dose CPT-11 regimen for gynecological cancers.	Irinotecan	138-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
24932285-13	2014	This finding indicates that the determination of UGT1A1 variants may be as useful in CPT-11 chemotherapy for gynecological conditions as it is in colorectal and lung cancer patients treated with this drug.	Irinotecan	85-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
25141892-0	2014	UGT1A1*28 polymorphisms: a potential pharmacological biomarker of irinotecan-based chemotherapies in colorectal cancer.	Irinotecan	66-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23959273-8	2014	Our findings support that intergenic polymorphisms in the AREG gene region might help to identify colorectal cancer patients that will benefit from irinotecan plus anti-EGFR therapy.	Irinotecan	148-158	amphiregulin	Homo sapiens	58-62
24959385-14	2014	Furthermore, both irinotecan and topotecan are the efflux pump ABCG2 substrates; cancer cells with high expression of ABCG2 showed strong irinotecan and topotecan resistance.	Irinotecan	18-28	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	63-68
24959385-14	2014	Furthermore, both irinotecan and topotecan are the efflux pump ABCG2 substrates; cancer cells with high expression of ABCG2 showed strong irinotecan and topotecan resistance.	Irinotecan	18-28	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	118-123
24959385-14	2014	Furthermore, both irinotecan and topotecan are the efflux pump ABCG2 substrates; cancer cells with high expression of ABCG2 showed strong irinotecan and topotecan resistance.	Irinotecan	138-148	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	63-68
24959385-14	2014	Furthermore, both irinotecan and topotecan are the efflux pump ABCG2 substrates; cancer cells with high expression of ABCG2 showed strong irinotecan and topotecan resistance.	Irinotecan	138-148	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	118-123
24798549-11	2014	Reovirus and irinotecan combination therapy is synergistic, p21 mediated, and represents a novel potential treatment for patients with CRC.	Irinotecan	13-23	H3 histone pseudogene 16	Homo sapiens	60-63
24611457-10	2014	Thus, MTHFR genetic polymorphisms may be screened to predict the clinical responses to irinotecan-based chemotherapy in CRC patients.	Irinotecan	87-97	methylenetetrahydrofolate reductase	Homo sapiens	6-11
24428790-0	2014	Targeted inhibition of IL-18 attenuates irinotecan-induced intestinal mucositis in mice.	Irinotecan	40-50	interleukin 18	Mus musculus	23-28
24428790-4	2014	Therefore, we have investigated the role of IL-18 in the pathogenesis of irinotecan-induced intestinal mucositis.	Irinotecan	73-83	interleukin 18	Mus musculus	44-49
24428790-9	2014	Additionally, irinotecan treatment increased MPO and iNOS activity, iNOS immunostaining and IL-18 expression in WT mice compared with saline treatment.	Irinotecan	14-24	myeloperoxidase	Mus musculus	45-48
24428790-9	2014	Additionally, irinotecan treatment increased MPO and iNOS activity, iNOS immunostaining and IL-18 expression in WT mice compared with saline treatment.	Irinotecan	14-24	nitric oxide synthase 2, inducible	Mus musculus	53-57
24428790-9	2014	Additionally, irinotecan treatment increased MPO and iNOS activity, iNOS immunostaining and IL-18 expression in WT mice compared with saline treatment.	Irinotecan	14-24	nitric oxide synthase 2, inducible	Mus musculus	68-72
24428790-9	2014	Additionally, irinotecan treatment increased MPO and iNOS activity, iNOS immunostaining and IL-18 expression in WT mice compared with saline treatment.	Irinotecan	14-24	interleukin 18	Mus musculus	92-97
24428790-13	2014	Furthermore, the Survival of irinotecan-treated mice was increased and iNOS immunoexpression and IL-18 production prevented in IL-18 knockout mice.	Irinotecan	29-39	interleukin 18	Mus musculus	127-132
24428790-14	2014	CONCLUSIONS AND IMPLICATIONS: Targeting IL-18 function may be a promising therapeutic approach to decreasing the severity of intestinal mucositis during irinotecan treatment regimens.	Irinotecan	153-163	interleukin 18	Mus musculus	40-45
24834123-1	2014	Uridine glucuronosyltransferase (UGT) gene polymorphisms have been linked to irinotecan toxicity.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	0-31
24834123-1	2014	Uridine glucuronosyltransferase (UGT) gene polymorphisms have been linked to irinotecan toxicity.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	33-36
24834123-2	2014	Our purpose was to study the association between UGT1A1*28, UGT1A7*2, and UGT1A7*3 polymorphisms and irinotecan toxicity in Greek patients receiving low-dose weekly irinotecan.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
24834123-2	2014	Our purpose was to study the association between UGT1A1*28, UGT1A7*2, and UGT1A7*3 polymorphisms and irinotecan toxicity in Greek patients receiving low-dose weekly irinotecan.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	74-80
24834123-8	2014	To conclude, UGT polymorphisms play a role in the toxicity of irinotecan, even if the drug is administered in low doses.	Irinotecan	62-72	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	13-16
24611457-0	2014	Effects of MTHFR genetic polymorphisms on toxicity and clinical response of irinotecan-based chemotherapy in patients with colorectal cancer.	Irinotecan	76-86	methylenetetrahydrofolate reductase	Homo sapiens	11-16
24611457-1	2014	AIMS: This meta-analysis aims to evaluate the effects of common polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene on the toxicity and clinical responses of irinotecan-based chemotherapy in patients with colorectal cancer (CRC).	Irinotecan	176-186	methylenetetrahydrofolate reductase	Homo sapiens	85-120
24611457-1	2014	AIMS: This meta-analysis aims to evaluate the effects of common polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene on the toxicity and clinical responses of irinotecan-based chemotherapy in patients with colorectal cancer (CRC).	Irinotecan	176-186	methylenetetrahydrofolate reductase	Homo sapiens	122-127
24611457-7	2014	RESULTS: The results from our meta-analysis suggested that MTHFR genetic polymorphisms might significantly decrease the rate of grade 3/4 toxicity of irinotecan-based chemotherapy in CRC patients (OR=0.53, 95% CI: 0.32-0.89, p=0.015).	Irinotecan	150-160	methylenetetrahydrofolate reductase	Homo sapiens	59-64
24611457-8	2014	Furthermore, we also demonstrated that MTHFR genetic polymorphisms strongly correlated with good clinical responses (complete response+partial response) to irinotecan-based chemotherapy in CRC patients (OR=1.47, 95% CI: 1.05-2.04, p=0.024).	Irinotecan	156-166	methylenetetrahydrofolate reductase	Homo sapiens	39-44
24611457-9	2014	CONCLUSIONS: Our findings provide empirical evidence that MTHFR genetic polymorphisms may decrease the toxicity of irinotecan-based chemotherapy and increase the clinical benefits for CRC patients.	Irinotecan	115-125	methylenetetrahydrofolate reductase	Homo sapiens	58-63
24382596-1	2014	Previous reports of the influence of UGT1A1 gene polymorphisms on the pharmacokinetics of irinotecan metabolism have not assessed Asian patients treated with FOLFIRI plus bevacizumab for advanced and recurrent colorectal cancer.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
24692733-0	2014	Multicenter phase II study of second-line cetuximab plus folinic acid/5-fluorouracil/irinotecan (FOLFIRI) in KRAS wild-type metastatic colorectal cancer: the FLIER study.	Irinotecan	85-95	KRAS proto-oncogene, GTPase	Homo sapiens	109-113
24683007-1	2014	Weekly cetuximab plus irinotecan-based regiments are standard first- and second-line chemotherapy for patients with KRAS wild-type metastatic colorectal cancer (mCRC).	Irinotecan	22-32	KRAS proto-oncogene, GTPase	Homo sapiens	116-120
24249672-2	2014	A phase I trial of the mTOR inhibitor temsirolimus (TEM) with irinotecan (IRN) and temozolomide (TMZ) was conducted in children with recurrent/refractory solid tumors, including central nervous system (CNS) tumors.	Irinotecan	62-72	mechanistic target of rapamycin kinase	Homo sapiens	23-27
24249672-2	2014	A phase I trial of the mTOR inhibitor temsirolimus (TEM) with irinotecan (IRN) and temozolomide (TMZ) was conducted in children with recurrent/refractory solid tumors, including central nervous system (CNS) tumors.	Irinotecan	74-77	mechanistic target of rapamycin kinase	Homo sapiens	23-27
24764659-5	2014	The CRYSTAL study showed that adding cetuximab to FOLFIRI (regimen of irinotecan, infusional fluorouracil and leucovorin) significantly improved results in the first-line treatment of KRAS wild-type mCRC.	Irinotecan	70-80	KRAS proto-oncogene, GTPase	Homo sapiens	184-188
24699684-1	2014	Two major forms of human carboxylesterase (CES), CES1A and CES2, dominate the pharmacokinetics of most prodrugs such as imidapril and irinotecan (CPT-11).	Irinotecan	134-144	carboxylesterase 2	Homo sapiens	59-63
24699684-1	2014	Two major forms of human carboxylesterase (CES), CES1A and CES2, dominate the pharmacokinetics of most prodrugs such as imidapril and irinotecan (CPT-11).	Irinotecan	146-152	carboxylesterase 2	Homo sapiens	59-63
24577941-0	2014	The use of Olaparib (AZD2281) potentiates SN-38 cytotoxicity in colon cancer cells by indirect inhibition of Rad51-mediated repair of DNA double-strand breaks.	Irinotecan	42-47	RAD51 recombinase	Mus musculus	109-114
24577941-5	2014	Furthermore, olaparib potentiated S-phase-specific double-strand DNA breaks (DSB) induced by SN-38, which is followed by Rad51 recruitment.	Irinotecan	93-98	RAD51 recombinase	Mus musculus	121-126
24577941-6	2014	siRNA-mediated knockdown of Rad51, but not Mre11 or Rad50, increased the sensitivity to olaparib and/or SN-38 treatment in colon cancer cells.	Irinotecan	104-109	RAD51 recombinase	Mus musculus	28-33
24772300-6	2014	The mPFS of the wild-type and mutated KRAS subgroups that had received irinotecan-based treatments was 7.7 and 9.7 months, respectively (P= 0.43).	Irinotecan	71-81	KRAS proto-oncogene, GTPase	Homo sapiens	38-42
24781822-3	2014	SLC6A6 knockdown (KD) attenuated cell survival and was accompanied by enhanced drug sensitivity to 5-fluorouracil (5-FU), doxycycline (DOX) and SN-38.	Irinotecan	144-149	solute carrier family 6 member 6	Homo sapiens	0-6
24781822-6	2014	Additionally, SLC6A6-siRNA treatment enhanced the cytotoxic effects of all 3 drugs, whereas the efficacy of ABCG2-siRNA treatment was limited to its 2 substrate drugs, DOX and SN-38.	Irinotecan	176-181	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	108-113
24692733-1	2014	BACKGROUND: This study was the first multicenter phase II study of cetuximab plus folinic acid/5-fluorouracil/irinotecan (FOLFIRI) in KRAS wild-type mCRC as a second-line treatment in Japan including BRAF and PIK3CA genotyping.	Irinotecan	110-120	KRAS proto-oncogene, GTPase	Homo sapiens	134-138
24287113-5	2014	The highest killing efficiency was observed after co-incubation of the cells with irinotecan and vitamin A (10muM), or vitamin E (25muM), respectively.	Irinotecan	82-92	latexin	Homo sapiens	110-113
24519753-0	2014	Associations between UGT1A1*6 or UGT1A1*6/*28 polymorphisms and irinotecan-induced neutropenia in Asian cancer patients.	Irinotecan	64-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
24519753-2	2014	Many studies have demonstrated that patients bearing UGT1A1*28 have a higher risk of severe neutropenia on toxicity of irinotecan.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
24519753-4	2014	Some researches reported that UGT1A1*28 and/or UGT1A1*6 could predict irinotecan-induced toxicities in Asian populations, but controversial conclusions still remained.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
24519753-4	2014	Some researches reported that UGT1A1*28 and/or UGT1A1*6 could predict irinotecan-induced toxicities in Asian populations, but controversial conclusions still remained.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
24519753-5	2014	This study aims to investigate the association between UGT1A1 gene polymorphisms *6, *6/*28 and irinotecan-related neutropenia in Asian cancer patients receiving irinotecan regimen chemotherapy.	Irinotecan	96-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
24519753-5	2014	This study aims to investigate the association between UGT1A1 gene polymorphisms *6, *6/*28 and irinotecan-related neutropenia in Asian cancer patients receiving irinotecan regimen chemotherapy.	Irinotecan	162-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
24519753-6	2014	EXPERIMENTAL DESIGN: Meta-analyses were done to assess the relationship between UGT1A1*6 or UGT1A1*6/*28 and irinotecan-induced neutropenia.	Irinotecan	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
24519753-6	2014	EXPERIMENTAL DESIGN: Meta-analyses were done to assess the relationship between UGT1A1*6 or UGT1A1*6/*28 and irinotecan-induced neutropenia.	Irinotecan	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
24519753-9	2014	CONCLUSIONS: In conclusion, the UGT1A1*6 and UGT1A1*6/*28 genotypes were associated with an increased risk of irinotecan-induced neutropenia in Asian cancer patients.	Irinotecan	110-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
24519753-9	2014	CONCLUSIONS: In conclusion, the UGT1A1*6 and UGT1A1*6/*28 genotypes were associated with an increased risk of irinotecan-induced neutropenia in Asian cancer patients.	Irinotecan	110-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
24242862-2	2014	Camptothecin analogues, including SN-38, have been shown to reduce the expression and transcriptional activity of HIF-1alpha in preclinical models.	Irinotecan	34-39	hypoxia inducible factor 1 subunit alpha	Homo sapiens	114-124
24242862-3	2014	We hypothesized that co-administration of pegylated SN-38 (EZN-2208) may offset the induction of HIF-1alpha following bevacizumab treatment, resulting in synergistic antitumor effects.	Irinotecan	52-57	hypoxia inducible factor 1 subunit alpha	Homo sapiens	97-107
24897286-0	2014	Association analysis of UGT1A genotype and haplotype with SN-38 glucuronidation in human livers.	Irinotecan	58-63	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	24-29
24897286-1	2014	AIM: 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, is mainly eliminated hepatically through glucuronidation by UGT1A1 and UGT1A9 enzymes.	Irinotecan	5-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
24897286-1	2014	AIM: 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, is mainly eliminated hepatically through glucuronidation by UGT1A1 and UGT1A9 enzymes.	Irinotecan	5-35	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	153-159
24897286-1	2014	AIM: 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, is mainly eliminated hepatically through glucuronidation by UGT1A1 and UGT1A9 enzymes.	Irinotecan	37-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
24897286-1	2014	AIM: 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, is mainly eliminated hepatically through glucuronidation by UGT1A1 and UGT1A9 enzymes.	Irinotecan	37-42	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	153-159
24897286-1	2014	AIM: 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, is mainly eliminated hepatically through glucuronidation by UGT1A1 and UGT1A9 enzymes.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
24897286-1	2014	AIM: 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, is mainly eliminated hepatically through glucuronidation by UGT1A1 and UGT1A9 enzymes.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	153-159
24897286-2	2014	This study comprehensively investigates the effects of UGT1A1 and UGT1A9 genetic polymorphism on SN-38 glucuronidation activity.	Irinotecan	97-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
24897286-2	2014	This study comprehensively investigates the effects of UGT1A1 and UGT1A9 genetic polymorphism on SN-38 glucuronidation activity.	Irinotecan	97-102	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	66-72
24897286-5	2014	The number of UGT1A1 reduced function alleles was associated with decreased SN-38G formation rates and UGT1A protein levels.	Irinotecan	76-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
24897286-5	2014	The number of UGT1A1 reduced function alleles was associated with decreased SN-38G formation rates and UGT1A protein levels.	Irinotecan	76-81	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	14-19
24897286-6	2014	UGT1A9 I399C&gt;T and UGT1A9*1b, which were highly linked, were associated with increased SN-38 glucuronidation activity and UGT1A protein levels.	Irinotecan	90-95	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	0-6
24897286-6	2014	UGT1A9 I399C&gt;T and UGT1A9*1b, which were highly linked, were associated with increased SN-38 glucuronidation activity and UGT1A protein levels.	Irinotecan	90-95	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	22-28
24897286-6	2014	UGT1A9 I399C&gt;T and UGT1A9*1b, which were highly linked, were associated with increased SN-38 glucuronidation activity and UGT1A protein levels.	Irinotecan	90-95	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	0-5
24897286-8	2014	CONCLUSION: UGT1A1 genetic polymorphisms have a more important function in human liver SN-38 glucuronidation activity than UGT1A9.	Irinotecan	87-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
24407191-0	2014	Sorafenib and irinotecan (NEXIRI) as second- or later-line treatment for patients with metastatic colorectal cancer and KRAS-mutated tumours: a multicentre Phase I/II trial.	Irinotecan	14-24	KRAS proto-oncogene, GTPase	Homo sapiens	120-124
24318863-5	2014	Target genes were XPD-751, GSTP-1-105, XRCC1-399 for oxaliplatin, UGT1A1 for irinotecan.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
23504048-5	2014	Single and combined use of paclitaxel and SN-38 produced significant cytolethality against the cervical adenocarcinoma cell line CAC-1.	Irinotecan	42-47	transmembrane protein 54	Homo sapiens	129-134
24215868-4	2014	Synergism was evident between LT-626 and cisplatin, oxaliplatin and SN-38 suggesting that PARP inhibitors in combination with DNA damaging agents may be a successful strategy for treatment of CRC.	Irinotecan	68-73	poly(ADP-ribose) polymerase 1	Homo sapiens	90-94
24462359-4	2014	In addition, P123-DOPE can inhibit breast cancer resistance protein (BCPR) mediated CPT-11 efflux in drug resistant MCF-7/BCRP breast cancer cells, thus acting as a "door blocker".	Irinotecan	84-90	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	35-67
24462359-4	2014	In addition, P123-DOPE can inhibit breast cancer resistance protein (BCPR) mediated CPT-11 efflux in drug resistant MCF-7/BCRP breast cancer cells, thus acting as a "door blocker".	Irinotecan	84-90	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	69-73
23384250-1	2014	ATP-Binding Cassette transporters such as ABCG2 confer resistance to various anticancer drugs including irinotecan and its active metabolite, SN38.	Irinotecan	104-114	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	42-47
23605141-1	2014	BACKGROUND: It was recently reported that genetic polymorphisms of UDP glucuronyltransferase-1 polypeptide A1 (UGT1A1), a glucuronidation enzyme, were associated with irinotecan (CPT-11) metabolism.	Irinotecan	167-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-109
23605141-1	2014	BACKGROUND: It was recently reported that genetic polymorphisms of UDP glucuronyltransferase-1 polypeptide A1 (UGT1A1), a glucuronidation enzyme, were associated with irinotecan (CPT-11) metabolism.	Irinotecan	167-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
23605141-1	2014	BACKGROUND: It was recently reported that genetic polymorphisms of UDP glucuronyltransferase-1 polypeptide A1 (UGT1A1), a glucuronidation enzyme, were associated with irinotecan (CPT-11) metabolism.	Irinotecan	179-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-109
23605141-1	2014	BACKGROUND: It was recently reported that genetic polymorphisms of UDP glucuronyltransferase-1 polypeptide A1 (UGT1A1), a glucuronidation enzyme, were associated with irinotecan (CPT-11) metabolism.	Irinotecan	179-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
23605141-2	2014	The active metabolite of CPT-11, 7-ethyl-10-hydroxycamptothecin (SN-38) was glucuronidated (SN-38G) by UGT1A1.	Irinotecan	65-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
23605141-2	2014	The active metabolite of CPT-11, 7-ethyl-10-hydroxycamptothecin (SN-38) was glucuronidated (SN-38G) by UGT1A1.	Irinotecan	92-97	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
23605141-4	2014	Several studies have suggested that the dose of CPT-11 should be decreased in patients homozygous for UGT1A1*6 or UGT1A1*28, or double heterozygotes (*6/*28).	Irinotecan	48-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108
23605141-4	2014	Several studies have suggested that the dose of CPT-11 should be decreased in patients homozygous for UGT1A1*6 or UGT1A1*28, or double heterozygotes (*6/*28).	Irinotecan	48-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
23605141-7	2014	RESULTS: The SN-38G/SN-38 concentration ratio was lower in patients who were homozygous for UGT1A1*6, heterozygous for UGT1A1*6 or UGT1A1*28, or were double heterozygotes compared with patients with wild-type genes.	Irinotecan	13-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
23605141-7	2014	RESULTS: The SN-38G/SN-38 concentration ratio was lower in patients who were homozygous for UGT1A1*6, heterozygous for UGT1A1*6 or UGT1A1*28, or were double heterozygotes compared with patients with wild-type genes.	Irinotecan	13-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
23605141-7	2014	RESULTS: The SN-38G/SN-38 concentration ratio was lower in patients who were homozygous for UGT1A1*6, heterozygous for UGT1A1*6 or UGT1A1*28, or were double heterozygotes compared with patients with wild-type genes.	Irinotecan	13-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
23605141-8	2014	The relative decreases in the SN-38G/SN-38 concentration ratio in patients homozygous for UGT1A1*6 and in double heterozygotes were greater than in patients heterozygous for UGT1A1*6 or UGT1A1*28.	Irinotecan	30-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
23605141-8	2014	The relative decreases in the SN-38G/SN-38 concentration ratio in patients homozygous for UGT1A1*6 and in double heterozygotes were greater than in patients heterozygous for UGT1A1*6 or UGT1A1*28.	Irinotecan	30-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
23605141-8	2014	The relative decreases in the SN-38G/SN-38 concentration ratio in patients homozygous for UGT1A1*6 and in double heterozygotes were greater than in patients heterozygous for UGT1A1*6 or UGT1A1*28.	Irinotecan	30-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	174-180
23609856-3	2014	Beside *28, UGT1A1*6 (*6) is another important variant allele in Japanese patients because it is associated with adverse events of irinotecan, metabolized by UGT1A1.	Irinotecan	131-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
23609856-3	2014	Beside *28, UGT1A1*6 (*6) is another important variant allele in Japanese patients because it is associated with adverse events of irinotecan, metabolized by UGT1A1.	Irinotecan	131-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
23529007-0	2014	Association of UGT1A1*28 polymorphisms with irinotecan-induced toxicities in colorectal cancer: a meta-analysis in Caucasians.	Irinotecan	44-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
23529007-1	2014	A meta-analysis in Caucasians was conducted to investigate the possible association of uridine diphosphate glucuronosyltransferase (UGT) 1A1 gene polymorphisms with irinotecan (IRI)-induced neutropenia and diarrhoea in colorectal cancer (CRC).	Irinotecan	165-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	87-140
24066723-2	2014	Nilotinib, a tyrosine kinase inhibitor, could potently inhibit SN-38 glucuronidation mainly catalyzed by UDP-glucuronosyltransferase (UGT) 1A1.	Irinotecan	63-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-142
24448639-0	2014	UGT1A1*6 polymorphisms are correlated with irinotecan-induced toxicity: a system review and meta-analysis in Asians.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24525731-6	2014	Irinotecan, another chemotherapeutic agent to induce DNA damaging used to treat patients with advanced gastric cancer that progressed on cisplatin, was found to inhibit the expression of XRCC1 effectively, and leading to an increase in the sensitivity of resistant cells to cisplatin.	Irinotecan	0-10	X-ray repair cross complementing 1	Homo sapiens	187-192
24523596-2	2014	ABCG2/BCRP is referred to as a "half-type" ABC transporter, functioning as a homodimer, and transports anticancer agents such as irinotecan, 7-ethyl-10-hydroxycamptothecin (SN-38), gefitinib, imatinib, methotrexate, and mitoxantrone from cells.	Irinotecan	129-139	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	6-10
24523596-2	2014	ABCG2/BCRP is referred to as a "half-type" ABC transporter, functioning as a homodimer, and transports anticancer agents such as irinotecan, 7-ethyl-10-hydroxycamptothecin (SN-38), gefitinib, imatinib, methotrexate, and mitoxantrone from cells.	Irinotecan	129-139	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
24523596-2	2014	ABCG2/BCRP is referred to as a "half-type" ABC transporter, functioning as a homodimer, and transports anticancer agents such as irinotecan, 7-ethyl-10-hydroxycamptothecin (SN-38), gefitinib, imatinib, methotrexate, and mitoxantrone from cells.	Irinotecan	141-171	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
24523596-2	2014	ABCG2/BCRP is referred to as a "half-type" ABC transporter, functioning as a homodimer, and transports anticancer agents such as irinotecan, 7-ethyl-10-hydroxycamptothecin (SN-38), gefitinib, imatinib, methotrexate, and mitoxantrone from cells.	Irinotecan	141-171	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	6-10
24523596-2	2014	ABCG2/BCRP is referred to as a "half-type" ABC transporter, functioning as a homodimer, and transports anticancer agents such as irinotecan, 7-ethyl-10-hydroxycamptothecin (SN-38), gefitinib, imatinib, methotrexate, and mitoxantrone from cells.	Irinotecan	173-178	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
24523596-2	2014	ABCG2/BCRP is referred to as a "half-type" ABC transporter, functioning as a homodimer, and transports anticancer agents such as irinotecan, 7-ethyl-10-hydroxycamptothecin (SN-38), gefitinib, imatinib, methotrexate, and mitoxantrone from cells.	Irinotecan	173-178	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	6-10
24316664-9	2014	mRNA levels of claudin-1 were significantly decreased early after irinotecan in the small and large intestines.	Irinotecan	66-76	claudin 1	Rattus norvegicus	15-24
24439671-0	2014	Regulation and expression of aberrant methylation on irinotecan metabolic genes CES2, UGT1A1 and GUSB in the in-vitro cultured colorectal cancer cells.	Irinotecan	53-63	carboxylesterase 2	Homo sapiens	80-84
24439671-0	2014	Regulation and expression of aberrant methylation on irinotecan metabolic genes CES2, UGT1A1 and GUSB in the in-vitro cultured colorectal cancer cells.	Irinotecan	53-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
24439671-0	2014	Regulation and expression of aberrant methylation on irinotecan metabolic genes CES2, UGT1A1 and GUSB in the in-vitro cultured colorectal cancer cells.	Irinotecan	53-63	glucuronidase beta	Homo sapiens	97-101
24439671-8	2014	CONCLUSION: Methylation in UGT1A1 gene expression silencing as an important mechanism; methylation could provide an effective target for methylation regulation intervening in the treatment of CPT-11.	Irinotecan	192-198	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
24308720-0	2014	The association of UGT1A1*6 and UGT1A1*28 with irinotecan-induced neutropenia in Asians: a meta-analysis.	Irinotecan	47-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
24308720-0	2014	The association of UGT1A1*6 and UGT1A1*28 with irinotecan-induced neutropenia in Asians: a meta-analysis.	Irinotecan	47-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
24308720-1	2014	BACKGROUND: The UGT1A1*28 polymorphism is known as a biomarker of irinotecan-induced neutropenia in Caucasians.	Irinotecan	66-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
24308720-5	2014	CONCLUSIONS: In Asians, a combination test of UGT1A1*6 and UGT1A1*28 might be a potential biomarker of irinotecan-induced neutropenia, an observation that will need additional trials for confirmation.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
24308720-5	2014	CONCLUSIONS: In Asians, a combination test of UGT1A1*6 and UGT1A1*28 might be a potential biomarker of irinotecan-induced neutropenia, an observation that will need additional trials for confirmation.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
24265452-10	2014	Finally, in irinotecan-induced enteritis, GLP-2 normalized epithelial barrier function in control (P &lt; .05) but not knockout animals.	Irinotecan	12-22	glucagon-like peptide 2 receptor	Mus musculus	42-47
24497922-1	2014	OBJECTIVE: To explore genes of the killer-cell immunoglobulin-like receptor (KIR) and of the HLA ligand and their relationship with the outcome of metastatic colorectal cancer (mCRC) patients treated with first-line 5-fluorouracil, leucovorin, and irinotecan (FOLFIRI).	Irinotecan	248-258	killer cell immunoglobulin like receptor, two Ig domains and short cytoplasmic tail 4	Homo sapiens	35-75
24194565-2	2014	Impaired hepatic clearance due to low-activity polymorphisms in human OATP1B1 may increase systemic exposure to SN-38, the active and toxic metabolite of the anticancer prodrug irinotecan.	Irinotecan	112-117	solute carrier organic anion transporter family member 1B1	Homo sapiens	70-77
24194565-2	2014	Impaired hepatic clearance due to low-activity polymorphisms in human OATP1B1 may increase systemic exposure to SN-38, the active and toxic metabolite of the anticancer prodrug irinotecan.	Irinotecan	177-187	solute carrier organic anion transporter family member 1B1	Homo sapiens	70-77
24701697-2	2014	Several recent phase III trials reported median overall survival data exceeding 30 months, an achievement inconceivable only 5 years ago.The first major step forward in the medical management of mCRC was provided by the addition of irinotecan and oxaliplatin to fluorouracil-based therapy; this increased survival from about 12 months to about 20 months.The introduction of biologic agents such as vascular endothelial growth factor inhibitors and epidermal growth factor inhibitors further increased survival--to more than 2 years in prospective trials.	Irinotecan	232-242	vascular endothelial growth factor A	Homo sapiens	398-432
24380837-0	2014	Optimization of irinotecan chronotherapy with P-glycoprotein inhibition.	Irinotecan	16-26	phosphoglycolate phosphatase	Mus musculus	46-60
24380837-1	2014	The relevance of P-glycoprotein (P-gp) for irinotecan chronopharmacology was investigated in female B6D2F1 mice.	Irinotecan	43-53	phosphoglycolate phosphatase	Mus musculus	33-37
24380837-7	2014	Non-tumor bearing mice lost an average of 17% or 9% of their body weight according to irinotecan administration at ZT3 or ZT15 respectively (p&lt;0.001).	Irinotecan	86-96	zinc finger protein 62	Mus musculus	115-118
24380837-12	2014	In conclusion, P-gp was an important determinant of the circadian balance between toxicity and efficacy of irinotecan.	Irinotecan	107-117	phosphoglycolate phosphatase	Mus musculus	15-19
24497922-1	2014	OBJECTIVE: To explore genes of the killer-cell immunoglobulin-like receptor (KIR) and of the HLA ligand and their relationship with the outcome of metastatic colorectal cancer (mCRC) patients treated with first-line 5-fluorouracil, leucovorin, and irinotecan (FOLFIRI).	Irinotecan	248-258	killer cell immunoglobulin like receptor, two Ig domains and short cytoplasmic tail 4	Homo sapiens	77-80
24195516-2	2014	The metabolism of CPT-11 is mainly controlled by carboxy-lesterase (CES), UDP-glucuronosyltransferase 1A (UGT1A), and beta-glucuronidase (GUSB).	Irinotecan	18-24	carboxylesterase 2	Homo sapiens	49-66
24815493-0	2014	Clinical observations on associations between the UGT1A1 genotype and severe toxicity of irinotecan.	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
24815493-2	2014	UDP glucuronosyltransferase1A1 (UGT1A1) catalyzes the glucuronidation of the active metabolite SN-38 but the relationship between UGT1A1 and severe toxicity remains unclear.	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-30
24815493-2	2014	UDP glucuronosyltransferase1A1 (UGT1A1) catalyzes the glucuronidation of the active metabolite SN-38 but the relationship between UGT1A1 and severe toxicity remains unclear.	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
24815493-2	2014	UDP glucuronosyltransferase1A1 (UGT1A1) catalyzes the glucuronidation of the active metabolite SN-38 but the relationship between UGT1A1 and severe toxicity remains unclear.	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
24815493-10	2014	CONCLUSIONS: Our study support the conclusion that patients with a UGT1A1*28 allele (s) will suffer an increased risk of severe irinotecan-induced diarrhea, whether with mid-or low-dosage.	Irinotecan	128-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
24815493-12	2014	Higher serum total bilirubin is an indication that patients UGT1A1 genotype is not wild-type, with significance for clinic usage of CPT-11.	Irinotecan	132-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
24172061-4	2014	In SW480 cells, DNMT inhibitors, such as decitabine (DAC), azacytidine and zebularine (Zeb), showed synergic effects on the cytotoxicity induced by anticancer drugs except for SN-38 plus Zeb, while HDAC inhibitors, trichostatin A, suberoylanilide hydroxamic acid and valproic acid, showed antagonistic effects.	Irinotecan	176-181	DNA methyltransferase 1	Homo sapiens	16-20
24172061-4	2014	In SW480 cells, DNMT inhibitors, such as decitabine (DAC), azacytidine and zebularine (Zeb), showed synergic effects on the cytotoxicity induced by anticancer drugs except for SN-38 plus Zeb, while HDAC inhibitors, trichostatin A, suberoylanilide hydroxamic acid and valproic acid, showed antagonistic effects.	Irinotecan	176-181	arylacetamide deacetylase	Homo sapiens	53-56
24172061-8	2014	However, synergic effects of DAC with 5-FU or CPT-11 (SN-38) were not observed in 4 CRC cell lines.	Irinotecan	54-59	arylacetamide deacetylase	Homo sapiens	29-32
22454224-15	2014	Combined treatment of olaparib with irinotecan might be effective in treatment of non-BRCA-related breast cancer.	Irinotecan	36-46	BRCA1 DNA repair associated	Homo sapiens	86-90
25967674-0	2014	Prevalence of the UGT1A1*6 (c.211G&gt;A) Polymorphism and Prediction of Irinotecan Toxicity in Iranian Populations of Different Ethnicities.	Irinotecan	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
25967674-1	2014	BACKGROUND: Pharmacogenetic studies on irinotecan treatment in patients with metastatic colorectal cancer have indicated that genetic polymorphisms in UGT1A1*6 can lead to decreased enzyme activity and accumulation of the toxic metabolite SN-38.	Irinotecan	39-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	151-157
25967674-1	2014	BACKGROUND: Pharmacogenetic studies on irinotecan treatment in patients with metastatic colorectal cancer have indicated that genetic polymorphisms in UGT1A1*6 can lead to decreased enzyme activity and accumulation of the toxic metabolite SN-38.	Irinotecan	239-244	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	151-157
25967674-9	2014	CONCLUSION: The identification of the UGT1A1*6 alleles is necessary among the different Iranian ethnic groups before irinotecan therapy, suggesting that genotyping would be helpful for clinicians to optimize chemotherapy or identify individuals at risk of adverse drug reactions before clinical trials.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
25016708-1	2014	BACKGROUND: Uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) is a key conjugating enzyme of bilirubin and the anti-tumor medication irinotecan.	Irinotecan	141-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-60
25016708-1	2014	BACKGROUND: Uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) is a key conjugating enzyme of bilirubin and the anti-tumor medication irinotecan.	Irinotecan	141-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
25016708-2	2014	Comprehensive analysis of UGT1A1 gene polymorphisms may provide benefit by predicting pharmacokinetics and outcomes of treatment with irinotecan and certain antiviral medications.	Irinotecan	134-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
24988246-3	2014	Polymorphisms of the CES1 gene have been reported to affect the metabolism of dabigatran etexilate, methylphenidate, oseltamivir, imidapril, and clopidogrel, whereas variants of the CES2 gene have been found to affect aspirin and irinotecan.	Irinotecan	230-240	carboxylesterase 1	Homo sapiens	21-25
24988246-3	2014	Polymorphisms of the CES1 gene have been reported to affect the metabolism of dabigatran etexilate, methylphenidate, oseltamivir, imidapril, and clopidogrel, whereas variants of the CES2 gene have been found to affect aspirin and irinotecan.	Irinotecan	230-240	carboxylesterase 2	Homo sapiens	182-186
24173769-4	2014	Inhibition of NF-kappaB activation by p65 small interfering RNA was shown to potentiate apoptosis induced by CPT-11.	Irinotecan	109-115	RELA proto-oncogene, NF-kB subunit	Homo sapiens	38-41
24173769-5	2014	Berberine suppressed CPT-11-induced NF-kappaB activation in a dose-dependent manner and enhanced chemosensitivity to CPT-11 by downregulating NF-kappaB activation of antiapoptotic genes, c-IAP1, c-IAP2, survivin and Bcl-xL.	Irinotecan	21-27	baculoviral IAP repeat containing 3	Homo sapiens	195-201
24173769-5	2014	Berberine suppressed CPT-11-induced NF-kappaB activation in a dose-dependent manner and enhanced chemosensitivity to CPT-11 by downregulating NF-kappaB activation of antiapoptotic genes, c-IAP1, c-IAP2, survivin and Bcl-xL.	Irinotecan	21-27	BCL2 like 1	Homo sapiens	216-222
24195503-11	2014	Analysis of UGT1A1 alleles may be the basis for modified dosing and reducing the potential toxicity of irinotecan.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
24368879-2	2014	Ziv-aflibercept is a fusion protein which acts as a decoy receptor for vascular endothelial growth factor (VEGF)-A, VEGF-B, and placental growth factor (PlGF); it was approved in combination with 5-fluorouracil, leucovorin, and irinotecan (FOLFIRI) for the treatment of patients with metastatic colorectal cancer that is resistant to or has progressed after an oxaliplatin-containing fluoropyrimidine-based regimen.	Irinotecan	228-238	placental growth factor	Homo sapiens	153-157
24594772-4	2014	The patient was treated with a combination of carboplatin and irinotecan, and achieved a partial response : size reduction of the prostate and the metastatic lesions, and decreased neuron specific enolase (NSE) level.	Irinotecan	62-72	enolase 2	Homo sapiens	181-204
24594772-4	2014	The patient was treated with a combination of carboplatin and irinotecan, and achieved a partial response : size reduction of the prostate and the metastatic lesions, and decreased neuron specific enolase (NSE) level.	Irinotecan	62-72	enolase 2	Homo sapiens	206-209
24190390-3	2014	In this study, we first demonstrate that a novel bFGF antagonist, peptide P7, previously isolated by phage display technology, reversed bFGF-induced resistance to irinotecan hydrochloride (CPT-11), and counteracted the anti-apoptotic effects of bFGF on CPT-11-treated HT-29 cells.	Irinotecan	163-187	fibroblast growth factor 2	Homo sapiens	49-53
24190390-3	2014	In this study, we first demonstrate that a novel bFGF antagonist, peptide P7, previously isolated by phage display technology, reversed bFGF-induced resistance to irinotecan hydrochloride (CPT-11), and counteracted the anti-apoptotic effects of bFGF on CPT-11-treated HT-29 cells.	Irinotecan	163-187	fibroblast growth factor 2	Homo sapiens	136-140
24190390-3	2014	In this study, we first demonstrate that a novel bFGF antagonist, peptide P7, previously isolated by phage display technology, reversed bFGF-induced resistance to irinotecan hydrochloride (CPT-11), and counteracted the anti-apoptotic effects of bFGF on CPT-11-treated HT-29 cells.	Irinotecan	163-187	fibroblast growth factor 2	Homo sapiens	136-140
24190390-3	2014	In this study, we first demonstrate that a novel bFGF antagonist, peptide P7, previously isolated by phage display technology, reversed bFGF-induced resistance to irinotecan hydrochloride (CPT-11), and counteracted the anti-apoptotic effects of bFGF on CPT-11-treated HT-29 cells.	Irinotecan	189-195	fibroblast growth factor 2	Homo sapiens	49-53
24190390-3	2014	In this study, we first demonstrate that a novel bFGF antagonist, peptide P7, previously isolated by phage display technology, reversed bFGF-induced resistance to irinotecan hydrochloride (CPT-11), and counteracted the anti-apoptotic effects of bFGF on CPT-11-treated HT-29 cells.	Irinotecan	189-195	fibroblast growth factor 2	Homo sapiens	136-140
24190390-3	2014	In this study, we first demonstrate that a novel bFGF antagonist, peptide P7, previously isolated by phage display technology, reversed bFGF-induced resistance to irinotecan hydrochloride (CPT-11), and counteracted the anti-apoptotic effects of bFGF on CPT-11-treated HT-29 cells.	Irinotecan	189-195	fibroblast growth factor 2	Homo sapiens	136-140
24190390-3	2014	In this study, we first demonstrate that a novel bFGF antagonist, peptide P7, previously isolated by phage display technology, reversed bFGF-induced resistance to irinotecan hydrochloride (CPT-11), and counteracted the anti-apoptotic effects of bFGF on CPT-11-treated HT-29 cells.	Irinotecan	253-259	fibroblast growth factor 2	Homo sapiens	49-53
24190390-3	2014	In this study, we first demonstrate that a novel bFGF antagonist, peptide P7, previously isolated by phage display technology, reversed bFGF-induced resistance to irinotecan hydrochloride (CPT-11), and counteracted the anti-apoptotic effects of bFGF on CPT-11-treated HT-29 cells.	Irinotecan	253-259	fibroblast growth factor 2	Homo sapiens	136-140
24190390-3	2014	In this study, we first demonstrate that a novel bFGF antagonist, peptide P7, previously isolated by phage display technology, reversed bFGF-induced resistance to irinotecan hydrochloride (CPT-11), and counteracted the anti-apoptotic effects of bFGF on CPT-11-treated HT-29 cells.	Irinotecan	253-259	fibroblast growth factor 2	Homo sapiens	136-140
24190390-4	2014	Further experiments indicated that the inhibition of Akt activation, the suppression of bFGF internalization, the increase in the Bax to Bcl-2 ratio and the downregulation of cytokeratin 8 (CK8) by P7 may contribute to the counteracting of the anti-apoptotic effects of bFGF, and further reversal of bFGF-induced resistance to CPT-11.	Irinotecan	327-333	keratin 8	Homo sapiens	190-193
24195516-2	2014	The metabolism of CPT-11 is mainly controlled by carboxy-lesterase (CES), UDP-glucuronosyltransferase 1A (UGT1A), and beta-glucuronidase (GUSB).	Irinotecan	18-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-104
24195516-2	2014	The metabolism of CPT-11 is mainly controlled by carboxy-lesterase (CES), UDP-glucuronosyltransferase 1A (UGT1A), and beta-glucuronidase (GUSB).	Irinotecan	18-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-111
24195516-2	2014	The metabolism of CPT-11 is mainly controlled by carboxy-lesterase (CES), UDP-glucuronosyltransferase 1A (UGT1A), and beta-glucuronidase (GUSB).	Irinotecan	18-24	glucuronidase beta	Homo sapiens	118-136
24195516-2	2014	The metabolism of CPT-11 is mainly controlled by carboxy-lesterase (CES), UDP-glucuronosyltransferase 1A (UGT1A), and beta-glucuronidase (GUSB).	Irinotecan	18-24	glucuronidase beta	Homo sapiens	138-142
24195516-11	2014	The promoter of the UGT1A1 gene in colorectal cancer cells is methylated, which is an important mechanism of UGT1A1 gene silencing and can be regarded as the target point of research for CPT-11 drug resistance and control mechanisms for the reversal of drug resistance.	Irinotecan	187-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
24548447-15	2013	Patients with down-regulated ERCC1 on Oxaliplatin or up-regulated TOPO Ion Irinotecan have longer survival and better curative effect.	Irinotecan	75-85	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	29-34
24968756-3	2014	This prospective study investigated the relationship between the mutation status of EGFR-related genes including KRAS and the response rate (RR) to cetuximab plus irinotecan therapy in Japanese mCRC patients.	Irinotecan	163-173	epidermal growth factor receptor	Homo sapiens	84-88
24968756-3	2014	This prospective study investigated the relationship between the mutation status of EGFR-related genes including KRAS and the response rate (RR) to cetuximab plus irinotecan therapy in Japanese mCRC patients.	Irinotecan	163-173	KRAS proto-oncogene, GTPase	Homo sapiens	113-117
24968756-7	2014	The RR to cetuximab plus irinotecan therapy was found to be 17.9 and 0% in the KRAS wild-type and mutant subgroups, respectively.	Irinotecan	25-35	KRAS proto-oncogene, GTPase	Homo sapiens	79-83
24968756-8	2014	CONCLUSION: Despite the identification of a lower-than-expected RR to treatment by the KRAS wild-type subgroup, KRAS mutation status appears to be a useful predictive marker of response to cetuximab plus irinotecan therapy in Japanese mCRC patients.	Irinotecan	204-214	KRAS proto-oncogene, GTPase	Homo sapiens	112-116
23921491-7	2014	Kinetic analyses for OATP-mediated transport revealed that the uptake of SN-38 by OATP1B1 was the highest, followed by OATP1B3.	Irinotecan	73-78	solute carrier organic anion transporter family member 1A2	Homo sapiens	21-25
23921491-7	2014	Kinetic analyses for OATP-mediated transport revealed that the uptake of SN-38 by OATP1B1 was the highest, followed by OATP1B3.	Irinotecan	73-78	solute carrier organic anion transporter family member 1B1	Homo sapiens	82-89
23921491-7	2014	Kinetic analyses for OATP-mediated transport revealed that the uptake of SN-38 by OATP1B1 was the highest, followed by OATP1B3.	Irinotecan	73-78	solute carrier organic anion transporter family member 1B3	Homo sapiens	119-126
23921491-8	2014	Among the uremic toxins, CMPF exhibited most potent inhibition of OATP1B1-mediated SN-38 uptake and directly inhibited the uptake of SN-38 also in hepatocytes.	Irinotecan	83-88	solute carrier organic anion transporter family member 1B1	Homo sapiens	66-73
23921491-10	2014	CONCLUSIONS: OATP1B1-mediated hepatic uptake of SN-38 was inhibited by uremic toxins, and gene expression of OATP1B1 was down-regulated by uremic plasma.	Irinotecan	48-53	solute carrier organic anion transporter family member 1B1	Homo sapiens	13-20
24359226-0	2013	Correlation between the methylation of SULF2 and WRN promoter and the irinotecan chemosensitivity in gastric cancer.	Irinotecan	70-80	sulfatase 2	Homo sapiens	39-44
24359226-0	2013	Correlation between the methylation of SULF2 and WRN promoter and the irinotecan chemosensitivity in gastric cancer.	Irinotecan	70-80	WRN RecQ like helicase	Homo sapiens	49-52
24359226-7	2013	Patients with SULF2 methylation were more sensitive to CPT-11 than those without SULF2 methylation (P &lt; 0.01).	Irinotecan	55-61	sulfatase 2	Homo sapiens	14-19
24359226-8	2013	Patients with both SULF2 and WRN methylation were also more sensitive to CPT-11 than others (P &lt; 0.05).	Irinotecan	73-79	sulfatase 2	Homo sapiens	19-24
24359226-8	2013	Patients with both SULF2 and WRN methylation were also more sensitive to CPT-11 than others (P &lt; 0.05).	Irinotecan	73-79	WRN RecQ like helicase	Homo sapiens	29-32
24359226-9	2013	CONCLUSION: SULF2 and WRN promoter methylation detection indicates potential predictive biomarkers to identify and target the most sensitive gastric cancer subpopulation for personalized CPT-11 therapy.	Irinotecan	187-193	WRN RecQ like helicase	Homo sapiens	22-25
24427321-11	2014	Curcumin may suppress GSTM5 expression to enhance the lethal effect of irinotecan on LOVO cells, and maybe their combination via the affection of PDI and PRDX4 to disturb the formation and reduction of disulfides results in inducing apoptosis of LOVO cell.	Irinotecan	71-81	glutathione S-transferase mu 5	Homo sapiens	22-27
24154875-5	2013	The application of a maximum-a-posteriori Bayesian inference method identified a linear model based on Rev-erbalpha and Bmal1 circadian expressions that accurately predicted for optimal irinotecan timing.	Irinotecan	186-196	nuclear receptor subfamily 1, group D, member 1	Mus musculus	103-115
24154875-5	2013	The application of a maximum-a-posteriori Bayesian inference method identified a linear model based on Rev-erbalpha and Bmal1 circadian expressions that accurately predicted for optimal irinotecan timing.	Irinotecan	186-196	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	120-125
24033692-1	2013	UNLABELLED: Retrospective studies have suggested that UDP-glucuronosyltransferase (UGT)1A1, UGT1A7, and UGT1A9 predict severe toxicity and efficacy of irinotecan-containing regimens.	Irinotecan	151-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-90
24263065-0	2013	KRAS-mutated plasma DNA as predictor of outcome from irinotecan monotherapy in metastatic colorectal cancer.	Irinotecan	53-63	KRAS proto-oncogene, GTPase	Homo sapiens	0-4
24263065-1	2013	BACKGROUND: We investigated the clinical implications of KRAS and BRAF mutations detected in both archival tumor tissue and plasma cell-free DNA in metastatic colorectal cancer patients treated with irinotecan monotherapy.	Irinotecan	199-209	KRAS proto-oncogene, GTPase	Homo sapiens	57-61
24324067-3	2013	To apply this strategy to the treatment of CNS lymphoma, we investigated the role of NSCs expressing carboxyl esterase (HB1.F3.CE), which activates irinotecan.	Irinotecan	148-158	histocompatibility minor HB-1	Homo sapiens	120-123
24324067-7	2013	RESULTS: The HB1.F3.CE cells significantly inhibited the growth of Raji cells with irinotecan treatment.	Irinotecan	83-93	histocompatibility minor HB-1	Homo sapiens	13-16
24033692-1	2013	UNLABELLED: Retrospective studies have suggested that UDP-glucuronosyltransferase (UGT)1A1, UGT1A7, and UGT1A9 predict severe toxicity and efficacy of irinotecan-containing regimens.	Irinotecan	151-161	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	92-98
24033692-1	2013	UNLABELLED: Retrospective studies have suggested that UDP-glucuronosyltransferase (UGT)1A1, UGT1A7, and UGT1A9 predict severe toxicity and efficacy of irinotecan-containing regimens.	Irinotecan	151-161	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	104-110
24311948-1	2013	BACKGROUND: The survival benefit for single-agent anti-epidermal growth factor receptor (egfr) therapy compared with combination therapy with irinotecan in KRAS wildtype (wt) metastatic colorectal cancer (mcrc) patients in the third-line treatment setting is not known.	Irinotecan	142-152	KRAS proto-oncogene, GTPase	Homo sapiens	156-160
24088669-0	2013	Polymorphisms in the UGT1A1 gene predict adverse effects of irinotecan in the treatment of gynecologic cancer in Japanese patients.	Irinotecan	60-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
24379067-0	2013	PEG-coated irinotecan cationic liposomes improve the therapeutic efficacy of breast cancer in animals.	Irinotecan	11-21	progestagen associated endometrial protein	Homo sapiens	0-3
24379067-2	2013	AIM: This study aimed to construct a kind of PEG-coated irinotecan cationic liposomes for investigating its efficacy and mechanism of action in the treatment of breast cancer in preclinical models.	Irinotecan	56-66	progestagen associated endometrial protein	Homo sapiens	45-48
24379067-5	2013	RESULTS: The zeta potential of PEG-coated irinotecan cationic liposomes was approximately 23 mV.	Irinotecan	42-52	progestagen associated endometrial protein	Homo sapiens	31-34
24379067-6	2013	The PEG-coated irinotecan cationic liposomes were approximately 66nm in diameter, significantly increased the intracellular uptake of irinotecan, and showed strong inhibitory effect on MDA-MB231 breast cancer cells.	Irinotecan	15-25	progestagen associated endometrial protein	Homo sapiens	4-7
24379067-6	2013	The PEG-coated irinotecan cationic liposomes were approximately 66nm in diameter, significantly increased the intracellular uptake of irinotecan, and showed strong inhibitory effect on MDA-MB231 breast cancer cells.	Irinotecan	134-144	progestagen associated endometrial protein	Homo sapiens	4-7
24379067-7	2013	A significant antitumor efficacy in the xenografted MDA-MB231 breast cancer cells in nude mice was evidenced by intravenous administration of PEG-coated irinotecan cationic liposomes.	Irinotecan	153-163	progestagen associated endometrial protein	Homo sapiens	142-145
24379067-8	2013	PEG-coated irinotecan cationic liposomes also improved the irinotecan blood circulation time and showed an enhanced drug concentration in tumor.	Irinotecan	11-21	progestagen associated endometrial protein	Homo sapiens	0-3
24379067-8	2013	PEG-coated irinotecan cationic liposomes also improved the irinotecan blood circulation time and showed an enhanced drug concentration in tumor.	Irinotecan	59-69	progestagen associated endometrial protein	Homo sapiens	0-3
24379067-9	2013	CONCLUSIONS: PEG-coated irinotecan cationic liposomes had significant inhibitory effect against breast cancer in vitro and in vivo, hence providing a new strategy for treating breast cancer.	Irinotecan	24-34	progestagen associated endometrial protein	Homo sapiens	13-16
24114122-0	2013	UGT1A1 genotype-guided phase I study of irinotecan, oxaliplatin, and capecitabine.	Irinotecan	40-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24114122-11	2013	UGT1A1 *1/*28 and *1/*1 patients treated with IRIN (150) had similar AUCs for the active irinotecan metabolite, SN38 (366 +/- 278 and 350 +/- 159 ng/ml*hr, respectively).	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24088669-6	2013	Homozygosity for UGT1A1*6/*6 and heterozygosity for UGT1A1*6/*28 were associated with an increased risk of absolute neutrophil count and/or diarrhea in Japanese gynecologic cancer patients, despite the lower doses of irinotecan used in these patients.	Irinotecan	217-227	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
24088669-7	2013	UGT1A1*6 and UGT1A1*28 are potential predictors of severe absolute neutrophil decrease and diarrhea caused by low-dose irinotecan in gynecologic cancer patients.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
24088669-7	2013	UGT1A1*6 and UGT1A1*28 are potential predictors of severe absolute neutrophil decrease and diarrhea caused by low-dose irinotecan in gynecologic cancer patients.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
24088669-1	2013	Irinotecan is a key chemotherapeutic drug used to treat many tumors, including cervical and ovarian cancers; however, irinotecan can cause toxicity, particularly in the presence of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene polymorphisms, which are associated with reduced enzyme activity.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	230-236
24088669-1	2013	Irinotecan is a key chemotherapeutic drug used to treat many tumors, including cervical and ovarian cancers; however, irinotecan can cause toxicity, particularly in the presence of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene polymorphisms, which are associated with reduced enzyme activity.	Irinotecan	118-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	230-236
24088669-2	2013	Here, we investigated the prevalence of three different variants of UGT1A1 (UGT1A1*6, UGT1A1*27 and UGT1A1*28) and their relationships with irinotecan-induced adverse events in patients with gynecologic cancer, who are treated with lower doses of irinotecan than patients with other types of solid tumors.	Irinotecan	140-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
24088669-2	2013	Here, we investigated the prevalence of three different variants of UGT1A1 (UGT1A1*6, UGT1A1*27 and UGT1A1*28) and their relationships with irinotecan-induced adverse events in patients with gynecologic cancer, who are treated with lower doses of irinotecan than patients with other types of solid tumors.	Irinotecan	247-257	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
23394826-14	2013	In clinical studies using midazolam or anticancer drugs (irinotecan and imatinib) as known CYP3A4 substrates in combination with SJW, decreased plasma levels of these drugs were observed, which was expected as a consequence of CYP3A4 induction.	Irinotecan	57-67	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	91-97
24132143-11	2013	We conclude that targeting ACLy may improve the therapeutic effects of irinotecan and that simultaneous targeting of ACLy and AKT may be warranted to overcome SN38 resistance.	Irinotecan	71-81	ATP citrate lyase	Homo sapiens	27-31
24129235-0	2013	A c-Met inhibitor increases the chemosensitivity of cancer stem cells to the irinotecan in gastric carcinoma.	Irinotecan	77-87	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	2-7
24129235-11	2013	The c-Met inhibitor may be a promising target molecule for irinotecan-based chemotherapy of gastric cancer.	Irinotecan	59-69	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-9
24081946-1	2013	PURPOSE: Etirinotecan pegol (NKTR-102) is a unique, long-acting topoisomerase-I inhibitor with prolonged systemic exposure to SN38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of irinotecan.	Irinotecan	126-130	natural killer cell triggering receptor	Homo sapiens	29-33
24081946-1	2013	PURPOSE: Etirinotecan pegol (NKTR-102) is a unique, long-acting topoisomerase-I inhibitor with prolonged systemic exposure to SN38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of irinotecan.	Irinotecan	132-162	natural killer cell triggering receptor	Homo sapiens	29-33
24081946-1	2013	PURPOSE: Etirinotecan pegol (NKTR-102) is a unique, long-acting topoisomerase-I inhibitor with prolonged systemic exposure to SN38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of irinotecan.	Irinotecan	11-21	natural killer cell triggering receptor	Homo sapiens	29-33
24191041-3	2013	CPT-11 is a prodrug that is hydrolyzed by hepatic and intestinal carboxylesterase to form SN-38, which in turn is detoxified primarily through UDP-glucuronosyltransferase 1A1 (UGT1A1)-catalyzed glucuronidation.	Irinotecan	0-6	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	143-174
24191041-3	2013	CPT-11 is a prodrug that is hydrolyzed by hepatic and intestinal carboxylesterase to form SN-38, which in turn is detoxified primarily through UDP-glucuronosyltransferase 1A1 (UGT1A1)-catalyzed glucuronidation.	Irinotecan	0-6	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	176-182
24191041-3	2013	CPT-11 is a prodrug that is hydrolyzed by hepatic and intestinal carboxylesterase to form SN-38, which in turn is detoxified primarily through UDP-glucuronosyltransferase 1A1 (UGT1A1)-catalyzed glucuronidation.	Irinotecan	90-95	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	143-174
24191041-3	2013	CPT-11 is a prodrug that is hydrolyzed by hepatic and intestinal carboxylesterase to form SN-38, which in turn is detoxified primarily through UDP-glucuronosyltransferase 1A1 (UGT1A1)-catalyzed glucuronidation.	Irinotecan	90-95	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	176-182
24191041-8	2013	CPT-11-treated Ugt1(DeltaHep) mice showed a similar lethality rate to the CPT-11-treated Ugt1(F/F) mice.	Irinotecan	0-6	UDP glucuronosyltransferase 1 family, polypeptide A2	Mus musculus	15-19
24191041-8	2013	CPT-11-treated Ugt1(DeltaHep) mice showed a similar lethality rate to the CPT-11-treated Ugt1(F/F) mice.	Irinotecan	74-80	UDP glucuronosyltransferase 1 family, polypeptide A2	Mus musculus	89-93
24191041-9	2013	However, Ugt1(DeltaGI) mice were highly susceptible to CPT-11-induced diarrhea, developing severe and lethal mucositis at much lower CPT-11 doses, a result of the proliferative cell loss and inflammation in the intestinal tract.	Irinotecan	55-61	UDP glucuronosyltransferase 1 family, polypeptide A2	Mus musculus	9-13
24191041-9	2013	However, Ugt1(DeltaGI) mice were highly susceptible to CPT-11-induced diarrhea, developing severe and lethal mucositis at much lower CPT-11 doses, a result of the proliferative cell loss and inflammation in the intestinal tract.	Irinotecan	133-139	UDP glucuronosyltransferase 1 family, polypeptide A2	Mus musculus	9-13
24191041-11	2013	Intestinal expression of the UGT1A proteins is critical toward the detoxification of SN-38, whereas induction of the UGT1A1 gene may serve to limit toxicity and improve the efficacy associated with CPT-11 treatment.	Irinotecan	85-90	Ugt1a@	Mus musculus	29-34
24191041-11	2013	Intestinal expression of the UGT1A proteins is critical toward the detoxification of SN-38, whereas induction of the UGT1A1 gene may serve to limit toxicity and improve the efficacy associated with CPT-11 treatment.	Irinotecan	198-204	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	117-123
23394826-14	2013	In clinical studies using midazolam or anticancer drugs (irinotecan and imatinib) as known CYP3A4 substrates in combination with SJW, decreased plasma levels of these drugs were observed, which was expected as a consequence of CYP3A4 induction.	Irinotecan	57-67	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	227-233
23850745-1	2013	Irinotecan is a camptothecin derivative with low oral bioavailability due to active efflux by intestinal P-glycoprotein receptors.	Irinotecan	0-10	ATP binding cassette subfamily B member 1	Homo sapiens	105-119
23850745-3	2013	However, an optimized Self micro emulsifying drug delivery system (SMEDDS), formulated to produce nano range oil droplets by using P-gp modulator excipients can tackle the issue and elevate the systemic availability of Irinotecan.	Irinotecan	219-229	phosphoglycolate phosphatase	Homo sapiens	131-135
23953030-3	2013	The canalicular transport of irinotecan and SN-38G is mediated by ABCC2 (MRP2) and ABCB1 (MDR1) which are both inhibited by ciclosporin.	Irinotecan	29-39	ATP binding cassette subfamily C member 2	Homo sapiens	66-71
23953030-3	2013	The canalicular transport of irinotecan and SN-38G is mediated by ABCC2 (MRP2) and ABCB1 (MDR1) which are both inhibited by ciclosporin.	Irinotecan	29-39	ATP binding cassette subfamily C member 2	Homo sapiens	73-77
23953030-3	2013	The canalicular transport of irinotecan and SN-38G is mediated by ABCC2 (MRP2) and ABCB1 (MDR1) which are both inhibited by ciclosporin.	Irinotecan	29-39	ATP binding cassette subfamily B member 1	Homo sapiens	83-88
23953030-3	2013	The canalicular transport of irinotecan and SN-38G is mediated by ABCC2 (MRP2) and ABCB1 (MDR1) which are both inhibited by ciclosporin.	Irinotecan	29-39	ATP binding cassette subfamily B member 1	Homo sapiens	90-94
23953030-3	2013	The canalicular transport of irinotecan and SN-38G is mediated by ABCC2 (MRP2) and ABCB1 (MDR1) which are both inhibited by ciclosporin.	Irinotecan	44-49	ATP binding cassette subfamily C member 2	Homo sapiens	66-71
23953030-3	2013	The canalicular transport of irinotecan and SN-38G is mediated by ABCC2 (MRP2) and ABCB1 (MDR1) which are both inhibited by ciclosporin.	Irinotecan	44-49	ATP binding cassette subfamily C member 2	Homo sapiens	73-77
23953030-3	2013	The canalicular transport of irinotecan and SN-38G is mediated by ABCC2 (MRP2) and ABCB1 (MDR1) which are both inhibited by ciclosporin.	Irinotecan	44-49	ATP binding cassette subfamily B member 1	Homo sapiens	83-88
24231711-2	2013	The patient was treated with a pancreaticoduodenectomy, ascending colectomy and postoperative chemotherapy of S-1 and irinotecan[IRIS; S-1, 80mg/m2(days 1-14); irinotecan, 100 mg/m2(days 1 and 15, every 4 weeks)].	Irinotecan	118-128	proteasome 26S subunit, non-ATPase 1	Homo sapiens	135-138
23953030-3	2013	The canalicular transport of irinotecan and SN-38G is mediated by ABCC2 (MRP2) and ABCB1 (MDR1) which are both inhibited by ciclosporin.	Irinotecan	44-49	ATP binding cassette subfamily B member 1	Homo sapiens	90-94
24124496-10	2013	SULF2 methylation was found to have a significant association with cisplatin efficacy(SULF2M: 57.14%, SULF2U: 80.56%, P = 0.02) and irinotecan efficacy(SULF2M: 89.29%, SULF2U: 62.50%, P = 0.01).	Irinotecan	132-142	sulfatase 2	Homo sapiens	0-5
24038068-7	2013	We finally compared the ability of a structurally related CHK1 inhibitor, GNE-900, to enhance the in vivo activity of gemcitabine, CPT-11, and temozolomide in xenograft models.	Irinotecan	131-137	checkpoint kinase 1	Homo sapiens	58-62
24038068-7	2013	We finally compared the ability of a structurally related CHK1 inhibitor, GNE-900, to enhance the in vivo activity of gemcitabine, CPT-11, and temozolomide in xenograft models.	Irinotecan	131-137	glucosamine (UDP-N-acetyl)-2-epimerase/N-acetylmannosamine kinase	Homo sapiens	74-77
23960095-0	2013	Sorafenib overcomes irinotecan resistance in colorectal cancer by inhibiting the ABCG2 drug-efflux pump.	Irinotecan	20-30	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	81-86
23401472-1	2013	Human uridine 5"-diphospho-glucuronosyltransferase (UGT) 1A1 catalyzes the metabolism of numerous clinically and pharmacologically important compounds, such as bilirubin and SN-38.	Irinotecan	174-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-60
22882086-2	2013	ABCG2 (BCRP) is an efflux transporter conferring cross-resistance to mitoxantrone (Mit), irinotecan (CPT11), and its active metabolite SN38.	Irinotecan	89-99	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
22882086-2	2013	ABCG2 (BCRP) is an efflux transporter conferring cross-resistance to mitoxantrone (Mit), irinotecan (CPT11), and its active metabolite SN38.	Irinotecan	89-99	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	7-11
22882086-2	2013	ABCG2 (BCRP) is an efflux transporter conferring cross-resistance to mitoxantrone (Mit), irinotecan (CPT11), and its active metabolite SN38.	Irinotecan	101-106	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
22882086-2	2013	ABCG2 (BCRP) is an efflux transporter conferring cross-resistance to mitoxantrone (Mit), irinotecan (CPT11), and its active metabolite SN38.	Irinotecan	101-106	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	7-11
22882086-2	2013	ABCG2 (BCRP) is an efflux transporter conferring cross-resistance to mitoxantrone (Mit), irinotecan (CPT11), and its active metabolite SN38.	Irinotecan	135-139	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
22882086-2	2013	ABCG2 (BCRP) is an efflux transporter conferring cross-resistance to mitoxantrone (Mit), irinotecan (CPT11), and its active metabolite SN38.	Irinotecan	135-139	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	7-11
24196082-8	2013	In November 2011, we started third-line chemotherapy using S-1/irinotecan (IRIS) with PSK.	Irinotecan	63-73	TAO kinase 2	Homo sapiens	86-89
23913164-5	2013	Critically, knockdown of TDP1 or inhibition of poly(ADP-ribose) polymerase-1 (PARP-1), an enzyme in the same complex as TDP1, sensitized rhabdomyosarcoma cell lines to analogues of irinotecan.	Irinotecan	181-191	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	25-29
23913164-5	2013	Critically, knockdown of TDP1 or inhibition of poly(ADP-ribose) polymerase-1 (PARP-1), an enzyme in the same complex as TDP1, sensitized rhabdomyosarcoma cell lines to analogues of irinotecan.	Irinotecan	181-191	poly(ADP-ribose) polymerase 1	Homo sapiens	47-76
23913164-5	2013	Critically, knockdown of TDP1 or inhibition of poly(ADP-ribose) polymerase-1 (PARP-1), an enzyme in the same complex as TDP1, sensitized rhabdomyosarcoma cell lines to analogues of irinotecan.	Irinotecan	181-191	poly(ADP-ribose) polymerase 1	Homo sapiens	78-84
23913164-5	2013	Critically, knockdown of TDP1 or inhibition of poly(ADP-ribose) polymerase-1 (PARP-1), an enzyme in the same complex as TDP1, sensitized rhabdomyosarcoma cell lines to analogues of irinotecan.	Irinotecan	181-191	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	120-124
23960095-2	2013	Therefore, new treatment options are needed to improve survival of patients with irinotecan-refractory CRCs, particularly those bearing KRAS mutations that preclude the use of anti-EGFR therapies.	Irinotecan	81-91	KRAS proto-oncogene, GTPase	Homo sapiens	136-140
23960095-2	2013	Therefore, new treatment options are needed to improve survival of patients with irinotecan-refractory CRCs, particularly those bearing KRAS mutations that preclude the use of anti-EGFR therapies.	Irinotecan	81-91	epidermal growth factor receptor	Homo sapiens	181-185
23960095-6	2013	By inhibiting the drug-efflux pump ABCG2, sorafenib favors irinotecan intracellular accumulation and enhances its toxicity.	Irinotecan	59-69	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	35-40
23960095-7	2013	Moreover, we found that sorafenib improved the efficacy of irinotecan by inhibiting the irinotecan-mediated p38 and ERK activation.	Irinotecan	59-69	mitogen-activated protein kinase 14	Homo sapiens	108-111
23960095-7	2013	Moreover, we found that sorafenib improved the efficacy of irinotecan by inhibiting the irinotecan-mediated p38 and ERK activation.	Irinotecan	59-69	mitogen-activated protein kinase 1	Homo sapiens	116-119
23960095-7	2013	Moreover, we found that sorafenib improved the efficacy of irinotecan by inhibiting the irinotecan-mediated p38 and ERK activation.	Irinotecan	88-98	mitogen-activated protein kinase 14	Homo sapiens	108-111
23960095-7	2013	Moreover, we found that sorafenib improved the efficacy of irinotecan by inhibiting the irinotecan-mediated p38 and ERK activation.	Irinotecan	88-98	mitogen-activated protein kinase 1	Homo sapiens	116-119
24069296-0	2013	Prognostic value of CD109+ circulating endothelial cells in recurrent glioblastomas treated with bevacizumab and irinotecan.	Irinotecan	113-123	CD109 molecule	Homo sapiens	20-25
24018773-2	2013	The aim of this study was to elucidate the predictive/prognostic role of ATP-binding cassette (ABC) and solute carrier (SLC) protein polymorphisms on irinotecan (FOLFIRI regimen) outcome.	Irinotecan	150-160	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	73-93
24018773-2	2013	The aim of this study was to elucidate the predictive/prognostic role of ATP-binding cassette (ABC) and solute carrier (SLC) protein polymorphisms on irinotecan (FOLFIRI regimen) outcome.	Irinotecan	150-160	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	95-98
24069296-7	2013	Patients treated with bevacizumab with or without irinotecan that were free from MRI progression after two months of treatment had significant decrease of CD109+ CECs: median PFS was 19 weeks; median OS 29 weeks.	Irinotecan	50-60	CD109 molecule	Homo sapiens	155-160
23859194-6	2013	We report that the DNA-damaging agents doxorubicin and 7-ethyl-10-hydroxycamptothecin were able to induce the formation of SAHF in some tumour cell types, and this induction was accompanied by activation of the retinoblastoma protein pathway.	Irinotecan	55-85	RB transcriptional corepressor 1	Homo sapiens	211-225
23835420-5	2013	OCT1-mediated morphine uptake was abolished by common loss-of-function polymorphisms in the OCT1 gene and was strongly inhibited by drug-drug interactions with irinotecan, verapamil and ondansetron.	Irinotecan	160-170	solute carrier family 22 member 1	Homo sapiens	0-4
23835420-5	2013	OCT1-mediated morphine uptake was abolished by common loss-of-function polymorphisms in the OCT1 gene and was strongly inhibited by drug-drug interactions with irinotecan, verapamil and ondansetron.	Irinotecan	160-170	solute carrier family 22 member 1	Homo sapiens	92-96
23359181-0	2013	Panitumumab and irinotecan every 3 weeks is an active and convenient regimen for second-line treatment of patients with wild-type K-RAS metastatic colorectal cancer.	Irinotecan	16-26	KRAS proto-oncogene, GTPase	Homo sapiens	130-135
23359181-1	2013	PURPOSE: To evaluate the efficacy and safety profile of the combination of panitumumab and irinotecan every 3 weeks in a phase II trial as second-line treatment in patients with advanced wild-type (WT) K-RAS colorectal cancer (CRC).	Irinotecan	91-101	KRAS proto-oncogene, GTPase	Homo sapiens	202-207
23359181-10	2013	CONCLUSION: This study shows that the administration of panitumumab plus irinotecan every 3 weeks is safe, active and feasible as second-line treatment in patients with advanced WT K-RAS CRC.	Irinotecan	73-83	KRAS proto-oncogene, GTPase	Homo sapiens	181-186
23978462-1	2013	BACKGROUND: Kirsten rat sarcoma virus (KRAS) wild-type status determined using a locked nucleic acid (LNA)-mediated quantitative polymerase chain reaction (qPCR) clamping assay (LNA assay) predicted response to therapy in the CRYSTAL (Cetuximab Combined With Irinotecan in First-Line Therapy for Metastatic Colorectal Cancer) study.	Irinotecan	259-269	KRAS proto-oncogene, GTPase	Homo sapiens	39-43
23859194-9	2013	In addition, we show that the mitogen-activated protein kinase p38 pathway was involved in tumour cell SAHF formation in response to doxorubicin and 7-ethyl-10-hydroxycamptothecin.	Irinotecan	149-179	mitogen-activated protein kinase 14	Homo sapiens	63-66
22643568-2	2013	In this study, we evaluated if there is any difference between first-line irinotecan-based and oxaliplatin-based chemotherapies in the duration of time to disease progression (TTP) in CRC patients with only liver metastasis.	Irinotecan	74-84	ZFP36 ring finger protein	Homo sapiens	176-179
23892411-0	2013	Analysis of UGT1A1*28 genotype and SN-38 pharmacokinetics for irinotecan-based chemotherapy in patients with advanced colorectal cancer: results from a multicenter, retrospective study in Shanghai.	Irinotecan	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
23892411-1	2013	BACKGROUND: The UGT1A1*28 polymorphism, although closely linked with CPT-11-related adverse effects, cannot be used alone to guide individualized treatment decisions.	Irinotecan	69-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
22643568-7	2013	TTP was significantly improved for patients who received irinotecan+5-FU+bevacizumab (median TTP, 13.73 +- 2.10 mo) when compared with irinotecan+5-FU (median TTP, 5.13 +- 0.70 mo).	Irinotecan	57-67	ZFP36 ring finger protein	Homo sapiens	0-3
22643568-7	2013	TTP was significantly improved for patients who received irinotecan+5-FU+bevacizumab (median TTP, 13.73 +- 2.10 mo) when compared with irinotecan+5-FU (median TTP, 5.13 +- 0.70 mo).	Irinotecan	57-67	ZFP36 ring finger protein	Homo sapiens	93-96
22643568-7	2013	TTP was significantly improved for patients who received irinotecan+5-FU+bevacizumab (median TTP, 13.73 +- 2.10 mo) when compared with irinotecan+5-FU (median TTP, 5.13 +- 0.70 mo).	Irinotecan	57-67	ZFP36 ring finger protein	Homo sapiens	93-96
23898114-0	2013	UDP-glucuronosyltransferase (UGT) 1A1*28 polymorphism-directed phase II study of irinotecan with 5"-deoxy-5-fluorouridine (5"-DFUR) for metastatic colorectal cancer.	Irinotecan	81-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-37
23898114-1	2013	AIM: We performed a phase II study of irinotecan with 5"-deoxy-5-fluorouridine (5"-DFUR) for metastatic colorectal cancer based on UDP-glucuronosyltransferase (UGT) 1A1 polymorphism.	Irinotecan	38-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	131-168
23898097-4	2013	In contrast, patient cohorts treated with irinotecan had significantly worse mOS (10.20 vs. 13.55 months, p=0.008, 35 vs. 810 cohorts) and a disadvantage compared to cohorts treated without irinotecan in survival gain analysis.	Irinotecan	42-52	Moloney sarcoma oncogene	Mus musculus	77-80
23800356-0	2013	Recurrent cervical cancer in a patient who was compound heterozygous for UGT1A1*6 and UGT1A1*28 presenting with serious adverse events during irinotecan hydrochloride/nedaplatin therapy.	Irinotecan	142-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
24156021-7	2013	Finally, we evaluated enhancement of cytotoxicity of S-1 by CPT-11 (7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin) which down-regulated TS in in vivo study.	Irinotecan	60-66	proteasome 26S subunit, non-ATPase 1	Homo sapiens	53-56
24156021-7	2013	Finally, we evaluated enhancement of cytotoxicity of S-1 by CPT-11 (7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin) which down-regulated TS in in vivo study.	Irinotecan	60-66	thymidylate synthetase	Homo sapiens	156-158
24156021-7	2013	Finally, we evaluated enhancement of cytotoxicity of S-1 by CPT-11 (7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin) which down-regulated TS in in vivo study.	Irinotecan	68-133	proteasome 26S subunit, non-ATPase 1	Homo sapiens	53-56
24156021-7	2013	Finally, we evaluated enhancement of cytotoxicity of S-1 by CPT-11 (7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin) which down-regulated TS in in vivo study.	Irinotecan	68-133	thymidylate synthetase	Homo sapiens	156-158
24156021-10	2013	Down-regulation of TS was observed after exposure to SN-38 (7-ethyl-10-hydroxycamptothecin) in a dose-dependent manner.	Irinotecan	53-58	thymidylate synthetase	Homo sapiens	19-21
24156021-10	2013	Down-regulation of TS was observed after exposure to SN-38 (7-ethyl-10-hydroxycamptothecin) in a dose-dependent manner.	Irinotecan	60-90	thymidylate synthetase	Homo sapiens	19-21
24156021-13	2013	Also, combined S-1 and CPT-11 dramatically inhibited tumor growth, compared to S-1 or CPT-11 alone in in vivo study.	Irinotecan	86-92	proteasome 26S subunit, non-ATPase 1	Homo sapiens	15-18
24156021-14	2013	In conclusion, CPT-11 down-regulated TS level and enhanced the effect of S-1.	Irinotecan	15-21	thymidylate synthetase	Homo sapiens	37-39
24156021-14	2013	In conclusion, CPT-11 down-regulated TS level and enhanced the effect of S-1.	Irinotecan	15-21	proteasome 26S subunit, non-ATPase 1	Homo sapiens	73-76
24156021-15	2013	Thus, the combination therapy with S-1 and CPT-11 might be a novel modality for bladder cancer, even with high TS level.	Irinotecan	43-49	thymidylate synthetase	Homo sapiens	111-113
23852648-3	2013	The aim of this trial is to evaluate the efficacy and safety of combination chemotherapy with trastuzumab and irinotecan in Japanese patients with advanced human epidermal growth factor receptor 2-positive chemo-refractory gastric cancer.	Irinotecan	110-120	erb-b2 receptor tyrosine kinase 2	Homo sapiens	162-196
23756919-8	2013	There was a strong correlation between hepatic CES-2 expression and activation of irinotecan (r (2) = 0.96, p &lt; 0.001).	Irinotecan	82-92	carboxylesterase 2	Homo sapiens	47-52
23756919-10	2013	Hepatic CES-2 mediated activation of irinotecan clearly correlated with tumour replacement by fibrosis (r (2) = 0.54, p = 0.01).	Irinotecan	37-47	carboxylesterase 2	Homo sapiens	8-13
23800356-0	2013	Recurrent cervical cancer in a patient who was compound heterozygous for UGT1A1*6 and UGT1A1*28 presenting with serious adverse events during irinotecan hydrochloride/nedaplatin therapy.	Irinotecan	142-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
23800356-6	2013	The findings in this patient indicate that CPT-11 should be administered with great care, even at a dose of 60 mg/m2, in patients receiving combined therapy with CPT-11 and NDP who are compound heterozygous for UGT1A1*6 and UGT1A1*28.	Irinotecan	43-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	211-217
23800356-6	2013	The findings in this patient indicate that CPT-11 should be administered with great care, even at a dose of 60 mg/m2, in patients receiving combined therapy with CPT-11 and NDP who are compound heterozygous for UGT1A1*6 and UGT1A1*28.	Irinotecan	43-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	224-230
23800356-6	2013	The findings in this patient indicate that CPT-11 should be administered with great care, even at a dose of 60 mg/m2, in patients receiving combined therapy with CPT-11 and NDP who are compound heterozygous for UGT1A1*6 and UGT1A1*28.	Irinotecan	162-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	211-217
23690068-0	2013	Molecular insights into microbial beta-glucuronidase inhibition to abrogate CPT-11 toxicity.	Irinotecan	76-82	glucuronidase beta	Homo sapiens	34-52
24511364-2	2013	In the present study curcumin inhibitory action on p-glycoprotein increased permeability of irinotecan, so in the colon cancer it would be beneficial if curcumin used as add on therapy.	Irinotecan	92-102	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	51-65
23180349-0	2013	Lack of Bax expression is associated with irinotecan-based treatment activity in advanced colorectal cancer patients.	Irinotecan	42-52	BCL2 associated X, apoptosis regulator	Homo sapiens	8-11
23180349-2	2013	Bax proapoptotic protein may correlate to chemosensitivity and differential response to irinotecan or oxaliplatin-based combinations.	Irinotecan	88-98	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
23180349-3	2013	METHODS: Bax expression was assessed by immunohistochemistry in 49 advanced colorectal cancer patients enrolled at our institution from 2002 to 2004 within a multicenter, phase II, randomized trial of first-line UFT/leucovorin/irinotecan (TEGAFIRI) versus UFT/leucovorin/oxaliplatin (TEGAFOX).	Irinotecan	227-237	BCL2 associated X, apoptosis regulator	Homo sapiens	9-12
23180349-8	2013	CONCLUSION: Bax-negative colorectal cancer may identify a specific phenotype of patients with significantly higher chance to respond to doublet irinotecan-based chemotherapy.	Irinotecan	144-154	BCL2 associated X, apoptosis regulator	Homo sapiens	12-15
27121781-1	2013	This study examined the effects of panitumumab, a human monoclonal antibody against epidermal growth factor receptor (EGFR), on irinotecan pharmacokinetics.	Irinotecan	128-138	epidermal growth factor receptor	Homo sapiens	84-116
23840132-0	2013	Severe irinotecan-induced toxicity in a patient with UGT1A1 28 and UGT1A1 6 polymorphisms.	Irinotecan	7-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-59
27121781-1	2013	This study examined the effects of panitumumab, a human monoclonal antibody against epidermal growth factor receptor (EGFR), on irinotecan pharmacokinetics.	Irinotecan	128-138	epidermal growth factor receptor	Homo sapiens	118-122
22791234-2	2013	Irinotecan demonstrates single-agent activity in head and neck cancer but activates NF-kappaB, promoting cell survival and resistance.	Irinotecan	0-10	nuclear factor kappa B subunit 1	Homo sapiens	84-93
23653048-0	2013	Influence of MLH1 on colon cancer sensitivity to poly(ADP-ribose) polymerase inhibitor combined with irinotecan.	Irinotecan	101-111	mutL homolog 1	Homo sapiens	13-17
23653048-5	2013	The results of in vitro and in vivo experiments indicated that MLH1, together with low levels of Top1, contributed to colon cancer resistance to irinotecan.	Irinotecan	145-155	mutL homolog 1	Homo sapiens	63-67
23653048-6	2013	In the MLH1-proficient cells SN-38, the active metabolite of irinotecan, induced lower levels of DNA damage than in MLH1-deficient cells, as shown by the weaker induction of gamma-H2AX and p53 phosphorylation.	Irinotecan	29-34	mutL homolog 1	Homo sapiens	7-11
23653048-6	2013	In the MLH1-proficient cells SN-38, the active metabolite of irinotecan, induced lower levels of DNA damage than in MLH1-deficient cells, as shown by the weaker induction of gamma-H2AX and p53 phosphorylation.	Irinotecan	29-34	tumor protein p53	Homo sapiens	189-192
23653048-6	2013	In the MLH1-proficient cells SN-38, the active metabolite of irinotecan, induced lower levels of DNA damage than in MLH1-deficient cells, as shown by the weaker induction of gamma-H2AX and p53 phosphorylation.	Irinotecan	61-71	mutL homolog 1	Homo sapiens	7-11
23653048-6	2013	In the MLH1-proficient cells SN-38, the active metabolite of irinotecan, induced lower levels of DNA damage than in MLH1-deficient cells, as shown by the weaker induction of gamma-H2AX and p53 phosphorylation.	Irinotecan	61-71	tumor protein p53	Homo sapiens	189-192
23653048-9	2013	Remarkably, inhibition of PARP function by PARPi or by PARP-1 gene silencing always increased the antitumor activity of irinotecan, even in the presence of low PARP-1 expression.	Irinotecan	120-130	poly(ADP-ribose) polymerase 1	Homo sapiens	26-30
23653048-9	2013	Remarkably, inhibition of PARP function by PARPi or by PARP-1 gene silencing always increased the antitumor activity of irinotecan, even in the presence of low PARP-1 expression.	Irinotecan	120-130	poly(ADP-ribose) polymerase 1	Homo sapiens	55-61
23653048-9	2013	Remarkably, inhibition of PARP function by PARPi or by PARP-1 gene silencing always increased the antitumor activity of irinotecan, even in the presence of low PARP-1 expression.	Irinotecan	120-130	poly(ADP-ribose) polymerase 1	Homo sapiens	160-166
23583082-10	2013	In the PET study in mice, the radioactivity levels in the brain, liver, and small intestine were slightly increased by inhibition of the Pgp/Bcrp function for more than 30 min after [(11)C]irinotecan injection.	Irinotecan	189-199	phosphoglycolate phosphatase	Mus musculus	137-140
23583082-10	2013	In the PET study in mice, the radioactivity levels in the brain, liver, and small intestine were slightly increased by inhibition of the Pgp/Bcrp function for more than 30 min after [(11)C]irinotecan injection.	Irinotecan	189-199	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	141-145
23583082-11	2013	This result demonstrated that in vivo behavior of [(11)C] irinotecan and radioactive metabolites are influenced by the Pgp/Bcrp function.	Irinotecan	58-68	phosphoglycolate phosphatase	Mus musculus	119-122
23583082-11	2013	This result demonstrated that in vivo behavior of [(11)C] irinotecan and radioactive metabolites are influenced by the Pgp/Bcrp function.	Irinotecan	58-68	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	123-127
23126525-6	2013	The combination of melatonin at concentrations of 50 muM with increasing doses of irinotecan (7.5, 15, 30, and 60 muM) resulted in an increase in the amount of DNA damage in A549 and HT29 cancer cells, but was not effective in inducing DNA damage in healthy human lymphocytes.	Irinotecan	82-92	latexin	Homo sapiens	114-117
23420304-11	2013	The subgroup of patients, who received irinotecan had a higher complication rate in the CTX group than in the BV + CTX group (55 % vs 41 %).	Irinotecan	39-49	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	88-91
23420304-11	2013	The subgroup of patients, who received irinotecan had a higher complication rate in the CTX group than in the BV + CTX group (55 % vs 41 %).	Irinotecan	39-49	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	115-118
23840132-0	2013	Severe irinotecan-induced toxicity in a patient with UGT1A1 28 and UGT1A1 6 polymorphisms.	Irinotecan	7-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
23840132-1	2013	Many studies have demonstrated the impact of UGT1A1 on toxicity of irinotecan.	Irinotecan	67-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
23840132-3	2013	Based on this, prescribers of irinotecan are advised that patients with UGT1A1 28 (TA 7/7) should start with a reduced dose of irinotecan, although a particular dose is not specified.	Irinotecan	30-40	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
23840132-3	2013	Based on this, prescribers of irinotecan are advised that patients with UGT1A1 28 (TA 7/7) should start with a reduced dose of irinotecan, although a particular dose is not specified.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
23840132-4	2013	Research in Asian countries has shown a lower incidence of UGT1A1 28 (TA 7/7), while UGT1A1 6 (A/A) is more often found and is associated with severe irinotecan-related neutropenia.	Irinotecan	150-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
23840132-7	2013	Simultaneous heterozygous UGT1A1 28 and UGT1A1 6 polymorphisms may produce higher exposure to SN-38 and a higher risk of adverse effects related to irinotecan.	Irinotecan	94-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
23840132-7	2013	Simultaneous heterozygous UGT1A1 28 and UGT1A1 6 polymorphisms may produce higher exposure to SN-38 and a higher risk of adverse effects related to irinotecan.	Irinotecan	94-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
23840132-7	2013	Simultaneous heterozygous UGT1A1 28 and UGT1A1 6 polymorphisms may produce higher exposure to SN-38 and a higher risk of adverse effects related to irinotecan.	Irinotecan	148-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
23840132-7	2013	Simultaneous heterozygous UGT1A1 28 and UGT1A1 6 polymorphisms may produce higher exposure to SN-38 and a higher risk of adverse effects related to irinotecan.	Irinotecan	148-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
23840132-8	2013	Additional studies will be necessary to determine the optimal starting dose of irinotecan for patients with both UGT1A1 28 and UGT1A1 6 polymorphisms.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
23840132-8	2013	Additional studies will be necessary to determine the optimal starting dose of irinotecan for patients with both UGT1A1 28 and UGT1A1 6 polymorphisms.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	127-133
23762305-9	2013	There were also weak but significant correlations between APTX mRNA expression levels and CPT-11 sensitivity (rho = -0.376, P = 0.017) or EVO sensitivity (rho = -0.322, P = 0.036).	Irinotecan	90-96	aprataxin	Homo sapiens	58-62
23514584-0	2013	Phase II trial of temsirolimus alone and in combination with irinotecan for KRAS mutant metastatic colorectal cancer: outcome and results of KRAS mutational analysis in plasma.	Irinotecan	61-71	KRAS proto-oncogene, GTPase	Homo sapiens	76-80
23595344-0	2013	A UGT1A1*28 and *6 genotype-directed phase I dose-escalation trial of irinotecan with fixed-dose capecitabine in Korean patients with metastatic colorectal cancer.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	2-8
22721392-0	2013	The role of autophagic cell death and apoptosis in irinotecan-treated p53 null colon cancer cells.	Irinotecan	51-61	tumor protein p53	Homo sapiens	70-73
22721392-1	2013	The roles of autophagic cell death and apoptosis induced by topoisomerase inhibitor irinotecan in colon cancer cells with deleted p53 were investigated during 48 h. We report that irinotecan-dependent cytotoxicity and proapoptotic activity were reduced in the present model while autophagy levels significantly increased.	Irinotecan	180-190	tumor protein p53	Homo sapiens	130-133
22721392-4	2013	These results suggest that different modes of cell death in p53 null colon cancer cells treated with cytostatics (irinotecan) may be activated simultaneously.	Irinotecan	114-124	tumor protein p53	Homo sapiens	60-63
23595344-10	2013	CONCLUSION: Irinotecan dosing based on UGT1A1*28 and *6 is feasible, and higher doses of irinotecan can be safely administered in patients with 0 or 1 DA, compared to those with 2 DA.	Irinotecan	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
23595344-1	2013	PURPOSE: UGT1A1 genotypes are important when considering treatment with irinotecan-containing regimens.	Irinotecan	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
23595344-2	2013	In this study, we determined the dose, efficacy, and tolerability of irinotecan according to UGT1A1 genotypes when combined with capecitabine in patients with metastatic colorectal cancer.	Irinotecan	69-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
23427296-9	2013	Despite much lower surface expression of CD74 than Trop-2 or CEACAM6, milatuzumab-SN-38 had similar efficacy in Capan-1 as anti-Trop-2-SN-38, but in NCI-N87, anti-CEACAM6 and anti-Trop-2 conjugates were superior.	Irinotecan	82-87	CEA cell adhesion molecule 6	Homo sapiens	163-170
23427296-11	2013	CD74 is a suitable target for ADCs in some solid tumor xenografts, with efficacy largely influenced by uniformity of CD74 expression and with SN-38 conjugates providing the best therapeutic responses; SN-38 conjugates were preferable in solid cancers, whereas doxorubicin ADC was better in lymphoma tested.	Irinotecan	142-147	CD74 molecule	Homo sapiens	0-4
23427296-11	2013	CD74 is a suitable target for ADCs in some solid tumor xenografts, with efficacy largely influenced by uniformity of CD74 expression and with SN-38 conjugates providing the best therapeutic responses; SN-38 conjugates were preferable in solid cancers, whereas doxorubicin ADC was better in lymphoma tested.	Irinotecan	201-206	CD74 molecule	Homo sapiens	0-4
23801203-0	2013	[Correlation of MDR1 and ABCG2 genetic polymorphisms with the efficacy and adverse events of irinotecan chemotherapy in patients with colorectal cancer].	Irinotecan	93-103	ATP binding cassette subfamily B member 1	Homo sapiens	16-20
23859115-0	2013	Cetuximab/irinotecan-chemotherapy in KRAS wild-type pretreated metastatic colorectal cancer: a pooled analysis and review of literature.	Irinotecan	10-20	KRAS proto-oncogene, GTPase	Homo sapiens	37-41
23859115-11	2013	CONCLUSION: In metastatic KRAS wild-type CRC patients pretreated with one or more lines of therapy, cetuximab plus irinotecan-based chemotherapy is an active treatment.	Irinotecan	115-125	KRAS proto-oncogene, GTPase	Homo sapiens	26-30
23730417-8	2013	In contrast, in patients who received first-line irinotecan-based regimens, the PFS was shorter in KRAS mutant patients (N = 15) than that in KRAS wild-type patients (N = 20).	Irinotecan	49-59	KRAS proto-oncogene, GTPase	Homo sapiens	99-103
23730417-8	2013	In contrast, in patients who received first-line irinotecan-based regimens, the PFS was shorter in KRAS mutant patients (N = 15) than that in KRAS wild-type patients (N = 20).	Irinotecan	49-59	KRAS proto-oncogene, GTPase	Homo sapiens	142-146
24119900-0	2013	[Correlation between the methylation of SULF2 and WRN promoter and chemosensitivity to irinotecan in gastric cancer].	Irinotecan	87-97	sulfatase 2	Homo sapiens	40-45
24119900-0	2013	[Correlation between the methylation of SULF2 and WRN promoter and chemosensitivity to irinotecan in gastric cancer].	Irinotecan	87-97	WRN RecQ like helicase	Homo sapiens	50-53
24119900-1	2013	OBJECTIVE: To explore the relationship between SULF2 and WRN promoter methylation and chemosensitivity to irinotecan, and also the clinicopathological features in patients with gastric cancer.	Irinotecan	106-116	sulfatase 2	Homo sapiens	47-52
24119900-1	2013	OBJECTIVE: To explore the relationship between SULF2 and WRN promoter methylation and chemosensitivity to irinotecan, and also the clinicopathological features in patients with gastric cancer.	Irinotecan	106-116	WRN RecQ like helicase	Homo sapiens	57-60
24119900-11	2013	The nude mice bearing human gastric cancer xenografts with SULF2 methylation were more sensitive to irrinotecan.	Irinotecan	100-111	sulfatase 2	Homo sapiens	59-64
24119900-12	2013	CONCLUSIONS: The detection of SULF2 and WRN promoter methylation may provide evidence for screening and targeting the most sensitive gastric cancer subpopulation suitable for personalized irrinotecan chemotherapy.	Irinotecan	188-199	sulfatase 2	Homo sapiens	30-35
24119900-12	2013	CONCLUSIONS: The detection of SULF2 and WRN promoter methylation may provide evidence for screening and targeting the most sensitive gastric cancer subpopulation suitable for personalized irrinotecan chemotherapy.	Irinotecan	188-199	WRN RecQ like helicase	Homo sapiens	40-43
23801203-12	2013	CONCLUSION: MDR1 2677 G&gt;T/A may be served as a biomarker in predicting the efficacy of irinotecan chemotherapy in patients with colorectal cancer.	Irinotecan	90-100	ATP binding cassette subfamily B member 1	Homo sapiens	12-16
23801203-0	2013	[Correlation of MDR1 and ABCG2 genetic polymorphisms with the efficacy and adverse events of irinotecan chemotherapy in patients with colorectal cancer].	Irinotecan	93-103	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	25-30
23801203-1	2013	OBJECTIVE: To investigate the correlation of MDR1 and ABCG2 genetic polymorphisms with the efficacy and adverse events of irinotecan chemotherapy in patients with colorectal cancer (CRC).	Irinotecan	122-132	ATP binding cassette subfamily B member 1	Homo sapiens	45-49
23801203-1	2013	OBJECTIVE: To investigate the correlation of MDR1 and ABCG2 genetic polymorphisms with the efficacy and adverse events of irinotecan chemotherapy in patients with colorectal cancer (CRC).	Irinotecan	122-132	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	54-59
23377825-0	2013	Identification of cetrimonium bromide and irinotecan as compounds with synthetic lethality against NDRG1 deficient prostate cancer cells.	Irinotecan	42-52	N-myc downstream regulated 1	Homo sapiens	99-104
23724141-7	2013	RESULTS: MSH3-deficient vs proficient CRC cells showed increased sensitivity to the irinotecan metabolite SN-38 and to oxaliplatin, but not 5-FU, as shown in assays for apoptosis and clonogenic survival.	Irinotecan	84-94	mutS homolog 3	Homo sapiens	9-13
23724141-7	2013	RESULTS: MSH3-deficient vs proficient CRC cells showed increased sensitivity to the irinotecan metabolite SN-38 and to oxaliplatin, but not 5-FU, as shown in assays for apoptosis and clonogenic survival.	Irinotecan	106-111	mutS homolog 3	Homo sapiens	9-13
23724141-9	2013	The impact of MSH3 knockdown on chemosensitivity to SN-38 and oxaliplatin was maintained independent of MLH1 status.	Irinotecan	52-57	mutS homolog 3	Homo sapiens	14-18
23724141-10	2013	In MSH3-deficient vs proficient cells, SN-38 and oxaliplatin induced higher levels of phosphorylated histone H2AX and Chk2, and similar results were found in MLH1-proficient SW480 cells.	Irinotecan	39-44	mutS homolog 3	Homo sapiens	3-7
23724141-10	2013	In MSH3-deficient vs proficient cells, SN-38 and oxaliplatin induced higher levels of phosphorylated histone H2AX and Chk2, and similar results were found in MLH1-proficient SW480 cells.	Irinotecan	39-44	checkpoint kinase 2	Homo sapiens	118-122
23724141-10	2013	In MSH3-deficient vs proficient cells, SN-38 and oxaliplatin induced higher levels of phosphorylated histone H2AX and Chk2, and similar results were found in MLH1-proficient SW480 cells.	Irinotecan	39-44	mutL homolog 1	Homo sapiens	158-162
23377825-6	2013	Screening of 3360 compounds revealed irinotecan and cetrimonium bromide (CTAB) as compounds that exhibited synthetic lethality against NDRG1 deficient PCa cells.	Irinotecan	37-47	N-myc downstream regulated 1	Homo sapiens	135-140
23377825-9	2013	Our results suggest that CTAB and irinotecan could be further explored for their potential clinical benefit in patients with NDRG1 deficient PCa.	Irinotecan	34-44	N-myc downstream regulated 1	Homo sapiens	125-130
24216984-3	2013	mTOR appears to enhance cancer cell survival following DNA damage, thus the inhibition of mTOR after irinotecan could theoretically show synergistic activities in patients.	Irinotecan	101-111	mechanistic target of rapamycin kinase	Homo sapiens	0-4
23439240-1	2013	Modified nanoprecipitation method was used for improved incorporation of hydrophilic drug (irinotecan hydrochloride) into the PLGA/PEO-PPO-PEO blended and blended/adsorbed nanoparticles.	Irinotecan	91-115	protoporphyrinogen oxidase	Homo sapiens	135-138
23461902-7	2013	RESULTS: We found that additional deficiency of Abcc4 in Abcb1a/b;Abcg2(-/-) mice significantly increased the brain concentration of all camptothecin analogues by 1.2-fold (gimatecan) to 5.8-fold (SN-38).	Irinotecan	197-202	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	48-53
23461902-8	2013	The presence of Abcb1a/b or Abcc4 alone was sufficient to reduce the brain concentration of SN-38 to the level in WT mice.	Irinotecan	92-97	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	16-22
23461902-8	2013	The presence of Abcb1a/b or Abcc4 alone was sufficient to reduce the brain concentration of SN-38 to the level in WT mice.	Irinotecan	92-97	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	28-33
24216984-3	2013	mTOR appears to enhance cancer cell survival following DNA damage, thus the inhibition of mTOR after irinotecan could theoretically show synergistic activities in patients.	Irinotecan	101-111	mechanistic target of rapamycin kinase	Homo sapiens	90-94
22124996-0	2013	Phase II study of bi-weekly irinotecan for patients with previously treated HER2-negative metastatic breast cancer: KMBOG0610B.	Irinotecan	28-38	erb-b2 receptor tyrosine kinase 2	Homo sapiens	76-80
23564776-0	2013	ABCG2 inhibitor YHO-13351 sensitizes cancer stem/initiating-like side population cells to irinotecan.	Irinotecan	90-100	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
23298313-7	2013	Second-line cetuximab plus irinotecan is a valid treatment strategy for mCRC patients with irinotecan-refractory and oxaliplatin-naive tumors harboring wild-type KRAS.	Irinotecan	27-37	KRAS proto-oncogene, GTPase	Homo sapiens	162-166
23358684-8	2013	Selection of irinotecan resistance in colon carcinoma cells led to a greater proportion of CSCs compared with parental cells, as measured by the CSC markers CD133 and ALDH1 activity (Aldefluor).	Irinotecan	13-23	prominin 1	Homo sapiens	157-162
23373735-0	2013	Regulation of carboxylesterase-2 expression by p53 family proteins and enhanced anti-cancer activities among 5-fluorouracil, irinotecan and doxazolidine prodrug.	Irinotecan	125-135	carboxylesterase 2	Homo sapiens	14-32
23373735-0	2013	Regulation of carboxylesterase-2 expression by p53 family proteins and enhanced anti-cancer activities among 5-fluorouracil, irinotecan and doxazolidine prodrug.	Irinotecan	125-135	tumor protein p53	Homo sapiens	47-50
23373735-3	2013	Irinotecan and many others such as PPD (pentyl carbamate of p-aminobenzyl carbamate of doxazolidine) require activation by carboxylesterase-2 (CES2).	Irinotecan	0-10	carboxylesterase 2	Homo sapiens	123-141
23373735-3	2013	Irinotecan and many others such as PPD (pentyl carbamate of p-aminobenzyl carbamate of doxazolidine) require activation by carboxylesterase-2 (CES2).	Irinotecan	0-10	carboxylesterase 2	Homo sapiens	143-147
23358684-8	2013	Selection of irinotecan resistance in colon carcinoma cells led to a greater proportion of CSCs compared with parental cells, as measured by the CSC markers CD133 and ALDH1 activity (Aldefluor).	Irinotecan	13-23	aldehyde dehydrogenase 1 family member A1	Homo sapiens	167-172
23770716-4	2013	Our data suggest that CPT-11 reduced the expression of IL-2/IFN-gamma and increased IL-10/TGF-beta expression in both peripheral blood and within the grafts.	Irinotecan	22-28	interleukin 2	Mus musculus	55-59
23770716-4	2013	Our data suggest that CPT-11 reduced the expression of IL-2/IFN-gamma and increased IL-10/TGF-beta expression in both peripheral blood and within the grafts.	Irinotecan	22-28	interferon gamma	Mus musculus	60-69
23770716-4	2013	Our data suggest that CPT-11 reduced the expression of IL-2/IFN-gamma and increased IL-10/TGF-beta expression in both peripheral blood and within the grafts.	Irinotecan	22-28	interleukin 10	Mus musculus	84-89
23770716-4	2013	Our data suggest that CPT-11 reduced the expression of IL-2/IFN-gamma and increased IL-10/TGF-beta expression in both peripheral blood and within the grafts.	Irinotecan	22-28	transforming growth factor, beta 1	Mus musculus	90-98
23770716-5	2013	CPT-11 could also inhibit alloresponses of memory T cells, while decreasing the proportion of CD4(+) memory T cells in the spleen of the recipients and significantly reducing serum alloantibody levels.	Irinotecan	0-6	CD4 antigen	Mus musculus	94-97
23328075-3	2013	The aim of this study was to examine any modulations in the DDC mRNA levels in gastric cancer cells after their treatment with the chemotherapeutic agents 5-fluorouracil, leucovorin, irinotecan, etoposide, cisplatin, and taxol.	Irinotecan	183-193	dopa decarboxylase	Homo sapiens	60-63
23364789-6	2013	The PRC stress response was also activated by the topoisomerase I inhibitor 7-ethyl-10-hydroxycamptothecin (SN-38), an inducer of premature senescence in tumor cells.	Irinotecan	76-106	PPARG related coactivator 1	Homo sapiens	4-7
23364789-6	2013	The PRC stress response was also activated by the topoisomerase I inhibitor 7-ethyl-10-hydroxycamptothecin (SN-38), an inducer of premature senescence in tumor cells.	Irinotecan	108-113	PPARG related coactivator 1	Homo sapiens	4-7
23364789-7	2013	Cells treated with SN-38 displayed morphological characteristics of senescence and express senescence-associated beta-galactosidase activity.	Irinotecan	19-24	galactosidase beta 1	Homo sapiens	113-131
23364789-8	2013	In contrast to menadione, the SN-38 induction of the PRC program occurred over an extended time course and was antioxidant-insensitive.	Irinotecan	30-35	PPARG related coactivator 1	Homo sapiens	53-56
23547747-19	2013	The base-case incremental cost-effectiveness ratio (ICER) for KRAS WT patients for cetuximab compared with best supportive care is $98,000 per quality-adjusted life-year (QALY), for panitumumab compared with best supportive care is $150,000 per QALY and for cetuximab plus irinotecan compared with best supportive care is $88,000 per QALY.	Irinotecan	273-283	KRAS proto-oncogene, GTPase	Homo sapiens	62-66
23547747-22	2013	For cetuximab plus irinotecan treatment for KRAS WT people, there is no direct evidence on progression-free survival, overall survival and duration of treatment.	Irinotecan	19-29	KRAS proto-oncogene, GTPase	Homo sapiens	44-48
23547747-24	2013	It would be useful to conduct a RCT for patients with KRAS WT status receiving cetuximab plus irinotecan.	Irinotecan	94-104	KRAS proto-oncogene, GTPase	Homo sapiens	54-58
23054213-0	2013	The PARP inhibitor ABT-888 synergizes irinotecan treatment of colon cancer cell lines.	Irinotecan	38-48	poly(ADP-ribose) polymerase 1	Homo sapiens	4-8
23386248-0	2013	Refining the UGT1A haplotype associated with irinotecan-induced hematological toxicity in metastatic colorectal cancer patients treated with 5-fluorouracil/irinotecan-based regimens.	Irinotecan	45-55	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	13-18
23386248-0	2013	Refining the UGT1A haplotype associated with irinotecan-induced hematological toxicity in metastatic colorectal cancer patients treated with 5-fluorouracil/irinotecan-based regimens.	Irinotecan	156-166	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	13-18
23386248-11	2013	Our results suggest that specific SNPs in UGT1A, other than UGT1A1*28, may influence irinotecan toxicity and should be considered to refine pharmacogenetic testing.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	42-47
23985249-0	2013	[Relationship between UGT1A and irinotecan-related toxicity].	Irinotecan	32-42	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	22-27
23517622-5	2013	RESULTS: Gene expression levels of APTX, BRCA1 and ERCC1 were significantly lower in irinotecan-sensitive gastric cancer samples than those irinotecan-resistant samples (P&lt;0.001 for all genes), while ISG15 (P=0.047) and Topo1 (P=0.002) were significantly higher.	Irinotecan	85-95	aprataxin	Mus musculus	35-39
23517622-5	2013	RESULTS: Gene expression levels of APTX, BRCA1 and ERCC1 were significantly lower in irinotecan-sensitive gastric cancer samples than those irinotecan-resistant samples (P&lt;0.001 for all genes), while ISG15 (P=0.047) and Topo1 (P=0.002) were significantly higher.	Irinotecan	85-95	breast cancer 1, early onset	Mus musculus	41-46
23517622-5	2013	RESULTS: Gene expression levels of APTX, BRCA1 and ERCC1 were significantly lower in irinotecan-sensitive gastric cancer samples than those irinotecan-resistant samples (P&lt;0.001 for all genes), while ISG15 (P=0.047) and Topo1 (P=0.002) were significantly higher.	Irinotecan	85-95	excision repair cross-complementing rodent repair deficiency, complementation group 1	Mus musculus	51-56
23517622-5	2013	RESULTS: Gene expression levels of APTX, BRCA1 and ERCC1 were significantly lower in irinotecan-sensitive gastric cancer samples than those irinotecan-resistant samples (P&lt;0.001 for all genes), while ISG15 (P=0.047) and Topo1 (P=0.002) were significantly higher.	Irinotecan	85-95	ISG15 ubiquitin-like modifier	Mus musculus	203-208
23517622-5	2013	RESULTS: Gene expression levels of APTX, BRCA1 and ERCC1 were significantly lower in irinotecan-sensitive gastric cancer samples than those irinotecan-resistant samples (P&lt;0.001 for all genes), while ISG15 (P=0.047) and Topo1 (P=0.002) were significantly higher.	Irinotecan	140-150	aprataxin	Mus musculus	35-39
23517622-5	2013	RESULTS: Gene expression levels of APTX, BRCA1 and ERCC1 were significantly lower in irinotecan-sensitive gastric cancer samples than those irinotecan-resistant samples (P&lt;0.001 for all genes), while ISG15 (P=0.047) and Topo1 (P=0.002) were significantly higher.	Irinotecan	140-150	excision repair cross-complementing rodent repair deficiency, complementation group 1	Mus musculus	51-56
23480903-1	2013	BACKGROUND/PURPOSE: Human carboxylesterase 2 (CES2) is the key enzyme for metabolic activation of irinotecan (CPT-11).	Irinotecan	98-108	carboxylesterase 2	Homo sapiens	26-44
23789755-0	2013	[Influence of genetic polymorphisms in UGT1A1, UGT1A7 and UGT1A9 on the pharmacokynetics of irinotecan, SN-38 and SN-38G].	Irinotecan	92-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
23789755-0	2013	[Influence of genetic polymorphisms in UGT1A1, UGT1A7 and UGT1A9 on the pharmacokynetics of irinotecan, SN-38 and SN-38G].	Irinotecan	92-102	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	47-53
23789755-0	2013	[Influence of genetic polymorphisms in UGT1A1, UGT1A7 and UGT1A9 on the pharmacokynetics of irinotecan, SN-38 and SN-38G].	Irinotecan	92-102	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	58-64
23789755-0	2013	[Influence of genetic polymorphisms in UGT1A1, UGT1A7 and UGT1A9 on the pharmacokynetics of irinotecan, SN-38 and SN-38G].	Irinotecan	104-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
23789755-0	2013	[Influence of genetic polymorphisms in UGT1A1, UGT1A7 and UGT1A9 on the pharmacokynetics of irinotecan, SN-38 and SN-38G].	Irinotecan	104-109	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	47-53
23789755-0	2013	[Influence of genetic polymorphisms in UGT1A1, UGT1A7 and UGT1A9 on the pharmacokynetics of irinotecan, SN-38 and SN-38G].	Irinotecan	104-109	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	58-64
23789755-0	2013	[Influence of genetic polymorphisms in UGT1A1, UGT1A7 and UGT1A9 on the pharmacokynetics of irinotecan, SN-38 and SN-38G].	Irinotecan	114-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
23789755-0	2013	[Influence of genetic polymorphisms in UGT1A1, UGT1A7 and UGT1A9 on the pharmacokynetics of irinotecan, SN-38 and SN-38G].	Irinotecan	114-119	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	47-53
23789755-0	2013	[Influence of genetic polymorphisms in UGT1A1, UGT1A7 and UGT1A9 on the pharmacokynetics of irinotecan, SN-38 and SN-38G].	Irinotecan	114-119	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	58-64
23789755-1	2013	OBJECTIVE: To evaluate the influence of genetic polymorphism in UGT1A1, UGT1A7 and UGT1A9 on the population pharmacokinetics of irinotecan and its metabolites, SN-38 and SN-38G.	Irinotecan	128-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
23789755-1	2013	OBJECTIVE: To evaluate the influence of genetic polymorphism in UGT1A1, UGT1A7 and UGT1A9 on the population pharmacokinetics of irinotecan and its metabolites, SN-38 and SN-38G.	Irinotecan	128-138	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	72-78
23789755-1	2013	OBJECTIVE: To evaluate the influence of genetic polymorphism in UGT1A1, UGT1A7 and UGT1A9 on the population pharmacokinetics of irinotecan and its metabolites, SN-38 and SN-38G.	Irinotecan	128-138	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	83-89
23789755-7	2013	The presence of UGT1A1*28, UGT1A7*3, UGT1A9*22 genotypes decreases SN-38 clearance between 20 and 36%.	Irinotecan	67-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
23789755-7	2013	The presence of UGT1A1*28, UGT1A7*3, UGT1A9*22 genotypes decreases SN-38 clearance between 20 and 36%.	Irinotecan	67-72	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	27-33
23789755-7	2013	The presence of UGT1A1*28, UGT1A7*3, UGT1A9*22 genotypes decreases SN-38 clearance between 20 and 36%.	Irinotecan	67-72	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	37-43
23789755-9	2013	CONCLUSION: The inclusion of pharmacokinetic-pharmacogenomic information can add value to the individualized dose adjustment of irinotecan, because it will let quantitatively handle dose reductions in patients with iatrogenic toxicity due to UGT1A1 genetic polymorphisms.	Irinotecan	128-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	242-248
23480903-1	2013	BACKGROUND/PURPOSE: Human carboxylesterase 2 (CES2) is the key enzyme for metabolic activation of irinotecan (CPT-11).	Irinotecan	98-108	carboxylesterase 2	Homo sapiens	46-50
23480903-1	2013	BACKGROUND/PURPOSE: Human carboxylesterase 2 (CES2) is the key enzyme for metabolic activation of irinotecan (CPT-11).	Irinotecan	110-116	carboxylesterase 2	Homo sapiens	26-44
23480903-1	2013	BACKGROUND/PURPOSE: Human carboxylesterase 2 (CES2) is the key enzyme for metabolic activation of irinotecan (CPT-11).	Irinotecan	110-116	carboxylesterase 2	Homo sapiens	46-50
23480903-8	2013	RESULTS: CES2 RNA expression was observed in neuroblastoma cells, and its expression in neuroblastoma cell lines was positively correlated with sensitivity to CPT-11 and apoptosis after CPT-11 exposure in vitro.	Irinotecan	159-165	carboxylesterase 2	Homo sapiens	9-13
23480903-8	2013	RESULTS: CES2 RNA expression was observed in neuroblastoma cells, and its expression in neuroblastoma cell lines was positively correlated with sensitivity to CPT-11 and apoptosis after CPT-11 exposure in vitro.	Irinotecan	186-192	carboxylesterase 2	Homo sapiens	9-13
23041588-1	2013	BACKGROUND: The purpose of this study was to evaluate the combination of panitumumab and irinotecan in patients with KRAS wild-type metastatic colorectal cancer refractory to standard chemotherapy (oxaliplatin, fluoropyrimidines-irinotecan and bevacizumab).	Irinotecan	89-99	KRAS proto-oncogene, GTPase	Homo sapiens	117-121
23041588-1	2013	BACKGROUND: The purpose of this study was to evaluate the combination of panitumumab and irinotecan in patients with KRAS wild-type metastatic colorectal cancer refractory to standard chemotherapy (oxaliplatin, fluoropyrimidines-irinotecan and bevacizumab).	Irinotecan	229-239	KRAS proto-oncogene, GTPase	Homo sapiens	117-121
23130636-2	2013	UGT1A1 (UDP-glucuronosyltransferase 1A1) is a critical gene for bilirubin metabolism and irinotecan detoxification.	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23108760-0	2013	Fatty acid synthase inhibitor cerulenin inhibits topoisomerase I catalytic activity and augments SN-38-induced apoptosis.	Irinotecan	97-102	fatty acid synthase	Homo sapiens	0-19
22934695-2	2013	This study aims to investigate the association between UGT1A1 gene polymorphisms and irinotecan related toxicities in Chinese Han gastrointestinal cancer patients receiving FOLFIRI regimen chemotherapy.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
23130636-2	2013	UGT1A1 (UDP-glucuronosyltransferase 1A1) is a critical gene for bilirubin metabolism and irinotecan detoxification.	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-39
22402322-5	2013	Here, we have used an established, genetically modified human NSC line (HB1.F3.CD) to deliver carboxylesterase (CE) to cerebellar tumor foci and locally activate the prodrug camptothecin-11 (CPT-11) (Irinotecan) to the potent topoisomerase I inhibitor SN-38.	Irinotecan	174-189	histocompatibility minor HB-1	Homo sapiens	72-75
23121194-5	2013	On the other hand, anti-CD 20 mAb-PEG-SN-38 via carbamate-bond as conventional immunoconjugate, enabled SN-38 to be released by a carboxylesterase inside of the tumor cell following the internalization, showed strong anti-tumor activity against malignant lymphoma as hypervascular and stroma-poor tumor.	Irinotecan	38-43	keratin 20	Homo sapiens	24-29
23348635-6	2013	Nonetheless, cells exposed to 5-FU, CPT-11, TNF-alpha or HSV-1 activate NF-kappaB.	Irinotecan	36-42	nuclear factor kappa B subunit 1	Homo sapiens	72-81
23121194-5	2013	On the other hand, anti-CD 20 mAb-PEG-SN-38 via carbamate-bond as conventional immunoconjugate, enabled SN-38 to be released by a carboxylesterase inside of the tumor cell following the internalization, showed strong anti-tumor activity against malignant lymphoma as hypervascular and stroma-poor tumor.	Irinotecan	104-109	keratin 20	Homo sapiens	24-29
22402322-5	2013	Here, we have used an established, genetically modified human NSC line (HB1.F3.CD) to deliver carboxylesterase (CE) to cerebellar tumor foci and locally activate the prodrug camptothecin-11 (CPT-11) (Irinotecan) to the potent topoisomerase I inhibitor SN-38.	Irinotecan	191-197	histocompatibility minor HB-1	Homo sapiens	72-75
22402322-5	2013	Here, we have used an established, genetically modified human NSC line (HB1.F3.CD) to deliver carboxylesterase (CE) to cerebellar tumor foci and locally activate the prodrug camptothecin-11 (CPT-11) (Irinotecan) to the potent topoisomerase I inhibitor SN-38.	Irinotecan	200-210	histocompatibility minor HB-1	Homo sapiens	72-75
22402322-5	2013	Here, we have used an established, genetically modified human NSC line (HB1.F3.CD) to deliver carboxylesterase (CE) to cerebellar tumor foci and locally activate the prodrug camptothecin-11 (CPT-11) (Irinotecan) to the potent topoisomerase I inhibitor SN-38.	Irinotecan	252-257	histocompatibility minor HB-1	Homo sapiens	72-75
23449330-5	2013	Then the kinetics of estradiol at 3-hydroxy position (E-3OH) and 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation by recombinant UGT1A1s as well as human and minipig liver microsomes were analyzed.	Irinotecan	65-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
23278696-5	2013	KEY FINDINGS: Genistein, as well as probenecid, significantly suppressed the MRP2-mediated biliary and intestinal secretion of CPT-11 and its metabolites and increased their plasma concentrations.	Irinotecan	127-133	ATP binding cassette subfamily C member 2	Rattus norvegicus	77-81
23303296-4	2013	Since SN-38 is metabolized to non-toxic SN-38-glucuronide by hepatic uridine diphosphate glucuronosyl transferase (UGT) 1A enzymes, UGT1A enzyme activities may influence adverse events of CPT-11.	Irinotecan	6-11	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	115-122
23303296-4	2013	Since SN-38 is metabolized to non-toxic SN-38-glucuronide by hepatic uridine diphosphate glucuronosyl transferase (UGT) 1A enzymes, UGT1A enzyme activities may influence adverse events of CPT-11.	Irinotecan	6-11	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	132-137
23303296-4	2013	Since SN-38 is metabolized to non-toxic SN-38-glucuronide by hepatic uridine diphosphate glucuronosyl transferase (UGT) 1A enzymes, UGT1A enzyme activities may influence adverse events of CPT-11.	Irinotecan	188-194	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	115-122
23303296-4	2013	Since SN-38 is metabolized to non-toxic SN-38-glucuronide by hepatic uridine diphosphate glucuronosyl transferase (UGT) 1A enzymes, UGT1A enzyme activities may influence adverse events of CPT-11.	Irinotecan	188-194	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	132-137
23303296-6	2013	Here, to identify the genetic factors that affect the adverse events of CPT-11, we determined the polymorphism in three UGT 1A isozyme genes in 45 inpatients with lung, colon, or stomach cancer.	Irinotecan	72-78	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	120-126
23303296-12	2013	In conclusion, UGT1A1*6/*28, UGT1A7*3/*3, and UGT1A9*1/*1 should be taken into consideration as markers for preventing severe adverse events of CPT-11 administration.	Irinotecan	144-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
23303296-12	2013	In conclusion, UGT1A1*6/*28, UGT1A7*3/*3, and UGT1A9*1/*1 should be taken into consideration as markers for preventing severe adverse events of CPT-11 administration.	Irinotecan	144-150	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	29-35
23303296-12	2013	In conclusion, UGT1A1*6/*28, UGT1A7*3/*3, and UGT1A9*1/*1 should be taken into consideration as markers for preventing severe adverse events of CPT-11 administration.	Irinotecan	144-150	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	46-52
23089672-11	2013	Regarding phase II enzyme polymorphism, the anticancer treatment with mercaptopurines and irinotecan is still considered important in relation to the polymorphism of TPMT and UGT1A1, respectively.	Irinotecan	90-100	thiopurine S-methyltransferase	Homo sapiens	166-170
23089672-11	2013	Regarding phase II enzyme polymorphism, the anticancer treatment with mercaptopurines and irinotecan is still considered important in relation to the polymorphism of TPMT and UGT1A1, respectively.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	175-181
23449330-7	2013	E-3OH and SN-38 glucuronidation by recombinant hUGT1A1 and mpUGT1A1 showed allosteric sigmoidal kinetics.	Irinotecan	10-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-54
23449330-5	2013	Then the kinetics of estradiol at 3-hydroxy position (E-3OH) and 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation by recombinant UGT1A1s as well as human and minipig liver microsomes were analyzed.	Irinotecan	97-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
22973964-0	2013	Irinotecan resistance is accompanied by upregulation of EGFR and Src signaling in human cancer models.	Irinotecan	0-10	epidermal growth factor receptor	Homo sapiens	56-60
22973964-6	2013	We now show that acquired resistance to SN-38 is accompanied by increased expression of EGFR, HER2, HER3 and Src proteins in two colorectal cancer cell models as well as by Src activation.	Irinotecan	40-45	erb-b2 receptor tyrosine kinase 2	Homo sapiens	94-98
23242585-13	2013	Immunostains of gammaH2AX and pChk1(S296) on serial tumor biopsies from four patients demonstrated an induction of DNA damage and Chk1 activation following irinotecan.	Irinotecan	156-166	checkpoint kinase 1	Homo sapiens	31-35
23053265-0	2013	Uridine diphosphate glucuronosyl transferase 1 family polypeptide A1 gene (UGT1A1) polymorphisms are associated with toxicity and efficacy in irinotecan monotherapy for refractory pancreatic cancer.	Irinotecan	142-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
24457609-0	2013	Gefitinib enhances the antitumor activity of CPT-11 in vitro and in vivo by inhibiting ABCG2 but not ABCB1: a new clue to circumvent gastrointestinal toxicity risk.	Irinotecan	45-51	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	87-92
24457609-2	2013	METHODS: We aimed to evaluate the inhibitory potency of gefitinib against the ABCB1- or ABCG2-mediated excretion of CPT-11 and its active metabolite SN-38 in vitro and in vivo.	Irinotecan	116-122	ATP binding cassette subfamily B member 1	Homo sapiens	78-83
24457609-2	2013	METHODS: We aimed to evaluate the inhibitory potency of gefitinib against the ABCB1- or ABCG2-mediated excretion of CPT-11 and its active metabolite SN-38 in vitro and in vivo.	Irinotecan	116-122	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	88-93
24457609-2	2013	METHODS: We aimed to evaluate the inhibitory potency of gefitinib against the ABCB1- or ABCG2-mediated excretion of CPT-11 and its active metabolite SN-38 in vitro and in vivo.	Irinotecan	149-154	ATP binding cassette subfamily B member 1	Homo sapiens	78-83
24457609-2	2013	METHODS: We aimed to evaluate the inhibitory potency of gefitinib against the ABCB1- or ABCG2-mediated excretion of CPT-11 and its active metabolite SN-38 in vitro and in vivo.	Irinotecan	149-154	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	88-93
24457609-3	2013	RESULTS: Gefitinib dose-dependently enhanced the antiproliferation activity of SN-38 in vitro by inhibiting ABCG2.	Irinotecan	79-84	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	108-113
22973964-6	2013	We now show that acquired resistance to SN-38 is accompanied by increased expression of EGFR, HER2, HER3 and Src proteins in two colorectal cancer cell models as well as by Src activation.	Irinotecan	40-45	erb-b2 receptor tyrosine kinase 3	Homo sapiens	100-104
22973964-6	2013	We now show that acquired resistance to SN-38 is accompanied by increased expression of EGFR, HER2, HER3 and Src proteins in two colorectal cancer cell models as well as by Src activation.	Irinotecan	40-45	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	109-112
22973964-6	2013	We now show that acquired resistance to SN-38 is accompanied by increased expression of EGFR, HER2, HER3 and Src proteins in two colorectal cancer cell models as well as by Src activation.	Irinotecan	40-45	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	173-176
22973964-0	2013	Irinotecan resistance is accompanied by upregulation of EGFR and Src signaling in human cancer models.	Irinotecan	0-10	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	65-68
22973964-4	2013	Exposure of tumor cells to irinotecan or its active metabolite SN-38 is accompanied by EGFR activation, either by stimulation of EGFR autophosphorylation or by Src-mediated phosphorylation.	Irinotecan	27-37	epidermal growth factor receptor	Homo sapiens	87-91
22973964-4	2013	Exposure of tumor cells to irinotecan or its active metabolite SN-38 is accompanied by EGFR activation, either by stimulation of EGFR autophosphorylation or by Src-mediated phosphorylation.	Irinotecan	27-37	epidermal growth factor receptor	Homo sapiens	129-133
22973964-4	2013	Exposure of tumor cells to irinotecan or its active metabolite SN-38 is accompanied by EGFR activation, either by stimulation of EGFR autophosphorylation or by Src-mediated phosphorylation.	Irinotecan	27-37	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	160-163
22973964-4	2013	Exposure of tumor cells to irinotecan or its active metabolite SN-38 is accompanied by EGFR activation, either by stimulation of EGFR autophosphorylation or by Src-mediated phosphorylation.	Irinotecan	63-68	epidermal growth factor receptor	Homo sapiens	87-91
22973964-4	2013	Exposure of tumor cells to irinotecan or its active metabolite SN-38 is accompanied by EGFR activation, either by stimulation of EGFR autophosphorylation or by Src-mediated phosphorylation.	Irinotecan	63-68	epidermal growth factor receptor	Homo sapiens	129-133
22973964-4	2013	Exposure of tumor cells to irinotecan or its active metabolite SN-38 is accompanied by EGFR activation, either by stimulation of EGFR autophosphorylation or by Src-mediated phosphorylation.	Irinotecan	63-68	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	160-163
22973964-6	2013	We now show that acquired resistance to SN-38 is accompanied by increased expression of EGFR, HER2, HER3 and Src proteins in two colorectal cancer cell models as well as by Src activation.	Irinotecan	40-45	epidermal growth factor receptor	Homo sapiens	88-92
23783485-0	2013	Associations between UGT1A1*6/*28 polymorphisms and irinotecan-induced severe toxicity in Chinese gastric or esophageal cancer patients.	Irinotecan	52-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	21-27
23089802-3	2013	Impaired or reduced UGT1A1 activity causes unconjugated hyperbilirubinemia (Gilbert"s syndrome and Crigler-Najjar syndrome) and side effects of drug treatment such as SN-38 (active metabolite of the anticancer drug irinotecan)-induced toxicity.	Irinotecan	167-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
23781580-0	2013	UGT1A1 genotype-specific phase I and pharmacokinetic study for combination chemotherapy with irinotecan and cisplatin: a Saitama Tumor Board study.	Irinotecan	93-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23781580-2	2013	The aim of the present study was to determine the RD of irinotecan in combination with cisplatin (CPT-P) for individuals with or without UGT1A1 polymorphisms.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
23781580-8	2013	CONCLUSION: UGT1A1 genotype-based RDs of irinotecan in CPT-P therapy were determined.	Irinotecan	41-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
23316441-3	2013	In this study, we focused on camptothecin and its derivatives, topotecan and irinotecan, which are type I topoisomerase inhibitors that create DNA double-strand breaks in rapidly dividing cells.	Irinotecan	77-87	Topoisomerase 1	Drosophila melanogaster	99-119
23686699-0	2013	UGT1A1 6/28 polymorphisms could predict irinotecan-induced severe neutropenia not diarrhea in Chinese colorectal cancer patients.	Irinotecan	40-50	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23686699-1	2013	The aim of this study was to investigate the associations between UDP-glucuronosyltransferase (UGT) 1A1 polymorphisms and irinotecan-induced toxicities in Chinese advanced colorectal cancer patients.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-103
23686699-9	2013	Both UGT1A1 6 and UGT1A1 28 variants were closely associated with irinotecan-induced severe neutropenia, but not diarrhea.	Irinotecan	66-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-11
23686699-9	2013	Both UGT1A1 6 and UGT1A1 28 variants were closely associated with irinotecan-induced severe neutropenia, but not diarrhea.	Irinotecan	66-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
23089802-3	2013	Impaired or reduced UGT1A1 activity causes unconjugated hyperbilirubinemia (Gilbert"s syndrome and Crigler-Najjar syndrome) and side effects of drug treatment such as SN-38 (active metabolite of the anticancer drug irinotecan)-induced toxicity.	Irinotecan	215-225	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
23648675-1	2013	Human carboxylesterase (CES) 1A and CES2, two major forms of human CES, dominate the pharmacokinetics of most prodrugs such as imidapril and irinotecan (CPT-11).	Irinotecan	141-151	carboxylesterase 2	Homo sapiens	36-40
23648675-1	2013	Human carboxylesterase (CES) 1A and CES2, two major forms of human CES, dominate the pharmacokinetics of most prodrugs such as imidapril and irinotecan (CPT-11).	Irinotecan	153-159	carboxylesterase 2	Homo sapiens	36-40
23783485-1	2013	The aim of this study was to investigate the associations between UDP-glucuronosyltransferase (UGT) 1A1 polymorphisms and irinotecan-induced toxicities in Chinese advanced gastric or esophageal cancer patients.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-103
23864251-2	2013	Therefore, we conducted this study to evaluate the effect of the combination of irinotecan and cisplatin in the treatment of GEP-NECs.	Irinotecan	80-90	granulin precursor	Homo sapiens	125-128
23864251-13	2013	The irinotecan plus cisplatin chemotherapy is moderately effective and tolerable well tolerated in advanced or metastatic GEP-NEC patients; octreotide LAR may be a good maintenance treatment and should be considered as a treatment option for these patients in the future.	Irinotecan	4-14	granulin precursor	Homo sapiens	122-125
23555046-9	2013	siRNA-mediated silencing of EGFR and Rictor reduced U251MG cell migration and increased sensitivity of the cells to irinotecan, temozolomide and vincristine.	Irinotecan	116-126	epidermal growth factor receptor	Homo sapiens	28-32
23422270-0	2013	The role of p38 in irinotecan-induced DNA damage and apoptosis of colon cancer cells.	Irinotecan	19-29	mitogen-activated protein kinase 14	Homo sapiens	12-15
23422270-1	2013	The role of p38 in irinotecan (CPT-11)-induced damage and cell death in colon cancer cell line SW620 was investigated.	Irinotecan	19-29	mitogen-activated protein kinase 14	Homo sapiens	12-15
23422270-2	2013	We demonstrate that CPT-11 treatment activates p38 in exposed cells, however with concentration dependent dynamics and differing consequences.	Irinotecan	20-26	mitogen-activated protein kinase 14	Homo sapiens	47-50
23422270-3	2013	Higher CPT-11 concentrations induce a massive early but relatively short-lasting p38 activity leading to apoptosis mediated by mitochondria and caspases.	Irinotecan	7-13	mitogen-activated protein kinase 14	Homo sapiens	81-84
23422270-4	2013	Pharmacological or siRNA inhibition of p38 then significantly prevents CPT-11-dependent cell death.	Irinotecan	71-77	mitogen-activated protein kinase 14	Homo sapiens	39-42
23422270-5	2013	Conversely, lower CPT-11 concentrations activate p38 in a delayed, however sustained manner, with apoptosis occurring only in a fraction of cells and in the absence of significant autophagy.	Irinotecan	18-24	mitogen-activated protein kinase 14	Homo sapiens	49-52
23422270-6	2013	Blocking p38 in thus treated cells increases their sensitivity toward CPT-11 and increases cell death.	Irinotecan	70-76	mitogen-activated protein kinase 14	Homo sapiens	9-12
23422270-7	2013	In summary, our results confirm the involvement of p38 in colon cancer cells response to CPT-11 while indicating a varying role of p38 in the final biological response.	Irinotecan	89-95	mitogen-activated protein kinase 14	Homo sapiens	51-54
23328486-0	2013	A phase II study of high-dose cetuximab plus irinotecan in colorectal cancer patients with KRAS wild-type tumors who progressed after standard dose of cetuximab plus irinotecan.	Irinotecan	45-55	KRAS proto-oncogene, GTPase	Homo sapiens	91-95
23328486-1	2013	OBJECTIVES: We conducted a phase II clinical trial of high-dose cetuximab plus irinotecan in KRAS wild-type patients who progressed on standard-dose cetuximab plus irinotecan.	Irinotecan	79-89	KRAS proto-oncogene, GTPase	Homo sapiens	93-97
23555046-9	2013	siRNA-mediated silencing of EGFR and Rictor reduced U251MG cell migration and increased sensitivity of the cells to irinotecan, temozolomide and vincristine.	Irinotecan	116-126	RPTOR independent companion of MTOR complex 2	Homo sapiens	37-43
23516488-0	2013	Association between UGT1A1*28 polymorphisms and clinical outcomes of irinotecan-based chemotherapies in colorectal cancer: a meta-analysis in Caucasians.	Irinotecan	69-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
23516488-1	2013	BACKGROUND: Whether UGT1A1*28 genotype is associated with clinical outcomes of irinotecan (IRI)-based chemotherapy in Colorectal cancer (CRC) is an important gap in existing knowledge to inform clinical utility.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
24292186-4	2013	UGT1A1*6 and *28 were significantly associated with altered pharmacokinetics of an irinotecan metabolite, SN-38, and with increased frequency of severe neutropenia.	Irinotecan	83-93	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	0-6
23520486-2	2013	As such, we sought to determine the ability of the mTOR inhibitor everolimus to potentiate the antitumor effects of irinotecan in colorectal cancer (CRC).	Irinotecan	116-126	mechanistic target of rapamycin kinase	Mus musculus	51-55
23520486-11	2013	CONCLUSIONS: Quantitative analysis of tumor growth and metabolomic data showed that the combination of everolimus and irinotecan was more beneficial in the BRAF/PIK3CA mutant HT29 tumor xenografts, which had an additive effect, than the KRAS/PIK3CA mutant HCT116 tumor xenografts, which had a less than additive effect.	Irinotecan	118-128	Braf transforming gene	Mus musculus	156-160
23520486-11	2013	CONCLUSIONS: Quantitative analysis of tumor growth and metabolomic data showed that the combination of everolimus and irinotecan was more beneficial in the BRAF/PIK3CA mutant HT29 tumor xenografts, which had an additive effect, than the KRAS/PIK3CA mutant HCT116 tumor xenografts, which had a less than additive effect.	Irinotecan	118-128	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Mus musculus	161-167
23520486-11	2013	CONCLUSIONS: Quantitative analysis of tumor growth and metabolomic data showed that the combination of everolimus and irinotecan was more beneficial in the BRAF/PIK3CA mutant HT29 tumor xenografts, which had an additive effect, than the KRAS/PIK3CA mutant HCT116 tumor xenografts, which had a less than additive effect.	Irinotecan	118-128	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	237-241
23520486-11	2013	CONCLUSIONS: Quantitative analysis of tumor growth and metabolomic data showed that the combination of everolimus and irinotecan was more beneficial in the BRAF/PIK3CA mutant HT29 tumor xenografts, which had an additive effect, than the KRAS/PIK3CA mutant HCT116 tumor xenografts, which had a less than additive effect.	Irinotecan	118-128	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Mus musculus	242-248
24036898-6	2013	Although SN-38-resistant SCLC cells lacking ICAM-1 expression were still refractory to trastuzumab, their in vivo growth was significantly suppressed by bevacizumab treatment due to dependence on their distinctive and abundant production of vascular endothelial growth factor.	Irinotecan	9-14	intercellular adhesion molecule 1	Homo sapiens	44-50
24036898-6	2013	Although SN-38-resistant SCLC cells lacking ICAM-1 expression were still refractory to trastuzumab, their in vivo growth was significantly suppressed by bevacizumab treatment due to dependence on their distinctive and abundant production of vascular endothelial growth factor.	Irinotecan	9-14	vascular endothelial growth factor A	Homo sapiens	241-275
23328499-6	2013	SN-38 glucuronidation in human and rat liver microsomes was inhibited dose-dependently by the presence of tacrolimus and the 50% inhibition concentration (IC50) values of tacrolimus in rat and human liver microsomes were 10.33 muM and 3.58 muM, respectively.	Irinotecan	0-5	latexin	Homo sapiens	227-230
23328499-6	2013	SN-38 glucuronidation in human and rat liver microsomes was inhibited dose-dependently by the presence of tacrolimus and the 50% inhibition concentration (IC50) values of tacrolimus in rat and human liver microsomes were 10.33 muM and 3.58 muM, respectively.	Irinotecan	0-5	latexin	Homo sapiens	240-243
23328499-8	2013	These findings suggest that tacrolimus inhibits UGT1A1-mediated SN-38 glucuronidation.	Irinotecan	64-69	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	48-54
23811769-8	2013	We also attempted to ameliorate the intestinal toxicity of irinotecan hydrochloride by modulating the hepatic and intestinal functions of MRP2.	Irinotecan	59-83	ATP binding cassette subfamily C member 2	Homo sapiens	138-142
24292186-4	2013	UGT1A1*6 and *28 were significantly associated with altered pharmacokinetics of an irinotecan metabolite, SN-38, and with increased frequency of severe neutropenia.	Irinotecan	106-111	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	0-6
23236239-0	2012	UGT1A1 predicts outcome in colorectal cancer treated with irinotecan and fluorouracil.	Irinotecan	58-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
23149859-10	2012	After SN-38 was released from TPGS/PLGA/SN-38 NPs in MDR cells, TPGS or/and PLGA may modulate the efflux microenvironment of the P-gp pump, such as mitochondria and the P-gp domain with an ATP-binding site.	Irinotecan	6-11	ATP binding cassette subfamily B member 1	Homo sapiens	129-133
23149859-10	2012	After SN-38 was released from TPGS/PLGA/SN-38 NPs in MDR cells, TPGS or/and PLGA may modulate the efflux microenvironment of the P-gp pump, such as mitochondria and the P-gp domain with an ATP-binding site.	Irinotecan	6-11	ATP binding cassette subfamily B member 1	Homo sapiens	169-173
23149859-10	2012	After SN-38 was released from TPGS/PLGA/SN-38 NPs in MDR cells, TPGS or/and PLGA may modulate the efflux microenvironment of the P-gp pump, such as mitochondria and the P-gp domain with an ATP-binding site.	Irinotecan	40-45	ATP binding cassette subfamily B member 1	Homo sapiens	129-133
23149859-10	2012	After SN-38 was released from TPGS/PLGA/SN-38 NPs in MDR cells, TPGS or/and PLGA may modulate the efflux microenvironment of the P-gp pump, such as mitochondria and the P-gp domain with an ATP-binding site.	Irinotecan	40-45	ATP binding cassette subfamily B member 1	Homo sapiens	169-173
20301284-8	1993	Agents/circumstances to avoid: Because TDP1 codes for a DNA repair enzyme, genotoxic anti-cancer drugs such as camptothecins (e.g., irinotecan and topotecan) and bleomycin are likely to be extremely harmful and possibly fatal; exposure to radiation is likely to be extremely harmful and possibly fatal.	Irinotecan	132-142	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	39-43
23236239-9	2012	Differences in irinotecan and its metabolites between UGT1A1 gene variants were compared.	Irinotecan	15-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
23236239-21	2012	Irinotecan PK was investigated in 34 patients, which showed high area under concentration curve (AUC) of irinotecan and SN-38, but low AUC ratio (SN-38G / SN-38) in those patients with UGT1A1*28 TA7/7.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	185-191
23236239-22	2012	CONCLUSION: A distinct distribution pattern of UGT1A1 genotypes in Chinese patients might contribute to relatively low toxicity associated with irinotecan and 5-fluorouracil in mCRC patients.	Irinotecan	144-154	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
23225456-7	2012	CONCLUSION: Our data demonstrate the efficacy of HAI of irinotecan combined with 5-fluorouracil and leucovorin for liver metastases from CRC, specifically in patients also treated with LDP.	Irinotecan	56-66	carboxypeptidase Q	Homo sapiens	185-188
23081779-6	2012	Upon exposure to irinotecan, the LGR5(+) cells transitioned into an LGR5(-) drug-resistant state.	Irinotecan	17-27	leucine rich repeat containing G protein-coupled receptor 5	Homo sapiens	33-37
23071293-0	2012	Clinical outcome of Japanese metastatic colorectal cancer patients harbouring the KRAS p.G13D mutation treated with cetuximab + irinotecan.	Irinotecan	128-138	KRAS proto-oncogene, GTPase	Homo sapiens	82-86
21844885-0	2012	Vascular endothelial growth factor polymorphisms and clinical outcome in colorectal cancer patients treated with irinotecan-based chemotherapy and bevacizumab.	Irinotecan	113-123	vascular endothelial growth factor A	Homo sapiens	0-34
21844885-10	2012	Our results support the potential predictive ability of VEGF genotypes in patients with metastatic colorectal cancer receiving irinotecan-based chemotherapy plus bevacizumab, in terms of RR and OS.	Irinotecan	127-137	vascular endothelial growth factor A	Homo sapiens	56-60
22753594-10	2012	We found that DPC4/SMAD4 inactivation sensitized pancreatic cancer cells to cisplatin and irinotecan by 2- to 4-fold, but they were modestly less sensitive to gemcitabine.	Irinotecan	90-100	SMAD family member 4	Homo sapiens	14-18
22753594-10	2012	We found that DPC4/SMAD4 inactivation sensitized pancreatic cancer cells to cisplatin and irinotecan by 2- to 4-fold, but they were modestly less sensitive to gemcitabine.	Irinotecan	90-100	SMAD family member 4	Homo sapiens	19-24
22270257-10	2012	Conversely potency of PP242 and the combination index for PP242 + irinotecan were unrelated, but synergy exists across all dose levels in PP242 and irinotecan sensitive, p53 wild-type cell lines.	Irinotecan	148-158	tumor protein p53	Homo sapiens	170-173
23271276-3	2012	Imidapril and irinotecan hydrochloride (CPT-11) were used as special substrates for CES1 and CES2, respectively.	Irinotecan	14-38	carboxylesterase 1E	Rattus norvegicus	84-88
23271276-3	2012	Imidapril and irinotecan hydrochloride (CPT-11) were used as special substrates for CES1 and CES2, respectively.	Irinotecan	14-38	carboxylesterase 2	Rattus norvegicus	93-97
23271276-3	2012	Imidapril and irinotecan hydrochloride (CPT-11) were used as special substrates for CES1 and CES2, respectively.	Irinotecan	40-46	carboxylesterase 1E	Rattus norvegicus	84-88
23271276-3	2012	Imidapril and irinotecan hydrochloride (CPT-11) were used as special substrates for CES1 and CES2, respectively.	Irinotecan	40-46	carboxylesterase 2	Rattus norvegicus	93-97
23081779-6	2012	Upon exposure to irinotecan, the LGR5(+) cells transitioned into an LGR5(-) drug-resistant state.	Irinotecan	17-27	leucine rich repeat containing G protein-coupled receptor 5	Homo sapiens	68-72
23233861-7	2012	Of the proposed gene/drug pairs the highest importance was assigned to HLA-B/abacavir, UGT1A1/irinotecan, and CYP2D6/tamoxifen.	Irinotecan	94-104	major histocompatibility complex, class I, B	Homo sapiens	71-76
23233861-7	2012	Of the proposed gene/drug pairs the highest importance was assigned to HLA-B/abacavir, UGT1A1/irinotecan, and CYP2D6/tamoxifen.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	87-93
23155248-5	2012	SN-38 induced different types of cell death in two OSCC cell lines: apoptosis (caspase-3 activation and internucleosomal DNA fragmentation) in HSC-2 cells and autophagy (formation of autophagosome and secondary lysosome) in HSC-4 cells.	Irinotecan	0-5	caspase 3	Homo sapiens	79-88
23162643-1	2012	This study retrospectively compared nedaplatin and irinotecan hydrochloride (NDP/CPT) combination therapy with cisplatin and irinotecan hydrochloride therapy (CDDP/CPT) for efficacy and adverse events in the treatment of clear cell adenocarcinoma of the ovary (CCC) and recurrent ovarian carcinoma.	Irinotecan	51-75	norrin cystine knot growth factor NDP	Homo sapiens	77-80
22909976-0	2012	K-Ras gene mutation status as a prognostic and predictive factor in patients with colorectal cancer undergoing irinotecan- or oxaliplatin-based chemotherapy.	Irinotecan	111-121	KRAS proto-oncogene, GTPase	Homo sapiens	0-5
22909976-7	2012	Multivariate analysis revealed a predictive significance for K-Ras mutations with respect to time to progression in patients treated with irinotecan and oxaliplatin as first-line chemotherapy.	Irinotecan	138-148	KRAS proto-oncogene, GTPase	Homo sapiens	61-66
22909976-11	2012	Also, K-Ras mutation status may predict time to progression in patients treated with irinotecan and oxaliplatin.	Irinotecan	85-95	KRAS proto-oncogene, GTPase	Homo sapiens	6-11
22922573-0	2012	The synergistic effects of low-dose irinotecan and TRAIL on TRAIL-resistant HT-29 colon carcinoma in vitro and in vivo.	Irinotecan	36-46	TNF superfamily member 10	Homo sapiens	60-65
22922573-3	2012	In this study, we investigated the synergistic effects of low-dose irinotecan (CPT-11) and TRAIL on TRAIL-resistant HT-29 colon carcinoma cells and explored potential mechanisms of apoptosis.	Irinotecan	67-77	TNF superfamily member 10	Homo sapiens	100-105
22922573-3	2012	In this study, we investigated the synergistic effects of low-dose irinotecan (CPT-11) and TRAIL on TRAIL-resistant HT-29 colon carcinoma cells and explored potential mechanisms of apoptosis.	Irinotecan	79-85	TNF superfamily member 10	Homo sapiens	100-105
22922573-8	2012	Our results showed that the antitumor effect of TRAIL could be enhanced significantly by low-dose CPT-11 on TRAIL-resistant HT-29 cells both in vitro and in vivo.	Irinotecan	98-104	TNF superfamily member 10	Homo sapiens	48-53
22922573-8	2012	Our results showed that the antitumor effect of TRAIL could be enhanced significantly by low-dose CPT-11 on TRAIL-resistant HT-29 cells both in vitro and in vivo.	Irinotecan	98-104	TNF superfamily member 10	Homo sapiens	108-113
22922573-9	2012	The synergistic apoptotic effect of CPT-11 and TRAIL was proposed to be mediated by upregulating DR5 mRNA expression and increasing expression of Bax and caspase-9 proteins.	Irinotecan	36-42	TNF receptor superfamily member 10b	Homo sapiens	97-100
22922573-9	2012	The synergistic apoptotic effect of CPT-11 and TRAIL was proposed to be mediated by upregulating DR5 mRNA expression and increasing expression of Bax and caspase-9 proteins.	Irinotecan	36-42	BCL2 associated X, apoptosis regulator	Homo sapiens	146-149
22922573-9	2012	The synergistic apoptotic effect of CPT-11 and TRAIL was proposed to be mediated by upregulating DR5 mRNA expression and increasing expression of Bax and caspase-9 proteins.	Irinotecan	36-42	caspase 9	Homo sapiens	154-163
22898888-6	2012	Further analyses showed that CPT-11 induced in both types of cells DNA damage and activated stress response pathways including p53 and p16 but with varying activity of stress kinase p38 and selected stress-associated microRNAs.	Irinotecan	29-35	tumor protein p53	Homo sapiens	127-130
23387089-1	2012	In this work, we developed PEO-PPO-PEO micelles loaded with irinotecan hydrochloride (CPT-11) using breast cancer resistance protein (BCRP) inhibitory material PEO20-PPO70-PEO20, and studied its mechanism of decreasing CPT-11 induced delayed diarrhea and intestinal toxicity.	Irinotecan	86-92	ATP binding cassette subfamily G member 2	Canis lupus familiaris	134-138
23387089-4	2012	The results showed that the obtained micelles could decrease the biliary excretion of CPT-11, ameliorate delayed diarrhea and intestinal toxicity of rats through inhibiting BCRP-mediated CPT-11 efflux.	Irinotecan	86-92	ATP binding cassette subfamily G member 2	Canis lupus familiaris	173-177
23387089-4	2012	The results showed that the obtained micelles could decrease the biliary excretion of CPT-11, ameliorate delayed diarrhea and intestinal toxicity of rats through inhibiting BCRP-mediated CPT-11 efflux.	Irinotecan	187-193	ATP binding cassette subfamily G member 2	Canis lupus familiaris	173-177
22929806-10	2012	The antitumor activity of both gemcitabine and irinotecan were significantly enhanced by CCT244747 in several human tumor xenografts, giving concomitant biomarker modulation indicative of CHK1 inhibition.	Irinotecan	47-57	checkpoint kinase 1	Homo sapiens	188-192
22898888-6	2012	Further analyses showed that CPT-11 induced in both types of cells DNA damage and activated stress response pathways including p53 and p16 but with varying activity of stress kinase p38 and selected stress-associated microRNAs.	Irinotecan	29-35	mitogen-activated protein kinase 14	Homo sapiens	182-185
22898888-6	2012	Further analyses showed that CPT-11 induced in both types of cells DNA damage and activated stress response pathways including p53 and p16 but with varying activity of stress kinase p38 and selected stress-associated microRNAs.	Irinotecan	29-35	cyclin dependent kinase inhibitor 2A	Homo sapiens	135-138
23335549-0	2012	Electrolyte abnormalities due to irinotecan administration in metastatic HER-2 positive breast  cancer patients.	Irinotecan	33-43	erb-b2 receptor tyrosine kinase 2	Homo sapiens	73-78
22770988-4	2012	Interestingly, when gef gene expression was combined with drugs of choice in the clinical treatment of colon cancer (5-fluorouracil, oxaliplatin and irinotecan), a strong synergistic effect was observed with approximately a 15-20% enhancement of the antiproliferative effect.	Irinotecan	149-159	Rho/Rac guanine nucleotide exchange factor 2	Homo sapiens	20-23
22167582-9	2012	Increased apoptosis monitored by caspase-3 was observed after day 15 with irinotecan treatment.	Irinotecan	74-84	caspase 3	Mus musculus	33-42
22614107-5	2012	Using the MTT assay, we found that zafirlukast enhanced the cytotoxicity of several anticancer drugs that are substrates of breast cancer resistance proteins (BCRP/ABCG2), including mitoxantrone and SN-38.	Irinotecan	199-204	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	164-169
22797812-13	2012	Transfection of siRNA against WRN             increased the sensitivity of the cells to CPT-11.	Irinotecan	88-94	WRN RecQ like helicase	Homo sapiens	30-33
22797812-14	2012	Aberrant DNA hypermethylation             of WRN also increased the sensitivity of cervical cancer cells to CPT-11.	Irinotecan	108-114	WRN RecQ like helicase	Homo sapiens	45-48
22797812-16	2012	This is the first report to show a relationship             between the methylation of the WRN gene and sensitivity to CPT-11 in gynecological             cancers.	Irinotecan	119-125	WRN RecQ like helicase	Homo sapiens	91-94
23202910-8	2012	The HB1.F3.CE, HB.F3.CD, or HB1.F3.CD.IFN-beta cells significantly reduced the LNCaP cell viability in the presence of the prodrugs 5-FC or CPT-11.	Irinotecan	140-146	histocompatibility minor HB-1	Homo sapiens	4-7
23202910-8	2012	The HB1.F3.CE, HB.F3.CD, or HB1.F3.CD.IFN-beta cells significantly reduced the LNCaP cell viability in the presence of the prodrugs 5-FC or CPT-11.	Irinotecan	140-146	histocompatibility minor HB-1	Homo sapiens	28-31
23202910-8	2012	The HB1.F3.CE, HB.F3.CD, or HB1.F3.CD.IFN-beta cells significantly reduced the LNCaP cell viability in the presence of the prodrugs 5-FC or CPT-11.	Irinotecan	140-146	interferon beta 1	Homo sapiens	38-46
22750060-4	2012	VKJP1 and VKJP3 significantly sensitized ABCG2-expressing cells to established substrates of ABCG2 including mitoxantrone, SN-38, and doxorubicin in a concentration-dependent manner, but not to the non-ABCG2 substrate cisplatin.	Irinotecan	123-128	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	41-46
22750060-4	2012	VKJP1 and VKJP3 significantly sensitized ABCG2-expressing cells to established substrates of ABCG2 including mitoxantrone, SN-38, and doxorubicin in a concentration-dependent manner, but not to the non-ABCG2 substrate cisplatin.	Irinotecan	123-128	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	93-98
22750060-4	2012	VKJP1 and VKJP3 significantly sensitized ABCG2-expressing cells to established substrates of ABCG2 including mitoxantrone, SN-38, and doxorubicin in a concentration-dependent manner, but not to the non-ABCG2 substrate cisplatin.	Irinotecan	123-128	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	93-98
23323463-8	2012	The prodrug irinotecan is biotransformed by carboxylesterase into its active metabolite SN-38, which is inactivated by UGT1 into the inactive compound SN-38G.	Irinotecan	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-123
23323463-8	2012	The prodrug irinotecan is biotransformed by carboxylesterase into its active metabolite SN-38, which is inactivated by UGT1 into the inactive compound SN-38G.	Irinotecan	88-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-123
23323463-8	2012	The prodrug irinotecan is biotransformed by carboxylesterase into its active metabolite SN-38, which is inactivated by UGT1 into the inactive compound SN-38G.	Irinotecan	151-156	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-123
22192364-3	2012	Anti-EGFR agents can be added to first-line FOLFIRI (5-fluorouracil, leucovorin [folinic acid], irinotecan) or FOLFOX (5-fluorouracil, leucovorin [folinic acid], oxaliplatin) in patients whose tumors express wild-type KRAS.	Irinotecan	96-106	epidermal growth factor receptor	Homo sapiens	5-9
23091446-8	2012	RESULTS: Anti-cancer drug-induced cell death was significantly enhanced by knockdown of MKP-1, and this effect was most prominent in cells treated with irinotecan and etoposide.	Irinotecan	152-162	dual specificity phosphatase 1	Homo sapiens	88-93
21706149-0	2012	Biweekly cetuximab plus irinotecan as second-line chemotherapy for patients with irinotecan-refractory and KRAS wild-type metastatic colorectal cancer according to epidermal growth factor receptor expression status.	Irinotecan	24-34	KRAS proto-oncogene, GTPase	Homo sapiens	107-111
22722827-2	2012	We previously found that a gefitinib-resistant cell line, PC-9/Met in which MET (MNNG-HOS transforming gene) is amplified, was more sensitive than its parent cell line (PC-9) to 7-ethyl-10-hydroxy-camptothecin (SN-38), an active metabolite of irinotecan.	Irinotecan	211-216	proprotein convertase subtilisin/kexin type 9	Homo sapiens	58-62
22722827-2	2012	We previously found that a gefitinib-resistant cell line, PC-9/Met in which MET (MNNG-HOS transforming gene) is amplified, was more sensitive than its parent cell line (PC-9) to 7-ethyl-10-hydroxy-camptothecin (SN-38), an active metabolite of irinotecan.	Irinotecan	243-253	proprotein convertase subtilisin/kexin type 9	Homo sapiens	58-62
22722827-4	2012	METHODS: The sensitivity of PC-9 and PC-9/Met to SN-38 was assessed by performing water soluble tetrazolium salt (WST-1) assays.	Irinotecan	49-54	proprotein convertase subtilisin/kexin type 9	Homo sapiens	28-41
22722827-9	2012	CONCLUSIONS: The increased sensitivity of PC-9/Met cells to SN-38 compared with that of PC-9 cells was partially because of topo I activities resulting from increased topo I mRNA and protein expression caused by MET signaling.	Irinotecan	60-65	proprotein convertase subtilisin/kexin type 9	Homo sapiens	42-46
22960892-1	2012	BACKGROUND &amp; OBJECTIVES: Genetic polymorphisms of uridine diphosphate glucuronyltransferase 1A1 (UGT1A1) have been associated with a wide variation of responses among patients prescribed with irinotecan.	Irinotecan	196-206	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
22960892-3	2012	The objective of this study was to investigate the prevalence of three different variants of UGT1A1 (UGT1A1*6, UGT1A1*27 and UGT1A1*28), which are associated with reduced enzyme activity and increased irinotecan toxicity, in the three main ethnic groups in Malaysia (Malays, Chinese and Indians).	Irinotecan	201-211	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
22960892-3	2012	The objective of this study was to investigate the prevalence of three different variants of UGT1A1 (UGT1A1*6, UGT1A1*27 and UGT1A1*28), which are associated with reduced enzyme activity and increased irinotecan toxicity, in the three main ethnic groups in Malaysia (Malays, Chinese and Indians).	Irinotecan	201-211	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
22960892-3	2012	The objective of this study was to investigate the prevalence of three different variants of UGT1A1 (UGT1A1*6, UGT1A1*27 and UGT1A1*28), which are associated with reduced enzyme activity and increased irinotecan toxicity, in the three main ethnic groups in Malaysia (Malays, Chinese and Indians).	Irinotecan	201-211	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
22960892-3	2012	The objective of this study was to investigate the prevalence of three different variants of UGT1A1 (UGT1A1*6, UGT1A1*27 and UGT1A1*28), which are associated with reduced enzyme activity and increased irinotecan toxicity, in the three main ethnic groups in Malaysia (Malays, Chinese and Indians).	Irinotecan	201-211	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
22960892-12	2012	Our results suggest that genotyping of UUGT1A1*6, UGT1A1*28 and UGT1A1*27 need to be performed before patients are prescribed with irinotecan due to their high prevalence of allelic variant which could lead to adverse drug reaction.	Irinotecan	131-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
21706149-11	2012	CONCLUSIONS: Biweekly cetuximab plus irinotecan as second-line treatment showed significant anti-tumor activity in patients with irinotecan-refractory mCRC and WT-KRAS regardless of EGFR expression status.	Irinotecan	37-47	KRAS proto-oncogene, GTPase	Homo sapiens	163-167
21706149-1	2012	BACKGROUND: Cetuximab plus irinotecan has been shown to be effective in metastatic colorectal cancer (mCRC) patients with wild-type (WT) KRAS and positive EGFR expressions (EGFR+).	Irinotecan	27-37	KRAS proto-oncogene, GTPase	Homo sapiens	137-141
21706149-1	2012	BACKGROUND: Cetuximab plus irinotecan has been shown to be effective in metastatic colorectal cancer (mCRC) patients with wild-type (WT) KRAS and positive EGFR expressions (EGFR+).	Irinotecan	27-37	epidermal growth factor receptor	Homo sapiens	155-159
21706149-1	2012	BACKGROUND: Cetuximab plus irinotecan has been shown to be effective in metastatic colorectal cancer (mCRC) patients with wild-type (WT) KRAS and positive EGFR expressions (EGFR+).	Irinotecan	27-37	epidermal growth factor receptor	Homo sapiens	173-177
22535688-2	2012	Intestinal bacteria convert the glucuronidated metabolite back to the toxic SN-38 using beta-glucuronidase (GUS), resulting in debilitating diarrhea.	Irinotecan	76-81	glucuronidase beta	Homo sapiens	88-106
22614251-13	2012	Neoadjuvant chemotherapy with irinotecan and nedaplatin was an effective             and well-tolerated treatment for patients with bulky stage Ib2 to IIb squamous             cell carcinoma of the uterine cervix.	Irinotecan	30-40	mitogen-activated protein kinase 8 interacting protein 2	Homo sapiens	144-147
22535688-2	2012	Intestinal bacteria convert the glucuronidated metabolite back to the toxic SN-38 using beta-glucuronidase (GUS), resulting in debilitating diarrhea.	Irinotecan	76-81	glucuronidase beta	Homo sapiens	108-111
22535688-3	2012	Inhibiting GUS activity may relieve this side effect of irinotecan.	Irinotecan	56-66	glucuronidase beta	Homo sapiens	11-14
22665525-1	2012	The topoisomerase I inhibitor irinotecan is used to treat advanced colorectal cancer and has been shown to have p53-independent anticancer activity.	Irinotecan	30-40	tumor protein p53	Homo sapiens	112-115
22665525-2	2012	The aim of this study was to identify the p53-independent signaling mechanisms activated by irinotecan.	Irinotecan	92-102	tumor protein p53	Homo sapiens	42-45
22665525-3	2012	Transcriptional profiling of isogenic HCT116 p53 wild-type and p53 null cells was carried out following treatment with the active metabolite of irinotecan, SN38.	Irinotecan	144-154	tumor protein p53	Homo sapiens	45-48
22665525-3	2012	Transcriptional profiling of isogenic HCT116 p53 wild-type and p53 null cells was carried out following treatment with the active metabolite of irinotecan, SN38.	Irinotecan	144-154	tumor protein p53	Homo sapiens	63-66
22535333-10	2012	CONCLUSION: The impact of increased risk of toxicity attributed to the UGT1A variants may be offset by irinotecan in clinical practice by dose reduction or the use of colony-stimulating factor.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	71-76
22112971-0	2012	Analysis of HER-3, insulin growth factor-1, nuclear factor-kB and epidermal growth factor receptor gene copy number in the prediction of clinical outcome for K-RAS wild-type colorectal cancer patients receiving irinotecan-cetuximab.	Irinotecan	211-221	epidermal growth factor receptor	Homo sapiens	66-98
21898389-4	2012	Use of KRAS testing (assuming KRAS mutant patients receive only irinotecan) was equally effective and saved $12,428 per patient in the United States.	Irinotecan	64-74	KRAS proto-oncogene, GTPase	Homo sapiens	7-11
22647487-0	2012	MAPK14/p38alpha confers irinotecan resistance to TP53-defective cells by inducing survival autophagy.	Irinotecan	24-34	mitogen-activated protein kinase 14	Homo sapiens	0-6
22647487-0	2012	MAPK14/p38alpha confers irinotecan resistance to TP53-defective cells by inducing survival autophagy.	Irinotecan	24-34	mitogen-activated protein kinase 14	Homo sapiens	7-15
22647487-0	2012	MAPK14/p38alpha confers irinotecan resistance to TP53-defective cells by inducing survival autophagy.	Irinotecan	24-34	tumor protein p53	Homo sapiens	49-53
22233275-3	2012	Val-SN-38 improved intracellular accumulation approximately 5-fold in MCF7 cells, compared with SN-38, and rather than changes in membrane permeability, the amino acid transporter ATB(0,+) played a role, whereas the dipeptide transporter PEPT1 did not.	Irinotecan	4-9	solute carrier family 15 member 1	Homo sapiens	238-243
22747970-4	2012	As the third line chemotherapy, a combination therapy of cetuximab with irinotecan was given, which markedly reduced his levels of serum CEA, and the size and number of liver tumors.	Irinotecan	72-82	CEA cell adhesion molecule 3	Homo sapiens	137-140
22415148-1	2012	PURPOSE: We conducted a phase I trial of irinotecan (CPT-11), a topoisomerase I inhibitor, combined with amrubicin, a topoisomerase II inhibitor, with recombinant human granulocyte colony-stimulating factor (rhG-CSF) support to overcome the neutropenia associated with this particular combination.	Irinotecan	41-51	colony stimulating factor 3	Homo sapiens	169-206
22415148-1	2012	PURPOSE: We conducted a phase I trial of irinotecan (CPT-11), a topoisomerase I inhibitor, combined with amrubicin, a topoisomerase II inhibitor, with recombinant human granulocyte colony-stimulating factor (rhG-CSF) support to overcome the neutropenia associated with this particular combination.	Irinotecan	53-59	colony stimulating factor 3	Homo sapiens	169-206
22521243-0	2012	ALDH+ tumor-initiating cells exhibiting gain in NOTCH1 gene copy number have enhanced regrowth sensitivity to a gamma-secretase inhibitor and irinotecan in colorectal cancer.	Irinotecan	142-152	notch receptor 1	Homo sapiens	48-54
22764771-5	2012	Important examples include ketoconazole inhibition of hepatic CYP3A4 in order to increase systemic exposure to docetaxel, irinotecan and etoposide, and cyclosporine inhibition of intestinal ATP-binding cassette transporters in order to decrease the toxicity of irinotecan and increase the bioavailability of oral docetaxel, paclitaxel and topotecan.	Irinotecan	122-132	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	62-68
22764771-5	2012	Important examples include ketoconazole inhibition of hepatic CYP3A4 in order to increase systemic exposure to docetaxel, irinotecan and etoposide, and cyclosporine inhibition of intestinal ATP-binding cassette transporters in order to decrease the toxicity of irinotecan and increase the bioavailability of oral docetaxel, paclitaxel and topotecan.	Irinotecan	261-271	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	62-68
22213127-2	2012	In GS the UGT1A1*28 variant reduces bilirubin conjugation by 70% and is associated with irinotecan and protease inhibitor side effects.	Irinotecan	88-98	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	10-16
25436684-0	2012	Inhibition of Stat3 by peptide aptamer rS3-PA enhances growth suppressive effects of irinotecan on colorectal cancer cells.	Irinotecan	85-95	signal transducer and activator of transcription 3	Homo sapiens	14-19
25436684-8	2012	Irinotecan has been used as a chemotherapeutic agent either as a single agent or in combination with 5-fluorouracil and targeted therapies directed against the epidermal growth factor receptor, such as cetuximab.	Irinotecan	0-10	epidermal growth factor receptor	Homo sapiens	160-192
22521243-10	2012	These results indicate the combination of PF-03084014 and irinotecan may be effective in reducing tumor recurrence in CRC patients whose tumors exhibit elevated levels of the Notch pathway.	Irinotecan	58-68	notch receptor 1	Homo sapiens	175-180
22741034-0	2012	Bax expression is predictive of favorable clinical outcome in chemonaive advanced gastric cancer patients treated with capecitabine, oxaliplatin, and irinotecan regimen.	Irinotecan	150-160	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
22676194-0	2012	Impact of the UGT1A1*28 allele on response to irinotecan: a systematic review and meta-analysis.	Irinotecan	46-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
22676194-1	2012	AIM: Pre-emptive irinotecan dose reduction for UGT1A1*28 homozygotes may result in reduced risk of severe neutropenia and diarrhea.	Irinotecan	17-27	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
22676194-3	2012	Whether UGT1A1*28 genotype is associated with irinotecan response therefore is an important gap in existing knowledge to inform clinical utility.	Irinotecan	46-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
22676194-4	2012	MATERIALS &amp; METHODS: A systematic review and meta-analysis was performed to analyze the difference in objective response rate (ORR) between irinotecan-administered cancer patients with different UGT1A1*28 genotypes: *28/*28 (homozygous variant), *1/*28 (heterozygous variant) or *1/*1 (wild-type).	Irinotecan	144-154	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	199-205
22676194-5	2012	The effect of irinotecan dose on the association between UGT1A1*28 and ORR was also assessed.	Irinotecan	14-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
22426819-3	2012	Breast cancer resistance protein (BCRP)/ABCG2,             a drug efflux pump, confers resistance to multiple anticancer agents such as SN-38             and topotecan.	Irinotecan	136-141	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
22426819-3	2012	Breast cancer resistance protein (BCRP)/ABCG2,             a drug efflux pump, confers resistance to multiple anticancer agents such as SN-38             and topotecan.	Irinotecan	136-141	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
22426819-3	2012	Breast cancer resistance protein (BCRP)/ABCG2,             a drug efflux pump, confers resistance to multiple anticancer agents such as SN-38             and topotecan.	Irinotecan	136-141	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	40-45
22426819-6	2012	LY294002, but not wortmannin, reversed the BCRP-mediated             SN-38 and topotecan resistance.	Irinotecan	69-74	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	43-47
22741034-2	2012	The purpose of this study was to evaluate the prognostic role of Bax in patients with advanced gastric cancer treated with triplet chemotherapy COI regimen (capecitabine, oxaliplatin, and irinotecan).	Irinotecan	188-198	BCL2 associated X, apoptosis regulator	Homo sapiens	65-68
22471369-7	2012	Increased activity of caspase-3 and caspase-9 was observed after treating with panaxadiol and irinotecan.	Irinotecan	94-104	caspase 3	Homo sapiens	22-31
22438565-11	2012	In both genders, AR was the main driver of TUBB3/TUBB6 expression, as constitutive silencing of AR was associated with downregulation of TUBB3/TUBB6 expression and increased sensitivity to oxaliplatin and SN-38.	Irinotecan	205-210	androgen receptor	Homo sapiens	96-98
22438565-11	2012	In both genders, AR was the main driver of TUBB3/TUBB6 expression, as constitutive silencing of AR was associated with downregulation of TUBB3/TUBB6 expression and increased sensitivity to oxaliplatin and SN-38.	Irinotecan	205-210	tubulin beta 3 class III	Homo sapiens	137-142
22328001-10	2012	Knockdown of CIP2A decreased the resistance of the cells to 5-fluorouracil, oxaliplatin, and SN38 (an active metabolite of irinotecan).	Irinotecan	123-133	cellular inhibitor of PP2A	Homo sapiens	13-18
22069124-9	2012	Thus, targeted therapies directed against calpain 2 may represent a novel strategy to enhance the anti-cancer efficacy of CPT-11.	Irinotecan	122-128	calpain 2	Homo sapiens	42-51
22516947-0	2012	Phase II and UGT1A1 genotype study of irinotecan dose escalation as salvage therapy for advanced gastric cancer.	Irinotecan	38-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
22069124-0	2012	Calpain 2-dependent IkappaBalpha degradation mediates CPT-11 secondary resistance in colorectal cancer xenografts.	Irinotecan	54-60	calpain 2	Homo sapiens	0-9
22069124-0	2012	Calpain 2-dependent IkappaBalpha degradation mediates CPT-11 secondary resistance in colorectal cancer xenografts.	Irinotecan	54-60	NFKB inhibitor alpha	Homo sapiens	20-32
22069124-6	2012	The decrease of NF-kappaB activation in HT-29R and RSN cells by stable transfections with the super-repressor form of IkappaBalpha augmented their sensitivity to CPT-11.	Irinotecan	162-168	NFKB inhibitor alpha	Homo sapiens	118-130
22069124-8	2012	SiRNA silencing of calpain 2 but not of S100A10 and/or annexin A2, resulted in a decrease in NF-kappaB activation, an increase in cellular levels of IkappaBalpha and a partial restoration of the CPT-11 sensitivity in both HT-29R and RSN cells, suggesting that calpain 2-dependent IkappaBalpha degradation mediates CPT-11 secondary resistance.	Irinotecan	195-201	calpain 2	Homo sapiens	19-28
22069124-8	2012	SiRNA silencing of calpain 2 but not of S100A10 and/or annexin A2, resulted in a decrease in NF-kappaB activation, an increase in cellular levels of IkappaBalpha and a partial restoration of the CPT-11 sensitivity in both HT-29R and RSN cells, suggesting that calpain 2-dependent IkappaBalpha degradation mediates CPT-11 secondary resistance.	Irinotecan	314-320	calpain 2	Homo sapiens	19-28
22471369-7	2012	Increased activity of caspase-3 and caspase-9 was observed after treating with panaxadiol and irinotecan.	Irinotecan	94-104	caspase 9	Homo sapiens	36-45
22471369-8	2012	The synergistic apoptotic effects were supported by docking analysis, which demonstrated that panaxadiol and irinotecan bound two different chains of the caspase-3 protein.	Irinotecan	109-119	caspase 3	Homo sapiens	154-163
22471369-9	2012	CONCLUSIONS: Data from this study suggested that caspase-3- and caspase-9-mediated apoptosis may play an important role in the panaxadiol enhanced antiproliferative effects of irinotecan on human colorectal cancer cells.	Irinotecan	176-186	caspase 3	Homo sapiens	49-73
22490361-3	2012	METHODS: We tested the interaction between phosphorylated AKT and MAPK expression in colorectal tumours and corresponding metastases and global outcome in K-RAS wild type patients receiving irinotecan-cetuximab.	Irinotecan	190-200	KRAS proto-oncogene, GTPase	Homo sapiens	155-160
22264223-8	2012	In third-line studies cetuximab-irinotecan is associated with a significant advantage in ORR, mTTP and OS.	Irinotecan	32-42	zinc finger protein 36	Mus musculus	94-98
22264223-10	2012	In third-line studies cetuximab-irinotecan is associated with a significant advantage in ORR, mTTP and OS.	Irinotecan	32-42	zinc finger protein 36	Mus musculus	94-98
22237959-0	2012	Ugt1a is required for the protective effect of selenium against irinotecan-induced toxicity.	Irinotecan	64-74	Ugt1a@	Rattus norvegicus	0-5
22101361-4	2012	The aim of this study was to investigate the role of NO on the pathogenesis of intestinal mucositis, as well as the participation of cytokines upon inducible nitric oxide synthase (iNOS) expression in irinotecan-induced intestinal mucositis.	Irinotecan	201-211	nitric oxide synthase 2, inducible	Mus musculus	148-179
22101361-4	2012	The aim of this study was to investigate the role of NO on the pathogenesis of intestinal mucositis, as well as the participation of cytokines upon inducible nitric oxide synthase (iNOS) expression in irinotecan-induced intestinal mucositis.	Irinotecan	201-211	nitric oxide synthase 2, inducible	Mus musculus	181-185
22101361-9	2012	Additionally, increased MPO and iNOS activity and iNOS immunoexpression were found in WT animals treated with irinotecan.	Irinotecan	110-120	myeloperoxidase	Mus musculus	24-27
22237959-4	2012	The objective of this study is to determine the role of a specific group of uridine diphosphate glucuronosyltransferases, which is coded by UGT1A, in detoxification process of irinotecan as well as selenium-associated protective effect against irinotecan-induced toxicity.	Irinotecan	176-186	Ugt1a@	Rattus norvegicus	140-145
22101361-9	2012	Additionally, increased MPO and iNOS activity and iNOS immunoexpression were found in WT animals treated with irinotecan.	Irinotecan	110-120	nitric oxide synthase 2, inducible	Mus musculus	32-36
22101361-9	2012	Additionally, increased MPO and iNOS activity and iNOS immunoexpression were found in WT animals treated with irinotecan.	Irinotecan	110-120	nitric oxide synthase 2, inducible	Mus musculus	50-54
22237959-11	2012	CONCLUSION: These data support the hypothesis that expression of UGT1A is critical for 5-methylselenocysteine to exert its protective effect against irinotecan-induced toxicity.	Irinotecan	149-159	Ugt1a@	Rattus norvegicus	65-70
22237959-4	2012	The objective of this study is to determine the role of a specific group of uridine diphosphate glucuronosyltransferases, which is coded by UGT1A, in detoxification process of irinotecan as well as selenium-associated protective effect against irinotecan-induced toxicity.	Irinotecan	244-254	Ugt1a@	Rattus norvegicus	140-145
22101361-11	2012	Moreover, through western blot, we verified that infliximab and pentoxifylline significantly inhibited irinotecan-induced iNOS expression.	Irinotecan	103-113	nitric oxide synthase 2, inducible	Mus musculus	122-126
22101361-12	2012	In addition, cytokine concentration was found only partially decreased in irinotecan-treated iNOS(-/-) mice when compared with wild-type animals that were given irinotecan.	Irinotecan	74-84	nitric oxide synthase 2, inducible	Mus musculus	93-97
22237959-9	2012	The enhanced sensitivity was specific to irinotecan and was not observed with other chemotherapeutic agents, such as docetaxel and cisplatin, where Ugt1a is not required for their metabolism.	Irinotecan	41-51	Ugt1a@	Rattus norvegicus	148-153
22202118-0	2012	Human organic cation transporter 1 is expressed in lymphoma cells and increases susceptibility to irinotecan and paclitaxel.	Irinotecan	98-108	solute carrier family 22 member 1	Homo sapiens	6-34
21174225-0	2012	Phase II study of combination chemotherapy with biweekly cetuximab and irinotecan for wild-type KRAS metastatic colorectal cancer refractory to irinotecan, oxaliplatin, and fluoropyrimidines.	Irinotecan	71-81	KRAS proto-oncogene, GTPase	Homo sapiens	96-100
21174225-12	2012	Combination chemotherapy with biweekly cetuximab and irinotecan was effective for pretreated metastatic colorectal cancer with wild-type KRAS.	Irinotecan	53-63	KRAS proto-oncogene, GTPase	Homo sapiens	137-141
22446188-5	2012	We therefore tested whether inhibition of Chk1 could potentiate the cytotoxicity of the DNA damaging agent irinotecan in TNBC using xenotransplant tumor models.	Irinotecan	107-117	checkpoint kinase 1	Homo sapiens	42-46
22202118-4	2012	Functionally, the antineoplastic agents irinotecan, mitoxantrone, and paclitaxel inhibited the uptake of the organic cation [(3)H]1-methyl-4-pyridinium iodide into OCT1-transfected Chinese hamster ovary model cells, with K(i) values of 1.7, 85, and 50 muM, respectively.	Irinotecan	40-50	solute carrier family 22 member 1	Homo sapiens	164-168
22202118-5	2012	Correspondingly, OCT1-positive cell lines and transfectants exhibited significantly higher susceptibilities to the cytotoxic effects of irinotecan and paclitaxel compared with those of OCT1-negative controls.	Irinotecan	136-146	solute carrier family 22 member 1	Homo sapiens	17-21
22200670-0	2012	Differential effects of calcium antagonists on ABCG2/BCRP-mediated drug             resistance and transport in SN-38-resistant HeLa cells.	Irinotecan	112-117	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	47-52
22389470-4	2012	We found that human epidermal growth factor receptor 2 (HER2) expressions are also upregulated in chemoresistant SBC-3/ETP, SBC-3/SN-38, and SBC-3/CDDP cells, compared with chemosensitive SBC-3 cells.	Irinotecan	130-135	erb-b2 receptor tyrosine kinase 2	Homo sapiens	20-54
22389470-4	2012	We found that human epidermal growth factor receptor 2 (HER2) expressions are also upregulated in chemoresistant SBC-3/ETP, SBC-3/SN-38, and SBC-3/CDDP cells, compared with chemosensitive SBC-3 cells.	Irinotecan	130-135	erb-b2 receptor tyrosine kinase 2	Homo sapiens	56-60
22389470-5	2012	Lapatinib, a tyrosine kinase inhibitor of HER2, could not suppress proliferation of these HER2-positive SCLC cells alone but successfully restored chemosensitivity to etoposide and SN-38 with a clinically applicable concentration.	Irinotecan	181-186	erb-b2 receptor tyrosine kinase 2	Homo sapiens	42-46
21176921-10	2012	Claudin-1 protein expression of both the small and large intestine decreased (P &lt; 0.05), occludin protein expression of the small intestine decreased (P &lt; 0.05), and occludin protein expression of the large intestine had decreasing tendency (P = 0.07) in irinotecan treated rats.	Irinotecan	261-271	occludin	Rattus norvegicus	172-180
21176921-11	2012	In irinotecan treated rats, claudin-1 mRNA of the small intestine decreased (P &lt; 0.05), claudin-1 mRNA of large intestine had a tendency to decrease (P = 0.05), occludin mRNA of both small and large intestine decreased (P &lt; 0.05).	Irinotecan	3-13	claudin 1	Rattus norvegicus	28-37
21176921-11	2012	In irinotecan treated rats, claudin-1 mRNA of the small intestine decreased (P &lt; 0.05), claudin-1 mRNA of large intestine had a tendency to decrease (P = 0.05), occludin mRNA of both small and large intestine decreased (P &lt; 0.05).	Irinotecan	3-13	claudin 1	Rattus norvegicus	91-100
21176921-11	2012	In irinotecan treated rats, claudin-1 mRNA of the small intestine decreased (P &lt; 0.05), claudin-1 mRNA of large intestine had a tendency to decrease (P = 0.05), occludin mRNA of both small and large intestine decreased (P &lt; 0.05).	Irinotecan	3-13	occludin	Rattus norvegicus	164-172
21176921-12	2012	CONCLUSIONS: Irinotecan injures claudin-1 and occludin.	Irinotecan	13-23	claudin 1	Rattus norvegicus	32-41
21176921-12	2012	CONCLUSIONS: Irinotecan injures claudin-1 and occludin.	Irinotecan	13-23	occludin	Rattus norvegicus	46-54
22469241-7	2012	For irinotecan-, oxaliplatin-, and bevacizumab-treated tumors, a significant correlation was established between the radiotracer uptake and caspase-3 immunostaining (r  =  .8, p &lt; .05; r  =  .9, p &lt; .001; r  =  .9, p &lt; .001, respectively).	Irinotecan	4-14	caspase 3	Mus musculus	140-149
22399605-0	2012	SN-38 overcomes chemoresistance of colorectal cancer cells induced by hypoxia, through HIF1alpha.	Irinotecan	0-5	hypoxia inducible factor 1 subunit alpha	Homo sapiens	87-96
22399605-7	2012	This effect was dependent on the significant inhibition of the accumulation of HIF-1alpha in cancer cells cultured under hypoxia by SN-38.	Irinotecan	132-137	hypoxia inducible factor 1 subunit alpha	Homo sapiens	79-89
22399605-9	2012	CONCLUSION: SN-38, through inhibition of HIF-1alpha can overcome chemoresistance under hypoxic conditions of colon cancer cells.	Irinotecan	12-17	hypoxia inducible factor 1 subunit alpha	Homo sapiens	41-51
22200670-0	2012	Differential effects of calcium antagonists on ABCG2/BCRP-mediated drug             resistance and transport in SN-38-resistant HeLa cells.	Irinotecan	112-117	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	53-57
22033674-5	2012	Unexpectedly, the in vivo antitumor activity of irinotecan was closely linked to a downregulation of hypoxia-inducible factor-1alpha (HIF1A) target genes along with an inhibition of HIF1A protein accumulation.	Irinotecan	48-58	hypoxia inducible factor 1 subunit alpha	Homo sapiens	101-132
22740978-0	2012	Correlation between plasma concentration ratios of SN-38 glucuronide and SN-38 and neutropenia induction in patients with colorectal cancer and wild-type UGT1A1 gene.	Irinotecan	51-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
22740978-3	2012	A total of 17 patients with colorectal cancer and wild-type UDP-glucuronosyltransferase (UGT)1A1 gene were enrolled and treated with CPT-11 as part of the FOLFIRI regimen [CPT-11 and fluorouracil (5-FU)].	Irinotecan	133-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-96
22740978-6	2012	The median, maximum and minimum values of plasma SN-38G/SN-38 ratios were 4.25, 7.09 and 1.03, respectively, indicating that UGT activities are variable among patients with the wild-type UGT1A1 gene.	Irinotecan	49-54	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	125-128
22740978-7	2012	The plasma SN-38G/SN-38 ratios decreased with an increase in the trial numbers of chemotherapy (r=0.741, p=0.000669), suggesting that CPT-11 treatment suppresses UGT activity, and the low plasma SN-38G/SN-38 ratios resulted in the induction of greater neutropenia.	Irinotecan	11-16	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	162-165
22740978-7	2012	The plasma SN-38G/SN-38 ratios decreased with an increase in the trial numbers of chemotherapy (r=0.741, p=0.000669), suggesting that CPT-11 treatment suppresses UGT activity, and the low plasma SN-38G/SN-38 ratios resulted in the induction of greater neutropenia.	Irinotecan	134-140	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	162-165
22740978-9	2012	In conclusion, UGT activity involved in SN-38 metabolism is variable among patients with the wild-type UGT1A1 gene, and each CPT-11 treatment suppresses UGT activity.	Irinotecan	40-45	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	15-18
22740978-9	2012	In conclusion, UGT activity involved in SN-38 metabolism is variable among patients with the wild-type UGT1A1 gene, and each CPT-11 treatment suppresses UGT activity.	Irinotecan	40-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
22740978-9	2012	In conclusion, UGT activity involved in SN-38 metabolism is variable among patients with the wild-type UGT1A1 gene, and each CPT-11 treatment suppresses UGT activity.	Irinotecan	40-45	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	103-106
22740978-9	2012	In conclusion, UGT activity involved in SN-38 metabolism is variable among patients with the wild-type UGT1A1 gene, and each CPT-11 treatment suppresses UGT activity.	Irinotecan	125-131	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	15-18
22740978-9	2012	In conclusion, UGT activity involved in SN-38 metabolism is variable among patients with the wild-type UGT1A1 gene, and each CPT-11 treatment suppresses UGT activity.	Irinotecan	125-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
22740978-9	2012	In conclusion, UGT activity involved in SN-38 metabolism is variable among patients with the wild-type UGT1A1 gene, and each CPT-11 treatment suppresses UGT activity.	Irinotecan	125-131	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	103-106
22033674-5	2012	Unexpectedly, the in vivo antitumor activity of irinotecan was closely linked to a downregulation of hypoxia-inducible factor-1alpha (HIF1A) target genes along with an inhibition of HIF1A protein accumulation.	Irinotecan	48-58	hypoxia inducible factor 1 subunit alpha	Homo sapiens	134-139
22033674-5	2012	Unexpectedly, the in vivo antitumor activity of irinotecan was closely linked to a downregulation of hypoxia-inducible factor-1alpha (HIF1A) target genes along with an inhibition of HIF1A protein accumulation.	Irinotecan	48-58	hypoxia inducible factor 1 subunit alpha	Homo sapiens	182-187
22788763-7	2012	Since irinotecan is increasingly being combined with radiotherapy, the potential for these proteins to act as predictive biomarkers for both Top I inhibitors and radiation is proposed, and the possibility of synergistic potentiation of chemoradiation regimes by Tdp1 and/or PARP inhibitors is considered.	Irinotecan	6-16	DNA topoisomerase I	Homo sapiens	141-146
22147942-11	2012	Additional studies are necessary to assess whether there is any predictive role of BRAF mutation for irinotecan-based therapy.	Irinotecan	101-111	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	83-87
22068817-3	2012	Three chemotherapeutic agents (5-fluorouracil, oxaliplatin and irinotecan) were tested by ATP-CRA and more sensitive agents were selected.	Irinotecan	63-73	myotubularin related protein 11	Homo sapiens	94-97
23631285-3	2012	The majority of the toxic manifestation is caused by the insufficient deactivation (glucuronidation) of irinotecan active metabolite SN-38 by UGT1A enzyme.	Irinotecan	104-114	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	142-147
23631285-3	2012	The majority of the toxic manifestation is caused by the insufficient deactivation (glucuronidation) of irinotecan active metabolite SN-38 by UGT1A enzyme.	Irinotecan	133-138	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	142-147
23631285-6	2012	The mutations in other enzyme systems also play role in the etiopathogenesis of the irinotecan toxicity: CYP3A (cytochrome P-450), ABC family of transmembrane transporters (adenosine-triphosphate binding cassette).	Irinotecan	84-94	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	105-110
22213294-1	2012	AIM: We investigated the effects of trastuzumab, an anti-HER2 humanized monoclonal antibody, on DNA breaks induced by SN-38, a topoisomerase-1 inhibitor, in gastric cancer cell lines positive or negative for HER2 expression.	Irinotecan	118-123	erb-b2 receptor tyrosine kinase 2	Homo sapiens	57-61
23481572-8	2012	While 5-florouracil did not inhibit the VEGF secretion of HT-29 cell line, irinotecan, oxaliplatin, docetaxel and paclitaxel significantly decreased the levels of secreted VEGF.	Irinotecan	75-85	vascular endothelial growth factor A	Homo sapiens	172-176
22229270-0	2012	Low-dosage metronomic chemotherapy and angiogenesis: topoisomerase inhibitors irinotecan and mitoxantrone stimulate VEGF-A-mediated angiogenesis.	Irinotecan	78-88	vascular endothelial growth factor A	Rattus norvegicus	116-122
22229270-4	2012	The aim of the present study was to assess the systemic effect of low-dosage metronomic treatment with either irinotecan or mitoxantrone on angiogenesis induced by VEGF-A.	Irinotecan	110-120	vascular endothelial growth factor A	Rattus norvegicus	164-170
21896304-6	2012	Cathepsin S expression levels are upregulated in HCT116, LoVo, Colo205 cell lines and HUVECs after exposure to CPT-11 in vitro.	Irinotecan	111-117	cathepsin S	Homo sapiens	0-11
22379477-4	2012	As hypoglossal nerve activity has been reported to be especially susceptible to cholinergic stimulation and irinotecan can cause cholinergic side effects by binding to and inactivating acetylcholinesterase, we suspect this mechanism to be responsible for irinotecan-induced dysarthria.	Irinotecan	108-118	acetylcholinesterase (Cartwright blood group)	Homo sapiens	185-205
22379477-4	2012	As hypoglossal nerve activity has been reported to be especially susceptible to cholinergic stimulation and irinotecan can cause cholinergic side effects by binding to and inactivating acetylcholinesterase, we suspect this mechanism to be responsible for irinotecan-induced dysarthria.	Irinotecan	255-265	acetylcholinesterase (Cartwright blood group)	Homo sapiens	185-205
21040359-6	2012	Hypermethylation of the DYPD gene (encodes the enzyme dihydropyrimidine dehydrogenase) and variation of the uridine diphosphate-glucuronosyltransferase 1A (UGT1A1) gene have predictive value for side effects and the efficacy of 5-fluoruracil and irinotecan, respectively.	Irinotecan	246-256	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	156-162
23176042-10	2012	Increased topoisomerase I expression and increased EGFR gene copy number as possible predictors of response to irinotecan- and cetuximab-based chemoradiation, respectively, deserve further studies.	Irinotecan	111-121	epidermal growth factor receptor	Homo sapiens	51-55
21901246-12	2012	In conclusion, silencing             of DEXI leads to resistance, but restored expression enhances susceptibility to             CPT in vitro and DEXI methylation results in poor response and outcome to CPT-11-based             chemotherapy, suggesting that DEXI is a potent therapeutic target and an epigenetic             biomarker for the selection of patients more likely to benefit from CPT-11-based             chemotherapy.	Irinotecan	203-209	Dexi homolog	Homo sapiens	40-44
22201120-2	2012	All patients harbored UDP-glucuronosyltransferase (UGT) 1A1*1/*1, *1/*6, or *1/*28 genotypes, which are associated with similar irinotecan pharmacokinetics and responses to FOLFIRI.	Irinotecan	128-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-59
22447115-4	2012	When cells were treated with a typical CYP3A substrate (triazolam), CYP2C9 substrate (diclofenac) or UGT1A1 substrate (SN-38), large amounts of their metabolites were detected in the medium of cells cultured on micro-space cell culture plates.	Irinotecan	119-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
22447115-5	2012	The formation of metabolites from triazolam, diclofenac and SN-38 was strongly inhibited by co-treatment with a CYP3A inhibitor (ketoconazole), CYP2C9 inhibitor (sulfaphenazole) and UGT1A1 inhibitor (ketoconazole), respectively.	Irinotecan	60-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
22447115-5	2012	The formation of metabolites from triazolam, diclofenac and SN-38 was strongly inhibited by co-treatment with a CYP3A inhibitor (ketoconazole), CYP2C9 inhibitor (sulfaphenazole) and UGT1A1 inhibitor (ketoconazole), respectively.	Irinotecan	60-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-188
21901246-12	2012	In conclusion, silencing             of DEXI leads to resistance, but restored expression enhances susceptibility to             CPT in vitro and DEXI methylation results in poor response and outcome to CPT-11-based             chemotherapy, suggesting that DEXI is a potent therapeutic target and an epigenetic             biomarker for the selection of patients more likely to benefit from CPT-11-based             chemotherapy.	Irinotecan	203-209	Dexi homolog	Homo sapiens	146-150
21901246-12	2012	In conclusion, silencing             of DEXI leads to resistance, but restored expression enhances susceptibility to             CPT in vitro and DEXI methylation results in poor response and outcome to CPT-11-based             chemotherapy, suggesting that DEXI is a potent therapeutic target and an epigenetic             biomarker for the selection of patients more likely to benefit from CPT-11-based             chemotherapy.	Irinotecan	203-209	Dexi homolog	Homo sapiens	146-150
22946345-2	2012	METHODS: Patients with RSCLC were treated with nedaplatin (NP) at 50 mg/m2 and irinotecan (CPT) at 50 mg/m2 on days 1 and 8 every 4 weeks for four cycles.	Irinotecan	79-89	choline phosphotransferase 1	Homo sapiens	91-94
22039078-4	2012	When SN-38 was stably linked to the anti-CD22 conjugate, its potency was reduced 40- to 55-fold.	Irinotecan	5-10	CD22 molecule	Homo sapiens	41-45
22862168-0	2012	Enhanced chemosensitivity to CPT-11 in colorectal carcinoma xenografts  by small hairpin RNA interference targeting PLK1.	Irinotecan	29-35	polo like kinase 1	Homo sapiens	116-120
22862168-7	2012	In vivo, employment of shRNA targeting PLK1 improved the sensitivity to treat SW620 nude mouse model toward CPT-11.	Irinotecan	108-114	polo like kinase 1	Mus musculus	39-43
22862168-10	2012	Taken together, combination of PLK1-specific shRNA interference with low-dose CPT-11 triggered a antitumor efficacy and represented a potential strategy to treat colon cancer.	Irinotecan	78-84	polo like kinase 1	Homo sapiens	31-35
22508373-0	2012	A phase I study of infusional 5-fluorouracil, leucovorin, oxaliplatin and irinotecan in Japanese patients with advanced colorectal cancer who harbor UGT1A1*1/*1,*1/*6 or *1/*28.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-155
22740861-0	2012	Sequential irinotecan hydrochloride/S-1 for S-1-resistant inoperable gastric cancer: A feasibility study.	Irinotecan	11-21	proteasome 26S subunit, non-ATPase 1	Homo sapiens	44-47
22740861-1	2012	Irinotecan hydrochloride (CPT-11) is reported to be involved in the downregulation of thymidylate synthase (TS), a target molecule of 5-fluorouracil (5-FU) and oral fluoropyrimidine S-1.	Irinotecan	0-24	thymidylate synthetase	Homo sapiens	86-106
22740861-1	2012	Irinotecan hydrochloride (CPT-11) is reported to be involved in the downregulation of thymidylate synthase (TS), a target molecule of 5-fluorouracil (5-FU) and oral fluoropyrimidine S-1.	Irinotecan	0-24	proteasome 26S subunit, non-ATPase 1	Homo sapiens	182-185
22740861-1	2012	Irinotecan hydrochloride (CPT-11) is reported to be involved in the downregulation of thymidylate synthase (TS), a target molecule of 5-fluorouracil (5-FU) and oral fluoropyrimidine S-1.	Irinotecan	26-32	thymidylate synthetase	Homo sapiens	86-106
22740861-1	2012	Irinotecan hydrochloride (CPT-11) is reported to be involved in the downregulation of thymidylate synthase (TS), a target molecule of 5-fluorouracil (5-FU) and oral fluoropyrimidine S-1.	Irinotecan	26-32	proteasome 26S subunit, non-ATPase 1	Homo sapiens	182-185
22740861-2	2012	Therefore, we hypothesized that a preceding administration of CPT-11 against S-1-resistant tumors may recover sensitivity to S-1.	Irinotecan	62-68	proteasome 26S subunit, non-ATPase 1	Homo sapiens	77-80
22740861-2	2012	Therefore, we hypothesized that a preceding administration of CPT-11 against S-1-resistant tumors may recover sensitivity to S-1.	Irinotecan	62-68	proteasome 26S subunit, non-ATPase 1	Homo sapiens	125-128
22777333-1	2012	OBJECTIVE: S-1 is effective in sequential combination with irinotecan (IRIS) in treating metastatic colorectal cancer.	Irinotecan	59-69	proteasome 26S subunit, non-ATPase 1	Homo sapiens	11-14
22206574-7	2011	The loss of cytoplasmic NF-kappa-B in response to irinotecan was diminished by sorafenib, providing evidence for a possible benefit for this drug combination.	Irinotecan	50-60	nuclear factor kappa B subunit 1	Homo sapiens	24-34
22927913-10	2012	Viability of both XB130-silenced SGC7901 cells and wild-type cells was suppressed by 5-fluorouracil (5-FU), cisplatin, and irinotecan in a dose-dependent way, but cisplatin and irinotecan were more sensitive against sXB130-silenced GC cells and 5-FU showed higher sensitivity to wild-type cells.	Irinotecan	123-133	actin filament associated protein 1 like 2	Homo sapiens	18-23
22927913-10	2012	Viability of both XB130-silenced SGC7901 cells and wild-type cells was suppressed by 5-fluorouracil (5-FU), cisplatin, and irinotecan in a dose-dependent way, but cisplatin and irinotecan were more sensitive against sXB130-silenced GC cells and 5-FU showed higher sensitivity to wild-type cells.	Irinotecan	177-187	actin filament associated protein 1 like 2	Homo sapiens	18-23
22293705-0	2012	[Examination of factors affecting adverse reactions and dosage reduction in UGT1A1 genotyped patients: a retrospective survey of irinotecan].	Irinotecan	129-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
22293705-1	2012	Our aim was to clarify the side effects of irinotecan which occurred in patients admitted to Showa University Hospital to investigate whether the UGT1A1 genetic polymorphism status was reflected in the discontinuation or dose reduction of irinotecan.	Irinotecan	239-249	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
22293705-8	2012	Our investigation confirmed that the UGT1A1 genetic polymorphism status of the patients was reflected in the discontinuance or dose reduction of irinotecan.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
22114188-7	2011	IF7 conjugated to the potent anticancer drug SN-38 and injected intravenously into nude mice carrying human colon HCT116 tumors efficiently suppressed tumor growth at low dosages with no apparent side effects.	Irinotecan	45-50	olfactory receptor family 2 subfamily V member 1	Mus musculus	0-3
22111927-4	2011	A potent and highly selective isoquinoline CHK1 inhibitor (SAR-020106) was identified, which potentiated the efficacies of irinotecan and gemcitabine in SW620 human colon carcinoma xenografts in nude mice.	Irinotecan	123-133	checkpoint kinase 1	Homo sapiens	43-47
21985641-5	2011	UGT1A1 activity correlation analyses using flavonoids-4"-O-glucuronidation vs beta-estradiol-3-glucuronidation (a well-recognized marker for UGT1A1) or vs SN-38 glucuronidation were performed using a bank of HLMs (n = 12) including three UGT1A1-genotyped HLMs (i.e., UGT1A1*1*1, UGT1A1*1*28, and UGT1A1*28*28).	Irinotecan	155-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
21985641-8	2011	In conclusion, UGT1A1-mediated 4"-O-glucuronidation of 3,3",4"-THF and 3,6,4"-THF was highly correlated with the glucuronidation of estradiol (3-OH) and SN-38.	Irinotecan	153-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
21840303-0	2011	Hepatocyte growth factor suppresses the anticancer effect of irinotecan by decreasing the level of active metabolite in HepG2 cells.	Irinotecan	61-71	hepatocyte growth factor	Homo sapiens	0-24
21840303-1	2011	In the liver, carboxylesterase (CES) converts irinotecan (CPT-11) to its active metabolite SN-38, which exerts anticancer effects.	Irinotecan	46-56	carboxylesterase 2	Homo sapiens	14-30
21840303-1	2011	In the liver, carboxylesterase (CES) converts irinotecan (CPT-11) to its active metabolite SN-38, which exerts anticancer effects.	Irinotecan	58-64	carboxylesterase 2	Homo sapiens	14-30
21840303-1	2011	In the liver, carboxylesterase (CES) converts irinotecan (CPT-11) to its active metabolite SN-38, which exerts anticancer effects.	Irinotecan	91-96	carboxylesterase 2	Homo sapiens	14-30
21840303-2	2011	SN-38 is metabolized to an inactive metabolite SN-38 glucuronide by uridine 5"-diphospho-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-116
21840303-2	2011	SN-38 is metabolized to an inactive metabolite SN-38 glucuronide by uridine 5"-diphospho-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-124
21840303-3	2011	Therefore, single nucleotide polymorphisms (SNPs) of the UGT1A1 gene are responsible for the severe adverse effects associated with the disruption of SN-38 metabolism.	Irinotecan	150-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
21840303-4	2011	However, despite having SNPs of the UGT1A1 gene, many patients metabolize SN-38 sufficiently to avoid severe adverse effects.	Irinotecan	74-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
21840303-6	2011	The aim of this study was to evaluate whether HGF alters the metabolism of CPT-11, resulting in a reduction in the anticancer effect of CPT11.	Irinotecan	75-81	hepatocyte growth factor	Homo sapiens	46-49
21840303-7	2011	The cytotoxicity of CPT-11 and SN-38 was evaluated in HepG2 cells pretreated with HGF.	Irinotecan	20-26	hepatocyte growth factor	Homo sapiens	82-85
21840303-7	2011	The cytotoxicity of CPT-11 and SN-38 was evaluated in HepG2 cells pretreated with HGF.	Irinotecan	31-36	hepatocyte growth factor	Homo sapiens	82-85
21840303-9	2011	HGF suppressed the cytotoxicity of CPT-11 by decreasing intracellular SN-38 levels that resulted from a decrease in CES2 and an increase in UGT1A1.	Irinotecan	35-41	hepatocyte growth factor	Homo sapiens	0-3
21840303-9	2011	HGF suppressed the cytotoxicity of CPT-11 by decreasing intracellular SN-38 levels that resulted from a decrease in CES2 and an increase in UGT1A1.	Irinotecan	35-41	carboxylesterase 2	Homo sapiens	116-120
21840303-9	2011	HGF suppressed the cytotoxicity of CPT-11 by decreasing intracellular SN-38 levels that resulted from a decrease in CES2 and an increase in UGT1A1.	Irinotecan	35-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
21840303-9	2011	HGF suppressed the cytotoxicity of CPT-11 by decreasing intracellular SN-38 levels that resulted from a decrease in CES2 and an increase in UGT1A1.	Irinotecan	70-75	hepatocyte growth factor	Homo sapiens	0-3
21840303-9	2011	HGF suppressed the cytotoxicity of CPT-11 by decreasing intracellular SN-38 levels that resulted from a decrease in CES2 and an increase in UGT1A1.	Irinotecan	70-75	carboxylesterase 2	Homo sapiens	116-120
21840303-9	2011	HGF suppressed the cytotoxicity of CPT-11 by decreasing intracellular SN-38 levels that resulted from a decrease in CES2 and an increase in UGT1A1.	Irinotecan	70-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
21840303-12	2011	These results suggest that HGF is a possible causative agent of acquired clinical resistance in chemotherapy with CPT-11 and could be useful as a predictor of clinical resistance.	Irinotecan	114-120	hepatocyte growth factor	Homo sapiens	27-30
21787264-5	2011	In this view, the uridine diphosphate glucuronosil transferase isoform 1A1 (UGT1A1) was associated with significant changes in disposition of CPT-11 and its metabolites, and consequently with treatment-induced toxicities.	Irinotecan	142-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-74
21787264-5	2011	In this view, the uridine diphosphate glucuronosil transferase isoform 1A1 (UGT1A1) was associated with significant changes in disposition of CPT-11 and its metabolites, and consequently with treatment-induced toxicities.	Irinotecan	142-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
21787264-6	2011	However, the complex pharmacokinetics of irinotecan and the involvement of several enzymes other than UGT (i.e., carboxyl estherases, CYP450 isoforms), and transmembrane transporters (ABCB1, ABCC1, ABCG2, SLCO1B1) make difficult the identification of patients with an optimal sensitivity and specificity, and a large part of variability among patients still remains unexplained.	Irinotecan	41-51	ATP binding cassette subfamily B member 1	Homo sapiens	184-189
21787264-6	2011	However, the complex pharmacokinetics of irinotecan and the involvement of several enzymes other than UGT (i.e., carboxyl estherases, CYP450 isoforms), and transmembrane transporters (ABCB1, ABCC1, ABCG2, SLCO1B1) make difficult the identification of patients with an optimal sensitivity and specificity, and a large part of variability among patients still remains unexplained.	Irinotecan	41-51	ATP binding cassette subfamily C member 1	Homo sapiens	191-196
21787264-6	2011	However, the complex pharmacokinetics of irinotecan and the involvement of several enzymes other than UGT (i.e., carboxyl estherases, CYP450 isoforms), and transmembrane transporters (ABCB1, ABCC1, ABCG2, SLCO1B1) make difficult the identification of patients with an optimal sensitivity and specificity, and a large part of variability among patients still remains unexplained.	Irinotecan	41-51	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	198-203
21787264-6	2011	However, the complex pharmacokinetics of irinotecan and the involvement of several enzymes other than UGT (i.e., carboxyl estherases, CYP450 isoforms), and transmembrane transporters (ABCB1, ABCC1, ABCG2, SLCO1B1) make difficult the identification of patients with an optimal sensitivity and specificity, and a large part of variability among patients still remains unexplained.	Irinotecan	41-51	solute carrier organic anion transporter family member 1B1	Homo sapiens	205-212
21652203-6	2011	Although exploratory nature and small sample size may be limitations of this study, these findings indicate that the efficacy of irinotecan plus cetuximab in MCRC patients with wild-type KRAS did not differ by previous sensitivity to irinotecan.	Irinotecan	129-139	KRAS proto-oncogene, GTPase	Homo sapiens	187-191
22077505-3	2011	METHODS: Published papers and publicly accessible genomic databases were searched up to August 2009 to obtain allele and genotype frequencies for UGT1A1*6 and *28, two common variants of UGT1A1, a gene that encodes for a key enzyme in the pathway of irinotecan metabolism.	Irinotecan	250-260	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
22077505-3	2011	METHODS: Published papers and publicly accessible genomic databases were searched up to August 2009 to obtain allele and genotype frequencies for UGT1A1*6 and *28, two common variants of UGT1A1, a gene that encodes for a key enzyme in the pathway of irinotecan metabolism.	Irinotecan	250-260	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
22077505-6	2011	Indians are at an elevated risk of irinotecan-induced neutropenia associated with UGT1A1*28 compared with Chinese and Japanese, and at an even higher risk compared with North American Caucasians.	Irinotecan	35-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
22077505-7	2011	On the other hand, Chinese and Japanese are at an elevated risk of irinotecan-induced neutropenia associated with UGT1A1*6 relative to Indians in Singapore or North American Caucasians.	Irinotecan	67-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
21744079-1	2011	We determined the maximum tolerated dose (MTD) and dose-limiting toxicities (DLT) of the oral vascular endothelial growth factor receptor (VEGFR) inhibitor, sunitinib, when administered with irinotecan among recurrent malignant glioma (MG) patients.	Irinotecan	191-201	kinase insert domain receptor	Homo sapiens	94-137
21744079-1	2011	We determined the maximum tolerated dose (MTD) and dose-limiting toxicities (DLT) of the oral vascular endothelial growth factor receptor (VEGFR) inhibitor, sunitinib, when administered with irinotecan among recurrent malignant glioma (MG) patients.	Irinotecan	191-201	kinase insert domain receptor	Homo sapiens	139-144
21997136-0	2011	An EGFR inhibitor enhances the efficacy of SN38, an active metabolite of irinotecan, in SN38-refractory gastric carcinoma cells.	Irinotecan	73-83	epidermal growth factor receptor	Homo sapiens	3-7
22333276-0	2011	[Study of irinotecan-induced toxicity and its correlation to UGT1A1 gene promoter polymorphisms].	Irinotecan	10-20	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
22333276-1	2011	OBJECTIVES: To investigate the distribution of uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1) gene promoter polymorphism and its relation to the toxicities caused by irinotecan in Chinese patients with cervical cancer and ovarian cancer.	Irinotecan	176-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-94
22333276-1	2011	OBJECTIVES: To investigate the distribution of uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1) gene promoter polymorphism and its relation to the toxicities caused by irinotecan in Chinese patients with cervical cancer and ovarian cancer.	Irinotecan	176-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
22333276-5	2011	The relationship between UGT1A1 gene promoter polymorphism and the toxicity caused by irinotecan was analyzed.	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
21990354-7	2011	Through the Nrf2-dependent increase of proteasomal gene expression and proteasome activity, the sensitivity of NCM460 cells to tumor necrosis factor-related apoptosis-inducing ligand- or irinotecan-induced apoptosis declined.	Irinotecan	187-197	NFE2 like bZIP transcription factor 2	Homo sapiens	12-16
22044840-0	2011	Anticancer drug irinotecan inhibits homomeric 5-HT3A and heteromeric 5-HT3AB receptor responses.	Irinotecan	16-26	5-hydroxytryptamine receptor 3A	Homo sapiens	46-52
21997136-2	2011	This study was performed to clarify the effect of epidermal growth factor receptor (EGFR) inhibitors in combination with SN38, an active metabolite of irinotecan, on the proliferation of irinotecan-refractory gastric cancer.	Irinotecan	187-197	epidermal growth factor receptor	Homo sapiens	50-82
21997136-2	2011	This study was performed to clarify the effect of epidermal growth factor receptor (EGFR) inhibitors in combination with SN38, an active metabolite of irinotecan, on the proliferation of irinotecan-refractory gastric cancer.	Irinotecan	187-197	epidermal growth factor receptor	Homo sapiens	84-88
21997136-7	2011	The combination of an EGFR inhibitor and SN38 significantly increased the levels of apoptosis-related molecules, caspase-6, p53, and DAPK-2, and resulted in the induction of apoptosis of irinotecan-resistant cells.	Irinotecan	187-197	epidermal growth factor receptor	Homo sapiens	22-26
21997136-7	2011	The combination of an EGFR inhibitor and SN38 significantly increased the levels of apoptosis-related molecules, caspase-6, p53, and DAPK-2, and resulted in the induction of apoptosis of irinotecan-resistant cells.	Irinotecan	187-197	death associated protein kinase 2	Homo sapiens	133-139
21997136-8	2011	The EGFR inhibitors increased the S-phase and decreased the UGT1A1 and ABCG expression in irinotecan-resistant cells.	Irinotecan	90-100	epidermal growth factor receptor	Homo sapiens	4-8
21997136-8	2011	The EGFR inhibitors increased the S-phase and decreased the UGT1A1 and ABCG expression in irinotecan-resistant cells.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
21997136-10	2011	CONCLUSION: The combination treatment with an EGFR inhibitor and irinotecan might produce synergistic anti-tumour effects for irinotecan-refractory gastric cancer cells.	Irinotecan	126-136	epidermal growth factor receptor	Homo sapiens	46-50
21869821-3	2011	We genetically modified HB1.F3 (F3) immortalized human NSCs to express rabbit carboxylesterase (rCE) enzyme, which efficiently converts the prodrug CPT-11 (Irinotecan) into an active anti-cancer agent (SN-38).	Irinotecan	148-154	coagulation factor III, tissue factor	Homo sapiens	28-30
21892003-0	2011	Single nucleotide polymorphisms of ABCC5 and ABCG1 transporter genes correlate to irinotecan-associated gastrointestinal toxicity in colorectal cancer patients: a DMET microarray profiling study.	Irinotecan	82-92	ATP binding cassette subfamily C member 5	Homo sapiens	35-40
21869821-3	2011	We genetically modified HB1.F3 (F3) immortalized human NSCs to express rabbit carboxylesterase (rCE) enzyme, which efficiently converts the prodrug CPT-11 (Irinotecan) into an active anti-cancer agent (SN-38).	Irinotecan	156-166	coagulation factor III, tissue factor	Homo sapiens	24-30
21892003-0	2011	Single nucleotide polymorphisms of ABCC5 and ABCG1 transporter genes correlate to irinotecan-associated gastrointestinal toxicity in colorectal cancer patients: a DMET microarray profiling study.	Irinotecan	82-92	ATP binding cassette subfamily G member 1	Homo sapiens	45-50
21892003-1	2011	Recent findings have disclosed the role of UDP-glucuronosyltransferase (UGT) 1A1*28 on the haematological toxicity induced by irinotecan (CPT-11), a drug commonly used in the treatment of metastatic colorectal cancer (mCRC).	Irinotecan	126-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-80
21892003-1	2011	Recent findings have disclosed the role of UDP-glucuronosyltransferase (UGT) 1A1*28 on the haematological toxicity induced by irinotecan (CPT-11), a drug commonly used in the treatment of metastatic colorectal cancer (mCRC).	Irinotecan	138-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-80
21869821-3	2011	We genetically modified HB1.F3 (F3) immortalized human NSCs to express rabbit carboxylesterase (rCE) enzyme, which efficiently converts the prodrug CPT-11 (Irinotecan) into an active anti-cancer agent (SN-38).	Irinotecan	148-154	coagulation factor III, tissue factor	Homo sapiens	24-30
21869821-3	2011	We genetically modified HB1.F3 (F3) immortalized human NSCs to express rabbit carboxylesterase (rCE) enzyme, which efficiently converts the prodrug CPT-11 (Irinotecan) into an active anti-cancer agent (SN-38).	Irinotecan	156-166	coagulation factor III, tissue factor	Homo sapiens	28-30
21892003-10	2011	We have identified 3 SNPs mapping in ABCG1, ABCC5 and OATP1B1/SLCO1B1 transporter genes associated with GI toxicity induced by irinotecan in mCRC patients expanding the available knowledge of irinogenomics.	Irinotecan	127-137	ATP binding cassette subfamily G member 1	Homo sapiens	37-42
21892003-10	2011	We have identified 3 SNPs mapping in ABCG1, ABCC5 and OATP1B1/SLCO1B1 transporter genes associated with GI toxicity induced by irinotecan in mCRC patients expanding the available knowledge of irinogenomics.	Irinotecan	127-137	ATP binding cassette subfamily C member 5	Homo sapiens	44-49
21869821-3	2011	We genetically modified HB1.F3 (F3) immortalized human NSCs to express rabbit carboxylesterase (rCE) enzyme, which efficiently converts the prodrug CPT-11 (Irinotecan) into an active anti-cancer agent (SN-38).	Irinotecan	202-207	coagulation factor III, tissue factor	Homo sapiens	24-30
21892003-10	2011	We have identified 3 SNPs mapping in ABCG1, ABCC5 and OATP1B1/SLCO1B1 transporter genes associated with GI toxicity induced by irinotecan in mCRC patients expanding the available knowledge of irinogenomics.	Irinotecan	127-137	solute carrier organic anion transporter family member 1B1	Homo sapiens	54-61
21869821-3	2011	We genetically modified HB1.F3 (F3) immortalized human NSCs to express rabbit carboxylesterase (rCE) enzyme, which efficiently converts the prodrug CPT-11 (Irinotecan) into an active anti-cancer agent (SN-38).	Irinotecan	202-207	coagulation factor III, tissue factor	Homo sapiens	28-30
21892003-10	2011	We have identified 3 SNPs mapping in ABCG1, ABCC5 and OATP1B1/SLCO1B1 transporter genes associated with GI toxicity induced by irinotecan in mCRC patients expanding the available knowledge of irinogenomics.	Irinotecan	127-137	solute carrier organic anion transporter family member 1B1	Homo sapiens	62-69
21816982-7	2011	Moreover, MDCKII/BCRP/PDZK1 cells are more resistant than MDCKII/BCRP cells to the cytotoxicity of the anticancer agent 7-ethyl-10-hydroxycamptothecin (SN-38), which is a substrate of BCRP.	Irinotecan	120-150	ATP binding cassette subfamily G member 2	Canis lupus familiaris	17-21
21816982-7	2011	Moreover, MDCKII/BCRP/PDZK1 cells are more resistant than MDCKII/BCRP cells to the cytotoxicity of the anticancer agent 7-ethyl-10-hydroxycamptothecin (SN-38), which is a substrate of BCRP.	Irinotecan	120-150	Na(+)/H(+) exchange regulatory cofactor NHE-RF3	Canis lupus familiaris	22-27
21816982-7	2011	Moreover, MDCKII/BCRP/PDZK1 cells are more resistant than MDCKII/BCRP cells to the cytotoxicity of the anticancer agent 7-ethyl-10-hydroxycamptothecin (SN-38), which is a substrate of BCRP.	Irinotecan	120-150	ATP binding cassette subfamily G member 2	Canis lupus familiaris	65-69
21816982-7	2011	Moreover, MDCKII/BCRP/PDZK1 cells are more resistant than MDCKII/BCRP cells to the cytotoxicity of the anticancer agent 7-ethyl-10-hydroxycamptothecin (SN-38), which is a substrate of BCRP.	Irinotecan	120-150	ATP binding cassette subfamily G member 2	Canis lupus familiaris	65-69
21816982-7	2011	Moreover, MDCKII/BCRP/PDZK1 cells are more resistant than MDCKII/BCRP cells to the cytotoxicity of the anticancer agent 7-ethyl-10-hydroxycamptothecin (SN-38), which is a substrate of BCRP.	Irinotecan	152-157	ATP binding cassette subfamily G member 2	Canis lupus familiaris	17-21
21816982-7	2011	Moreover, MDCKII/BCRP/PDZK1 cells are more resistant than MDCKII/BCRP cells to the cytotoxicity of the anticancer agent 7-ethyl-10-hydroxycamptothecin (SN-38), which is a substrate of BCRP.	Irinotecan	152-157	Na(+)/H(+) exchange regulatory cofactor NHE-RF3	Canis lupus familiaris	22-27
21948564-8	2011	Surprisingly, expression of miR-451 caused a decrease in self-renewal, tumorigenicity, and chemoresistance to irinotecan of colonspheres.	Irinotecan	110-120	microRNA 451a	Homo sapiens	28-35
22045708-10	2011	SPECT analyses demonstrated a significant increase in tumoral (99m)Tc-(CO)(3) His-annexin A5 uptake 4 d after bevacizumab treatment and 24 h after irinotecan administration (232.78 +- 24.82 percentage injected dose/tumor weight [g]/body weight [kg], P &lt; 0.05), compared with each monotherapy, indicating a synergistic effect of both therapies.	Irinotecan	147-157	annexin A5	Mus musculus	82-92
22045708-11	2011	CONCLUSION: (99m)Tc-(CO)(3) His-annexin A5 micro-SPECT demonstrates increased antitumor activity of irinotecan during the transient vascular normalization period caused by bevacizumab.	Irinotecan	100-110	annexin A5	Mus musculus	32-42
21529984-6	2011	The expression status of Klotho, and of the ATP-binding cassette (ABC) transporters MRP1, MDR and breast cancer resistant protein (BCRP), which can cause resistance to anticancer drugs, including irinotecan, was assessed by immunohistochemical analysis in resected surgical specimens of patients with early-stage SCLC.	Irinotecan	196-206	ATP binding cassette subfamily C member 1	Homo sapiens	84-88
22045708-0	2011	(99)mTc-(CO)(3) His-annexin A5 micro-SPECT demonstrates increased cell death by irinotecan during the vascular normalization window caused by bevacizumab.	Irinotecan	80-90	annexin A5	Mus musculus	20-30
21948564-12	2011	Furthermore, miR-451 restoration decreases expression of the ATP-binding cassette drug transporter ABCB1 and results in irinotecan sensitization.	Irinotecan	120-130	microRNA 451a	Homo sapiens	13-20
21948564-13	2011	These findings correlate well with the lower expression of miR-451 observed in patients who did not respond to irinotecan-based first-line therapy compared with patients who did.	Irinotecan	111-121	microRNA 451a	Homo sapiens	59-66
21948564-14	2011	Our data suggest that miR-451 is a novel candidate to circumvent recurrence and drug resistance in colorectal cancer and could be used as a marker to predict response to irinotecan in patients with colon carcinoma.	Irinotecan	170-180	microRNA 451a	Homo sapiens	22-29
21918342-14	2011	Cox regression analysis showed that irinotecan-containing regimens were associated with improved overall survival(hazard ratio: 0.	Irinotecan	36-46	cytochrome c oxidase subunit 8A	Homo sapiens	0-3
21210765-2	2011	Irinotecan and topotecan are currently used to treat various types of cancers and many CPT derivatives are being developed.	Irinotecan	0-10	choline phosphotransferase 1	Homo sapiens	87-90
21210765-9	2011	Thus, the present study has identified RECQL5 as a major determinant for CPT resistance in colorectal cancer cells and a potential candidate as a biomarker for irinotecan-based treatment for colon cancer.	Irinotecan	160-170	RecQ like helicase 5	Homo sapiens	39-45
21286718-0	2011	Cetuximab enhances the activities of irinotecan on gastric cancer cell lines through downregulating the EGFR pathway upregulated by irinotecan.	Irinotecan	37-47	epidermal growth factor receptor	Homo sapiens	104-108
21286718-0	2011	Cetuximab enhances the activities of irinotecan on gastric cancer cell lines through downregulating the EGFR pathway upregulated by irinotecan.	Irinotecan	132-142	epidermal growth factor receptor	Homo sapiens	104-108
21286718-6	2011	The effects of cetuximab or irinotecan as single agents or the combination on the expression of p53, p16, and EGFR signaling pathways were also studied.	Irinotecan	28-38	tumor protein p53	Homo sapiens	96-99
21286718-6	2011	The effects of cetuximab or irinotecan as single agents or the combination on the expression of p53, p16, and EGFR signaling pathways were also studied.	Irinotecan	28-38	cyclin dependent kinase inhibitor 2A	Homo sapiens	101-104
21286718-6	2011	The effects of cetuximab or irinotecan as single agents or the combination on the expression of p53, p16, and EGFR signaling pathways were also studied.	Irinotecan	28-38	epidermal growth factor receptor	Homo sapiens	110-114
21286718-8	2011	Irinotecan increases phosphorylation of EGFR, MAPK, and AKT and decreases the expression of P27(Kip1), which could be all abrogated by its combination with cetuximab.	Irinotecan	0-10	epidermal growth factor receptor	Homo sapiens	40-44
21286718-8	2011	Irinotecan increases phosphorylation of EGFR, MAPK, and AKT and decreases the expression of P27(Kip1), which could be all abrogated by its combination with cetuximab.	Irinotecan	0-10	AKT serine/threonine kinase 1	Homo sapiens	56-59
21286718-8	2011	Irinotecan increases phosphorylation of EGFR, MAPK, and AKT and decreases the expression of P27(Kip1), which could be all abrogated by its combination with cetuximab.	Irinotecan	0-10	interferon alpha inducible protein 27	Homo sapiens	92-95
21286718-8	2011	Irinotecan increases phosphorylation of EGFR, MAPK, and AKT and decreases the expression of P27(Kip1), which could be all abrogated by its combination with cetuximab.	Irinotecan	0-10	cyclin dependent kinase inhibitor 1B	Homo sapiens	96-100
21286718-10	2011	CONCLUSIONS                         :                          Cetuximab enhances the activities of irinotecan on GC cells via the downregulation of the EGFR pathway upregulated by irinotecan.	Irinotecan	100-110	epidermal growth factor receptor	Homo sapiens	153-157
21286718-10	2011	CONCLUSIONS                         :                          Cetuximab enhances the activities of irinotecan on GC cells via the downregulation of the EGFR pathway upregulated by irinotecan.	Irinotecan	181-191	epidermal growth factor receptor	Homo sapiens	153-157
20467885-10	2011	Irinotecan and simvastatin combination treatment of A549 and H460 cells increased G(1) phase arrest, which was associated with up-regulation of p21(WAF1/CIP) and p53 compared with irinotecan alone.	Irinotecan	0-10	cyclin dependent kinase inhibitor 1A	Homo sapiens	144-147
20467885-10	2011	Irinotecan and simvastatin combination treatment of A549 and H460 cells increased G(1) phase arrest, which was associated with up-regulation of p21(WAF1/CIP) and p53 compared with irinotecan alone.	Irinotecan	0-10	tumor protein p53	Homo sapiens	162-165
21850716-0	2011	Total synthesis of 7-ethyl-10-hydroxycamptothecin (SN38) and its application to the development of C18-functionalized camptothecin derivatives.	Irinotecan	19-49	Bardet-Biedl syndrome 9	Homo sapiens	99-102
21868538-1	2011	The present study has investigated the effect of panipenem, a widely used antibiotic, on the pharmacokinetics of an active metabolite of irinotecan (CPT-11), 7-ethyl-10-hydroxy-camptothecin (SN-38) and SN-38 glucuronide (SN-38G) produced by uridine-diphosphate glucuronosyltransferase (UGT) 1A isoform-mediated glucuronidation in rats.	Irinotecan	137-147	Ugt1a@	Rattus norvegicus	241-293
21868538-1	2011	The present study has investigated the effect of panipenem, a widely used antibiotic, on the pharmacokinetics of an active metabolite of irinotecan (CPT-11), 7-ethyl-10-hydroxy-camptothecin (SN-38) and SN-38 glucuronide (SN-38G) produced by uridine-diphosphate glucuronosyltransferase (UGT) 1A isoform-mediated glucuronidation in rats.	Irinotecan	149-155	Ugt1a@	Rattus norvegicus	241-293
21868538-3	2011	When the effect of pretreatment with panipenem on glucuronidation activities of substrates for hepatic UGT1A isoforms was investigated using substrates 4-methylumbelliferone (4MU), estradiol and SN-38, the rate of 4MU glucuronide formation was significantly increased, but that of estradiol glucuronide formation was unchanged.	Irinotecan	195-200	Ugt1a@	Rattus norvegicus	103-108
21855038-1	2011	BACKGROUND: This prospective analysis evaluated the effect of tumor KRAS status on efficacy of second-line panitumumab plus folinic acid/5-fluorouracil/irinotecan (FOLFIRI).	Irinotecan	152-162	KRAS proto-oncogene, GTPase	Homo sapiens	68-72
21945893-14	2011	Cox regression analysis showed that irinotecan-containing regimens were associated with improved overall survival(hazard ratio: 0.	Irinotecan	36-46	cytochrome c oxidase subunit 8A	Homo sapiens	0-3
21945437-3	2011	As an early response to DNA damage following CPT-11 treatment, we found that there was an increase in the gammaH2AX(S139) foci number and that total phosphorylation levels were reduced in PC-3 cells following ectopic NKX3.1 expression as well as in LNCaP cells following androgen administration.	Irinotecan	45-51	NK3 homeobox 1	Homo sapiens	217-223
21965746-0	2011	ERas enhances resistance to CPT-11 in gastric cancer.	Irinotecan	28-34	ES cell expressed Ras	Homo sapiens	0-4
21965746-5	2011	RESULTS: ERas-overexpressing clones were significantly more resistant to CPT-11 than were the control (p&lt;0.001).	Irinotecan	73-79	ES cell expressed Ras	Homo sapiens	9-13
21965746-9	2011	CONCLUSION: ERas induces chemoresistance to CPT-11 via activation of phosphatidylinositol-3 kinase-protein kinase beta mTOR pathway and NF-kappaB, and consequently results in up-regulation of ABCG2.	Irinotecan	44-50	ES cell expressed Ras	Homo sapiens	12-16
21965746-9	2011	CONCLUSION: ERas induces chemoresistance to CPT-11 via activation of phosphatidylinositol-3 kinase-protein kinase beta mTOR pathway and NF-kappaB, and consequently results in up-regulation of ABCG2.	Irinotecan	44-50	mechanistic target of rapamycin kinase	Homo sapiens	119-123
21965746-9	2011	CONCLUSION: ERas induces chemoresistance to CPT-11 via activation of phosphatidylinositol-3 kinase-protein kinase beta mTOR pathway and NF-kappaB, and consequently results in up-regulation of ABCG2.	Irinotecan	44-50	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	192-197
21740478-0	2011	Genotype-directed, dose-finding study of irinotecan in cancer patients with UGT1A1*28 and/or UGT1A1*6 polymorphisms.	Irinotecan	41-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
21740478-0	2011	Genotype-directed, dose-finding study of irinotecan in cancer patients with UGT1A1*28 and/or UGT1A1*6 polymorphisms.	Irinotecan	41-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
21740478-1	2011	Irinotecan-induced severe neutropenia is associated with homozygosity for the UGT1A1*28 or UGT1A1*6 alleles.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
21740478-1	2011	Irinotecan-induced severe neutropenia is associated with homozygosity for the UGT1A1*28 or UGT1A1*6 alleles.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
21740478-2	2011	In this study, we determined the maximum-tolerated dose (MTD) of irinotecan in patients with UGT1A1 polymorphisms.	Irinotecan	65-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
21740478-14	2011	Patients homozygous for the UGT1A1*28 or UGT1A1*6 allele can receive irinotecan in a starting dose of 150 mg/m(2), but many required dose reductions or delayed treatment in subsequent cycles.	Irinotecan	69-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
21740478-14	2011	Patients homozygous for the UGT1A1*28 or UGT1A1*6 allele can receive irinotecan in a starting dose of 150 mg/m(2), but many required dose reductions or delayed treatment in subsequent cycles.	Irinotecan	69-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
21452059-8	2011	Further, western blot analyses of xenograft tumors demonstrated that EZN-2208 had significantly more effect than CPT-11 in down-regulating HIF-1alpha, VEGF, Glut1 and MMP2 protein levels.	Irinotecan	113-119	hypoxia inducible factor 1, alpha subunit	Mus musculus	139-149
21452059-8	2011	Further, western blot analyses of xenograft tumors demonstrated that EZN-2208 had significantly more effect than CPT-11 in down-regulating HIF-1alpha, VEGF, Glut1 and MMP2 protein levels.	Irinotecan	113-119	vascular endothelial growth factor A	Mus musculus	151-155
21452059-8	2011	Further, western blot analyses of xenograft tumors demonstrated that EZN-2208 had significantly more effect than CPT-11 in down-regulating HIF-1alpha, VEGF, Glut1 and MMP2 protein levels.	Irinotecan	113-119	solute carrier family 2 (facilitated glucose transporter), member 1	Mus musculus	157-162
21452059-8	2011	Further, western blot analyses of xenograft tumors demonstrated that EZN-2208 had significantly more effect than CPT-11 in down-regulating HIF-1alpha, VEGF, Glut1 and MMP2 protein levels.	Irinotecan	113-119	matrix metallopeptidase 2	Mus musculus	167-171
21771946-2	2011	The UGT1A1 promoter genotype also correlates with toxicity induced by the chemotherapeutic drug irinotecan.	Irinotecan	96-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
22866151-0	2011	Prevalence of topoisomerase I genetic mutations and UGT1A1 polymorphisms associated with irinotecan in individuals of Asian descent.	Irinotecan	89-99	DNA topoisomerase I	Homo sapiens	14-29
21687948-4	2011	Polymorphisms of MRP2, a protein involved in methotrexate, cisplatin and irinotecan active metabolite glucuronide transport, negatively affect platinum-based chemotherapy response.	Irinotecan	73-83	ATP binding cassette subfamily C member 2	Homo sapiens	17-21
22866151-0	2011	Prevalence of topoisomerase I genetic mutations and UGT1A1 polymorphisms associated with irinotecan in individuals of Asian descent.	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
22866151-1	2011	Topoisomerase I (TOP-I) mutations have been shown to be correlated to irinotecan resistance in vitro.	Irinotecan	70-80	DNA topoisomerase I	Homo sapiens	0-15
22866151-1	2011	Topoisomerase I (TOP-I) mutations have been shown to be correlated to irinotecan resistance in vitro.	Irinotecan	70-80	DNA topoisomerase I	Homo sapiens	17-22
22866151-3	2011	On the other hand, polymorphisms of UGT1A1 have been shown to be associated with CPT-11 toxicity in clinical situations.	Irinotecan	81-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
22866151-4	2011	The primary aim of this study was to investigate the prevalence of mutations in the TOP-I exons associated with CPT-11 resistance, including untreated cancer tissue.	Irinotecan	112-118	DNA topoisomerase I	Homo sapiens	84-89
22866151-12	2011	In conclusion, TOP-I genetic mutations correlated to CPT-11 resistance were not detected in any of the subjects and untreated lung cancer tissues.	Irinotecan	53-59	DNA topoisomerase I	Homo sapiens	15-20
21829065-3	2011	In this study, we tested the point mutation of codon 12 and 13 in the KRAS gene by Luminex(xMAP)flow cytometry with sequence-specific oligonucleotide probes for 39 out of 64 unresectable mCRC patients enrolled from Sep 2008 to Oct 2009, who were administered cetuximab in combination with irinotecan(CPT-11)as third-line therapy.	Irinotecan	289-299	KRAS proto-oncogene, GTPase	Homo sapiens	70-74
21046105-10	2011	[(18)F]FLT-PET imaging revealed a 64% decrease in [(18)F]FLT uptake in tumors of HCT116 xenograft-bearing mice treated with a combination of PXD101 and irinotecan, indicating a decrease in thymidine kinase 1 (TK1) activity.	Irinotecan	152-162	thymidine kinase 1	Mus musculus	189-207
21046105-10	2011	[(18)F]FLT-PET imaging revealed a 64% decrease in [(18)F]FLT uptake in tumors of HCT116 xenograft-bearing mice treated with a combination of PXD101 and irinotecan, indicating a decrease in thymidine kinase 1 (TK1) activity.	Irinotecan	152-162	thymidine kinase 1	Mus musculus	209-212
21829065-3	2011	In this study, we tested the point mutation of codon 12 and 13 in the KRAS gene by Luminex(xMAP)flow cytometry with sequence-specific oligonucleotide probes for 39 out of 64 unresectable mCRC patients enrolled from Sep 2008 to Oct 2009, who were administered cetuximab in combination with irinotecan(CPT-11)as third-line therapy.	Irinotecan	300-306	KRAS proto-oncogene, GTPase	Homo sapiens	70-74
21829065-33	2011	Therefore, we concluded that the KRAS mutation in mCRC is a predictive factor for the lack of response to combination therapy with cetuximab plus CPT- 11, as reported in previous clinical studies.	Irinotecan	146-153	KRAS proto-oncogene, GTPase	Homo sapiens	33-37
20072801-0	2011	Phase II study of combination chemotherapy with irinotecan and cetuximab for pretreated metastatic colorectal cancer harboring wild-type KRAS.	Irinotecan	48-58	KRAS proto-oncogene, GTPase	Homo sapiens	137-141
20072801-1	2011	The aim of this study was to prospectively evaluate the efficacy of combination irinotecan and cetuximab chemotherapy in patients with pretreated metastatic colorectal cancer harboring wild-type KRAS.	Irinotecan	80-90	KRAS proto-oncogene, GTPase	Homo sapiens	195-199
21287524-2	2011	The UGT1A1 gene encodes for an enzyme that metabolizes irinotecan, and its genetic variants were shown to be associated with increased drug toxicity.	Irinotecan	55-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
21585235-6	2011	This achievement has led to personalized irinotecan therapy, reflecting ethnic differences in UGT1A1 genotypes, and possible benefits of genetic testing have also been suggested for gemcitabine and tamoxifen therapy, which still requires further validation.	Irinotecan	41-51	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
21868346-1	2011	OBJECTIVE: To evaluate the safety and efficacy of trsatuzumab (Herceptin) combined with FOLFIRI regimen (irinotecan plus 5-FU/LV) in the treatment of HER2-positive advanced gastric cancer.	Irinotecan	105-115	erb-b2 receptor tyrosine kinase 2	Homo sapiens	150-154
21287524-12	2011	CONCLUSIONS: The UGT1A1*28 7/7 genotype is strongly associated with severe hematological toxicity and higher hospitalization rate and predicts lower survival of colorectal cancer in users of irinotecan.	Irinotecan	191-201	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
21733184-0	2011	Irinotecan induces steroid and xenobiotic receptor (SXR) signaling to detoxification pathway in colon cancer cells.	Irinotecan	0-10	nuclear receptor subfamily 1 group I member 2	Homo sapiens	19-50
21733184-0	2011	Irinotecan induces steroid and xenobiotic receptor (SXR) signaling to detoxification pathway in colon cancer cells.	Irinotecan	0-10	nuclear receptor subfamily 1 group I member 2	Homo sapiens	52-55
21733184-5	2011	RESULTS: In this study, we have shown that endogenous SXR is activated in response to SN-38, the active metabolite of the anticancer drug irinotecan, in human colon cancer cell lines.	Irinotecan	86-91	nuclear receptor subfamily 1 group I member 2	Homo sapiens	54-57
21733184-5	2011	RESULTS: In this study, we have shown that endogenous SXR is activated in response to SN-38, the active metabolite of the anticancer drug irinotecan, in human colon cancer cell lines.	Irinotecan	138-148	nuclear receptor subfamily 1 group I member 2	Homo sapiens	54-57
21733184-6	2011	We have found that endogenous SXR translocates into the nucleus and associates with RXR upon SN-38 treatment.	Irinotecan	93-98	nuclear receptor subfamily 1 group I member 2	Homo sapiens	30-33
21733184-6	2011	We have found that endogenous SXR translocates into the nucleus and associates with RXR upon SN-38 treatment.	Irinotecan	93-98	retinoid X receptor alpha	Homo sapiens	84-87
21733184-9	2011	As a consequence, cells overexpressing SXR were found to be less sensitive to irinotecan treatment.	Irinotecan	78-88	nuclear receptor subfamily 1 group I member 2	Homo sapiens	39-42
21733184-10	2011	CONCLUSIONS: Altogether, these results suggest that the SXR pathway is involved in colon cancer irinotecan resistance in colon cancer cell line via the upregulation of select detoxification genes.	Irinotecan	96-106	nuclear receptor subfamily 1 group I member 2	Homo sapiens	56-59
21459094-10	2011	Inhibition of the drug-efflux pump ABCB1 by PSC-833 allowed irinotecan to eradicate tumor-initiating cells.	Irinotecan	60-70	ATP binding cassette subfamily B member 1	Homo sapiens	35-40
21459094-15	2011	CONCLUSIONS: The resistance of colorectal tumors to irinotecan requires the cooperative action of tumor-initiating ALDHhigh/ABCB1negative cells and their differentiated, drug-expelling, ALDHlow/ABCB1positive daughter cells.	Irinotecan	52-62	ATP binding cassette subfamily B member 1	Homo sapiens	124-129
21459094-15	2011	CONCLUSIONS: The resistance of colorectal tumors to irinotecan requires the cooperative action of tumor-initiating ALDHhigh/ABCB1negative cells and their differentiated, drug-expelling, ALDHlow/ABCB1positive daughter cells.	Irinotecan	52-62	ATP binding cassette subfamily B member 1	Homo sapiens	194-199
21464197-6	2011	FLB-12 significantly inhibits the PXR-activated loss of righting reflex to 2,2,2-tribromoethanol (Avertin) in vivo, abrogates PXR-mediated resistance to 7-ethyl-10-hydroxycamptothecin (SN-38) in colon cancer cells in vitro, and attenuates PXR-mediated acetaminophen hepatotoxicity in vivo.	Irinotecan	153-183	nuclear receptor subfamily 1, group I, member 2	Mus musculus	34-37
21566063-8	2011	Coadministration of irinotecan with YHO-13351 significantly increased the survival time of mice inoculated with BCRP-transduced murine leukemia P388 cells and suppressed the tumor growth in an HCT116/BCRP xenograft model, whereas irinotecan alone had little effect in these tumor models.	Irinotecan	20-30	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	112-116
21566063-8	2011	Coadministration of irinotecan with YHO-13351 significantly increased the survival time of mice inoculated with BCRP-transduced murine leukemia P388 cells and suppressed the tumor growth in an HCT116/BCRP xenograft model, whereas irinotecan alone had little effect in these tumor models.	Irinotecan	20-30	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	193-204
21566063-8	2011	Coadministration of irinotecan with YHO-13351 significantly increased the survival time of mice inoculated with BCRP-transduced murine leukemia P388 cells and suppressed the tumor growth in an HCT116/BCRP xenograft model, whereas irinotecan alone had little effect in these tumor models.	Irinotecan	230-240	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	112-116
21566063-1	2011	Breast cancer resistance protein (BCRP/ABCG2) confers resistance to anticancer drugs such as 7-ethyl-10-hydroxycamptothecin (SN-38, an active metabolite of irinotecan), mitoxantrone, and topotecan.	Irinotecan	93-123	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
21566063-1	2011	Breast cancer resistance protein (BCRP/ABCG2) confers resistance to anticancer drugs such as 7-ethyl-10-hydroxycamptothecin (SN-38, an active metabolite of irinotecan), mitoxantrone, and topotecan.	Irinotecan	93-123	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
21566063-1	2011	Breast cancer resistance protein (BCRP/ABCG2) confers resistance to anticancer drugs such as 7-ethyl-10-hydroxycamptothecin (SN-38, an active metabolite of irinotecan), mitoxantrone, and topotecan.	Irinotecan	93-123	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	39-44
21566063-1	2011	Breast cancer resistance protein (BCRP/ABCG2) confers resistance to anticancer drugs such as 7-ethyl-10-hydroxycamptothecin (SN-38, an active metabolite of irinotecan), mitoxantrone, and topotecan.	Irinotecan	125-130	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
21566063-1	2011	Breast cancer resistance protein (BCRP/ABCG2) confers resistance to anticancer drugs such as 7-ethyl-10-hydroxycamptothecin (SN-38, an active metabolite of irinotecan), mitoxantrone, and topotecan.	Irinotecan	125-130	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
21566063-1	2011	Breast cancer resistance protein (BCRP/ABCG2) confers resistance to anticancer drugs such as 7-ethyl-10-hydroxycamptothecin (SN-38, an active metabolite of irinotecan), mitoxantrone, and topotecan.	Irinotecan	125-130	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	39-44
21566063-1	2011	Breast cancer resistance protein (BCRP/ABCG2) confers resistance to anticancer drugs such as 7-ethyl-10-hydroxycamptothecin (SN-38, an active metabolite of irinotecan), mitoxantrone, and topotecan.	Irinotecan	156-166	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
21464197-6	2011	FLB-12 significantly inhibits the PXR-activated loss of righting reflex to 2,2,2-tribromoethanol (Avertin) in vivo, abrogates PXR-mediated resistance to 7-ethyl-10-hydroxycamptothecin (SN-38) in colon cancer cells in vitro, and attenuates PXR-mediated acetaminophen hepatotoxicity in vivo.	Irinotecan	153-183	nuclear receptor subfamily 1, group I, member 2	Mus musculus	126-129
21566063-1	2011	Breast cancer resistance protein (BCRP/ABCG2) confers resistance to anticancer drugs such as 7-ethyl-10-hydroxycamptothecin (SN-38, an active metabolite of irinotecan), mitoxantrone, and topotecan.	Irinotecan	156-166	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
21566063-1	2011	Breast cancer resistance protein (BCRP/ABCG2) confers resistance to anticancer drugs such as 7-ethyl-10-hydroxycamptothecin (SN-38, an active metabolite of irinotecan), mitoxantrone, and topotecan.	Irinotecan	156-166	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	39-44
21566063-3	2011	YHO-13177 potentiated the cytotoxicity of SN-38, mitoxantrone, and topotecan in both BCRP-transduced human colon cancer HCT116 (HCT116/BCRP) cells and SN-38-resistant human lung cancer A549 (A549/SN4) cells that express BCRP, but had little effect in the parental cells.	Irinotecan	42-47	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	85-89
21566063-4	2011	In addition, YHO-13177 potentiated the cytotoxicity of SN-38 in human lung cancer NCI-H460 and NCI-H23, myeloma RPMI-8226, and pancreatic cancer AsPC-1 cells that intrinsically expressed BCRP.	Irinotecan	55-60	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	187-191
21464197-6	2011	FLB-12 significantly inhibits the PXR-activated loss of righting reflex to 2,2,2-tribromoethanol (Avertin) in vivo, abrogates PXR-mediated resistance to 7-ethyl-10-hydroxycamptothecin (SN-38) in colon cancer cells in vitro, and attenuates PXR-mediated acetaminophen hepatotoxicity in vivo.	Irinotecan	153-183	nuclear receptor subfamily 1, group I, member 2	Mus musculus	126-129
21464197-6	2011	FLB-12 significantly inhibits the PXR-activated loss of righting reflex to 2,2,2-tribromoethanol (Avertin) in vivo, abrogates PXR-mediated resistance to 7-ethyl-10-hydroxycamptothecin (SN-38) in colon cancer cells in vitro, and attenuates PXR-mediated acetaminophen hepatotoxicity in vivo.	Irinotecan	185-190	nuclear receptor subfamily 1, group I, member 2	Mus musculus	34-37
21654688-2	2011	Irinotecan is converted into 7-ethyl-10-hydroxycamptothecin (SN-38) by a carboxylsterase and metabolised through uridine diphosphate glucuronosyl transferase (UGT1A1).	Irinotecan	29-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
21576795-3	2011	Therefore, we used the poly(NIPA-co-DMAEMA) nanoparticles as a carrier for the controlled release of a hydrophobic anticancer agent, 7-ethyl-10-hydroxy-camptothecin (SN-38).	Irinotecan	166-171	zinc finger C3HC-type containing 1	Homo sapiens	28-32
21576795-6	2011	The cytotoxicity of the SN-38-loaded poly(NIPA-co-DMAEMA) nanoparticles was investigated in human colon cancer cells (HT-29) to compare with the treatment of an anticancer drug, Irinotecan( ) (CPT-11).	Irinotecan	24-29	zinc finger C3HC-type containing 1	Homo sapiens	42-46
21654688-2	2011	Irinotecan is converted into 7-ethyl-10-hydroxycamptothecin (SN-38) by a carboxylsterase and metabolised through uridine diphosphate glucuronosyl transferase (UGT1A1).	Irinotecan	61-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
21654688-2	2011	Irinotecan is converted into 7-ethyl-10-hydroxycamptothecin (SN-38) by a carboxylsterase and metabolised through uridine diphosphate glucuronosyl transferase (UGT1A1).	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
21486216-4	2011	We show that ONCOFID -S exerts a strong in vitro anti-proliferative activity on CD44 over-expressing rat DHD/K12/trb colon adenocarcinoma cells, as well as on gastric, breast, oesophageal, ovarian and lung human cancer cells, higher than that exerted by unconjugated SN-38.	Irinotecan	267-272	CD44 molecule (Indian blood group)	Rattus norvegicus	80-84
21350582-0	2011	Enhancement of CPT-11 antitumor activity by adenovirus-mediated expression of beta-glucuronidase in tumors.	Irinotecan	15-21	glucuronidase beta	Homo sapiens	78-96
21350582-3	2011	Here, we investigated if local expression of beta-glucuronidase (betaG) on cancer cells to catalytically convert SN38G to SN38 could enhance the antitumor activity of CPT-11.	Irinotecan	167-173	glucuronidase beta	Homo sapiens	45-63
21350582-5	2011	Surface beta-glucuronidase-expressing cells were 20 to 80-fold more sensitive to SN-38G than the parental cells.	Irinotecan	81-86	glucuronidase beta	Homo sapiens	8-26
21350582-6	2011	Intravenous CPT-11 produced significantly greater suppression of CL1-5 and LS174 T tumors that expressed betaG as compared with unmodified tumors.	Irinotecan	12-18	adhesion G protein-coupled receptor L1	Homo sapiens	65-70
21559018-2	2011	The primary aim of our study was to verify a possible correlation between EGFR gene promoter methylation and clinical outcome in metastatic colorectal cancer patients receiving chemotherapy with irinotecan and cetuximab.	Irinotecan	195-205	epidermal growth factor receptor	Homo sapiens	74-78
20949523-11	2011	CONCLUSIONS: Tumor tissue lines established via subrenal capsule xenografting provide models with clinical relevance and the present study suggests that irinotecan could be useful for therapy of refractory prostatic SCC, in particular in combination with cisplatin.	Irinotecan	153-163	serpin family B member 3	Homo sapiens	216-219
21372224-0	2011	Humanized anti-Trop-2 IgG-SN-38 conjugate for effective treatment of diverse epithelial cancers: preclinical studies in human cancer xenograft models and monkeys.	Irinotecan	26-31	tumor associated calcium signal transducer 2	Homo sapiens	15-21
21372224-1	2011	PURPOSE: Evaluate the efficacy of an SN-38-anti-Trop-2 antibody-drug conjugate (ADC) against several human solid tumor types, and to assess its tolerability in mice and monkeys, the latter with tissue cross-reactivity to hRS7 similar to humans.	Irinotecan	37-42	tumor associated calcium signal transducer 2	Homo sapiens	48-54
21372224-2	2011	EXPERIMENTAL DESIGN: Two SN-38 derivatives, CL2-SN-38 and CL2A-SN-38, were conjugated to the anti-Trop-2-humanized antibody, hRS7.	Irinotecan	25-30	endogenous retrovirus group W member 5	Homo sapiens	44-47
21372224-2	2011	EXPERIMENTAL DESIGN: Two SN-38 derivatives, CL2-SN-38 and CL2A-SN-38, were conjugated to the anti-Trop-2-humanized antibody, hRS7.	Irinotecan	25-30	tumor associated calcium signal transducer 2	Homo sapiens	98-104
21372224-7	2011	Exposure of cells to the ADC demonstrated signaling pathways leading to PARP cleavage, but differences versus free SN-38 in p53 and p21 upregulation were noted.	Irinotecan	115-120	tumor protein p53	Homo sapiens	124-127
21372224-7	2011	Exposure of cells to the ADC demonstrated signaling pathways leading to PARP cleavage, but differences versus free SN-38 in p53 and p21 upregulation were noted.	Irinotecan	115-120	H3 histone pseudogene 16	Homo sapiens	132-135
21372224-9	2011	Mice tolerated a dose of 2 x 12 mg/kg (SN-38 equivalents) with only short-lived elevations in ALT and AST liver enzyme levels.	Irinotecan	39-44	transmembrane protease, serine 11d	Mus musculus	102-105
21372224-11	2011	CONCLUSIONS: The anti-Trop-2 hRS7-CL2A-SN-38 ADC provides significant and specific antitumor effects against a range of human solid tumor types.	Irinotecan	39-44	tumor associated calcium signal transducer 2	Homo sapiens	22-28
21721861-11	2011	However, the average expression of Rev-erbalpha, Per2, and Bmal1 were down-regulated 2- to 10-fold with irinotecan at the worst ZT, while being minimally or unaffected at the best ZT, irrespective of sex.	Irinotecan	104-114	nuclear receptor subfamily 1, group D, member 1	Mus musculus	35-47
21721861-11	2011	However, the average expression of Rev-erbalpha, Per2, and Bmal1 were down-regulated 2- to 10-fold with irinotecan at the worst ZT, while being minimally or unaffected at the best ZT, irrespective of sex.	Irinotecan	104-114	period circadian clock 2	Mus musculus	49-53
21721861-11	2011	However, the average expression of Rev-erbalpha, Per2, and Bmal1 were down-regulated 2- to 10-fold with irinotecan at the worst ZT, while being minimally or unaffected at the best ZT, irrespective of sex.	Irinotecan	104-114	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	59-64
21721861-13	2011	The mRNA expressions of irinotecan clock-controlled metabolism genes Ce2, Ugt1a1, and Top1 were unchanged or down-regulated according to irinotecan timing and sex.	Irinotecan	24-34	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	74-80
21721861-13	2011	The mRNA expressions of irinotecan clock-controlled metabolism genes Ce2, Ugt1a1, and Top1 were unchanged or down-regulated according to irinotecan timing and sex.	Irinotecan	137-147	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	74-80
21507240-8	2011	Specific depletion of Mcl-1 from HepG2 cells by RNA interference increases sensitivity of HepG2 cells to chemotherapeutic drugs (i.e. cisplatin and irinotecan).	Irinotecan	148-158	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	22-27
21387285-12	2011	In conclusion, administration of PDGF-R tyrosine kinase inhibitor in combination with irinotecan appears to impair the progressive growth of gastric carcinoma by blockade of PDGF-R signaling pathways in stromal cells.	Irinotecan	86-96	platelet derived growth factor receptor, beta polypeptide	Mus musculus	174-180
21298326-7	2011	Furthermore, the CD26 effect was enhanced when apigenin was paired with chemotherapeutic agents utilized in the treatment of advanced colorectal cancer including irinotecan, 5-fluorouracil and oxaliplatin.	Irinotecan	162-172	dipeptidyl peptidase 4	Homo sapiens	17-21
21166471-8	2011	These findings indicated that Oct-targeted liposomes loaded with CPT-11 may offer considerable potential for MTC chemotherapy because cytotoxicity of both CPT-11 and Oct was enhanced by effective cellular uptake via SSTR2.	Irinotecan	65-71	somatostatin receptor 2	Homo sapiens	216-221
21166471-8	2011	These findings indicated that Oct-targeted liposomes loaded with CPT-11 may offer considerable potential for MTC chemotherapy because cytotoxicity of both CPT-11 and Oct was enhanced by effective cellular uptake via SSTR2.	Irinotecan	155-161	somatostatin receptor 2	Homo sapiens	216-221
21216137-2	2011	In vitro studies have shown that omeprazole can alter the function of metabolic enzymes and transporters that are involved in the metabolism of irinotecan, such as uridine diphosphate glucuronosyltransferase subfamily 1A1 (UGT1A1), cytochrome P-450 enzymes subfamily 3A (CYP3A) and ATP-binding cassette drug-transporter G2 (ABCG2).	Irinotecan	144-154	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	223-229
21635994-6	2011	RESULTS: For the metastatic colorectal cancer LLD population with K-ras wild-type genotype, mean overall survival estimates were 37.7 months for first-line treatment with cetuximab plus FOLFIRI (irinotecan, leucovorin, fluorouracil) and 30.4 months for bevacizumab plus FOLFOX (oxaliplatin, leucovorin, fluorouracil).	Irinotecan	195-205	KRAS proto-oncogene, GTPase	Homo sapiens	66-71
21216137-2	2011	In vitro studies have shown that omeprazole can alter the function of metabolic enzymes and transporters that are involved in the metabolism of irinotecan, such as uridine diphosphate glucuronosyltransferase subfamily 1A1 (UGT1A1), cytochrome P-450 enzymes subfamily 3A (CYP3A) and ATP-binding cassette drug-transporter G2 (ABCG2).	Irinotecan	144-154	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	282-322
21216137-2	2011	In vitro studies have shown that omeprazole can alter the function of metabolic enzymes and transporters that are involved in the metabolism of irinotecan, such as uridine diphosphate glucuronosyltransferase subfamily 1A1 (UGT1A1), cytochrome P-450 enzymes subfamily 3A (CYP3A) and ATP-binding cassette drug-transporter G2 (ABCG2).	Irinotecan	144-154	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	324-329
21499002-7	2011	The patient was started on combined chemotherapy with S-1/CPT-11(S-1 80 mg/body, po, day 1-14 and CPT-11 120 mg/body iv day 1), serum CEA levels returned to normal range, and marked reduction of lymph node size was observed on CT.	Irinotecan	58-64	proteasome 26S subunit, non-ATPase 1	Homo sapiens	65-68
21499002-7	2011	The patient was started on combined chemotherapy with S-1/CPT-11(S-1 80 mg/body, po, day 1-14 and CPT-11 120 mg/body iv day 1), serum CEA levels returned to normal range, and marked reduction of lymph node size was observed on CT.	Irinotecan	58-64	CEA cell adhesion molecule 3	Homo sapiens	134-137
21242184-3	2011	Although she achieved long-term survival of more than 2 years, the last-line chemotherapy, consisting of irinotecan, induced grade 4 febrile neutropenia and her performance status deteriorated even with a reduced dose according to the analysis of UDP-glucuronosyltransferase 1A1.	Irinotecan	105-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	247-278
21366639-4	2011	SN-38 is subsequently detoxified by uridine diphosphate-glycosyltransferase 1, encoded by the UGT1A1 gene.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
21366639-5	2011	It is well known that the variant allele UGT1A*18 is associated with the more common adverse effects of irinotecan.	Irinotecan	104-114	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	41-46
21104178-0	2011	Serum matrilysin correlates with poor survival independently of KRAS and BRAF status in refractory advanced colorectal cancer patients treated with irinotecan plus cetuximab.	Irinotecan	148-158	matrix metallopeptidase 7	Homo sapiens	6-16
22214020-0	2011	[Treatment with CPT-11 based on the UGT1A1 genetic polymorphism].	Irinotecan	16-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
21439039-0	2011	EGFR related mutational status and association to clinical outcome of third-line cetuximab-irinotecan in metastatic colorectal cancer.	Irinotecan	91-101	epidermal growth factor receptor	Homo sapiens	0-4
21468552-5	2011	It has been demonstrated that the UGT1A1*28 polymorphism plays a predictive role in patients administered an irinotecan-containing regimen.	Irinotecan	109-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
21309756-1	2011	Variation of a short (TA)(n) repeat sequence (rs8175347) covering the TATA box of UGT1A1 (UDP-glucuronosyltransferase1A1) is associated with hyperbilirubinaemia (Gilbert"s syndrome) and adverse drug reactions, and is used for dosage advice for irinotecan.	Irinotecan	244-254	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
21309756-1	2011	Variation of a short (TA)(n) repeat sequence (rs8175347) covering the TATA box of UGT1A1 (UDP-glucuronosyltransferase1A1) is associated with hyperbilirubinaemia (Gilbert"s syndrome) and adverse drug reactions, and is used for dosage advice for irinotecan.	Irinotecan	244-254	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-120
21193546-6	2011	In contrast, anti-DLL4 was efficacious against both wild-type and mutant KRAS colon tumors as a single agent and in combination with irinotecan.	Irinotecan	133-143	delta like canonical Notch ligand 4	Homo sapiens	18-22
21193546-7	2011	Further analysis of mutant KRAS tumors indicated that the anti-DLL4/irinotecan combination produced a significant decrease in colon cancer stem cell frequency while promoting apoptosis in tumor cells.	Irinotecan	68-78	KRAS proto-oncogene, GTPase	Homo sapiens	27-31
21193546-7	2011	Further analysis of mutant KRAS tumors indicated that the anti-DLL4/irinotecan combination produced a significant decrease in colon cancer stem cell frequency while promoting apoptosis in tumor cells.	Irinotecan	68-78	delta like canonical Notch ligand 4	Homo sapiens	63-67
21216589-1	2011	The breast cancer resistance protein ABCG2 confers cellular resistance to irinotecan (CPT-11) and its active metabolite SN-38.	Irinotecan	74-84	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	37-42
21216589-1	2011	The breast cancer resistance protein ABCG2 confers cellular resistance to irinotecan (CPT-11) and its active metabolite SN-38.	Irinotecan	86-92	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	37-42
21216589-1	2011	The breast cancer resistance protein ABCG2 confers cellular resistance to irinotecan (CPT-11) and its active metabolite SN-38.	Irinotecan	120-125	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	37-42
21216589-4	2011	Addition of MBLI-87, an acridone derivative inhibitor, significantly increased the irinotecan effect against the growth of ABCG2-expressing xenografts.	Irinotecan	83-93	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	123-128
21216589-5	2011	In vitro, MBLI-87 was as potent as GF120918 against ABCG2-mediated irinotecan efflux, and additionally was specific for ABCG2.	Irinotecan	67-77	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	52-57
21205068-4	2011	The combination of low-dose irinotecan and US irradiation significantly inhibited the tube formation of HUVEC and vascular endothelial growth factor expression of tumor cells in vitro.	Irinotecan	28-38	vascular endothelial growth factor A	Homo sapiens	114-148
21617725-0	2011	Concurrence of UGT1A polymorphism and end-stage renal disease leads to severe toxicities of irinotecan in a patient with metastatic colon cancer.	Irinotecan	92-102	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	15-20
21617725-9	2011	Sequencing analysis of the UGT1A genes found that the patient had variant alleles of UGT1A1*28, UGT1A1*60 and UGT1A9*22, which may lead to decreased glucuronidation and excretion of SN-38, and may account for increased irinotecan-related toxicity.	Irinotecan	182-187	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	27-32
21617725-9	2011	Sequencing analysis of the UGT1A genes found that the patient had variant alleles of UGT1A1*28, UGT1A1*60 and UGT1A9*22, which may lead to decreased glucuronidation and excretion of SN-38, and may account for increased irinotecan-related toxicity.	Irinotecan	182-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
21617725-9	2011	Sequencing analysis of the UGT1A genes found that the patient had variant alleles of UGT1A1*28, UGT1A1*60 and UGT1A9*22, which may lead to decreased glucuronidation and excretion of SN-38, and may account for increased irinotecan-related toxicity.	Irinotecan	182-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
21617725-9	2011	Sequencing analysis of the UGT1A genes found that the patient had variant alleles of UGT1A1*28, UGT1A1*60 and UGT1A9*22, which may lead to decreased glucuronidation and excretion of SN-38, and may account for increased irinotecan-related toxicity.	Irinotecan	182-187	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	110-116
21617725-9	2011	Sequencing analysis of the UGT1A genes found that the patient had variant alleles of UGT1A1*28, UGT1A1*60 and UGT1A9*22, which may lead to decreased glucuronidation and excretion of SN-38, and may account for increased irinotecan-related toxicity.	Irinotecan	219-229	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	27-32
21617725-9	2011	Sequencing analysis of the UGT1A genes found that the patient had variant alleles of UGT1A1*28, UGT1A1*60 and UGT1A9*22, which may lead to decreased glucuronidation and excretion of SN-38, and may account for increased irinotecan-related toxicity.	Irinotecan	219-229	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
21617725-9	2011	Sequencing analysis of the UGT1A genes found that the patient had variant alleles of UGT1A1*28, UGT1A1*60 and UGT1A9*22, which may lead to decreased glucuronidation and excretion of SN-38, and may account for increased irinotecan-related toxicity.	Irinotecan	219-229	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
21617725-9	2011	Sequencing analysis of the UGT1A genes found that the patient had variant alleles of UGT1A1*28, UGT1A1*60 and UGT1A9*22, which may lead to decreased glucuronidation and excretion of SN-38, and may account for increased irinotecan-related toxicity.	Irinotecan	219-229	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	110-116
21617725-11	2011	CONCLUSIONS: UGT1A polymorphisms and renal failure may lead to accumulation of SN-38, which may have played a role in the death of this patient.	Irinotecan	79-84	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	13-18
21617725-12	2011	Irinotecan should be used cautiously in dialysis patients with metastatic colorectal cancer and screening for UGT1A polymorphisms may help in identifying patients with lower SN-38 glucuronidation rates and greater susceptibility to irinotecan-induced toxicity.	Irinotecan	174-179	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	110-115
21617725-12	2011	Irinotecan should be used cautiously in dialysis patients with metastatic colorectal cancer and screening for UGT1A polymorphisms may help in identifying patients with lower SN-38 glucuronidation rates and greater susceptibility to irinotecan-induced toxicity.	Irinotecan	232-242	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	110-115
21390185-8	2011	Axitinib and SN-38 combined treatment greatly inhibited the expression of the ATP7A and ABCG2 genes in endothelial and cancer cells, increasing the SN-38 intracellular concentration.	Irinotecan	13-18	ATPase copper transporting alpha	Homo sapiens	78-83
21390185-8	2011	Axitinib and SN-38 combined treatment greatly inhibited the expression of the ATP7A and ABCG2 genes in endothelial and cancer cells, increasing the SN-38 intracellular concentration.	Irinotecan	13-18	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	88-93
21390185-8	2011	Axitinib and SN-38 combined treatment greatly inhibited the expression of the ATP7A and ABCG2 genes in endothelial and cancer cells, increasing the SN-38 intracellular concentration.	Irinotecan	148-153	ATPase copper transporting alpha	Homo sapiens	78-83
21390185-8	2011	Axitinib and SN-38 combined treatment greatly inhibited the expression of the ATP7A and ABCG2 genes in endothelial and cancer cells, increasing the SN-38 intracellular concentration.	Irinotecan	148-153	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	88-93
21030469-11	2011	In addition, 7-ethyl-10-hydroxycamptothecin, a substrate of UGT1A1 (reported K(m) = 24 muM) seemed to be a weak inhibitor of bilirubin glucuronidation (IC(50) = 356.4 muM) but a partial inhibitor of estradiol-3-glucuronidation.	Irinotecan	13-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
21030469-11	2011	In addition, 7-ethyl-10-hydroxycamptothecin, a substrate of UGT1A1 (reported K(m) = 24 muM) seemed to be a weak inhibitor of bilirubin glucuronidation (IC(50) = 356.4 muM) but a partial inhibitor of estradiol-3-glucuronidation.	Irinotecan	13-43	latexin	Homo sapiens	87-90
21030469-11	2011	In addition, 7-ethyl-10-hydroxycamptothecin, a substrate of UGT1A1 (reported K(m) = 24 muM) seemed to be a weak inhibitor of bilirubin glucuronidation (IC(50) = 356.4 muM) but a partial inhibitor of estradiol-3-glucuronidation.	Irinotecan	13-43	latexin	Homo sapiens	167-170
21194879-5	2011	The chemosensitivity of cell lines with various expression levels of PTEN was evaluated using 5-flurouracil (5-FU), oxaliplatin and irinotecan (CPT), and clinical significance was evaluated by immunohistochemical analysis of 133 CRC specimens.	Irinotecan	132-142	phosphatase and tensin homolog	Homo sapiens	69-73
21188390-0	2011	Predictive value of VEGF gene polymorphisms for metastatic colorectal cancer patients receiving first-line treatment including fluorouracil, irinotecan, and bevacizumab.	Irinotecan	141-151	vascular endothelial growth factor A	Homo sapiens	20-24
20177420-2	2011	Irinotecan"s active metabolite is inactivated by UDP-glucuronosyltransferase 1A1 (UGT1A1), which is deficient in Gilbert"s syndrome.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-80
21159664-0	2011	Targeting the p38 MAPK pathway inhibits irinotecan resistance in colon adenocarcinoma.	Irinotecan	40-50	mitogen-activated protein kinase 14	Homo sapiens	14-17
21159664-6	2011	Moreover, p38 inhibition sensitized tumor cells derived from both SN38-sensitive and -resistant HCT116 cells to irinotecan treatment in xenograft models.	Irinotecan	112-122	mitogen-activated protein kinase 14	Homo sapiens	10-13
21159664-7	2011	Finally, we detected less phosphorylated p38 in primary colon cancer of patients sensitive to irinotecan-based treatment, compared with nonresponder patients.	Irinotecan	94-104	mitogen-activated protein kinase 14	Homo sapiens	41-44
21159664-8	2011	This indicates that enhanced level of phosphorylated p38 could predict the absence of clinical response to irinotecan.	Irinotecan	107-117	mitogen-activated protein kinase 14	Homo sapiens	53-56
21159664-9	2011	Altogether, our results show that the p38 MAPK pathway is involved in irinotecan sensitivity and suggest that phosphorylated p38 expression level could be used as a marker of clinical resistance to irinotecan.	Irinotecan	70-80	mitogen-activated protein kinase 14	Homo sapiens	38-41
21159664-9	2011	Altogether, our results show that the p38 MAPK pathway is involved in irinotecan sensitivity and suggest that phosphorylated p38 expression level could be used as a marker of clinical resistance to irinotecan.	Irinotecan	198-208	mitogen-activated protein kinase 14	Homo sapiens	38-41
21159664-9	2011	Altogether, our results show that the p38 MAPK pathway is involved in irinotecan sensitivity and suggest that phosphorylated p38 expression level could be used as a marker of clinical resistance to irinotecan.	Irinotecan	198-208	mitogen-activated protein kinase 14	Homo sapiens	125-128
21159664-10	2011	They further suggest that targeting the p38 pathway may be a potential strategy to overcome resistance to irinotecan-based chemotherapies in colorectal cancer.	Irinotecan	106-116	mitogen-activated protein kinase 14	Homo sapiens	40-43
20177420-2	2011	Irinotecan"s active metabolite is inactivated by UDP-glucuronosyltransferase 1A1 (UGT1A1), which is deficient in Gilbert"s syndrome.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
20177420-3	2011	Irinotecan and metabolites are transported by P-glycoprotein, encoded by ABCB1.	Irinotecan	0-10	ATP binding cassette subfamily B member 1	Homo sapiens	46-60
20177420-3	2011	Irinotecan and metabolites are transported by P-glycoprotein, encoded by ABCB1.	Irinotecan	0-10	ATP binding cassette subfamily B member 1	Homo sapiens	73-78
21297369-4	2011	Irinotecan, now used for treatments of many cancers, is metabolically activated to SN-38 and then inactivated to SN-38 glucuronide by a UDP-glucuronosyltransferase UGT1A1.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	164-170
20854796-9	2011	Cells incubated with anticancer drugs susceptible to glucuronidation, such as tamoxifen or irinotecan, together with methotrexate, showed a lesser degree of cytotoxicity, due to UGT1A6 induction.	Irinotecan	91-101	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	178-184
21283624-8	2011	We report that the phenotypes arising in mice globally deleted for the Cdc25s are due to the failure of small intestinal stem and progenitor cells to proliferate and that blocking cell division by inhibiting the cell cycle engine (through Cdc25 loss) versus by inducing DNA damage (via irinotecan) provokes a markedly different response of small intestinal epithelial cells.	Irinotecan	286-296	cell division cycle 25C	Mus musculus	71-76
20833148-5	2011	These studies confirm that hiCE demonstrates the most efficient kinetic parameters for CPT-11 activation, however, due to the high levels of hCE1 that are expressed in liver, the latter enzyme can contribute up to 50% of the total of drug hydrolysis in this tissue.	Irinotecan	87-93	carboxylesterase 1	Homo sapiens	141-145
20833148-6	2011	Conversely, in human duodenum, jejunum, ileum and kidney, where hCE1 expression is very low, greater than 99% of the conversion of CPT-11 to SN-38 was mediated by hiCE.	Irinotecan	141-146	carboxylesterase 1	Homo sapiens	64-68
20833148-8	2011	Overall, our studies demonstrate that hCE1 plays a significant role in CPT-11 hydrolysis even though it is up to 100-fold less efficient at drug activation than hiCE, and that drug activation in the intestine and kidney are likely major contributors to SN-38 production in vivo.	Irinotecan	71-77	carboxylesterase 1	Homo sapiens	38-42
20680278-8	2011	CONCLUSIONS: Additional in vitro experiments suggest that these results can be explained by induction of UGT1A1 by methimazole, leading to higher SN-38G concentrations.	Irinotecan	146-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
20833148-8	2011	Overall, our studies demonstrate that hCE1 plays a significant role in CPT-11 hydrolysis even though it is up to 100-fold less efficient at drug activation than hiCE, and that drug activation in the intestine and kidney are likely major contributors to SN-38 production in vivo.	Irinotecan	253-258	carboxylesterase 1	Homo sapiens	38-42
20814789-0	2011	The small-molecule tyrosine kinase inhibitor nilotinib is a potent noncompetitive inhibitor of the SN-38 glucuronidation by human UGT1A1.	Irinotecan	99-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
20354702-2	2011	CPT-11 is mainly activated to SN-38 by carboxylesterase (CES) and then detoxified to SN-38 glucuronide (SN-38G) by UDP-glucuronosyltransferase (UGT) in the liver.	Irinotecan	0-6	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	115-142
20354702-2	2011	CPT-11 is mainly activated to SN-38 by carboxylesterase (CES) and then detoxified to SN-38 glucuronide (SN-38G) by UDP-glucuronosyltransferase (UGT) in the liver.	Irinotecan	0-6	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	144-147
20354702-2	2011	CPT-11 is mainly activated to SN-38 by carboxylesterase (CES) and then detoxified to SN-38 glucuronide (SN-38G) by UDP-glucuronosyltransferase (UGT) in the liver.	Irinotecan	85-90	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	115-142
20354702-2	2011	CPT-11 is mainly activated to SN-38 by carboxylesterase (CES) and then detoxified to SN-38 glucuronide (SN-38G) by UDP-glucuronosyltransferase (UGT) in the liver.	Irinotecan	85-90	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	144-147
20354702-3	2011	SN-38G is excreted via bile and de-conjugated to SN-38 by beta-glucuronidase (beta-GLU) in the intestinal content.	Irinotecan	0-5	glucuronidase, beta	Rattus norvegicus	58-76
20354702-3	2011	SN-38G is excreted via bile and de-conjugated to SN-38 by beta-glucuronidase (beta-GLU) in the intestinal content.	Irinotecan	0-5	glucuronidase, beta	Rattus norvegicus	78-86
20814789-1	2011	PURPOSE: Inhibition of the UDP-glucuronosyltransferase (UGT) 1A1 by nilotinib was examined in vitro with SN-38 as a substrate, to estimate the possibility of drug-drug interaction of nilotinib with other medicines predominantly detoxified by UGT1A1.	Irinotecan	105-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-64
20354702-3	2011	SN-38G is excreted via bile and de-conjugated to SN-38 by beta-glucuronidase (beta-GLU) in the intestinal content.	Irinotecan	49-54	glucuronidase, beta	Rattus norvegicus	58-76
20814789-2	2011	METHODS: Inhibition of UGT1A1-catalyzed SN-38 glucuronidation by nilotinib was examined with human liver microsomes (HLM) and recombinant human UGT1A1 as enzyme sources.	Irinotecan	40-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
20354702-3	2011	SN-38G is excreted via bile and de-conjugated to SN-38 by beta-glucuronidase (beta-GLU) in the intestinal content.	Irinotecan	49-54	glucuronidase, beta	Rattus norvegicus	78-86
20814789-4	2011	RESULTS: Nilotinib potently inhibited the SN-38 glucuronidation by human liver microsomal UGT1A1 and recombinant UGT1A1 in a noncompetitive manner, with K(i) values of 0.286 +- 0.0094 and 0.079 +- 0.0029 muM, respectively.	Irinotecan	42-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
20814789-4	2011	RESULTS: Nilotinib potently inhibited the SN-38 glucuronidation by human liver microsomal UGT1A1 and recombinant UGT1A1 in a noncompetitive manner, with K(i) values of 0.286 +- 0.0094 and 0.079 +- 0.0029 muM, respectively.	Irinotecan	42-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
21609311-3	2011	SN-38 collapsed the mitochondrial membrane potential (MMP), arrested cells in S- and G2-phases of the cell cycle, and induced apoptosis via activation of caspase 3 and PARP.	Irinotecan	0-5	caspase 3	Homo sapiens	154-163
21634054-0	2011	Efficacy of irinotecan in combination with  5-fluorouracil (FOLFIRI) for metastatic gastric or  gastroesophageal junction adenocarcinomas (MGA)  treatment.	Irinotecan	12-22	MAX dimerization protein MGA	Homo sapiens	139-142
22149660-8	2011	RESULTS: We found a significant inhibition of MATE1-mediated MPP uptake by several antineoplastic agents and pH dependent IC(50)values for mitoxantrone (7.8 muM at pH 7.4 and 0.6 muM at pH 8.5) as well as for irinotecan (4.4 muM at pH 7.4 and 1.1 muM at pH 8.5), respectively.	Irinotecan	209-219	solute carrier family 47 member 1	Homo sapiens	46-51
21282945-10	2011	SDHA and GAPDH were the most variable genes in the jejunum and colon where they were 4.4 and 3.2 fold upregulated following irinotecan, respectively.	Irinotecan	124-134	succinate dehydrogenase complex flavoprotein subunit A	Rattus norvegicus	0-4
21282945-10	2011	SDHA and GAPDH were the most variable genes in the jejunum and colon where they were 4.4 and 3.2 fold upregulated following irinotecan, respectively.	Irinotecan	124-134	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	9-14
21609311-3	2011	SN-38 collapsed the mitochondrial membrane potential (MMP), arrested cells in S- and G2-phases of the cell cycle, and induced apoptosis via activation of caspase 3 and PARP.	Irinotecan	0-5	poly(ADP-ribose) polymerase 1	Homo sapiens	168-172
21212430-0	2011	The role of HER-3 expression in the prediction of clinical outcome for advanced colorectal cancer patients receiving irinotecan and cetuximab.	Irinotecan	117-127	erb-b2 receptor tyrosine kinase 3	Homo sapiens	12-17
22016648-9	2011	The acute heart and kidney toxicity of the active metabolite SN-38 from its less toxic prodrug, irinotecan could be differentiated, and two novel gene markers for hormone replacement therapy were identified, namely fabp4 and pparg, which were down-regulated by estradiol treatment.	Irinotecan	61-66	fatty acid binding protein 4, adipocyte	Mus musculus	215-220
22016648-9	2011	The acute heart and kidney toxicity of the active metabolite SN-38 from its less toxic prodrug, irinotecan could be differentiated, and two novel gene markers for hormone replacement therapy were identified, namely fabp4 and pparg, which were down-regulated by estradiol treatment.	Irinotecan	61-66	peroxisome proliferator activated receptor gamma	Mus musculus	225-230
21733405-0	2011	In Situ intestinal perfusion of irinotecan: application to P-gp mediated drug interaction and introduction of an improved HPLC assay.	Irinotecan	32-42	phosphoglycolate phosphatase	Rattus norvegicus	59-63
21733405-1	2011	PURPOSE: To determine experimentally the intestinal permeability of the anticancer prodrug irinotecan, and to quantify the amount of its cytotoxic metabolite SN-38 that is intestinally excreted (exsorped) as a predictor of intestinal toxicity, and to assess the effect of p-glycoprotein (p-gp) inhibitors (verapamil as a model) on the permeability and toxicity of irinotecan.	Irinotecan	158-163	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	272-286
21733405-1	2011	PURPOSE: To determine experimentally the intestinal permeability of the anticancer prodrug irinotecan, and to quantify the amount of its cytotoxic metabolite SN-38 that is intestinally excreted (exsorped) as a predictor of intestinal toxicity, and to assess the effect of p-glycoprotein (p-gp) inhibitors (verapamil as a model) on the permeability and toxicity of irinotecan.	Irinotecan	158-163	phosphoglycolate phosphatase	Rattus norvegicus	288-292
21733405-9	2011	P-gp inhibition using verapamil found to significantly enhance the intestinal permeability of irinotecan and potentially decrease the intestinal toxicity due to SN-38 exposure.	Irinotecan	94-104	phosphoglycolate phosphatase	Rattus norvegicus	0-4
21733405-9	2011	P-gp inhibition using verapamil found to significantly enhance the intestinal permeability of irinotecan and potentially decrease the intestinal toxicity due to SN-38 exposure.	Irinotecan	161-166	phosphoglycolate phosphatase	Rattus norvegicus	0-4
21150467-13	2011	The UGT1A1*6 and UGT1A1*27 genotypes might be useful predictors of grade 4 neutropenia in patients who receive irinotecan-based chemotherapy.	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
21150467-13	2011	The UGT1A1*6 and UGT1A1*27 genotypes might be useful predictors of grade 4 neutropenia in patients who receive irinotecan-based chemotherapy.	Irinotecan	111-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
21473286-2	2011	Especially, SNPs of UTG1A1 and CYP2C19 are important for patients who are treated with irinotecan and proton pump inhibitors, respectively.	Irinotecan	87-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	31-38
21212430-3	2011	The aim of our analysis was to investigate a possible correlation between HER-3 expression and clinical outcome in wild-type K-RAS advanced colorectal cancer patients receiving cetuximab and irinotecan.	Irinotecan	191-201	erb-b2 receptor tyrosine kinase 3	Homo sapiens	74-79
21212430-3	2011	The aim of our analysis was to investigate a possible correlation between HER-3 expression and clinical outcome in wild-type K-RAS advanced colorectal cancer patients receiving cetuximab and irinotecan.	Irinotecan	191-201	KRAS proto-oncogene, GTPase	Homo sapiens	125-130
21985855-0	2011	Successful treatment of a patient with HER2-positive metastatic gastric cancer with third-line combination therapy with irinotecan, 5-fluorouracil, leucovorin and trastuzumab (FOLFIRI-T).	Irinotecan	120-130	erb-b2 receptor tyrosine kinase 2	Homo sapiens	39-43
21212430-4	2011	We retrospectively analyzed immunoreactivity for HER-3 in wild-type K-RAS advanced colorectal cancer patients receiving irinotecan and cetuximab.	Irinotecan	120-130	erb-b2 receptor tyrosine kinase 3	Homo sapiens	49-54
20872237-8	2010	We found that a clinically approved camptothecin analog, irinotecan suppressed the migration, Cdc42 activity, and autophosphorylation of FAK, and attenuated integrin beta1 distribution selectively in LM8 cells.	Irinotecan	57-67	cell division cycle 42	Mus musculus	94-99
21674030-0	2011	Strain- and sex-dependent circadian changes in abcc2 transporter expression: implications for irinotecan chronotolerance in mouse ileum.	Irinotecan	94-104	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	47-52
21674030-1	2011	BACKGROUND: ATP-binding cassette transporter abcc2 is involved in the cellular efflux of irinotecan.	Irinotecan	89-99	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	45-50
21674030-3	2011	Here, we investigate whether circadian changes in local abcc2 expression participate in the circadian rhythm of irinotecan toxicity for ileum mucosa, and further assess whether genetic background or sex modify this relation.	Irinotecan	112-122	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	56-61
21674030-13	2011	CONCLUSIONS/SIGNIFICANCE: Strain- and sex-dependent circadian patterns in abcc2 expressions displayed robust relations with the chronotolerance of ileum mucosa for irinotecan.	Irinotecan	164-174	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	74-79
21355292-9	2011	CONCLUSION: GSTA and ZNF subunit genes might play an important regulation role in the irinotecan resistance of colon cancer.	Irinotecan	86-96	zinc finger protein 763	Homo sapiens	21-24
22041697-3	2011	Organic anion transporting polypeptide 1B1 (OATP1B1, gene SLCO1B1) is expressed on the basolateral membrane of hepatocytes and can facilitate hepatic uptake of certain clinically relevant drugs such as statins except for fluvastatin, angiotensin converting enzyme inhibitors, angiotensin II receptor antagonists, antidiabetic drug (repaglinide) and anticancer drugs (SN-38 and methotrexate).	Irinotecan	367-372	solute carrier organic anion transporter family member 1B1	Homo sapiens	0-42
22041697-3	2011	Organic anion transporting polypeptide 1B1 (OATP1B1, gene SLCO1B1) is expressed on the basolateral membrane of hepatocytes and can facilitate hepatic uptake of certain clinically relevant drugs such as statins except for fluvastatin, angiotensin converting enzyme inhibitors, angiotensin II receptor antagonists, antidiabetic drug (repaglinide) and anticancer drugs (SN-38 and methotrexate).	Irinotecan	367-372	solute carrier organic anion transporter family member 1B1	Homo sapiens	44-51
22041697-3	2011	Organic anion transporting polypeptide 1B1 (OATP1B1, gene SLCO1B1) is expressed on the basolateral membrane of hepatocytes and can facilitate hepatic uptake of certain clinically relevant drugs such as statins except for fluvastatin, angiotensin converting enzyme inhibitors, angiotensin II receptor antagonists, antidiabetic drug (repaglinide) and anticancer drugs (SN-38 and methotrexate).	Irinotecan	367-372	solute carrier organic anion transporter family member 1B1	Homo sapiens	58-65
22041697-5	2011	For examples, the SLCO1B1*15 haplotype (or 521T&gt;C genotype) results in decreased uptake activity of SN-38 from systemic circulation, leading to increased plasma concentration of SN-38 and an enhanced risk of neutropenia.	Irinotecan	103-108	solute carrier organic anion transporter family member 1B1	Homo sapiens	18-25
22041697-5	2011	For examples, the SLCO1B1*15 haplotype (or 521T&gt;C genotype) results in decreased uptake activity of SN-38 from systemic circulation, leading to increased plasma concentration of SN-38 and an enhanced risk of neutropenia.	Irinotecan	181-186	solute carrier organic anion transporter family member 1B1	Homo sapiens	18-25
21208842-1	2010	BACKGROUND: The aim of this multicenter phase II study was to demonstrate the activity of the epidermal growth factor receptor (EGFR)-targeting monoclonal antibody cetuximab combined with irinotecan in the treatment of Latin American patients with EGFR-expressing metastatic colorectal cancer (mCRC) in whom previous treatment with an irinotecan-containing regimen had failed.	Irinotecan	335-345	epidermal growth factor receptor	Homo sapiens	94-126
21208842-1	2010	BACKGROUND: The aim of this multicenter phase II study was to demonstrate the activity of the epidermal growth factor receptor (EGFR)-targeting monoclonal antibody cetuximab combined with irinotecan in the treatment of Latin American patients with EGFR-expressing metastatic colorectal cancer (mCRC) in whom previous treatment with an irinotecan-containing regimen had failed.	Irinotecan	335-345	epidermal growth factor receptor	Homo sapiens	128-132
20872237-8	2010	We found that a clinically approved camptothecin analog, irinotecan suppressed the migration, Cdc42 activity, and autophosphorylation of FAK, and attenuated integrin beta1 distribution selectively in LM8 cells.	Irinotecan	57-67	PTK2 protein tyrosine kinase 2	Mus musculus	137-140
20872237-8	2010	We found that a clinically approved camptothecin analog, irinotecan suppressed the migration, Cdc42 activity, and autophosphorylation of FAK, and attenuated integrin beta1 distribution selectively in LM8 cells.	Irinotecan	57-67	integrin beta 1 (fibronectin receptor beta)	Mus musculus	157-171
20847137-3	2010	In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine.	Irinotecan	233-243	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	77-83
20583968-1	2010	The ATP-binding cassette transporters P-glycoprotein (ABCB1, MDR1) and multidrug resistance protein 4 (MRP4) efflux irinotecan and its active metabolite SN-38 in vitro, and thus may contribute to system clearance of these compounds.	Irinotecan	116-126	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	61-65
20583968-1	2010	The ATP-binding cassette transporters P-glycoprotein (ABCB1, MDR1) and multidrug resistance protein 4 (MRP4) efflux irinotecan and its active metabolite SN-38 in vitro, and thus may contribute to system clearance of these compounds.	Irinotecan	116-126	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	71-101
20583968-1	2010	The ATP-binding cassette transporters P-glycoprotein (ABCB1, MDR1) and multidrug resistance protein 4 (MRP4) efflux irinotecan and its active metabolite SN-38 in vitro, and thus may contribute to system clearance of these compounds.	Irinotecan	116-126	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	103-107
20583968-1	2010	The ATP-binding cassette transporters P-glycoprotein (ABCB1, MDR1) and multidrug resistance protein 4 (MRP4) efflux irinotecan and its active metabolite SN-38 in vitro, and thus may contribute to system clearance of these compounds.	Irinotecan	153-158	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	54-59
20583968-1	2010	The ATP-binding cassette transporters P-glycoprotein (ABCB1, MDR1) and multidrug resistance protein 4 (MRP4) efflux irinotecan and its active metabolite SN-38 in vitro, and thus may contribute to system clearance of these compounds.	Irinotecan	116-126	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	54-59
20847137-3	2010	In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine.	Irinotecan	233-243	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	99-105
20583968-1	2010	The ATP-binding cassette transporters P-glycoprotein (ABCB1, MDR1) and multidrug resistance protein 4 (MRP4) efflux irinotecan and its active metabolite SN-38 in vitro, and thus may contribute to system clearance of these compounds.	Irinotecan	153-158	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	61-65
20583968-1	2010	The ATP-binding cassette transporters P-glycoprotein (ABCB1, MDR1) and multidrug resistance protein 4 (MRP4) efflux irinotecan and its active metabolite SN-38 in vitro, and thus may contribute to system clearance of these compounds.	Irinotecan	153-158	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	71-101
20847137-5	2010	CYP3A4.16 exhibited intrinsic clearances (V(max)/K(m)) that were lowered considerably (by 84-60%) for metabolism of midazolam, carbamazepine, atorvastatin, paclitaxel, and irinotecan compared with CYP3A4.1 due to increased K(m) with or without decreased V(max) values, whereas no apparent decrease in intrinsic clearance was observed for docetaxel.	Irinotecan	172-182	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
20583968-1	2010	The ATP-binding cassette transporters P-glycoprotein (ABCB1, MDR1) and multidrug resistance protein 4 (MRP4) efflux irinotecan and its active metabolite SN-38 in vitro, and thus may contribute to system clearance of these compounds.	Irinotecan	153-158	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	103-107
20583968-4	2010	Mdr1a/b genotype was a significant covariate for the clearance of both irinotecan lactone and SN-38 lactone.	Irinotecan	71-89	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	0-5
20847137-5	2010	CYP3A4.16 exhibited intrinsic clearances (V(max)/K(m)) that were lowered considerably (by 84-60%) for metabolism of midazolam, carbamazepine, atorvastatin, paclitaxel, and irinotecan compared with CYP3A4.1 due to increased K(m) with or without decreased V(max) values, whereas no apparent decrease in intrinsic clearance was observed for docetaxel.	Irinotecan	172-182	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	197-203
20583968-4	2010	Mdr1a/b genotype was a significant covariate for the clearance of both irinotecan lactone and SN-38 lactone.	Irinotecan	94-107	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	0-5
20583968-5	2010	Exposures to irinotecan lactone and SN-38 lactone after a 40 mg/kg dose were 1.6-fold higher in Mdr1a/b(-/-) mice compared to wild-type mice.	Irinotecan	13-31	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	96-101
20583968-5	2010	Exposures to irinotecan lactone and SN-38 lactone after a 40 mg/kg dose were 1.6-fold higher in Mdr1a/b(-/-) mice compared to wild-type mice.	Irinotecan	36-49	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	96-101
20583968-7	2010	These results suggest that P-gp plays a role in irinotecan and SN-38 elimination, but Mrp4 does not affect irinotecan or SN-38 plasma pharmacokinetics.	Irinotecan	48-58	phosphoglycolate phosphatase	Mus musculus	27-31
20583968-7	2010	These results suggest that P-gp plays a role in irinotecan and SN-38 elimination, but Mrp4 does not affect irinotecan or SN-38 plasma pharmacokinetics.	Irinotecan	63-68	phosphoglycolate phosphatase	Mus musculus	27-31
20847137-6	2010	On the other hand, K(m) values for CYP3A4.18 were comparable to those for CYP3A4.1 for all substrates except terfenadine; but V(max) values were lower for midazolam, paclitaxel, docetaxel, and irinotecan, resulting in partially reduced intrinsic clearance values (by 34-52%).	Irinotecan	193-203	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	35-41
20889729-8	2010	This synergy was not universal but, when observed (Susa S/R, H1975, H358, and MDA-MB-231 cell lines), was related to SN-38 intracellular accumulation (2.2- to 4.8-fold increase, P &lt; 0.05 for each), attributable to the inhibition of the breast cancer-related protein (BCRP) efflux pump by lapatinib.	Irinotecan	117-122	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	239-268
20198621-0	2010	Synergistic antitumor activity of the SN-38-incorporating polymeric micelles NK012 with S-1 in a mouse model of non-small cell lung cancer.	Irinotecan	38-43	proteasome (prosome, macropain) 26S subunit, non-ATPase, 1	Mus musculus	88-91
20198621-1	2010	The combination therapy of CPT-11, a prodrug of SN-38, with S-1, a dihydropyrimidine dehydrogenase inhibitory fluoropyrimidine, shows a high clinical response rate in non-small cell lung cancer (NSCLC).	Irinotecan	27-33	proteasome (prosome, macropain) 26S subunit, non-ATPase, 1	Mus musculus	60-63
19862647-0	2010	MDR1 polymorphism role in patients treated with cetuximab and irinotecan in irinotecan refractory colorectal cancer.	Irinotecan	62-72	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
19862647-0	2010	MDR1 polymorphism role in patients treated with cetuximab and irinotecan in irinotecan refractory colorectal cancer.	Irinotecan	76-86	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
19862647-1	2010	The aim of the study was to evaluate the influence of the MDR1 C3435T polymorphism on the therapeutic response in 23 patients treated with cetuximab plus irinotecan for irinotecan refractory liver metastatic colorectal cancer considering their KRAS status.	Irinotecan	154-164	ATP binding cassette subfamily B member 1	Homo sapiens	58-62
19862647-1	2010	The aim of the study was to evaluate the influence of the MDR1 C3435T polymorphism on the therapeutic response in 23 patients treated with cetuximab plus irinotecan for irinotecan refractory liver metastatic colorectal cancer considering their KRAS status.	Irinotecan	169-179	ATP binding cassette subfamily B member 1	Homo sapiens	58-62
19862647-2	2010	Indeed, irinotecan and its active metabolite (SN-38) are both substrates of P-glycoprotein (P-gp) encoded by MDR1.	Irinotecan	8-18	ATP binding cassette subfamily B member 1	Homo sapiens	76-90
19862647-2	2010	Indeed, irinotecan and its active metabolite (SN-38) are both substrates of P-glycoprotein (P-gp) encoded by MDR1.	Irinotecan	8-18	ATP binding cassette subfamily B member 1	Homo sapiens	92-96
19862647-2	2010	Indeed, irinotecan and its active metabolite (SN-38) are both substrates of P-glycoprotein (P-gp) encoded by MDR1.	Irinotecan	8-18	ATP binding cassette subfamily B member 1	Homo sapiens	109-113
19862647-2	2010	Indeed, irinotecan and its active metabolite (SN-38) are both substrates of P-glycoprotein (P-gp) encoded by MDR1.	Irinotecan	46-51	ATP binding cassette subfamily B member 1	Homo sapiens	76-90
19862647-2	2010	Indeed, irinotecan and its active metabolite (SN-38) are both substrates of P-glycoprotein (P-gp) encoded by MDR1.	Irinotecan	46-51	ATP binding cassette subfamily B member 1	Homo sapiens	92-96
19862647-2	2010	Indeed, irinotecan and its active metabolite (SN-38) are both substrates of P-glycoprotein (P-gp) encoded by MDR1.	Irinotecan	46-51	ATP binding cassette subfamily B member 1	Homo sapiens	109-113
19862647-9	2010	These results suggest that EGFR inhibition by cetuximab may overcome this irinotecan resistance by abrogating drug efflux depending on MDR1 3435 polymorphism.	Irinotecan	74-84	epidermal growth factor receptor	Homo sapiens	27-31
19862647-9	2010	These results suggest that EGFR inhibition by cetuximab may overcome this irinotecan resistance by abrogating drug efflux depending on MDR1 3435 polymorphism.	Irinotecan	74-84	ATP binding cassette subfamily B member 1	Homo sapiens	135-139
20889729-8	2010	This synergy was not universal but, when observed (Susa S/R, H1975, H358, and MDA-MB-231 cell lines), was related to SN-38 intracellular accumulation (2.2- to 4.8-fold increase, P &lt; 0.05 for each), attributable to the inhibition of the breast cancer-related protein (BCRP) efflux pump by lapatinib.	Irinotecan	117-122	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	270-274
21151408-2	2010	This paper uses a case-based approach to summarize the consensus recommendations developed during that meeting.These are the consensus recommendations:Testing for the KRAS status of the tumour should be performed as soon as an egfr inhibitor is being considered as an option for treatment.Anti-egfr therapies are not recommended for the treatment of patients with tumours showing mutated KRAS status.For a patient with wild-type KRAS and an Eastern Cooperative Oncology Group status of 0-2, whose mcrc has previously been treated with a fluoropyrimidine, irinotecan, and oxaliplatin, switching to an egfr inhibitor is a recommended strategy.Cetuximab, cetuximab plus irinotecan, and panitumumab are all options for third-line therapy in patients with wild-type KRAS, provided that tolerability is acceptable.	Irinotecan	555-565	KRAS proto-oncogene, GTPase	Homo sapiens	167-171
21042746-5	2010	Combinations of CG2 with SN38 (the active form of irinotecan), 5FU, or oxaliplatin were more effective than the agents alone when used to inhibit the growth of HCT116 cells.	Irinotecan	50-60	transmembrane protein 245	Homo sapiens	16-19
21042746-6	2010	The protein expressions of acetyl-H3, p21, caspase-3, -8, and -9, PARP, and XIAP were affected in a time- and dose-dependent manner in HCT116 cells treated with the CG2 alone or combined CG2 and SN-38.	Irinotecan	195-200	caspase 3	Homo sapiens	43-64
21042746-6	2010	The protein expressions of acetyl-H3, p21, caspase-3, -8, and -9, PARP, and XIAP were affected in a time- and dose-dependent manner in HCT116 cells treated with the CG2 alone or combined CG2 and SN-38.	Irinotecan	195-200	transmembrane protein 245	Homo sapiens	165-168
21151408-2	2010	This paper uses a case-based approach to summarize the consensus recommendations developed during that meeting.These are the consensus recommendations:Testing for the KRAS status of the tumour should be performed as soon as an egfr inhibitor is being considered as an option for treatment.Anti-egfr therapies are not recommended for the treatment of patients with tumours showing mutated KRAS status.For a patient with wild-type KRAS and an Eastern Cooperative Oncology Group status of 0-2, whose mcrc has previously been treated with a fluoropyrimidine, irinotecan, and oxaliplatin, switching to an egfr inhibitor is a recommended strategy.Cetuximab, cetuximab plus irinotecan, and panitumumab are all options for third-line therapy in patients with wild-type KRAS, provided that tolerability is acceptable.	Irinotecan	667-677	KRAS proto-oncogene, GTPase	Homo sapiens	167-171
21472350-1	2010	Irinotecan (CTP-11) is a topoisomerase I inhibitor used in the treatment of colorectal cancer and non-small cell lung cancer (NSCLC).	Irinotecan	0-10	SPANX family member C	Homo sapiens	12-18
20829196-7	2010	Interestingly, multidrug-resistant cell lines that overexpressed P-glycoprotein (P-gp), multidrug resistance-associated proteins, and breast cancer resistance protein were rendered resistant to docetaxel, vinblastine, SN-38, and doxorubicin, but not to I-387.	Irinotecan	218-223	ATP binding cassette subfamily B member 1	Homo sapiens	65-79
20829196-7	2010	Interestingly, multidrug-resistant cell lines that overexpressed P-glycoprotein (P-gp), multidrug resistance-associated proteins, and breast cancer resistance protein were rendered resistant to docetaxel, vinblastine, SN-38, and doxorubicin, but not to I-387.	Irinotecan	218-223	ATP binding cassette subfamily B member 1	Homo sapiens	81-85
20829196-7	2010	Interestingly, multidrug-resistant cell lines that overexpressed P-glycoprotein (P-gp), multidrug resistance-associated proteins, and breast cancer resistance protein were rendered resistant to docetaxel, vinblastine, SN-38, and doxorubicin, but not to I-387.	Irinotecan	218-223	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	134-166
21472350-3	2010	We isolated irinotecan-resistant human NSCLC A549 cells, termed A549/CTP-11R cells.	Irinotecan	12-22	SPANX family member C	Homo sapiens	69-75
21472350-4	2010	A549/CTP-11R cells were resistant to irinotecan, as well as paclitaxel, gemcitabine and carboplatin.	Irinotecan	37-47	SPANX family member C	Homo sapiens	5-11
21472350-5	2010	Curcumin, a nuclear factor-kappaB (NF-kappaB) inhibitor, increased the sensitivity to irinotecan of A549/CTP-11R cells.	Irinotecan	86-96	nuclear factor kappa B subunit 1	Homo sapiens	35-44
21472350-5	2010	Curcumin, a nuclear factor-kappaB (NF-kappaB) inhibitor, increased the sensitivity to irinotecan of A549/CTP-11R cells.	Irinotecan	86-96	SPANX family member C	Homo sapiens	105-111
20039040-1	2010	BACKGROUND: Expression of the DNA repair protein O (6)-methylguanine-DNA methyltransferase (MGMT) correlates with resistance to irinotecan in colorectal cancer cell lines.	Irinotecan	128-138	O-6-methylguanine-DNA methyltransferase	Homo sapiens	92-96
20924375-0	2010	Activity of irinotecan and temozolomide in the presence of O6-methylguanine-DNA methyltransferase inhibition in neuroblastoma pre-clinical models.	Irinotecan	12-22	O-6-methylguanine-DNA methyltransferase	Homo sapiens	59-97
20924375-3	2010	Using neuroblastoma pre-clinical models, we determined whether the inhibition of MGMT by O(6)-benzylguanine (O6-BG) could enhance the anti-tumour activity of TMZ and irinotecan.	Irinotecan	166-176	O-6-methylguanine-DNA methyltransferase	Homo sapiens	81-85
19967559-1	2010	Breast cancer resistance protein (BCRP/ABCG2), an ATP-binding cassette half transporter, confers multidrug resistance (MDR) to a series of antitumor agents such as mitoxantrone, daunorubicin, SN-38, and topotecan, and often limits the efficacy of chemotherapy.	Irinotecan	192-197	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
19967559-1	2010	Breast cancer resistance protein (BCRP/ABCG2), an ATP-binding cassette half transporter, confers multidrug resistance (MDR) to a series of antitumor agents such as mitoxantrone, daunorubicin, SN-38, and topotecan, and often limits the efficacy of chemotherapy.	Irinotecan	192-197	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
19967559-1	2010	Breast cancer resistance protein (BCRP/ABCG2), an ATP-binding cassette half transporter, confers multidrug resistance (MDR) to a series of antitumor agents such as mitoxantrone, daunorubicin, SN-38, and topotecan, and often limits the efficacy of chemotherapy.	Irinotecan	192-197	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	39-44
20099280-0	2010	Insulin-like growth factor 1 expression correlates with clinical outcome in K-RAS wild type colorectal cancer patients treated with cetuximab and irinotecan.	Irinotecan	146-156	insulin like growth factor 1	Homo sapiens	0-28
20099280-0	2010	Insulin-like growth factor 1 expression correlates with clinical outcome in K-RAS wild type colorectal cancer patients treated with cetuximab and irinotecan.	Irinotecan	146-156	KRAS proto-oncogene, GTPase	Homo sapiens	76-81
20099280-4	2010	IGF-1 expression and K-RAS mutational status was assessed in advanced colorectal cancer patients receiving irinotecan/cetuximab.	Irinotecan	107-117	insulin like growth factor 1	Homo sapiens	0-5
20099280-9	2010	Among K-RAS wild type patients, IGF-1 negative and positive tumors showed a partial response to cetuximab-irinotecan in 13 (65%) and 11 (22%) cases, respectively (p = 0.002).	Irinotecan	106-116	insulin like growth factor 1	Homo sapiens	32-37
21036743-4	2010	RESULTS: High intratumoral gene expression levels of EGFR, VEGFR2 and NRP1 were associated with longer overall survival (OS) in patients receiving combined monoclonal antibodies with or without irinotecan.	Irinotecan	194-204	epidermal growth factor receptor	Homo sapiens	53-57
21036743-4	2010	RESULTS: High intratumoral gene expression levels of EGFR, VEGFR2 and NRP1 were associated with longer overall survival (OS) in patients receiving combined monoclonal antibodies with or without irinotecan.	Irinotecan	194-204	kinase insert domain receptor	Homo sapiens	59-65
21036743-4	2010	RESULTS: High intratumoral gene expression levels of EGFR, VEGFR2 and NRP1 were associated with longer overall survival (OS) in patients receiving combined monoclonal antibodies with or without irinotecan.	Irinotecan	194-204	neuropilin 1	Homo sapiens	70-74
20066420-0	2010	Se-methylselenocysteine sensitizes hypoxic tumor cells to irinotecan by targeting hypoxia-inducible factor 1alpha.	Irinotecan	58-68	hypoxia inducible factor 1 subunit alpha	Homo sapiens	82-113
20066420-8	2010	CONCLUSIONS: Our results show that HIF-1alpha is a critical target for MSC and its inhibition was associated with enhanced antitumor activity of irinotecan.	Irinotecan	145-155	hypoxia inducible factor 1 subunit alpha	Homo sapiens	35-45
20811661-0	2010	Irinotecan overcomes the resistance to 5-fluorouracil in human colon cancer xenografts by down-regulation of intratumoral thymidylate synthase.	Irinotecan	0-10	thymidylate synthetase	Homo sapiens	122-142
20682600-4	2010	This study aims to characterize the expression of multiple MMPs including MMP-1, -2, -3, -9 and -12 and their inhibitors, tissue inhibitor of metalloproteinase (TIMP)-1 and -2, in a rat model of irinotecan-induced mucositis.	Irinotecan	195-205	matrix metallopeptidase 1	Rattus norvegicus	59-63
20682600-4	2010	This study aims to characterize the expression of multiple MMPs including MMP-1, -2, -3, -9 and -12 and their inhibitors, tissue inhibitor of metalloproteinase (TIMP)-1 and -2, in a rat model of irinotecan-induced mucositis.	Irinotecan	195-205	matrix metallopeptidase 1	Rattus norvegicus	74-99
20682600-4	2010	This study aims to characterize the expression of multiple MMPs including MMP-1, -2, -3, -9 and -12 and their inhibitors, tissue inhibitor of metalloproteinase (TIMP)-1 and -2, in a rat model of irinotecan-induced mucositis.	Irinotecan	195-205	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	122-175
20682600-8	2010	A significant alteration in both gene expression and tissue levels of MMPs and TIMPs was noted following irinotecan.	Irinotecan	105-115	matrix metallopeptidase 1	Rattus norvegicus	70-74
20682600-11	2010	TIMP-1 and -2 levels were significantly altered in the jejunum following irinotecan.	Irinotecan	73-83	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	0-13
20682600-12	2010	The augmentation in the expression profiles of MMPs and their inhibitors correlated with histopathological alterations observed in the tissue following irinotecan.	Irinotecan	152-162	matrix metallopeptidase 1	Rattus norvegicus	47-51
20811661-6	2010	CPT-11, but not l-OHP, induced a decrease in activities and protein levels of TS and an increase in those of RNR in KM12C/5-FU tumors only, which was likely related to decreased expressions of several proteins in G1/S phase of the cells including CDK4, pRB, and E2F1 in these tumors.	Irinotecan	0-6	thymidylate synthetase	Homo sapiens	78-80
20811661-6	2010	CPT-11, but not l-OHP, induced a decrease in activities and protein levels of TS and an increase in those of RNR in KM12C/5-FU tumors only, which was likely related to decreased expressions of several proteins in G1/S phase of the cells including CDK4, pRB, and E2F1 in these tumors.	Irinotecan	0-6	cyclin dependent kinase 4	Homo sapiens	247-251
20811661-6	2010	CPT-11, but not l-OHP, induced a decrease in activities and protein levels of TS and an increase in those of RNR in KM12C/5-FU tumors only, which was likely related to decreased expressions of several proteins in G1/S phase of the cells including CDK4, pRB, and E2F1 in these tumors.	Irinotecan	0-6	RB transcriptional corepressor 1	Homo sapiens	253-256
20811661-6	2010	CPT-11, but not l-OHP, induced a decrease in activities and protein levels of TS and an increase in those of RNR in KM12C/5-FU tumors only, which was likely related to decreased expressions of several proteins in G1/S phase of the cells including CDK4, pRB, and E2F1 in these tumors.	Irinotecan	0-6	E2F transcription factor 1	Homo sapiens	262-266
20716241-1	2010	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: The anticancer agent irinotecan is a prodrug that is hydrolyzed by hepatic carboxylesterase to its active and toxic metabolite SN-38 and oxidized by CYP3A4 to its inactive metabolite APC.	Irinotecan	63-73	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	191-197
20716241-1	2010	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: The anticancer agent irinotecan is a prodrug that is hydrolyzed by hepatic carboxylesterase to its active and toxic metabolite SN-38 and oxidized by CYP3A4 to its inactive metabolite APC.	Irinotecan	169-174	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	191-197
20716241-2	2010	Irinotecan therapy is complicated by co-administered drugs that inhibit CYP3A4 and decrease APC formation and that indirectly increase SN-38 formation.	Irinotecan	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	72-78
20716241-4	2010	WHAT THIS STUDY ADDS: In microsomal fractions from patients with severe hepatic dysfunction both APC and SN-38 formation were decreased due to down-regulation of CYP3A4 and carboxylesterase enzymes.	Irinotecan	105-110	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	162-168
20716241-14	2010	CONCLUSIONS: Down-regulation of CYP3A4 in liver disease decreased APC formation from irinotecan.	Irinotecan	85-95	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	32-38
20716241-16	2010	However, in a subset of disease samples SN-38 production was relatively high because CYP3A4 activity was markedly impaired.	Irinotecan	40-45	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	85-91
20628391-0	2010	UGT1A and TYMS genetic variants predict toxicity and response of colorectal cancer patients treated with first-line irinotecan and fluorouracil combination therapy.	Irinotecan	116-126	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	0-5
20504912-4	2010	In contrast, one of its analogs, irinotecan (CPT-11), was found to be an hPXR agonist in the same tests.	Irinotecan	33-43	nuclear receptor subfamily 1 group I member 2	Homo sapiens	73-77
20504912-4	2010	In contrast, one of its analogs, irinotecan (CPT-11), was found to be an hPXR agonist in the same tests.	Irinotecan	45-51	nuclear receptor subfamily 1 group I member 2	Homo sapiens	73-77
21098876-12	2010	Our results indicate that rHuEpo acts via EpoR to directly inhibit DLD-1 cell growth and indirectly modulate the cytostatics effects of 5-FU and SN-38.	Irinotecan	145-150	erythropoietin receptor	Homo sapiens	42-46
19951251-7	2010	Exposure of melanoma cells to conditioned media from the HB1.F3.CD.rCE cells in the presence of CPT-11 increased the tumor cell-killing effect by approximately 100-fold when compared to CPT-11 alone.	Irinotecan	96-102	histocompatibility minor HB-1	Homo sapiens	57-60
19951251-7	2010	Exposure of melanoma cells to conditioned media from the HB1.F3.CD.rCE cells in the presence of CPT-11 increased the tumor cell-killing effect by approximately 100-fold when compared to CPT-11 alone.	Irinotecan	186-192	histocompatibility minor HB-1	Homo sapiens	57-60
20619636-3	2010	In this study, we demonstrated that enforced expression of Aven blocks UV-irradiation-, SN-38- or cisplatin-induced apoptosis upstream of mitochondria by stabilising Bcl-xL protein levels in breast cancer cells.	Irinotecan	88-93	apoptosis and caspase activation inhibitor	Homo sapiens	59-63
20619636-3	2010	In this study, we demonstrated that enforced expression of Aven blocks UV-irradiation-, SN-38- or cisplatin-induced apoptosis upstream of mitochondria by stabilising Bcl-xL protein levels in breast cancer cells.	Irinotecan	88-93	BCL2 like 1	Homo sapiens	166-172
20066473-6	2010	We found that metronomic administration of CPT-11 significantly inhibited malignant glioma growth by inhibiting angiogenesis; this treatment procedure reduced the number of tumor vessels and the area of hypoxic lesions and reduced expression of VEGF and HIF-1alpha, the most important angiogenic factors in gliomas.	Irinotecan	43-49	vascular endothelial growth factor A	Homo sapiens	245-249
20066473-6	2010	We found that metronomic administration of CPT-11 significantly inhibited malignant glioma growth by inhibiting angiogenesis; this treatment procedure reduced the number of tumor vessels and the area of hypoxic lesions and reduced expression of VEGF and HIF-1alpha, the most important angiogenic factors in gliomas.	Irinotecan	43-49	hypoxia inducible factor 1 subunit alpha	Homo sapiens	254-264
22966396-7	2010	Among the genes, Bcl-2/adenovirus E1B 19 kDa protein interacting protein 3 (BNIP3), a Bcl-2 family pro-apoptotic protein, was identified as being involved in CPT-11 resistance following methylation of its promoter.	Irinotecan	158-164	BCL2 interacting protein 3	Homo sapiens	17-74
22966396-7	2010	Among the genes, Bcl-2/adenovirus E1B 19 kDa protein interacting protein 3 (BNIP3), a Bcl-2 family pro-apoptotic protein, was identified as being involved in CPT-11 resistance following methylation of its promoter.	Irinotecan	158-164	BCL2 interacting protein 3	Homo sapiens	76-81
22966396-7	2010	Among the genes, Bcl-2/adenovirus E1B 19 kDa protein interacting protein 3 (BNIP3), a Bcl-2 family pro-apoptotic protein, was identified as being involved in CPT-11 resistance following methylation of its promoter.	Irinotecan	158-164	BCL2 apoptosis regulator	Homo sapiens	17-22
22966396-10	2010	The results suggest that methylation of BNIP3 is a predictive factor in the prognosis and response to CPT-11 treatment in CRC patients.	Irinotecan	102-108	BCL2 interacting protein 3	Homo sapiens	40-45
20620155-5	2010	The enzymatic properties of UGT1A1 proteins were characterized by kinetic analysis of 7-hydroxy-4-trifluoromethylcoumarin (7-HFC), estradiol at 3-hydroxy position (E-3OH) and 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation.	Irinotecan	175-205	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
20620155-5	2010	The enzymatic properties of UGT1A1 proteins were characterized by kinetic analysis of 7-hydroxy-4-trifluoromethylcoumarin (7-HFC), estradiol at 3-hydroxy position (E-3OH) and 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation.	Irinotecan	207-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
20620155-9	2010	In recombinant UGT1A1 enzymes expressed in insect cells, the kinetics of 7-HFC, E-3OH and SN-38 glucuronidation fitted the substrate inhibition (7-HFC glucuronidation) or Hill equation (E-3OH and SN-38 glucuronidation), and each glucuronidation showed the same kinetic profile between humans and cynomolgus monkeys.	Irinotecan	90-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
20628391-9	2010	CONCLUSION: TYMS and UGT1A polymorphisms influence on tumour response and toxicities derived from irinotecan/5FU treatment in CRC patients.	Irinotecan	98-108	thymidylate synthetase	Homo sapiens	12-16
20628391-9	2010	CONCLUSION: TYMS and UGT1A polymorphisms influence on tumour response and toxicities derived from irinotecan/5FU treatment in CRC patients.	Irinotecan	98-108	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	21-26
20628391-0	2010	UGT1A and TYMS genetic variants predict toxicity and response of colorectal cancer patients treated with first-line irinotecan and fluorouracil combination therapy.	Irinotecan	116-126	thymidylate synthetase	Homo sapiens	10-14
20666740-0	2010	Prospective evaluation of angiogenic, hypoxic and EGFR-related biomarkers in recurrent glioblastoma multiforme treated with cetuximab, bevacizumab and irinotecan.	Irinotecan	151-161	epidermal growth factor receptor	Homo sapiens	50-54
20649590-1	2010	BACKGROUND AND PURPOSE: Carboxylesterases (CEs) metabolize a wide range of xenobiotic substrates including heroin, cocaine, meperidine and the anticancer agent CPT-11.	Irinotecan	160-166	carboxylesterase 1	Homo sapiens	24-41
20649590-7	2010	However, cocaine, heroin and CPT-11 were all substrates for the intestinal CE, hiCE (CES2), as determined using both the recombinant protein and the tissue fractions.	Irinotecan	29-35	carboxylesterase 2	Homo sapiens	85-89
20653675-0	2010	Association of carboxylesterase 1A genotypes with irinotecan pharmacokinetics in Japanese cancer patients.	Irinotecan	50-60	carboxylesterase 1	Homo sapiens	15-33
20406168-5	2010	In recent years, genetic polymorphisms in UDP-glucuronosyltransferase (UGT) 1A1, an enzyme involved in SN-38 glucuronidation, has been linked to interindividual pharmacokinetic variability and irinotecan toxicity.	Irinotecan	103-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-79
20653675-1	2010	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * Association of UDP-glucuronosyltransferase 1A1 (UGT1A1) genetic polymorphisms *6 and *28 with reduced clearance of SN-38 and severe neutropenia in irinotecan therapy was demonstrated in Japanese cancer patients.	Irinotecan	158-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-89
20653675-1	2010	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * Association of UDP-glucuronosyltransferase 1A1 (UGT1A1) genetic polymorphisms *6 and *28 with reduced clearance of SN-38 and severe neutropenia in irinotecan therapy was demonstrated in Japanese cancer patients.	Irinotecan	158-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
20653675-1	2010	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * Association of UDP-glucuronosyltransferase 1A1 (UGT1A1) genetic polymorphisms *6 and *28 with reduced clearance of SN-38 and severe neutropenia in irinotecan therapy was demonstrated in Japanese cancer patients.	Irinotecan	190-200	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-89
20653675-1	2010	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * Association of UDP-glucuronosyltransferase 1A1 (UGT1A1) genetic polymorphisms *6 and *28 with reduced clearance of SN-38 and severe neutropenia in irinotecan therapy was demonstrated in Japanese cancer patients.	Irinotecan	190-200	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
20653675-4	2010	WHAT THIS STUDY ADDS * Association of functional CES1 gene number with AUC ratio [(SN-38 + SN-38G)/irinotecan], an in vivo index of CES activity, was observed in patients with irinotecan monotherapy.	Irinotecan	83-88	carboxylesterase 1	Homo sapiens	49-53
20653675-4	2010	WHAT THIS STUDY ADDS * Association of functional CES1 gene number with AUC ratio [(SN-38 + SN-38G)/irinotecan], an in vivo index of CES activity, was observed in patients with irinotecan monotherapy.	Irinotecan	99-109	carboxylesterase 1	Homo sapiens	49-53
20653675-4	2010	WHAT THIS STUDY ADDS * Association of functional CES1 gene number with AUC ratio [(SN-38 + SN-38G)/irinotecan], an in vivo index of CES activity, was observed in patients with irinotecan monotherapy.	Irinotecan	176-186	carboxylesterase 1	Homo sapiens	49-53
20653675-6	2010	AIMS Human carboxylesterase 1 (CES1) hydrolyzes irinotecan to produce an active metabolite SN-38 in the liver.	Irinotecan	48-58	carboxylesterase 1	Homo sapiens	11-29
20653675-6	2010	AIMS Human carboxylesterase 1 (CES1) hydrolyzes irinotecan to produce an active metabolite SN-38 in the liver.	Irinotecan	48-58	carboxylesterase 1	Homo sapiens	31-35
20653675-6	2010	AIMS Human carboxylesterase 1 (CES1) hydrolyzes irinotecan to produce an active metabolite SN-38 in the liver.	Irinotecan	91-96	carboxylesterase 1	Homo sapiens	11-29
20653675-6	2010	AIMS Human carboxylesterase 1 (CES1) hydrolyzes irinotecan to produce an active metabolite SN-38 in the liver.	Irinotecan	91-96	carboxylesterase 1	Homo sapiens	31-35
20653675-11	2010	Associations of CES1 genotypes, number of functional CES1 genes (1A1, 1A2 and var1A1) and major SNPs, with the AUC ratio of (SN-38 + SN-38G)/irinotecan, a parameter of in vivo CES activity, were analyzed for 58 patients treated with irinotecan monotherapy.	Irinotecan	125-130	carboxylesterase 1	Homo sapiens	16-20
20653675-11	2010	Associations of CES1 genotypes, number of functional CES1 genes (1A1, 1A2 and var1A1) and major SNPs, with the AUC ratio of (SN-38 + SN-38G)/irinotecan, a parameter of in vivo CES activity, were analyzed for 58 patients treated with irinotecan monotherapy.	Irinotecan	141-151	carboxylesterase 1	Homo sapiens	16-20
20562211-0	2010	Dose-dependent association between UGT1A1*28 genotype and irinotecan-induced neutropenia: low doses also increase risk.	Irinotecan	58-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
20562211-1	2010	PURPOSE: A previous meta-analysis showed that the association between the UGT1A1*28 genotype and irinotecan-induced neutropenia was influenced by irinotecan dose and that the risk of neutropenia was similar at low doses for patients with all genotypes.	Irinotecan	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
20562211-1	2010	PURPOSE: A previous meta-analysis showed that the association between the UGT1A1*28 genotype and irinotecan-induced neutropenia was influenced by irinotecan dose and that the risk of neutropenia was similar at low doses for patients with all genotypes.	Irinotecan	146-156	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
20562211-5	2010	The association between UGT1A1*28 and the relative extent of glucuronidation (REG) of SN-38 was also examined.	Irinotecan	86-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
20562211-5	2010	The association between UGT1A1*28 and the relative extent of glucuronidation (REG) of SN-38 was also examined.	Irinotecan	86-91	regenerating family member 1 alpha	Homo sapiens	78-81
20562211-11	2010	We found the weighted mean difference of REG (UGT1A1*1/*1 or UGT1A1*1/*28 versus UGT1A1*28/*28) increased with increasing dose of irinotecan.	Irinotecan	130-140	regenerating family member 1 alpha	Homo sapiens	41-44
20562211-11	2010	We found the weighted mean difference of REG (UGT1A1*1/*1 or UGT1A1*1/*28 versus UGT1A1*28/*28) increased with increasing dose of irinotecan.	Irinotecan	130-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
20562211-11	2010	We found the weighted mean difference of REG (UGT1A1*1/*1 or UGT1A1*1/*28 versus UGT1A1*28/*28) increased with increasing dose of irinotecan.	Irinotecan	130-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
20562211-11	2010	We found the weighted mean difference of REG (UGT1A1*1/*1 or UGT1A1*1/*28 versus UGT1A1*28/*28) increased with increasing dose of irinotecan.	Irinotecan	130-140	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
20562211-12	2010	CONCLUSIONS: In conclusion, the UGT1A1*28/*28 genotype was associated with an increased risk of neutropenia not only at medium or high doses of irinotecan but also at low doses.	Irinotecan	144-154	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
20562211-13	2010	The dose-dependent manner of SN-38 glucuronidation explained why the association between UGT1A1*28 and neutropenia was dose dependent.	Irinotecan	29-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
20406168-5	2010	In recent years, genetic polymorphisms in UDP-glucuronosyltransferase (UGT) 1A1, an enzyme involved in SN-38 glucuronidation, has been linked to interindividual pharmacokinetic variability and irinotecan toxicity.	Irinotecan	193-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-79
20580994-0	2010	The UGT1A1*28 polymorphism correlates with erlotinib"s effect on SN-38 glucuronidation.	Irinotecan	65-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
20663031-3	2010	In addition, we have investigated the potential involvement of breast cancer resistance protein (BCRP) in biliary excretion, pharmacokinetics, and intestinal toxicity of CPT-11.	Irinotecan	170-176	ATP binding cassette subfamily G member 2	Canis lupus familiaris	97-101
20663031-5	2010	The effect of PEO-PPO-PEO micelles on BCRP-mediated cellular accumulation and transport efflux of CPT-11 was evaluated in MDCKII/BCRP cells.	Irinotecan	98-104	ATP binding cassette subfamily G member 2	Canis lupus familiaris	38-42
20663031-5	2010	The effect of PEO-PPO-PEO micelles on BCRP-mediated cellular accumulation and transport efflux of CPT-11 was evaluated in MDCKII/BCRP cells.	Irinotecan	98-104	ATP binding cassette subfamily G member 2	Canis lupus familiaris	129-133
20663031-7	2010	KEY FINDINGS: The obtained micelles could effectively inhibit BCRP-mediated CPT-11 efflux in MDCKII/BCRP cells, and significantly decrease the drug biliary excretion in rats.	Irinotecan	76-82	ATP binding cassette subfamily G member 2	Canis lupus familiaris	62-66
20663031-7	2010	KEY FINDINGS: The obtained micelles could effectively inhibit BCRP-mediated CPT-11 efflux in MDCKII/BCRP cells, and significantly decrease the drug biliary excretion in rats.	Irinotecan	76-82	ATP binding cassette subfamily G member 2	Canis lupus familiaris	100-104
20663031-11	2010	The study indicated a potential involvement of BCRP in CPT-11 pharmacokinetics and CPT-11-induced intestinal toxicity.	Irinotecan	55-61	ATP binding cassette subfamily G member 2	Canis lupus familiaris	47-51
20663031-11	2010	The study indicated a potential involvement of BCRP in CPT-11 pharmacokinetics and CPT-11-induced intestinal toxicity.	Irinotecan	83-89	ATP binding cassette subfamily G member 2	Canis lupus familiaris	47-51
20661248-1	2010	BACKGROUND: Accurate description of current practice within advanced colorectal cancer (CRC) specialties were needed to inform an economic evaluation of the UGT1A1 pharmacogenetic test for irinotecan in the United Kingdom.	Irinotecan	189-199	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	157-163
20637356-4	2010	The phenotyping of DPD and UGT1A1 activities, and to a lesser extent, its genotyping, appears as the most useful tool in terms of prediction of toxicities induced by two major drugs: 5-FU and irinotecan.	Irinotecan	192-202	dihydropyrimidine dehydrogenase	Homo sapiens	19-22
20637356-4	2010	The phenotyping of DPD and UGT1A1 activities, and to a lesser extent, its genotyping, appears as the most useful tool in terms of prediction of toxicities induced by two major drugs: 5-FU and irinotecan.	Irinotecan	192-202	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
20630823-2	2010	This trial was designed to evaluate irinotecan/cisplatin plus maintenance imatinib in patients with c-Kit-positive disease (the transmembrane receptor c-Kit is the product of the c-KIT protooncogene).	Irinotecan	36-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	100-105
20630823-2	2010	This trial was designed to evaluate irinotecan/cisplatin plus maintenance imatinib in patients with c-Kit-positive disease (the transmembrane receptor c-Kit is the product of the c-KIT protooncogene).	Irinotecan	36-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	151-156
20630823-2	2010	This trial was designed to evaluate irinotecan/cisplatin plus maintenance imatinib in patients with c-Kit-positive disease (the transmembrane receptor c-Kit is the product of the c-KIT protooncogene).	Irinotecan	36-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	179-184
20063115-3	2010	The MTD for patients receiving enzyme-inducing anticonvulsants (EIAC) was as follows: irinotecan 400 mg/m(2)/week on Days 1, 8, 22 and 29 during RT, followed by BCNU 100 mg/m(2) Day 1, and irinotecan, 400 mg/m(2) on Days 1, 8, 22 and 29, every 6 weeks.	Irinotecan	86-96	metallothionein 1E	Homo sapiens	4-7
20063115-10	2010	SN-38 C(max) and AUC in EIAC patients receiving 400 mg/m(2) irinotecan were 20.9 ng/ml and 212 ng/ml h, and in non-EIAC patients receiving 125 mg/m(2), 15.5 ng/ml and 207 ng/ml h. SN-38 AUC varied by UGT1A1*28 status in non-EIAC patients.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	200-206
20063115-12	2010	Non-EIAC patients with UGT1A1*28 variant alleles appear particularly sensitive to toxicity from irinotecan.	Irinotecan	96-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
20580994-2	2010	We aimed to investigate the effect of erlotinib on SN-38 glucuronidation and the association between UGT1A polymorphisms and SN-38 glucuronidation activity in the presence of erlotinib.	Irinotecan	125-130	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	101-106
20580994-6	2010	Our data showed that erlotinib exhibited potent non-competitive inhibition against SN-38 glucuronidation in pooled HLMs and UGT1A1.	Irinotecan	83-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
20580994-9	2010	Significant correlations were observed between SN-38 glucuronidation activity in the presence of erlotinib and UGT1A1*28 in 52 Caucasian liver microsomes.	Irinotecan	47-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
20580994-10	2010	Our results suggest that erlotinib is a potent inhibitor of SN-38 glucuronidation via UGT1A1 inhibition.	Irinotecan	60-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
20580994-12	2010	UGT1A1*28 polymorphism correlates with erlotinib"s effect on SN-38 glucuronidation.	Irinotecan	61-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19739070-2	2010	We investigated the influence of the essential component of MMR, the hMLH1 protein, on the cellular response to DNA-double strand breaks induced by treatment with SN-38, the active metabolite of topoisomerase I inhibitor irinotecan, in a strictly isogenic cell system (p53(wt), hMLH1(+)/p53(wt), hMLH1(-)).	Irinotecan	163-168	mutL homolog 1	Homo sapiens	69-74
20335017-0	2010	Dose-dependent association between UGT1A1*28 polymorphism and irinotecan-induced diarrhoea: a meta-analysis.	Irinotecan	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
20335017-2	2010	The associations between the UGT1A1*28 polymorphism and irinotecan-induced diarrhoea remains controversial because of conflicting data in the literature.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
20304778-0	2010	Phase II study of combination chemotherapy with biweekly cetuximab and irinotecan for pre-treated metastatic colorectal cancer harboring wild-type KRAS.	Irinotecan	71-81	KRAS proto-oncogene, GTPase	Homo sapiens	147-151
20602618-3	2010	Although multiple genes may play a role in irinotecan activity, the majority of evidence to date suggests that variation in expression of UGT1A1 caused by a common promoter polymorphism (UGT1A1*28) is strongly associated with toxicity; however, this link is dose dependent.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	138-144
20602618-3	2010	Although multiple genes may play a role in irinotecan activity, the majority of evidence to date suggests that variation in expression of UGT1A1 caused by a common promoter polymorphism (UGT1A1*28) is strongly associated with toxicity; however, this link is dose dependent.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
20602618-4	2010	Variations in other pharmacokinetic genes, particularly the transporter ABCC2, also contribute to irinotecan toxicity.	Irinotecan	98-108	ATP binding cassette subfamily C member 2	Homo sapiens	72-77
20335017-9	2010	The risk of severe diarrhoea at medium and high irinotecan doses was higher among patients with a UGT1A1*28/*28 genotype than among those with a UGT1A1*1/*1 genotype (OR=3.69, 95% confidence interval [CI]=2.00-6.83; P&lt;0.001).	Irinotecan	48-58	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
20335017-12	2010	In conclusion, patients carrying UGT1A1*28 allele(s) are at an increased risk of irinotecan-induced severe diarrhoea.	Irinotecan	81-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
19739070-3	2010	By using hMLH1 expressing clones or cells transduced with the hMLH1-expressing adenovirus as well as siRNA technology, we show that in response to SN-38-induced DNA damage the MMR proficient (MMR(+)) cells make: (i) a stronger G2/M arrest, (ii) a subsequent longer tetraploid G1 arrest, (iii) a stronger activation of Chk1 and Chk2 kinases than the MMR deficient (MMR(-)) counterparts.	Irinotecan	147-152	mutL homolog 1	Homo sapiens	9-14
19739070-3	2010	By using hMLH1 expressing clones or cells transduced with the hMLH1-expressing adenovirus as well as siRNA technology, we show that in response to SN-38-induced DNA damage the MMR proficient (MMR(+)) cells make: (i) a stronger G2/M arrest, (ii) a subsequent longer tetraploid G1 arrest, (iii) a stronger activation of Chk1 and Chk2 kinases than the MMR deficient (MMR(-)) counterparts.	Irinotecan	147-152	mutL homolog 1	Homo sapiens	62-67
19739070-3	2010	By using hMLH1 expressing clones or cells transduced with the hMLH1-expressing adenovirus as well as siRNA technology, we show that in response to SN-38-induced DNA damage the MMR proficient (MMR(+)) cells make: (i) a stronger G2/M arrest, (ii) a subsequent longer tetraploid G1 arrest, (iii) a stronger activation of Chk1 and Chk2 kinases than the MMR deficient (MMR(-)) counterparts.	Irinotecan	147-152	checkpoint kinase 1	Homo sapiens	318-322
19739070-3	2010	By using hMLH1 expressing clones or cells transduced with the hMLH1-expressing adenovirus as well as siRNA technology, we show that in response to SN-38-induced DNA damage the MMR proficient (MMR(+)) cells make: (i) a stronger G2/M arrest, (ii) a subsequent longer tetraploid G1 arrest, (iii) a stronger activation of Chk1 and Chk2 kinases than the MMR deficient (MMR(-)) counterparts.	Irinotecan	147-152	checkpoint kinase 2	Homo sapiens	327-331
19739070-2	2010	We investigated the influence of the essential component of MMR, the hMLH1 protein, on the cellular response to DNA-double strand breaks induced by treatment with SN-38, the active metabolite of topoisomerase I inhibitor irinotecan, in a strictly isogenic cell system (p53(wt), hMLH1(+)/p53(wt), hMLH1(-)).	Irinotecan	221-231	mutL homolog 1	Homo sapiens	69-74
20124398-3	2010	The well characterized substrate for UGT1A1, 7-ethyl-10-hydroxy-camptothecin (SN-38), showed the greatest difference in parent drug exposure ( approximately 3-fold increase) and clearance ( approximately 3-fold decrease) in Tg(UGT1(A1*28)) Ugt1(-/-) mice after intravenous administration compared with wild-type and phenobarbital-treated animals.	Irinotecan	78-83	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	37-43
19908066-11	2010	CONCLUSIONS: XRCC1 genotype independently predicted overall survival in metastatic colorectal carcinoma patients treated with irinotecan-based chemotherapy.	Irinotecan	126-136	X-ray repair cross complementing 1	Homo sapiens	13-18
20211505-1	2010	BACKGROUND AND PURPOSE: The aim of this study is to evaluate the efficacy and safety of preoperative radiation therapy combined with S-1 and irinotecan (SI) in LARC.	Irinotecan	141-151	C-C motif chemokine ligand 20	Homo sapiens	160-164
20121626-0	2010	Carcinoembryonic antigen surge in metastatic colorectal cancer patients responding to irinotecan combination chemotherapy.	Irinotecan	86-96	CEA cell adhesion molecule 3	Homo sapiens	0-24
20121626-2	2010	The aim of this study was to investigate the phenomenon of CEA surge in irinotecan-based chemotherapy.	Irinotecan	72-82	CEA cell adhesion molecule 3	Homo sapiens	59-62
20121626-7	2010	CONCLUSION: A CEA surge can be induced by irinotecan-based chemotherapy.	Irinotecan	42-52	CEA cell adhesion molecule 3	Homo sapiens	14-17
20121626-8	2010	An early increase in CEA after irinotecan-based chemotherapy does not usually indicate progression of disease and failure of therapy, and should not lead to a change of chemotherapy.	Irinotecan	31-41	CEA cell adhesion molecule 3	Homo sapiens	21-24
20164124-0	2010	Secreted protein acidic and rich in cysteine-induced cellular senescence in colorectal cancers in response to irinotecan is mediated by P53.	Irinotecan	110-120	secreted protein acidic and cysteine rich	Homo sapiens	0-44
20164124-0	2010	Secreted protein acidic and rich in cysteine-induced cellular senescence in colorectal cancers in response to irinotecan is mediated by P53.	Irinotecan	110-120	tumor protein p53	Homo sapiens	136-139
20164124-6	2010	However, CPT-11-resistant cells exposed to endogenous or exogenous SPARC can also be triggered into cellular senescence.	Irinotecan	9-15	secreted protein acidic and cysteine rich	Homo sapiens	67-72
20651349-12	2010	Silencing of beta-catenin decreased transcription of these ABC transporter genes; beta-catenin-silenced cells became relatively sensitive to paclitaxel and irinotecan.	Irinotecan	156-166	catenin beta 1	Homo sapiens	13-25
20651349-12	2010	Silencing of beta-catenin decreased transcription of these ABC transporter genes; beta-catenin-silenced cells became relatively sensitive to paclitaxel and irinotecan.	Irinotecan	156-166	catenin beta 1	Homo sapiens	82-94
19771428-2	2010	METHODS: Associations between transporter haplotypes/variations along with UGT1A1*28 or *6 and SN-38 area under the time-concentration curve (AUC) or neutropenia were examined in irinotecan monotherapy (55 patients) and irinotecan-cisplatin-combination therapy (62 patients).	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
19771428-3	2010	RESULTS: Higher SN-38 AUC values were observed in ABCB1 2677G&gt;T (A893S) (*2 group) for both regimens.	Irinotecan	16-21	ATP binding cassette subfamily B member 1	Homo sapiens	50-55
20124398-8	2010	These differences are consistent with SN-38 glucuronidation activities using HLMs isolated from individuals genotyped as UGT1A1*1 or UGT1A1*28.	Irinotecan	38-43	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	121-127
20124398-3	2010	The well characterized substrate for UGT1A1, 7-ethyl-10-hydroxy-camptothecin (SN-38), showed the greatest difference in parent drug exposure ( approximately 3-fold increase) and clearance ( approximately 3-fold decrease) in Tg(UGT1(A1*28)) Ugt1(-/-) mice after intravenous administration compared with wild-type and phenobarbital-treated animals.	Irinotecan	78-83	UDP glucuronosyltransferase 1 family, polypeptide A2	Mus musculus	37-41
20124398-3	2010	The well characterized substrate for UGT1A1, 7-ethyl-10-hydroxy-camptothecin (SN-38), showed the greatest difference in parent drug exposure ( approximately 3-fold increase) and clearance ( approximately 3-fold decrease) in Tg(UGT1(A1*28)) Ugt1(-/-) mice after intravenous administration compared with wild-type and phenobarbital-treated animals.	Irinotecan	78-83	UDP glucuronosyltransferase 1 family, polypeptide A2	Mus musculus	240-244
20124398-7	2010	For SN-38 glucuronidation, V(max) decreased 5-fold in Tg(UGT1(A1*28)) Ugt1(-/-) mouse liver microsomes compared with microsomes prepared from wild-type mice, and decreased 10-fold compared with phenobarbital-treated Tg(UGT1(A1*28)) Ugt1(-/-) mice.	Irinotecan	4-9	UDP glucuronosyltransferase 1 family, polypeptide A2	Mus musculus	57-61
20124398-7	2010	For SN-38 glucuronidation, V(max) decreased 5-fold in Tg(UGT1(A1*28)) Ugt1(-/-) mouse liver microsomes compared with microsomes prepared from wild-type mice, and decreased 10-fold compared with phenobarbital-treated Tg(UGT1(A1*28)) Ugt1(-/-) mice.	Irinotecan	4-9	UDP glucuronosyltransferase 1 family, polypeptide A2	Mus musculus	70-74
20124398-7	2010	For SN-38 glucuronidation, V(max) decreased 5-fold in Tg(UGT1(A1*28)) Ugt1(-/-) mouse liver microsomes compared with microsomes prepared from wild-type mice, and decreased 10-fold compared with phenobarbital-treated Tg(UGT1(A1*28)) Ugt1(-/-) mice.	Irinotecan	4-9	UDP glucuronosyltransferase 1 family, polypeptide A2	Mus musculus	219-223
20124398-7	2010	For SN-38 glucuronidation, V(max) decreased 5-fold in Tg(UGT1(A1*28)) Ugt1(-/-) mouse liver microsomes compared with microsomes prepared from wild-type mice, and decreased 10-fold compared with phenobarbital-treated Tg(UGT1(A1*28)) Ugt1(-/-) mice.	Irinotecan	4-9	UDP glucuronosyltransferase 1 family, polypeptide A2	Mus musculus	232-236
20085586-8	2010	Patients that were homozygous for the reference alleles SSTR4 rs2567608 (AA) and EPHA7 rs2278107 (TT) showed lower disease control rates in response to irinotecan and oxaliplatin regimens, respectively, than those with substitution alleles (P = 0.022 and 0.014, respectively).	Irinotecan	152-162	somatostatin receptor 4	Homo sapiens	56-61
20395318-2	2010	We investigated the kinetics of (18)F-FLT during treatment of malignant glioma with bevacizumab and irinotecan.	Irinotecan	100-110	fms related receptor tyrosine kinase 1	Homo sapiens	38-41
20371676-0	2010	Aprataxin tumor levels predict response of colorectal cancer patients to irinotecan-based treatment.	Irinotecan	73-83	aprataxin	Homo sapiens	0-9
20371676-4	2010	RESULTS: A good correlation was observed between irinotecan sensitivity and the expression of aprataxin (APTX), a histidine triad domain superfamily protein involved in DNA repair.	Irinotecan	49-59	aprataxin	Homo sapiens	94-103
20371676-4	2010	RESULTS: A good correlation was observed between irinotecan sensitivity and the expression of aprataxin (APTX), a histidine triad domain superfamily protein involved in DNA repair.	Irinotecan	49-59	aprataxin	Homo sapiens	105-109
20371676-5	2010	Moreover, using an isogenic in vitro system deficient in APTX, we show that aprataxin directly regulates the cellular sensitivity to camptothecin, suggesting that it could be used to predict patient response to irinotecan.	Irinotecan	211-221	aprataxin	Homo sapiens	76-85
20371676-10	2010	CONCLUSIONS: These results show that aprataxin tumor levels can be used to identify patients with low probability of response to irinotecan-based therapy who are ideal candidates to receive treatment with alternative agents in an attempt to improve patient survival.	Irinotecan	129-139	aprataxin	Homo sapiens	37-46
20513938-3	2010	Patients with genetic variations in UGT1A1 and DPYD genes are hypersensitive to Irinotecan and 5-Fluorouracil (5FU) respectively.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
20513938-3	2010	Patients with genetic variations in UGT1A1 and DPYD genes are hypersensitive to Irinotecan and 5-Fluorouracil (5FU) respectively.	Irinotecan	80-90	dihydropyrimidine dehydrogenase	Homo sapiens	47-51
20530432-2	2010	MATERIALS AND METHODS: We evaluated the influence of hepatocyte growth factor, vascular endothelial growth factor and epidermal growth factor on the effect of 5-fluorouracil, oxaliplatin and SN-38 (the active metabolite of irinotecan) on WiDr cells.	Irinotecan	191-196	vascular endothelial growth factor A	Homo sapiens	79-113
20530432-2	2010	MATERIALS AND METHODS: We evaluated the influence of hepatocyte growth factor, vascular endothelial growth factor and epidermal growth factor on the effect of 5-fluorouracil, oxaliplatin and SN-38 (the active metabolite of irinotecan) on WiDr cells.	Irinotecan	191-196	epidermal growth factor	Homo sapiens	118-141
20085586-8	2010	Patients that were homozygous for the reference alleles SSTR4 rs2567608 (AA) and EPHA7 rs2278107 (TT) showed lower disease control rates in response to irinotecan and oxaliplatin regimens, respectively, than those with substitution alleles (P = 0.022 and 0.014, respectively).	Irinotecan	152-162	EPH receptor A7	Homo sapiens	81-86
20704575-5	2010	Combined treatments with CPT-11 or SN-38 significantly increased caspase 3/7 activity compared with RET siRNA, CPT-11 or SN-38 treatment alone.	Irinotecan	25-31	caspase 3	Homo sapiens	65-74
20047821-7	2010	In comparison with bare CS-g-PCL nanomicelles, the corresponding SN-38-loaded nanomicelles showed increased particle sizes and a little reduced zeta potentials.	Irinotecan	65-70	polycystic kidney disease 2-like 1	Mus musculus	29-32
20704575-5	2010	Combined treatments with CPT-11 or SN-38 significantly increased caspase 3/7 activity compared with RET siRNA, CPT-11 or SN-38 treatment alone.	Irinotecan	25-31	ret proto-oncogene	Homo sapiens	100-103
20704575-5	2010	Combined treatments with CPT-11 or SN-38 significantly increased caspase 3/7 activity compared with RET siRNA, CPT-11 or SN-38 treatment alone.	Irinotecan	35-40	caspase 3	Homo sapiens	65-74
20704575-5	2010	Combined treatments with CPT-11 or SN-38 significantly increased caspase 3/7 activity compared with RET siRNA, CPT-11 or SN-38 treatment alone.	Irinotecan	35-40	ret proto-oncogene	Homo sapiens	100-103
20704575-7	2010	These findings that RET siRNA enhanced sensitivity for CPT-11 will provide a novel strategy for the treatment of MTC with RET mutation.	Irinotecan	55-61	ret proto-oncogene	Homo sapiens	20-23
20704575-7	2010	These findings that RET siRNA enhanced sensitivity for CPT-11 will provide a novel strategy for the treatment of MTC with RET mutation.	Irinotecan	55-61	ret proto-oncogene	Homo sapiens	122-125
20047821-6	2010	Water-insoluble antitumor drug, SN-38, was easily encapsulated into CS-g-PCL nanomicelles by lyophilization method.	Irinotecan	32-37	polycystic kidney disease 2-like 1	Mus musculus	73-76
20047821-9	2010	Also, the CS-g-PCL nanomicelles effectively protected the active lactone ring of SN-38 from hydrolysis under physiological condition, due to the encapsulation of SN-38 into the hydrophobic cores in the nanomicelles.	Irinotecan	81-86	polycystic kidney disease 2-like 1	Mus musculus	15-18
20047821-9	2010	Also, the CS-g-PCL nanomicelles effectively protected the active lactone ring of SN-38 from hydrolysis under physiological condition, due to the encapsulation of SN-38 into the hydrophobic cores in the nanomicelles.	Irinotecan	162-167	polycystic kidney disease 2-like 1	Mus musculus	15-18
20511137-3	2010	Numerous variants have been found in UGT1A1 , the main conjugating enzyme of bilirubin and drugs such as the anticancer drug irinotecan.	Irinotecan	125-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
20511137-4	2010	Recently, the US Food and Drug Administration (FDA) recommended testing for the presence of UGT1A1*28 , an allele correlated with decreased transcriptional activity, to predict patients at risk of irinotecan toxicity.	Irinotecan	197-207	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
20179984-0	2010	Indispensability of UGT1A1*6 genotyping in Japanese cancer patients treated with irinotecan.	Irinotecan	81-91	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
20726333-7	2010	In cocultures, IL-1beta induced HGF release, while CPT-11 alone or combined with IL-1beta decreased HGF secretion.	Irinotecan	51-57	hepatocyte growth factor	Homo sapiens	100-103
20726333-8	2010	An immunoblotting analysis followed by densitometry revealed that the combination of IL-1beta plus CPT-11 added to the cocultures led to a decrease in HSPs and MRP levels.	Irinotecan	99-105	ATP binding cassette subfamily C member 1	Homo sapiens	160-163
19859084-0	2010	Association of SUMO1 and UBC9 genotypes with tumor response in non-small-cell lung cancer treated with irinotecan-based chemotherapy.	Irinotecan	103-113	small ubiquitin like modifier 1	Homo sapiens	15-20
20216081-3	2010	The purpose of this study is to determine the toxicity and response rate to the addition of the selective oral COX-2 inhibitor, celecoxib, to gemcitabine and irinotecan in patients with inoperable pancreatic cancer.	Irinotecan	158-168	prostaglandin-endoperoxide synthase 2	Homo sapiens	111-116
19859084-0	2010	Association of SUMO1 and UBC9 genotypes with tumor response in non-small-cell lung cancer treated with irinotecan-based chemotherapy.	Irinotecan	103-113	ubiquitin conjugating enzyme E2 I	Homo sapiens	25-29
19859084-1	2010	Irinotecan induces small ubiquitin-like modifier (SUMO)-1 conjugation to topoisomerase-I, leading to enhanced sensitivity to irinotecan.	Irinotecan	0-10	small ubiquitin like modifier 1	Homo sapiens	19-57
19859084-1	2010	Irinotecan induces small ubiquitin-like modifier (SUMO)-1 conjugation to topoisomerase-I, leading to enhanced sensitivity to irinotecan.	Irinotecan	125-135	small ubiquitin like modifier 1	Homo sapiens	19-57
19859084-7	2010	This finding suggests that the UBC9 10920CG genotype enhances sensitivity to irinotecan chemotherapy in advanced NSCLC through upregulation of SUMO1 in tumor cells.	Irinotecan	77-87	ubiquitin conjugating enzyme E2 I	Homo sapiens	31-35
19859084-7	2010	This finding suggests that the UBC9 10920CG genotype enhances sensitivity to irinotecan chemotherapy in advanced NSCLC through upregulation of SUMO1 in tumor cells.	Irinotecan	77-87	small ubiquitin like modifier 1	Homo sapiens	143-148
20213647-3	2010	We adapted an "in vivo complexes of enzyme to DNA" (ICE) bioassay to assess irinotecan activity in the stomach, duodenum, colon and liver of male Wistar rats after a single treatment with irinotecan (100 mg/kg body weight, intraperitoneally).	Irinotecan	188-198	caspase 1	Rattus norvegicus	52-55
20238327-19	2010	Two and three-drug regimens including 5-FU, cisplatin, with or without an anthracycline, as well as irinotecan or docetaxel-containing regimens are reasonable treatment options for HER-2 negative patients.	Irinotecan	100-110	erb-b2 receptor tyrosine kinase 2	Homo sapiens	181-186
20196838-0	2010	Pregnane X Receptor (PXR) expression in colorectal cancer cells restricts irinotecan chemosensitivity through enhanced SN-38 glucuronidation.	Irinotecan	74-84	nuclear receptor subfamily 1 group I member 2	Homo sapiens	0-19
20196838-0	2010	Pregnane X Receptor (PXR) expression in colorectal cancer cells restricts irinotecan chemosensitivity through enhanced SN-38 glucuronidation.	Irinotecan	74-84	nuclear receptor subfamily 1 group I member 2	Homo sapiens	21-24
20196838-0	2010	Pregnane X Receptor (PXR) expression in colorectal cancer cells restricts irinotecan chemosensitivity through enhanced SN-38 glucuronidation.	Irinotecan	119-124	nuclear receptor subfamily 1 group I member 2	Homo sapiens	0-19
20196838-0	2010	Pregnane X Receptor (PXR) expression in colorectal cancer cells restricts irinotecan chemosensitivity through enhanced SN-38 glucuronidation.	Irinotecan	119-124	nuclear receptor subfamily 1 group I member 2	Homo sapiens	21-24
20196838-4	2010	Considering the metabolic pathway of irinotecan and the tissue distribution of Pregnane x Receptor (PXR), we hypothesized that PXR could play a key role in colon cancer cell response to irinotecan.	Irinotecan	37-47	nuclear receptor subfamily 1 group I member 2	Homo sapiens	127-130
20196838-4	2010	Considering the metabolic pathway of irinotecan and the tissue distribution of Pregnane x Receptor (PXR), we hypothesized that PXR could play a key role in colon cancer cell response to irinotecan.	Irinotecan	186-196	nuclear receptor subfamily 1 group I member 2	Homo sapiens	79-98
20196838-4	2010	Considering the metabolic pathway of irinotecan and the tissue distribution of Pregnane x Receptor (PXR), we hypothesized that PXR could play a key role in colon cancer cell response to irinotecan.	Irinotecan	186-196	nuclear receptor subfamily 1 group I member 2	Homo sapiens	100-103
20196838-4	2010	Considering the metabolic pathway of irinotecan and the tissue distribution of Pregnane x Receptor (PXR), we hypothesized that PXR could play a key role in colon cancer cell response to irinotecan.	Irinotecan	186-196	nuclear receptor subfamily 1 group I member 2	Homo sapiens	127-130
20196838-7	2010	Cellular response to irinotecan and its active metabolic SN38 was assessed by cell viability assays, HPLC metabolic profiles and mRNA quantification of PXR target genes.	Irinotecan	21-31	nuclear receptor subfamily 1 group I member 2	Homo sapiens	152-155
20196838-13	2010	CONCLUSION: Our results demonstrate that tumoral metabolism of SN38 is affected by PXR and point to potential therapeutic significance of PXR quantification in the prediction of irinotecan response.	Irinotecan	178-188	nuclear receptor subfamily 1 group I member 2	Homo sapiens	138-141
20009028-8	2010	When gavaged with fat (trioleate), RS4 stimulated a lower postprandial glucose-dependent insulinotropic polypeptide (GIP; incretin) response than RS2.	Irinotecan	35-38	gastric inhibitory polypeptide	Mus musculus	71-115
20009028-8	2010	When gavaged with fat (trioleate), RS4 stimulated a lower postprandial glucose-dependent insulinotropic polypeptide (GIP; incretin) response than RS2.	Irinotecan	35-38	gastric inhibitory polypeptide	Mus musculus	117-120
20009028-10	2010	In conclusion, dietary supplementation with RS4-type resistant starch attenuates high-fat diet-induced obesity more effectively than RS2 in C57BL/6J mice, which may be attributable to lower postprandial GIP and increased fat catabolism in the liver.	Irinotecan	44-47	gastric inhibitory polypeptide	Mus musculus	203-206
20235794-5	2010	This article provides an overview of recent progress in irinotecan pharmacogenetics and discusses the clinical significance of the UGT1A1 genotype/haplotype with regard to severe irinotecan toxicity.	Irinotecan	179-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	131-137
20028383-1	2010	Although individuals carrying the UGT1A1 allele *28 have an increased risk of severe toxicities associated with irinotecan, no phase I study has been conducted based on the polymorphism.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
20028383-12	2010	The recommended starting doses of biweekly irinotecan for phase II/III were 150 mg/m(2) for patients with the UGT1A1 6/6 genotype and 70 mg/m(2) for those with the 6/7 genotype, respectively.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
19931604-0	2010	Relations between strain and gender dependencies of irinotecan toxicity and UGT1A1, CES2 and TOP1 expressions in mice.	Irinotecan	52-62	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	76-82
20235794-2	2010	Irinotecan is one of the models for personalized medicine based on pharmacogenetics, and a number of clinical studies have revealed significant associations between UGT1A1*28 and irinotecan toxicity.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	165-171
20235794-2	2010	Irinotecan is one of the models for personalized medicine based on pharmacogenetics, and a number of clinical studies have revealed significant associations between UGT1A1*28 and irinotecan toxicity.	Irinotecan	179-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	165-171
19931604-0	2010	Relations between strain and gender dependencies of irinotecan toxicity and UGT1A1, CES2 and TOP1 expressions in mice.	Irinotecan	52-62	carboxylesterase 2C	Mus musculus	84-88
19931604-2	2010	CPT-11 is bio-activated through CES, detoxified through UGT1A1 and inhibits TOP1.	Irinotecan	0-6	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	56-62
19931604-11	2010	Genetic background and gender significantly altered the molecular prediction of irinotecan toxicity by UGT1A1, CES2 and TOP1 mRNA expressions.	Irinotecan	80-90	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	103-109
19931604-11	2010	Genetic background and gender significantly altered the molecular prediction of irinotecan toxicity by UGT1A1, CES2 and TOP1 mRNA expressions.	Irinotecan	80-90	carboxylesterase 2C	Mus musculus	111-115
20038727-1	2010	PURPOSE We aimed to identify the maximum-tolerated dose (MTD) of irinotecan in patients with cancer with UGT1A1*1/*1 and *1/*28 genotypes.	Irinotecan	65-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
19889793-7	2010	In addition to 4MUG, the PS(serosal) of the glucuronide conjugates of 7-ethyl-10-hydroxycamptothecin (SN-38) and acetaminophen in the jejunal everted sacs were also significantly reduced in Mrp3(-/-) mice compared with wild-type mice.	Irinotecan	70-100	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	190-194
19652968-0	2010	Dynamic monitoring the TCR CDR3 spectratypes in patients with metastatic CRC treated with a combination of bevacizumab, irinotecan, fluorouracil, and leucovorin.	Irinotecan	120-130	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	23-26
19932091-2	2010	In addition, homozygous subjects for UGT1A128 genotype may suffer from severe irinotecan toxicity or jaundice during treatment with the protease inhibitor atazanavir.	Irinotecan	78-88	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	37-42
19889793-7	2010	In addition to 4MUG, the PS(serosal) of the glucuronide conjugates of 7-ethyl-10-hydroxycamptothecin (SN-38) and acetaminophen in the jejunal everted sacs were also significantly reduced in Mrp3(-/-) mice compared with wild-type mice.	Irinotecan	102-107	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	190-194
20068078-0	2010	A CYP3A4 phenotype-based dosing algorithm for individualized treatment of irinotecan.	Irinotecan	74-84	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	2-8
20096102-1	2010	BACKGROUND: UDP-glucuronosyltransferase 1A1 (UGT1A1) is a pivotal enzyme involved in metabolism of SN-38, the active metabolite of irinotecan commonly used to treat metastatic colorectal cancer.	Irinotecan	99-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-43
20096102-1	2010	BACKGROUND: UDP-glucuronosyltransferase 1A1 (UGT1A1) is a pivotal enzyme involved in metabolism of SN-38, the active metabolite of irinotecan commonly used to treat metastatic colorectal cancer.	Irinotecan	99-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
20096102-1	2010	BACKGROUND: UDP-glucuronosyltransferase 1A1 (UGT1A1) is a pivotal enzyme involved in metabolism of SN-38, the active metabolite of irinotecan commonly used to treat metastatic colorectal cancer.	Irinotecan	131-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-43
20096102-1	2010	BACKGROUND: UDP-glucuronosyltransferase 1A1 (UGT1A1) is a pivotal enzyme involved in metabolism of SN-38, the active metabolite of irinotecan commonly used to treat metastatic colorectal cancer.	Irinotecan	131-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
20068078-1	2010	PURPOSE: Irinotecan, the prodrug of SN-38, is extensively metabolized by cytochrome P450-3A4 (CYP3A4).	Irinotecan	9-19	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	73-92
20068078-1	2010	PURPOSE: Irinotecan, the prodrug of SN-38, is extensively metabolized by cytochrome P450-3A4 (CYP3A4).	Irinotecan	9-19	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	94-100
20068078-1	2010	PURPOSE: Irinotecan, the prodrug of SN-38, is extensively metabolized by cytochrome P450-3A4 (CYP3A4).	Irinotecan	36-41	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	73-92
20068078-1	2010	PURPOSE: Irinotecan, the prodrug of SN-38, is extensively metabolized by cytochrome P450-3A4 (CYP3A4).	Irinotecan	36-41	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	94-100
20068078-2	2010	A randomized trial was done to assess the utility of an algorithm for individualized irinotecan dose calculation based on a priori CYP3A4 activity measurements by the midazolam clearance test.	Irinotecan	85-95	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	131-137
20068078-11	2010	CONCLUSIONS: Incorporation of CYP3A4 phenotyping in dose calculation resulted in an improved predictability of the pharmacokinetic and toxicity profile of irinotecan, thereby lowering the incidence of severe neutropenia.	Irinotecan	155-165	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	30-36
20068078-12	2010	In combination with UGT1A1*28 genotyping, CYP3A4 phenotype determination should be explored further as a strategy for the individualization of irinotecan treatment.	Irinotecan	143-153	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-48
20551639-5	2010	Treatment of FaDu tumor with a therapeutic dose of irinotecan resulted in depression of xCT protein levels, leading to tumor growth retardation and downregulation of GSH with increased reactive oxygen species (ROS).	Irinotecan	51-61	solute carrier family 7 member 11	Homo sapiens	88-91
19495753-9	2010	In mouse xenograft models, TP300 showed antitumor activity against both BCRP-positive and -negative xenografts, whereas CPT-11 was less active against BCRP-positive xenografts.	Irinotecan	120-126	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	151-155
20551639-7	2010	CONCLUSION: Depression of xCT protein by irinotecan resulted in downregulation of GSH and increase in ROS, which could be the other possible mechanisms of DNA damage by irinotecan.	Irinotecan	41-51	solute carrier family 7 member 11	Homo sapiens	26-29
20551639-7	2010	CONCLUSION: Depression of xCT protein by irinotecan resulted in downregulation of GSH and increase in ROS, which could be the other possible mechanisms of DNA damage by irinotecan.	Irinotecan	169-179	solute carrier family 7 member 11	Homo sapiens	26-29
19835560-6	2010	Variant alleles of UGT1A1 are less capable of conjugating and eliminating SN-38, the active form of the topoisomerase inhibitor irinotecan, and defective alleles for NAT2 are responsible for the well-described acetylation polymorphism that leads to impaired clearance of isoniazid and other agents.	Irinotecan	74-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
20205661-6	2010	Furthermore variations in the UGT1A gene and the ABCB1 gene influence irinotecan metabolism and disposition.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	30-35
19835560-6	2010	Variant alleles of UGT1A1 are less capable of conjugating and eliminating SN-38, the active form of the topoisomerase inhibitor irinotecan, and defective alleles for NAT2 are responsible for the well-described acetylation polymorphism that leads to impaired clearance of isoniazid and other agents.	Irinotecan	128-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
20205661-6	2010	Furthermore variations in the UGT1A gene and the ABCB1 gene influence irinotecan metabolism and disposition.	Irinotecan	70-80	ATP binding cassette subfamily B member 1	Homo sapiens	49-54
20067946-3	2010	Cetuximab, a chimeric monoclonal antibody (mAb) against the epidermal growth factor receptor (EGFR) is FDA approved as a single agent, or in combination with irinotecan, in both irinotecan-naive and refractory patients, and has additional efficacy in combination with oxaliplatin.	Irinotecan	178-188	epidermal growth factor receptor	Homo sapiens	60-92
19819285-7	2010	Adding EPO in human lymphocyte cultures in vitro and in P388 leukemia bearing mice in vivo in the presence of CPT-11 decreased SCEs levels and increased PRIs and MIs were observed compared with cells treated either in vitro or in vivo with CPT-11 alone, which shows that EPO protected cells from the toxic action of CPT-11.	Irinotecan	110-116	erythropoietin	Homo sapiens	7-10
19819285-7	2010	Adding EPO in human lymphocyte cultures in vitro and in P388 leukemia bearing mice in vivo in the presence of CPT-11 decreased SCEs levels and increased PRIs and MIs were observed compared with cells treated either in vitro or in vivo with CPT-11 alone, which shows that EPO protected cells from the toxic action of CPT-11.	Irinotecan	110-116	erythropoietin	Mus musculus	271-274
19819285-7	2010	Adding EPO in human lymphocyte cultures in vitro and in P388 leukemia bearing mice in vivo in the presence of CPT-11 decreased SCEs levels and increased PRIs and MIs were observed compared with cells treated either in vitro or in vivo with CPT-11 alone, which shows that EPO protected cells from the toxic action of CPT-11.	Irinotecan	240-246	erythropoietin	Homo sapiens	7-10
19819285-7	2010	Adding EPO in human lymphocyte cultures in vitro and in P388 leukemia bearing mice in vivo in the presence of CPT-11 decreased SCEs levels and increased PRIs and MIs were observed compared with cells treated either in vitro or in vivo with CPT-11 alone, which shows that EPO protected cells from the toxic action of CPT-11.	Irinotecan	240-246	erythropoietin	Homo sapiens	7-10
19819285-8	2010	EPO"s protective action on human peripheral lymphocytes in vitro and P388 cells in vivo from the topoisomerase I inhibitor CPT-11, lead us to propose it as a geno- and cytoprotective agent.	Irinotecan	123-129	erythropoietin	Homo sapiens	0-3
20798767-8	2010	The iAUC for glucose and insulin were lower following ingestion of RS4 compared with the GLU and PWB trials.	Irinotecan	67-70	insulin	Homo sapiens	25-32
20798767-10	2010	These data illustrate, for the first time, that directly substituting standard starch with RS4(XL), while matched for available carbohydrates, attenuated postprandial glucose and insulin levels in humans.	Irinotecan	91-94	insulin	Homo sapiens	179-186
21486535-1	2010	PURPOSE: Functional polymorphisms of the UGT1A1 gene, particularly the UGT1A1*28 variant, are associated with the severity of the bone marrow suppression in patients with metastatic colorectal cancer receiving irinotecan.	Irinotecan	210-220	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
21486535-1	2010	PURPOSE: Functional polymorphisms of the UGT1A1 gene, particularly the UGT1A1*28 variant, are associated with the severity of the bone marrow suppression in patients with metastatic colorectal cancer receiving irinotecan.	Irinotecan	210-220	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
20053762-10	2010	Irinotecan and gemcitabine antitumor activity was enhanced by SAR-020106 in vivo with minimal toxicity.	Irinotecan	0-10	sarcosine dehydrogenase	Homo sapiens	62-65
20377135-0	2010	The UGT1A1*28 genotype and the toxicity of low-dose irinotecan in patients with advanced lung cancer.	Irinotecan	52-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
20377135-1	2010	The association between the UGT1A1*28 genotype and the severe toxicity of low-dose irinotecan has been controversial, and few studies have examined this association in patients with lung cancer.	Irinotecan	83-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-34
20377135-2	2010	The aim of this study was to assess the association between the UGT1A1*28 genotype and the severe toxicity of low-dose irinotecan in Japanese patients with lung cancer.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
20377135-11	2010	Therefore, low-dose irinotecan could be administered without reducing starting dose in patients with UGT1A1*28 genotype.	Irinotecan	20-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
20067946-3	2010	Cetuximab, a chimeric monoclonal antibody (mAb) against the epidermal growth factor receptor (EGFR) is FDA approved as a single agent, or in combination with irinotecan, in both irinotecan-naive and refractory patients, and has additional efficacy in combination with oxaliplatin.	Irinotecan	178-188	epidermal growth factor receptor	Homo sapiens	94-98
20930093-0	2010	Effects of mannose-binding lectin polymorphisms on irinotecan-induced febrile neutropenia.	Irinotecan	51-61	mannose binding lectin 2	Homo sapiens	11-33
23074403-38	2010	CONCLUSIONS: KRAS status is predictive of outcomes in cetuximab and panitumumab monotherapy, and in cetuximab-irinotecan combination therapy.	Irinotecan	110-120	KRAS proto-oncogene, GTPase	Homo sapiens	13-17
20930093-4	2010	Here, we investigated the effects of MBL2 genotypes on irinotecan-induced febrile neutropenia in patients with solid tumors.	Irinotecan	55-65	mannose binding lectin 2	Homo sapiens	37-41
20930093-5	2010	PATIENTS AND METHODS: Irinotecan-treated patients were genotyped for the MBL2 gene.	Irinotecan	22-32	mannose binding lectin 2	Homo sapiens	73-77
23074403-32	2010	CETUXIMAB-IRINOTECAN COMBINATION THERAPY: There is low GRADE evidence that testing for KRAS may optimize survival benefits in patients without the KRAS mutation (KRAS wildtype, or KRAS WT) compared to those with the mutation.	Irinotecan	10-20	KRAS proto-oncogene, GTPase	Homo sapiens	87-91
23074403-33	2010	However, cetuximab-irinotecan combination treatments based on KRAS status discount any effect of cetuximab in possibly reversing resistance to irinotecan in patients with the mutation, as observed effects were lower than for patients without the mutation.	Irinotecan	19-29	KRAS proto-oncogene, GTPase	Homo sapiens	62-66
20054236-10	2009	Interestingly, under normoxia, Plk2 deficient tumor cells demonstrated increased apoptosis in response to various chemotherapeutic agents including CPT -11 but increased resistance to apoptotic death after CPT-11 treatment under hypoxia, and tumor xenografts comprised of these Plk2-deficient cells were resistant to CPT -11.	Irinotecan	148-155	polo like kinase 2	Homo sapiens	31-35
19920821-1	2009	BACKGROUND: Both irinotecan (CPT-11) and S-1 are active against colorectal cancer; however, as S-1 is a prodrug of 5-fluorouracil (5-FU), 5-FU and its metabolites might inhibit the antitumour effect of CPT-11.	Irinotecan	202-208	proteasome 26S subunit, non-ATPase 1	Homo sapiens	41-44
19920821-1	2009	BACKGROUND: Both irinotecan (CPT-11) and S-1 are active against colorectal cancer; however, as S-1 is a prodrug of 5-fluorouracil (5-FU), 5-FU and its metabolites might inhibit the antitumour effect of CPT-11.	Irinotecan	202-208	proteasome 26S subunit, non-ATPase 1	Homo sapiens	95-98
19920821-1	2009	BACKGROUND: Both irinotecan (CPT-11) and S-1 are active against colorectal cancer; however, as S-1 is a prodrug of 5-fluorouracil (5-FU), 5-FU and its metabolites might inhibit the antitumour effect of CPT-11.	Irinotecan	17-27	proteasome 26S subunit, non-ATPase 1	Homo sapiens	95-98
19920821-1	2009	BACKGROUND: Both irinotecan (CPT-11) and S-1 are active against colorectal cancer; however, as S-1 is a prodrug of 5-fluorouracil (5-FU), 5-FU and its metabolites might inhibit the antitumour effect of CPT-11.	Irinotecan	29-35	proteasome 26S subunit, non-ATPase 1	Homo sapiens	95-98
20054236-10	2009	Interestingly, under normoxia, Plk2 deficient tumor cells demonstrated increased apoptosis in response to various chemotherapeutic agents including CPT -11 but increased resistance to apoptotic death after CPT-11 treatment under hypoxia, and tumor xenografts comprised of these Plk2-deficient cells were resistant to CPT -11.	Irinotecan	206-212	polo like kinase 2	Homo sapiens	31-35
20054236-10	2009	Interestingly, under normoxia, Plk2 deficient tumor cells demonstrated increased apoptosis in response to various chemotherapeutic agents including CPT -11 but increased resistance to apoptotic death after CPT-11 treatment under hypoxia, and tumor xenografts comprised of these Plk2-deficient cells were resistant to CPT -11.	Irinotecan	317-324	polo like kinase 2	Homo sapiens	31-35
19536776-0	2009	The dual EGFR/HER-2 tyrosine kinase inhibitor lapatinib sensitizes colon and gastric cancer cells to the irinotecan active metabolite SN-38.	Irinotecan	105-115	epidermal growth factor receptor	Mus musculus	9-13
19536776-0	2009	The dual EGFR/HER-2 tyrosine kinase inhibitor lapatinib sensitizes colon and gastric cancer cells to the irinotecan active metabolite SN-38.	Irinotecan	105-115	erb-b2 receptor tyrosine kinase 2	Mus musculus	14-19
19536776-0	2009	The dual EGFR/HER-2 tyrosine kinase inhibitor lapatinib sensitizes colon and gastric cancer cells to the irinotecan active metabolite SN-38.	Irinotecan	134-139	epidermal growth factor receptor	Mus musculus	9-13
19536776-0	2009	The dual EGFR/HER-2 tyrosine kinase inhibitor lapatinib sensitizes colon and gastric cancer cells to the irinotecan active metabolite SN-38.	Irinotecan	134-139	erb-b2 receptor tyrosine kinase 2	Mus musculus	14-19
19608554-0	2009	Prolonged neutropenia after irinotecan-based chemotherapy in a child with polymorphisms of UGT1A1 and SLCO1B1.	Irinotecan	28-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
19608554-0	2009	Prolonged neutropenia after irinotecan-based chemotherapy in a child with polymorphisms of UGT1A1 and SLCO1B1.	Irinotecan	28-38	solute carrier organic anion transporter family member 1B1	Homo sapiens	102-109
19608554-1	2009	Genetic polymorphisms of uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1), and SLCO1B1 coding organic anion-transporter polypeptide 1B1, are independent risk factors known to increase irinotecan toxicity in adults.	Irinotecan	193-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-73
19608554-1	2009	Genetic polymorphisms of uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1), and SLCO1B1 coding organic anion-transporter polypeptide 1B1, are independent risk factors known to increase irinotecan toxicity in adults.	Irinotecan	193-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
19608554-1	2009	Genetic polymorphisms of uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1), and SLCO1B1 coding organic anion-transporter polypeptide 1B1, are independent risk factors known to increase irinotecan toxicity in adults.	Irinotecan	193-203	solute carrier organic anion transporter family member 1B1	Homo sapiens	88-95
19608554-5	2009	To our knowledge, this is the first case report of combined genotyping of both UGT1A1 and SLCO1B1 in a child with severe irinotecan toxicity.	Irinotecan	121-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	79-85
19608554-5	2009	To our knowledge, this is the first case report of combined genotyping of both UGT1A1 and SLCO1B1 in a child with severe irinotecan toxicity.	Irinotecan	121-131	solute carrier organic anion transporter family member 1B1	Homo sapiens	90-97
19415281-2	2009	Exploratory analyses of the impact of variability in uridine diphosphate glucuronosyltransferase 1A (UGT1A) genes on irinotecan metabolism and toxicity were conducted.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	53-99
19663821-5	2009	Both HI-6 and irinotecan inhibited ChE/AChE activity but showed different levels of ChE inhibition in plasma and AChE inhibition in the liver and brain tissue.	Irinotecan	14-24	butyrylcholinesterase	Homo sapiens	35-38
19663821-5	2009	Both HI-6 and irinotecan inhibited ChE/AChE activity but showed different levels of ChE inhibition in plasma and AChE inhibition in the liver and brain tissue.	Irinotecan	14-24	acetylcholinesterase (Cartwright blood group)	Homo sapiens	39-43
19663821-5	2009	Both HI-6 and irinotecan inhibited ChE/AChE activity but showed different levels of ChE inhibition in plasma and AChE inhibition in the liver and brain tissue.	Irinotecan	14-24	butyrylcholinesterase	Homo sapiens	40-43
19663821-5	2009	Both HI-6 and irinotecan inhibited ChE/AChE activity but showed different levels of ChE inhibition in plasma and AChE inhibition in the liver and brain tissue.	Irinotecan	14-24	acetylcholinesterase (Cartwright blood group)	Homo sapiens	113-117
19415281-2	2009	Exploratory analyses of the impact of variability in uridine diphosphate glucuronosyltransferase 1A (UGT1A) genes on irinotecan metabolism and toxicity were conducted.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	101-106
19415281-8	2009	UGT1A1 polymorphisms were associated with variability in irinotecan PK.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19885570-7	2009	The combination of safingol/irinotecan at 1:1 molar ratio was found to be additive in HT-29 cells (CI=0.94) and synergistic in LS-174T cells (CI=0.68), and resulted in concentration- and time-dependent down-regulation of p-PKC and p-MARCKS.	Irinotecan	28-38	myristoylated alanine rich protein kinase C substrate	Homo sapiens	233-239
19909340-5	2009	When ABCG2 wild type-expressing cells were incubated with various N-linked glycosylation inhibitors, tunicamycin profoundly suppressed the protein expression level of ABCG2 and, accordingly, reduced the ABCG2-mediated cellular resistance to the cancer chemotherapeutic SN-38.	Irinotecan	269-274	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	5-10
19909340-5	2009	When ABCG2 wild type-expressing cells were incubated with various N-linked glycosylation inhibitors, tunicamycin profoundly suppressed the protein expression level of ABCG2 and, accordingly, reduced the ABCG2-mediated cellular resistance to the cancer chemotherapeutic SN-38.	Irinotecan	269-274	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	167-172
19909340-5	2009	When ABCG2 wild type-expressing cells were incubated with various N-linked glycosylation inhibitors, tunicamycin profoundly suppressed the protein expression level of ABCG2 and, accordingly, reduced the ABCG2-mediated cellular resistance to the cancer chemotherapeutic SN-38.	Irinotecan	269-274	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	167-172
19883083-4	2009	Tdp1 inhibitors have been regarded as potential therapeutics in combination with Top1 inhibitors, such as the camptothecin derivatives, topotecan, and irinotecan, which are used to treat human cancers.	Irinotecan	151-161	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	0-4
20093746-12	2009	rhTGF-beta1 and/or CPT-11 may potentate resistance to chemotherapy by increasing HSP and MRP expression but, on the other hand, they may limit tumour cell spread by decreasing the level of some soluble mediators of inflammation (IL-6 and NO).	Irinotecan	19-25	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	81-84
20093746-12	2009	rhTGF-beta1 and/or CPT-11 may potentate resistance to chemotherapy by increasing HSP and MRP expression but, on the other hand, they may limit tumour cell spread by decreasing the level of some soluble mediators of inflammation (IL-6 and NO).	Irinotecan	19-25	ATP binding cassette subfamily C member 1	Homo sapiens	89-92
20093746-12	2009	rhTGF-beta1 and/or CPT-11 may potentate resistance to chemotherapy by increasing HSP and MRP expression but, on the other hand, they may limit tumour cell spread by decreasing the level of some soluble mediators of inflammation (IL-6 and NO).	Irinotecan	19-25	interleukin 6	Homo sapiens	229-233
20071295-2	2009	Its active metabolite, 7-ethyl-10 hydroxycamptothecin (SN-38) is glucuronidated by a uridine-diphosphoglucuronosyltransferase (UGT1A1) to form an inactive metabolite.	Irinotecan	23-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	127-133
20071295-2	2009	Its active metabolite, 7-ethyl-10 hydroxycamptothecin (SN-38) is glucuronidated by a uridine-diphosphoglucuronosyltransferase (UGT1A1) to form an inactive metabolite.	Irinotecan	55-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	127-133
19915942-3	2009	The immoglobulin (Ig) G1 EGFR-targeting monoclonal antibody (mAb), cetuximab, has been shown to provide significant clinical benefits when added to standard irinotecan- and oxaliplatin-containing chemotherapy regimens, first-line, in patients with KRAS wild-type mCRC.	Irinotecan	157-167	epidermal growth factor receptor	Homo sapiens	25-29
19770637-0	2009	UGT1A1 genotyping: a predictor of irinotecan-associated side effects and drug efficacy?	Irinotecan	34-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19858398-10	2009	Trends (of doubtful significance) were seen for associations of XRCC1, ERCC2, and GSTP1 with toxicity during irinotecan regimens: XRCC1, primary end point, any irinotecan-containing regimen (P = .045); ERCC2, secondary end point, irinotecan alone (P = .003); GSTP1, secondary end point; IrFU (P = .039); and irinotecan alone (P = .05).	Irinotecan	109-119	glutathione S-transferase pi 1	Homo sapiens	82-87
19858398-13	2009	Further investigation of XRCC1, ERCC2, and GSTP1 as potential predictors of irinotecan toxicity is warranted.	Irinotecan	76-86	glutathione S-transferase pi 1	Homo sapiens	43-48
19770637-3	2009	SN-38 is inactivated by uridine disphosphate glucuronosyl transferase 1 (UGT1A1) into the inactive compound SN-38G, which is excreted with the bile.This review concentrates on a critical evaluation of UGT1A1 gene polymorphism as a predictor of toxicity and treatment efficacy in patients who received irinotecan for metastatic colorectal cancer.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
19770637-3	2009	SN-38 is inactivated by uridine disphosphate glucuronosyl transferase 1 (UGT1A1) into the inactive compound SN-38G, which is excreted with the bile.This review concentrates on a critical evaluation of UGT1A1 gene polymorphism as a predictor of toxicity and treatment efficacy in patients who received irinotecan for metastatic colorectal cancer.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	201-207
19770637-3	2009	SN-38 is inactivated by uridine disphosphate glucuronosyl transferase 1 (UGT1A1) into the inactive compound SN-38G, which is excreted with the bile.This review concentrates on a critical evaluation of UGT1A1 gene polymorphism as a predictor of toxicity and treatment efficacy in patients who received irinotecan for metastatic colorectal cancer.	Irinotecan	301-311	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
19673886-0	2009	Prolonged low-dose administration of the cyclooxygenase-2 inhibitor celecoxib enhances the antitumor activity of irinotecan against neuroblastoma xenografts.	Irinotecan	113-123	prostaglandin-endoperoxide synthase 2	Homo sapiens	41-57
19796956-3	2009	Results have also shown that 2,9-bis(3-(dimethylamino)propoxy)-6-(4-(3-(dimethylamino)propoxy)phenyl)-11H-indeno[1,2-c]quinolin-11-one (17), which exhibited GI(50) of 0.60 and 0.68 microM against the growth of Hep G2 and A549, respectively, was more active than the positive topotecan and irinotecan.	Irinotecan	289-299	DNL-type zinc finger	Homo sapiens	210-213
19673886-6	2009	Induction of apoptosis by CPT-11 with and without celecoxib was associated with the up-regulation of Bax expression and the down-regulation of Bcl-2 expression.	Irinotecan	26-32	BCL2 associated X, apoptosis regulator	Homo sapiens	101-104
19673886-6	2009	Induction of apoptosis by CPT-11 with and without celecoxib was associated with the up-regulation of Bax expression and the down-regulation of Bcl-2 expression.	Irinotecan	26-32	BCL2 apoptosis regulator	Homo sapiens	143-148
20037407-10	2009	In spite of combined S-1 and CPT-11 chemotherapy, the CEA level increased, and lymph nodes were getting larger.	Irinotecan	29-35	CEA cell adhesion molecule 3	Homo sapiens	54-57
19917537-1	2009	Therapy for metastatic colorectal cancer has been improved in terms of response rate, time to progression and overall survival by the emergence of anti-EGFR monoclonal antibodies (cetuximab and panitumumab) in combination with standard cytotoxic chemotherapy (oxaliplatin or CPT-11-based combinations).	Irinotecan	275-281	epidermal growth factor receptor	Homo sapiens	152-156
19738126-1	2009	PURPOSE: To study the power of the epidermal growth factor receptor (EGFR) epiregulin (EREG) and amphiregulin (AREG) ligands" expression in primary tumors to predict the outcome in patients with chemorefractory metastatic colorectal cancer (cmCRC) treated with the combination of cetuximab and irinotecan.	Irinotecan	294-304	epidermal growth factor receptor	Homo sapiens	35-67
19859999-0	2009	UGT1A1 gene polymorphism: impact on toxicity and efficacy of irinotecan-based regimens in metastatic colorectal cancer.	Irinotecan	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19859999-1	2009	AIM: To investigate the correlation between uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) gene polymorphisms and irinotecan-associated side effects and parameters of drug efficacy in patients with metastatic colorectal cancer (mCRC) receiving a low-dose weekly irinotecan chemotherapeutic regimen.	Irinotecan	125-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-92
19859999-1	2009	AIM: To investigate the correlation between uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) gene polymorphisms and irinotecan-associated side effects and parameters of drug efficacy in patients with metastatic colorectal cancer (mCRC) receiving a low-dose weekly irinotecan chemotherapeutic regimen.	Irinotecan	125-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
19859999-2	2009	METHODS: Genotypes were retrospectively evaluated by gene scan analysis on the ABI 310 sequencer of the TATAA box in the promoter region of the UGT1A1 gene in blood samples from 105 patients who had received 1st line irinotecan-based chemotherapy for mCRC.	Irinotecan	217-227	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
19859999-7	2009	CONCLUSION: This analysis demonstrates the non-significant influence of the UGT1A1 gene polymorphism on efficacy and rate of irinotecan-associated toxicity in mCRC patients receiving low-dose irinotecan based chemotherapy.	Irinotecan	125-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
19738126-1	2009	PURPOSE: To study the power of the epidermal growth factor receptor (EGFR) epiregulin (EREG) and amphiregulin (AREG) ligands" expression in primary tumors to predict the outcome in patients with chemorefractory metastatic colorectal cancer (cmCRC) treated with the combination of cetuximab and irinotecan.	Irinotecan	294-304	epidermal growth factor receptor	Homo sapiens	69-73
19738126-13	2009	CONCLUSION: Expression of EGFR ligands in primary tumors significantly predicts outcome in KRAS WT cmCRC treated with cetuximab and irinotecan.	Irinotecan	132-142	epidermal growth factor receptor	Homo sapiens	26-30
19738126-13	2009	CONCLUSION: Expression of EGFR ligands in primary tumors significantly predicts outcome in KRAS WT cmCRC treated with cetuximab and irinotecan.	Irinotecan	132-142	KRAS proto-oncogene, GTPase	Homo sapiens	91-95
19765103-0	2009	Irinotecan-induced mucositis manifesting as diarrhoea corresponds with an amended intestinal flora and mucin profile.	Irinotecan	0-10	solute carrier family 13 member 2	Rattus norvegicus	103-108
19765103-3	2009	Bacterial beta-glucuronidase is thought to be involved in the metabolism of irinotecan, implicating the intestinal flora.	Irinotecan	76-86	glucuronidase, beta	Rattus norvegicus	10-28
19765103-12	2009	In conclusion, irinotecan-induced diarrhoea may be caused by an increase in some beta-glucuronidase-producing bacteria, especially E. coli, exacerbating the toxicity of active metabolites.	Irinotecan	15-25	glucuronidase, beta	Rattus norvegicus	81-99
19696792-0	2009	Single nucleotide polymorphism in ABCG2 is associated with irinotecan-induced severe myelosuppression.	Irinotecan	59-69	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-39
19696792-6	2009	Although only limited subjects were investigated, our results suggested that a genetic polymorphism in ABCG2 might alter the transport activity for the drug and elevate the systemic circulation level of irinotecan, leading to severe myelosuppression.	Irinotecan	203-213	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	103-108
19332770-1	2009	Bevacizumab is a humanized monoclonal antibody against vascular endothelial growth factor (VEGF) that has efficacy in recurrent malignant gliomas, particularly in combination with irinotecan.	Irinotecan	180-190	vascular endothelial growth factor A	Homo sapiens	55-89
19789330-0	2009	CEACAM5-targeted therapy of human colonic and pancreatic cancer xenografts with potent labetuzumab-SN-38 immunoconjugates.	Irinotecan	99-104	CEA cell adhesion molecule 5	Homo sapiens	0-7
19789330-1	2009	PURPOSE: To improve the efficacy and reduce the gastrointestinal toxicity of the cancer prodrug, CPT-11, we have developed immunoconjugates of its active form, SN-38, and an anti-CEACAM5 antibody for targeted chemotherapy.	Irinotecan	97-103	CEA cell adhesion molecule 5	Homo sapiens	179-186
19789330-2	2009	EXPERIMENTAL DESIGN: SN-38 conjugates of the anti-CEACAM5 monoclonal antibody, labetuzumab (hMN-14), varying in the nature of the cross-linker attachment at the drug"s 20-hydroxyl position, were evaluated in vitro, in metastatic and/or s.c. human colonic and pancreatic cancer xenografts in nude mice using appropriate controls, and in a CEACAM5-negative tumor model.	Irinotecan	21-26	CEA cell adhesion molecule 5	Homo sapiens	50-57
20021826-8	2009	Under hypoxic conditions, the expression of HIF-1alpha and VEGF increased as time accumulated, Bevacizumab combined with SN-38 almost completely inhibited the expression of HIF-1alpha and VEGF.	Irinotecan	121-126	hypoxia inducible factor 1 subunit alpha	Homo sapiens	44-54
20021826-8	2009	Under hypoxic conditions, the expression of HIF-1alpha and VEGF increased as time accumulated, Bevacizumab combined with SN-38 almost completely inhibited the expression of HIF-1alpha and VEGF.	Irinotecan	121-126	hypoxia inducible factor 1 subunit alpha	Homo sapiens	173-183
20021826-8	2009	Under hypoxic conditions, the expression of HIF-1alpha and VEGF increased as time accumulated, Bevacizumab combined with SN-38 almost completely inhibited the expression of HIF-1alpha and VEGF.	Irinotecan	121-126	vascular endothelial growth factor A	Homo sapiens	188-192
20021826-10	2009	CONCLUSION: These findings suggest the anti-proliferation effect of bevacizumab and SN-38 was schedule-dependent, and the synergistic effect of Bevacizumab and SN-38 was related to drug modulation of the HIF-1alpha and MAP kinase pathway.	Irinotecan	160-165	hypoxia inducible factor 1 subunit alpha	Homo sapiens	204-214
19332770-1	2009	Bevacizumab is a humanized monoclonal antibody against vascular endothelial growth factor (VEGF) that has efficacy in recurrent malignant gliomas, particularly in combination with irinotecan.	Irinotecan	180-190	vascular endothelial growth factor A	Homo sapiens	91-95
19785749-1	2009	BACKGROUND: The anti-VEGF antibody bevacizumab associated with an irinotecan or oxaliplatin-based chemotherapy was proved to be superior to the chemotherapy alone in first or second line treatment of metastatic colorectal cancer (mCRC).	Irinotecan	66-76	vascular endothelial growth factor A	Homo sapiens	21-25
19644023-4	2009	Irinotecan toxicity in colorectal cancer is more common in patients with reduced-activity UGT1A alleles, resulting in excessive exposure to the potent SN-38 metabolite.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	90-95
19687340-0	2009	Tyrosine kinase inhibitor enhances the bioavailability of oral irinotecan in pediatric patients with refractory solid tumors.	Irinotecan	63-73	TXK tyrosine kinase	Homo sapiens	0-15
19728911-12	2009	CONCLUSIONS: Transient CEA surges can be observed in Chinese MCRC patients receiving oxaplatin or irinotecan-based chemotherapy, which does not indicate tumor progression, but good therapeutic efficacy.	Irinotecan	98-108	CEA cell adhesion molecule 3	Homo sapiens	23-26
19517472-1	2009	BACKGROUND: The objective of this study was to examine the cost effectiveness of using a pharmacogenetic test for uridine diphosphate glycosyltransferase 1A1*28 (UGT1A1*28) variant homozygosity before administering irinotecan to patients with metastatic colorectal cancer.	Irinotecan	215-225	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	162-168
19517472-4	2009	With genetic testing, irinotecan dosage was reduced 25% in homozygotes with the UGT1A1*28 variant allele.	Irinotecan	22-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
19755821-1	2009	SN-38, an active metabolite of irinotecan (CPT-11), is glucuronidated into SN-38G mainly by UGT1A1, during detoxification.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
19755821-1	2009	SN-38, an active metabolite of irinotecan (CPT-11), is glucuronidated into SN-38G mainly by UGT1A1, during detoxification.	Irinotecan	31-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
19755821-1	2009	SN-38, an active metabolite of irinotecan (CPT-11), is glucuronidated into SN-38G mainly by UGT1A1, during detoxification.	Irinotecan	43-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
19755821-1	2009	SN-38, an active metabolite of irinotecan (CPT-11), is glucuronidated into SN-38G mainly by UGT1A1, during detoxification.	Irinotecan	75-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
19755821-2	2009	However, significant interindividual pharmacokinetic variability in SN-38 is caused by factors, including inherited predispositions that may affect the function and expression of UGT1A1.	Irinotecan	68-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	179-185
20084161-8	2009	The US Food and Drug Administration has approved the UDP-glucuronosyltransferase 1A1 test in patients treated with irinotecan, and additional approval of newer tests is anticipated.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	53-84
19493273-4	2009	As with gefitinib, erlotinib effectively reversed BCRP-mediated resistance to SN-38 (7-ethyl-10-hydroxycamptothecin) and mitoxantrone.	Irinotecan	78-83	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	50-54
19493273-4	2009	As with gefitinib, erlotinib effectively reversed BCRP-mediated resistance to SN-38 (7-ethyl-10-hydroxycamptothecin) and mitoxantrone.	Irinotecan	85-115	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	50-54
19644023-4	2009	Irinotecan toxicity in colorectal cancer is more common in patients with reduced-activity UGT1A alleles, resulting in excessive exposure to the potent SN-38 metabolite.	Irinotecan	151-156	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	90-95
19712476-0	2009	Epidermal Growth Factor Receptor (EGFR) gene copy number (GCN) correlates with clinical activity of irinotecan-cetuximab in K-RAS wild-type colorectal cancer: a fluorescence in situ (FISH) and chromogenic in situ hybridization (CISH) analysis.	Irinotecan	100-110	KRAS proto-oncogene, GTPase	Homo sapiens	124-129
19603018-0	2009	KRAS codon 61, 146 and BRAF mutations predict resistance to cetuximab plus irinotecan in KRAS codon 12 and 13 wild-type metastatic colorectal cancer.	Irinotecan	75-85	KRAS proto-oncogene, GTPase	Homo sapiens	0-4
20719167-2	2009	Irinotecan, oxidized by CYP3A4 to produce inactive compounds, is used for treatment of various cancers including advanced non small cell lung cancer (NSCLC) patients.	Irinotecan	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	24-30
20719167-3	2009	CYP3A4(*)16B polymorphism was associated with decreased metabolism of irrinotecan.	Irinotecan	70-81	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
20719167-4	2009	Irinotecan is also metabolized by carboxylesterase to its principal active metabolite, SN-38, which is subsequently glucuronidated by UGT1As to form the inactive compound SN-38G.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-138
20719167-4	2009	Irinotecan is also metabolized by carboxylesterase to its principal active metabolite, SN-38, which is subsequently glucuronidated by UGT1As to form the inactive compound SN-38G.	Irinotecan	87-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-138
20719167-4	2009	Irinotecan is also metabolized by carboxylesterase to its principal active metabolite, SN-38, which is subsequently glucuronidated by UGT1As to form the inactive compound SN-38G.	Irinotecan	171-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	134-138
20719167-5	2009	UGT1A1(*)28 and UGT1A1(*)6 polymorphisms were useful for predicting severe toxicity with NSCLC patients treated with irinotecan-based chemotherapy.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
20719167-5	2009	UGT1A1(*)28 and UGT1A1(*)6 polymorphisms were useful for predicting severe toxicity with NSCLC patients treated with irinotecan-based chemotherapy.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
19603018-0	2009	KRAS codon 61, 146 and BRAF mutations predict resistance to cetuximab plus irinotecan in KRAS codon 12 and 13 wild-type metastatic colorectal cancer.	Irinotecan	75-85	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	23-27
19603018-0	2009	KRAS codon 61, 146 and BRAF mutations predict resistance to cetuximab plus irinotecan in KRAS codon 12 and 13 wild-type metastatic colorectal cancer.	Irinotecan	75-85	KRAS proto-oncogene, GTPase	Homo sapiens	89-93
19433978-17	2009	Our case is the first clinical piece of evidence that demonstrates an increased sensitivity to camptothecin-11 and a reduced topoisomerase I relaxation activity in BRCA2 associated pancreatic cancer.	Irinotecan	95-110	BRCA2 DNA repair associated	Homo sapiens	164-169
19664991-5	2009	Furthermore, we found that specifically inhibiting human DLL4 in the tumor, either alone or in combination with the chemotherapeutic agent irinotecan, reduced cancer stem cell frequency, as shown by flow cytometric and in vivo tumorigenicity studies.	Irinotecan	139-149	delta like canonical Notch ligand 4	Homo sapiens	57-61
19491654-7	2009	In SK-OV-3 cells, but not in OVCAR-3 cells, CPT-11/SN-38 exposures alone increased p21(waf1/cip1) expression.	Irinotecan	44-50	cyclin dependent kinase inhibitor 1A	Homo sapiens	83-96
19653336-6	2009	Irinotecan sensitizes p53 wild type, mutant and null cells to Fas-mediated cell apoptosis in CRC cells.	Irinotecan	0-10	tumor protein p53	Homo sapiens	22-25
19653336-7	2009	Wild type p53 cells were more sensitive to irinotecan than mutated p53.	Irinotecan	43-53	tumor protein p53	Homo sapiens	10-13
19653336-8	2009	Irinotecan has an anti-VEGF effect inhibiting endothelial cell proliferation, increasing apoptosis and reducing microvascular density which is only limited by irinotecan toxicity levels.	Irinotecan	0-10	vascular endothelial growth factor A	Homo sapiens	23-27
19653336-10	2009	p53 and VEGF status of the patients" tumour is likely to affect the responsiveness of CRC to irinotecan.	Irinotecan	93-103	tumor protein p53	Homo sapiens	0-3
19653336-10	2009	p53 and VEGF status of the patients" tumour is likely to affect the responsiveness of CRC to irinotecan.	Irinotecan	93-103	vascular endothelial growth factor A	Homo sapiens	8-12
19491654-5	2009	In OVCAR-3 cells, p53 gene therapy inhibited the cell growth and sensitized cells to CPT-11/SN-38, but not to docetaxel.	Irinotecan	85-91	tumor protein p53	Homo sapiens	18-21
19491654-7	2009	In SK-OV-3 cells, but not in OVCAR-3 cells, CPT-11/SN-38 exposures alone increased p21(waf1/cip1) expression.	Irinotecan	51-56	cyclin dependent kinase inhibitor 1A	Homo sapiens	83-96
19491654-5	2009	In OVCAR-3 cells, p53 gene therapy inhibited the cell growth and sensitized cells to CPT-11/SN-38, but not to docetaxel.	Irinotecan	92-97	tumor protein p53	Homo sapiens	18-21
19457654-6	2009	In conclusion, in this largest study on capecitabine with or without irinotecan to date we found a predictive value of DPD expression.	Irinotecan	69-79	dihydropyrimidine dehydrogenase	Homo sapiens	119-122
19359405-2	2009	For example, irinotecan, a carbamate prodrug used in the treatment of colorectal cancer, is biotransformed in vivo by CES2 in intestine and liver, thereby producing a potent topoisomerase I inhibitor.	Irinotecan	13-23	carboxylesterase 2H	Mus musculus	118-122
19491654-11	2009	These results support the combination of p53 gene therapy with topoisomerase I inhibitors SN-38/CPT-11 when tumour cells contain mutated p53.	Irinotecan	90-95	tumor protein p53	Homo sapiens	137-140
19491654-11	2009	These results support the combination of p53 gene therapy with topoisomerase I inhibitors SN-38/CPT-11 when tumour cells contain mutated p53.	Irinotecan	96-102	tumor protein p53	Homo sapiens	137-140
19622774-5	2009	Depletion of Drg1 by small interfering RNA induced up-regulation of Bim and its accumulation in the mitochondria, which correlated with loss of mitochondrial membrane potential and induction of apoptosis in cells exposed to SN-38.	Irinotecan	224-229	developmentally regulated GTP binding protein 1	Homo sapiens	13-17
19622774-5	2009	Depletion of Drg1 by small interfering RNA induced up-regulation of Bim and its accumulation in the mitochondria, which correlated with loss of mitochondrial membrane potential and induction of apoptosis in cells exposed to SN-38.	Irinotecan	224-229	BCL2 like 11	Homo sapiens	68-71
19436196-2	2009	We hypothesized that the expression of topoisomerase I (Topo I) and thymidylate synthase (TS) may help predict the treatment response in patients undergoing irinotecan and capecitabine-based chemoradiation.	Irinotecan	157-167	thymidylate synthetase	Homo sapiens	68-88
19436196-2	2009	We hypothesized that the expression of topoisomerase I (Topo I) and thymidylate synthase (TS) may help predict the treatment response in patients undergoing irinotecan and capecitabine-based chemoradiation.	Irinotecan	157-167	thymidylate synthetase	Homo sapiens	90-92
19620803-1	2009	UNLABELLED: Irinotecan hydrochloride (CPT-11) is converted to SN-38 by carboxylesterase, SN-38 is conjugated by UDP-glucuronosyl- transferase (UGT) to SN-38G.	Irinotecan	62-67	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	112-141
19620803-1	2009	UNLABELLED: Irinotecan hydrochloride (CPT-11) is converted to SN-38 by carboxylesterase, SN-38 is conjugated by UDP-glucuronosyl- transferase (UGT) to SN-38G.	Irinotecan	38-44	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	143-146
19620803-1	2009	UNLABELLED: Irinotecan hydrochloride (CPT-11) is converted to SN-38 by carboxylesterase, SN-38 is conjugated by UDP-glucuronosyl- transferase (UGT) to SN-38G.	Irinotecan	62-67	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	143-146
19620803-1	2009	UNLABELLED: Irinotecan hydrochloride (CPT-11) is converted to SN-38 by carboxylesterase, SN-38 is conjugated by UDP-glucuronosyl- transferase (UGT) to SN-38G.	Irinotecan	12-36	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	112-141
19620803-1	2009	UNLABELLED: Irinotecan hydrochloride (CPT-11) is converted to SN-38 by carboxylesterase, SN-38 is conjugated by UDP-glucuronosyl- transferase (UGT) to SN-38G.	Irinotecan	89-94	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	112-141
19620803-1	2009	UNLABELLED: Irinotecan hydrochloride (CPT-11) is converted to SN-38 by carboxylesterase, SN-38 is conjugated by UDP-glucuronosyl- transferase (UGT) to SN-38G.	Irinotecan	12-36	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	143-146
19620803-1	2009	UNLABELLED: Irinotecan hydrochloride (CPT-11) is converted to SN-38 by carboxylesterase, SN-38 is conjugated by UDP-glucuronosyl- transferase (UGT) to SN-38G.	Irinotecan	38-44	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	112-141
19620803-1	2009	UNLABELLED: Irinotecan hydrochloride (CPT-11) is converted to SN-38 by carboxylesterase, SN-38 is conjugated by UDP-glucuronosyl- transferase (UGT) to SN-38G.	Irinotecan	89-94	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	143-146
19620803-1	2009	UNLABELLED: Irinotecan hydrochloride (CPT-11) is converted to SN-38 by carboxylesterase, SN-38 is conjugated by UDP-glucuronosyl- transferase (UGT) to SN-38G.	Irinotecan	89-94	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	112-141
19620803-1	2009	UNLABELLED: Irinotecan hydrochloride (CPT-11) is converted to SN-38 by carboxylesterase, SN-38 is conjugated by UDP-glucuronosyl- transferase (UGT) to SN-38G.	Irinotecan	89-94	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	143-146
19620808-1	2009	Severe neutropenia attributable to irinotecan hydrochloride (CPT-11) is reportedly associated with gene polymorphism of UGT1A1 related to its metabolism.	Irinotecan	35-59	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	120-126
19620808-1	2009	Severe neutropenia attributable to irinotecan hydrochloride (CPT-11) is reportedly associated with gene polymorphism of UGT1A1 related to its metabolism.	Irinotecan	61-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	120-126
19620808-9	2009	Nine days following administration of the first course, we found neutropenia of grade 3 and a fever of 38 degrees C. Analysis of the UGT1A1 gene polymorphism after symptom improvement revealed UGT1A1(*)28 homozygosity in both cases, which suggests that when FOLFIRI is conducted on a patient with homozygous UGT1A1(*)28, it is necessary to pay attention to neutropenia even with a CPT-11 dosage of 120 mg/m(2).	Irinotecan	381-387	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	133-139
19620808-9	2009	Nine days following administration of the first course, we found neutropenia of grade 3 and a fever of 38 degrees C. Analysis of the UGT1A1 gene polymorphism after symptom improvement revealed UGT1A1(*)28 homozygosity in both cases, which suggests that when FOLFIRI is conducted on a patient with homozygous UGT1A1(*)28, it is necessary to pay attention to neutropenia even with a CPT-11 dosage of 120 mg/m(2).	Irinotecan	381-387	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	193-199
19620808-9	2009	Nine days following administration of the first course, we found neutropenia of grade 3 and a fever of 38 degrees C. Analysis of the UGT1A1 gene polymorphism after symptom improvement revealed UGT1A1(*)28 homozygosity in both cases, which suggests that when FOLFIRI is conducted on a patient with homozygous UGT1A1(*)28, it is necessary to pay attention to neutropenia even with a CPT-11 dosage of 120 mg/m(2).	Irinotecan	381-387	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	193-199
19531575-1	2009	Irinotecan is a topoisomerase-I (Top-I) inhibitor used for the treatment of colorectal cancer.	Irinotecan	0-10	DNA topoisomerase I	Homo sapiens	16-31
19531575-13	2009	If confirmed in other models, these results suggest that p16 and p53 status affects the 5-aza-irinotecan interaction.	Irinotecan	94-104	cyclin dependent kinase inhibitor 2A	Homo sapiens	57-60
19513514-14	2009	However, significant genotypic variation of UGT1A1, which was assumed to affect irinotecan toxicity, was not observed to affect RR, toxicity or survival.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
19604089-1	2009	AIMS: A recent study found that variation in camptothecin pharmacodynamic genes (TOP1, PARP1, TDP1 and XRCC1) correlated with efficacy and risk of neutropenia in irinotecan-treated cancer patients (median dose: 180 mg/m2), which suggests that these genes might predict outcomes to irinotecan-based therapies.	Irinotecan	162-172	poly(ADP-ribose) polymerase 1	Homo sapiens	87-92
19604089-1	2009	AIMS: A recent study found that variation in camptothecin pharmacodynamic genes (TOP1, PARP1, TDP1 and XRCC1) correlated with efficacy and risk of neutropenia in irinotecan-treated cancer patients (median dose: 180 mg/m2), which suggests that these genes might predict outcomes to irinotecan-based therapies.	Irinotecan	162-172	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	94-98
19604089-1	2009	AIMS: A recent study found that variation in camptothecin pharmacodynamic genes (TOP1, PARP1, TDP1 and XRCC1) correlated with efficacy and risk of neutropenia in irinotecan-treated cancer patients (median dose: 180 mg/m2), which suggests that these genes might predict outcomes to irinotecan-based therapies.	Irinotecan	162-172	X-ray repair cross complementing 1	Homo sapiens	103-108
19604089-1	2009	AIMS: A recent study found that variation in camptothecin pharmacodynamic genes (TOP1, PARP1, TDP1 and XRCC1) correlated with efficacy and risk of neutropenia in irinotecan-treated cancer patients (median dose: 180 mg/m2), which suggests that these genes might predict outcomes to irinotecan-based therapies.	Irinotecan	281-291	X-ray repair cross complementing 1	Homo sapiens	103-108
19531575-13	2009	If confirmed in other models, these results suggest that p16 and p53 status affects the 5-aza-irinotecan interaction.	Irinotecan	94-104	tumor protein p53	Homo sapiens	65-68
19531575-1	2009	Irinotecan is a topoisomerase-I (Top-I) inhibitor used for the treatment of colorectal cancer.	Irinotecan	0-10	DNA topoisomerase I	Homo sapiens	33-38
19531575-3	2009	5-Aza may enhance irinotecan cytotoxicity by at least one of the following mechanisms: (a) Top-I promoter demethylation, (b) activation of genes involved in Top-I transcriptional regulation (p16 or Sp1), and (c) modulation of the cell cycle and apoptosis after DNA damage.	Irinotecan	18-28	DNA topoisomerase I	Homo sapiens	91-96
19531575-3	2009	5-Aza may enhance irinotecan cytotoxicity by at least one of the following mechanisms: (a) Top-I promoter demethylation, (b) activation of genes involved in Top-I transcriptional regulation (p16 or Sp1), and (c) modulation of the cell cycle and apoptosis after DNA damage.	Irinotecan	18-28	DNA topoisomerase I	Homo sapiens	157-162
19531575-3	2009	5-Aza may enhance irinotecan cytotoxicity by at least one of the following mechanisms: (a) Top-I promoter demethylation, (b) activation of genes involved in Top-I transcriptional regulation (p16 or Sp1), and (c) modulation of the cell cycle and apoptosis after DNA damage.	Irinotecan	18-28	cyclin dependent kinase inhibitor 2A	Homo sapiens	191-194
19531575-10	2009	p16 demethylation was also associated with enhanced cell cycle arrest after irinotecan treatment.	Irinotecan	76-86	cyclin dependent kinase inhibitor 2A	Homo sapiens	0-3
19217207-3	2009	Accordingly, TRAP1 levels were increased in HT-29 colorectal carcinoma cells resistant to 5-fluorouracil, oxaliplatin and irinotecan.	Irinotecan	122-132	TNF receptor associated protein 1	Homo sapiens	13-18
19217207-5	2009	Interestingly, TRAP1 overexpression leads to 5-fluorouracil-, oxaliplatin- and irinotecan-resistant phenotypes in different neoplastic cells.	Irinotecan	79-89	TNF receptor associated protein 1	Homo sapiens	15-20
19217207-6	2009	Conversely, the inhibition of TRAP1 activity by TRAP1 ATPase antagonist, shepherdin, increased the sensitivity to oxaliplatin and irinotecan in colorectal carcinoma cells resistant to the single agents.	Irinotecan	130-140	TNF receptor associated protein 1	Homo sapiens	30-35
19217207-6	2009	Conversely, the inhibition of TRAP1 activity by TRAP1 ATPase antagonist, shepherdin, increased the sensitivity to oxaliplatin and irinotecan in colorectal carcinoma cells resistant to the single agents.	Irinotecan	130-140	TNF receptor associated protein 1	Homo sapiens	48-53
19217207-6	2009	Conversely, the inhibition of TRAP1 activity by TRAP1 ATPase antagonist, shepherdin, increased the sensitivity to oxaliplatin and irinotecan in colorectal carcinoma cells resistant to the single agents.	Irinotecan	130-140	dynein axonemal heavy chain 8	Homo sapiens	54-60
19201079-10	2009	The overexpression of ABCG2/BCRP was involved in the mechanism of resistance in SN-38-tolerant cells, and ABCC1/MRP1, ABCC3/MRP3, ABCC5/MRP5, and GGT1 may also have participated.	Irinotecan	80-85	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	22-27
19201079-10	2009	The overexpression of ABCG2/BCRP was involved in the mechanism of resistance in SN-38-tolerant cells, and ABCC1/MRP1, ABCC3/MRP3, ABCC5/MRP5, and GGT1 may also have participated.	Irinotecan	80-85	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	28-32
19528468-8	2009	TS protein level significantly decreased after exposure to SN-38.	Irinotecan	59-64	thymidylate synthetase	Homo sapiens	0-2
19528468-9	2009	CONCLUSION: The sequence dependency between SN-38 and 5-FU against colon cancer cells may be related to the dual action on cell cycle regulation by 5-FU and to the down-regulation of TS level by SN-38.	Irinotecan	44-49	thymidylate synthetase	Homo sapiens	183-185
19528468-9	2009	CONCLUSION: The sequence dependency between SN-38 and 5-FU against colon cancer cells may be related to the dual action on cell cycle regulation by 5-FU and to the down-regulation of TS level by SN-38.	Irinotecan	195-200	thymidylate synthetase	Homo sapiens	183-185
19581859-0	2009	Epidermal growth factor receptor expression discrepancies in metastatic colorectal cancer patients treated with cetuximab plus irinotecan-based chemotherapy refractory to irinotecan and oxaliplatin.	Irinotecan	127-137	epidermal growth factor receptor	Homo sapiens	0-32
18998135-2	2009	Irinotecan is used to treat a variety of solid tumours, through the inhibition of DNA topoisomerase I and is linked with severe mucositis and diarrhoea.	Irinotecan	0-10	DNA topoisomerase I	Rattus norvegicus	82-101
18998135-11	2009	CONCLUSIONS: Irinotecan causes an increase in mucin secretion and a net decrease in mucin-producing goblet cells, and the expression of Muc2 and Muc4 in the gastrointestinal tract is altered following treatment.	Irinotecan	13-23	solute carrier family 13 member 2	Rattus norvegicus	46-51
18998135-11	2009	CONCLUSIONS: Irinotecan causes an increase in mucin secretion and a net decrease in mucin-producing goblet cells, and the expression of Muc2 and Muc4 in the gastrointestinal tract is altered following treatment.	Irinotecan	13-23	solute carrier family 13 member 2	Rattus norvegicus	84-89
19581859-0	2009	Epidermal growth factor receptor expression discrepancies in metastatic colorectal cancer patients treated with cetuximab plus irinotecan-based chemotherapy refractory to irinotecan and oxaliplatin.	Irinotecan	171-181	epidermal growth factor receptor	Homo sapiens	0-32
19349540-7	2009	Almost 30% of the variability in SN-38 (the active metabolite of CPT-11) AUC is explained by ABCC1 1684T&gt;C, ABCB1 IVS9 -44A&gt;G, and UGT1A1*93 (P = .004).	Irinotecan	65-71	ATP binding cassette subfamily C member 1	Homo sapiens	93-98
19398573-0	2009	PTEN expression and KRAS mutations on primary tumors and metastases in the prediction of benefit from cetuximab plus irinotecan for patients with metastatic colorectal cancer.	Irinotecan	117-127	phosphatase and tensin homolog	Homo sapiens	0-4
19398573-14	2009	CONCLUSION: PTEN loss in metastases may be predictive of resistance to cetuximab plus irinotecan.	Irinotecan	86-96	phosphatase and tensin homolog	Homo sapiens	12-16
19349540-7	2009	Almost 30% of the variability in SN-38 (the active metabolite of CPT-11) AUC is explained by ABCC1 1684T&gt;C, ABCB1 IVS9 -44A&gt;G, and UGT1A1*93 (P = .004).	Irinotecan	65-71	ATP binding cassette subfamily B member 1	Homo sapiens	111-116
19349540-7	2009	Almost 30% of the variability in SN-38 (the active metabolite of CPT-11) AUC is explained by ABCC1 1684T&gt;C, ABCB1 IVS9 -44A&gt;G, and UGT1A1*93 (P = .004).	Irinotecan	65-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
19349540-10	2009	CONCLUSION: On the basis of this exploratory analysis, common polymorphisms in genes encoding for ABC and SLC transporters may have a significant impact on the pharmacokinetics and pharmacodynamics of CPT-11.	Irinotecan	201-207	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	98-101
19349540-10	2009	CONCLUSION: On the basis of this exploratory analysis, common polymorphisms in genes encoding for ABC and SLC transporters may have a significant impact on the pharmacokinetics and pharmacodynamics of CPT-11.	Irinotecan	201-207	C-C motif chemokine ligand 21	Homo sapiens	106-109
19264971-6	2009	To determine the possible compensatory UGT isoforms, we first verified that UGT1A activities were significantly lower (p &lt; 0.05) in Gunn rats by using UGT1A-specific probes 7-ethyl-10-hydroxycamptothecin (SN-38) and prunetin.	Irinotecan	176-206	Ugt1a@	Rattus norvegicus	76-81
19264971-6	2009	To determine the possible compensatory UGT isoforms, we first verified that UGT1A activities were significantly lower (p &lt; 0.05) in Gunn rats by using UGT1A-specific probes 7-ethyl-10-hydroxycamptothecin (SN-38) and prunetin.	Irinotecan	208-213	Ugt1a@	Rattus norvegicus	76-81
19417717-0	2009	Effects of oral administration of S-1 on the pharmacokinetics of SN-38, irinotecan active metabolite, in patients with advanced colorectal cancer.	Irinotecan	65-70	proteasome 26S subunit, non-ATPase 1	Homo sapiens	34-37
19349540-1	2009	PURPOSE: We aim to identify genetic variation, in addition to the UGT1A1*28 polymorphism, that can explain the variability in irinotecan (CPT-11) pharmacokinetics and neutropenia in cancer patients.	Irinotecan	126-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
19349540-1	2009	PURPOSE: We aim to identify genetic variation, in addition to the UGT1A1*28 polymorphism, that can explain the variability in irinotecan (CPT-11) pharmacokinetics and neutropenia in cancer patients.	Irinotecan	138-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
19349540-6	2009	More than 40% of the variation in CPT-11 area under the curve (AUC) is explained by ABCC2 -24C&gt;T, SLCO1B1*5, HNF1A 79A&gt;C, age, and CPT-11 dose (P &lt; .0001).	Irinotecan	34-40	ATP binding cassette subfamily C member 2	Homo sapiens	84-89
19349540-6	2009	More than 40% of the variation in CPT-11 area under the curve (AUC) is explained by ABCC2 -24C&gt;T, SLCO1B1*5, HNF1A 79A&gt;C, age, and CPT-11 dose (P &lt; .0001).	Irinotecan	34-40	solute carrier organic anion transporter family member 1B1	Homo sapiens	101-108
19349540-6	2009	More than 40% of the variation in CPT-11 area under the curve (AUC) is explained by ABCC2 -24C&gt;T, SLCO1B1*5, HNF1A 79A&gt;C, age, and CPT-11 dose (P &lt; .0001).	Irinotecan	34-40	HNF1 homeobox A	Homo sapiens	112-117
19349540-7	2009	Almost 30% of the variability in SN-38 (the active metabolite of CPT-11) AUC is explained by ABCC1 1684T&gt;C, ABCB1 IVS9 -44A&gt;G, and UGT1A1*93 (P = .004).	Irinotecan	33-38	ATP binding cassette subfamily C member 1	Homo sapiens	93-98
19349540-7	2009	Almost 30% of the variability in SN-38 (the active metabolite of CPT-11) AUC is explained by ABCC1 1684T&gt;C, ABCB1 IVS9 -44A&gt;G, and UGT1A1*93 (P = .004).	Irinotecan	33-38	ATP binding cassette subfamily B member 1	Homo sapiens	111-116
19349540-7	2009	Almost 30% of the variability in SN-38 (the active metabolite of CPT-11) AUC is explained by ABCC1 1684T&gt;C, ABCB1 IVS9 -44A&gt;G, and UGT1A1*93 (P = .004).	Irinotecan	33-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
19417717-0	2009	Effects of oral administration of S-1 on the pharmacokinetics of SN-38, irinotecan active metabolite, in patients with advanced colorectal cancer.	Irinotecan	72-82	proteasome 26S subunit, non-ATPase 1	Homo sapiens	34-37
19417717-2	2009	The objective of this study was to describe the interaction between CPT-11 and S-1 in 4 patients with colorectal cancer.	Irinotecan	68-74	proteasome 26S subunit, non-ATPase 1	Homo sapiens	79-82
19417717-3	2009	Coadministration of S-1 changed the pharmacokinetic behavior of CPT-11 and its metabolites.	Irinotecan	64-70	proteasome 26S subunit, non-ATPase 1	Homo sapiens	20-23
19417717-4	2009	In particular, maximum plasma concentration (Cmax) and area under the plasma concentration curve (AUC) of 7-ethyl-10-hydroxycampothecin (SN-38) was markedly decreased by coadministration of S-1.	Irinotecan	106-135	proteasome 26S subunit, non-ATPase 1	Homo sapiens	190-193
19417717-4	2009	In particular, maximum plasma concentration (Cmax) and area under the plasma concentration curve (AUC) of 7-ethyl-10-hydroxycampothecin (SN-38) was markedly decreased by coadministration of S-1.	Irinotecan	137-142	proteasome 26S subunit, non-ATPase 1	Homo sapiens	190-193
19417717-5	2009	For SN-38, the median ratio of Cmax and AUC with S-1 to those without S-1 was median 0.34 (range 0.24-0.78) and 0.56 (range 0.23-0.68), respectively.	Irinotecan	4-9	proteasome 26S subunit, non-ATPase 1	Homo sapiens	49-52
19417717-5	2009	For SN-38, the median ratio of Cmax and AUC with S-1 to those without S-1 was median 0.34 (range 0.24-0.78) and 0.56 (range 0.23-0.68), respectively.	Irinotecan	4-9	proteasome 26S subunit, non-ATPase 1	Homo sapiens	70-73
19417717-7	2009	We conclude that the plasma concentration of SN-38 was decreased by oral administration of S-1 in patients with colorectal cancer.	Irinotecan	45-50	proteasome 26S subunit, non-ATPase 1	Homo sapiens	91-94
19642458-5	2009	The anti-VEGFR bevacizumab is the standard first line treatment in metastatic colorectal cancer with irinotecan based chemotherapy.	Irinotecan	101-111	kinase insert domain receptor	Homo sapiens	9-14
19364970-1	2009	PURPOSE: UGT1A1*28 is considered the main pharmacogenetic predictor of the toxicity outcome of irinotecan-treated patients.	Irinotecan	95-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
18998132-0	2009	Life-threatening toxicities in a patient with UGT1A1*6/*28 and SLCO1B1*15/*15 genotypes after irinotecan-based chemotherapy.	Irinotecan	94-104	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
18998132-0	2009	Life-threatening toxicities in a patient with UGT1A1*6/*28 and SLCO1B1*15/*15 genotypes after irinotecan-based chemotherapy.	Irinotecan	94-104	solute carrier organic anion transporter family member 1B1	Homo sapiens	63-70
18998132-6	2009	CONCLUSION: The severe toxicities in this patient are attributable to the extensive accumulation of SN-38, which may result from a synergistic or additive effect of low metabolic (UGT1A1*6/*28) and transport (SLCO1B1*15/*15) capabilities.	Irinotecan	100-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
18998132-6	2009	CONCLUSION: The severe toxicities in this patient are attributable to the extensive accumulation of SN-38, which may result from a synergistic or additive effect of low metabolic (UGT1A1*6/*28) and transport (SLCO1B1*15/*15) capabilities.	Irinotecan	100-105	solute carrier organic anion transporter family member 1B1	Homo sapiens	209-216
19461176-0	2009	[Evaluation of irinotecan hydrochloride (CPT-11) and trastuzumab combination therapy as salvage treatment in patients with HER2 overexpressing metastatic breast cancer].	Irinotecan	15-39	erb-b2 receptor tyrosine kinase 2	Homo sapiens	123-127
19461176-4	2009	PURPOSE: To evaluate retrospectively the efficacy of CPT-11 and trastuzumab combination therapy as salvage treatment in patients with human epidermal growth factor receptor 2 (HER2)overexpressing MBC.	Irinotecan	53-59	erb-b2 receptor tyrosine kinase 2	Homo sapiens	140-174
19461176-4	2009	PURPOSE: To evaluate retrospectively the efficacy of CPT-11 and trastuzumab combination therapy as salvage treatment in patients with human epidermal growth factor receptor 2 (HER2)overexpressing MBC.	Irinotecan	53-59	erb-b2 receptor tyrosine kinase 2	Homo sapiens	176-180
19450125-0	2009	UGT1A1*28 genotype predicts gastrointestinal toxicity in patients treated with intermediate-dose irinotecan.	Irinotecan	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19450125-1	2009	AIMS: Variants in UGT1A1 have previously been associated with toxicity from irinotecan chemotherapy.	Irinotecan	76-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
19450125-2	2009	We conducted a pragmatic prospective cohort study to establish the relevance of UGT1A1 variants in the prediction of severe diarrhea and neutropenia in patients with colorectal cancer receiving irinotecan in a routine clinical setting.	Irinotecan	194-204	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
19671328-8	2009	Cetuximab plus irinotecan as second-line therapy for patients with EGFR-expressing metastatic colorectal cancer who had previously failed to respond to irinotecan-added therapy could reach a tumor response rate of 16.4% - 23.0%, and median overall survival duration of 8.6 - 10.7 months.	Irinotecan	15-25	epidermal growth factor receptor	Homo sapiens	67-71
19225040-5	2009	Hydrolysis of imidapril and irinotecan hydrochloride (CPT-11) is catalyzed mainly by CES1 and CES2, respectively.	Irinotecan	28-52	carboxylesterase 1	Homo sapiens	85-89
19225040-5	2009	Hydrolysis of imidapril and irinotecan hydrochloride (CPT-11) is catalyzed mainly by CES1 and CES2, respectively.	Irinotecan	28-52	carboxylesterase 2	Homo sapiens	94-98
19225040-5	2009	Hydrolysis of imidapril and irinotecan hydrochloride (CPT-11) is catalyzed mainly by CES1 and CES2, respectively.	Irinotecan	54-60	carboxylesterase 1	Homo sapiens	85-89
19225040-5	2009	Hydrolysis of imidapril and irinotecan hydrochloride (CPT-11) is catalyzed mainly by CES1 and CES2, respectively.	Irinotecan	54-60	carboxylesterase 2	Homo sapiens	94-98
19390945-0	2009	UGT1A1*6 polymorphism is most predictive of severe neutropenia induced by irinotecan in Japanese cancer patients.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19262372-0	2009	Inhibition of P-glycoprotein-mediated docetaxel efflux sensitizes ovarian cancer cells to concomitant docetaxel and SN-38 exposure.	Irinotecan	116-121	ATP binding cassette subfamily B member 1	Homo sapiens	14-28
19262372-8	2009	SN-38 increased P-gp expression in all cell lines.	Irinotecan	0-5	ATP binding cassette subfamily B member 1	Homo sapiens	16-20
19390945-1	2009	BACKGROUND: Gene polymorphisms of the UDP-glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) contribute to individual variations in adverse events among patients administered irinotecan, and the distribution of the polymorphisms shows large interethnic differences.	Irinotecan	182-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-90
19390945-1	2009	BACKGROUND: Gene polymorphisms of the UDP-glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) contribute to individual variations in adverse events among patients administered irinotecan, and the distribution of the polymorphisms shows large interethnic differences.	Irinotecan	182-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
19287947-5	2009	Intraperitoneal injection of CPT-11, an anticancer topoisomerase I inhibitor that causes granulosa cell-specific apoptosis partly through Fas-Fas ligand (FasL) interactions in MCH mice, induced follicular apoptosis in both the wild-type and DAPK-mutant mice.	Irinotecan	29-35	Fas ligand (TNF superfamily, member 6)	Mus musculus	138-152
19390945-2	2009	Variation in the solute carrier organic anion-transporter family, member 1B1 (SLCO1B1) gene also has a significant effect on the disposition of irinotecan in Asian cancer patients.	Irinotecan	144-154	solute carrier organic anion transporter family member 1B1	Homo sapiens	17-76
19287947-5	2009	Intraperitoneal injection of CPT-11, an anticancer topoisomerase I inhibitor that causes granulosa cell-specific apoptosis partly through Fas-Fas ligand (FasL) interactions in MCH mice, induced follicular apoptosis in both the wild-type and DAPK-mutant mice.	Irinotecan	29-35	Fas ligand (TNF superfamily, member 6)	Mus musculus	154-158
19287947-7	2009	The Fas and FasL expression levels in the CPT-11-injected mice did not differ significantly between the wild-type and DAPK-mutant mice.	Irinotecan	42-48	Fas ligand (TNF superfamily, member 6)	Mus musculus	12-16
19390945-2	2009	Variation in the solute carrier organic anion-transporter family, member 1B1 (SLCO1B1) gene also has a significant effect on the disposition of irinotecan in Asian cancer patients.	Irinotecan	144-154	solute carrier organic anion transporter family member 1B1	Homo sapiens	78-85
19390945-12	2009	CONCLUSION: These findings suggest that the UGT1A1*6 polymorphism is a potential predictor of severe neutropenia caused by irinotecan in Japanese cancer patients.	Irinotecan	123-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
19212674-3	2009	Although Akt activity seemed to be involved with the sensitivity of SCLC cells to chemotherapeutic agents (cisplatin, etoposide, SN38 and amrubicin), in Akt-activated N417 cells, only amrubicin exerted synergistic cell growth inhibition when combined with an Akt inhibitor, LY294002.	Irinotecan	129-133	AKT serine/threonine kinase 1	Homo sapiens	9-12
19372567-5	2009	EJ human bladder carcinoma cells expressing membrane-tethered beta-glucuronidase (EJ/mbetaG cells) were used to selectively hydrolyze SN-38G to SN-38.	Irinotecan	134-139	glucuronidase beta	Homo sapiens	62-80
19372567-5	2009	EJ human bladder carcinoma cells expressing membrane-tethered beta-glucuronidase (EJ/mbetaG cells) were used to selectively hydrolyze SN-38G to SN-38.	Irinotecan	144-149	glucuronidase beta	Homo sapiens	62-80
19372567-11	2009	The high concentrations of SN-38G found in the serum of patients treated with CPT-11 suggest that clinical response to CPT-11 may be improved by elevating beta-glucuronidase activity in tumors.	Irinotecan	27-32	glucuronidase beta	Homo sapiens	155-173
19372567-11	2009	The high concentrations of SN-38G found in the serum of patients treated with CPT-11 suggest that clinical response to CPT-11 may be improved by elevating beta-glucuronidase activity in tumors.	Irinotecan	78-84	glucuronidase beta	Homo sapiens	155-173
19372567-11	2009	The high concentrations of SN-38G found in the serum of patients treated with CPT-11 suggest that clinical response to CPT-11 may be improved by elevating beta-glucuronidase activity in tumors.	Irinotecan	119-125	glucuronidase beta	Homo sapiens	155-173
19135530-0	2009	Effect of P-glycoprotein inhibitor, verapamil, on oral bioavailability and pharmacokinetics of irinotecan in rats.	Irinotecan	95-105	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	10-24
19135530-1	2009	The objective of present investigation was to study the effect of verapamil on the pharmacokinetics of irinotecan in order to evaluate the role of P-glycoprotein (P-gp) in irinotecan disposition.	Irinotecan	172-182	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	147-161
19135530-1	2009	The objective of present investigation was to study the effect of verapamil on the pharmacokinetics of irinotecan in order to evaluate the role of P-glycoprotein (P-gp) in irinotecan disposition.	Irinotecan	172-182	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	163-167
19135530-5	2009	Bi-directional transport and inhibition studies in Caco-2 cells indicated irinotecan to be a P-gp substrate and the function of intestinal P-gp was significantly inhibited in presence of verapamil.	Irinotecan	74-84	phosphoglycolate phosphatase	Homo sapiens	93-97
19135530-5	2009	Bi-directional transport and inhibition studies in Caco-2 cells indicated irinotecan to be a P-gp substrate and the function of intestinal P-gp was significantly inhibited in presence of verapamil.	Irinotecan	74-84	phosphoglycolate phosphatase	Homo sapiens	139-143
19135530-13	2009	These results are quite stimulating for further development of a clinically useful oral formulation of irinotecan based on P-gp inhibition.	Irinotecan	103-113	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	123-127
19212674-3	2009	Although Akt activity seemed to be involved with the sensitivity of SCLC cells to chemotherapeutic agents (cisplatin, etoposide, SN38 and amrubicin), in Akt-activated N417 cells, only amrubicin exerted synergistic cell growth inhibition when combined with an Akt inhibitor, LY294002.	Irinotecan	129-133	AKT serine/threonine kinase 1	Homo sapiens	153-156
19212674-3	2009	Although Akt activity seemed to be involved with the sensitivity of SCLC cells to chemotherapeutic agents (cisplatin, etoposide, SN38 and amrubicin), in Akt-activated N417 cells, only amrubicin exerted synergistic cell growth inhibition when combined with an Akt inhibitor, LY294002.	Irinotecan	129-133	AKT serine/threonine kinase 1	Homo sapiens	153-156
19190342-6	2009	Uptake of the organic cation [(3)H]MPP (4-methyl-pyridinium iodide) into these cells and also into hOCT3 stably transfected Chinese hamster ovary (CHO) cells was inhibited by irinotecan, vincristine, and melphalan.	Irinotecan	175-185	solute carrier family 22 member 3	Homo sapiens	99-104
19190131-0	2009	Marked activity of irinotecan and rapamycin combination toward colon cancer cells in vivo and in vitro is mediated through cooperative modulation of the mammalian target of rapamycin/hypoxia-inducible factor-1alpha axis.	Irinotecan	19-29	hypoxia inducible factor 1 subunit alpha	Homo sapiens	183-214
19164213-4	2009	We investigated the association of FcgammaR polymorphisms and KRAS mutation with the outcome of irinotecan-refractory mCRC patients treated with cetuximab plus irinotecan.	Irinotecan	96-106	KRAS proto-oncogene, GTPase	Homo sapiens	62-66
19164213-11	2009	CONCLUSION: Combined FcgammaRIIa/FcgammaRIIIa polymorphisms are prognostic factors for disease progression in mCRC patients treated with cetuximab plus irinotecan.	Irinotecan	152-162	Fc gamma receptor IIa	Homo sapiens	21-32
19164213-11	2009	CONCLUSION: Combined FcgammaRIIa/FcgammaRIIIa polymorphisms are prognostic factors for disease progression in mCRC patients treated with cetuximab plus irinotecan.	Irinotecan	152-162	Fc gamma receptor IIIa	Homo sapiens	33-45
21475811-1	2009	This study aimed to clarify the mechanism by which apoptosis and Fas ligand (FasL) expression are induced in the ovarian granulosa cells of mice injected with irinotecan HCl (CPT-11).	Irinotecan	159-173	Fas ligand (TNF superfamily, member 6)	Mus musculus	65-75
21475811-1	2009	This study aimed to clarify the mechanism by which apoptosis and Fas ligand (FasL) expression are induced in the ovarian granulosa cells of mice injected with irinotecan HCl (CPT-11).	Irinotecan	159-173	Fas ligand (TNF superfamily, member 6)	Mus musculus	77-81
21475811-1	2009	This study aimed to clarify the mechanism by which apoptosis and Fas ligand (FasL) expression are induced in the ovarian granulosa cells of mice injected with irinotecan HCl (CPT-11).	Irinotecan	175-181	Fas ligand (TNF superfamily, member 6)	Mus musculus	65-75
21475811-1	2009	This study aimed to clarify the mechanism by which apoptosis and Fas ligand (FasL) expression are induced in the ovarian granulosa cells of mice injected with irinotecan HCl (CPT-11).	Irinotecan	175-181	Fas ligand (TNF superfamily, member 6)	Mus musculus	77-81
21475811-7	2009	In conclusion, apoptosis and FasL expression induced in the ovarian granulosa cells of mice injected with CPT-11 is not caused by direct stimulation with CPT-11 or SN38.	Irinotecan	106-112	Fas ligand (TNF superfamily, member 6)	Mus musculus	29-33
21475811-8	2009	Therefore, systemic CPT-11 administration appears to induce apoptosis and FasL expression in granulosa cells via currently unknown endogenous FasL-inducing factors or by active metabolites of CPT-11 other than SN38.	Irinotecan	20-26	Fas ligand (TNF superfamily, member 6)	Mus musculus	74-78
21475811-8	2009	Therefore, systemic CPT-11 administration appears to induce apoptosis and FasL expression in granulosa cells via currently unknown endogenous FasL-inducing factors or by active metabolites of CPT-11 other than SN38.	Irinotecan	20-26	Fas ligand (TNF superfamily, member 6)	Mus musculus	142-146
19190131-4	2009	A second class are topoisomerase I inhibitors, such as irinotecan, which are able to inhibit the accumulation of HIF-1alpha.	Irinotecan	55-65	hypoxia inducible factor 1 subunit alpha	Homo sapiens	113-123
19190131-11	2009	CONCLUSION: These results identify HIF-1alpha as a promising target and provide a rationale for clinical trials of low-dose irinotecan and rapamycin combination toward metastatic colon cancer.	Irinotecan	124-134	hypoxia inducible factor 1 subunit alpha	Homo sapiens	35-45
19190342-9	2009	The growth of CHO-hOCT3 was inhibited by 20% more with irinotecan and by 50% more with vincristine compared with nontransfected CHO cells.	Irinotecan	55-65	solute carrier family 22 member 3	Homo sapiens	18-23
18685565-0	2009	Phase I/II pharmacokinetic and pharmacogenomic study of UGT1A1 polymorphism in elderly patients with advanced non-small cell lung cancer treated with irinotecan.	Irinotecan	150-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
18929442-0	2009	Inhibition of Akt signaling by SN-38 induces apoptosis in cervical cancer.	Irinotecan	31-36	AKT serine/threonine kinase 1	Homo sapiens	14-17
18929442-6	2009	Western Blot showed that SN-38 down-regulated protein expression of p-Akt and increased protein expression of p53 and p21, but it had no effects on protein expression of Bax, Bcl-2 and Akt.	Irinotecan	25-30	AKT serine/threonine kinase 1	Homo sapiens	70-73
18929442-6	2009	Western Blot showed that SN-38 down-regulated protein expression of p-Akt and increased protein expression of p53 and p21, but it had no effects on protein expression of Bax, Bcl-2 and Akt.	Irinotecan	25-30	tumor protein p53	Homo sapiens	110-113
18929442-6	2009	Western Blot showed that SN-38 down-regulated protein expression of p-Akt and increased protein expression of p53 and p21, but it had no effects on protein expression of Bax, Bcl-2 and Akt.	Irinotecan	25-30	H3 histone pseudogene 16	Homo sapiens	118-121
18929442-7	2009	Transfection of the full-length Akt cDNA into HeLa and SiHa cells resulted in the reduction of apoptosis induced by SN-38, and Akt kinase activity regulated the p53 pathway, indicating that inhibition of the Akt pathway played an important role in exhibition of SN-38-mediated cytotoxic effect.	Irinotecan	116-121	AKT serine/threonine kinase 1	Homo sapiens	32-35
18929442-7	2009	Transfection of the full-length Akt cDNA into HeLa and SiHa cells resulted in the reduction of apoptosis induced by SN-38, and Akt kinase activity regulated the p53 pathway, indicating that inhibition of the Akt pathway played an important role in exhibition of SN-38-mediated cytotoxic effect.	Irinotecan	262-267	AKT serine/threonine kinase 1	Homo sapiens	32-35
18929442-7	2009	Transfection of the full-length Akt cDNA into HeLa and SiHa cells resulted in the reduction of apoptosis induced by SN-38, and Akt kinase activity regulated the p53 pathway, indicating that inhibition of the Akt pathway played an important role in exhibition of SN-38-mediated cytotoxic effect.	Irinotecan	262-267	tumor protein p53	Homo sapiens	161-164
18929442-8	2009	Our data suggested that SN-38 could induce apoptosis through a p53 pathway and that activation of p53 in response to S-38 is governed by Akt.	Irinotecan	24-29	tumor protein p53	Homo sapiens	63-66
18929442-8	2009	Our data suggested that SN-38 could induce apoptosis through a p53 pathway and that activation of p53 in response to S-38 is governed by Akt.	Irinotecan	24-29	tumor protein p53	Homo sapiens	98-101
18685565-9	2009	An analysis of the influence of UGT1A1*28 and *6 polymorphisms provides useful information for the prediction of CPT-11-related hematological toxicity.	Irinotecan	113-119	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-38
19208748-11	2009	Further, EFEMP1 expression decreased apoptosis and promoted cell cycle progression in response to serum starvation or exposure to gemcitabine, 5-fluorouracil, and irinotecan.	Irinotecan	163-173	EGF containing fibulin extracellular matrix protein 1	Homo sapiens	9-15
18981166-0	2009	Close association of UGT1A9 IVS1+399C&gt;T with UGT1A1*28, *6, or *60 haplotype and its apparent influence on 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation in Japanese.	Irinotecan	110-140	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	21-27
18981166-0	2009	Close association of UGT1A9 IVS1+399C&gt;T with UGT1A1*28, *6, or *60 haplotype and its apparent influence on 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation in Japanese.	Irinotecan	142-147	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	21-27
18981166-0	2009	Close association of UGT1A9 IVS1+399C&gt;T with UGT1A1*28, *6, or *60 haplotype and its apparent influence on 7-ethyl-10-hydroxycamptothecin (SN-38) glucuronidation in Japanese.	Irinotecan	142-147	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
18981166-1	2009	The anticancer prodrug, irinotecan, is converted to its active form 7-ethyl-10-hydroxycamptothecin (SN-38) by carboxylesterases, and SN-38 is inactivated by UDP-glucuronosyltransferase (UGT)1A1-mediated glucuronidation.	Irinotecan	24-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	186-193
18981166-1	2009	The anticancer prodrug, irinotecan, is converted to its active form 7-ethyl-10-hydroxycamptothecin (SN-38) by carboxylesterases, and SN-38 is inactivated by UDP-glucuronosyltransferase (UGT)1A1-mediated glucuronidation.	Irinotecan	68-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	186-193
18981166-1	2009	The anticancer prodrug, irinotecan, is converted to its active form 7-ethyl-10-hydroxycamptothecin (SN-38) by carboxylesterases, and SN-38 is inactivated by UDP-glucuronosyltransferase (UGT)1A1-mediated glucuronidation.	Irinotecan	100-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	186-193
18981166-1	2009	The anticancer prodrug, irinotecan, is converted to its active form 7-ethyl-10-hydroxycamptothecin (SN-38) by carboxylesterases, and SN-38 is inactivated by UDP-glucuronosyltransferase (UGT)1A1-mediated glucuronidation.	Irinotecan	133-138	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	186-193
18981166-3	2009	In a recent study, it was reported that the UGT1A9 IVS1+399 (I399)C&gt;T polymorphism is associated with increased SN-38 glucuronidation both in vitro and in vivo.	Irinotecan	115-120	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	44-50
18981166-11	2009	Thus, at least in Japanese populations, influence of I399C&gt;T on SN-38 glucuronidation is attributable to its close association with either UGT1A1*6, *28, or *60.	Irinotecan	67-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
19234367-0	2009	Role of glucocorticoid receptor in the regulation of cellular sensitivity to irinotecan hydrochloride.	Irinotecan	77-101	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	8-31
19111841-1	2009	The breast cancer resistance protein, BCRP/ABCG2, is a half-molecule ATP-binding cassette transporter that facilitates the efflux of various anticancer agents from the cell, including 7-ethyl-10-hydroxycamptothecin, topotecan and mitoxantrone.	Irinotecan	184-214	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	4-36
19111841-1	2009	The breast cancer resistance protein, BCRP/ABCG2, is a half-molecule ATP-binding cassette transporter that facilitates the efflux of various anticancer agents from the cell, including 7-ethyl-10-hydroxycamptothecin, topotecan and mitoxantrone.	Irinotecan	184-214	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	38-42
19111841-1	2009	The breast cancer resistance protein, BCRP/ABCG2, is a half-molecule ATP-binding cassette transporter that facilitates the efflux of various anticancer agents from the cell, including 7-ethyl-10-hydroxycamptothecin, topotecan and mitoxantrone.	Irinotecan	184-214	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	43-48
19118001-7	2009	In this drug-sensitive cellular background, MRP7 conferred high levels of resistance to docetaxel (46-fold), paclitaxel (116-fold), SN-38 (65-fold), daunorubicin (7.5-fold), etoposide (11-fold), and vincristine (56-fold).	Irinotecan	132-137	ATP binding cassette subfamily C member 10	Homo sapiens	44-48
19147571-3	2009	We then report that chemotherapy induces Notch-1, as oxaliplatin, 5-fluorouracil (5-FU), or SN-38 (the active metabolite of irinotecan) induced Notch-1 intracellular domain (NICD) protein and activated Hes-1.	Irinotecan	92-97	notch receptor 1	Homo sapiens	41-48
19147571-3	2009	We then report that chemotherapy induces Notch-1, as oxaliplatin, 5-fluorouracil (5-FU), or SN-38 (the active metabolite of irinotecan) induced Notch-1 intracellular domain (NICD) protein and activated Hes-1.	Irinotecan	92-97	notch receptor 1	Homo sapiens	144-151
19147571-3	2009	We then report that chemotherapy induces Notch-1, as oxaliplatin, 5-fluorouracil (5-FU), or SN-38 (the active metabolite of irinotecan) induced Notch-1 intracellular domain (NICD) protein and activated Hes-1.	Irinotecan	92-97	hes family bHLH transcription factor 1	Homo sapiens	202-207
19147571-3	2009	We then report that chemotherapy induces Notch-1, as oxaliplatin, 5-fluorouracil (5-FU), or SN-38 (the active metabolite of irinotecan) induced Notch-1 intracellular domain (NICD) protein and activated Hes-1.	Irinotecan	124-134	notch receptor 1	Homo sapiens	41-48
19147571-3	2009	We then report that chemotherapy induces Notch-1, as oxaliplatin, 5-fluorouracil (5-FU), or SN-38 (the active metabolite of irinotecan) induced Notch-1 intracellular domain (NICD) protein and activated Hes-1.	Irinotecan	124-134	notch receptor 1	Homo sapiens	144-151
19147571-3	2009	We then report that chemotherapy induces Notch-1, as oxaliplatin, 5-fluorouracil (5-FU), or SN-38 (the active metabolite of irinotecan) induced Notch-1 intracellular domain (NICD) protein and activated Hes-1.	Irinotecan	124-134	hes family bHLH transcription factor 1	Homo sapiens	202-207
19147571-6	2009	Blocking the activation of Notch signaling with GSI34 sensitized cells to chemotherapy and was synergistic with oxaliplatin, 5-FU, and SN-38.	Irinotecan	135-140	notch receptor 1	Homo sapiens	27-32
19414151-4	2009	UGT1A1*28 leads to reduced conjugation of SN-38, the active metabolite of irinotecan, resulting in an increased rate of adverse effects, especially neutropenia.	Irinotecan	42-47	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19414151-4	2009	UGT1A1*28 leads to reduced conjugation of SN-38, the active metabolite of irinotecan, resulting in an increased rate of adverse effects, especially neutropenia.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
19208614-3	2009	Potent and specific inhibitors of PARP are available; these have been shown to increase the cytotoxicity of a range of anti-cancer agents including temozolomide, irinotecan and radiation.	Irinotecan	162-172	poly(ADP-ribose) polymerase 1	Homo sapiens	34-38
19147776-1	2009	PURPOSE: CPX-1 is a novel, liposome-encapsulated formulation of irinotecan and floxuridine designed to prolong in vitro optimized synergistic molar ratios of both drugs postinfusion.	Irinotecan	64-74	complexin 1	Homo sapiens	9-14
19151561-3	2009	To identify the optimal therapy candidates, EGFR (epidermal growth factor receptor)mutations are biomarkers available as predictive factors for EGFR tyrosine kinase inhibitors and UGT(uridine diphosphate glucuronosyltransferase)1A1 as a risk predictor of irinotecan in the present practice.	Irinotecan	255-265	epidermal growth factor receptor	Homo sapiens	44-48
19571434-10	2009	In the present study, Kampo was clarified to inhibit beta-estradiol and SN-38 glucuronidation mainly catalyzed by UGT1A1.	Irinotecan	72-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
19151561-3	2009	To identify the optimal therapy candidates, EGFR (epidermal growth factor receptor)mutations are biomarkers available as predictive factors for EGFR tyrosine kinase inhibitors and UGT(uridine diphosphate glucuronosyltransferase)1A1 as a risk predictor of irinotecan in the present practice.	Irinotecan	255-265	epidermal growth factor receptor	Homo sapiens	50-82
19151561-3	2009	To identify the optimal therapy candidates, EGFR (epidermal growth factor receptor)mutations are biomarkers available as predictive factors for EGFR tyrosine kinase inhibitors and UGT(uridine diphosphate glucuronosyltransferase)1A1 as a risk predictor of irinotecan in the present practice.	Irinotecan	255-265	epidermal growth factor receptor	Homo sapiens	144-148
19151561-3	2009	To identify the optimal therapy candidates, EGFR (epidermal growth factor receptor)mutations are biomarkers available as predictive factors for EGFR tyrosine kinase inhibitors and UGT(uridine diphosphate glucuronosyltransferase)1A1 as a risk predictor of irinotecan in the present practice.	Irinotecan	255-265	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	180-231
18221820-5	2009	The UGT1A1*6/*6, UGT1A9*1/*1 or *1/*22, and SLCO1B1 521TC or CC genotypes, and female-gender were predictive for higher AUC(SN-38) in multivariate analysis.	Irinotecan	124-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
19125128-0	2009	Recommendations from the EGAPP Working Group: can UGT1A1 genotyping reduce morbidity and mortality in patients with metastatic colorectal cancer treated with irinotecan?	Irinotecan	158-168	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
19125128-8	2009	CLINICAL VALIDITY: The EWG found adequate evidence of a significant association between UGT1A1 genotype and the incidence of severe neutropenia at standard doses of irinotecan.	Irinotecan	165-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
19125128-16	2009	Further rigorous evaluation of UGT1A1 genotyping using current and promising irinotecan treatment protocols is warranted.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
19125129-0	2009	Can UGT1A1 genotyping reduce morbidity and mortality in patients with metastatic colorectal cancer treated with irinotecan?	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
19125129-2	2009	This evidence-based review addresses the question of whether testing for UGT1A1 mutations in patients with metastatic colorectal cancer treated with irinotecan leads to improvement in outcomes (e.g., irinotecan toxicity, response to treatment, morbidity, and mortality), when compared with no testing.	Irinotecan	149-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
19125129-2	2009	This evidence-based review addresses the question of whether testing for UGT1A1 mutations in patients with metastatic colorectal cancer treated with irinotecan leads to improvement in outcomes (e.g., irinotecan toxicity, response to treatment, morbidity, and mortality), when compared with no testing.	Irinotecan	200-210	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
19125129-16	2009	Given the large number of colorectal cancer cases diagnosed each year, a randomized controlled trial of the effects of irinotecan dose modifications in patients with colorectal cancer based on their UGT1A1 genotype is feasible and could clarify the tradeoffs between possible reductions in severe neutropenia and improved tumor response and/or survival in patients with various UGT1A1 genotypes.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	199-205
19125129-16	2009	Given the large number of colorectal cancer cases diagnosed each year, a randomized controlled trial of the effects of irinotecan dose modifications in patients with colorectal cancer based on their UGT1A1 genotype is feasible and could clarify the tradeoffs between possible reductions in severe neutropenia and improved tumor response and/or survival in patients with various UGT1A1 genotypes.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	378-384
19404408-13	2009	In contrast, the MTD was determined to be dose level 4 (200 mg/m(2) for irinotecan and AUC 5 for carboplatin) by modified-Fibonacci simulation.	Irinotecan	72-82	metallothionein 1E	Homo sapiens	17-20
19534437-1	2009	BACKGROUND: Combination of cetuximab and irinotecan is an efficacious second- (and further-)-line treatment-alternative in patients with EGFR-positive metastatic colorectal cancer refractory to irinotecan.	Irinotecan	41-51	epidermal growth factor receptor	Homo sapiens	137-141
18221820-5	2009	The UGT1A1*6/*6, UGT1A9*1/*1 or *1/*22, and SLCO1B1 521TC or CC genotypes, and female-gender were predictive for higher AUC(SN-38) in multivariate analysis.	Irinotecan	124-129	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	17-23
18221820-5	2009	The UGT1A1*6/*6, UGT1A9*1/*1 or *1/*22, and SLCO1B1 521TC or CC genotypes, and female-gender were predictive for higher AUC(SN-38) in multivariate analysis.	Irinotecan	124-129	solute carrier organic anion transporter family member 1B1	Homo sapiens	44-51
19712005-3	2009	METHODS: Here, we assess the genome of 469 individuals from Sao Miguel Island (Azores, Portugal) in order to determine the frequencies of polymorphisms and haplotypes in UGT1A1, UGT1A6, and UGT1A7, the co-occurrence of reduced enzyme activity UGT1A variants related to irinotecan toxicity, and to calculate the extent of linkage disequilibrium (LD) in the genomic region encompassing these genes.	Irinotecan	269-279	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	170-176
18820127-2	2009	Herein, we report that treatment with the 90-kDa heat shock protein (Hsp90) molecular chaperone inhibitor 17-allylamino-17-demethoxygeldanamycin (17AAG) selectively abrogates the G(2)/M checkpoint induced by 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan, in p53-null compared with p53-intact HCT116 colon cancer cells.	Irinotecan	208-238	heat shock protein 90 alpha family class A member 1	Homo sapiens	69-74
18820127-2	2009	Herein, we report that treatment with the 90-kDa heat shock protein (Hsp90) molecular chaperone inhibitor 17-allylamino-17-demethoxygeldanamycin (17AAG) selectively abrogates the G(2)/M checkpoint induced by 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan, in p53-null compared with p53-intact HCT116 colon cancer cells.	Irinotecan	208-238	N-methylpurine DNA glycosylase	Homo sapiens	148-151
19712005-3	2009	METHODS: Here, we assess the genome of 469 individuals from Sao Miguel Island (Azores, Portugal) in order to determine the frequencies of polymorphisms and haplotypes in UGT1A1, UGT1A6, and UGT1A7, the co-occurrence of reduced enzyme activity UGT1A variants related to irinotecan toxicity, and to calculate the extent of linkage disequilibrium (LD) in the genomic region encompassing these genes.	Irinotecan	269-279	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	170-175
18820127-2	2009	Herein, we report that treatment with the 90-kDa heat shock protein (Hsp90) molecular chaperone inhibitor 17-allylamino-17-demethoxygeldanamycin (17AAG) selectively abrogates the G(2)/M checkpoint induced by 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan, in p53-null compared with p53-intact HCT116 colon cancer cells.	Irinotecan	240-245	heat shock protein 90 alpha family class A member 1	Homo sapiens	69-74
18820127-2	2009	Herein, we report that treatment with the 90-kDa heat shock protein (Hsp90) molecular chaperone inhibitor 17-allylamino-17-demethoxygeldanamycin (17AAG) selectively abrogates the G(2)/M checkpoint induced by 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan, in p53-null compared with p53-intact HCT116 colon cancer cells.	Irinotecan	240-245	N-methylpurine DNA glycosylase	Homo sapiens	148-151
19032367-1	2008	ATP-binding cassette transporter G2 (ABCG2) is the most recently described transporter of the multidrug-resistance pump and it promotes resistance to anticancer drugs such as doxorubicin, mitoxantrone, topotecan, and SN-38.	Irinotecan	217-222	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-35
18820127-2	2009	Herein, we report that treatment with the 90-kDa heat shock protein (Hsp90) molecular chaperone inhibitor 17-allylamino-17-demethoxygeldanamycin (17AAG) selectively abrogates the G(2)/M checkpoint induced by 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan, in p53-null compared with p53-intact HCT116 colon cancer cells.	Irinotecan	272-282	heat shock protein 90 alpha family class A member 1	Homo sapiens	69-74
18820127-2	2009	Herein, we report that treatment with the 90-kDa heat shock protein (Hsp90) molecular chaperone inhibitor 17-allylamino-17-demethoxygeldanamycin (17AAG) selectively abrogates the G(2)/M checkpoint induced by 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan, in p53-null compared with p53-intact HCT116 colon cancer cells.	Irinotecan	272-282	N-methylpurine DNA glycosylase	Homo sapiens	148-151
18820127-8	2009	Knockdown of Chk1 and Wee1 by short interfering RNA each resulted in abrogation of the G(2)/M checkpoint induced by SN-38.	Irinotecan	116-121	checkpoint kinase 1	Homo sapiens	13-17
18820127-8	2009	Knockdown of Chk1 and Wee1 by short interfering RNA each resulted in abrogation of the G(2)/M checkpoint induced by SN-38.	Irinotecan	116-121	WEE1 G2 checkpoint kinase	Homo sapiens	22-26
18820127-9	2009	The combination of SN-38 and 17AAG was shown to be synergistic in p53-null but not in parental HCT116 cells by median effect/combination index analysis.	Irinotecan	19-24	tumor protein p53	Homo sapiens	66-69
19738388-0	2009	The role of KRAS mutations in predicting the efficacy of cetuximab-plus-irinotecan therapy in irinotecan-refractory Korean metastatic colorectal cancer patients.	Irinotecan	72-82	KRAS proto-oncogene, GTPase	Homo sapiens	12-16
19738388-0	2009	The role of KRAS mutations in predicting the efficacy of cetuximab-plus-irinotecan therapy in irinotecan-refractory Korean metastatic colorectal cancer patients.	Irinotecan	94-104	KRAS proto-oncogene, GTPase	Homo sapiens	12-16
19738388-9	2009	CONCLUSIONS: This study indicates the clinical relevance of KRAS mutations in predicting the efficacy of cetuximab-plus-irinotecan-based chemotherapy in irinotecan-refractory Korean mCRC patients.	Irinotecan	120-130	KRAS proto-oncogene, GTPase	Homo sapiens	60-64
19738388-9	2009	CONCLUSIONS: This study indicates the clinical relevance of KRAS mutations in predicting the efficacy of cetuximab-plus-irinotecan-based chemotherapy in irinotecan-refractory Korean mCRC patients.	Irinotecan	153-163	KRAS proto-oncogene, GTPase	Homo sapiens	60-64
19299905-0	2009	Clinical significance of UDP-glucuronosyltransferase 1A1*6 for toxicities of combination chemotherapy with irinotecan and cisplatin in gynecologic cancers: a prospective multi-institutional study.	Irinotecan	107-117	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-56
19299905-1	2009	BACKGROUND: To investigate the effects of UDP-glucuronosyltransferase 1A1 (UGT1A1) *28, *6 and *27 in patients with gynecologic cancer who received chemotherapy with irinotecan and cisplatin.	Irinotecan	166-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-73
19299905-9	2009	CONCLUSION: In addition to UGT1A1*28, UGT1A1*6 might also be a key candidate to determine the dose of combination chemotherapy with irinotecan and cisplatin.	Irinotecan	132-142	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
19366055-1	2009	BACKGROUND: Capecitabine in combination with oxaliplatin and irinotecan (COI regimen) is active and well tolerated in metastatic colorectal cancer.	Irinotecan	61-71	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	73-76
19440006-0	2009	Treatment of gastric cancer cells with 5-fluorouracil/leucovorin and irinotecan induces distinct alterations in the mRNA expression of the apoptosis-related genes, including the novel gene BCL2L12.	Irinotecan	69-79	BCL2 like 12	Homo sapiens	189-196
19440006-3	2009	The aim of this study was to investigate the modulations in the BAX, BCL2 and BCL2L12 mRNA levels in gastric cancer cells, after their treatment with the anticancer drugs 5-fluorouracil and irinotecan as well as the antioxidant substance leucovorin.	Irinotecan	190-200	BCL2 associated X, apoptosis regulator	Homo sapiens	64-67
19440006-3	2009	The aim of this study was to investigate the modulations in the BAX, BCL2 and BCL2L12 mRNA levels in gastric cancer cells, after their treatment with the anticancer drugs 5-fluorouracil and irinotecan as well as the antioxidant substance leucovorin.	Irinotecan	190-200	BCL2 apoptosis regulator	Homo sapiens	69-73
19440006-3	2009	The aim of this study was to investigate the modulations in the BAX, BCL2 and BCL2L12 mRNA levels in gastric cancer cells, after their treatment with the anticancer drugs 5-fluorouracil and irinotecan as well as the antioxidant substance leucovorin.	Irinotecan	190-200	BCL2 like 12	Homo sapiens	78-85
19521145-6	2009	In combination therapy experiments, antibodies to PrP enhanced the effect of irinotecan, 5-FU, cisplatin and doxorubicin to varying degrees.	Irinotecan	77-87	prion protein	Homo sapiens	50-53
19088028-9	2008	CPT-11 treatment up-regulated Noxa expression, as did bortezomib, and enhanced Noxa/Mcl-1 complexes.	Irinotecan	0-6	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	30-34
19088028-9	2008	CPT-11 treatment up-regulated Noxa expression, as did bortezomib, and enhanced Noxa/Mcl-1 complexes.	Irinotecan	0-6	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	79-83
19088028-9	2008	CPT-11 treatment up-regulated Noxa expression, as did bortezomib, and enhanced Noxa/Mcl-1 complexes.	Irinotecan	0-6	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	84-89
19088028-10	2008	CPT-11 also disrupted the Mcl-1/Bak interaction.	Irinotecan	0-6	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	26-31
19088028-10	2008	CPT-11 also disrupted the Mcl-1/Bak interaction.	Irinotecan	0-6	BCL2 antagonist/killer 1	Homo sapiens	32-35
19088028-11	2008	Knockdown of Noxa using short hairpin RNA lentiviral constructs was shown to significantly attenuate the cytotoxic effect of CPT-11 or bortezomib combined with ABT-737 and inhibited caspase-3 cleavage.	Irinotecan	125-131	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	13-17
19088028-12	2008	CONCLUSIONS: Induction of Noxa by CPT-11 or bortezomib can sensitize colorectal cancer cells expressing Mcl-1 to ABT-737.	Irinotecan	34-40	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	26-30
19088028-12	2008	CONCLUSIONS: Induction of Noxa by CPT-11 or bortezomib can sensitize colorectal cancer cells expressing Mcl-1 to ABT-737.	Irinotecan	34-40	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	104-109
18953066-0	2008	Genetic testing for UGT1A1*28 and *6 in Japanese patients who receive irinotecan chemotherapy.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
18927500-0	2008	Faecal microflora and beta-glucuronidase expression are altered in an irinotecan-induced diarrhea model in rats.	Irinotecan	70-80	glucuronidase, beta	Rattus norvegicus	22-40
18927500-3	2008	Irinotecan causes cholinergic and delayed onset diarrhea in patients, in which beta-glucuronidase produced by gut bacteria is thought to be involved.	Irinotecan	0-10	glucuronidase beta	Homo sapiens	79-97
18927500-13	2008	CONCLUSIONS: Irinotecan-induced diarrhea may be caused by an increase in beta-glucuronidase producing bacteria.	Irinotecan	13-23	glucuronidase, beta	Rattus norvegicus	73-91
19032367-1	2008	ATP-binding cassette transporter G2 (ABCG2) is the most recently described transporter of the multidrug-resistance pump and it promotes resistance to anticancer drugs such as doxorubicin, mitoxantrone, topotecan, and SN-38.	Irinotecan	217-222	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	37-42
19047118-1	2008	PURPOSE: Recently, an objective response rate of 12% was reported in a phase II study of cetuximab in patients with epidermal growth factor receptor (EGFR)-expressing metastatic colorectal cancer (mCRC) refractory to fluoropyrimidine-, oxaliplatin-, and irinotecan-based chemotherapy (IMC-0144).	Irinotecan	254-264	epidermal growth factor receptor	Homo sapiens	116-148
19047118-1	2008	PURPOSE: Recently, an objective response rate of 12% was reported in a phase II study of cetuximab in patients with epidermal growth factor receptor (EGFR)-expressing metastatic colorectal cancer (mCRC) refractory to fluoropyrimidine-, oxaliplatin-, and irinotecan-based chemotherapy (IMC-0144).	Irinotecan	254-264	epidermal growth factor receptor	Homo sapiens	150-154
19059062-3	2008	Irinotecan toxicity in patients who have colorectal cancer has been linked to reduced activity of uridine diphosphate-glucuronyltransferase 1A1 (UGT1A1).	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-143
19059062-3	2008	Irinotecan toxicity in patients who have colorectal cancer has been linked to reduced activity of uridine diphosphate-glucuronyltransferase 1A1 (UGT1A1).	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	145-151
18335219-1	2008	PURPOSE: A multicenter phase I trial to establish the recommended dose of CPT-11/docetaxel plus cisplatin in advanced esophagogastric cancer patients and to correlate the efficacy and toxicity with genetic polymorphisms in DNA repair genes (XPD and XRCC3) and the UGT1A1 gene.	Irinotecan	74-80	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	241-244
18981587-0	2008	Association of ATP-binding cassette, sub-family C, number 2 (ABCC2) genotype with pharmacokinetics of irinotecan in Japanese patients with metastatic colorectal cancer treated with irinotecan plus infusional 5-fluorouracil/leucovorin (FOLFIRI).	Irinotecan	102-112	ATP binding cassette subfamily C member 2	Homo sapiens	15-59
18981587-0	2008	Association of ATP-binding cassette, sub-family C, number 2 (ABCC2) genotype with pharmacokinetics of irinotecan in Japanese patients with metastatic colorectal cancer treated with irinotecan plus infusional 5-fluorouracil/leucovorin (FOLFIRI).	Irinotecan	102-112	ATP binding cassette subfamily C member 2	Homo sapiens	61-66
18981587-1	2008	ATP-binding cassette, sub-family C, number 2 (ABCC2) is involved in the biliary excretion of irinotecan and its metabolites, SN-38 and SN-38 glucuronide.	Irinotecan	93-103	ATP binding cassette subfamily C member 2	Homo sapiens	0-44
18981587-1	2008	ATP-binding cassette, sub-family C, number 2 (ABCC2) is involved in the biliary excretion of irinotecan and its metabolites, SN-38 and SN-38 glucuronide.	Irinotecan	93-103	ATP binding cassette subfamily C member 2	Homo sapiens	46-51
19028276-2	2008	In the present study, mRNA expression of PDGFRbeta and c-kit in 33 patients with locally advanced rectal cancer undergoing preoperative chemoradiotherapy with cetuximab/capecitabine/irinotecan in correlation with the tumor regression rate was investigated.	Irinotecan	182-192	platelet derived growth factor receptor beta	Homo sapiens	41-50
18941461-5	2008	hMLH1-deficient cell lines due to either epigenetic silencing or mutation showed very similar IC(50) and were four- to nine-fold more sensitive to CPT-11 than the MSS line.	Irinotecan	147-153	mutL homolog 1	Homo sapiens	0-5
18941461-6	2008	Cell lines harbouring mutations in both MRE11 and RAD50 were most sensitive to CPT-11.	Irinotecan	79-85	MRE11 homolog, double strand break repair nuclease	Homo sapiens	40-45
18941461-6	2008	Cell lines harbouring mutations in both MRE11 and RAD50 were most sensitive to CPT-11.	Irinotecan	79-85	RAD50 double strand break repair protein	Homo sapiens	50-55
18981587-1	2008	ATP-binding cassette, sub-family C, number 2 (ABCC2) is involved in the biliary excretion of irinotecan and its metabolites, SN-38 and SN-38 glucuronide.	Irinotecan	125-130	ATP binding cassette subfamily C member 2	Homo sapiens	0-44
18981587-1	2008	ATP-binding cassette, sub-family C, number 2 (ABCC2) is involved in the biliary excretion of irinotecan and its metabolites, SN-38 and SN-38 glucuronide.	Irinotecan	125-130	ATP binding cassette subfamily C member 2	Homo sapiens	46-51
18981587-2	2008	Effects of the ABCC2 genotype on the pharmacokinetics (PK) of irinotecan and the metabolites were examined in Japanese patients with metastatic colorectal cancer receiving irinotecan plus infusional 5-fluorouracil/leucovorin (FOLFIRI).	Irinotecan	62-72	ATP binding cassette subfamily C member 2	Homo sapiens	15-20
18981587-5	2008	Relationship between the ABCC2 genotypes or diplotypes and area under the time-concentration curve (AUC) of irinotecan and the metabolites normalized by irinotecan dose was analyzed.	Irinotecan	108-118	ATP binding cassette subfamily C member 2	Homo sapiens	25-30
18981587-6	2008	The lower AUC of irinotecan was seen in patients with A/A or G/A genotypes at 1249 of the ABCC2 gene than others (p=0.011, Mann-Whitney U teat).	Irinotecan	17-27	ATP binding cassette subfamily C member 2	Homo sapiens	90-95
18981587-12	2008	Thus, ABCC2 genotype is one of the predictors of the variability of irinotecan PK in Japanese patients with metastatic colorectal cancer receiving FOLFIRI.	Irinotecan	68-78	ATP binding cassette subfamily C member 2	Homo sapiens	6-11
18278496-10	2008	RESULTS: The best structural model for irinotecan and its metabolites consisted of six-compartments: two compartments for irinotecan and SN-38, and one each for APC and SN-38G.	Irinotecan	39-49	APC regulator of WNT signaling pathway	Homo sapiens	161-164
18771527-0	2008	Overexpression of carboxylesterase-2 results in enhanced efficacy of topoisomerase I inhibitor, irinotecan (CPT-11), for multiple myeloma.	Irinotecan	96-106	carboxylesterase 2	Homo sapiens	18-36
18771527-0	2008	Overexpression of carboxylesterase-2 results in enhanced efficacy of topoisomerase I inhibitor, irinotecan (CPT-11), for multiple myeloma.	Irinotecan	108-114	carboxylesterase 2	Homo sapiens	18-36
18771527-5	2008	Interestingly, high expression of hCE-2 represented the nature of normal plasma cells, suggesting that hCE-2 could efficiently generate SN-38 within the plasma cells.	Irinotecan	136-141	carboxylesterase 2	Homo sapiens	34-39
18771527-5	2008	Interestingly, high expression of hCE-2 represented the nature of normal plasma cells, suggesting that hCE-2 could efficiently generate SN-38 within the plasma cells.	Irinotecan	136-141	carboxylesterase 2	Homo sapiens	103-108
18558463-6	2008	UGT1A1 *28 homozygosity is strongly associated with irinotecan-induced neutropenia and polymorphisms in the transporting peptides ABCB1 and OATP1B1 have also been associated with gastrointestinal toxicity and irinotecan pharmacokinetics, respectively.	Irinotecan	52-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18558463-6	2008	UGT1A1 *28 homozygosity is strongly associated with irinotecan-induced neutropenia and polymorphisms in the transporting peptides ABCB1 and OATP1B1 have also been associated with gastrointestinal toxicity and irinotecan pharmacokinetics, respectively.	Irinotecan	209-219	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18558463-6	2008	UGT1A1 *28 homozygosity is strongly associated with irinotecan-induced neutropenia and polymorphisms in the transporting peptides ABCB1 and OATP1B1 have also been associated with gastrointestinal toxicity and irinotecan pharmacokinetics, respectively.	Irinotecan	209-219	ATP binding cassette subfamily B member 1	Homo sapiens	130-135
18558463-6	2008	UGT1A1 *28 homozygosity is strongly associated with irinotecan-induced neutropenia and polymorphisms in the transporting peptides ABCB1 and OATP1B1 have also been associated with gastrointestinal toxicity and irinotecan pharmacokinetics, respectively.	Irinotecan	209-219	solute carrier organic anion transporter family member 1B1	Homo sapiens	140-147
18558463-7	2008	In the irinotecan product label, it is advised to reduce the irinotecan starting dose for UGT1A1 *28 homozygotes.	Irinotecan	7-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
18558463-7	2008	In the irinotecan product label, it is advised to reduce the irinotecan starting dose for UGT1A1 *28 homozygotes.	Irinotecan	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
18771527-6	2008	As expected, higher sensitivity to CPT-11 was observed in hCE-2-overexpressing U266 cells than mock U266 cells.	Irinotecan	35-41	carboxylesterase 2	Homo sapiens	58-63
18335219-1	2008	PURPOSE: A multicenter phase I trial to establish the recommended dose of CPT-11/docetaxel plus cisplatin in advanced esophagogastric cancer patients and to correlate the efficacy and toxicity with genetic polymorphisms in DNA repair genes (XPD and XRCC3) and the UGT1A1 gene.	Irinotecan	74-80	X-ray repair cross complementing 3	Homo sapiens	249-254
18335219-1	2008	PURPOSE: A multicenter phase I trial to establish the recommended dose of CPT-11/docetaxel plus cisplatin in advanced esophagogastric cancer patients and to correlate the efficacy and toxicity with genetic polymorphisms in DNA repair genes (XPD and XRCC3) and the UGT1A1 gene.	Irinotecan	74-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	264-270
18801934-8	2008	Markers available for identifying drug-induced adverse reactions include thiopurine methyltransferase (TPMT) to predict toxicity from thiopurines in the treatment of acute lymphoblastic leukemia and uridine diphosphate glucuronyltransferase to predict toxicity from irinotecan in the treatment of colorectal cancer.	Irinotecan	266-276	thiopurine S-methyltransferase	Homo sapiens	103-107
19260480-0	2008	TACE of liver metastases from colorectal cancer adopting irinotecan-eluting beads: beneficial effect of palliative intra-arterial lidocaine and post-procedure supportive therapy on the control of side effects.	Irinotecan	57-67	ADAM metallopeptidase domain 17	Homo sapiens	0-4
19004723-5	2008	Among the most conclusive examples one is that of the prediction of severe neutropenia induced by the irinotecan among patients homozygous for * 28 allele of UGT1A1 enzyme which conjugates SN38 active compound of irinotecan, the other one is the presence of a KRAS mutated allele in tumor cell to predict resistance to anti EGFR antibodies in the treatment of colorectal metastatic cancer.	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
18832463-3	2008	Homozygous carriers of UGT1A1*28 as well as those with additional UGT1A variants can suffer from severe irinotecan toxicity or jaundice during treatment with the protease inhibitor atazanavir.	Irinotecan	104-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18832463-3	2008	Homozygous carriers of UGT1A1*28 as well as those with additional UGT1A variants can suffer from severe irinotecan toxicity or jaundice during treatment with the protease inhibitor atazanavir.	Irinotecan	104-114	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	23-28
18797455-0	2008	GSTP1 Ile105Val polymorphism correlates with progression-free survival in MCRC patients treated with or without irinotecan: a study of the Dutch Colorectal Cancer Group.	Irinotecan	112-122	glutathione S-transferase pi 1	Homo sapiens	0-5
18797455-2	2008	As nuclear GSTP1 activity decreases irinotecan cytotoxicity, Val-allele carriers may benefit more from irinotecan chemotherapy.	Irinotecan	36-46	glutathione S-transferase pi 1	Homo sapiens	11-16
18797455-2	2008	As nuclear GSTP1 activity decreases irinotecan cytotoxicity, Val-allele carriers may benefit more from irinotecan chemotherapy.	Irinotecan	103-113	glutathione S-transferase pi 1	Homo sapiens	11-16
18797455-3	2008	Our aim was to investigate the association of GSTP1 genotype with treatment outcome of irinotecan.	Irinotecan	87-97	glutathione S-transferase pi 1	Homo sapiens	46-51
18797455-10	2008	GSTP1 codon 105 polymorphism may be predictive for the response to irinotecan-based chemotherapy in patients with MCRC, with the Val-allele being associated with a better outcome.	Irinotecan	67-77	glutathione S-transferase pi 1	Homo sapiens	0-5
18797458-2	2008	We included 49 patients treated for metastatic colorectal cancer with a combination of 5-fluorouracil and irinotecan; a polymorphism in the UGT1A1 gene (TA repeat in the TATA box) and one in the CES2 gene promoter (830C&gt;G) were studied as potential markers for SN-38 glucuronidation and irinotecan activation, respectively; and the potential activity of CYP3A4 was estimated from cortisol biotransformation into 6beta-hydroxycortisol.	Irinotecan	106-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
18797458-10	2008	UGT1A1 genotyping plus cortisol 6beta-hydroxylation determination could help to determine the optimal dose of irinotecan.	Irinotecan	110-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18927314-2	2008	We conducted a phase I study of irinotecan and the Hsp90 inhibitor 17AAG, which can also down-regulate Chk1, in patients with solid tumors.	Irinotecan	32-42	checkpoint kinase 1	Homo sapiens	103-107
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-141
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	143-149
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	325-331
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	203-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-141
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	203-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	143-149
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	203-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	325-331
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	235-245	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-141
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	235-245	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	143-149
18720361-1	2008	Pharmacogenetic research indicates a relationship between a polymorphism in the gene encoding uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and irinotecan inactivation, in that degradation of SN-38, the active metabolite of irinotecan, correlates inversely with the number of TA repeats in the TATA element of the UGT1A1 promoter region.	Irinotecan	235-245	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	325-331
18720361-2	2008	Individuals who are homozygous for the UGT1A1*28 allele (7 repeats) may exhibit reduced degradation of SN-38 and increased probability of severe toxicities.	Irinotecan	103-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
18720361-5	2008	Irinotecan labeling recommends testing for the UGT1A1*28 allele and reducing irinotecan dosing in patients who are positive to reduce the likelihood of dose-limiting neutropenia only, but not diarrhea.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
18703021-7	2008	A number of Pgp substrates (quinidine, amprenavir, irinotecan, topotecan, atorvastatin and erythromycin) induced net digoxin secretion, as did the non-Pgp substrate artemisinin.	Irinotecan	51-61	ATP binding cassette subfamily B member 1	Homo sapiens	12-15
19004723-5	2008	Among the most conclusive examples one is that of the prediction of severe neutropenia induced by the irinotecan among patients homozygous for * 28 allele of UGT1A1 enzyme which conjugates SN38 active compound of irinotecan, the other one is the presence of a KRAS mutated allele in tumor cell to predict resistance to anti EGFR antibodies in the treatment of colorectal metastatic cancer.	Irinotecan	102-112	KRAS proto-oncogene, GTPase	Homo sapiens	260-264
19004723-5	2008	Among the most conclusive examples one is that of the prediction of severe neutropenia induced by the irinotecan among patients homozygous for * 28 allele of UGT1A1 enzyme which conjugates SN38 active compound of irinotecan, the other one is the presence of a KRAS mutated allele in tumor cell to predict resistance to anti EGFR antibodies in the treatment of colorectal metastatic cancer.	Irinotecan	102-112	epidermal growth factor receptor	Homo sapiens	324-328
19004723-5	2008	Among the most conclusive examples one is that of the prediction of severe neutropenia induced by the irinotecan among patients homozygous for * 28 allele of UGT1A1 enzyme which conjugates SN38 active compound of irinotecan, the other one is the presence of a KRAS mutated allele in tumor cell to predict resistance to anti EGFR antibodies in the treatment of colorectal metastatic cancer.	Irinotecan	213-223	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-164
19004723-5	2008	Among the most conclusive examples one is that of the prediction of severe neutropenia induced by the irinotecan among patients homozygous for * 28 allele of UGT1A1 enzyme which conjugates SN38 active compound of irinotecan, the other one is the presence of a KRAS mutated allele in tumor cell to predict resistance to anti EGFR antibodies in the treatment of colorectal metastatic cancer.	Irinotecan	213-223	KRAS proto-oncogene, GTPase	Homo sapiens	260-264
19004723-5	2008	Among the most conclusive examples one is that of the prediction of severe neutropenia induced by the irinotecan among patients homozygous for * 28 allele of UGT1A1 enzyme which conjugates SN38 active compound of irinotecan, the other one is the presence of a KRAS mutated allele in tumor cell to predict resistance to anti EGFR antibodies in the treatment of colorectal metastatic cancer.	Irinotecan	213-223	epidermal growth factor receptor	Homo sapiens	324-328
18794444-3	2008	Recent studies show that imatinib reverses ABCG2-mediated drug resistance to topotecan hydrochloride and SN-38.	Irinotecan	105-110	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	43-48
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	31-37
18765539-0	2008	Thymidine selectively enhances growth suppressive effects of camptothecin/irinotecan in MSI+ cells and tumors containing a mutation of MRE11.	Irinotecan	74-84	phenylalkylamine Ca2+ antagonist (emopamil) binding protein	Mus musculus	88-91
18765539-10	2008	Increased sensitivity to this combination is also evident in vivo as thymidine enhances irinotecan-induced growth suppression of MMR-deficient tumors carrying the MRE11 mutation in mouse xenografts.	Irinotecan	88-98	MRE11A homolog A, double strand break repair nuclease	Mus musculus	163-168
18765539-11	2008	CONCLUSION: Irinotecan-thymidine combinations may be particularly effective when targeted to MSI+ tumors containing this readily detectable MRE11 mutation.	Irinotecan	12-22	phenylalkylamine Ca2+ antagonist (emopamil) binding protein	Mus musculus	93-96
18765539-11	2008	CONCLUSION: Irinotecan-thymidine combinations may be particularly effective when targeted to MSI+ tumors containing this readily detectable MRE11 mutation.	Irinotecan	12-22	MRE11A homolog A, double strand break repair nuclease	Mus musculus	140-145
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	43-49
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	31-37
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	31-37
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	43-49
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	43-49
18418374-8	2008	The component characterizing irinotecan"s compartments was associated with HNF1alpha and ABCC2 polymorphisms.	Irinotecan	29-39	HNF1 homeobox A	Homo sapiens	75-84
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	126-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18418374-8	2008	The component characterizing irinotecan"s compartments was associated with HNF1alpha and ABCC2 polymorphisms.	Irinotecan	29-39	ATP binding cassette subfamily C member 2	Homo sapiens	89-94
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	126-131	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	31-37
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	126-131	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	43-49
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	31-37
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	43-49
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	31-37
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	43-49
18418374-7	2008	Polymorphisms in genes UGT1A1, UGT1A7, and UGT1A9 had strong associations with a component corresponding to the irinotecan-to-SN-38 pathway and SN-38 recirculation and to a component relating to SN-38-to-SN-38G conversion and elimination of SN-38G.	Irinotecan	144-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18619980-1	2008	P-glycoprotein (P-gp) is found to play a very significant role in intestinal and biliary transport of irinotecan and its active metabolite, SN-38.	Irinotecan	102-112	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-14
18509065-5	2008	In particular, SN-38 arrested cells in S phase, enhanced the accumulation of gemcitabine metabolites, and diminished checkpoint kinase 1, thereby sensitizing cells in the SN-38 --&gt; gemcitabine sequence.	Irinotecan	15-20	checkpoint kinase 1	Homo sapiens	117-136
18695900-10	2008	The results from the present subcutaneously implanted tumor model suggested that a higher efficacy may be expected when bevacizumab is combined with the cytotoxic agent CPT-11, compared to bevacizumab alone, against tumors with a variety of VEGF production levels in clinical situations.	Irinotecan	169-175	vascular endothelial growth factor A	Homo sapiens	241-245
18619980-1	2008	P-glycoprotein (P-gp) is found to play a very significant role in intestinal and biliary transport of irinotecan and its active metabolite, SN-38.	Irinotecan	102-112	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	16-20
18619980-1	2008	P-glycoprotein (P-gp) is found to play a very significant role in intestinal and biliary transport of irinotecan and its active metabolite, SN-38.	Irinotecan	140-145	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-14
18619980-1	2008	P-glycoprotein (P-gp) is found to play a very significant role in intestinal and biliary transport of irinotecan and its active metabolite, SN-38.	Irinotecan	140-145	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	16-20
18619980-2	2008	This makes P-gp inhibition a logical strategy for improving irinotecan"s oral efficacy and reducing its toxicity.	Irinotecan	60-70	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	11-15
18619980-10	2008	Our studies not only propose a safe approach for bioavailability enhancement and reducing toxicity of irinotecan by P-gp inhibition but in another way also reiterate the significance of elucidating herb-drug interactions for future insights.	Irinotecan	102-112	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	116-120
17992531-7	2008	RESULTS: Area under the concentration-time curve ratios of APC/irinotecan, an in vivo parameter for CYP3A4 activity, were significantly higher in females than in males.	Irinotecan	63-73	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	100-106
18816295-2	2008	UGT1A9 is a UGT that catalyses the conjugation of endogenous oestrogenic and thyroid hormones, acetaminophen, SN-38 (an active metabolite of irinotecan) and phenols.	Irinotecan	110-115	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	0-6
18816295-2	2008	UGT1A9 is a UGT that catalyses the conjugation of endogenous oestrogenic and thyroid hormones, acetaminophen, SN-38 (an active metabolite of irinotecan) and phenols.	Irinotecan	141-151	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	0-6
18579105-9	2008	The blood to bile distribution ratio (AUC(bile)/AUC(blood)) was significantly reduced after group coadministration of EGCG, it can be seen that the bile efflux transport system of CPT-11 and SN-38 may be markedly reduced by the treatment of EGCG which plays the role of P-gp inhibitor.	Irinotecan	180-186	ATP binding cassette subfamily B member 1	Homo sapiens	270-274
18579105-9	2008	The blood to bile distribution ratio (AUC(bile)/AUC(blood)) was significantly reduced after group coadministration of EGCG, it can be seen that the bile efflux transport system of CPT-11 and SN-38 may be markedly reduced by the treatment of EGCG which plays the role of P-gp inhibitor.	Irinotecan	191-196	ATP binding cassette subfamily B member 1	Homo sapiens	270-274
17992531-0	2008	Impact of CYP3A4 haplotypes on irinotecan pharmacokinetics in Japanese cancer patients.	Irinotecan	31-41	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	10-16
17992531-1	2008	BACKGROUND AND PURPOSE: Cytochrome P450 3A4 (CYP3A4) converts an anticancer prodrug, irinotecan, to inactive metabolites such as APC.	Irinotecan	85-95	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	24-43
17992531-1	2008	BACKGROUND AND PURPOSE: Cytochrome P450 3A4 (CYP3A4) converts an anticancer prodrug, irinotecan, to inactive metabolites such as APC.	Irinotecan	85-95	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	45-51
17992531-12	2008	CONCLUSION: This study suggested that CYP3A4*16B was associated with decreased metabolism of irinotecan to APC.	Irinotecan	93-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	38-44
17992531-2	2008	However, the contribution of CYP3A4 genetic polymorphisms to irinotecan pharmacokinetics (PK) and pharmacodynamics (PD) is not fully elucidated.	Irinotecan	61-71	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	29-35
18690847-3	2008	The aim of the study was to investigate the induction by celecoxib of some multidrug resistance proteins, MRP1, MRP2, MRP4 and MRP5, involved in the transport of irinotecan and 5-FU.	Irinotecan	162-172	ATP binding cassette subfamily C member 1	Homo sapiens	106-110
17992531-4	2008	In this study, the effects of CYP3A4 haplotypes including *16B on irinotecan PK/PD were investigated in irinotecan-administered patients.	Irinotecan	66-76	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	30-36
17992531-5	2008	METHODS: The CYP3A4 genotypes for 177 Japanese cancer patients who received irinotecan were defined in terms of 4 major haplotypes, i.e., *1A (wild type), *1G (IVS10 + 12G &gt; A), *16B [554C &gt; G (Thr185Ser) and IVS10 + 12G &gt; A], and *18B [878T &gt; C (Leu293Pro) and IVS10 + 12G &gt; A].	Irinotecan	76-86	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	13-19
17992531-6	2008	Associations of CYP3A4 genotypes with irinotecan PK and severe toxicities (grade 3 diarrhea and grade 3 or 4 neutropenia) were investigated.	Irinotecan	38-48	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	16-22
18690847-3	2008	The aim of the study was to investigate the induction by celecoxib of some multidrug resistance proteins, MRP1, MRP2, MRP4 and MRP5, involved in the transport of irinotecan and 5-FU.	Irinotecan	162-172	ATP binding cassette subfamily C member 2	Homo sapiens	112-116
18690847-3	2008	The aim of the study was to investigate the induction by celecoxib of some multidrug resistance proteins, MRP1, MRP2, MRP4 and MRP5, involved in the transport of irinotecan and 5-FU.	Irinotecan	162-172	ATP binding cassette subfamily C member 4	Homo sapiens	118-122
18690847-3	2008	The aim of the study was to investigate the induction by celecoxib of some multidrug resistance proteins, MRP1, MRP2, MRP4 and MRP5, involved in the transport of irinotecan and 5-FU.	Irinotecan	162-172	ATP binding cassette subfamily C member 5	Homo sapiens	127-131
18633245-0	2008	[Role of UGT1A1*28 and UGT1A1*6 for irinotecan-induced adverse drug reaction].	Irinotecan	36-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
18594531-1	2008	The aim of the study was to investigate the associations between UGT1A1(*)28 genotype and (1) response rates, (2) febrile neutropenia and (3) dose intensity in patients with metastatic colorectal cancer treated with irinotecan.	Irinotecan	216-226	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	65-71
18594531-2	2008	UGT1A1(*)28 genotype was determined in 218 patients receiving irinotecan (either first-line therapy with capecitabine or second-line as monotherapy) for metastatic colorectal cancer.	Irinotecan	62-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18632807-0	2008	Colorectal tumor cells treated with 5-FU, oxaliplatin, irinotecan, and cetuximab exhibit changes in 18F-FDG incorporation corresponding to hexokinase activity and glucose transport.	Irinotecan	55-65	hexokinase 1	Homo sapiens	139-149
18708359-7	2008	Resistance of TuBEC to chemotherapeutic agents such as CPT-11, etoposide, and temozolomide can be overcome by knockdown of GRP78 using small interfering RNA or chemical inhibition of its catalytic site.	Irinotecan	55-61	heat shock protein family A (Hsp70) member 5	Homo sapiens	123-128
19343150-8	2008	In a randomized trial comparing 5-FU vs. irinotecan plus cisplatin vs. S-1, conducted by the Japan Clinical Oncology Group, S-1 was associated with a favorable safety profile, response rate, and time-to-treatment failure with longer survival compared with 5-FU.	Irinotecan	41-51	proteasome 26S subunit, non-ATPase 1	Homo sapiens	124-127
18633245-0	2008	[Role of UGT1A1*28 and UGT1A1*6 for irinotecan-induced adverse drug reaction].	Irinotecan	36-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
18633245-3	2008	Irinotecan is metabolized by carboxylesterase to form an active metabolite, 7-ethyl-10-hydroxycamptothecin(SN-38), which in turn is subsequently conjugated by UGT-glucuronosyltransferase 1A1(UGT1A1)to yield an inactive form, SN-38 glucuronide(SN-38 G).	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
18633245-3	2008	Irinotecan is metabolized by carboxylesterase to form an active metabolite, 7-ethyl-10-hydroxycamptothecin(SN-38), which in turn is subsequently conjugated by UGT-glucuronosyltransferase 1A1(UGT1A1)to yield an inactive form, SN-38 glucuronide(SN-38 G).	Irinotecan	76-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
18633245-3	2008	Irinotecan is metabolized by carboxylesterase to form an active metabolite, 7-ethyl-10-hydroxycamptothecin(SN-38), which in turn is subsequently conjugated by UGT-glucuronosyltransferase 1A1(UGT1A1)to yield an inactive form, SN-38 glucuronide(SN-38 G).	Irinotecan	107-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	191-197
18633245-4	2008	The UGT1A1 gene polymorphisms contribute to the individual variation in adverse events among patients administered irinotecan.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
18633245-7	2008	Recently, it has been demonstrated that genetic variants of UGT1A1*6 in addition to UGT1A1*28 are associated with the occurrence of adverse events in irinotecan chemotherapy in Asians.	Irinotecan	150-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
18633245-7	2008	Recently, it has been demonstrated that genetic variants of UGT1A1*6 in addition to UGT1A1*28 are associated with the occurrence of adverse events in irinotecan chemotherapy in Asians.	Irinotecan	150-160	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
18633245-8	2008	This review summarizes recent studies to outline the role of UGT1A1*28 and UGT1A1*6 for irinotecan-induced adverse drug reaction in Japanese cancer patients.	Irinotecan	88-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
18633245-8	2008	This review summarizes recent studies to outline the role of UGT1A1*28 and UGT1A1*6 for irinotecan-induced adverse drug reaction in Japanese cancer patients.	Irinotecan	88-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
18609706-11	2008	Furthermore, cells with reduced Bcl-x(L) or Mcl-1 expression was more sensitive towards oxaliplatin- and irinotecan-induced apoptosis, and in the case of Bcl-x(L) also towards 5-FU-induced apoptosis.	Irinotecan	105-115	BCL2 like 1	Homo sapiens	32-40
18320294-1	2008	PURPOSE: The inter/intramolecular interactions between drugs (floxuridine, irinotecan) and excipients (copper gluconate, triethanolamine) in the dual-drug liposomal formulation CPX-1 were elucidated in order to identify the physicochemical properties that allow coordinated release of irinotecan and floxuridine and maintenance of the two agents at a fixed, synergistic 1:1 molar ratio.	Irinotecan	75-85	complexin 1	Homo sapiens	177-182
18320294-5	2008	Approximately 45% of the total irinotecan was detectable in the copper-containing CPX-1 formulation by NMR, which decreased to 19% without copper present in the liposomal interior.	Irinotecan	31-41	complexin 1	Homo sapiens	82-87
18609706-11	2008	Furthermore, cells with reduced Bcl-x(L) or Mcl-1 expression was more sensitive towards oxaliplatin- and irinotecan-induced apoptosis, and in the case of Bcl-x(L) also towards 5-FU-induced apoptosis.	Irinotecan	105-115	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	44-49
18384433-0	2008	Vascular endothelial growth factor expression is closely related to irinotecan-mediated inhibition of tumor growth and angiogenesis in neuroblastoma xenografts.	Irinotecan	68-78	vascular endothelial growth factor A	Mus musculus	0-34
17703303-3	2008	The aim of this study was to determine the expression of nuclear factor-kappaB (NF-kappaB), tumor necrosis factor (TNF) and interleukins-1beta (IL-1beta) and -6 (IL-6) in the AT following the administration of the chemotherapeutic agent irinotecan.	Irinotecan	237-247	interleukin 6	Rattus norvegicus	162-166
18384433-8	2008	Our data demonstrate that diminished VEGF gene and protein expression is closely correlated with tumor growth inhibition and inhibition of angiogenesis by CPT-11 in NB xenografts.	Irinotecan	155-161	vascular endothelial growth factor A	Mus musculus	37-41
18633223-1	2008	Irinotecan hydrochloride is an inhibitor of DNA topoisomerase I enzyme by its main active metabolite SN-38.	Irinotecan	0-24	DNA topoisomerase I	Rattus norvegicus	44-63
18445521-7	2008	In conclusion, ST1968 exhibited an outstanding antitumour activity superior to that of irinotecan against SCC.	Irinotecan	87-97	serpin family B member 3	Homo sapiens	106-109
18633223-1	2008	Irinotecan hydrochloride is an inhibitor of DNA topoisomerase I enzyme by its main active metabolite SN-38.	Irinotecan	101-106	DNA topoisomerase I	Rattus norvegicus	44-63
18633225-1	2008	We encountered a 64-year-old UGT1A1*28 heterotype patient who received CPT-11 and CDDP chemotherapy for Stage III A small-cell lung-cancer and developed grade 4 neutropenia as assessed by CTCAE v3.0 in Pharmaceutical Management.	Irinotecan	71-77	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
18503403-5	2008	By performing uridine diphosphate glucuronosyltransferase (UGT) 1A1 genetic testing, some studies have been able to predict which patients receiving irinotecan will experience the toxicity.	Irinotecan	149-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-67
18497997-8	2008	Furthermore, quantitative real-time PCR demonstrated that mRNA changes of selected novel genes (CENPB, H2AFX, MCM5, ZADH1 and NGB) in irinotecan-resistant clones vs. parental clone were in agreement with array-CGH results.	Irinotecan	134-144	centromere protein B	Homo sapiens	96-101
18497997-8	2008	Furthermore, quantitative real-time PCR demonstrated that mRNA changes of selected novel genes (CENPB, H2AFX, MCM5, ZADH1 and NGB) in irinotecan-resistant clones vs. parental clone were in agreement with array-CGH results.	Irinotecan	134-144	H2A.X variant histone	Homo sapiens	103-108
18497997-8	2008	Furthermore, quantitative real-time PCR demonstrated that mRNA changes of selected novel genes (CENPB, H2AFX, MCM5, ZADH1 and NGB) in irinotecan-resistant clones vs. parental clone were in agreement with array-CGH results.	Irinotecan	134-144	minichromosome maintenance complex component 5	Homo sapiens	110-114
18497997-8	2008	Furthermore, quantitative real-time PCR demonstrated that mRNA changes of selected novel genes (CENPB, H2AFX, MCM5, ZADH1 and NGB) in irinotecan-resistant clones vs. parental clone were in agreement with array-CGH results.	Irinotecan	134-144	prostaglandin reductase 2	Homo sapiens	116-121
18497997-8	2008	Furthermore, quantitative real-time PCR demonstrated that mRNA changes of selected novel genes (CENPB, H2AFX, MCM5, ZADH1 and NGB) in irinotecan-resistant clones vs. parental clone were in agreement with array-CGH results.	Irinotecan	134-144	neuroglobin	Homo sapiens	126-129
17700594-0	2008	Influence of UGT1A9 intronic I399C&gt;T polymorphism on SN-38 glucuronidation in Asian cancer patients.	Irinotecan	56-61	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	13-19
17700594-1	2008	Genetic polymorphisms in hepatically expressed UGT1A1 and UGT1A9 contribute to the interindividual variability i-n irinotecan disposition and toxicity.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-53
17700594-1	2008	Genetic polymorphisms in hepatically expressed UGT1A1 and UGT1A9 contribute to the interindividual variability i-n irinotecan disposition and toxicity.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	58-64
17700594-5	2008	UGT1A1-1A9 diplotype analysis showed that patients harbouring the H1/H2 (TG6GT(10)T/GG6GT(9)C) diplotype had 2.4-fold lower systemic exposure to SN-38 glucuronide (SN-38G) compared with patients harbouring the H1/H5 (TG6GT(10)T/GG6GT(10)C) diplotype (P=0.025).	Irinotecan	145-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
17700594-7	2008	and suggests that the UGT1A9 I399C&gt;T variant may be an important glucuronidating allele affecting the pharmacokinetics of SN-38 and SN-38G in Asian cancer patients receiving irinotecan chemotherapy.	Irinotecan	125-130	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	22-28
17700594-7	2008	and suggests that the UGT1A9 I399C&gt;T variant may be an important glucuronidating allele affecting the pharmacokinetics of SN-38 and SN-38G in Asian cancer patients receiving irinotecan chemotherapy.	Irinotecan	135-140	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	22-28
17700594-7	2008	and suggests that the UGT1A9 I399C&gt;T variant may be an important glucuronidating allele affecting the pharmacokinetics of SN-38 and SN-38G in Asian cancer patients receiving irinotecan chemotherapy.	Irinotecan	177-187	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	22-28
17943230-1	2008	Clinically relevant resistance to the currently approved camptothecins, irinotecan and topotecan, is poorly understood but may involve increased expression of ATP-dependent drug transporters such as ABCG2 (breast cancer resistant protein, BCRP).	Irinotecan	72-82	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	199-204
17943230-1	2008	Clinically relevant resistance to the currently approved camptothecins, irinotecan and topotecan, is poorly understood but may involve increased expression of ATP-dependent drug transporters such as ABCG2 (breast cancer resistant protein, BCRP).	Irinotecan	72-82	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	239-243
18172616-1	2008	Human UDP-glucuronosyltransferase (UGT)1A1 is a critical enzyme responsible for detoxification and metabolism of endogenous and exogenous lipophilic compounds, such as potentially neurotoxic bilirubin and the anticancer drug irinotecan SN-38, via conjugation with glucuronic acid.	Irinotecan	225-235	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-42
18172616-1	2008	Human UDP-glucuronosyltransferase (UGT)1A1 is a critical enzyme responsible for detoxification and metabolism of endogenous and exogenous lipophilic compounds, such as potentially neurotoxic bilirubin and the anticancer drug irinotecan SN-38, via conjugation with glucuronic acid.	Irinotecan	236-241	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	6-42
18652401-4	2008	Polymorphisms of UGT 1A1 are considered as potential indicators of a risk of toxicity treatment by irinotecan.	Irinotecan	99-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-24
17624531-7	2008	RESULTS: CPT-11 caused significant diarrhea, histopathological alterations (inflammatory cell infiltration, loss of crypt architecture and villus shortening) and increased intestinal tissue MPO activity, TNF-alpha, IL-1beta and KC level and TNF-alpha immuno-staining.	Irinotecan	9-15	tumor necrosis factor	Mus musculus	241-250
18443598-6	2008	SN-38 preferentially inhibited endothelial cell proliferation alone and interacted synergistically with semaxinib; it induced apoptosis and increased the expression and secretion of TSP-1.	Irinotecan	0-5	thrombospondin 1	Homo sapiens	182-187
18443598-7	2008	Metronomic CPT-11 alone and combined with semaxinib significantly inhibits tumour growth in the absence of toxicity, which was accompanied by decreases in microvessel density and increases in TSP-1 gene expression in tumour tissues.	Irinotecan	11-17	thrombospondin 1	Homo sapiens	192-197
18443598-8	2008	In vitro results show the antiangiogenic properties of low-concentration SN-38, suggesting a key role of TSP-1 in this effect.	Irinotecan	73-78	thrombospondin 1	Homo sapiens	105-110
18472966-6	2008	Therapy with PKI166 alone or with irinotecan produced apoptosis of these endothelial cells and necrosis of the EGFR-negative tumors.	Irinotecan	34-44	epidermal growth factor receptor	Homo sapiens	111-115
18248513-6	2008	Both of naringenin and elacridar separately enhanced the sensitivity for CPT-11 and SN-38 in KYN-2 cells abundantly expressing BCRP, CYP3A4/5 and UGT1A1, but not in KYN-1 cells expressing lower levels.	Irinotecan	73-79	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	127-131
18248513-6	2008	Both of naringenin and elacridar separately enhanced the sensitivity for CPT-11 and SN-38 in KYN-2 cells abundantly expressing BCRP, CYP3A4/5 and UGT1A1, but not in KYN-1 cells expressing lower levels.	Irinotecan	84-89	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	127-131
18248513-6	2008	Both of naringenin and elacridar separately enhanced the sensitivity for CPT-11 and SN-38 in KYN-2 cells abundantly expressing BCRP, CYP3A4/5 and UGT1A1, but not in KYN-1 cells expressing lower levels.	Irinotecan	84-89	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	133-139
18248513-6	2008	Both of naringenin and elacridar separately enhanced the sensitivity for CPT-11 and SN-38 in KYN-2 cells abundantly expressing BCRP, CYP3A4/5 and UGT1A1, but not in KYN-1 cells expressing lower levels.	Irinotecan	84-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
18248513-8	2008	On the other hand, naringenin and elacridar significantly increased the chemosensitivity for CPT-11 and SN-38 in the KYN-1-derived cells artificially overexpressing BCRP.	Irinotecan	93-99	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	165-169
18248513-8	2008	On the other hand, naringenin and elacridar significantly increased the chemosensitivity for CPT-11 and SN-38 in the KYN-1-derived cells artificially overexpressing BCRP.	Irinotecan	104-109	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	165-169
18248513-10	2008	Those results suggest that BCRP is one of the chemosensitivity determinants of CPT-11 in HCC cells and its inhibition might be critical for cells expressing abundant BCRP.	Irinotecan	79-85	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	27-31
18248513-10	2008	Those results suggest that BCRP is one of the chemosensitivity determinants of CPT-11 in HCC cells and its inhibition might be critical for cells expressing abundant BCRP.	Irinotecan	79-85	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	166-170
17624531-1	2008	INTRODUCTION: Irinotecan (CPT-11) is an inhibitor of DNA topoisomerase I and is clinically effective against several cancers.	Irinotecan	14-24	topoisomerase (DNA) I	Mus musculus	53-72
17624531-1	2008	INTRODUCTION: Irinotecan (CPT-11) is an inhibitor of DNA topoisomerase I and is clinically effective against several cancers.	Irinotecan	26-32	topoisomerase (DNA) I	Mus musculus	53-72
17624531-7	2008	RESULTS: CPT-11 caused significant diarrhea, histopathological alterations (inflammatory cell infiltration, loss of crypt architecture and villus shortening) and increased intestinal tissue MPO activity, TNF-alpha, IL-1beta and KC level and TNF-alpha immuno-staining.	Irinotecan	9-15	myeloperoxidase	Mus musculus	190-193
17624531-7	2008	RESULTS: CPT-11 caused significant diarrhea, histopathological alterations (inflammatory cell infiltration, loss of crypt architecture and villus shortening) and increased intestinal tissue MPO activity, TNF-alpha, IL-1beta and KC level and TNF-alpha immuno-staining.	Irinotecan	9-15	tumor necrosis factor	Mus musculus	204-213
17624531-7	2008	RESULTS: CPT-11 caused significant diarrhea, histopathological alterations (inflammatory cell infiltration, loss of crypt architecture and villus shortening) and increased intestinal tissue MPO activity, TNF-alpha, IL-1beta and KC level and TNF-alpha immuno-staining.	Irinotecan	9-15	interleukin 1 beta	Mus musculus	215-223
18541046-12	2008	We also estimates the potential effects of genetic variations: the AUC and Cmax of SN-38 may increase to 208% and 165% respectively with the genetic variation UGT1A1*28/*28 which reduces the expression of UGT1A1 down to 30%.	Irinotecan	83-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	159-165
18541046-12	2008	We also estimates the potential effects of genetic variations: the AUC and Cmax of SN-38 may increase to 208% and 165% respectively with the genetic variation UGT1A1*28/*28 which reduces the expression of UGT1A1 down to 30%.	Irinotecan	83-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	205-211
18300238-0	2008	UGT1A1*28 polymorphism predicts irinotecan-induced severe toxicities without affecting treatment outcome and survival in patients with metastatic colorectal carcinoma.	Irinotecan	32-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18300238-1	2008	BACKGROUND: It is known that the uridine-diphosphoglucuronosyl transferase 1A1 (UGT1A1)*28 polymorphism reduces UGT1A1 enzyme activity, which may lead to severe toxicities in patients who receive irinotecan.	Irinotecan	196-206	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-78
18300238-1	2008	BACKGROUND: It is known that the uridine-diphosphoglucuronosyl transferase 1A1 (UGT1A1)*28 polymorphism reduces UGT1A1 enzyme activity, which may lead to severe toxicities in patients who receive irinotecan.	Irinotecan	196-206	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
18300238-1	2008	BACKGROUND: It is known that the uridine-diphosphoglucuronosyl transferase 1A1 (UGT1A1)*28 polymorphism reduces UGT1A1 enzyme activity, which may lead to severe toxicities in patients who receive irinotecan.	Irinotecan	196-206	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	112-118
18300238-11	2008	CONCLUSIONS: The current data suggested that the UGT1A1*28 polymorphism may be a key determinant for predicting irinotecan-induced severe toxicities without affecting treatment outcome for patients with metastatic CRC.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
18425325-0	2008	A novel molecular mechanism for anticancer drug-induced ovarian failure: Irinotecan HCl, an anticancer topoisomerase I inhibitor, induces specific FasL expression in granulosa cells of large ovarian follicles to enhance follicular apoptosis.	Irinotecan	73-87	Fas ligand (TNF superfamily, member 6)	Mus musculus	147-151
18425325-3	2008	Clinically therapeutic doses of CPT-11 were injected intraperitoneally into 8-week-old female MCH mice, and their ovaries were examined by the TUNEL assay to detect dead cells.	Irinotecan	32-38	modifier of chinchilla	Mus musculus	94-97
18425325-6	2008	Intraperitoneal CPT-11 injections induced specific TUNEL-positive cells and cell death with cleaved caspase 3 expression among large ovarian follicular granulosa cells.	Irinotecan	16-22	caspase 3	Mus musculus	100-109
18425325-11	2008	Although no FasL expression was detected in normal ovarian tissues, CPT-11 injections significantly induced specific FasL expression in granulosa cells.	Irinotecan	68-74	Fas ligand (TNF superfamily, member 6)	Mus musculus	117-121
18425325-13	2008	In conclusion, CPT-11 dose-dependently induced specific FasL expression in granulosa cells of developing ovarian follicles.	Irinotecan	15-21	Fas ligand (TNF superfamily, member 6)	Mus musculus	56-60
18437170-4	2008	In addition, the Food and Drug Administration of the United States now requires a "black box" warning on the packaging of irinotecan for evaluation of germline polymorphism in UGT1A1, the gene mutated in Gilbert"s syndrome, for potential reduction of drug dosage in patients with the UGT1A1*28 polymorphism.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	176-182
18437170-4	2008	In addition, the Food and Drug Administration of the United States now requires a "black box" warning on the packaging of irinotecan for evaluation of germline polymorphism in UGT1A1, the gene mutated in Gilbert"s syndrome, for potential reduction of drug dosage in patients with the UGT1A1*28 polymorphism.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	284-290
18466101-0	2008	Cost-effectiveness of UGT1A1 genotyping in second-line, high-dose, once every 3 weeks irinotecan monotherapy treatment of colorectal cancer.	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28
18466101-1	2008	AIM: The aim of the present study was to evaluate the cost-effectiveness of UGT1A1 genotyping in second-line, high-dose, once every 3 weeks irinotecan monotherapy treatment of colorectal cancer.	Irinotecan	140-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
18466101-5	2008	RESULTS &amp; CONCLUSION: Genotyping in combination with a subsequent reduction of initial irinotecan dose for UGT1A1 7/7 genotype patients was cost-saving for the population of African and Caucasian origin.	Irinotecan	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
18466101-8	2008	Finally, the application of a 3-weekly high-dose treatment regimen with a 20% reduced dosage compared with the low-dose weekly irinotecan regimen in patients with UGT1A1 7/7 genotype was less expensive and is more convenient for the patient.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	163-169
17549477-0	2008	Involvement of UDP-glucuronosyltransferase activity in irinotecan-induced delayed-onset diarrhea in rats.	Irinotecan	55-65	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	15-42
17549477-1	2008	We assessed the involvement of UDP-glucuronosyltransferase (UGT) activity in episodes of irinotecan hydrochloride (CPT-11)-induced delayed-onset diarrhea using a mutant rat strain with an inherited deficiency of UGT1A (Gunn rats).	Irinotecan	89-113	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	31-58
17549477-1	2008	We assessed the involvement of UDP-glucuronosyltransferase (UGT) activity in episodes of irinotecan hydrochloride (CPT-11)-induced delayed-onset diarrhea using a mutant rat strain with an inherited deficiency of UGT1A (Gunn rats).	Irinotecan	89-113	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	60-63
17549477-1	2008	We assessed the involvement of UDP-glucuronosyltransferase (UGT) activity in episodes of irinotecan hydrochloride (CPT-11)-induced delayed-onset diarrhea using a mutant rat strain with an inherited deficiency of UGT1A (Gunn rats).	Irinotecan	115-121	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	31-58
17549477-1	2008	We assessed the involvement of UDP-glucuronosyltransferase (UGT) activity in episodes of irinotecan hydrochloride (CPT-11)-induced delayed-onset diarrhea using a mutant rat strain with an inherited deficiency of UGT1A (Gunn rats).	Irinotecan	115-121	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	60-63
17549477-10	2008	These results clarified that the deficiency of UGT activity contributed greatly to the induction of the CPT-11-induced delayed-onset diarrhea and epithelial impairment in the intestine.	Irinotecan	104-110	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	47-50
17549477-11	2008	In the clinic, great care is needed when using chemotherapy with CPT-11 in patients with poor UGT activity.	Irinotecan	65-71	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	94-97
18381438-3	2008	With the combination therapy of SN-38 (the active metabolite of CPT-11) followed by flavopiridol, the induction of apoptosis was 5-fold greater in the p53+/+ cells compared with the p53-/- cells.	Irinotecan	64-70	tumor protein p53	Homo sapiens	151-154
18381438-3	2008	With the combination therapy of SN-38 (the active metabolite of CPT-11) followed by flavopiridol, the induction of apoptosis was 5-fold greater in the p53+/+ cells compared with the p53-/- cells.	Irinotecan	64-70	tumor protein p53	Homo sapiens	182-185
18381438-3	2008	With the combination therapy of SN-38 (the active metabolite of CPT-11) followed by flavopiridol, the induction of apoptosis was 5-fold greater in the p53+/+ cells compared with the p53-/- cells.	Irinotecan	32-37	tumor protein p53	Homo sapiens	151-154
17624531-10	2008	CONCLUSION: These results suggest an important role of TNF-alpha, IL-1beta and KC in the pathogenesis of intestinal mucositis induced by CPT-11.	Irinotecan	137-143	tumor necrosis factor	Mus musculus	55-64
18381438-3	2008	With the combination therapy of SN-38 (the active metabolite of CPT-11) followed by flavopiridol, the induction of apoptosis was 5-fold greater in the p53+/+ cells compared with the p53-/- cells.	Irinotecan	32-37	tumor protein p53	Homo sapiens	182-185
18381438-7	2008	Depletion of Rad51 by small interfering RNA (siRNA) sensitized both p53+/+ and p53-/- cells to SN-38-induced apoptosis with increase of gamma H2AX, a marker of DNA damage.	Irinotecan	95-100	RAD51 recombinase	Homo sapiens	13-18
18381438-7	2008	Depletion of Rad51 by small interfering RNA (siRNA) sensitized both p53+/+ and p53-/- cells to SN-38-induced apoptosis with increase of gamma H2AX, a marker of DNA damage.	Irinotecan	95-100	tumor protein p53	Homo sapiens	79-82
17624531-10	2008	CONCLUSION: These results suggest an important role of TNF-alpha, IL-1beta and KC in the pathogenesis of intestinal mucositis induced by CPT-11.	Irinotecan	137-143	interleukin 1 beta	Mus musculus	66-74
18082937-0	2008	Importance of UDP-glucuronosyltransferase 1A1*6 for irinotecan toxicities in Japanese cancer patients.	Irinotecan	52-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-45
18467239-0	2008	UGT1A1*28 and other UGT1A polymorphisms as determinants of irinotecan toxicity.	Irinotecan	59-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
18467239-0	2008	UGT1A1*28 and other UGT1A polymorphisms as determinants of irinotecan toxicity.	Irinotecan	59-69	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	0-5
18413798-9	2008	The antitumor effect of RGD-L-TRAIL was further enhanced by combination with CPT-11 in both TRAIL-sensitive COLO-205 and TRAIL-resistive HT-29 tumor xenograft models.	Irinotecan	77-83	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	30-35
18413798-9	2008	The antitumor effect of RGD-L-TRAIL was further enhanced by combination with CPT-11 in both TRAIL-sensitive COLO-205 and TRAIL-resistive HT-29 tumor xenograft models.	Irinotecan	77-83	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	92-97
18413798-9	2008	The antitumor effect of RGD-L-TRAIL was further enhanced by combination with CPT-11 in both TRAIL-sensitive COLO-205 and TRAIL-resistive HT-29 tumor xenograft models.	Irinotecan	77-83	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	92-97
18379174-2	2008	Irinotecan, an anticancer drug, is one of the models for personalized medicine, and a number of clinical studies have revealed significant associations between UGT1A1(*)28 and irinotecan toxicity.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
18379174-2	2008	Irinotecan, an anticancer drug, is one of the models for personalized medicine, and a number of clinical studies have revealed significant associations between UGT1A1(*)28 and irinotecan toxicity.	Irinotecan	176-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	160-166
18379174-6	2008	This mini-review outlines our recent studies on irinotecan pharmacogenetics and discusses the clinical significance of UGT1A1(*)6 and (*)28 markers for personalized irinotecan therapy in Japanese cancer patients.	Irinotecan	165-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	119-125
18381960-1	2008	PURPOSE: This study was designed to evaluate the in vitro cytotoxicity and in vivo efficacy of TRA-8, a mouse monoclonal antibody that binds to the DR5 death receptor for tumor necrosis factor-related apoptosis-inducing ligand (also called Apo2L), alone and in combination with CPT-11, against human colon cancer cells and xenografts.	Irinotecan	278-284	TNF receptor superfamily member 10b	Homo sapiens	148-151
18357380-9	2008	The effects of 5-FU and SN-38 on thymidylate synthase (TS) protein expression, an important determinant of 5-FU sensitivity, were assessed by Western blot analysis in H69 cells.	Irinotecan	24-29	thymidylate synthetase	Homo sapiens	33-53
18357380-9	2008	The effects of 5-FU and SN-38 on thymidylate synthase (TS) protein expression, an important determinant of 5-FU sensitivity, were assessed by Western blot analysis in H69 cells.	Irinotecan	24-29	thymidylate synthetase	Homo sapiens	55-57
18357380-10	2008	Treatment with SN-38 for 24 h suppressed TS protein expression and this low level of TS was maintained for at least 72 h. Pretreatment with SN-38 inhibited the 5-FU-induced increase of TS protein.	Irinotecan	15-20	thymidylate synthetase	Homo sapiens	41-43
18357380-10	2008	Treatment with SN-38 for 24 h suppressed TS protein expression and this low level of TS was maintained for at least 72 h. Pretreatment with SN-38 inhibited the 5-FU-induced increase of TS protein.	Irinotecan	140-145	thymidylate synthetase	Homo sapiens	41-43
18357380-10	2008	Treatment with SN-38 for 24 h suppressed TS protein expression and this low level of TS was maintained for at least 72 h. Pretreatment with SN-38 inhibited the 5-FU-induced increase of TS protein.	Irinotecan	140-145	thymidylate synthetase	Homo sapiens	85-87
18357380-10	2008	Treatment with SN-38 for 24 h suppressed TS protein expression and this low level of TS was maintained for at least 72 h. Pretreatment with SN-38 inhibited the 5-FU-induced increase of TS protein.	Irinotecan	140-145	thymidylate synthetase	Homo sapiens	85-87
18357380-11	2008	The synergistic effect induced by the combination of SN-38 and 5-FU may be attributable to the SN-38-induced suppression of TS protein.	Irinotecan	53-58	thymidylate synthetase	Homo sapiens	124-126
18357380-11	2008	The synergistic effect induced by the combination of SN-38 and 5-FU may be attributable to the SN-38-induced suppression of TS protein.	Irinotecan	95-100	thymidylate synthetase	Homo sapiens	124-126
18082937-1	2008	Recent pharmacogenetic studies on irinotecan have revealed the impact of UDP glucuronosyltransferase (UGT) 1A1*28 on severe irinotecan toxicities.	Irinotecan	34-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-110
18082937-1	2008	Recent pharmacogenetic studies on irinotecan have revealed the impact of UDP glucuronosyltransferase (UGT) 1A1*28 on severe irinotecan toxicities.	Irinotecan	124-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-110
18082937-2	2008	Although the clinical role of UGT1A1*6, which is specifically detected in East Asian patients, in irinotecan toxicities is suggested, clear evidence remains limited.	Irinotecan	98-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	30-36
18082937-3	2008	To examine the impact of *6, the association of UGT1A1 genotypes with severe irinotecan toxicities was retrospectively investigated in Japanese cancer patients.	Irinotecan	77-87	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
17483951-1	2008	PURPOSE: Carboxylesterase 2 (CES2) is involved in the activation of the anticancer drug irinotecan to its active metabolite SN-38.	Irinotecan	88-98	carboxylesterase 2	Homo sapiens	9-27
18347181-3	2008	CDC45L, NFKB1, PARP1, TDP1, and XRCC1 have been shown to influence the cytotoxic action of camptothecins, including irinotecan.	Irinotecan	116-126	cell division cycle 45	Homo sapiens	0-6
18347181-3	2008	CDC45L, NFKB1, PARP1, TDP1, and XRCC1 have been shown to influence the cytotoxic action of camptothecins, including irinotecan.	Irinotecan	116-126	nuclear factor kappa B subunit 1	Homo sapiens	8-13
18347181-3	2008	CDC45L, NFKB1, PARP1, TDP1, and XRCC1 have been shown to influence the cytotoxic action of camptothecins, including irinotecan.	Irinotecan	116-126	poly(ADP-ribose) polymerase 1	Homo sapiens	15-20
18347181-3	2008	CDC45L, NFKB1, PARP1, TDP1, and XRCC1 have been shown to influence the cytotoxic action of camptothecins, including irinotecan.	Irinotecan	116-126	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	22-26
18347181-3	2008	CDC45L, NFKB1, PARP1, TDP1, and XRCC1 have been shown to influence the cytotoxic action of camptothecins, including irinotecan.	Irinotecan	116-126	X-ray repair cross complementing 1	Homo sapiens	32-37
17998284-2	2008	PATIENTS AND METHODS: We studied the KRAS mutation status of 113 patients with irinotecan refractory mCRC treated with CTX in clinical trials.	Irinotecan	79-89	KRAS proto-oncogene, GTPase	Homo sapiens	37-41
17483951-1	2008	PURPOSE: Carboxylesterase 2 (CES2) is involved in the activation of the anticancer drug irinotecan to its active metabolite SN-38.	Irinotecan	88-98	carboxylesterase 2	Homo sapiens	29-33
17483951-1	2008	PURPOSE: Carboxylesterase 2 (CES2) is involved in the activation of the anticancer drug irinotecan to its active metabolite SN-38.	Irinotecan	124-129	carboxylesterase 2	Homo sapiens	9-27
17483951-1	2008	PURPOSE: Carboxylesterase 2 (CES2) is involved in the activation of the anticancer drug irinotecan to its active metabolite SN-38.	Irinotecan	124-129	carboxylesterase 2	Homo sapiens	29-33
17483951-4	2008	CES2 genotypes were tentatively related to irinotecan cytotoxicity and CES2 expression in the NCI-60 panel; to response to treatment and event-free survival in colorectal cancer patients; and to CES2 expression and catalytic activity in subsets of the human liver collection.	Irinotecan	43-53	carboxylesterase 2	Homo sapiens	0-4
18349289-3	2008	METHODS: Genotyping of the UGT1A1*28, UGT1A7 N129K/R131K, and UGT1A7-57T/G variants was done in 105 irinotecan-treated patients with metastatic colorectal cancer; adverse events were documented during all 297 treatment cycles and analyzed by Cochran-Mantel-Haenszel, Mann-Whitney, and chi2 tests.	Irinotecan	100-110	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	62-68
18188187-4	2008	Therefore, we have developed a mutant human CE (hCE1m6), based on the human liver CE hCE1, that can activate CPT-11 approximately 70-fold more efficiently than the wild-type protein and can be expressed at high levels in mammalian cells.	Irinotecan	109-115	carboxylesterase 1	Homo sapiens	48-52
18219662-2	2008	Topoisomerase I inhibitors, including 7-ethyl-10-hydroxycamptothecin (SN-38), are substrates effluxed by BCRP.	Irinotecan	38-68	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	105-109
18219662-2	2008	Topoisomerase I inhibitors, including 7-ethyl-10-hydroxycamptothecin (SN-38), are substrates effluxed by BCRP.	Irinotecan	70-75	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	105-109
18219662-6	2008	Subsequently, bisulfite sequencing analysis in both PC-6 cells and SN-38-resistant PC-6/SN2-5H, highly expressing BCRP cells was performed to identify the methylated region in the BCRP promoter.	Irinotecan	67-72	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	114-118
18219662-6	2008	Subsequently, bisulfite sequencing analysis in both PC-6 cells and SN-38-resistant PC-6/SN2-5H, highly expressing BCRP cells was performed to identify the methylated region in the BCRP promoter.	Irinotecan	67-72	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	180-184
18349289-1	2008	BACKGROUND: Gilbert"s syndrome is characterized by a functional promoter single nucleotide polymorphism (SNP) of the UDP-glucuronosyltransferase (UGT) 1A1 gene and represents a pharmacogenetic risk factor for irinotecan toxicity, but study data remain controversial.	Irinotecan	209-219	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	117-154
18349289-2	2008	The active CPT-11 metabolite 7-ethyl-10-hydroxycamptothecin is detoxified by several UGT1A proteins, which include UGT1A7 with a high specific activity that may contribute to the risk of irinotecan toxicity in Gilbert"s syndrome patients.	Irinotecan	11-17	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	85-90
18349289-7	2008	CONCLUSIONS: Irinotecan toxicity is more likely in patients with Gilbert"s syndrome carrying the UGT1A1*28 allele combined with reduced function UGT1A7 N129K/R131K and UGT1A7-57T/G SNP.	Irinotecan	13-23	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-103
18349289-2	2008	The active CPT-11 metabolite 7-ethyl-10-hydroxycamptothecin is detoxified by several UGT1A proteins, which include UGT1A7 with a high specific activity that may contribute to the risk of irinotecan toxicity in Gilbert"s syndrome patients.	Irinotecan	11-17	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	115-121
18349289-2	2008	The active CPT-11 metabolite 7-ethyl-10-hydroxycamptothecin is detoxified by several UGT1A proteins, which include UGT1A7 with a high specific activity that may contribute to the risk of irinotecan toxicity in Gilbert"s syndrome patients.	Irinotecan	29-59	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	85-90
18349289-7	2008	CONCLUSIONS: Irinotecan toxicity is more likely in patients with Gilbert"s syndrome carrying the UGT1A1*28 allele combined with reduced function UGT1A7 N129K/R131K and UGT1A7-57T/G SNP.	Irinotecan	13-23	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	145-151
18349289-2	2008	The active CPT-11 metabolite 7-ethyl-10-hydroxycamptothecin is detoxified by several UGT1A proteins, which include UGT1A7 with a high specific activity that may contribute to the risk of irinotecan toxicity in Gilbert"s syndrome patients.	Irinotecan	29-59	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	115-121
18349289-7	2008	CONCLUSIONS: Irinotecan toxicity is more likely in patients with Gilbert"s syndrome carrying the UGT1A1*28 allele combined with reduced function UGT1A7 N129K/R131K and UGT1A7-57T/G SNP.	Irinotecan	13-23	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	168-174
18349289-2	2008	The active CPT-11 metabolite 7-ethyl-10-hydroxycamptothecin is detoxified by several UGT1A proteins, which include UGT1A7 with a high specific activity that may contribute to the risk of irinotecan toxicity in Gilbert"s syndrome patients.	Irinotecan	187-197	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	85-90
18349289-2	2008	The active CPT-11 metabolite 7-ethyl-10-hydroxycamptothecin is detoxified by several UGT1A proteins, which include UGT1A7 with a high specific activity that may contribute to the risk of irinotecan toxicity in Gilbert"s syndrome patients.	Irinotecan	187-197	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	115-121
18349289-8	2008	Based on the ability of UGT1A7 to metabolize and eliminate the active irinotecan metabolite 7-ethyl-10-hydroxycamptothecin, the UGT1A1/UGT1A7 SNP combination haplotype appears to be a superior risk predictor than Gilbert"s syndrome alone.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	24-30
18349289-8	2008	Based on the ability of UGT1A7 to metabolize and eliminate the active irinotecan metabolite 7-ethyl-10-hydroxycamptothecin, the UGT1A1/UGT1A7 SNP combination haplotype appears to be a superior risk predictor than Gilbert"s syndrome alone.	Irinotecan	92-122	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	24-30
18349289-8	2008	Based on the ability of UGT1A7 to metabolize and eliminate the active irinotecan metabolite 7-ethyl-10-hydroxycamptothecin, the UGT1A1/UGT1A7 SNP combination haplotype appears to be a superior risk predictor than Gilbert"s syndrome alone.	Irinotecan	92-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	128-134
18349289-8	2008	Based on the ability of UGT1A7 to metabolize and eliminate the active irinotecan metabolite 7-ethyl-10-hydroxycamptothecin, the UGT1A1/UGT1A7 SNP combination haplotype appears to be a superior risk predictor than Gilbert"s syndrome alone.	Irinotecan	92-122	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	135-141
17786445-8	2008	With irinotecan and 5-FU, mOS around 8 months were reported and with cetuximab combined with irinotecan, the highest mOS was 9.8 months.	Irinotecan	5-15	Moloney sarcoma oncogene	Mus musculus	26-29
17905465-7	2008	In summary, we showed that a ERCC1-negative protein status was significantly related to tumor responsiveness to neoadjuvant chemotherapy with cisplatin and irinotecan, but such a status was not a clear prognostic predictor to cisplatin-based neoadjuvant therapy in NSCLC patients.	Irinotecan	156-166	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	29-34
18082941-5	2008	Antineoplastic screening demonstrated that five candidates agents, docetaxel, actinomycin D, mitoxantrone, paclitaxel, and SN-38, exhibited potent inhibitory effects on OATP1B3-mediated transport of CDCA-NBD.	Irinotecan	123-128	solute carrier organic anion transporter family member 1B3	Homo sapiens	169-176
18082941-7	2008	We determined that SN-38 is a novel substrate for OATP1B3.	Irinotecan	19-24	solute carrier organic anion transporter family member 1B3	Homo sapiens	50-57
18023188-1	2008	Carboxylesterases metabolize numerous exogenous and endogenous ester-containing compounds including the chemotherapeutic agent CPT-11, anti-influenza viral agent oseltamivir, and many agrochemicals.	Irinotecan	127-133	carboxylesterase 1	Homo sapiens	0-17
18157147-0	2008	Tumor targeting carboxylesterase fused with anti-CEA scFv improve the anticancer effect with a less toxic dose of irinotecan.	Irinotecan	114-124	pregnancy specific beta-1-glycoprotein 2	Homo sapiens	49-52
18157147-0	2008	Tumor targeting carboxylesterase fused with anti-CEA scFv improve the anticancer effect with a less toxic dose of irinotecan.	Irinotecan	114-124	immunglobulin heavy chain variable region	Homo sapiens	53-57
18157147-6	2008	The recombinant enzyme anchors onto the tumor cell surface CEA, and thus metabolize CPT-11 extracellularly.	Irinotecan	84-90	pregnancy specific beta-1-glycoprotein 2	Homo sapiens	59-62
18182997-0	2008	Pharmacological targeting of NF-kappaB potentiates the effect of the topoisomerase inhibitor CPT-11 on colon cancer cells.	Irinotecan	93-99	nuclear factor kappa B subunit 1	Homo sapiens	29-38
18182997-4	2008	In human colon cancer cells, inhibition of NF-kappaB using 10 microM AS602868 induced a 30-50% growth inhibitory effect and strongly enhanced the action of SN-38, the topoisomerase I inhibitor and CPT-11 active metabolite.	Irinotecan	156-161	nuclear factor kappa B subunit 1	Homo sapiens	43-52
18182997-4	2008	In human colon cancer cells, inhibition of NF-kappaB using 10 microM AS602868 induced a 30-50% growth inhibitory effect and strongly enhanced the action of SN-38, the topoisomerase I inhibitor and CPT-11 active metabolite.	Irinotecan	197-203	nuclear factor kappa B subunit 1	Homo sapiens	43-52
18182997-6	2008	In xenografts experiments, inhibition of NF-kappaB potentiated the antitumoural effect of CPT-11 in a dose-dependent manner.	Irinotecan	90-96	nuclear factor kappa B subunit 1	Homo sapiens	41-50
18182997-8	2008	Ex vivo tumour analyses as well as in vitro studies showed that AS602868 impaired CPT-11-induced NF-kappaB activation, and enhanced tumour cell cycle arrest and apoptosis.	Irinotecan	82-88	nuclear factor kappa B subunit 1	Homo sapiens	97-106
18182667-2	2008	The aim of these retrospective studies was to evaluate tumor vascularity and expression of components of the VEGF pathway and hypoxic responses as predictive markers for radiographic response and survival benefit from the bevacizumab and irinotecan therapy.	Irinotecan	238-248	vascular endothelial growth factor A	Homo sapiens	109-113
18230579-2	2008	This chimeric antibody inhibiting the Epidermal Growth receptor (EGFR) has been demonstrated to be efficient in the treatment of irinotecan-resistant metastatic CRC expressing the EGFR.	Irinotecan	129-139	epidermal growth factor receptor	Homo sapiens	65-69
18230579-2	2008	This chimeric antibody inhibiting the Epidermal Growth receptor (EGFR) has been demonstrated to be efficient in the treatment of irinotecan-resistant metastatic CRC expressing the EGFR.	Irinotecan	129-139	epidermal growth factor receptor	Homo sapiens	180-184
18231104-5	2008	In patients given first-line cisplatin-based regimens (combined with S-1 or irinotecan) (43 patients), low ERCC1 correlated with a higher response rate (low: 55.6% vs high: 18.8%; P=0.008).	Irinotecan	76-86	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	107-112
18281753-1	2008	CPT-11 is activated by hydrolysis to SN-38 that is primarily inactivated through biotrans-formation into SN-38 glucuronide ( SN-38 G) by UGT1As.	Irinotecan	0-6	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-141
18281753-1	2008	CPT-11 is activated by hydrolysis to SN-38 that is primarily inactivated through biotrans-formation into SN-38 glucuronide ( SN-38 G) by UGT1As.	Irinotecan	37-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-141
18281753-1	2008	CPT-11 is activated by hydrolysis to SN-38 that is primarily inactivated through biotrans-formation into SN-38 glucuronide ( SN-38 G) by UGT1As.	Irinotecan	105-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-141
18281753-3	2008	The toxicities of CPT-11 have been reported to correlate with the polymorphism of the number of TA repeats in UGT1A1 gene because of its gene transcriptional efficiency.	Irinotecan	18-24	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
18281776-6	2008	She was also treated with cisplatin and S-1 as fourth-line chemotherapy after treatment with nedaplatin and gemcitabine, docetaxel and irinotecan, and gefitinib.	Irinotecan	135-145	proteasome 26S subunit, non-ATPase 1	Homo sapiens	40-43
18778115-1	2008	Bevacizumab (Avastin) is a recombinant, humanized monoclonal antibody against vascular endothelial growth factor (VEGF) that is used to inhibit VEGF function in vascular endothelial cells and thereby inhibit tumor angiogenesis, upon which solid tumors depend for growth and metastasis.The addition of bevacizumab to fluoropyrimidine-based chemotherapy, with or without irinotecan or oxaliplatin, in both the first- and second-line treatment of metastatic colorectal cancer, significantly increased median progression-free survival or time to disease progression in most randomized controlled trials.	Irinotecan	369-379	vascular endothelial growth factor A	Homo sapiens	78-112
18778115-1	2008	Bevacizumab (Avastin) is a recombinant, humanized monoclonal antibody against vascular endothelial growth factor (VEGF) that is used to inhibit VEGF function in vascular endothelial cells and thereby inhibit tumor angiogenesis, upon which solid tumors depend for growth and metastasis.The addition of bevacizumab to fluoropyrimidine-based chemotherapy, with or without irinotecan or oxaliplatin, in both the first- and second-line treatment of metastatic colorectal cancer, significantly increased median progression-free survival or time to disease progression in most randomized controlled trials.	Irinotecan	369-379	vascular endothelial growth factor A	Homo sapiens	114-118
19075668-13	2008	Using an ex vivo drug sensitivity assay, the histoculture drug response assay (HDRA), the expression of ATP7A in human surgically resected colon cancer cells correlated with sensitivity to 7-ethyl-10-hydroxy-camptothecin (SN-38).	Irinotecan	222-227	ATPase copper transporting alpha	Homo sapiens	104-109
19075668-14	2008	ATP7A-overexpressing cells are resistant to many anticancer drugs including SN-38, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11), vincristine, paclitaxel, etoposide, doxorubicin (Dox), and mitoxantron.	Irinotecan	76-81	ATPase copper transporting alpha	Homo sapiens	0-5
19075668-14	2008	ATP7A-overexpressing cells are resistant to many anticancer drugs including SN-38, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11), vincristine, paclitaxel, etoposide, doxorubicin (Dox), and mitoxantron.	Irinotecan	83-149	ATPase copper transporting alpha	Homo sapiens	0-5
19075668-14	2008	ATP7A-overexpressing cells are resistant to many anticancer drugs including SN-38, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11), vincristine, paclitaxel, etoposide, doxorubicin (Dox), and mitoxantron.	Irinotecan	151-157	ATPase copper transporting alpha	Homo sapiens	0-5
17786445-8	2008	With irinotecan and 5-FU, mOS around 8 months were reported and with cetuximab combined with irinotecan, the highest mOS was 9.8 months.	Irinotecan	93-103	Moloney sarcoma oncogene	Mus musculus	117-120
17766002-0	2008	Influence of the organic anion-transporting polypeptide 1B1 (OATP1B1) polymorphisms on irinotecan-pharmacokinetics and clinical outcome of patients with advanced non-small cell lung cancer.	Irinotecan	87-97	solute carrier organic anion transporter family member 1B1	Homo sapiens	17-59
18370855-1	2008	ABCG2 was discovered in multi-drug-resistant cancer cells, with the identification of chemotherapeutic agents, such as mitoxantrone, flavopiridol, methotrexate and irinotecan as substrates.	Irinotecan	164-174	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
18714167-7	2008	CONCLUSION: These results indicate that both Apo2L/TRAIL-sensitive and -resistant colon tumors will respond to a combination of CPT-11 and Apo2L/TRAIL and predict that this will be useful in the treatment of human colon cancers in a clinical setting.	Irinotecan	128-134	TNF superfamily member 10	Homo sapiens	45-50
18714167-7	2008	CONCLUSION: These results indicate that both Apo2L/TRAIL-sensitive and -resistant colon tumors will respond to a combination of CPT-11 and Apo2L/TRAIL and predict that this will be useful in the treatment of human colon cancers in a clinical setting.	Irinotecan	128-134	TNF superfamily member 10	Homo sapiens	51-56
17766002-0	2008	Influence of the organic anion-transporting polypeptide 1B1 (OATP1B1) polymorphisms on irinotecan-pharmacokinetics and clinical outcome of patients with advanced non-small cell lung cancer.	Irinotecan	87-97	solute carrier organic anion transporter family member 1B1	Homo sapiens	61-68
18852492-3	2008	This model was applied to data from phase II/III trials of first-line bevacizumab plus 5-FU/LV with/without irinotecan (IFL).	Irinotecan	108-118	interferon alpha 1	Homo sapiens	120-123
17766002-1	2008	To investigate whether the OATP1B1 polymorphisms affect irinotecan-pharmacokinetics and subsequent toxicity and tumor response of patients with advanced NSCLC.	Irinotecan	56-66	solute carrier organic anion transporter family member 1B1	Homo sapiens	27-34
17766002-8	2008	These findings suggest that OATP1B1 variants are involved in SN-38 disposition and highly predictive for severe toxicity of NSCLC patients treated with irinotecan-based chemotherapy.	Irinotecan	61-66	solute carrier organic anion transporter family member 1B1	Homo sapiens	28-35
17766002-8	2008	These findings suggest that OATP1B1 variants are involved in SN-38 disposition and highly predictive for severe toxicity of NSCLC patients treated with irinotecan-based chemotherapy.	Irinotecan	152-162	solute carrier organic anion transporter family member 1B1	Homo sapiens	28-35
17345086-9	2007	Among these active compounds, 3",4",7-trimethoxyflavone showed the strongest anti-BCRP activity with RI(50) values of 0.012 microM for SN-38 and 0.044 muM for mitoxantrone.	Irinotecan	135-140	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	82-86
17898154-1	2007	The UGT1A1*28 polymorphism is known to correlate with altered clearance of bilirubin (Gilbert syndrome) and drugs such as 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxy camptothecin (CPT-11).	Irinotecan	122-189	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
17898154-1	2007	The UGT1A1*28 polymorphism is known to correlate with altered clearance of bilirubin (Gilbert syndrome) and drugs such as 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxy camptothecin (CPT-11).	Irinotecan	191-197	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
17898154-5	2007	Bilirubin, estradiol (3-OH), ethinyl estradiol (3-OH), and 7-ethyl-10-hydroxycamptothecin (SN-38) were found to show significantly lower rates of metabolism in the UGT1A1*28/*28 microsomes with no change in K(m) values.	Irinotecan	59-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	164-170
17978195-4	2007	Strain-specific differences in the rate of 16 alpha-hydroxytestosterone generation and irinotecan glucuronidation correlated with the pattern of genetic variation within Cyp2b9 and Ugt1a loci, respectively.	Irinotecan	87-97	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	170-176
17978195-4	2007	Strain-specific differences in the rate of 16 alpha-hydroxytestosterone generation and irinotecan glucuronidation correlated with the pattern of genetic variation within Cyp2b9 and Ugt1a loci, respectively.	Irinotecan	87-97	Ugt1a@	Mus musculus	181-186
18361806-3	2007	The anti-EGFR monoclonal antibody cetuximab has been shown to reverse chemotherapy resistance in patients with irinotecan-refractory mCRC, to improve survival compared with best supportive care (BSC) alone, and to prolong progression free-survival (PFS) in the first- and second-line settings.	Irinotecan	111-121	epidermal growth factor receptor	Homo sapiens	9-13
18478930-1	2007	OBJECTIVE: To assess the polymorphism of UGT1A gene in Chinese, and to investigate the correlation between UGT1A polymorphism and irinotecan toxicity in colorectal cancer patients.	Irinotecan	130-140	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	107-112
18478930-8	2007	CONCLUSION: Chinese patients exhibit less irinotecan-related diarrhea due to higher frequence of UGT1A A1 * 28 wild genotype TA6/6.	Irinotecan	42-52	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	97-102
17273826-5	2007	A decrease in Bcl-xL sensitised cells to the small molecule inhibitor of Bcl-xL, Antimycin A3 and the DNA topoisomerase I inhibitors, SN-38 and camptothecin, but not to doxorubicin.	Irinotecan	134-139	BCL2 like 1	Homo sapiens	14-20
29793274-2	2007	: Role ofUGT1A1*6, UGT1A1*28 and ABCG2 c.421C&gt;A polymorphisms in irinotecan-induced neutropenia in Asian cancer patients.	Irinotecan	68-78	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	33-38
29793274-7	2007	In that study, a statistically significantly higher level of SN-38 and a relatively lower degree of glucuronidation occurred in patients with the UGT1A1*6 homozygote genotype than in patients with the reference genotype.	Irinotecan	61-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
17942911-9	2007	Knockdown of GRP78 also sensitizes glioma cells to 5-fluorouracil and CPT-11.	Irinotecan	70-76	heat shock protein family A (Hsp70) member 5	Homo sapiens	13-18
17273826-0	2007	Short hairpin RNAs targeting Bcl-xL modulate senescence and apoptosis following SN-38 and irinotecan exposure in a colon cancer model.	Irinotecan	80-85	BCL2 like 1	Homo sapiens	29-35
17273826-0	2007	Short hairpin RNAs targeting Bcl-xL modulate senescence and apoptosis following SN-38 and irinotecan exposure in a colon cancer model.	Irinotecan	90-100	BCL2 like 1	Homo sapiens	29-35
17273826-10	2007	Antimycin A3, in combination with SN-38 recapitulated this phenotype in HCT 116 cells, suggesting a potential role for small molecule inhibitors of Bcl-xL/Bcl-2 in the treatment of colorectal cancer, potentially in combination with irinotecan.	Irinotecan	34-39	BCL2 like 1	Homo sapiens	148-154
17728214-7	2007	The risk of experiencing irinotecan-induced hematologic toxicity for patients with a UGT1A1*28/*28 genotype thus appears to be a function of the dose of irinotecan administered.	Irinotecan	25-35	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
17393318-11	2007	MEK activation suppressed CPT-11-induced apoptosis in IEC-caMEK cells via a COX-2- dependent mechanism.	Irinotecan	26-32	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	76-81
17898662-0	2007	Severe toxicities after irinotecan-based chemotherapy in a patient with lung cancer: a homozygote for the SLCO1B1*15 allele.	Irinotecan	24-34	solute carrier organic anion transporter family member 1B1	Homo sapiens	106-113
17898662-2	2007	Polymorphism of the UGT1A1 gene is one of the likely reasons for interindividual differences in irinotecan pharmacokinetics and severe toxicity.	Irinotecan	96-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
17898662-3	2007	Also, polymorphic organic anion-transporting polypeptide 1B1 (OATP1B1, SLCO1B1) is reported to be involved in the hepatocellular uptake of SN-38.	Irinotecan	139-144	solute carrier organic anion transporter family member 1B1	Homo sapiens	18-60
17898662-3	2007	Also, polymorphic organic anion-transporting polypeptide 1B1 (OATP1B1, SLCO1B1) is reported to be involved in the hepatocellular uptake of SN-38.	Irinotecan	139-144	solute carrier organic anion transporter family member 1B1	Homo sapiens	62-69
17898662-3	2007	Also, polymorphic organic anion-transporting polypeptide 1B1 (OATP1B1, SLCO1B1) is reported to be involved in the hepatocellular uptake of SN-38.	Irinotecan	139-144	solute carrier organic anion transporter family member 1B1	Homo sapiens	71-78
17898662-6	2007	Analysis of genetic variants in genes encoding the drug-metabolizing enzyme (UGT1A1) and transporter (SLCO1B1) involving irinotecan disposition revealed that this patient was homozygous for the SLCO1B1*15 allele, which may result in severe toxicities attributable to the extensive accumulation of SN-38.	Irinotecan	121-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
17898662-6	2007	Analysis of genetic variants in genes encoding the drug-metabolizing enzyme (UGT1A1) and transporter (SLCO1B1) involving irinotecan disposition revealed that this patient was homozygous for the SLCO1B1*15 allele, which may result in severe toxicities attributable to the extensive accumulation of SN-38.	Irinotecan	121-131	solute carrier organic anion transporter family member 1B1	Homo sapiens	102-109
17898662-6	2007	Analysis of genetic variants in genes encoding the drug-metabolizing enzyme (UGT1A1) and transporter (SLCO1B1) involving irinotecan disposition revealed that this patient was homozygous for the SLCO1B1*15 allele, which may result in severe toxicities attributable to the extensive accumulation of SN-38.	Irinotecan	121-131	solute carrier organic anion transporter family member 1B1	Homo sapiens	194-201
17898662-6	2007	Analysis of genetic variants in genes encoding the drug-metabolizing enzyme (UGT1A1) and transporter (SLCO1B1) involving irinotecan disposition revealed that this patient was homozygous for the SLCO1B1*15 allele, which may result in severe toxicities attributable to the extensive accumulation of SN-38.	Irinotecan	297-302	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
17898662-6	2007	Analysis of genetic variants in genes encoding the drug-metabolizing enzyme (UGT1A1) and transporter (SLCO1B1) involving irinotecan disposition revealed that this patient was homozygous for the SLCO1B1*15 allele, which may result in severe toxicities attributable to the extensive accumulation of SN-38.	Irinotecan	297-302	solute carrier organic anion transporter family member 1B1	Homo sapiens	102-109
17898662-6	2007	Analysis of genetic variants in genes encoding the drug-metabolizing enzyme (UGT1A1) and transporter (SLCO1B1) involving irinotecan disposition revealed that this patient was homozygous for the SLCO1B1*15 allele, which may result in severe toxicities attributable to the extensive accumulation of SN-38.	Irinotecan	297-302	solute carrier organic anion transporter family member 1B1	Homo sapiens	194-201
17898662-7	2007	Screening of SLCO1B1*15 is suggested to be useful in irinotecan chemotherapy to avoid unpredicted severe toxicity, although the homozygous genotype is rare among the Japanese.	Irinotecan	53-63	solute carrier organic anion transporter family member 1B1	Homo sapiens	13-20
17728214-1	2007	The Food and Drug Administration and Pfizer changed the package insert for irinotecan to include a patient"s UGT1A1*28 genotype as a risk factor for severe neutropenia on the basis of the findings of four pharmacogenetic studies, which found that irinotecan-treated patients who were homozygous for the UGT1A1*28 allele had a greater risk of hematologic toxic effects than patients who had one or two copies of the wild-type allele (UGT1A1*1).	Irinotecan	75-85	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
17728214-1	2007	The Food and Drug Administration and Pfizer changed the package insert for irinotecan to include a patient"s UGT1A1*28 genotype as a risk factor for severe neutropenia on the basis of the findings of four pharmacogenetic studies, which found that irinotecan-treated patients who were homozygous for the UGT1A1*28 allele had a greater risk of hematologic toxic effects than patients who had one or two copies of the wild-type allele (UGT1A1*1).	Irinotecan	247-257	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
17640957-2	2007	hCE-2 also activates an anticancer drug, irinotecan (7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothecin, CPT-11), into its active metabolite, 7-ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	41-51	carboxylesterase 2	Homo sapiens	0-5
17640957-2	2007	hCE-2 also activates an anticancer drug, irinotecan (7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothecin, CPT-11), into its active metabolite, 7-ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	53-119	carboxylesterase 2	Homo sapiens	0-5
17640957-2	2007	hCE-2 also activates an anticancer drug, irinotecan (7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothecin, CPT-11), into its active metabolite, 7-ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	121-127	carboxylesterase 2	Homo sapiens	0-5
17640957-2	2007	hCE-2 also activates an anticancer drug, irinotecan (7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothecin, CPT-11), into its active metabolite, 7-ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	158-188	carboxylesterase 2	Homo sapiens	0-5
17640957-2	2007	hCE-2 also activates an anticancer drug, irinotecan (7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothecin, CPT-11), into its active metabolite, 7-ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	190-195	carboxylesterase 2	Homo sapiens	0-5
17060921-1	2007	Variants within the human UGT1A1 gene are associated with irinotecan induced severely adverse reactions and hyperbilirubinemia.	Irinotecan	58-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
17875772-11	2007	Both in vitro and in vivo studies suggest inactivation of MGMT with O(6)-benzylguanine may increase the activity of temozolomide and irinotecan against neuroblastoma.	Irinotecan	133-143	O-6-methylguanine-DNA methyltransferase	Mus musculus	58-62
17728214-7	2007	The risk of experiencing irinotecan-induced hematologic toxicity for patients with a UGT1A1*28/*28 genotype thus appears to be a function of the dose of irinotecan administered.	Irinotecan	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
19262706-1	2007	PURPOSE: To evaluate the association between dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) levels in primary gastric tumors and clinical response to S-1 or S-1 plus irinotecan in patients with unresectable advanced gastric cancer, and to investigate the molecular mechanism of augmented antitumor activity of the combination using human gastric cancer xenografts with high TS activity.	Irinotecan	187-197	dihydropyrimidine dehydrogenase	Homo sapiens	45-76
17627617-7	2007	These exploratory findings suggest that homozygosity for UGT1A1*6 allele may be associated with altered SN-38 disposition and may increase the risk of severe neutropenia in Asian cancer patients, particularly in the Chinese cancer patients who comprised 80% (n = 36) of the patient population in the present study.	Irinotecan	104-109	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
17406868-0	2007	Genetic linkage of UGT1A7 and UGT1A9 polymorphisms to UGT1A1*6 is associated with reduced activity for SN-38 in Japanese patients with cancer.	Irinotecan	103-108	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	19-25
17406868-0	2007	Genetic linkage of UGT1A7 and UGT1A9 polymorphisms to UGT1A1*6 is associated with reduced activity for SN-38 in Japanese patients with cancer.	Irinotecan	103-108	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	30-36
17406868-0	2007	Genetic linkage of UGT1A7 and UGT1A9 polymorphisms to UGT1A1*6 is associated with reduced activity for SN-38 in Japanese patients with cancer.	Irinotecan	103-108	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	54-60
17406868-1	2007	PURPOSE: The phenotypic effects of UGT1A7 and UGT1A9 genetic polymorphisms on the in vivo pharmacokinetics of irinotecan were examined.	Irinotecan	110-120	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	35-41
17406868-1	2007	PURPOSE: The phenotypic effects of UGT1A7 and UGT1A9 genetic polymorphisms on the in vivo pharmacokinetics of irinotecan were examined.	Irinotecan	110-120	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	46-52
17406868-9	2007	CONCLUSION: Genetic linkage of UGT1A7 and UGT1A9 polymorphisms to UGT1A1*6, related to reduced catalytic and transcriptional activities of UGTs, is associated with the decreased glucuronosyltransferase activity for SN-38 in Japanese patients with cancer.	Irinotecan	215-220	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	31-37
17406868-9	2007	CONCLUSION: Genetic linkage of UGT1A7 and UGT1A9 polymorphisms to UGT1A1*6, related to reduced catalytic and transcriptional activities of UGTs, is associated with the decreased glucuronosyltransferase activity for SN-38 in Japanese patients with cancer.	Irinotecan	215-220	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	42-48
17406868-9	2007	CONCLUSION: Genetic linkage of UGT1A7 and UGT1A9 polymorphisms to UGT1A1*6, related to reduced catalytic and transcriptional activities of UGTs, is associated with the decreased glucuronosyltransferase activity for SN-38 in Japanese patients with cancer.	Irinotecan	215-220	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
17873515-1	2007	PURPOSE: Because of its supposed inhibiting capacities of uridine-diphosphate glucuronosyltransferase 1A (UGT1A)-mediated glucuronidation in rats, the antiepileptic drug valproic acid has been investigated as modulator of irinotecan-induced delayed-type diarrhea in rats.	Irinotecan	222-232	Ugt1a@	Rattus norvegicus	106-111
19262706-1	2007	PURPOSE: To evaluate the association between dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) levels in primary gastric tumors and clinical response to S-1 or S-1 plus irinotecan in patients with unresectable advanced gastric cancer, and to investigate the molecular mechanism of augmented antitumor activity of the combination using human gastric cancer xenografts with high TS activity.	Irinotecan	187-197	dihydropyrimidine dehydrogenase	Homo sapiens	78-81
19262706-5	2007	In the experimental studies, S-1 plus irinotecan showed augmented antitumor activity against tumors with high TS activity (P &lt; .01) compared with either agent alone.	Irinotecan	38-48	thymidylate synthetase	Homo sapiens	110-112
19262706-6	2007	A potential mechanism for this effect was suggested by the significant reduction in TS activity observed following irinotecan administration in tumors with high TS activity.	Irinotecan	115-125	thymidylate synthetase	Homo sapiens	84-86
19262706-6	2007	A potential mechanism for this effect was suggested by the significant reduction in TS activity observed following irinotecan administration in tumors with high TS activity.	Irinotecan	115-125	thymidylate synthetase	Homo sapiens	161-163
19262706-7	2007	CONCLUSION: This study suggests that, via down-regulation of TS by irinotecan treatment, combination chemotherapy with S-1 and irinotecan could be effective in gastric cancer patients with high TS levels.	Irinotecan	67-77	thymidylate synthetase	Homo sapiens	61-63
19262706-7	2007	CONCLUSION: This study suggests that, via down-regulation of TS by irinotecan treatment, combination chemotherapy with S-1 and irinotecan could be effective in gastric cancer patients with high TS levels.	Irinotecan	67-77	thymidylate synthetase	Homo sapiens	194-196
19262706-7	2007	CONCLUSION: This study suggests that, via down-regulation of TS by irinotecan treatment, combination chemotherapy with S-1 and irinotecan could be effective in gastric cancer patients with high TS levels.	Irinotecan	127-137	thymidylate synthetase	Homo sapiens	61-63
19262706-7	2007	CONCLUSION: This study suggests that, via down-regulation of TS by irinotecan treatment, combination chemotherapy with S-1 and irinotecan could be effective in gastric cancer patients with high TS levels.	Irinotecan	127-137	thymidylate synthetase	Homo sapiens	194-196
17634538-0	2007	TIMP-1 is significantly associated with objective response and survival in metastatic colorectal cancer patients receiving combination of irinotecan, 5-fluorouracil, and folinic acid.	Irinotecan	138-148	TIMP metallopeptidase inhibitor 1	Homo sapiens	0-6
17691917-5	2007	So far, the candidate gene approach has provided important clues for pharmacogenomic-based personalized chemotherapy with 6-mercaptopurine (6-MP), solely metabolized by thiopurine S-methyltransferase (TPMT), and irinotecan, mainly detoxified by UDP-glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	212-222	thiopurine S-methyltransferase	Homo sapiens	201-205
17691917-6	2007	Reduced activity of TPMT caused by polymorphisms in the TPMT gene and decreased activity of UGT1A1 caused by UGT1A1*28 are related to severe toxic effects of 6-MP and irinotecan, respectively.	Irinotecan	167-177	thiopurine S-methyltransferase	Homo sapiens	20-24
17691917-6	2007	Reduced activity of TPMT caused by polymorphisms in the TPMT gene and decreased activity of UGT1A1 caused by UGT1A1*28 are related to severe toxic effects of 6-MP and irinotecan, respectively.	Irinotecan	167-177	thiopurine S-methyltransferase	Homo sapiens	56-60
17691917-6	2007	Reduced activity of TPMT caused by polymorphisms in the TPMT gene and decreased activity of UGT1A1 caused by UGT1A1*28 are related to severe toxic effects of 6-MP and irinotecan, respectively.	Irinotecan	167-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	92-98
17691917-6	2007	Reduced activity of TPMT caused by polymorphisms in the TPMT gene and decreased activity of UGT1A1 caused by UGT1A1*28 are related to severe toxic effects of 6-MP and irinotecan, respectively.	Irinotecan	167-177	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	109-115
17537833-0	2007	Interleukin-6 alters the cellular responsiveness to clopidogrel, irinotecan, and oseltamivir by suppressing the expression of carboxylesterases HCE1 and HCE2.	Irinotecan	65-75	interleukin 6	Homo sapiens	0-13
17537833-0	2007	Interleukin-6 alters the cellular responsiveness to clopidogrel, irinotecan, and oseltamivir by suppressing the expression of carboxylesterases HCE1 and HCE2.	Irinotecan	65-75	carboxylesterase 2	Homo sapiens	126-143
17537833-0	2007	Interleukin-6 alters the cellular responsiveness to clopidogrel, irinotecan, and oseltamivir by suppressing the expression of carboxylesterases HCE1 and HCE2.	Irinotecan	65-75	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	144-148
17537833-0	2007	Interleukin-6 alters the cellular responsiveness to clopidogrel, irinotecan, and oseltamivir by suppressing the expression of carboxylesterases HCE1 and HCE2.	Irinotecan	65-75	carboxylesterase 2	Homo sapiens	153-157
17666793-0	2007	Irinotecan-induced apoptosis is inhibited by increased P-glycoprotein expression and decreased p53 in human hepatocellular carcinoma cells.	Irinotecan	0-10	ATP binding cassette subfamily B member 1	Homo sapiens	55-69
17666793-0	2007	Irinotecan-induced apoptosis is inhibited by increased P-glycoprotein expression and decreased p53 in human hepatocellular carcinoma cells.	Irinotecan	0-10	tumor protein p53	Homo sapiens	95-98
17666793-7	2007	SN-38 significantly induced apoptosis in Huh7 cells at 24 h. SN-38 also increased the expression of p53, Bax, and caspase-9 and decreased Bcl-xL expression in Huh7 cells.	Irinotecan	0-5	tumor protein p53	Homo sapiens	100-103
17666793-7	2007	SN-38 significantly induced apoptosis in Huh7 cells at 24 h. SN-38 also increased the expression of p53, Bax, and caspase-9 and decreased Bcl-xL expression in Huh7 cells.	Irinotecan	0-5	BCL2 associated X, apoptosis regulator	Homo sapiens	105-108
17666793-7	2007	SN-38 significantly induced apoptosis in Huh7 cells at 24 h. SN-38 also increased the expression of p53, Bax, and caspase-9 and decreased Bcl-xL expression in Huh7 cells.	Irinotecan	0-5	caspase 9	Homo sapiens	114-123
17666793-7	2007	SN-38 significantly induced apoptosis in Huh7 cells at 24 h. SN-38 also increased the expression of p53, Bax, and caspase-9 and decreased Bcl-xL expression in Huh7 cells.	Irinotecan	0-5	BCL2 like 1	Homo sapiens	138-144
17666793-7	2007	SN-38 significantly induced apoptosis in Huh7 cells at 24 h. SN-38 also increased the expression of p53, Bax, and caspase-9 and decreased Bcl-xL expression in Huh7 cells.	Irinotecan	61-66	tumor protein p53	Homo sapiens	100-103
17666793-7	2007	SN-38 significantly induced apoptosis in Huh7 cells at 24 h. SN-38 also increased the expression of p53, Bax, and caspase-9 and decreased Bcl-xL expression in Huh7 cells.	Irinotecan	61-66	BCL2 associated X, apoptosis regulator	Homo sapiens	105-108
17666793-7	2007	SN-38 significantly induced apoptosis in Huh7 cells at 24 h. SN-38 also increased the expression of p53, Bax, and caspase-9 and decreased Bcl-xL expression in Huh7 cells.	Irinotecan	61-66	caspase 9	Homo sapiens	114-123
17666793-7	2007	SN-38 significantly induced apoptosis in Huh7 cells at 24 h. SN-38 also increased the expression of p53, Bax, and caspase-9 and decreased Bcl-xL expression in Huh7 cells.	Irinotecan	61-66	BCL2 like 1	Homo sapiens	138-144
17666793-8	2007	SN-38 decreased p53 expression and increased P-gp expression after 120 h, resulting in inhibition of apoptosis.	Irinotecan	0-5	tumor protein p53	Homo sapiens	16-19
17666793-8	2007	SN-38 decreased p53 expression and increased P-gp expression after 120 h, resulting in inhibition of apoptosis.	Irinotecan	0-5	ATP binding cassette subfamily B member 1	Homo sapiens	45-49
17666793-10	2007	SN-38-induced P-gp expression was additionally enhanced by p53 decoy oligodeoxynucleotide.	Irinotecan	0-5	ATP binding cassette subfamily B member 1	Homo sapiens	14-18
17666793-10	2007	SN-38-induced P-gp expression was additionally enhanced by p53 decoy oligodeoxynucleotide.	Irinotecan	0-5	tumor protein p53	Homo sapiens	59-62
17622938-6	2007	RESULTS: A strong correlation was observed between the glucuronidation of T4 and SN-38, a UGT1A1 substrate (r=0.82, P&lt;0.0001).	Irinotecan	81-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
17762398-2	2007	The presence of an additional TA repeat in the TATA sequence of the UGT1A1 promoter leads to a significant decrease in SN-38 glucuronidation.	Irinotecan	119-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
17762398-3	2007	Patients with the UGT1A1 (TA)7 allele are more likely to experience severe neutropenia and diarrhea following irinotecan chemotherapy.	Irinotecan	110-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
17577039-0	2007	UGT1A1 promoter genotype correlates with SN-38 pharmacokinetics, but not severe toxicity in patients receiving low-dose irinotecan.	Irinotecan	41-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
17534875-0	2007	Associations of ABCB1, ABCC2, and ABCG2 polymorphisms with irinotecan-pharmacokinetics and clinical outcome in patients with advanced non-small cell lung cancer.	Irinotecan	59-69	ATP binding cassette subfamily B member 1	Homo sapiens	16-21
17534875-0	2007	Associations of ABCB1, ABCC2, and ABCG2 polymorphisms with irinotecan-pharmacokinetics and clinical outcome in patients with advanced non-small cell lung cancer.	Irinotecan	59-69	ATP binding cassette subfamily C member 2	Homo sapiens	23-28
17534875-0	2007	Associations of ABCB1, ABCC2, and ABCG2 polymorphisms with irinotecan-pharmacokinetics and clinical outcome in patients with advanced non-small cell lung cancer.	Irinotecan	59-69	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-39
17534875-1	2007	BACKGROUND: The authors investigated whether ABCB1, ABCC2, and ABCG2 genetic polymorphisms affect pharmacokinetics (PK) of irinotecan and treatment outcome of patients with advanced nonsmall cell lung cancer (NSCLC).	Irinotecan	123-133	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	63-68
17534875-11	2007	CONCLUSIONS: Specific polymorphisms of ABCB1 and ABCC2 can influence disposition and tumor response to irinotecan by regulating transporter activity.	Irinotecan	103-113	ATP binding cassette subfamily B member 1	Homo sapiens	39-44
17534875-11	2007	CONCLUSIONS: Specific polymorphisms of ABCB1 and ABCC2 can influence disposition and tumor response to irinotecan by regulating transporter activity.	Irinotecan	103-113	ATP binding cassette subfamily C member 2	Homo sapiens	49-54
17681105-1	2007	BACKGROUND: Uridine diphosphate glucuronosyltransferase (UGT) 1A1 7/7 polymorphism has been linked with an increased risk of irinotecan-induced severe toxicities.	Irinotecan	125-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-65
17681105-2	2007	We evaluated UGT1A1 polymorphism in patients developing grade 3/4 toxicity after initiation of irinotecan to determine the frequency of this polymorphism in this population.	Irinotecan	95-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
17681105-3	2007	PATIENTS AND METHODS: Twenty patients with grade 3/4 irinotecan-induced toxicity underwent UGT1A1 genotyping in an exploratory study.	Irinotecan	53-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97
17681105-8	2007	Our data support the need for more prospective studies that evaluate the predictive value of UGT1A1 as well as UGT1A1-based dosing in patients receiving irinotecan.	Irinotecan	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
17681105-8	2007	Our data support the need for more prospective studies that evaluate the predictive value of UGT1A1 as well as UGT1A1-based dosing in patients receiving irinotecan.	Irinotecan	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
17609585-6	2007	SN-38 binding motifs were detected in the proximal promoter of p53 (bases -433 to -317 and -814 to -711).	Irinotecan	0-5	tumor protein p53	Homo sapiens	63-66
17609585-7	2007	These results suggest that the p53-mediated apoptosis pathway is important in the anticancer effects of irinotecan in hepatocellular carcinoma.	Irinotecan	104-114	tumor protein p53	Homo sapiens	31-34
17558305-1	2007	OBJECTIVES: SN-38, an active metabolite of irinotecan, is detoxified by glucuronidation with UGT1A isoforms, 1A1, 1A7, 1A9, and 1A10.	Irinotecan	12-17	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	93-98
17558305-1	2007	OBJECTIVES: SN-38, an active metabolite of irinotecan, is detoxified by glucuronidation with UGT1A isoforms, 1A1, 1A7, 1A9, and 1A10.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	93-98
17558305-2	2007	The pharmacogenetic information on UGT1A haplotypes covering all these isoforms is important for the individualized therapy of irinotecan.	Irinotecan	127-137	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	35-40
17558305-3	2007	Associations between UGT1A haplotypes and pharmacokinetics/pharmacodynamics of irinotecan were investigated to identify pharmacogenetic markers.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	21-26
17558305-4	2007	METHODS: Associations between UGT1A haplotypes and the area under concentration curve ratio (SN-38 glucuronide/SN-38) or toxicities were analyzed in 177 Japanese cancer patients treated with irinotecan as a single agent or in combination chemotherapy.	Irinotecan	93-98	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	30-35
17558305-10	2007	CONCLUSIONS: The haplotypes significantly associated with reduced area under concentration curve ratios and neutropenia contained UGT1A1*6 or *28, and both of them should be genotyped before irinotecan is given to Japanese and probably other Asian patients.	Irinotecan	191-201	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	130-136
17609585-0	2007	Irinotecan activates p53 with its active metabolite, resulting in human hepatocellular carcinoma apoptosis.	Irinotecan	0-10	tumor protein p53	Homo sapiens	21-24
17609585-4	2007	SN-38 significantly increased the expression of p53 protein and its phosphorylation at Ser(15) in the nucleus and apoptosis-inducing proteins Bax, caspase-9, and caspase-3, while it significantly decreased the antiapoptosis protein Bcl-xL of Huh7 cells.	Irinotecan	0-5	tumor protein p53	Homo sapiens	48-51
17609585-4	2007	SN-38 significantly increased the expression of p53 protein and its phosphorylation at Ser(15) in the nucleus and apoptosis-inducing proteins Bax, caspase-9, and caspase-3, while it significantly decreased the antiapoptosis protein Bcl-xL of Huh7 cells.	Irinotecan	0-5	BCL2 associated X, apoptosis regulator	Homo sapiens	142-145
17609585-4	2007	SN-38 significantly increased the expression of p53 protein and its phosphorylation at Ser(15) in the nucleus and apoptosis-inducing proteins Bax, caspase-9, and caspase-3, while it significantly decreased the antiapoptosis protein Bcl-xL of Huh7 cells.	Irinotecan	0-5	caspase 9	Homo sapiens	147-156
17609585-4	2007	SN-38 significantly increased the expression of p53 protein and its phosphorylation at Ser(15) in the nucleus and apoptosis-inducing proteins Bax, caspase-9, and caspase-3, while it significantly decreased the antiapoptosis protein Bcl-xL of Huh7 cells.	Irinotecan	0-5	caspase 3	Homo sapiens	162-171
17609585-4	2007	SN-38 significantly increased the expression of p53 protein and its phosphorylation at Ser(15) in the nucleus and apoptosis-inducing proteins Bax, caspase-9, and caspase-3, while it significantly decreased the antiapoptosis protein Bcl-xL of Huh7 cells.	Irinotecan	0-5	BCL2 like 1	Homo sapiens	232-238
17609585-5	2007	SN-38-induced apoptosis was recovered after p53 antisense oligodeoxynucleotide (AS ODN) pretreatment, while Huh7 cells were precultured with p53 AS ODN, followed by the addition of SN-38 for 24 h. Furthermore, increases in p53 DNA-binding activity were observed in the nuclei of Huh7 cells after SN-38 treatment as shown by electrophoretic mobility shift analysis.	Irinotecan	0-5	tumor protein p53	Homo sapiens	44-47
17609585-5	2007	SN-38-induced apoptosis was recovered after p53 antisense oligodeoxynucleotide (AS ODN) pretreatment, while Huh7 cells were precultured with p53 AS ODN, followed by the addition of SN-38 for 24 h. Furthermore, increases in p53 DNA-binding activity were observed in the nuclei of Huh7 cells after SN-38 treatment as shown by electrophoretic mobility shift analysis.	Irinotecan	0-5	tumor protein p53	Homo sapiens	141-144
17609585-5	2007	SN-38-induced apoptosis was recovered after p53 antisense oligodeoxynucleotide (AS ODN) pretreatment, while Huh7 cells were precultured with p53 AS ODN, followed by the addition of SN-38 for 24 h. Furthermore, increases in p53 DNA-binding activity were observed in the nuclei of Huh7 cells after SN-38 treatment as shown by electrophoretic mobility shift analysis.	Irinotecan	0-5	tumor protein p53	Homo sapiens	141-144
17549342-1	2007	Tumor sensitivity to anticancer drugs such as CPT-11 and platinum derivatives was investigated by assessing Topo-1 and Bax/ERCC-1 expression in patients with stage I/II breast, lung, and gastric cancer who were positive for ONCs, and tumor sensitivity was compared between CPT-11 and platinum derivatives.	Irinotecan	46-52	BCL2 associated X, apoptosis regulator	Homo sapiens	119-122
17549342-1	2007	Tumor sensitivity to anticancer drugs such as CPT-11 and platinum derivatives was investigated by assessing Topo-1 and Bax/ERCC-1 expression in patients with stage I/II breast, lung, and gastric cancer who were positive for ONCs, and tumor sensitivity was compared between CPT-11 and platinum derivatives.	Irinotecan	46-52	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	123-129
17725105-0	2007	Schedule-dependent cytotoxicity of 5-fluorouracil and irinotecan in p53 mutant human colon cancer.	Irinotecan	54-64	tumor protein p53	Homo sapiens	68-71
17516995-10	2007	Inhibitory effects of irinotecan on enzyme acetylcholinesterase (AChE) were studied in erythrocytes.	Irinotecan	22-32	acetylcholinesterase (Cartwright blood group)	Homo sapiens	43-63
17516995-10	2007	Inhibitory effects of irinotecan on enzyme acetylcholinesterase (AChE) were studied in erythrocytes.	Irinotecan	22-32	acetylcholinesterase (Cartwright blood group)	Homo sapiens	65-69
17516995-12	2007	Irinotecan was found to be strong inhibitor of the acetylcholine hydrolysis and to cause a continuous decrease of catalytic activity of AChE.	Irinotecan	0-10	acetylcholinesterase (Cartwright blood group)	Homo sapiens	136-140
17441964-5	2007	We also confirmed that the phosphorylated form of DNA-PK was increased by treatment with both etoposide and SN-38.	Irinotecan	108-113	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	50-56
17510208-0	2007	UGT1A1 polymorphism can predict hematologic toxicity in patients treated with irinotecan.	Irinotecan	78-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
17487378-0	2007	The interactive transcript abundance index [c-myc*p73alpha]/[p21*Bcl-2] correlates with baseline level of apoptosis and response to CPT-11 in human bronchogenic carcinoma cell lines.	Irinotecan	132-138	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	44-49
17487378-0	2007	The interactive transcript abundance index [c-myc*p73alpha]/[p21*Bcl-2] correlates with baseline level of apoptosis and response to CPT-11 in human bronchogenic carcinoma cell lines.	Irinotecan	132-138	BCL2 apoptosis regulator	Homo sapiens	65-70
17487378-6	2007	In addition, the interactive transcript abundance index (ITAI) [c-myc*p73alpha]/[p21*Bcl-2] was directly correlated with baseline apoptosis (p&lt;0.01) and CPT-11 response (p&lt;0.05).	Irinotecan	156-162	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	64-69
17487378-6	2007	In addition, the interactive transcript abundance index (ITAI) [c-myc*p73alpha]/[p21*Bcl-2] was directly correlated with baseline apoptosis (p&lt;0.01) and CPT-11 response (p&lt;0.05).	Irinotecan	156-162	BCL2 apoptosis regulator	Homo sapiens	85-90
17487378-7	2007	The ITAI was also correlated with CPT-11 response among cell lines derived from a variety of tissues that had inactivating p53 mutations or deletions, supporting its applicability for predicting response to camptothecins in other tissues regardless of p53 status.	Irinotecan	34-40	tumor protein p53	Homo sapiens	123-126
17608024-0	2007	UGT1AI*6 and UGT1A1*27 for individualized irinotecan chemotherapy.	Irinotecan	42-52	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	0-6
17608024-0	2007	UGT1AI*6 and UGT1A1*27 for individualized irinotecan chemotherapy.	Irinotecan	42-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
17608024-1	2007	Genetic polymorphisms of uridine 5"-diphospho-glucuronosyl-transferase (UGT)1A1, a crucial drug-metabolizing enzyme of the anticancer drug irinotecan, are essential determinants of individual variation in susceptibility to irinotecan-related toxicity.	Irinotecan	139-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-79
17608024-1	2007	Genetic polymorphisms of uridine 5"-diphospho-glucuronosyl-transferase (UGT)1A1, a crucial drug-metabolizing enzyme of the anticancer drug irinotecan, are essential determinants of individual variation in susceptibility to irinotecan-related toxicity.	Irinotecan	223-233	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-79
17608024-4	2007	Therefore, it is reasonable to assume that the presence of UGT1A1*6 or UGTIA1*27 would also increase the risk of irinotecan toxicity.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
17146732-12	2007	A DLT of grade 3 abdominal pain was seen at dose 600 mg BID of LY293111 with irinotecan 250 mg/m(2).	Irinotecan	77-87	BH3 interacting domain death agonist	Homo sapiens	56-59
17725105-2	2007	We evaluated cytotoxic effects of a sequentially administered a combination of 5-FU with CPT-11 in human p53 mutant colon cancer.	Irinotecan	89-95	tumor protein p53	Homo sapiens	105-108
17575116-7	2007	Four minimally toxic compounds--BIM IV, BIM V, arcyriaflavin A, and K252c-reduced the relative resistance of ABCG2-transfected cells to SN-38 in cytotoxicity assays.	Irinotecan	136-141	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	109-114
17534441-7	2007	In vivo, 4-IBP increased the antitumor effects of temozolomide and irinotecan in immunodeficient mice that were orthotopically grafted with invasive cancer cells.	Irinotecan	67-77	translocator protein	Mus musculus	11-14
17510416-0	2007	Copper-transporting P-type ATPase, ATP7A, confers multidrug resistance and its expression is related to resistance to SN-38 in clinical colon cancer.	Irinotecan	118-123	ATPase copper transporting alpha	Homo sapiens	35-40
17510416-5	2007	ATP7A expression also enhanced the efflux rates of doxorubicin and SN-38 from cells and increased the uptake of SN-38 in membrane vesicles.	Irinotecan	67-72	ATPase copper transporting alpha	Homo sapiens	0-5
17510416-5	2007	ATP7A expression also enhanced the efflux rates of doxorubicin and SN-38 from cells and increased the uptake of SN-38 in membrane vesicles.	Irinotecan	112-117	ATPase copper transporting alpha	Homo sapiens	0-5
17510416-8	2007	Using the histoculture drug response assay that is useful for the prediction of drug sensitivity of clinical cancers, ATP7A-expressing colon cancer cells were significantly more resistant to SN-38 than ATP7A-negative cells.	Irinotecan	191-196	ATPase copper transporting alpha	Homo sapiens	118-123
17513603-9	2007	Furthermore, c-FLIP gene silencing sensitized MDA435 cells to other chemotherapies, including etoposide, mitoxantrone, and SN-38.	Irinotecan	123-128	CASP8 and FADD like apoptosis regulator	Homo sapiens	13-19
17529881-4	2007	SN-38 is further metabolized to SN-38G by various hepatic and extrahepatic UGT1A isozymes, mainly UGT1A1.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	75-80
17529881-4	2007	SN-38 is further metabolized to SN-38G by various hepatic and extrahepatic UGT1A isozymes, mainly UGT1A1.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
17529881-4	2007	SN-38 is further metabolized to SN-38G by various hepatic and extrahepatic UGT1A isozymes, mainly UGT1A1.	Irinotecan	32-37	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	75-80
17529881-4	2007	SN-38 is further metabolized to SN-38G by various hepatic and extrahepatic UGT1A isozymes, mainly UGT1A1.	Irinotecan	32-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	98-104
17529881-5	2007	Impaired glucuronidation activity of the UGT1A1 enzyme has been linked with elevated levels of SN-38, leading to toxicities.	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
17529881-6	2007	UGT1A1*28 involves an extra TA repeat in the UGT1A1 promoter region and is the variant most frequently contributing to interpatient variability in irinotecan pharmacokinetics and toxicities.	Irinotecan	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
17529881-6	2007	UGT1A1*28 involves an extra TA repeat in the UGT1A1 promoter region and is the variant most frequently contributing to interpatient variability in irinotecan pharmacokinetics and toxicities.	Irinotecan	147-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
17529881-8	2007	Recently, UGT1A1*6 seems to contribute to the risk of toxicity of irinotecan in Asian patients.	Irinotecan	66-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
17409690-8	2007	hCE2 preferentially hydrolyzes substrates with a small acyl moiety such as CPT-11, due to conformational steric hindrance in its active site.	Irinotecan	75-81	carboxylesterase 2	Homo sapiens	0-4
17390033-2	2007	Gefitinib and imatinib are tyrosine kinase inhibitors which have clinical activities in several malignancies and they are also potent inhibitors of breast cancer resistance protein (BCRP) transporter, which confers the resistance of topoisomerase I inhibitors including SN-38 and topotecan.	Irinotecan	270-275	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	148-180
17390033-2	2007	Gefitinib and imatinib are tyrosine kinase inhibitors which have clinical activities in several malignancies and they are also potent inhibitors of breast cancer resistance protein (BCRP) transporter, which confers the resistance of topoisomerase I inhibitors including SN-38 and topotecan.	Irinotecan	270-275	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	182-186
17390033-10	2007	BCRP was equally overexpressed in the SBC-3/SN-38 with and without gefitinib or imatinib.	Irinotecan	44-49	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-4
17390033-11	2007	In addition, the BCRP expression on the SBC-3/SN-38 cell membrane with and without gefitinib seemed to be equal.	Irinotecan	46-51	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	17-21
17390039-1	2007	The sensitivity of LN metastases to anticancer drugs such as CPT-11 and platinum agents was investigated by assessing Topo-1 and Bax/ERCC-1 expression in patients who had stage III/Dukes" C colorectal cancer with ONCs.	Irinotecan	61-67	BCL2 associated X, apoptosis regulator	Homo sapiens	129-132
17390039-1	2007	The sensitivity of LN metastases to anticancer drugs such as CPT-11 and platinum agents was investigated by assessing Topo-1 and Bax/ERCC-1 expression in patients who had stage III/Dukes" C colorectal cancer with ONCs.	Irinotecan	61-67	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	133-139
17431115-7	2007	Thus, Apo2L/TRAIL + CPT-11 treatment-induced apoptosis is regulated through an S-phase checkpoint controlled by the Chk2-Cdc25A and Chk1-Cdc25A pathways and inhibition of Cdk2-associated kinase activity.	Irinotecan	20-26	cyclin dependent kinase 2	Homo sapiens	171-175
17431115-8	2007	Low-dose CPT-11 and aphidicolin increased the proportion of S-phase cells and sensitized cells to Apo2L/TRAIL, by inducing phosphatidylserine externalization, caspase activation, and poly(ADP-ribose) polymerase 1 cleavage.	Irinotecan	9-15	TNF superfamily member 10	Homo sapiens	98-103
17431115-8	2007	Low-dose CPT-11 and aphidicolin increased the proportion of S-phase cells and sensitized cells to Apo2L/TRAIL, by inducing phosphatidylserine externalization, caspase activation, and poly(ADP-ribose) polymerase 1 cleavage.	Irinotecan	9-15	TNF superfamily member 10	Homo sapiens	104-109
17431115-8	2007	Low-dose CPT-11 and aphidicolin increased the proportion of S-phase cells and sensitized cells to Apo2L/TRAIL, by inducing phosphatidylserine externalization, caspase activation, and poly(ADP-ribose) polymerase 1 cleavage.	Irinotecan	9-15	poly(ADP-ribose) polymerase 1	Homo sapiens	183-212
17391070-0	2007	Circulating VEGF reduction, response and outcome in advanced colorectal cancer patients treated with cetuximab plus irinotecan.	Irinotecan	116-126	vascular endothelial growth factor A	Homo sapiens	12-16
17391070-1	2007	OBJECTIVE: We designed this trial to investigate if modifications in levels of circulating vascular endothelial growth factor (VEGF) may be related to clinical response and outcome in advanced colorectal cancer patients during treatment with a weekly combination of cetuximab plus irinotecan.	Irinotecan	281-291	vascular endothelial growth factor A	Homo sapiens	91-125
17391070-1	2007	OBJECTIVE: We designed this trial to investigate if modifications in levels of circulating vascular endothelial growth factor (VEGF) may be related to clinical response and outcome in advanced colorectal cancer patients during treatment with a weekly combination of cetuximab plus irinotecan.	Irinotecan	281-291	vascular endothelial growth factor A	Homo sapiens	127-131
17391070-9	2007	CONCLUSION: These data represent the first evidence that suggests a role of VEGF reduction in the prediction of efficacy of treatment with cetuximab plus weekly irinotecan in heavily pretreated advanced colorectal cancer patients.	Irinotecan	161-171	vascular endothelial growth factor A	Homo sapiens	76-80
17395183-0	2007	Heat shock protein 27 is associated with irinotecan resistance in human colorectal cancer cells.	Irinotecan	41-51	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	0-18
17395183-2	2007	In the present study, we investigated the influence of Hsp expression on the irinotecan resistance of human colorectal cancer cells.	Irinotecan	77-87	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	55-58
17395183-3	2007	Among eight Hsp genes tested in this study, we confirmed that the expression of Hsp27 correlated with irinotecan resistance in colorectal cancer cells.	Irinotecan	102-112	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	12-15
17395183-3	2007	Among eight Hsp genes tested in this study, we confirmed that the expression of Hsp27 correlated with irinotecan resistance in colorectal cancer cells.	Irinotecan	102-112	heat shock protein family B (small) member 1	Homo sapiens	80-85
17395183-4	2007	Specific inhibition of Hsp27 expression using an antisense oliogodeoxynucleotide increased the irinotecan sensitivity.	Irinotecan	95-105	heat shock protein family B (small) member 1	Homo sapiens	23-28
17395183-5	2007	On the contrary, an overexpression of Hsp27 decreased the irinotecan sensitivity in colorectal cancer cells.	Irinotecan	58-68	heat shock protein family B (small) member 1	Homo sapiens	38-43
17395183-7	2007	The expression level of Hsp27 determined by immunohistochemical analysis correlated with the clinical response to irinotecan in colorectal cancer patients.	Irinotecan	114-124	heat shock protein family B (small) member 1	Homo sapiens	24-29
17395183-8	2007	Hsp27 expression levels of irinotecan-non-responder (mean staining score, 6.28; proportion of high staining score, 64.2%) were significantly higher compared to those of irinotecan-responder (mean staining score, 3.16; proportion of high staining score, 33.3%) (P for t-test=0.045).	Irinotecan	27-37	heat shock protein family B (small) member 1	Homo sapiens	0-5
17395183-8	2007	Hsp27 expression levels of irinotecan-non-responder (mean staining score, 6.28; proportion of high staining score, 64.2%) were significantly higher compared to those of irinotecan-responder (mean staining score, 3.16; proportion of high staining score, 33.3%) (P for t-test=0.045).	Irinotecan	169-179	heat shock protein family B (small) member 1	Homo sapiens	0-5
17395183-9	2007	These findings suggest that Hsp27 is involved in the irinotecan resistance of colorectal cancer cells possibly by reducing caspase-3 activity.	Irinotecan	53-63	heat shock protein family B (small) member 1	Homo sapiens	28-33
17395183-9	2007	These findings suggest that Hsp27 is involved in the irinotecan resistance of colorectal cancer cells possibly by reducing caspase-3 activity.	Irinotecan	53-63	caspase 3	Homo sapiens	123-132
17431115-2	2007	Previously, we reported that the cytotoxic effect of a zinc-bound form of Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL), which is currently evaluated in clinical trials, in combination with low-dose CPT-11, induces apoptosis of C4-2 human prostate cancer cells and tissues.	Irinotecan	235-241	TNF receptor superfamily member 10a	Homo sapiens	74-78
17431115-2	2007	Previously, we reported that the cytotoxic effect of a zinc-bound form of Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL), which is currently evaluated in clinical trials, in combination with low-dose CPT-11, induces apoptosis of C4-2 human prostate cancer cells and tissues.	Irinotecan	235-241	TNF superfamily member 10	Homo sapiens	143-148
17431115-2	2007	Previously, we reported that the cytotoxic effect of a zinc-bound form of Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL), which is currently evaluated in clinical trials, in combination with low-dose CPT-11, induces apoptosis of C4-2 human prostate cancer cells and tissues.	Irinotecan	235-241	TNF superfamily member 10	Homo sapiens	149-154
17431115-7	2007	Thus, Apo2L/TRAIL + CPT-11 treatment-induced apoptosis is regulated through an S-phase checkpoint controlled by the Chk2-Cdc25A and Chk1-Cdc25A pathways and inhibition of Cdk2-associated kinase activity.	Irinotecan	20-26	TNF superfamily member 10	Homo sapiens	6-11
17431115-7	2007	Thus, Apo2L/TRAIL + CPT-11 treatment-induced apoptosis is regulated through an S-phase checkpoint controlled by the Chk2-Cdc25A and Chk1-Cdc25A pathways and inhibition of Cdk2-associated kinase activity.	Irinotecan	20-26	TNF superfamily member 10	Homo sapiens	12-17
17431115-7	2007	Thus, Apo2L/TRAIL + CPT-11 treatment-induced apoptosis is regulated through an S-phase checkpoint controlled by the Chk2-Cdc25A and Chk1-Cdc25A pathways and inhibition of Cdk2-associated kinase activity.	Irinotecan	20-26	checkpoint kinase 2	Homo sapiens	116-120
17431115-7	2007	Thus, Apo2L/TRAIL + CPT-11 treatment-induced apoptosis is regulated through an S-phase checkpoint controlled by the Chk2-Cdc25A and Chk1-Cdc25A pathways and inhibition of Cdk2-associated kinase activity.	Irinotecan	20-26	cell division cycle 25A	Homo sapiens	121-127
17431115-7	2007	Thus, Apo2L/TRAIL + CPT-11 treatment-induced apoptosis is regulated through an S-phase checkpoint controlled by the Chk2-Cdc25A and Chk1-Cdc25A pathways and inhibition of Cdk2-associated kinase activity.	Irinotecan	20-26	checkpoint kinase 1	Homo sapiens	132-136
17431115-7	2007	Thus, Apo2L/TRAIL + CPT-11 treatment-induced apoptosis is regulated through an S-phase checkpoint controlled by the Chk2-Cdc25A and Chk1-Cdc25A pathways and inhibition of Cdk2-associated kinase activity.	Irinotecan	20-26	cell division cycle 25A	Homo sapiens	137-143
17410034-3	2007	Genetic polymorphisms in the UGT1A1 gene have been identified as one of the causes of the increased diarrhea seen in white patients treated with irinotecan when compared with Japanese patients.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
17531109-0	2007	Reversible grade 4 hyperbilirubinemia in a patient with UGT1A1 7/7 genotype treated with irinotecan and cetuximab.	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
17531109-5	2007	This case outlines the possibility of severe hepatic toxicity with moderate doses of irinotecan in patients with a UGT1A1 7/7 genotype.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-121
17471158-6	2007	The anticancer agent irinotecan is metabolized to the active SN-38, which is further glucuronidated and detoxified by UGT 1A1.	Irinotecan	21-31	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-125
17471158-6	2007	The anticancer agent irinotecan is metabolized to the active SN-38, which is further glucuronidated and detoxified by UGT 1A1.	Irinotecan	61-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-125
17159606-0	2007	Role of p53 in irinotecan-induced intestinal cell death and mucosal damage.	Irinotecan	15-25	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	8-11
17159606-3	2007	The aim of this study was to investigate the role of the p53 protein in the onset of intestinal damage following irinotecan treatment in two different settings.	Irinotecan	113-123	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	57-60
17159606-10	2007	Irinotecan may act through upregulation of proapoptotic proteins Bax and Bak to induce cell death.	Irinotecan	0-10	BCL2 associated X, apoptosis regulator	Rattus norvegicus	65-68
16799812-12	2007	RT-PCR was used to confirm effects of irinotecan on caspase-1 expression in jejunal tissue and was significantly increased 6 h after treatment with irinotecan.	Irinotecan	38-48	caspase 1	Rattus norvegicus	52-61
16799812-12	2007	RT-PCR was used to confirm effects of irinotecan on caspase-1 expression in jejunal tissue and was significantly increased 6 h after treatment with irinotecan.	Irinotecan	148-158	caspase 1	Rattus norvegicus	52-61
17465213-0	2007	CPT-11 (SN-38) chemotherapy may be selectively applicable to biliary tract cancer with low hMLH1 expression.	Irinotecan	0-6	mutL homolog 1	Homo sapiens	91-96
17465213-0	2007	CPT-11 (SN-38) chemotherapy may be selectively applicable to biliary tract cancer with low hMLH1 expression.	Irinotecan	8-13	mutL homolog 1	Homo sapiens	91-96
17465213-8	2007	The hMLH1 expression was correlated with the IC50 for SN-38, although the relationship was not statistically significant (R = 0.717, p = 0.0715).	Irinotecan	54-59	mutL homolog 1	Homo sapiens	4-9
17465213-11	2007	The cell growth of the hMLH1 dsRNA transfected group was decreased by approximately 50% by SN-38 exposure.	Irinotecan	91-96	mutL homolog 1	Homo sapiens	23-28
17465213-14	2007	In conclusion, a low expression of hMLH1 in biliary tract cancer may aid in predicting its responsiveness to CPT-11 (SN38).	Irinotecan	109-115	mutL homolog 1	Homo sapiens	35-40
17323127-5	2007	ABCG2 is the most recently described of the three major multidrug-resistance pumps, and its substrates include mitoxantrone, topotecan, irinotecan, flavopiridol, and methotrexate.	Irinotecan	136-146	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
17367069-8	2007	In the animal model, irinotecan treatment led to a statistically significant decrease in tumor growth that was accompanied by a decrease in Bcl-2 and survivin levels and an increase in apoptotic cell death.	Irinotecan	21-31	BCL2 apoptosis regulator	Homo sapiens	140-145
17273745-1	2007	The aim of this study was to investigate the influence of combining thymidylate synthase (TS), X-ray cross complementing factor 1 (XRCC1) and uridine diphosphate glucoronosyltransferase (UGT1A1 *28) polymorphism genotypes in response rate and time to progression (TTP) in metastatic colorectal cancer patients treated with 5-fluorouracil (5-FU) plus irinotecan or oxaliplatin (OXA).	Irinotecan	350-360	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	187-193
17159606-10	2007	Irinotecan may act through upregulation of proapoptotic proteins Bax and Bak to induce cell death.	Irinotecan	0-10	BCL2-antagonist/killer 1	Rattus norvegicus	73-76
17255282-6	2007	CHIR-124 interacts synergistically with topoisomerase poisons (e.g., camptothecin or SN-38) in causing growth inhibition in several p53-mutant solid tumor cell lines as determined by isobologram or response surface analysis.	Irinotecan	85-90	tumor protein p53	Homo sapiens	132-135
17965001-4	2007	The clinical application currently the most successful is the association of the anti-EGFR monoclonal antibody cetuximab with irinotecan in metastatic colorectal cancer.	Irinotecan	126-136	epidermal growth factor receptor	Homo sapiens	86-90
17713603-0	2007	Evaluation of HI-6 oxime: potential use in protection of human acetylcholinesterase inhibited by antineoplastic drug irinotecan and its cyto/genotoxicity in vitro.	Irinotecan	117-127	acetylcholinesterase (Cartwright blood group)	Homo sapiens	63-83
17713603-4	2007	Since their adverse effects are not well elucidated, in this study the efficiency of HI-6 oxime in protection and/or reactivation of human erythrocyte AChE inhibited by the antineoplastic drug irinotecan as well as its cyto/genotoxicity in vitro were investigated.	Irinotecan	193-203	acetylcholinesterase (Cartwright blood group)	Homo sapiens	151-155
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.	Irinotecan	257-267	thiopurine S-methyltransferase	Homo sapiens	29-59
17185998-0	2007	Irinotecan-induced diarrhea: functional significance of the polymorphic ABCC2 transporter protein.	Irinotecan	0-10	ATP binding cassette subfamily C member 2	Homo sapiens	72-77
17185998-2	2007	Life-threatening diarrhea is observed in up to 25% of patients receiving irinotecan and has been related with irinotecan pharmacokinetics and UGT1A1 genotype status.	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
17185998-3	2007	Here, we explore the association of ABCC2 (MRP2) polymorphisms and haplotypes with irinotecan disposition and diarrhea.	Irinotecan	83-93	ATP binding cassette subfamily C member 2	Homo sapiens	36-41
17185998-6	2007	The haplotype ABCC2*2 was associated with lower irinotecan clearance (28.3 versus 31.6 l/h; P=0.020).	Irinotecan	48-58	ATP binding cassette subfamily C member 2	Homo sapiens	14-19
17185998-9	2007	This study suggests that the presence of the ABCC2*2 haplotype is associated with less irinotecan-related diarrhea, maybe as a consequence of reduced hepatobiliary secretion of irinotecan.	Irinotecan	87-97	ATP binding cassette subfamily C member 2	Homo sapiens	45-50
17185998-9	2007	This study suggests that the presence of the ABCC2*2 haplotype is associated with less irinotecan-related diarrhea, maybe as a consequence of reduced hepatobiliary secretion of irinotecan.	Irinotecan	177-187	ATP binding cassette subfamily C member 2	Homo sapiens	45-50
17185998-10	2007	As the association was seen in patients not genetically predisposed at risk for diarrhea due to UGT1A1*28, confirmatory studies of the relationships of ABCC2 genotypes and irinotecan disposition and toxicity are warranted.	Irinotecan	172-182	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
17185998-10	2007	As the association was seen in patients not genetically predisposed at risk for diarrhea due to UGT1A1*28, confirmatory studies of the relationships of ABCC2 genotypes and irinotecan disposition and toxicity are warranted.	Irinotecan	172-182	ATP binding cassette subfamily C member 2	Homo sapiens	152-157
17520583-3	2007	Cetuximab, a chimeric mouse-human monoclonal antibody targeting the extracellular domain of the epidermal growth factor receptor (EGFR), has shown low but detectable activity when employed in pretreated patients either as a single agent or in combination with irinotecan.	Irinotecan	260-270	epidermal growth factor receptor	Homo sapiens	96-128
19356014-0	2007	ABCB1, SLCO1B1 and UGT1A1 gene polymorphisms are associated with toxicity in metastatic colorectal cancer patients treated with first-line irinotecan.	Irinotecan	139-149	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
19356014-0	2007	ABCB1, SLCO1B1 and UGT1A1 gene polymorphisms are associated with toxicity in metastatic colorectal cancer patients treated with first-line irinotecan.	Irinotecan	139-149	solute carrier organic anion transporter family member 1B1	Homo sapiens	7-14
19356014-0	2007	ABCB1, SLCO1B1 and UGT1A1 gene polymorphisms are associated with toxicity in metastatic colorectal cancer patients treated with first-line irinotecan.	Irinotecan	139-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
28207116-3	2007	Cetuximab, a chimeric mouse-human monoclonal antibody targeting the extracellular domain of the epidermal growth factor receptor (EGFR), has shown low but detectable activity when employed in pretreated patients either as a single agent or in combination with irinotecan.	Irinotecan	260-270	epidermal growth factor receptor	Homo sapiens	96-128
28207116-3	2007	Cetuximab, a chimeric mouse-human monoclonal antibody targeting the extracellular domain of the epidermal growth factor receptor (EGFR), has shown low but detectable activity when employed in pretreated patients either as a single agent or in combination with irinotecan.	Irinotecan	260-270	epidermal growth factor receptor	Homo sapiens	130-134
28207116-4	2007	Cetuximab in combination with irinotecan has been registered in the USA and Europe for the treatment of patients with metastatic colorectal cancer expressing the EGFR after failure of prior irinotecan-based cytotoxic therapy.	Irinotecan	30-40	epidermal growth factor receptor	Homo sapiens	162-166
28207119-3	2007	The chimeric anti- EGFR monoclonal antibody cetuximab has been approved for EGFR-expressing colorectal tumors in patients who progress after irinotecan-based chemotherapy in combination with irinotecan and in squamous cell head and neck carcinomas for patients with locally advanced disease in combination with radiation therapy or after failure of platinum-based chemotherapy in recurrent or metastatic disease (FDA).	Irinotecan	141-151	epidermal growth factor receptor	Homo sapiens	19-23
17520583-3	2007	Cetuximab, a chimeric mouse-human monoclonal antibody targeting the extracellular domain of the epidermal growth factor receptor (EGFR), has shown low but detectable activity when employed in pretreated patients either as a single agent or in combination with irinotecan.	Irinotecan	260-270	epidermal growth factor receptor	Homo sapiens	130-134
17520583-4	2007	Cetuximab in combination with irinotecan has been registered in the USA and Europe for the treatment of patients with metastatic colorectal cancer expressing the EGFR after failure of prior irinotecan-based cytotoxic therapy.	Irinotecan	30-40	epidermal growth factor receptor	Homo sapiens	162-166
17520586-3	2007	The chimeric anti- EGFR monoclonal antibody cetuximab has been approved for EGFR-expressing colorectal tumors in patients who progress after irinotecan-based chemotherapy in combination with irinotecan and in squamous cell head and neck carcinomas for patients with locally advanced disease in combination with radiation therapy or after failure of platinum-based chemotherapy in recurrent or metastatic disease (FDA).	Irinotecan	141-151	epidermal growth factor receptor	Homo sapiens	19-23
17913044-3	2007	In vivo delivery of irinotecan and floxuridine coencapsulated inside liposomes at the synergistic 1:1 molar ratio (referred to as CPX-1) lead to greatly enhanced efficacy compared to the two drugs administered as a saline-based cocktail in a number of human xenograft and murine tumor models.	Irinotecan	20-30	complexin 1	Homo sapiens	130-135
17192505-3	2007	This analysis extended the work of a previous study that examined the effect of UGT1A1 genotypes on the incidence of severe neutropenia in 86 advanced cancer patients following irinotecan treatment.	Irinotecan	177-187	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
17192505-7	2007	Based on these findings and other reports, the irinotecan label was modified to indicate the role of UGT1A1*28 polymorphism in the metabolism of irinotecan and the associated increased risk of severe neutropenia.	Irinotecan	47-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
17192505-7	2007	Based on these findings and other reports, the irinotecan label was modified to indicate the role of UGT1A1*28 polymorphism in the metabolism of irinotecan and the associated increased risk of severe neutropenia.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
17192505-8	2007	The label modifications also included recommendations for lower starting doses of irinotecan in patients homozygous for the UGT1A1*28 (7/7) polymorphism.	Irinotecan	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	124-130
17552365-1	2007	We retrospectively analyzed the outcome of high-risk patients with non-small cell lung cancer (NSCLC) treated with nedaplatin (NP) and irinotecan (CPT) combination chemotherapy.	Irinotecan	135-145	choline phosphotransferase 1	Homo sapiens	147-150
17913044-6	2007	Synergistic antitumor activity observed for CPX-1 was associated with maintenance of the 1:1 irinotecan:floxuridine molar ratio in plasma and tumor tissue over 16-24 h. In contrast, injection of the drugs combined in saline resulted in irinotecan:floxuridine ratios that changed 10-fold within 1 h in plasma and sevenfold within 4 h in tumor tissue.	Irinotecan	93-103	complexin 1	Homo sapiens	44-49
17264798-1	2007	BACKGROUND: The conversion of CPT-11 to its active form, SN-38, by carboxylesterases (CESs) is a critical event in CPT-11-induced cytotoxicity.	Irinotecan	30-36	carboxylesterase 1	Homo sapiens	67-84
17264798-2	2007	Among the CESs, CES1 and CES2 probably play a major role in the metabolism, but the functional significance and molecular basis of CES1 on CPT-11 response remain unclear.	Irinotecan	139-145	carboxylesterase 1	Homo sapiens	131-135
17264798-1	2007	BACKGROUND: The conversion of CPT-11 to its active form, SN-38, by carboxylesterases (CESs) is a critical event in CPT-11-induced cytotoxicity.	Irinotecan	57-62	carboxylesterase 1	Homo sapiens	67-84
17264798-1	2007	BACKGROUND: The conversion of CPT-11 to its active form, SN-38, by carboxylesterases (CESs) is a critical event in CPT-11-induced cytotoxicity.	Irinotecan	115-121	carboxylesterase 1	Homo sapiens	67-84
17264798-3	2007	METHODS AND RESULTS: We investigated CES1A1 (AB119997) and CES1A2 (AB187225), whose coding sequences were recently registered in GenBank, for CPT-11-induced cytotoxicity, anticipating novel biomarkers of CPT-11 response.	Irinotecan	142-148	carboxylesterase 1 pseudogene 1	Homo sapiens	59-65
17090741-5	2006	The labeling of irinotecan was recently changed and now includes a warning of greater neutropenia risk in patients with reduced activity in the drug-metabolizing enzyme uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	169-216
17106441-1	2006	This is the first phase II study of S-1 monotherapy for patients with metastatic colorectal cancer after failure of both irinotecan- and oxaliplatin-containing regimens.	Irinotecan	121-131	proteasome 26S subunit, non-ATPase 1	Homo sapiens	36-39
17089053-2	2006	Our aim was to evaluate the effects of combination therapy with irinotecan hydrochloride and cisplatin (CPT-P), comparing to regimen with paclitaxel and platinum (TP).	Irinotecan	64-88	ceramide-1-phosphate transfer protein	Homo sapiens	104-109
17207039-2	2007	After receiving cisplatin/irinotecan, serum progastrin-releasing peptide (ProGRP) levels decreased to within the reference values and the lesions were markedly reduced in size.	Irinotecan	26-36	gastrin releasing peptide	Homo sapiens	44-72
17207039-2	2007	After receiving cisplatin/irinotecan, serum progastrin-releasing peptide (ProGRP) levels decreased to within the reference values and the lesions were markedly reduced in size.	Irinotecan	26-36	gastrin releasing peptide	Homo sapiens	74-80
17183650-5	2006	To test this hypothesis, we injected HB1.F3.C1 cells transduced to express an enzyme that efficiently activates the anti-cancer prodrug CPT-11 intravenously into mice bearing disseminated neuroblastoma tumors.	Irinotecan	136-142	paternally expressed 10	Mus musculus	37-40
17183650-8	2006	Mice treated with the combination of HB1.F3.C1 cells expressing the CPT-11-activating enzyme and this prodrug produced tumor-free survival of 100% of the mice for &gt;6 months (P&lt;0.001 compared to control groups).	Irinotecan	68-74	paternally expressed 10	Mus musculus	37-40
17148668-8	2006	Imatinib alone or in combination with irinotecan inhibited phosphorylation of PDGF-Rbeta of tumor-associated stromal cells and pericytes.	Irinotecan	38-48	platelet derived growth factor receptor beta	Homo sapiens	78-88
17184208-1	2006	Depending upon the UDP glucuronosyltransferase 1A1 (UGT1A1) genotype, patients are more or less susceptible to the risk of severe toxicity of irinotecan.	Irinotecan	142-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-50
17184208-1	2006	Depending upon the UDP glucuronosyltransferase 1A1 (UGT1A1) genotype, patients are more or less susceptible to the risk of severe toxicity of irinotecan.	Irinotecan	142-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
17184208-2	2006	As the US FDA-approved label of irinotecan (CPT-11, Camptosar) has been recently revised to include UGT1A1 genotype among potential risk factors for toxicity, it is expected that UGT1A1 genotyping will be increasingly used in patients undergoing irinotecan treatment.	Irinotecan	32-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	179-185
17090741-5	2006	The labeling of irinotecan was recently changed and now includes a warning of greater neutropenia risk in patients with reduced activity in the drug-metabolizing enzyme uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	218-224
16894565-8	2006	High intratumoral mRNA levels of EGFR, ERCC1 and GSPT-P1 were each significantly associated with response to CPT-11 based chemotherapy.	Irinotecan	109-115	epidermal growth factor receptor	Homo sapiens	33-37
16894565-8	2006	High intratumoral mRNA levels of EGFR, ERCC1 and GSPT-P1 were each significantly associated with response to CPT-11 based chemotherapy.	Irinotecan	109-115	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	39-44
17090741-7	2006	Numerous studies have demonstrated the effects of genetic factors, especially UGT1A1*28, that contribute to interpatient variability in irinotecan pharmacokinetics and toxicity.	Irinotecan	136-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
16894565-12	2006	This small retrospective study suggests that gene expression levels of EGFR, ERCC1 and GST-P1 may be useful in predicting the clinical outcome of patients with metastatic CRC treated with first-line CPT-11 based chemotherapy.	Irinotecan	199-205	epidermal growth factor receptor	Homo sapiens	71-75
17090741-8	2006	Irinotecan"s new labeling recommends that clinicians consider reducing the dosage of irinotecan in patients homozygous for UGT1A1*28.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
16894565-12	2006	This small retrospective study suggests that gene expression levels of EGFR, ERCC1 and GST-P1 may be useful in predicting the clinical outcome of patients with metastatic CRC treated with first-line CPT-11 based chemotherapy.	Irinotecan	199-205	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	77-82
16894565-12	2006	This small retrospective study suggests that gene expression levels of EGFR, ERCC1 and GST-P1 may be useful in predicting the clinical outcome of patients with metastatic CRC treated with first-line CPT-11 based chemotherapy.	Irinotecan	199-205	glutathione S-transferase pi 1	Homo sapiens	87-93
17090741-8	2006	Irinotecan"s new labeling recommends that clinicians consider reducing the dosage of irinotecan in patients homozygous for UGT1A1*28.	Irinotecan	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
17090741-9	2006	CONCLUSION: At least part of the interpatient variability of irinotecan toxicity can be explained by the UGT1A1*28 polymorphism.	Irinotecan	61-71	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
17090741-10	2006	Patients who are homozygous for the UGT1A1*28 allele have an increased risk of developing severe neutropenia when receiving irinotecan, especially the 300-350- mg/m2 regimen.	Irinotecan	124-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	36-42
17185519-4	2006	The irinotecan/UGT1A1 issue and the development of molecular diagnostic testing are now to be translated into clinical practice.	Irinotecan	4-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
16965601-4	2006	Pharmacogenetic relationships were explored between the UGT1A1 genotype and the ratio of the area under the plasma concentration-time curve (AUC) of the active metabolite of irinotecan (SN-38) to that of SN-38 glucuronide (SN-38G), used as a surrogate for UGT1A1 activity (AUC(SN-38)/AUC(SN-38G)).	Irinotecan	204-209	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
17185519-1	2006	This article focuses on pharmacogenetic associations between genetic polymorphism of uridine diphosphate glucuronosyltransferase (UGT) 1A1 gene and irinotecan toxicity.	Irinotecan	148-158	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-138
17185519-3	2006	On the basis of these backgrounds, the irinotecan label was updated in 2005 in the United States to provide pharmacogenetic information, and a dose reduction of irinotecan should be considered for patients known to be homozygous for the UGT1A1*28 allele when administered in combination with other agents or a single agent.	Irinotecan	161-171	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	237-243
16965601-4	2006	Pharmacogenetic relationships were explored between the UGT1A1 genotype and the ratio of the area under the plasma concentration-time curve (AUC) of the active metabolite of irinotecan (SN-38) to that of SN-38 glucuronide (SN-38G), used as a surrogate for UGT1A1 activity (AUC(SN-38)/AUC(SN-38G)).	Irinotecan	204-209	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
16965601-4	2006	Pharmacogenetic relationships were explored between the UGT1A1 genotype and the ratio of the area under the plasma concentration-time curve (AUC) of the active metabolite of irinotecan (SN-38) to that of SN-38 glucuronide (SN-38G), used as a surrogate for UGT1A1 activity (AUC(SN-38)/AUC(SN-38G)).	Irinotecan	204-209	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
16965601-10	2006	The two patients simultaneously heterozygous for UGT1A1*28 and UGT1A1*6 and the two patients homozygous for UGT1A1*6 had significantly higher AUC(SN-38)/AUC(SN-38G) ratios than the others (P = 0.0039).	Irinotecan	146-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
16965601-10	2006	The two patients simultaneously heterozygous for UGT1A1*28 and UGT1A1*6 and the two patients homozygous for UGT1A1*6 had significantly higher AUC(SN-38)/AUC(SN-38G) ratios than the others (P = 0.0039).	Irinotecan	146-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
16965601-10	2006	The two patients simultaneously heterozygous for UGT1A1*28 and UGT1A1*6 and the two patients homozygous for UGT1A1*6 had significantly higher AUC(SN-38)/AUC(SN-38G) ratios than the others (P = 0.0039).	Irinotecan	146-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
16965601-10	2006	The two patients simultaneously heterozygous for UGT1A1*28 and UGT1A1*6 and the two patients homozygous for UGT1A1*6 had significantly higher AUC(SN-38)/AUC(SN-38G) ratios than the others (P = 0.0039).	Irinotecan	157-162	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
16965601-11	2006	Concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, altered the disposition of irinotecan remarkably, potentially increasing susceptibility to toxicity.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
16965601-11	2006	Concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, altered the disposition of irinotecan remarkably, potentially increasing susceptibility to toxicity.	Irinotecan	90-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
16965601-13	2006	UGT1A1 polymorphisms in the coding region of the UGT1A1 gene should be genotyped in addition to testing for UGT1A1*28 to more accurately predict irinotecan-related toxicity, at least in Asian patients.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
16965601-13	2006	UGT1A1 polymorphisms in the coding region of the UGT1A1 gene should be genotyped in addition to testing for UGT1A1*28 to more accurately predict irinotecan-related toxicity, at least in Asian patients.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
16965601-13	2006	UGT1A1 polymorphisms in the coding region of the UGT1A1 gene should be genotyped in addition to testing for UGT1A1*28 to more accurately predict irinotecan-related toxicity, at least in Asian patients.	Irinotecan	145-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
16965601-0	2006	Pharmacogenetic impact of polymorphisms in the coding region of the UGT1A1 gene on SN-38 glucuronidation in Japanese patients with cancer.	Irinotecan	83-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	68-74
16965601-1	2006	Pharmacogenetic testing for UDP-glucuronosyltransferase (UGT) 1A1*28, a promoter variant of the UGT1A1 gene, is now carried out clinically to estimate the risk of irinotecan-associated toxicity.	Irinotecan	163-173	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-65
16965601-1	2006	Pharmacogenetic testing for UDP-glucuronosyltransferase (UGT) 1A1*28, a promoter variant of the UGT1A1 gene, is now carried out clinically to estimate the risk of irinotecan-associated toxicity.	Irinotecan	163-173	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
16965601-4	2006	Pharmacogenetic relationships were explored between the UGT1A1 genotype and the ratio of the area under the plasma concentration-time curve (AUC) of the active metabolite of irinotecan (SN-38) to that of SN-38 glucuronide (SN-38G), used as a surrogate for UGT1A1 activity (AUC(SN-38)/AUC(SN-38G)).	Irinotecan	174-184	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
16965601-4	2006	Pharmacogenetic relationships were explored between the UGT1A1 genotype and the ratio of the area under the plasma concentration-time curve (AUC) of the active metabolite of irinotecan (SN-38) to that of SN-38 glucuronide (SN-38G), used as a surrogate for UGT1A1 activity (AUC(SN-38)/AUC(SN-38G)).	Irinotecan	186-191	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
29788595-0	2006	Novel personalized medicine technology: UGT1A1 testing for irinotecan as a case study.	Irinotecan	59-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	Irinotecan	169-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	Irinotecan	169-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	Irinotecan	169-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
17016579-3	2006	We present a colon cancer patient with the UGT1A1 polymorphism (UGT1A1 *28) as a known high risk for irinotecan, who was treated with a combination of doxifluridine and irinotecan for peritoneal dissemination resulting in stable disease for 2 years without adverse reactions, although the patient initially developed severe adverse effects to the combination of the protracted venous infusion of 5-FU and irinotecan.	Irinotecan	169-179	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
29788595-1	2006	Third Wave"s Invader  UDP glucuronosyltransferase 1A1 (UGT1A1) Molecular Assay, a genotyping system to predict adverse drug reactions in patients receiving the chemotherapeutic agent irinotecan (Camptosar , Pzifer, NY, USA) for the treatment of metastatic colorectal cancer (mCRC), was recently approved by the US FDA.	Irinotecan	183-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-53
29788595-1	2006	Third Wave"s Invader  UDP glucuronosyltransferase 1A1 (UGT1A1) Molecular Assay, a genotyping system to predict adverse drug reactions in patients receiving the chemotherapeutic agent irinotecan (Camptosar , Pzifer, NY, USA) for the treatment of metastatic colorectal cancer (mCRC), was recently approved by the US FDA.	Irinotecan	183-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
29788595-1	2006	Third Wave"s Invader  UDP glucuronosyltransferase 1A1 (UGT1A1) Molecular Assay, a genotyping system to predict adverse drug reactions in patients receiving the chemotherapeutic agent irinotecan (Camptosar , Pzifer, NY, USA) for the treatment of metastatic colorectal cancer (mCRC), was recently approved by the US FDA.	Irinotecan	195-204	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	55-61
29788595-3	2006	This descriptive analysis highlight these data and the issues for the translation of this test to practice, including gaps in the evidence base, issues regarding adoption of the test to clinical practice and the potential societal impact of UGT1A1 testing for irinotecan prescribing.	Irinotecan	260-270	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	241-247
16437251-2	2006	We have demonstrated from a rat model that intestinal beta-glucuronidase may play a key role in the development of CPT-11-induced delayed diarrhea by the deconjugation of the luminal SN-38 glucuronide, and the elimination of the intestinal microflora by antibiotics or dosing of TJ-14, a Kampo medicine that contains beta-glucuronidase inhibitor baicalin, exerted a protective effect.	Irinotecan	115-121	glucuronidase, beta	Rattus norvegicus	54-72
17047068-0	2006	Novel SN-38-incorporating polymeric micelles, NK012, eradicate vascular endothelial growth factor-secreting bulky tumors.	Irinotecan	6-11	vascular endothelial growth factor A	Homo sapiens	63-97
17047068-4	2006	The purpose of this study is to investigate the pharmacologic character of NK012 as an anticancer agent, especially in a vascular endothelial growth factor (VEGF)-secreting tumor model.	Irinotecan	75-80	vascular endothelial growth factor A	Homo sapiens	121-155
17047068-4	2006	The purpose of this study is to investigate the pharmacologic character of NK012 as an anticancer agent, especially in a vascular endothelial growth factor (VEGF)-secreting tumor model.	Irinotecan	75-80	vascular endothelial growth factor A	Homo sapiens	157-161
17047068-11	2006	In the drug distribution analysis, an increased accumulation of SN-38 in SBC-3/VEGF tumors was observed as compared with that in SBC-3/Neo tumors.	Irinotecan	64-69	vascular endothelial growth factor A	Homo sapiens	79-83
17047068-12	2006	NK012 markedly enhanced the antitumor activity of SN-38, especially in highly VEGF-secreting tumors, and could be a promising SN-38-based formulation.	Irinotecan	50-55	vascular endothelial growth factor A	Homo sapiens	78-82
16437251-2	2006	We have demonstrated from a rat model that intestinal beta-glucuronidase may play a key role in the development of CPT-11-induced delayed diarrhea by the deconjugation of the luminal SN-38 glucuronide, and the elimination of the intestinal microflora by antibiotics or dosing of TJ-14, a Kampo medicine that contains beta-glucuronidase inhibitor baicalin, exerted a protective effect.	Irinotecan	115-121	glucuronidase, beta	Rattus norvegicus	317-335
16896007-9	2006	Both 99mTc-DIDA/DISIDA and MIBI 1-hour RET correlated with SN-38 area under the curve (AUC; P &lt; .01).	Irinotecan	59-64	ret proto-oncogene	Homo sapiens	39-42
16982469-3	2006	Recent FDA approval of genetic testing for mutations in the UGT1A1 gene that predict adverse reactions to irinotecan is ushering in a new era that will increasingly rely on genotyping to individualize treatment decisions for patients with cancer as well as for patients at high risk who may be candidates for chemoprevention agents.	Irinotecan	106-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
17030643-2	2006	Monoclonal antibodies against the epidermal growth factor receptor (EGFR) are active against EGFR-expressing mCRC that is refractory to irinotecan.	Irinotecan	136-146	epidermal growth factor receptor	Homo sapiens	34-66
17030643-2	2006	Monoclonal antibodies against the epidermal growth factor receptor (EGFR) are active against EGFR-expressing mCRC that is refractory to irinotecan.	Irinotecan	136-146	epidermal growth factor receptor	Homo sapiens	68-72
17015060-0	2006	Effect of S-1 on pharmacokinetics of irinotecan in a patient with colorectal cancer.	Irinotecan	37-47	proteasome 26S subunit, non-ATPase 1	Homo sapiens	10-13
16815871-0	2006	A mechanistic study on reduced toxicity of irinotecan by coadministered thalidomide, a tumor necrosis factor-alpha inhibitor.	Irinotecan	43-53	tumor necrosis factor	Rattus norvegicus	87-114
16815871-14	2006	Thalidomide and PGA also significantly inhibited P-glycoprotein (PgP/MDR1), multidrug resistance-associated protein (MRP1)- and MRP2-mediated CPT-11 and SN-38 transport in MDCKII cells.	Irinotecan	142-148	ATP binding cassette subfamily C member 1	Canis lupus familiaris	76-121
16815871-14	2006	Thalidomide and PGA also significantly inhibited P-glycoprotein (PgP/MDR1), multidrug resistance-associated protein (MRP1)- and MRP2-mediated CPT-11 and SN-38 transport in MDCKII cells.	Irinotecan	142-148	ATP binding cassette subfamily C member 2	Canis lupus familiaris	128-132
16815871-14	2006	Thalidomide and PGA also significantly inhibited P-glycoprotein (PgP/MDR1), multidrug resistance-associated protein (MRP1)- and MRP2-mediated CPT-11 and SN-38 transport in MDCKII cells.	Irinotecan	153-158	ATP binding cassette subfamily C member 1	Canis lupus familiaris	76-121
16815871-14	2006	Thalidomide and PGA also significantly inhibited P-glycoprotein (PgP/MDR1), multidrug resistance-associated protein (MRP1)- and MRP2-mediated CPT-11 and SN-38 transport in MDCKII cells.	Irinotecan	153-158	ATP binding cassette subfamily C member 2	Canis lupus familiaris	128-132
16896007-10	2006	On multiple regression analysis, SN-38 AUC = -215 + 18.68 x bilirubin + 4.27 x MIBI 1-hour RET (P = .009, R2 = 44.2%).	Irinotecan	33-38	ret proto-oncogene	Homo sapiens	91-94
16943524-0	2006	Thymidine phosphorylase expression is associated with response to capecitabine plus irinotecan in patients with metastatic colorectal cancer.	Irinotecan	84-94	thymidine phosphorylase	Homo sapiens	0-23
16404634-1	2006	PURPOSE: Several studies have demonstrated significant interactions between immunosuppressants (e.g., cyclosporin A) and chemotherapeutic drugs that are BCRP substrates (e.g., irinotecan), resulting in increased bioavailability and reduced clearance of these agents.	Irinotecan	176-186	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	153-157
16969123-1	2006	BACKGROUND: Irinotecan is metabolized by various enzymes, including carboxylesterases, cytochrome P450 3A isozymes (CYP3A) and uridine-diphosphate glucuronosyltransferase 1A isoforms (UGT1A).	Irinotecan	12-22	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	184-189
18666754-5	2006	Furthermore, the analysis of the conversion of irinotecan into SN-38 by carboxylesterase, the detoxification of irinotecan and SN-38 by CYP3A4 and UDP-glucuronosyl transferases, and the activity of excretory systems (i.e., cMOAT, P-gp and MRP) seems able to predict the interindividual variability in pharmacokinetics and pharmacodynamics, being possible to predict untolerable toxicities.	Irinotecan	127-132	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	136-142
17086870-3	2006	The purpose of this study was to evaluate the cytotoxic effect of CPT-11 alone and in combination with mitomycin C (MMC) and hyperthermia on three colorectal cancer cell lines: CACO-2, HT-29, and DHD/K12/TRb (PROb).	Irinotecan	66-72	T cell receptor beta locus	Homo sapiens	204-207
16865249-8	2006	Our data suggest that GSTT1-null is associated with a greater probability of developing toxicity to 5-Fu/CPT-11/Lv treatments, indicating a potential application of this genetic analysis in predicting adverse effects of this regimen.	Irinotecan	105-111	glutathione S-transferase theta 1	Homo sapiens	22-27
16951398-12	2006	It is suggested that the UGT1A1*28 genotype status could be used as a screening tool for a priori prevention of irinotecan-induced delayed-type diarrhea.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
16842384-0	2006	The in vitro metabolism of irinotecan (CPT-11) by carboxylesterase and beta-glucuronidase in human colorectal tumours.	Irinotecan	27-37	glucuronidase beta	Homo sapiens	71-89
16545899-4	2006	7-Ethyl-10-hydroxycamptothecin (SN-38) glucuronidation, used as a probe for UGT1A1, showed sigmoidal kinetics with a Hill coefficient (n) of 1.2-1.3 in control and BNF-pretreated HepG2 cells.	Irinotecan	0-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
16545899-4	2006	7-Ethyl-10-hydroxycamptothecin (SN-38) glucuronidation, used as a probe for UGT1A1, showed sigmoidal kinetics with a Hill coefficient (n) of 1.2-1.3 in control and BNF-pretreated HepG2 cells.	Irinotecan	32-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
16906022-1	2006	OBJECTIVE: To investigate the pharmacogenetic effect of SLCO1B1 *1a, *1b, *5 and *15 polymorphisms on irinotecan disposition in Asian cancer patients.	Irinotecan	102-112	solute carrier organic anion transporter family member 1B1	Homo sapiens	56-63
16906022-8	2006	CONCLUSION: These findings suggest that (1) SLCO1B1 haplotypes may have a significant influence on the disposition of irinotecan and its metabolites in Asian cancer patients, and (2) patients with SLCO1B1*15 haplotype may be susceptible to increased sensitivity to irinotecan, which may manifest itself either by increased efficacy or toxicity or both owing to the increased exposure levels to 7-ethyl-10-hydroxycamptothecin.	Irinotecan	118-128	solute carrier organic anion transporter family member 1B1	Homo sapiens	44-51
16906022-8	2006	CONCLUSION: These findings suggest that (1) SLCO1B1 haplotypes may have a significant influence on the disposition of irinotecan and its metabolites in Asian cancer patients, and (2) patients with SLCO1B1*15 haplotype may be susceptible to increased sensitivity to irinotecan, which may manifest itself either by increased efficacy or toxicity or both owing to the increased exposure levels to 7-ethyl-10-hydroxycamptothecin.	Irinotecan	118-128	solute carrier organic anion transporter family member 1B1	Homo sapiens	197-204
16906022-8	2006	CONCLUSION: These findings suggest that (1) SLCO1B1 haplotypes may have a significant influence on the disposition of irinotecan and its metabolites in Asian cancer patients, and (2) patients with SLCO1B1*15 haplotype may be susceptible to increased sensitivity to irinotecan, which may manifest itself either by increased efficacy or toxicity or both owing to the increased exposure levels to 7-ethyl-10-hydroxycamptothecin.	Irinotecan	265-275	solute carrier organic anion transporter family member 1B1	Homo sapiens	44-51
16906022-8	2006	CONCLUSION: These findings suggest that (1) SLCO1B1 haplotypes may have a significant influence on the disposition of irinotecan and its metabolites in Asian cancer patients, and (2) patients with SLCO1B1*15 haplotype may be susceptible to increased sensitivity to irinotecan, which may manifest itself either by increased efficacy or toxicity or both owing to the increased exposure levels to 7-ethyl-10-hydroxycamptothecin.	Irinotecan	265-275	solute carrier organic anion transporter family member 1B1	Homo sapiens	197-204
16906022-8	2006	CONCLUSION: These findings suggest that (1) SLCO1B1 haplotypes may have a significant influence on the disposition of irinotecan and its metabolites in Asian cancer patients, and (2) patients with SLCO1B1*15 haplotype may be susceptible to increased sensitivity to irinotecan, which may manifest itself either by increased efficacy or toxicity or both owing to the increased exposure levels to 7-ethyl-10-hydroxycamptothecin.	Irinotecan	394-424	solute carrier organic anion transporter family member 1B1	Homo sapiens	44-51
16906022-8	2006	CONCLUSION: These findings suggest that (1) SLCO1B1 haplotypes may have a significant influence on the disposition of irinotecan and its metabolites in Asian cancer patients, and (2) patients with SLCO1B1*15 haplotype may be susceptible to increased sensitivity to irinotecan, which may manifest itself either by increased efficacy or toxicity or both owing to the increased exposure levels to 7-ethyl-10-hydroxycamptothecin.	Irinotecan	394-424	solute carrier organic anion transporter family member 1B1	Homo sapiens	197-204
16809434-0	2006	Inhibition of poly(ADP-ribose) polymerase prevents irinotecan-induced intestinal damage and enhances irinotecan/temozolomide efficacy against colon carcinoma.	Irinotecan	51-61	poly(ADP-ribose) polymerase 1	Homo sapiens	14-41
16809434-0	2006	Inhibition of poly(ADP-ribose) polymerase prevents irinotecan-induced intestinal damage and enhances irinotecan/temozolomide efficacy against colon carcinoma.	Irinotecan	101-111	poly(ADP-ribose) polymerase 1	Homo sapiens	14-41
16809434-1	2006	Poly(ADP-ribose) polymerase (PARP) inhibitors enhance the antitumor activity of the topoisomerase I inhibitor irinotecan (CPT-11), which is used to treat advanced colorectal carcinoma.	Irinotecan	110-120	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
16809434-1	2006	Poly(ADP-ribose) polymerase (PARP) inhibitors enhance the antitumor activity of the topoisomerase I inhibitor irinotecan (CPT-11), which is used to treat advanced colorectal carcinoma.	Irinotecan	110-120	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
16809434-1	2006	Poly(ADP-ribose) polymerase (PARP) inhibitors enhance the antitumor activity of the topoisomerase I inhibitor irinotecan (CPT-11), which is used to treat advanced colorectal carcinoma.	Irinotecan	122-128	poly(ADP-ribose) polymerase 1	Homo sapiens	0-27
16809434-1	2006	Poly(ADP-ribose) polymerase (PARP) inhibitors enhance the antitumor activity of the topoisomerase I inhibitor irinotecan (CPT-11), which is used to treat advanced colorectal carcinoma.	Irinotecan	122-128	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
16809434-6	2006	Oral administration of GPI 15427 (40 mg/kg/q2x3 days) prevented intestinal injury and diarrhea induced by CPT-11 (30 mg/kg/day x 3 days) reducing inflammation and PARP-1 overactivation, as evidenced by immunohistochemical staining of intestinal tissue with antipoly(ADP-ribose) antibody (Ab).	Irinotecan	106-112	poly(ADP-ribose) polymerase 1	Homo sapiens	163-169
16781005-3	2006	Therefore, we conducted a prospective feasibility study designed specifically to evaluate the efficacy of carboplatin (day 1) and irinotecan (days 1, 8, 15) with granulocyte colony-stimulating factor (G-CSF) support in elderly SCLC patients.	Irinotecan	130-140	colony stimulating factor 3	Homo sapiens	162-199
16781005-3	2006	Therefore, we conducted a prospective feasibility study designed specifically to evaluate the efficacy of carboplatin (day 1) and irinotecan (days 1, 8, 15) with granulocyte colony-stimulating factor (G-CSF) support in elderly SCLC patients.	Irinotecan	130-140	colony stimulating factor 3	Homo sapiens	201-206
16928820-5	2006	Nontoxic concentration of curcumin I, II, and III sensitized the ABCG2-expressing cells to mitoxantrone, topotecan, SN-38, and doxorubicin.	Irinotecan	116-121	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	65-70
16857004-7	2006	After four courses of irinotecan, metastatic lesions were remarkably reduced in size, and the serum level of AFP decreased from 0.7 million to 927 ng/mL.	Irinotecan	22-32	alpha fetoprotein	Homo sapiens	109-112
16842384-0	2006	The in vitro metabolism of irinotecan (CPT-11) by carboxylesterase and beta-glucuronidase in human colorectal tumours.	Irinotecan	39-45	glucuronidase beta	Homo sapiens	71-89
16842384-4	2006	The aim of this study was to determine, the reactivation of SN-38 from SN-38 glucuronide by beta-glucuronidase may represent a significant pathway of SN-38 formation.	Irinotecan	60-65	glucuronidase beta	Homo sapiens	92-110
16842384-4	2006	The aim of this study was to determine, the reactivation of SN-38 from SN-38 glucuronide by beta-glucuronidase may represent a significant pathway of SN-38 formation.	Irinotecan	71-76	glucuronidase beta	Homo sapiens	92-110
16842384-6	2006	RESULTS: The rate of conversion of irinotecan (9.6 microm) was lower in tumour tissue than matched normal colon mucosa samples (0.30+/-0.14 pmol min-1 mg-1 protein and 0.77+/-0.59 pmol min-1 mg-1 protein, respectively; P&lt;0.005).	Irinotecan	35-45	CD59 molecule (CD59 blood group)	Homo sapiens	145-155
16842384-6	2006	RESULTS: The rate of conversion of irinotecan (9.6 microm) was lower in tumour tissue than matched normal colon mucosa samples (0.30+/-0.14 pmol min-1 mg-1 protein and 0.77+/-0.59 pmol min-1 mg-1 protein, respectively; P&lt;0.005).	Irinotecan	35-45	CD59 molecule (CD59 blood group)	Homo sapiens	185-195
16842384-9	2006	At equal concentrations of irinotecan and SN-38 glucuronide, the rate of beta-glucuronidase-mediated SN-38 production was higher than that formed from irinotecan in both tumour and normal tissue (P&lt;0.05).	Irinotecan	27-37	glucuronidase beta	Homo sapiens	73-91
16842384-9	2006	At equal concentrations of irinotecan and SN-38 glucuronide, the rate of beta-glucuronidase-mediated SN-38 production was higher than that formed from irinotecan in both tumour and normal tissue (P&lt;0.05).	Irinotecan	42-47	glucuronidase beta	Homo sapiens	73-91
16842384-9	2006	At equal concentrations of irinotecan and SN-38 glucuronide, the rate of beta-glucuronidase-mediated SN-38 production was higher than that formed from irinotecan in both tumour and normal tissue (P&lt;0.05).	Irinotecan	101-106	glucuronidase beta	Homo sapiens	73-91
16842384-11	2006	CONCLUSIONS: Tumour beta-glucuronidase may play a significant role in the exposure of tumours to SN-38 in vivo.	Irinotecan	97-102	glucuronidase beta	Homo sapiens	20-38
16595709-0	2006	The novel UGT1A9 intronic I399 polymorphism appears as a predictor of 7-ethyl-10-hydroxycamptothecin glucuronidation levels in the liver.	Irinotecan	70-100	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	10-16
16824027-0	2006	Screening for adverse reactions to irinotecan treatment using the Invader UGT1A1 Molecular Assay.	Irinotecan	35-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
16824027-1	2006	Accumulating evidence provides support for the idea that determination of UGT1A1 polymorphisms before irinotecan (CPT-11) treatment is clinically useful and important for predicting and avoiding related toxicities.	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
16824027-1	2006	Accumulating evidence provides support for the idea that determination of UGT1A1 polymorphisms before irinotecan (CPT-11) treatment is clinically useful and important for predicting and avoiding related toxicities.	Irinotecan	114-120	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
16824027-3	2006	A dose reduction of irinotecan should be considered for patients known to be homozygous for the UGT1A1*28 allele when administered in combination with other agents or as a single agent.	Irinotecan	20-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
16824027-6	2006	This newly developed method for detecting UGT1A1 polymorphisms is feasible and has the potential to be widely used for rapid and accurate screening before irinotecan treatment.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
16595709-4	2006	Of all the variants, the UGT1A9 I399C&gt;T was associated with the most dramatic change in SN-38-glucuronide (SN-38G) (2.64-fold; p = 0.0007).	Irinotecan	91-96	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	25-31
16595709-1	2006	Polymorphisms in UGT1A9 were associated with reduced toxicity and increased response to irinotecan in cancer patients.	Irinotecan	88-98	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	17-23
16595709-6	2006	The very low linkage disequilibrium (r(2) &lt; 0.19) between UGT1A9 I399 and all the other UGT1A1 and UGT1A9 variants suggests a direct effect or linkage to unknown functional variant(s) relevant to SN-38 glucuronidation.	Irinotecan	199-204	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	61-67
16595709-7	2006	The UGT1A9 -118T(9/10) was also linked to alteration of SN-38 glucuronidation profiles in the liver (p &lt; 0.05) and was associated with higher UGT1A1 protein (p = 0.03).	Irinotecan	56-61	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	4-10
16713012-7	2006	When administered concurrently, gefitinib and SN-38 had a synergistic effect in five of the seven cell lines expressing wild-type EGFR, whereas the combination was antagonistic in PC-9 cells and a PC-9 subline resistant to gefitinib and expressing deletional mutant EGFR (PC-9/ZD).	Irinotecan	46-51	epidermal growth factor receptor	Homo sapiens	130-134
16595709-10	2006	Despite limitations resulting from sample size, results indicate that UGT1A9 I399 and -118T(9/10) may represent additional candidates in combination with UGT1A1 promoter haplotypes for the prediction of SN-38 glucuronidation profile in vivo.	Irinotecan	203-208	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	70-76
16595709-10	2006	Despite limitations resulting from sample size, results indicate that UGT1A9 I399 and -118T(9/10) may represent additional candidates in combination with UGT1A1 promoter haplotypes for the prediction of SN-38 glucuronidation profile in vivo.	Irinotecan	203-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-160
16809730-0	2006	The role of UGT1A1*28 polymorphism in the pharmacodynamics and pharmacokinetics of irinotecan in patients with metastatic colorectal cancer.	Irinotecan	83-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
16809730-1	2006	PURPOSE: UGT1A1*28 polymorphism has been associated with decreased glucuronidation of SN38, the active metabolite of irinotecan.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	9-15
16809730-11	2006	In particular, the possibility of a dose reduction for irinotecan in patients with a UGT1A1*28 polymorphism is not supported by the result of this analysis.	Irinotecan	55-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
16713012-7	2006	When administered concurrently, gefitinib and SN-38 had a synergistic effect in five of the seven cell lines expressing wild-type EGFR, whereas the combination was antagonistic in PC-9 cells and a PC-9 subline resistant to gefitinib and expressing deletional mutant EGFR (PC-9/ZD).	Irinotecan	46-51	epidermal growth factor receptor	Homo sapiens	266-270
16713012-8	2006	When administered sequentially, treatment with SN-38 followed by gefitinib had remarkable synergistic effects in the PC-9 and PC-9/ZD cells.	Irinotecan	47-52	proprotein convertase subtilisin/kexin type 9	Homo sapiens	117-121
16713012-8	2006	When administered sequentially, treatment with SN-38 followed by gefitinib had remarkable synergistic effects in the PC-9 and PC-9/ZD cells.	Irinotecan	47-52	proprotein convertase subtilisin/kexin type 9	Homo sapiens	126-130
16723399-9	2006	Most importantly, WRN hypermethylation in colorectal tumors was a predictor of good clinical response to the camptothecin analogue irinotecan, a topoisomerase inhibitor commonly used in the clinical setting for the treatment of this tumor type.	Irinotecan	131-141	WRN RecQ like helicase	Homo sapiens	18-21
16897987-10	2006	It will be essential to prove that the combination of S-1 plus CPT-11 can replace the combination of infusional 5-FU and LV plus CPT-11 without negatively affecting efficacy and toxicity.	Irinotecan	129-135	proteasome 26S subunit, non-ATPase 1	Homo sapiens	54-57
16897973-3	2006	S-1 based combination therapies with other promising drugs like cisplatin, irinotecan and taxanes, are expected to yield good results.	Irinotecan	75-85	proteasome 26S subunit, non-ATPase 1	Homo sapiens	0-3
16897977-7	2006	Among various CPT-11 based chemotherapy, S-1 +CPT-11 appears to be the most effective and less toxic treatment.	Irinotecan	14-20	proteasome 26S subunit, non-ATPase 1	Homo sapiens	41-52
16897989-3	2006	One of the combination therapies with S-1 plus irinotecan (CPT-11) has also been expected to have a better therapeutic value.	Irinotecan	59-65	proteasome 26S subunit, non-ATPase 1	Homo sapiens	38-41
16187112-3	2006	The aim of this study was to ascertain whether two polymorphisms in the MTHFR gene (677C&gt;T and 1298 A&gt;C) could be used as genomic predictors of clinical response to fluoropyrimidine-based chemotherapy (in combination with irinotecan or oxaliplatin).	Irinotecan	228-238	methylenetetrahydrofolate reductase	Homo sapiens	72-77
16897968-5	2006	In combination with other anticancer drugs such as CPT-11 and taxanes, S-1 exercised synergistic antitumor efficacy not only on 5-FU-sensitive tumors with low expression levels of thymidylate synthase (TS) but also on 5-FU-resistant tumors with originally higher and/or elevated levels of TS expression.	Irinotecan	51-57	proteasome 26S subunit, non-ATPase 1	Homo sapiens	71-74
16897968-6	2006	As one of the reasonable mechanism of antitumor synergism by the combination, CPT-11 and taxanes were found to reduce the expression of TS in human tumor resistant to 5-FU with high expression TS levels.	Irinotecan	78-84	thymidylate synthetase	Homo sapiens	136-138
16897968-6	2006	As one of the reasonable mechanism of antitumor synergism by the combination, CPT-11 and taxanes were found to reduce the expression of TS in human tumor resistant to 5-FU with high expression TS levels.	Irinotecan	78-84	thymidylate synthetase	Homo sapiens	193-195
16508919-5	2006	Many enzymes are involved in controlling the disposition of irinotecan, including the cellular target (TOP1), metabolism enzymes (CES2, UGT1A1, CYP3A4, CYP3A5), and cellular transporters of the anti-cancer agent (ABCB1, ABCC1, ABCC2, ABCC3, ABCC5, ABCG2).	Irinotecan	60-70	carboxylesterase 2	Homo sapiens	130-134
16508919-5	2006	Many enzymes are involved in controlling the disposition of irinotecan, including the cellular target (TOP1), metabolism enzymes (CES2, UGT1A1, CYP3A4, CYP3A5), and cellular transporters of the anti-cancer agent (ABCB1, ABCC1, ABCC2, ABCC3, ABCC5, ABCG2).	Irinotecan	60-70	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	136-142
16508919-5	2006	Many enzymes are involved in controlling the disposition of irinotecan, including the cellular target (TOP1), metabolism enzymes (CES2, UGT1A1, CYP3A4, CYP3A5), and cellular transporters of the anti-cancer agent (ABCB1, ABCC1, ABCC2, ABCC3, ABCC5, ABCG2).	Irinotecan	60-70	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	144-150
16508919-5	2006	Many enzymes are involved in controlling the disposition of irinotecan, including the cellular target (TOP1), metabolism enzymes (CES2, UGT1A1, CYP3A4, CYP3A5), and cellular transporters of the anti-cancer agent (ABCB1, ABCC1, ABCC2, ABCC3, ABCC5, ABCG2).	Irinotecan	60-70	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	152-158
16508919-5	2006	Many enzymes are involved in controlling the disposition of irinotecan, including the cellular target (TOP1), metabolism enzymes (CES2, UGT1A1, CYP3A4, CYP3A5), and cellular transporters of the anti-cancer agent (ABCB1, ABCC1, ABCC2, ABCC3, ABCC5, ABCG2).	Irinotecan	60-70	ATP binding cassette subfamily B member 1	Homo sapiens	213-218
16508919-5	2006	Many enzymes are involved in controlling the disposition of irinotecan, including the cellular target (TOP1), metabolism enzymes (CES2, UGT1A1, CYP3A4, CYP3A5), and cellular transporters of the anti-cancer agent (ABCB1, ABCC1, ABCC2, ABCC3, ABCC5, ABCG2).	Irinotecan	60-70	ATP binding cassette subfamily C member 1	Homo sapiens	220-225
16508919-5	2006	Many enzymes are involved in controlling the disposition of irinotecan, including the cellular target (TOP1), metabolism enzymes (CES2, UGT1A1, CYP3A4, CYP3A5), and cellular transporters of the anti-cancer agent (ABCB1, ABCC1, ABCC2, ABCC3, ABCC5, ABCG2).	Irinotecan	60-70	ATP binding cassette subfamily C member 2	Homo sapiens	227-232
16508919-5	2006	Many enzymes are involved in controlling the disposition of irinotecan, including the cellular target (TOP1), metabolism enzymes (CES2, UGT1A1, CYP3A4, CYP3A5), and cellular transporters of the anti-cancer agent (ABCB1, ABCC1, ABCC2, ABCC3, ABCC5, ABCG2).	Irinotecan	60-70	ATP binding cassette subfamily C member 3	Homo sapiens	234-239
16508919-5	2006	Many enzymes are involved in controlling the disposition of irinotecan, including the cellular target (TOP1), metabolism enzymes (CES2, UGT1A1, CYP3A4, CYP3A5), and cellular transporters of the anti-cancer agent (ABCB1, ABCC1, ABCC2, ABCC3, ABCC5, ABCG2).	Irinotecan	60-70	ATP binding cassette subfamily C member 5	Homo sapiens	241-246
16508919-5	2006	Many enzymes are involved in controlling the disposition of irinotecan, including the cellular target (TOP1), metabolism enzymes (CES2, UGT1A1, CYP3A4, CYP3A5), and cellular transporters of the anti-cancer agent (ABCB1, ABCC1, ABCC2, ABCC3, ABCC5, ABCG2).	Irinotecan	60-70	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	248-253
16794239-3	2006	DESIGN: This review summarizes current clinical data for EGFR-TKIs as monotherapy or in combination with 5-fluorouracil/leucovorin, irinotecan, or oxaliplatin, focusing on the rapidly developing area of colorectal, gastroesophageal, and pancreatic cancers.	Irinotecan	132-142	epidermal growth factor receptor	Homo sapiens	57-61
16818517-5	2006	We envisioned that dp-VP16 would be converted to the active chemotherapeutic agent VP-16 by the same rabbit carboxylesterase (rCE) that we have previously shown to efficiently activate the prodrug irinotecan (CPT-11).	Irinotecan	197-207	host cell factor C1	Homo sapiens	22-26
16818517-5	2006	We envisioned that dp-VP16 would be converted to the active chemotherapeutic agent VP-16 by the same rabbit carboxylesterase (rCE) that we have previously shown to efficiently activate the prodrug irinotecan (CPT-11).	Irinotecan	209-215	host cell factor C1	Homo sapiens	22-26
16818517-6	2006	This dp-VP16 prodrug might then be used in combination with CPT-11, with both drugs activated by a single enzyme.	Irinotecan	60-66	host cell factor C1	Homo sapiens	8-12
16507564-3	2006	We designed this trial to investigate the modification of the vascular endothelial growth factor (VEGF) and interferon-gamma (IFN-gamma) in advanced colorectal cancer patients during treatment with a weekly combination of cetuximab plus irinotecan.	Irinotecan	237-247	vascular endothelial growth factor A	Homo sapiens	62-96
16501609-0	2006	Pleiotrophin, a candidate gene for poor tumor vasculature and in vivo neuroblastoma sensitivity to irinotecan.	Irinotecan	99-109	pleiotrophin	Homo sapiens	0-12
16501609-6	2006	PTN thus appeared to be a likely candidate gene associated with resistance to CPT-11 in this in vivo model.	Irinotecan	78-84	pleiotrophin	Homo sapiens	0-3
16501609-8	2006	PTN failed to demonstrate implication in resistance to CPT-11 in vitro but could influence sensitivity to CPT-11 exclusively through an in vivo mechanism.	Irinotecan	106-112	pleiotrophin	Homo sapiens	0-3
16636344-0	2006	Comprehensive analysis of UGT1A polymorphisms predictive for pharmacokinetics and treatment outcome in patients with non-small-cell lung cancer treated with irinotecan and cisplatin.	Irinotecan	157-167	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	26-31
16636344-4	2006	We analyzed the association of UGT1A genotypes with irinotecan PK and clinical outcomes.	Irinotecan	52-62	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	31-36
16636344-11	2006	CONCLUSION: These findings suggest that UGT1A1*6 and UGT1A9*22 genotypes may be important for SN-38 glucuronidation and associate with irinotecan-related severe toxicity.	Irinotecan	94-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
16636344-11	2006	CONCLUSION: These findings suggest that UGT1A1*6 and UGT1A9*22 genotypes may be important for SN-38 glucuronidation and associate with irinotecan-related severe toxicity.	Irinotecan	94-99	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	53-59
16636344-11	2006	CONCLUSION: These findings suggest that UGT1A1*6 and UGT1A9*22 genotypes may be important for SN-38 glucuronidation and associate with irinotecan-related severe toxicity.	Irinotecan	135-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	40-46
16636344-11	2006	CONCLUSION: These findings suggest that UGT1A1*6 and UGT1A9*22 genotypes may be important for SN-38 glucuronidation and associate with irinotecan-related severe toxicity.	Irinotecan	135-145	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	53-59
16636344-12	2006	Specifically, UGT1A1*6 might be useful for predicting tumor response and survival outcome of Korean patients with NSCLC treated with irinotecan-based chemotherapy.	Irinotecan	133-143	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
16685247-0	2006	Invader UGT1A1 molecular assay for irinotecan toxicity.	Irinotecan	35-45	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
16827119-6	2006	In contrast to the cells transfected with wild-type survivin, or the control NSCLC-3/neo, those cells transfected with mutant survivin and treated with SN-38 --&gt; PS-341 exhibited enhanced caspase 9 activity (&gt; 2-fold), caspase 3 (&gt; 2- to 3-fold) activity and cytotoxicity compared to the NSCLC-3/neo cells.	Irinotecan	152-157	caspase 9	Homo sapiens	191-200
16827119-6	2006	In contrast to the cells transfected with wild-type survivin, or the control NSCLC-3/neo, those cells transfected with mutant survivin and treated with SN-38 --&gt; PS-341 exhibited enhanced caspase 9 activity (&gt; 2-fold), caspase 3 (&gt; 2- to 3-fold) activity and cytotoxicity compared to the NSCLC-3/neo cells.	Irinotecan	152-157	caspase 3	Homo sapiens	225-234
16682733-4	2006	For example, pharmacogenetic tests currently used in cancer therapy, such as genotyping UGT1A1 to reduce the incidence of severe toxicity of irinotecan and sequencing epidermal growth factor receptor from tumors to identify somatic mutations conferring sensitivity to tyrosine kinase inhibitors, were developed without initial identification of interpopulation differences.	Irinotecan	141-151	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
16641252-4	2006	An assay is available for genotypic testing of the enzyme UGT1A1, which is predictive of toxicity from irinotecan.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
16821585-4	2006	RESULTS: Three independent lines of enquiry indicated that, in the tumour specimens, SN-38 was glucuronidated primarily by UGT1A1, the isozyme generally recognised as being responsible for hepatic detoxification of this compound, while with NU/ICRF 505 two candidate isoforms emerged - UGT1A8 and/or UGT1A10 - both of which are not normally expressed in the liver.	Irinotecan	85-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	123-129
16821585-4	2006	RESULTS: Three independent lines of enquiry indicated that, in the tumour specimens, SN-38 was glucuronidated primarily by UGT1A1, the isozyme generally recognised as being responsible for hepatic detoxification of this compound, while with NU/ICRF 505 two candidate isoforms emerged - UGT1A8 and/or UGT1A10 - both of which are not normally expressed in the liver.	Irinotecan	85-90	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	286-292
16821585-4	2006	RESULTS: Three independent lines of enquiry indicated that, in the tumour specimens, SN-38 was glucuronidated primarily by UGT1A1, the isozyme generally recognised as being responsible for hepatic detoxification of this compound, while with NU/ICRF 505 two candidate isoforms emerged - UGT1A8 and/or UGT1A10 - both of which are not normally expressed in the liver.	Irinotecan	85-90	UDP glucuronosyltransferase family 1 member A10	Homo sapiens	300-307
16507564-3	2006	We designed this trial to investigate the modification of the vascular endothelial growth factor (VEGF) and interferon-gamma (IFN-gamma) in advanced colorectal cancer patients during treatment with a weekly combination of cetuximab plus irinotecan.	Irinotecan	237-247	interferon gamma	Homo sapiens	108-124
16507564-3	2006	We designed this trial to investigate the modification of the vascular endothelial growth factor (VEGF) and interferon-gamma (IFN-gamma) in advanced colorectal cancer patients during treatment with a weekly combination of cetuximab plus irinotecan.	Irinotecan	237-247	interferon gamma	Homo sapiens	126-135
16494624-0	2006	Bcr-abl positive blast crisis of chronic myeloid leukemia emerging in a case of metastatic colorectal cancer 3 months after completion of an 8-month course of cetuximab and irinotecan.	Irinotecan	173-183	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
16364925-4	2006	Interestingly, while the susceptibilities of Tbeta4 overexpressers to 5-FU and irinotecan remained unchanged, they were more resistant to doxorubicin and etoposide which triggered apoptosis via a mitochondrial pathway.	Irinotecan	79-89	thymosin beta 4 X-linked	Homo sapiens	45-51
16724931-2	2006	Recent clinical studies indicate that thalidomide, a known tumor necrosis factor-alpha inhibitor, ameliorated the toxicities induced by CPT-11.	Irinotecan	136-142	tumor necrosis factor	Rattus norvegicus	59-86
16446370-1	2006	DNA damage induced by the topoisomerase I inhibitor irinotecan (CPT-11) triggers in p53(WT) colorectal carcinoma cells a long term cell cycle arrest and in p53MUT cells a transient arrest followed by apoptosis (Magrini, R., Bhonde, M. R., Hanski, M. L., Notter, M., Scherubl, H., Boland, C. R., Zeitz, M., and Hanski, C. (2002) Int.	Irinotecan	52-62	tumor protein p53	Homo sapiens	84-87
16618113-1	2006	ABCG2 is an ATP-binding cassette half-transporter conferring resistance to chemotherapeutic agents such as mitoxantrone, irinotecan, and flavopiridol.	Irinotecan	121-131	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	12-49
16702730-1	2006	The ATP-binding cassette transporter, ABCG2, which is expressed at high levels in the intestine and liver, functions as an efflux transporter for many drugs, including clinically used anticancer agents such as topotecan and the active metabolite of irinotecan (SN-38).	Irinotecan	249-259	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	38-43
16702730-1	2006	The ATP-binding cassette transporter, ABCG2, which is expressed at high levels in the intestine and liver, functions as an efflux transporter for many drugs, including clinically used anticancer agents such as topotecan and the active metabolite of irinotecan (SN-38).	Irinotecan	261-266	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	38-43
16702730-2	2006	In this study, to elucidate the linkage disequilibrium (LD) profiles and haplotype structures of ABCG2, we have comprehensively searched for genetic variations in the putative promoter region, all the exons, and their flanking introns of ABCG2 from 177 Japanese cancer patients treated with irinotecan.	Irinotecan	291-301	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	97-102
16525652-12	2006	in vivo results demonstrated that DPA enhanced the in vivo anticancer activity of the chemotherapeutic agent, CPT-11, by elevation of p53-independent p21/Cip1 and p27/Kip1 expression.	Irinotecan	110-116	H3 histone pseudogene 16	Homo sapiens	150-153
16525652-12	2006	in vivo results demonstrated that DPA enhanced the in vivo anticancer activity of the chemotherapeutic agent, CPT-11, by elevation of p53-independent p21/Cip1 and p27/Kip1 expression.	Irinotecan	110-116	cyclin dependent kinase inhibitor 1A	Homo sapiens	154-158
16525652-12	2006	in vivo results demonstrated that DPA enhanced the in vivo anticancer activity of the chemotherapeutic agent, CPT-11, by elevation of p53-independent p21/Cip1 and p27/Kip1 expression.	Irinotecan	110-116	interferon alpha inducible protein 27	Homo sapiens	163-166
16525652-12	2006	in vivo results demonstrated that DPA enhanced the in vivo anticancer activity of the chemotherapeutic agent, CPT-11, by elevation of p53-independent p21/Cip1 and p27/Kip1 expression.	Irinotecan	110-116	cyclin dependent kinase inhibitor 1B	Homo sapiens	167-171
16777630-6	2006	Moreover the association of the irinotecan with the anti EGFR antibody (Erbitux)), cetixumab) has show a efficacy in third line after progression under an protocol with irinotecan.	Irinotecan	32-42	epidermal growth factor receptor	Homo sapiens	57-61
16777630-6	2006	Moreover the association of the irinotecan with the anti EGFR antibody (Erbitux)), cetixumab) has show a efficacy in third line after progression under an protocol with irinotecan.	Irinotecan	169-179	epidermal growth factor receptor	Homo sapiens	57-61
16618113-1	2006	ABCG2 is an ATP-binding cassette half-transporter conferring resistance to chemotherapeutic agents such as mitoxantrone, irinotecan, and flavopiridol.	Irinotecan	121-131	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
16518418-0	2006	Potentiation of irinotecan sensitivity by Se-methylselenocysteine in an in vivo tumor model is associated with downregulation of cyclooxygenase-2, inducible nitric oxide synthase, and hypoxia-inducible factor 1alpha expression, resulting in reduced angiogenesis.	Irinotecan	16-26	prostaglandin-endoperoxide synthase 2	Homo sapiens	129-145
16518418-0	2006	Potentiation of irinotecan sensitivity by Se-methylselenocysteine in an in vivo tumor model is associated with downregulation of cyclooxygenase-2, inducible nitric oxide synthase, and hypoxia-inducible factor 1alpha expression, resulting in reduced angiogenesis.	Irinotecan	16-26	nitric oxide synthase 2	Homo sapiens	147-178
16518418-0	2006	Potentiation of irinotecan sensitivity by Se-methylselenocysteine in an in vivo tumor model is associated with downregulation of cyclooxygenase-2, inducible nitric oxide synthase, and hypoxia-inducible factor 1alpha expression, resulting in reduced angiogenesis.	Irinotecan	16-26	hypoxia inducible factor 1 subunit alpha	Homo sapiens	184-215
16518418-3	2006	In FaDu xenografts, a poorly differentiated tumor-expressing mutant p53, the cure rate was increased from 30% with irinotecan alone to 100% with the combination of irinotecan and MSC.	Irinotecan	115-125	tumor protein p53	Homo sapiens	68-71
16518418-3	2006	In FaDu xenografts, a poorly differentiated tumor-expressing mutant p53, the cure rate was increased from 30% with irinotecan alone to 100% with the combination of irinotecan and MSC.	Irinotecan	164-174	tumor protein p53	Homo sapiens	68-71
16518418-7	2006	In contrast, significant downregulation of cyclooxygenase-2 (COX-2) expression and activity was observed in the cells exposed to SN-38 in combination with MSC compared to SN-38 alone.	Irinotecan	129-134	prostaglandin-endoperoxide synthase 2	Homo sapiens	43-59
16518418-7	2006	In contrast, significant downregulation of cyclooxygenase-2 (COX-2) expression and activity was observed in the cells exposed to SN-38 in combination with MSC compared to SN-38 alone.	Irinotecan	129-134	prostaglandin-endoperoxide synthase 2	Homo sapiens	61-66
16518418-7	2006	In contrast, significant downregulation of cyclooxygenase-2 (COX-2) expression and activity was observed in the cells exposed to SN-38 in combination with MSC compared to SN-38 alone.	Irinotecan	171-176	prostaglandin-endoperoxide synthase 2	Homo sapiens	43-59
16518418-7	2006	In contrast, significant downregulation of cyclooxygenase-2 (COX-2) expression and activity was observed in the cells exposed to SN-38 in combination with MSC compared to SN-38 alone.	Irinotecan	171-176	prostaglandin-endoperoxide synthase 2	Homo sapiens	61-66
16518418-9	2006	Analysis of tumor tissues at 24 h after treatment with synergistic modality of irinotecan and MSC revealed significant downregulation of COX-2, inducible nitric oxide synthase (iNOS) and hypoxia-induced factor-1alpha expression (HIF 1alpha).	Irinotecan	79-89	prostaglandin-endoperoxide synthase 2	Homo sapiens	137-142
16518418-9	2006	Analysis of tumor tissues at 24 h after treatment with synergistic modality of irinotecan and MSC revealed significant downregulation of COX-2, inducible nitric oxide synthase (iNOS) and hypoxia-induced factor-1alpha expression (HIF 1alpha).	Irinotecan	79-89	nitric oxide synthase 2	Homo sapiens	144-175
16518418-9	2006	Analysis of tumor tissues at 24 h after treatment with synergistic modality of irinotecan and MSC revealed significant downregulation of COX-2, inducible nitric oxide synthase (iNOS) and hypoxia-induced factor-1alpha expression (HIF 1alpha).	Irinotecan	79-89	nitric oxide synthase 2	Homo sapiens	177-181
16518418-9	2006	Analysis of tumor tissues at 24 h after treatment with synergistic modality of irinotecan and MSC revealed significant downregulation of COX-2, inducible nitric oxide synthase (iNOS) and hypoxia-induced factor-1alpha expression (HIF 1alpha).	Irinotecan	79-89	hypoxia inducible factor 1 subunit alpha	Homo sapiens	229-239
16446370-1	2006	DNA damage induced by the topoisomerase I inhibitor irinotecan (CPT-11) triggers in p53(WT) colorectal carcinoma cells a long term cell cycle arrest and in p53MUT cells a transient arrest followed by apoptosis (Magrini, R., Bhonde, M. R., Hanski, M. L., Notter, M., Scherubl, H., Boland, C. R., Zeitz, M., and Hanski, C. (2002) Int.	Irinotecan	52-62	tumor protein p53	Homo sapiens	156-159
16446370-1	2006	DNA damage induced by the topoisomerase I inhibitor irinotecan (CPT-11) triggers in p53(WT) colorectal carcinoma cells a long term cell cycle arrest and in p53MUT cells a transient arrest followed by apoptosis (Magrini, R., Bhonde, M. R., Hanski, M. L., Notter, M., Scherubl, H., Boland, C. R., Zeitz, M., and Hanski, C. (2002) Int.	Irinotecan	64-70	tumor protein p53	Homo sapiens	84-87
16446370-1	2006	DNA damage induced by the topoisomerase I inhibitor irinotecan (CPT-11) triggers in p53(WT) colorectal carcinoma cells a long term cell cycle arrest and in p53MUT cells a transient arrest followed by apoptosis (Magrini, R., Bhonde, M. R., Hanski, M. L., Notter, M., Scherubl, H., Boland, C. R., Zeitz, M., and Hanski, C. (2002) Int.	Irinotecan	64-70	tumor protein p53	Homo sapiens	156-159
16446370-5	2006	Here we used five p53WT and five p53MUT established colon carcinoma cell lines to identify gene expression alterations associated with apoptosis in p53MUT cells after treatment with SN-38, the irinotecan metabolite.	Irinotecan	182-187	tumor protein p53	Homo sapiens	18-21
16446370-5	2006	Here we used five p53WT and five p53MUT established colon carcinoma cell lines to identify gene expression alterations associated with apoptosis in p53MUT cells after treatment with SN-38, the irinotecan metabolite.	Irinotecan	182-187	tumor protein p53	Homo sapiens	33-36
16446370-10	2006	Together, these data indicate that the high expression of mitotic genes in p53MUT cells after SN-38 treatment contributes to DNA damage-induced apoptosis, whereas their suppression in p53WT cells acts as a safeguard mechanism preventing mitosis initiation and the subsequent apoptosis.	Irinotecan	94-99	tumor protein p53	Homo sapiens	75-78
16309825-2	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	121-127	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	39-42
16551870-0	2006	Irinotecan inactivation is modulated by epigenetic silencing of UGT1A1 in colon cancer.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	64-70
16551870-2	2006	The UGT1A1-metabolizing enzyme, expressed in liver and colon, is primarily involved in the inactivation of its active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	129-159	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
16551870-2	2006	The UGT1A1-metabolizing enzyme, expressed in liver and colon, is primarily involved in the inactivation of its active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	161-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
16551870-9	2006	Loss of UGT1A1 methylation was further associated with an increase in UGT1A1 protein content and with an enhanced inactivation of SN-38 by 300% in HCT-116 cells.	Irinotecan	130-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
16551870-10	2006	CONCLUSIONS: We conclude that DNA methylation represses UGT1A1 expression in colon cancer and that this process may contribute to the level of tumoral inactivation of the anticancer agent SN-38 and potentially influence clinical response.	Irinotecan	188-193	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
16303243-1	2006	Breast cancer resistance protein (BCRP) is a half-molecule ATP-binding cassette transporter that pumps out various anticancer agents such as 7-ethyl-10-hydroxycamptothecin, topotecan and mitoxantrone.	Irinotecan	141-171	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
16303243-1	2006	Breast cancer resistance protein (BCRP) is a half-molecule ATP-binding cassette transporter that pumps out various anticancer agents such as 7-ethyl-10-hydroxycamptothecin, topotecan and mitoxantrone.	Irinotecan	141-171	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
16309825-2	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	95-100	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	27-32
16309825-2	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	95-100	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
16309825-2	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	95-100	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	39-42
16309825-2	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	95-100	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	43-47
16309825-2	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	121-127	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	27-32
16309825-2	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	121-127	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
16309825-2	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	121-127	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	43-47
16343744-5	2006	In this review, the role of genetic polymorphisms in the main enzyme-systems (carboxylesterase, cytochrome P450 3A, and uridine diphosphate-glucuronosyltransferase) and ABC-transporters (ABCB1, ABCC2, and ABCG2) involved in irinotecan metabolism, are discussed.	Irinotecan	224-234	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	120-163
16343744-5	2006	In this review, the role of genetic polymorphisms in the main enzyme-systems (carboxylesterase, cytochrome P450 3A, and uridine diphosphate-glucuronosyltransferase) and ABC-transporters (ABCB1, ABCC2, and ABCG2) involved in irinotecan metabolism, are discussed.	Irinotecan	224-234	ATP binding cassette subfamily B member 1	Homo sapiens	187-192
16343744-5	2006	In this review, the role of genetic polymorphisms in the main enzyme-systems (carboxylesterase, cytochrome P450 3A, and uridine diphosphate-glucuronosyltransferase) and ABC-transporters (ABCB1, ABCC2, and ABCG2) involved in irinotecan metabolism, are discussed.	Irinotecan	224-234	ATP binding cassette subfamily C member 2	Homo sapiens	194-199
16343744-5	2006	In this review, the role of genetic polymorphisms in the main enzyme-systems (carboxylesterase, cytochrome P450 3A, and uridine diphosphate-glucuronosyltransferase) and ABC-transporters (ABCB1, ABCC2, and ABCG2) involved in irinotecan metabolism, are discussed.	Irinotecan	224-234	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	205-210
16619577-0	2006	Feasibility study of biweekly CPT-11 plus CDDP for S-1- and paclitaxel-refractory, metastatic gastric cancer.	Irinotecan	30-36	proteasome 26S subunit, non-ATPase 1	Homo sapiens	51-54
16303861-0	2006	Cetuximab and irinotecan/5-fluorouracil/folinic acid is a safe combination for the first-line treatment of patients with epidermal growth factor receptor expressing metastatic colorectal carcinoma.	Irinotecan	14-24	epidermal growth factor receptor	Homo sapiens	121-153
16619577-9	2006	CONCLUSION: Biweekly CPT-11 plus CDDP was feasible for S-1- and paclitaxel-refractory metastatic gastric cancer, with moderate activity and favorable toxicity.	Irinotecan	21-27	proteasome 26S subunit, non-ATPase 1	Homo sapiens	55-58
16542215-0	2006	Role of ABCG2 as a biomarker for predicting resistance to CPT-11/SN-38 in lung cancer.	Irinotecan	58-64	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	8-13
16456808-1	2006	BACKGROUND: In the current Phase II study, the authors evaluated the association between genomic polymorphic variants in uridine diphosphate glucuronosyl transferase (UGT1A1), methylenetetrahydrofolate reductase (MTHFR), and thymidylate synthase (TS) genes, and the incidence of the adverse effects of irinotecan and raltitrexed in previously heavily treated patients with metastatic colorectal carcinoma.	Irinotecan	302-312	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-173
16456808-10	2006	CONCLUSIONS: In the current study, UGT1A1 promoter polymorphism was found to be predictive of the risk of diarrhea, emesis, and fatigue caused by chemotherapy with irinotecan and raltitrexed.	Irinotecan	164-174	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
16456808-11	2006	Screening for UGT1A1 promoter polymorphism may be clinically useful for identifying patients at a higher risk of developing a severe or potentially life-threatening toxicity after irinotecan-based chemotherapy.	Irinotecan	180-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
16542215-7	2006	These results indicate that the upregulation of ABCG2 was functional, and related to the resistance of H23/SN-38 cells to SN-38.	Irinotecan	107-112	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	48-53
16542215-0	2006	Role of ABCG2 as a biomarker for predicting resistance to CPT-11/SN-38 in lung cancer.	Irinotecan	65-70	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	8-13
16542215-7	2006	These results indicate that the upregulation of ABCG2 was functional, and related to the resistance of H23/SN-38 cells to SN-38.	Irinotecan	122-127	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	48-53
16541742-6	2006	The standard chemotherapy for extensive SCLC is the combination of cisplatin and irinotecan or etoposide.	Irinotecan	81-91	SCLC1	Homo sapiens	40-44
16542215-8	2006	Moreover, we found that gene expression levels of ABCG2 were significantly correlated with the concentration of SN-38 for 50% cell survival in 13 NSCLC cells (r=0.592, P&lt;0.05).	Irinotecan	112-117	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	50-55
16542215-9	2006	The present results indicate that the induction of ABCG2 by SN-38 does confer acquired resistance to CPT-11/SN-38, but the induction of ABCG2 and subsequent drug resistance are reversible.	Irinotecan	60-65	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	51-56
16542215-9	2006	The present results indicate that the induction of ABCG2 by SN-38 does confer acquired resistance to CPT-11/SN-38, but the induction of ABCG2 and subsequent drug resistance are reversible.	Irinotecan	101-107	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	51-56
16542215-9	2006	The present results indicate that the induction of ABCG2 by SN-38 does confer acquired resistance to CPT-11/SN-38, but the induction of ABCG2 and subsequent drug resistance are reversible.	Irinotecan	108-113	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	51-56
16542215-10	2006	However, the expression level of ABCG2 may be a useful indicator of CPT-11/SN-38 activity in lung cancer.	Irinotecan	68-74	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	33-38
16542215-10	2006	However, the expression level of ABCG2 may be a useful indicator of CPT-11/SN-38 activity in lung cancer.	Irinotecan	75-80	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	33-38
16517957-1	2006	BACKGROUND: Irinotecan hydrochloride (CPT-11), a topoisomerase I inhibitor highly effective for various cancers, has its dosage limited by diffuse mucosal damage with increased prostaglandin (PG) E(2).	Irinotecan	12-36	topoisomerase I	Zea mays	49-64
16517957-1	2006	BACKGROUND: Irinotecan hydrochloride (CPT-11), a topoisomerase I inhibitor highly effective for various cancers, has its dosage limited by diffuse mucosal damage with increased prostaglandin (PG) E(2).	Irinotecan	38-44	topoisomerase I	Zea mays	49-64
16465425-4	2006	MVP protein levels were enhanced in SW-620 cells after a 72 h treatment with doxorubicin (Adr), etoposide (VP-16), cis-platinum (II) diammine dichloride (CDDP) or SN-38, but not vincristine (VCR) or paclitaxel (Taxol) at their IC50 concentration.	Irinotecan	163-168	major vault protein	Homo sapiens	0-3
16535772-0	2006	Re: Yin MB, Li Z-R, Cao S, Durrani FA, Azrak RG, Frank C, and Rustum YM (2004) Enhanced 7-ethyl-10-hydroxycamptothecin (SN-38) lethality by methylselenocysteine is associated with Chk2 phosphorylation at threonin-68 and down-regulation of Cdc6 expression.	Irinotecan	88-118	checkpoint kinase 2	Homo sapiens	180-184
16535772-0	2006	Re: Yin MB, Li Z-R, Cao S, Durrani FA, Azrak RG, Frank C, and Rustum YM (2004) Enhanced 7-ethyl-10-hydroxycamptothecin (SN-38) lethality by methylselenocysteine is associated with Chk2 phosphorylation at threonin-68 and down-regulation of Cdc6 expression.	Irinotecan	88-118	cell division cycle 6	Homo sapiens	239-243
16535772-0	2006	Re: Yin MB, Li Z-R, Cao S, Durrani FA, Azrak RG, Frank C, and Rustum YM (2004) Enhanced 7-ethyl-10-hydroxycamptothecin (SN-38) lethality by methylselenocysteine is associated with Chk2 phosphorylation at threonin-68 and down-regulation of Cdc6 expression.	Irinotecan	120-125	checkpoint kinase 2	Homo sapiens	180-184
16535772-0	2006	Re: Yin MB, Li Z-R, Cao S, Durrani FA, Azrak RG, Frank C, and Rustum YM (2004) Enhanced 7-ethyl-10-hydroxycamptothecin (SN-38) lethality by methylselenocysteine is associated with Chk2 phosphorylation at threonin-68 and down-regulation of Cdc6 expression.	Irinotecan	120-125	cell division cycle 6	Homo sapiens	239-243
16465425-5	2006	Treatment for 48 h with Adr, VP-16 and SN-38 at their IC50 concentration also enhanced the expression of MVP mRNA.	Irinotecan	39-44	major vault protein	Homo sapiens	105-108
16476837-10	2006	Irinotecan and agents like gefitinib, erlotinib, and imatinib targeting the epidermal growth factor receptor and platelet-derived growth factor receptor have shown some promise in recurrent malignant glioma.	Irinotecan	0-10	epidermal growth factor receptor	Homo sapiens	76-108
16444269-3	2006	A cytotoxin-armed antibody reactive with one of these drug-induced surface proteins, the LY6D/E48 antigen, originally identified as the target of a monoclonal antibody reactive with squamous cell carcinomas, caused complete regression of colorectal tumor xenografts in mice treated with CPT-11, whereas either agent alone was less effective.	Irinotecan	287-293	lymphocyte antigen 6 complex, locus D	Mus musculus	89-93
16271446-3	2006	Irinotecan is subject to extensive metabolism by various polymorphic enzymes, including CES2 to form SN-38, members of the UGT1A subfamily, and CYP3A4 and CYP3A5, which form several pharmacologically inactive oxidation products.	Irinotecan	0-10	carboxylesterase 2	Homo sapiens	88-92
16271446-3	2006	Irinotecan is subject to extensive metabolism by various polymorphic enzymes, including CES2 to form SN-38, members of the UGT1A subfamily, and CYP3A4 and CYP3A5, which form several pharmacologically inactive oxidation products.	Irinotecan	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	144-150
16271446-3	2006	Irinotecan is subject to extensive metabolism by various polymorphic enzymes, including CES2 to form SN-38, members of the UGT1A subfamily, and CYP3A4 and CYP3A5, which form several pharmacologically inactive oxidation products.	Irinotecan	0-10	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	155-161
16271446-3	2006	Irinotecan is subject to extensive metabolism by various polymorphic enzymes, including CES2 to form SN-38, members of the UGT1A subfamily, and CYP3A4 and CYP3A5, which form several pharmacologically inactive oxidation products.	Irinotecan	101-106	carboxylesterase 2	Homo sapiens	88-92
16271446-4	2006	Elimination of irinotecan is also dependent on drug-transporting proteins, notably ABCB1 (P-glycoprotein), ABCC2 (cMOAT) and ABCG2 (BCRP), present on the bile canalicular membrane.	Irinotecan	15-25	ATP binding cassette subfamily B member 1	Homo sapiens	83-88
16271446-4	2006	Elimination of irinotecan is also dependent on drug-transporting proteins, notably ABCB1 (P-glycoprotein), ABCC2 (cMOAT) and ABCG2 (BCRP), present on the bile canalicular membrane.	Irinotecan	15-25	ATP binding cassette subfamily C member 2	Homo sapiens	107-112
16271446-4	2006	Elimination of irinotecan is also dependent on drug-transporting proteins, notably ABCB1 (P-glycoprotein), ABCC2 (cMOAT) and ABCG2 (BCRP), present on the bile canalicular membrane.	Irinotecan	15-25	ATP binding cassette subfamily C member 2	Homo sapiens	114-119
16271446-4	2006	Elimination of irinotecan is also dependent on drug-transporting proteins, notably ABCB1 (P-glycoprotein), ABCC2 (cMOAT) and ABCG2 (BCRP), present on the bile canalicular membrane.	Irinotecan	15-25	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	125-130
16271446-4	2006	Elimination of irinotecan is also dependent on drug-transporting proteins, notably ABCB1 (P-glycoprotein), ABCC2 (cMOAT) and ABCG2 (BCRP), present on the bile canalicular membrane.	Irinotecan	15-25	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	132-136
15893418-5	2006	In HeLa cells, genistein inhibited CDK1 phosphorylation after irinotecan treatment.	Irinotecan	62-72	cyclin dependent kinase 1	Homo sapiens	35-39
16501908-5	2006	The EGF receptor antibody cetuximab shows activity as single agent and in combination with irinotecan.	Irinotecan	91-101	epidermal growth factor receptor	Homo sapiens	4-16
16877259-0	2006	Pharmacogenetics of uridine diphosphoglucuronosyltransferase (UGT) 1A family members and its role in patient response to irinotecan.	Irinotecan	121-131	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	20-69
16170360-6	2006	Irinotecan treatment also induced in mouse tumours derived from the p53(wt) cell lines a tetraploid G1 arrest and in those derived from the p53-deficient cell lines a transient G2/M arrest and apoptosis.	Irinotecan	0-10	transformation related protein 53, pseudogene	Mus musculus	68-71
16170360-6	2006	Irinotecan treatment also induced in mouse tumours derived from the p53(wt) cell lines a tetraploid G1 arrest and in those derived from the p53-deficient cell lines a transient G2/M arrest and apoptosis.	Irinotecan	0-10	transformation related protein 53, pseudogene	Mus musculus	140-143
16454746-3	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	95-100	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	27-32
16454746-3	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	95-100	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
16454746-3	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	95-100	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	39-42
16454746-3	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	95-100	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	43-47
16454746-3	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	121-127	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	27-32
16454746-3	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	121-127	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
16454746-3	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	121-127	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	39-42
16454746-3	2006	However, overexpression of ABCG2 (BCRP/MXR/ABCP) reportedly confers cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	121-127	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	43-47
17163168-9	2006	Tumors with high TS, TP, and DPD expression levels should be treated with such non-TS-directed anticancer drugs as irinotecan or oxaliplatin, or in combination with 5-FU.	Irinotecan	115-125	dihydropyrimidine dehydrogenase	Homo sapiens	29-32
16251201-0	2006	Phase II study of tailored chemotherapy for advanced colorectal cancer with either 5-fluouracil and leucovorin or oxaliplatin and irinotecan based on the expression of thymidylate synthase and dihydropyrimidine dehydrogenase.	Irinotecan	130-140	thymidylate synthetase	Homo sapiens	168-188
16251201-0	2006	Phase II study of tailored chemotherapy for advanced colorectal cancer with either 5-fluouracil and leucovorin or oxaliplatin and irinotecan based on the expression of thymidylate synthase and dihydropyrimidine dehydrogenase.	Irinotecan	130-140	dihydropyrimidine dehydrogenase	Homo sapiens	193-224
16877259-4	2006	SN-38 is inactivated via glucuronidation catalyzed by various hepatic and extrahepatic UGT1A isozymes.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	87-92
16877259-5	2006	Although the role of the UGT1A1 *28 genetic variant has received much attention in altered toxicity upon irinotecan treatment, other UGT1A enzymes also play an important role.	Irinotecan	105-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
16877259-5	2006	Although the role of the UGT1A1 *28 genetic variant has received much attention in altered toxicity upon irinotecan treatment, other UGT1A enzymes also play an important role.	Irinotecan	105-115	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	25-30
16409125-4	2006	The objective of this study was to determine whether the chemotherapeutic agent irinotecan, by enhancing nuclear localization of YB-1, and the histone deacetylase inhibitor trichostatin A, by upregulating coxsackievirus-adenovirus receptor (CAR) expression, could augment replication of and cell lysis by adenovirus dl520 in glioblastomas in vitro.	Irinotecan	80-90	Y-box binding protein 1	Homo sapiens	129-133
16409125-4	2006	The objective of this study was to determine whether the chemotherapeutic agent irinotecan, by enhancing nuclear localization of YB-1, and the histone deacetylase inhibitor trichostatin A, by upregulating coxsackievirus-adenovirus receptor (CAR) expression, could augment replication of and cell lysis by adenovirus dl520 in glioblastomas in vitro.	Irinotecan	80-90	CXADR Ig-like cell adhesion molecule	Homo sapiens	241-244
16409125-5	2006	We found that trichostatin A upregulated CAR expression and that irinotecan caused increased nuclear localization of YB-1 in both glioblastoma cell lines.	Irinotecan	65-75	Y-box binding protein 1	Homo sapiens	117-121
17878748-1	2006	OBJECTIVES: Breast cancer resistance protein (BCRP) confers resistance to certain anticancer drugs such as mitoxantrone, topotecan and SN-38.	Irinotecan	135-140	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	12-44
17878748-1	2006	OBJECTIVES: Breast cancer resistance protein (BCRP) confers resistance to certain anticancer drugs such as mitoxantrone, topotecan and SN-38.	Irinotecan	135-140	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	46-50
16314881-1	2006	Common polymorphisms within the human UGT1A gene locus are associated with irinotecan and tranilast toxicity.	Irinotecan	75-85	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	38-43
16267624-0	2005	Pharmacogenetics of irinotecan: a promoter polymorphism of UGT1A1 gene and severe adverse reactions to irinotecan.	Irinotecan	20-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	59-65
15918039-6	2005	Consistent with the pharmacokinetic data, four to fivefold more CPT-11 was required to induce regressions in human Rh30 xenografts grown in esterase-deficient scid mice, as opposed to those grown in scid animals.	Irinotecan	64-70	Rh blood group D antigen	Homo sapiens	115-119
16257398-0	2005	Inhibition of acetylcholinesterase by the anticancer prodrug CPT-11.	Irinotecan	61-67	acetylcholinesterase (Cartwright blood group)	Homo sapiens	14-34
16257398-6	2005	Kinetic studies indicated that CPT-11 was primarily responsible for AChE inhibition with the 4-piperidinopiperidine moiety, the major determinant in the loss of enzyme activity.	Irinotecan	31-37	acetylcholinesterase (Cartwright blood group)	Homo sapiens	68-72
16367905-5	2005	PA317 cells transfected with C603S-BCRP (PA/C603S) showed either similar or only marginally lower SN-38 resistance than PA/WT cells, despite the reduced levels of BCRP dimer in these cells.	Irinotecan	98-103	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	34-39
16367905-5	2005	PA317 cells transfected with C603S-BCRP (PA/C603S) showed either similar or only marginally lower SN-38 resistance than PA/WT cells, despite the reduced levels of BCRP dimer in these cells.	Irinotecan	98-103	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	35-39
16367905-6	2005	Moreover, the degree of SN-38 resistance in the mutant BCRP transfectants was found to be associated with the monomer expression levels under reducing conditions.	Irinotecan	24-29	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	55-59
16123050-0	2005	Gefitinib (Iressa) inhibits the CYP3A4-mediated formation of 7-ethyl-10-(4-amino-1-piperidino)carbonyloxycamptothecin but activates that of 7-ethyl-10-[4-N-(5-aminopentanoic acid)-1-piperidino]carbonyloxycamptothecin from irinotecan.	Irinotecan	222-232	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	32-38
16267624-1	2005	This review focuses on a pharmacogenetic association between genetic polymorphism of UGT1A1 gene and severe adverse reactions to irinotecan.	Irinotecan	129-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	85-91
16267624-4	2005	A case-control study of Japanese cancer patients revealed that those with the variant UGT1A1 alleles were at significantly higher risk of severe adverse reactions to irinotecan, suggesting that the genotyping strategy would be clinically useful.	Irinotecan	166-176	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	86-92
16400742-3	2005	(2) Cetuximab, an antibody directed against the epidermal growth factor receptor (EGFR), is indicated for patients with EGF-expressing metastatic colorectal cancer, after failure of irinotecan-based chemotherapy.	Irinotecan	182-192	epidermal growth factor receptor	Homo sapiens	48-80
16369175-8	2005	PTK787 alone or in combination with CPT-11 reduced the phosphorylation of VEGF-R in tumor cells and tumor-associated endothelial cells, was associated with decreased microvessel density, a decreased proliferative index, and an increased apoptotic index.	Irinotecan	36-42	vascular endothelial growth factor A	Mus musculus	74-78
16373718-2	2005	We assessed the roles of p53, TRAIL receptors, and cellular Fas-associated death domain-like interleukin-1beta-converting enzyme inhibitory protein (c-FLIP) in regulating the cytotoxic effects of recombinant TRAIL (rTRAIL) alone and in combination with chemotherapy [5-fluorouracil (5-FU), oxaliplatin, and irinotecan] in a panel of colon cancer cell lines.	Irinotecan	307-317	CASP8 and FADD like apoptosis regulator	Homo sapiens	149-155
16491625-0	2005	UGT1A1 genotyping in patients undergoing treatment with irinotecan.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
16095811-0	2005	The radical scavenger edaravone enhances the anti-tumor effects of CPT-11 in murine colon cancer by increasing apoptosis via inhibition of NF-kappaB.	Irinotecan	67-73	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	139-148
16095811-4	2005	In vitro, SN38, the active metabolite of CPT-11, induced activation of NF-kB, the production of intracellular reactive oxygen species, the activation of caspase-3, and apoptosis in colon26 cells.	Irinotecan	41-47	caspase 3	Mus musculus	153-162
16399432-4	2005	Patients who have failed first-line therapy have benefited from 5-FU, leucovorin, and irinotecan (IFL), 5-FU, leucovorin, and oxaliplatin (FOLFOX), and 5-FU, leucovorin, and irinotecan (FOLFIRI) in the second-line treatment setting.	Irinotecan	86-96	interferon alpha 1	Homo sapiens	98-101
16222152-0	2005	The epidermal growth factor receptor tyrosine kinase inhibitor gefitinib sensitizes colon cancer cells to irinotecan.	Irinotecan	106-116	epidermal growth factor receptor	Homo sapiens	4-36
16222152-3	2005	We investigated the effects of the EGFR tyrosine kinase inhibitor gefitinib on cellular determinants of irinotecan resistance in human colon cancer cells.	Irinotecan	104-114	epidermal growth factor receptor	Homo sapiens	35-39
15947933-8	2005	CPT-11 80 mg/m(2) produced a mean increase in S-phase by IHC for cyclin A of 137%.	Irinotecan	0-6	cyclin A2	Homo sapiens	65-73
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	126-132	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
16132345-12	2005	In addition, the accumulation of CPT-11 and SN-38 over 120 min in MRP4/HepG2 cells was significantly reduced compared to V/HepG2 cells, whereas the addition of celecoxib, MK571, or BSO significantly increased their accumulation in MRP4/HepG2 cells.	Irinotecan	33-39	ATP binding cassette subfamily C member 4	Homo sapiens	66-70
16132345-12	2005	In addition, the accumulation of CPT-11 and SN-38 over 120 min in MRP4/HepG2 cells was significantly reduced compared to V/HepG2 cells, whereas the addition of celecoxib, MK571, or BSO significantly increased their accumulation in MRP4/HepG2 cells.	Irinotecan	33-39	ATP binding cassette subfamily C member 4	Homo sapiens	231-235
16132345-12	2005	In addition, the accumulation of CPT-11 and SN-38 over 120 min in MRP4/HepG2 cells was significantly reduced compared to V/HepG2 cells, whereas the addition of celecoxib, MK571, or BSO significantly increased their accumulation in MRP4/HepG2 cells.	Irinotecan	44-49	ATP binding cassette subfamily C member 4	Homo sapiens	66-70
16270098-4	2005	For the treatment of metastatic colorectal cancer, improved response rates and prolonged survival have been reported when irinotecan or oxaliplatin was added to 5-FU/FA; a further increase in efficacy was shown when bevacizumab, an antibody to vascular endothelial growth factor, was added to chemotherapy.	Irinotecan	122-132	vascular endothelial growth factor A	Homo sapiens	244-278
16132345-17	2005	CPT-11 and SN-38 are substrates for MRP4.	Irinotecan	0-6	ATP binding cassette subfamily C member 4	Homo sapiens	36-40
16132345-17	2005	CPT-11 and SN-38 are substrates for MRP4.	Irinotecan	11-16	ATP binding cassette subfamily C member 4	Homo sapiens	36-40
16132345-12	2005	In addition, the accumulation of CPT-11 and SN-38 over 120 min in MRP4/HepG2 cells was significantly reduced compared to V/HepG2 cells, whereas the addition of celecoxib, MK571, or BSO significantly increased their accumulation in MRP4/HepG2 cells.	Irinotecan	44-49	ATP binding cassette subfamily C member 4	Homo sapiens	231-235
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	126-132	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	16-48
16132345-16	2005	CONCLUSIONS: Human MRP4 rendered significant resistance to cyclophosphamide, CPT, CPT-11, SN-38, rubitecan, and 10-OH-CPT.	Irinotecan	82-88	ATP binding cassette subfamily C member 4	Homo sapiens	19-23
16132345-16	2005	CONCLUSIONS: Human MRP4 rendered significant resistance to cyclophosphamide, CPT, CPT-11, SN-38, rubitecan, and 10-OH-CPT.	Irinotecan	90-95	ATP binding cassette subfamily C member 4	Homo sapiens	19-23
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	126-132	ATP binding cassette subfamily C member 1	Homo sapiens	50-54
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	126-132	ATP binding cassette subfamily C member 2	Homo sapiens	60-64
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	134-144	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	134-144	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	16-48
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	134-144	ATP binding cassette subfamily C member 1	Homo sapiens	50-54
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	134-144	ATP binding cassette subfamily C member 2	Homo sapiens	60-64
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	147-152	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	147-152	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	16-48
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	147-152	ATP binding cassette subfamily C member 1	Homo sapiens	50-54
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	147-152	ATP binding cassette subfamily C member 2	Homo sapiens	60-64
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	179-185	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	179-185	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	16-48
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	179-185	ATP binding cassette subfamily C member 1	Homo sapiens	50-54
16132345-3	2005	P-glycoprotein, breast cancer resistance protein, MRP1, and MRP2 have been implicated in resistance to various CPTs including CPT-11 (irinotecan), SN-38 (the active metabolite of CPT-11), and topotecan.	Irinotecan	179-185	ATP binding cassette subfamily C member 2	Homo sapiens	60-64
16098482-0	2005	MRP1 mutated in the L0 region transports SN-38 but not leukotriene C4 or estradiol-17 (beta-D-glucuronate).	Irinotecan	41-46	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
16315940-5	2005	A weekly CPT-11 infusion therapy was effective to the recurrent skin and soft tissue lesions (CR and PR), and the tumor markers (CEA and CA15-3) markedly declined.	Irinotecan	9-15	mucin 1, cell surface associated	Homo sapiens	137-143
16204068-3	2005	In contrast, irinotecan (CPT-11) and tomudex sensitized p53 WT, mutant, and null cells to Fas-mediated cell death.	Irinotecan	13-23	tumor protein p53	Homo sapiens	56-59
16204068-3	2005	In contrast, irinotecan (CPT-11) and tomudex sensitized p53 WT, mutant, and null cells to Fas-mediated cell death.	Irinotecan	25-31	tumor protein p53	Homo sapiens	56-59
16204068-4	2005	Furthermore, CPT-11 and tomudex, but not 5-FU or oxaliplatin, up-regulated Fas cell surface expression in a p53-independent manner.	Irinotecan	13-19	tumor protein p53	Homo sapiens	108-111
16204068-5	2005	In addition, increased Fas cell surface expression in p53 mutant and null cell lines in response to CPT-11 and tomudex was accompanied by only a slight increase in total Fas mRNA and protein expression, suggesting that these agents trigger p53-independent trafficking of Fas to the plasma membrane.	Irinotecan	100-106	tumor protein p53	Homo sapiens	54-57
16204068-6	2005	Treatment with CPT-11 or tomudex induced STAT1 phosphorylation (Ser727) in the p53-null HCT116 cell line but not the p53 WT cell line.	Irinotecan	15-21	signal transducer and activator of transcription 1	Homo sapiens	41-46
16204068-6	2005	Treatment with CPT-11 or tomudex induced STAT1 phosphorylation (Ser727) in the p53-null HCT116 cell line but not the p53 WT cell line.	Irinotecan	15-21	tumor protein p53	Homo sapiens	79-82
16204068-7	2005	Furthermore, STAT1-targeted small interfering RNA (siRNA) inhibited up-regulation of Fas cell surface expression in response to CPT-11 and tomudex in these cells.	Irinotecan	128-134	signal transducer and activator of transcription 1	Homo sapiens	13-18
16204068-9	2005	This suggests that STAT1 regulates expression of gene(s) involved in cell surface trafficking of Fas in response to CPT-11 or tomudex.	Irinotecan	116-122	signal transducer and activator of transcription 1	Homo sapiens	19-24
16204068-10	2005	We conclude that CPT-11 and tomudex may be more effective than 5-FU and oxaliplatin in the treatment of p53 mutant colorectal cancer tumors by sensitizing them to Fas-mediated apoptosis in a STAT1-dependent manner.	Irinotecan	17-23	tumor protein p53	Homo sapiens	104-107
16204068-10	2005	We conclude that CPT-11 and tomudex may be more effective than 5-FU and oxaliplatin in the treatment of p53 mutant colorectal cancer tumors by sensitizing them to Fas-mediated apoptosis in a STAT1-dependent manner.	Irinotecan	17-23	signal transducer and activator of transcription 1	Homo sapiens	191-196
16203781-1	2005	PURPOSE: Irinotecan (CPT11) is a prodrug activated in humans mainly by carboxylesterase 2 (CES2) generating the SN38 metabolite responsible for the drug efficacy and toxicity.	Irinotecan	9-19	carboxylesterase 2	Homo sapiens	71-89
16203781-1	2005	PURPOSE: Irinotecan (CPT11) is a prodrug activated in humans mainly by carboxylesterase 2 (CES2) generating the SN38 metabolite responsible for the drug efficacy and toxicity.	Irinotecan	9-19	carboxylesterase 2	Homo sapiens	91-95
16203781-1	2005	PURPOSE: Irinotecan (CPT11) is a prodrug activated in humans mainly by carboxylesterase 2 (CES2) generating the SN38 metabolite responsible for the drug efficacy and toxicity.	Irinotecan	21-26	carboxylesterase 2	Homo sapiens	71-89
16203781-1	2005	PURPOSE: Irinotecan (CPT11) is a prodrug activated in humans mainly by carboxylesterase 2 (CES2) generating the SN38 metabolite responsible for the drug efficacy and toxicity.	Irinotecan	21-26	carboxylesterase 2	Homo sapiens	91-95
16251801-3	2005	By treating fresh human colonic explants with 5-Fluorouracil (200 microg/ml), CPT-11 (100 microg/ml) and/or TRAIL (100 ng/ml) we readily detected a signal in situ using FITC-VAD-FMK at different time points, whereas labeling of colonic explants with EGFP-conjugated Annexin V proved less specific.	Irinotecan	78-84	annexin A5	Homo sapiens	266-275
16166450-3	2005	A recent study found that coadministration of irinotecan and ketoconazole led to a significant increase in the formation of SN-38 (7-ethyl-10-hydroxycamptothecine), an UGT1A substrate.	Irinotecan	46-56	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	168-173
16166450-3	2005	A recent study found that coadministration of irinotecan and ketoconazole led to a significant increase in the formation of SN-38 (7-ethyl-10-hydroxycamptothecine), an UGT1A substrate.	Irinotecan	124-129	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	168-173
16166450-3	2005	A recent study found that coadministration of irinotecan and ketoconazole led to a significant increase in the formation of SN-38 (7-ethyl-10-hydroxycamptothecine), an UGT1A substrate.	Irinotecan	131-162	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	168-173
16166450-5	2005	EXPERIMENTAL DESIGN: SN-38 glucuronidation activities were determined by measuring the rate of SN-38 glucuronide (SN-38G) formation using pooled human liver microsomes and cDNA-expressed UGT1A isoforms (1A1, 1A7 and 1A9) in the presence of ketoconazole.	Irinotecan	21-26	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	187-192
16166450-11	2005	CONCLUSIONS: These results show that ketoconazole is a potent UGT1A1 inhibitor, which seems the basis for increased exposure to SN-38 when coadministered with irinotecan.	Irinotecan	128-133	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
16166450-11	2005	CONCLUSIONS: These results show that ketoconazole is a potent UGT1A1 inhibitor, which seems the basis for increased exposure to SN-38 when coadministered with irinotecan.	Irinotecan	159-169	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
16144935-10	2005	In conclusion, low SMAD4 tumor levels identified a subset of patients with poor prognosis following surgery and 5-FU-based adjuvant therapy; therefore, these patients could be good candidates to receive combined treatment with additional chemotherapeutic agents such as CPT-11 and/or oxaliplatin.	Irinotecan	270-276	SMAD family member 4	Homo sapiens	19-24
15828025-5	2005	The main aim of this review is to provide an overview of the known polymorphisms present in the genes which codify for factors (thymidylate synthase dihydropyrimidine dehydrogenase, uridine diphosphate (UDP)-glucuronosyl-transferase 1A1, enzymes implicated in DNA repair) involved in the action mechanisms of the drugs now utilized in chemotherapeutic treatment of colorectal carcinoma, such as fluoropyrimidines, irinotecan, and platinum agents.	Irinotecan	414-424	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	182-236
16184937-0	2005	[A case of colon cancer with liver and lung metastases-efficacy of CPT-11/5-FU/l-LV (IFL) as part of ambulatory treatment].	Irinotecan	67-73	interferon alpha 1	Homo sapiens	85-88
16101140-2	2005	PATIENTS AND METHODS: The impact of gemcitabine, irinotecan and oxaliplatin + 5-FU upon the serum markers vascular endothelial growth factor (VEGF) (pro-angiogenic) and IFN-gamma-inducible protein (IP)-10 (anti-angiogenic) was evaluated by ELISA in locally advanced and/or metastatic cancer versus clinical efficacy and survival.	Irinotecan	49-59	vascular endothelial growth factor A	Homo sapiens	106-140
16187025-4	2005	Irinotecan is metabolized by carboxylesterase to form an active SN-38, which is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) to yield its beta-glucuronide.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	117-144
16187025-4	2005	Irinotecan is metabolized by carboxylesterase to form an active SN-38, which is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) to yield its beta-glucuronide.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	146-149
16187025-4	2005	Irinotecan is metabolized by carboxylesterase to form an active SN-38, which is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) to yield its beta-glucuronide.	Irinotecan	64-69	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	117-144
16187025-4	2005	Irinotecan is metabolized by carboxylesterase to form an active SN-38, which is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) to yield its beta-glucuronide.	Irinotecan	64-69	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	146-149
16187025-5	2005	The polymorphic UGT isoenzyme, UGT1A1 has genetic variants which decrease in SN-38 glucuronidating capacity and could help predict irinotecan-associated toxicity.	Irinotecan	77-82	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	16-19
16187025-5	2005	The polymorphic UGT isoenzyme, UGT1A1 has genetic variants which decrease in SN-38 glucuronidating capacity and could help predict irinotecan-associated toxicity.	Irinotecan	77-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
16187025-5	2005	The polymorphic UGT isoenzyme, UGT1A1 has genetic variants which decrease in SN-38 glucuronidating capacity and could help predict irinotecan-associated toxicity.	Irinotecan	131-141	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	16-19
16187025-5	2005	The polymorphic UGT isoenzyme, UGT1A1 has genetic variants which decrease in SN-38 glucuronidating capacity and could help predict irinotecan-associated toxicity.	Irinotecan	131-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
16187025-7	2005	We suggest that irinotecan offers an effective treatment option for children with recurrent brain stem glioma and other genetic variants except UGT1A1 may be a risk factor for irinotecan-induced toxicity.	Irinotecan	176-186	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	144-150
16010439-0	2005	Increased anticancer activity of the thymidylate synthase inhibitor BGC9331 combined with the topoisomerase I inhibitor SN-38 in human colorectal and breast cancer cells: induction of apoptosis and ROCK cleavage through caspase-3-dependent and -independent mechanisms.	Irinotecan	120-125	caspase 3	Homo sapiens	220-229
16077970-2	2005	We examined TS expression in tumours from 86 patients with advanced colorectal cancer who received one of two chemotherapy regimes (either irinotecan alone or irinotecan and 5-flurouracil with folinic acid).	Irinotecan	139-149	thymidylate synthetase	Homo sapiens	12-14
16077970-2	2005	We examined TS expression in tumours from 86 patients with advanced colorectal cancer who received one of two chemotherapy regimes (either irinotecan alone or irinotecan and 5-flurouracil with folinic acid).	Irinotecan	159-169	thymidylate synthetase	Homo sapiens	12-14
16077970-6	2005	A significant association was found between tumour TS expression and response to treatment with 5-FU plus FA with irinotecan (p=0.05).	Irinotecan	114-124	thymidylate synthetase	Homo sapiens	51-53
16108826-1	2005	Breast cancer resistance protein (BCRP) is a half-molecule ATP-binding cassette transporter that forms a functional homodimer and pumps out various anticancer agents, such as 7-ethyl-10-hydroxycamptothecin, topotecan, mitoxantrone and flavopiridol, from cells.	Irinotecan	175-205	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
16108826-1	2005	Breast cancer resistance protein (BCRP) is a half-molecule ATP-binding cassette transporter that forms a functional homodimer and pumps out various anticancer agents, such as 7-ethyl-10-hydroxycamptothecin, topotecan, mitoxantrone and flavopiridol, from cells.	Irinotecan	175-205	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
16108826-1	2005	Breast cancer resistance protein (BCRP) is a half-molecule ATP-binding cassette transporter that forms a functional homodimer and pumps out various anticancer agents, such as 7-ethyl-10-hydroxycamptothecin, topotecan, mitoxantrone and flavopiridol, from cells.	Irinotecan	175-205	ATP binding cassette subfamily A member 4	Homo sapiens	59-91
16103093-3	2005	The combination IFN-beta and irinotecan (CPT-11) cooperatively inhibits cell growth and IRF-5 synergizes with it to further promote apoptosis.	Irinotecan	29-39	interferon regulatory factor 5	Homo sapiens	88-93
16103093-3	2005	The combination IFN-beta and irinotecan (CPT-11) cooperatively inhibits cell growth and IRF-5 synergizes with it to further promote apoptosis.	Irinotecan	41-47	interferon beta 1	Homo sapiens	16-24
15838659-3	2005	In 4-day cytotoxicity assays with mitoxantrone, topotecan, SN-38 or diflomotecan, cells transfected with wild-type R482 ABCG2 showed IC50 values up to 1.2-fold to 5-fold higher than cells expressing comparable levels of Q141K ABCG2, suggesting that the Q141K SNP affects drug transport.	Irinotecan	59-64	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	120-125
16010439-5	2005	Treatment of HT-29 cells with either BGC9331 or SN-38 increased caspase-3 activity and the percentage of apoptotic cells from 3 to 13%.	Irinotecan	48-53	caspase 3	Homo sapiens	64-73
16022921-1	2005	Irinotecan is a topoisomerase I inhibitor that is highly active against small cell lung cancer (SCLC).	Irinotecan	0-10	SCLC1	Homo sapiens	96-100
16022921-11	2005	This irinotecan and etoposide regimen is active against ED-SCLC with relatively mild toxicity.	Irinotecan	5-15	SCLC1	Homo sapiens	59-63
15944780-4	2005	The tumor weights with MTD of CPM or CPT-11 in combination with anti-IL-6 antibody treatment, which decreases serum IL-6 level and improves cachexia status, were significantly smaller than those in the MTD treatment-alone group with clone 20, but not with clone 5.	Irinotecan	37-43	interleukin 6	Mus musculus	116-120
15833930-4	2005	The stability of SN-38 lactone and carboxylate in incubation mixtures of microsomes and UDP-glucuronosyltransferase (UGT) isoforms was used to determine optimal incubation times.	Irinotecan	17-30	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	88-115
16104527-0	2005	[Assessment of immunotoxicity of irinotecan determined by the novel method, by which productivity of TNF-alpha from whole blood is stimulated by lipopolysaccharide].	Irinotecan	33-43	tumor necrosis factor	Homo sapiens	101-110
15772291-4	2005	Previous studies have indicated that CPT-11 can inhibit acetylcholinesterase (AChE), and here, we provide a detailed analysis of the inhibition of AChE by CPT-11 and by structural analogs.	Irinotecan	37-43	acetylcholinesterase (Cartwright blood group)	Homo sapiens	78-82
15846114-6	2005	In contrast, doxorubicin and paclitaxel caused no up-regulation in vitro, while irinotecan caused inhibition of COX-2 (2.7-fold decrease, p&lt;0.01).	Irinotecan	80-90	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	112-117
15984515-2	2005	The standard chemotherapy for extensive SCLC in Japan is the combination of irinotecan and cisplatin.	Irinotecan	76-86	SCLC1	Homo sapiens	40-44
15902309-3	2005	We were able to achieve restoration of their radiosensitivity and sensitivity to 5-fluorouracil and irinotecan by reexpression of SPARC in tumor xenografts.	Irinotecan	100-110	secreted protein acidic and cysteine rich	Homo sapiens	130-135
15723219-2	2005	In the experiments described here using AGS gastric cancer cells, SN38 (the active metabolite of CPT-11) induced tyrosine phosphorylation of EGFR within 5 min, and this was followed by the induction of transcripts and/or proteins of heparin-binding EGF-like growth factor, amphiregulin, transforming growth factor-alpha, and interlukin-8 (IL-8).	Irinotecan	97-103	epidermal growth factor receptor	Homo sapiens	141-145
15930350-8	2005	Patients with UDP-glucuronosyltransferase (UGT1A1; TA)6/6 promoter genotype had a lower ratio of free to glucuronide form of SN-38 than in patients with &gt;/=1 (TA)7 allele.	Irinotecan	125-130	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
15956246-7	2005	Many gene expression changes observed following in vitro SN-38 exposure were also seen following in vivo administration of 10 or 15 mg/m(2) CPT-11; notably, proapoptotic changes included reduced transcription of survivin pathway-associated genes and increased transcription of death receptor 5.	Irinotecan	57-62	TNF receptor superfamily member 10b	Homo sapiens	277-293
15956246-7	2005	Many gene expression changes observed following in vitro SN-38 exposure were also seen following in vivo administration of 10 or 15 mg/m(2) CPT-11; notably, proapoptotic changes included reduced transcription of survivin pathway-associated genes and increased transcription of death receptor 5.	Irinotecan	140-146	TNF receptor superfamily member 10b	Homo sapiens	277-293
15772291-4	2005	Previous studies have indicated that CPT-11 can inhibit acetylcholinesterase (AChE), and here, we provide a detailed analysis of the inhibition of AChE by CPT-11 and by structural analogs.	Irinotecan	37-43	acetylcholinesterase (Cartwright blood group)	Homo sapiens	147-151
15772291-4	2005	Previous studies have indicated that CPT-11 can inhibit acetylcholinesterase (AChE), and here, we provide a detailed analysis of the inhibition of AChE by CPT-11 and by structural analogs.	Irinotecan	155-161	acetylcholinesterase (Cartwright blood group)	Homo sapiens	147-151
15772291-5	2005	These studies demonstrate that the terminal dipiperidino moiety in CPT-11 plays a major role in enzyme inhibition, and this has been confirmed by X-ray crystallographic studies of a complex of the drug with Torpedo californica AChE.	Irinotecan	67-73	acetylcholinesterase (Cartwright blood group)	Homo sapiens	227-231
15772291-7	2005	The 3D structure of the CPT-11/AChE complex also permits modeling of CPT-11 complexed with mammalian butyrylcholinesterase and carboxylesterase, both of which are known to hydrolyze the drug to the active metabolite.	Irinotecan	24-30	acetylcholinesterase (Cartwright blood group)	Homo sapiens	31-35
15772291-7	2005	The 3D structure of the CPT-11/AChE complex also permits modeling of CPT-11 complexed with mammalian butyrylcholinesterase and carboxylesterase, both of which are known to hydrolyze the drug to the active metabolite.	Irinotecan	69-75	acetylcholinesterase (Cartwright blood group)	Homo sapiens	31-35
15772291-8	2005	Overall, the results presented here clarify the mechanism of AChE inhibition by CPT-11 and detail the interaction of the drug with the protein.	Irinotecan	80-86	acetylcholinesterase (Cartwright blood group)	Homo sapiens	61-65
15948034-1	2005	CPT-11 is a DNA topoisomerase I inhibitor for the therapy of colorectal cancer, whereas St. John"s Wort (Hypericum perforatum, SJW) is a widely used herbal anti-depressant.	Irinotecan	0-6	DNA topoisomerase I	Rattus norvegicus	12-31
15867226-3	2005	Drg1 expression is also associated with resistance to irinotecan therapy in preclinical colorectal cancer models.	Irinotecan	54-64	developmentally regulated GTP binding protein 1	Homo sapiens	0-4
15886469-5	2005	However, in HT-29 cells, the CPT-11/5-FU combination enhanced Mn-SOD activity when compared to cells treated with CPT-11 alone.	Irinotecan	29-35	superoxide dismutase 2	Homo sapiens	62-68
15886469-5	2005	However, in HT-29 cells, the CPT-11/5-FU combination enhanced Mn-SOD activity when compared to cells treated with CPT-11 alone.	Irinotecan	114-120	superoxide dismutase 2	Homo sapiens	62-68
15886469-7	2005	CONCLUSION: Treatment with the CPT-11/5-FU combination may promote in HT-29 cell apoptosis by enhancing Mn-SOD activity.	Irinotecan	31-37	superoxide dismutase 2	Homo sapiens	104-110
15867367-7	2005	AEE788 alone or in combination with CPT-11 inhibited pEGFR, pVEGFR, and phosphorylated Akt expression on tumor-associated endothelial cells as well as on tumor cells.	Irinotecan	36-42	thymoma viral proto-oncogene 1	Mus musculus	87-90
15867226-7	2005	We correlated expression of Drg1 to numerous clinical and tumor related variables and to patient outcomes, including a subset of patients who recurred and received irinotecan-based therapy.	Irinotecan	164-174	developmentally regulated GTP binding protein 1	Homo sapiens	28-32
15867226-10	2005	High Drg1 expression suggested irinotecan resistance (P = 0.07).	Irinotecan	31-41	developmentally regulated GTP binding protein 1	Homo sapiens	5-9
15867226-12	2005	High Drg1 may also be associated with relative resistance to irinotecan.	Irinotecan	61-71	developmentally regulated GTP binding protein 1	Homo sapiens	5-9
15867226-5	2005	We performed this study to evaluate the role of Drg1 in a large cohort of patients with metastatic colorectal cancer who were irinotecan naive.	Irinotecan	126-136	developmentally regulated GTP binding protein 1	Homo sapiens	48-52
15716465-10	2005	We identified a novel reduced-function TATA box SNP of the UGT1A7 gene that catalyzes irinotecan metabolite detoxification.	Irinotecan	86-96	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	59-65
15809721-0	2005	Blocking of PI3K/Akt pathway enhances apoptosis induced by SN-38, an active form of CPT-11, in human hepatoma cells.	Irinotecan	59-64	AKT serine/threonine kinase 1	Homo sapiens	17-20
15809721-0	2005	Blocking of PI3K/Akt pathway enhances apoptosis induced by SN-38, an active form of CPT-11, in human hepatoma cells.	Irinotecan	84-90	AKT serine/threonine kinase 1	Homo sapiens	17-20
15809721-3	2005	CPT-11, a derivative of camptothecin, works as type-I DNA topoisomerase inhibitor and showed a major objective response rate in patients with metastatic colorectal cancer.	Irinotecan	0-6	DNA topoisomerase I	Homo sapiens	47-71
15809721-4	2005	In this study, the mechanism underlying chemo-resistance to SN-38, an active form of CPT-11, in HCC was investigated in relation to anti-apoptotic pathways NF-kappaB and PI3K/Akt.	Irinotecan	60-65	nuclear factor kappa B subunit 1	Homo sapiens	156-165
15809721-4	2005	In this study, the mechanism underlying chemo-resistance to SN-38, an active form of CPT-11, in HCC was investigated in relation to anti-apoptotic pathways NF-kappaB and PI3K/Akt.	Irinotecan	60-65	AKT serine/threonine kinase 1	Homo sapiens	175-178
15809721-4	2005	In this study, the mechanism underlying chemo-resistance to SN-38, an active form of CPT-11, in HCC was investigated in relation to anti-apoptotic pathways NF-kappaB and PI3K/Akt.	Irinotecan	85-91	nuclear factor kappa B subunit 1	Homo sapiens	156-165
15809721-4	2005	In this study, the mechanism underlying chemo-resistance to SN-38, an active form of CPT-11, in HCC was investigated in relation to anti-apoptotic pathways NF-kappaB and PI3K/Akt.	Irinotecan	85-91	AKT serine/threonine kinase 1	Homo sapiens	175-178
15809721-6	2005	NF-kappaB was constitutively activated in Hep3B, and SN-38 further enhanced the nuclear translocation of NF-kappaB.	Irinotecan	53-58	nuclear factor kappa B subunit 1	Homo sapiens	105-114
15809721-8	2005	On the other hand, SN-38 phosphorylated Akt and pretreatment with PI3K inhibitors increased SN-38-induced apoptosis, indicating that resistance to SN-38 in Hep3B occurs partly through the PI3K/Akt not the NF-kappaB pathway.	Irinotecan	19-24	AKT serine/threonine kinase 1	Homo sapiens	40-43
15809721-8	2005	On the other hand, SN-38 phosphorylated Akt and pretreatment with PI3K inhibitors increased SN-38-induced apoptosis, indicating that resistance to SN-38 in Hep3B occurs partly through the PI3K/Akt not the NF-kappaB pathway.	Irinotecan	92-97	AKT serine/threonine kinase 1	Homo sapiens	193-196
15809721-8	2005	On the other hand, SN-38 phosphorylated Akt and pretreatment with PI3K inhibitors increased SN-38-induced apoptosis, indicating that resistance to SN-38 in Hep3B occurs partly through the PI3K/Akt not the NF-kappaB pathway.	Irinotecan	92-97	nuclear factor kappa B subunit 1	Homo sapiens	205-214
15809721-8	2005	On the other hand, SN-38 phosphorylated Akt and pretreatment with PI3K inhibitors increased SN-38-induced apoptosis, indicating that resistance to SN-38 in Hep3B occurs partly through the PI3K/Akt not the NF-kappaB pathway.	Irinotecan	92-97	AKT serine/threonine kinase 1	Homo sapiens	193-196
15809721-8	2005	On the other hand, SN-38 phosphorylated Akt and pretreatment with PI3K inhibitors increased SN-38-induced apoptosis, indicating that resistance to SN-38 in Hep3B occurs partly through the PI3K/Akt not the NF-kappaB pathway.	Irinotecan	92-97	nuclear factor kappa B subunit 1	Homo sapiens	205-214
15858133-3	2005	A heterozygous G &gt; A transition at the 5" splicing donor consensus sequence in intron 14 leading to exon 14 skipping (IVS14+1 G &gt; A, DPYD*2A) with partial loss of enzyme activity may be partly responsible for 5FU induced toxicity, whereas irinotecan associated toxicity may in part be explained by an aberrant UGT1A1 promoter (TA)(n) genotype underlying Gilbert"s syndrome with reduced liver glucuronidation activity.	Irinotecan	245-255	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	316-322
15716465-2	2005	UGT1A1*28 is a functional UGT promoter polymorphism associated with Gilbert"s disease and severe irinotecan toxicity, which also occurs in the absence of UGT1A1*28.	Irinotecan	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
15716465-2	2005	UGT1A1*28 is a functional UGT promoter polymorphism associated with Gilbert"s disease and severe irinotecan toxicity, which also occurs in the absence of UGT1A1*28.	Irinotecan	97-107	beta-1,3-glucuronyltransferase 2	Homo sapiens	0-3
15716465-3	2005	The aim of this study was to identify and characterize UGT promoter variants relevant for irinotecan detoxification.	Irinotecan	90-100	beta-1,3-glucuronyltransferase 2	Homo sapiens	55-58
15716465-11	2005	Its association with variants of the UGT1A1 promoter and UGT1A7 gene may influence irinotecan metabolism.	Irinotecan	83-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
15716465-11	2005	Its association with variants of the UGT1A1 promoter and UGT1A7 gene may influence irinotecan metabolism.	Irinotecan	83-93	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	57-63
15864130-2	2005	SN-38, the active metabolite of the anticancer agent irinotecan, is metabolized by both UGT1A1 and UGT1A9.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
15864130-2	2005	SN-38, the active metabolite of the anticancer agent irinotecan, is metabolized by both UGT1A1 and UGT1A9.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	99-105
15864130-2	2005	SN-38, the active metabolite of the anticancer agent irinotecan, is metabolized by both UGT1A1 and UGT1A9.	Irinotecan	53-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
15864130-2	2005	SN-38, the active metabolite of the anticancer agent irinotecan, is metabolized by both UGT1A1 and UGT1A9.	Irinotecan	53-63	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	99-105
15864130-9	2005	Common UGT1A9-UGT1A1 diplotypes were defined, and a difference was observed across the SN-38 glucuronidation rates in Caucasian livers stratified by diplotypes.	Irinotecan	87-92	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	7-13
15864130-11	2005	If the functional effect of these haplotypes can be confirmed, this haplotypic information would be applicable to the correct design of prospective clinical studies of irinotecan, as well as of other drugs primarily metabolized by both UGT1A1 and UGT1A9.	Irinotecan	168-178	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	247-253
15699047-5	2005	Colony forming assays demonstrated that down-regulation of ATR or Chk1 sensitized cells to SN-38 and camptothecin.	Irinotecan	91-96	ATR serine/threonine kinase	Homo sapiens	59-62
15897249-10	2005	In conclusion, the significant increase in the cure rate after methylselenocysteine/CPT-11 could be related to increased drug delivery into both tumors (CES1), reduced resistance to SN-38 (ABCC1 and DRG1) in FaDu, and induced Fas ligand apoptosis (TNFSF6) in A253.	Irinotecan	84-90	carboxylesterase 1	Homo sapiens	153-157
15897249-10	2005	In conclusion, the significant increase in the cure rate after methylselenocysteine/CPT-11 could be related to increased drug delivery into both tumors (CES1), reduced resistance to SN-38 (ABCC1 and DRG1) in FaDu, and induced Fas ligand apoptosis (TNFSF6) in A253.	Irinotecan	84-90	ATP binding cassette subfamily C member 1	Homo sapiens	189-194
15897249-10	2005	In conclusion, the significant increase in the cure rate after methylselenocysteine/CPT-11 could be related to increased drug delivery into both tumors (CES1), reduced resistance to SN-38 (ABCC1 and DRG1) in FaDu, and induced Fas ligand apoptosis (TNFSF6) in A253.	Irinotecan	84-90	developmentally regulated GTP binding protein 1	Homo sapiens	199-203
15897249-10	2005	In conclusion, the significant increase in the cure rate after methylselenocysteine/CPT-11 could be related to increased drug delivery into both tumors (CES1), reduced resistance to SN-38 (ABCC1 and DRG1) in FaDu, and induced Fas ligand apoptosis (TNFSF6) in A253.	Irinotecan	84-90	Fas ligand	Homo sapiens	226-236
15897249-10	2005	In conclusion, the significant increase in the cure rate after methylselenocysteine/CPT-11 could be related to increased drug delivery into both tumors (CES1), reduced resistance to SN-38 (ABCC1 and DRG1) in FaDu, and induced Fas ligand apoptosis (TNFSF6) in A253.	Irinotecan	84-90	Fas ligand	Homo sapiens	248-254
15897249-10	2005	In conclusion, the significant increase in the cure rate after methylselenocysteine/CPT-11 could be related to increased drug delivery into both tumors (CES1), reduced resistance to SN-38 (ABCC1 and DRG1) in FaDu, and induced Fas ligand apoptosis (TNFSF6) in A253.	Irinotecan	182-187	ATP binding cassette subfamily C member 1	Homo sapiens	189-194
15897249-7	2005	After methylselenocysteine treatment, the intratumor area under the concentration-time curve of SN-38 increased to a significantly higher level in A253 than in FaDu and was associated with increased expression of CES1 in both tumors.	Irinotecan	96-101	carboxylesterase 1	Homo sapiens	213-217
15897249-8	2005	Methylselenocysteine/CPT-11 treatment, compared with CPT-11 alone, resulted in a significant decrease in levels of ABCC1 and DRG1 in FaDu tumors and an increase in levels of CYP3A5 and TNFSF6 in A253 tumors.	Irinotecan	21-27	ATP binding cassette subfamily C member 1	Homo sapiens	115-120
15897249-8	2005	Methylselenocysteine/CPT-11 treatment, compared with CPT-11 alone, resulted in a significant decrease in levels of ABCC1 and DRG1 in FaDu tumors and an increase in levels of CYP3A5 and TNFSF6 in A253 tumors.	Irinotecan	21-27	developmentally regulated GTP binding protein 1	Homo sapiens	125-129
15897249-8	2005	Methylselenocysteine/CPT-11 treatment, compared with CPT-11 alone, resulted in a significant decrease in levels of ABCC1 and DRG1 in FaDu tumors and an increase in levels of CYP3A5 and TNFSF6 in A253 tumors.	Irinotecan	21-27	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	174-180
15897249-8	2005	Methylselenocysteine/CPT-11 treatment, compared with CPT-11 alone, resulted in a significant decrease in levels of ABCC1 and DRG1 in FaDu tumors and an increase in levels of CYP3A5 and TNFSF6 in A253 tumors.	Irinotecan	21-27	Fas ligand	Homo sapiens	185-191
15996331-0	2005	[Prognostic value of thymidylate synthase, topoisomerase-1 and Ki-67 in advanced colorectal cancer patients on irinotecan and fluorouracil treatment].	Irinotecan	111-121	thymidylate synthetase	Homo sapiens	21-41
15846298-7	2005	Combination of HGS-ETR1 with chemotherapeutic agents (topotecan, 5-fluorouracil, and irinotecan) in three independent colon cancer xenograft models resulted in an enhanced antitumour efficacy compared to either agent alone.	Irinotecan	85-95	CUGBP Elav-like family member 3	Homo sapiens	19-23
15699047-5	2005	Colony forming assays demonstrated that down-regulation of ATR or Chk1 sensitized cells to SN-38 and camptothecin.	Irinotecan	91-96	checkpoint kinase 1	Homo sapiens	66-70
15699047-6	2005	In contrast, ATM and Chk2 had minimal effect of sensitivity to SN-38 or camptothecin.	Irinotecan	63-68	checkpoint kinase 2	Homo sapiens	21-25
15699047-7	2005	Additional experiments demonstrated that the Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin, which down-regulates Chk1, also sensitized a variety of human carcinoma cell lines to SN-38.	Irinotecan	187-192	heat shock protein 90 alpha family class A member 1	Homo sapiens	45-50
15723263-2	2005	The findings reported here demonstrate that SN38 (the active metabolite of CPT-11) induces the tyrosine phosphorylation of EGFR within 5 min, followed by the induction of transcripts and/or proteins of the heparin-binding EGF-like growth factor, amphiregulin, transforming growth factor-alpha, and interlukin-8 (IL-8) in AGS gastric cancer cells.	Irinotecan	44-48	epidermal growth factor receptor	Homo sapiens	123-127
15801936-3	2005	All patients were genotyped for allelic variants in genes encoding drug metabolizing enzymes (CYP3A4, CYP3A5, UGT1A1) and drug transporters (ABCB1, ABCC2 and ABCG2) that are involved in irinotecan disposition.	Irinotecan	186-196	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
15801936-3	2005	All patients were genotyped for allelic variants in genes encoding drug metabolizing enzymes (CYP3A4, CYP3A5, UGT1A1) and drug transporters (ABCB1, ABCC2 and ABCG2) that are involved in irinotecan disposition.	Irinotecan	186-196	ATP binding cassette subfamily B member 1	Homo sapiens	141-146
15801936-3	2005	All patients were genotyped for allelic variants in genes encoding drug metabolizing enzymes (CYP3A4, CYP3A5, UGT1A1) and drug transporters (ABCB1, ABCC2 and ABCG2) that are involved in irinotecan disposition.	Irinotecan	186-196	ATP binding cassette subfamily C member 2	Homo sapiens	148-153
15801936-3	2005	All patients were genotyped for allelic variants in genes encoding drug metabolizing enzymes (CYP3A4, CYP3A5, UGT1A1) and drug transporters (ABCB1, ABCC2 and ABCG2) that are involved in irinotecan disposition.	Irinotecan	186-196	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	158-163
15723263-2	2005	The findings reported here demonstrate that SN38 (the active metabolite of CPT-11) induces the tyrosine phosphorylation of EGFR within 5 min, followed by the induction of transcripts and/or proteins of the heparin-binding EGF-like growth factor, amphiregulin, transforming growth factor-alpha, and interlukin-8 (IL-8) in AGS gastric cancer cells.	Irinotecan	75-81	epidermal growth factor receptor	Homo sapiens	123-127
15801936-6	2005	The C(max) of irinotecan was significantly lower in patients carrying the CC genotype at exon 26 of the ABCB1 gene compared with those harbouring at least one variant allele (P = 0.047).	Irinotecan	14-24	ATP binding cassette subfamily B member 1	Homo sapiens	104-109
15801936-7	2005	Patients harbouring the wild type ABCG2 CTCA genotype were associated with significantly higher values for relative extent of conversion (REC) of irinotecan to SN-38 compared with patients carrying at least one deletion CTCA allele (P = 0.019).	Irinotecan	146-156	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-39
15855893-5	2005	Chimeric monoclonal antibody therapy directed at the epidermal growth factor receptor was associated with radiographic responses in a significant minority of patients with irinotecan-refractory colon cancer in a randomized phase II study of patients with irinotecan-refractory disease.	Irinotecan	172-182	epidermal growth factor receptor	Homo sapiens	53-85
15801936-7	2005	Patients harbouring the wild type ABCG2 CTCA genotype were associated with significantly higher values for relative extent of conversion (REC) of irinotecan to SN-38 compared with patients carrying at least one deletion CTCA allele (P = 0.019).	Irinotecan	160-165	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-39
15801936-8	2005	CONCLUSIONS: The present exploratory study shows that genetic polymorphisms in drug transporter genes, particularly in ABCB1 and ABCG2 genes, may be important in influencing the pharmacokinetics of irinotecan and its metabolites.	Irinotecan	198-208	ATP binding cassette subfamily B member 1	Homo sapiens	119-124
15801936-8	2005	CONCLUSIONS: The present exploratory study shows that genetic polymorphisms in drug transporter genes, particularly in ABCB1 and ABCG2 genes, may be important in influencing the pharmacokinetics of irinotecan and its metabolites.	Irinotecan	198-208	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	129-134
15801936-9	2005	The predictive value of the identified allelic variants in the ABCG2 and ABCB1 genes on irinotecan disposition should be further investigated in a larger patient population as well as in other ethnic populations.	Irinotecan	88-98	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	63-68
15801936-9	2005	The predictive value of the identified allelic variants in the ABCG2 and ABCB1 genes on irinotecan disposition should be further investigated in a larger patient population as well as in other ethnic populations.	Irinotecan	88-98	ATP binding cassette subfamily B member 1	Homo sapiens	73-78
15855893-5	2005	Chimeric monoclonal antibody therapy directed at the epidermal growth factor receptor was associated with radiographic responses in a significant minority of patients with irinotecan-refractory colon cancer in a randomized phase II study of patients with irinotecan-refractory disease.	Irinotecan	255-265	epidermal growth factor receptor	Homo sapiens	53-85
15583935-0	2005	Anti-angiogenic effects of SN38 (active metabolite of irinotecan): inhibition of hypoxia-inducible factor 1 alpha (HIF-1alpha)/vascular endothelial growth factor (VEGF) expression of glioma and growth of endothelial cells.	Irinotecan	27-31	hypoxia inducible factor 1 subunit alpha	Homo sapiens	81-113
15827327-0	2005	Expression of multidrug transporter MRP4/ABCC4 is a marker of poor prognosis in neuroblastoma and confers resistance to irinotecan in vitro.	Irinotecan	120-130	ATP binding cassette subfamily C member 4	Homo sapiens	36-40
15827327-0	2005	Expression of multidrug transporter MRP4/ABCC4 is a marker of poor prognosis in neuroblastoma and confers resistance to irinotecan in vitro.	Irinotecan	120-130	ATP binding cassette subfamily C member 4	Homo sapiens	41-46
15583935-0	2005	Anti-angiogenic effects of SN38 (active metabolite of irinotecan): inhibition of hypoxia-inducible factor 1 alpha (HIF-1alpha)/vascular endothelial growth factor (VEGF) expression of glioma and growth of endothelial cells.	Irinotecan	27-31	hypoxia inducible factor 1 subunit alpha	Homo sapiens	115-125
15583935-0	2005	Anti-angiogenic effects of SN38 (active metabolite of irinotecan): inhibition of hypoxia-inducible factor 1 alpha (HIF-1alpha)/vascular endothelial growth factor (VEGF) expression of glioma and growth of endothelial cells.	Irinotecan	27-31	vascular endothelial growth factor A	Homo sapiens	127-161
15583935-0	2005	Anti-angiogenic effects of SN38 (active metabolite of irinotecan): inhibition of hypoxia-inducible factor 1 alpha (HIF-1alpha)/vascular endothelial growth factor (VEGF) expression of glioma and growth of endothelial cells.	Irinotecan	27-31	vascular endothelial growth factor A	Homo sapiens	163-167
15583935-0	2005	Anti-angiogenic effects of SN38 (active metabolite of irinotecan): inhibition of hypoxia-inducible factor 1 alpha (HIF-1alpha)/vascular endothelial growth factor (VEGF) expression of glioma and growth of endothelial cells.	Irinotecan	54-64	hypoxia inducible factor 1 subunit alpha	Homo sapiens	81-113
15583935-0	2005	Anti-angiogenic effects of SN38 (active metabolite of irinotecan): inhibition of hypoxia-inducible factor 1 alpha (HIF-1alpha)/vascular endothelial growth factor (VEGF) expression of glioma and growth of endothelial cells.	Irinotecan	54-64	hypoxia inducible factor 1 subunit alpha	Homo sapiens	115-125
15583935-0	2005	Anti-angiogenic effects of SN38 (active metabolite of irinotecan): inhibition of hypoxia-inducible factor 1 alpha (HIF-1alpha)/vascular endothelial growth factor (VEGF) expression of glioma and growth of endothelial cells.	Irinotecan	54-64	vascular endothelial growth factor A	Homo sapiens	127-161
15583935-0	2005	Anti-angiogenic effects of SN38 (active metabolite of irinotecan): inhibition of hypoxia-inducible factor 1 alpha (HIF-1alpha)/vascular endothelial growth factor (VEGF) expression of glioma and growth of endothelial cells.	Irinotecan	54-64	vascular endothelial growth factor A	Homo sapiens	163-167
15788689-7	2005	The JNK inhibitor SP600125 substantially decreased the activation of caspases and apoptosis induced by MSeA combination with SN38 or etoposide and completely blocked these events induced by MSeA/paclitaxel.	Irinotecan	125-129	mitogen-activated protein kinase 8	Homo sapiens	4-7
15788689-7	2005	The JNK inhibitor SP600125 substantially decreased the activation of caspases and apoptosis induced by MSeA combination with SN38 or etoposide and completely blocked these events induced by MSeA/paclitaxel.	Irinotecan	125-129	caspase 8	Homo sapiens	69-77
15788689-10	2005	A JNK-independent suppression of survivin by SN38 and etoposide, but not by paclitaxel, was also observed.	Irinotecan	45-49	mitogen-activated protein kinase 8	Homo sapiens	2-5
15608127-7	2005	Among the variants examined, OATP1B1*15 (N130D and V174A; reported allele frequency 10-15%) exhibited decreased transport activities for SN-38 as well as pravastatin, estrone-3-sulfate, and estradiol-17beta-glucuronide.	Irinotecan	137-142	solute carrier organic anion transporter family member 1B1	Homo sapiens	29-36
15572581-10	2005	The intrinsic clearance of 7-ethyl-10-hydroxycamptothecin (SN-38) by P229L UGT1A1 expressed in COS-1 cells was about 3% of the wild type.	Irinotecan	27-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
15572581-10	2005	The intrinsic clearance of 7-ethyl-10-hydroxycamptothecin (SN-38) by P229L UGT1A1 expressed in COS-1 cells was about 3% of the wild type.	Irinotecan	59-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	75-81
15608127-0	2005	Role of organic anion transporter OATP1B1 (OATP-C) in hepatic uptake of irinotecan and its active metabolite, 7-ethyl-10-hydroxycamptothecin: in vitro evidence and effect of single nucleotide polymorphisms.	Irinotecan	72-82	solute carrier organic anion transporter family member 1B1	Homo sapiens	34-41
15608127-0	2005	Role of organic anion transporter OATP1B1 (OATP-C) in hepatic uptake of irinotecan and its active metabolite, 7-ethyl-10-hydroxycamptothecin: in vitro evidence and effect of single nucleotide polymorphisms.	Irinotecan	72-82	solute carrier organic anion transporter family member 1B1	Homo sapiens	43-49
15608127-8	2005	This study is the first to yield evidence that OATP1B1 is involved in the hepatic disposition of SN-38 and that genetic polymorphisms of OATP1B1 may contribute to the known interpatient variability in disposition of irinotecan.	Irinotecan	97-102	solute carrier organic anion transporter family member 1B1	Homo sapiens	47-54
15608127-0	2005	Role of organic anion transporter OATP1B1 (OATP-C) in hepatic uptake of irinotecan and its active metabolite, 7-ethyl-10-hydroxycamptothecin: in vitro evidence and effect of single nucleotide polymorphisms.	Irinotecan	110-140	solute carrier organic anion transporter family member 1B1	Homo sapiens	34-41
15608127-0	2005	Role of organic anion transporter OATP1B1 (OATP-C) in hepatic uptake of irinotecan and its active metabolite, 7-ethyl-10-hydroxycamptothecin: in vitro evidence and effect of single nucleotide polymorphisms.	Irinotecan	110-140	solute carrier organic anion transporter family member 1B1	Homo sapiens	43-49
15608127-8	2005	This study is the first to yield evidence that OATP1B1 is involved in the hepatic disposition of SN-38 and that genetic polymorphisms of OATP1B1 may contribute to the known interpatient variability in disposition of irinotecan.	Irinotecan	216-226	solute carrier organic anion transporter family member 1B1	Homo sapiens	137-144
15608127-3	2005	Here, we examined the contribution of an organic anion-transporting polypeptide, OATP1B1 (OATP-C), which transports a variety of drugs and their metabolites from blood to liver in humans, to the hepatic disposition of irinotecan, SN-38, and its glucuronide conjugate (SN-38G) by using HEK293 cells stably transfected with SLCO1B1*1a (OATP-C*1a) coding wild-type OATP1B1.	Irinotecan	218-228	solute carrier organic anion transporter family member 1B1	Homo sapiens	81-88
15608127-3	2005	Here, we examined the contribution of an organic anion-transporting polypeptide, OATP1B1 (OATP-C), which transports a variety of drugs and their metabolites from blood to liver in humans, to the hepatic disposition of irinotecan, SN-38, and its glucuronide conjugate (SN-38G) by using HEK293 cells stably transfected with SLCO1B1*1a (OATP-C*1a) coding wild-type OATP1B1.	Irinotecan	218-228	solute carrier organic anion transporter family member 1B1	Homo sapiens	90-96
15608127-3	2005	Here, we examined the contribution of an organic anion-transporting polypeptide, OATP1B1 (OATP-C), which transports a variety of drugs and their metabolites from blood to liver in humans, to the hepatic disposition of irinotecan, SN-38, and its glucuronide conjugate (SN-38G) by using HEK293 cells stably transfected with SLCO1B1*1a (OATP-C*1a) coding wild-type OATP1B1.	Irinotecan	230-235	solute carrier organic anion transporter family member 1B1	Homo sapiens	81-88
15608127-3	2005	Here, we examined the contribution of an organic anion-transporting polypeptide, OATP1B1 (OATP-C), which transports a variety of drugs and their metabolites from blood to liver in humans, to the hepatic disposition of irinotecan, SN-38, and its glucuronide conjugate (SN-38G) by using HEK293 cells stably transfected with SLCO1B1*1a (OATP-C*1a) coding wild-type OATP1B1.	Irinotecan	230-235	solute carrier organic anion transporter family member 1B1	Homo sapiens	90-96
15608127-3	2005	Here, we examined the contribution of an organic anion-transporting polypeptide, OATP1B1 (OATP-C), which transports a variety of drugs and their metabolites from blood to liver in humans, to the hepatic disposition of irinotecan, SN-38, and its glucuronide conjugate (SN-38G) by using HEK293 cells stably transfected with SLCO1B1*1a (OATP-C*1a) coding wild-type OATP1B1.	Irinotecan	268-273	solute carrier organic anion transporter family member 1B1	Homo sapiens	81-88
15608127-3	2005	Here, we examined the contribution of an organic anion-transporting polypeptide, OATP1B1 (OATP-C), which transports a variety of drugs and their metabolites from blood to liver in humans, to the hepatic disposition of irinotecan, SN-38, and its glucuronide conjugate (SN-38G) by using HEK293 cells stably transfected with SLCO1B1*1a (OATP-C*1a) coding wild-type OATP1B1.	Irinotecan	268-273	solute carrier organic anion transporter family member 1B1	Homo sapiens	90-96
15608127-6	2005	Moreover, SN-38 exhibited a significant inhibitory effect on OATP1B1-mediated uptake of [(3)H]estrone-3-sulfate.	Irinotecan	10-15	solute carrier organic anion transporter family member 1B1	Homo sapiens	61-68
15668287-9	2005	CONCLUSIONS: The administration of irinotecan with docetaxel in platinum-refractory NSCLC prolonged TTP, but did not improve significantly RR, median survival or 1-year survival.	Irinotecan	35-45	ZFP36 ring finger protein	Homo sapiens	100-103
15686910-3	2005	Furthermore bisbenzyl 4 potentiated the cytotoxicity of SN-38 in BCRP-transduced K562 (K562/BCRP) cells.	Irinotecan	56-61	BCR pseudogene 1	Homo sapiens	65-69
15686910-3	2005	Furthermore bisbenzyl 4 potentiated the cytotoxicity of SN-38 in BCRP-transduced K562 (K562/BCRP) cells.	Irinotecan	56-61	BCR pseudogene 1	Homo sapiens	92-96
15709193-0	2005	UGT1A7 and UGT1A9 polymorphisms predict response and toxicity in colorectal cancer patients treated with capecitabine/irinotecan.	Irinotecan	118-128	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	0-6
15709193-0	2005	UGT1A7 and UGT1A9 polymorphisms predict response and toxicity in colorectal cancer patients treated with capecitabine/irinotecan.	Irinotecan	118-128	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	11-17
15709193-2	2005	We hypothesized that germline polymorphisms within genes related to drug target (thymidylate synthase) or metabolizing enzymes (UDP-glucuronosyltransferase, UGT) would impact response and toxicity to the combination of capecitabine plus irinotecan (CPT-11).	Irinotecan	237-247	thymidylate synthetase	Homo sapiens	81-101
15709193-2	2005	We hypothesized that germline polymorphisms within genes related to drug target (thymidylate synthase) or metabolizing enzymes (UDP-glucuronosyltransferase, UGT) would impact response and toxicity to the combination of capecitabine plus irinotecan (CPT-11).	Irinotecan	237-247	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	157-160
15709193-2	2005	We hypothesized that germline polymorphisms within genes related to drug target (thymidylate synthase) or metabolizing enzymes (UDP-glucuronosyltransferase, UGT) would impact response and toxicity to the combination of capecitabine plus irinotecan (CPT-11).	Irinotecan	249-255	thymidylate synthetase	Homo sapiens	81-101
15709193-2	2005	We hypothesized that germline polymorphisms within genes related to drug target (thymidylate synthase) or metabolizing enzymes (UDP-glucuronosyltransferase, UGT) would impact response and toxicity to the combination of capecitabine plus irinotecan (CPT-11).	Irinotecan	249-255	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	157-160
15709193-10	2005	CONCLUSIONS: These data strongly suggest that UGT1A7 and/or UGT1A9 genotypes may be predictors of response and toxicity in CRC patients treated with capecitabine plus irinotecan.	Irinotecan	167-177	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	46-52
15709193-10	2005	CONCLUSIONS: These data strongly suggest that UGT1A7 and/or UGT1A9 genotypes may be predictors of response and toxicity in CRC patients treated with capecitabine plus irinotecan.	Irinotecan	167-177	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	60-66
15757419-4	2005	S-1-based combination therapies with other promising drugs, including cis-platin, irinotecan and taxanes, are expected to yield good results.	Irinotecan	82-92	proteasome 26S subunit, non-ATPase 1	Homo sapiens	0-3
15821783-23	2005	Results of a large phase II study have shown response when used in combination with irinotecan in 22.9% of patients with EGFR-expressing, irinotecan-refractory, colorectal cancer.	Irinotecan	84-94	epidermal growth factor receptor	Homo sapiens	121-125
15821783-23	2005	Results of a large phase II study have shown response when used in combination with irinotecan in 22.9% of patients with EGFR-expressing, irinotecan-refractory, colorectal cancer.	Irinotecan	138-148	epidermal growth factor receptor	Homo sapiens	121-125
15558802-1	2005	BACKGROUND: In the current study, the authors report a Phase II trial of irinotecan (CPT-11), a topoisomerase I inhibitor active against malignant glioma (MG), with celecoxib, a selective COX-2 inhibitor, among MG patients with recurrent disease.	Irinotecan	73-83	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	188-193
15709211-14	2005	There it was reported that the combination of 5-fluorouracil, leucovorin, and irinotecan (Camptosar; Pfizer Pharmaceuticals; New York, NY) with anti-vascular endothelial growth factor antibody (bevacizumab-Avastin; Genentech, Inc.; South San Francisco, CA) was superior to the chemotherapy regimen alone when used to treat patients with metastatic colorectal cancer.	Irinotecan	78-88	vascular endothelial growth factor A	Homo sapiens	149-183
15709211-14	2005	There it was reported that the combination of 5-fluorouracil, leucovorin, and irinotecan (Camptosar; Pfizer Pharmaceuticals; New York, NY) with anti-vascular endothelial growth factor antibody (bevacizumab-Avastin; Genentech, Inc.; South San Francisco, CA) was superior to the chemotherapy regimen alone when used to treat patients with metastatic colorectal cancer.	Irinotecan	90-99	vascular endothelial growth factor A	Homo sapiens	149-183
15709212-4	2005	There exist several clinically relevant examples of the utility of pharmacogenomics that associate specific genetic polymorphisms in drug metabolizing enzymes (e.g., TPMT, UGT1A1, DPD), drug transporters (MDR1), and drug target enzymes (TS) with clinical outcomes in patients treated with commonly prescribed chemotherapy drugs, such as 5-fluorouracil and irinotecan (Camptosar; Pfizer Pharmaceuticals; New York, NY http://www.pfizer.com).	Irinotecan	356-366	thiopurine S-methyltransferase	Homo sapiens	166-170
15709212-4	2005	There exist several clinically relevant examples of the utility of pharmacogenomics that associate specific genetic polymorphisms in drug metabolizing enzymes (e.g., TPMT, UGT1A1, DPD), drug transporters (MDR1), and drug target enzymes (TS) with clinical outcomes in patients treated with commonly prescribed chemotherapy drugs, such as 5-fluorouracil and irinotecan (Camptosar; Pfizer Pharmaceuticals; New York, NY http://www.pfizer.com).	Irinotecan	368-377	thiopurine S-methyltransferase	Homo sapiens	166-170
15695404-1	2005	Breast cancer resistance protein (BCRP)/ABCG2 mediates concurrent resistance to chemotherapeutic agents, such as 7-ethyl-10-hydroxycamptothecin (SN-38), mitoxantrone, and topotecan, by pumping them out of cells.	Irinotecan	113-143	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
15695404-1	2005	Breast cancer resistance protein (BCRP)/ABCG2 mediates concurrent resistance to chemotherapeutic agents, such as 7-ethyl-10-hydroxycamptothecin (SN-38), mitoxantrone, and topotecan, by pumping them out of cells.	Irinotecan	113-143	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
15695404-1	2005	Breast cancer resistance protein (BCRP)/ABCG2 mediates concurrent resistance to chemotherapeutic agents, such as 7-ethyl-10-hydroxycamptothecin (SN-38), mitoxantrone, and topotecan, by pumping them out of cells.	Irinotecan	113-143	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	40-45
15695404-1	2005	Breast cancer resistance protein (BCRP)/ABCG2 mediates concurrent resistance to chemotherapeutic agents, such as 7-ethyl-10-hydroxycamptothecin (SN-38), mitoxantrone, and topotecan, by pumping them out of cells.	Irinotecan	145-150	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
15695404-1	2005	Breast cancer resistance protein (BCRP)/ABCG2 mediates concurrent resistance to chemotherapeutic agents, such as 7-ethyl-10-hydroxycamptothecin (SN-38), mitoxantrone, and topotecan, by pumping them out of cells.	Irinotecan	145-150	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
15695404-1	2005	Breast cancer resistance protein (BCRP)/ABCG2 mediates concurrent resistance to chemotherapeutic agents, such as 7-ethyl-10-hydroxycamptothecin (SN-38), mitoxantrone, and topotecan, by pumping them out of cells.	Irinotecan	145-150	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	40-45
15695404-5	2005	E(2) potentiates the cytotoxicity of SN-38, but not vincristine, in MCF-7/BCRP cells significantly, and increases cellular topotecan uptake in MCF-7 and MCF-7/BCRP cells.	Irinotecan	37-42	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	74-78
15727486-10	2005	The enzymes responsible for the activation, metabolism and mechanism of action of irinotecan, namely carboxylesterase 2, cytochrome P450 (CYP) 3A4, uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1), and topoisomerase-I, also exhibit variable interindividual activity.	Irinotecan	82-92	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	121-146
15727486-10	2005	The enzymes responsible for the activation, metabolism and mechanism of action of irinotecan, namely carboxylesterase 2, cytochrome P450 (CYP) 3A4, uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1), and topoisomerase-I, also exhibit variable interindividual activity.	Irinotecan	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	148-203
15727486-10	2005	The enzymes responsible for the activation, metabolism and mechanism of action of irinotecan, namely carboxylesterase 2, cytochrome P450 (CYP) 3A4, uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1), and topoisomerase-I, also exhibit variable interindividual activity.	Irinotecan	82-92	carboxylesterase 2	Homo sapiens	101-119
15727486-10	2005	The enzymes responsible for the activation, metabolism and mechanism of action of irinotecan, namely carboxylesterase 2, cytochrome P450 (CYP) 3A4, uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1), and topoisomerase-I, also exhibit variable interindividual activity.	Irinotecan	82-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	205-211
15727486-13	2005	CYP3A4 and UGT1A1 activity levels might be predictive of irinotecan toxicity rather than efficacy.	Irinotecan	57-67	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
15727486-13	2005	CYP3A4 and UGT1A1 activity levels might be predictive of irinotecan toxicity rather than efficacy.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
15813675-2	2005	Cancer cells overexpressing the ABCG2 gene show multidrug resistance to mitoxantrone-, methotrexate-, doxorubicin-, and camptothecin-based anticancer drugs, such as topotecan and SN-38.	Irinotecan	179-184	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	32-37
15720263-8	2005	Uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1) genotype has been reported to be associated with time to progression and survival in patients treated with irinotecan.	Irinotecan	172-182	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-55
15613901-11	2005	This retrospective study showed a high resectability rate, and a prolonged TTP and OS in patients with ACRC after induction treatment with irinotecan-based chemotherapy.	Irinotecan	139-149	ZFP36 ring finger protein	Homo sapiens	75-78
15720263-8	2005	Uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1) genotype has been reported to be associated with time to progression and survival in patients treated with irinotecan.	Irinotecan	172-182	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
16280599-6	2005	Moreover, both resveratrol and CPT-11, which are known to arrest cell-cycle progression, elevated egr-1 mRNA levels in glioma cells.	Irinotecan	31-37	early growth response 1	Rattus norvegicus	98-103
16257834-2	2005	Irinotecan undergoes drug metabolism to form an active SN-38, which is further converted to its beta-glucuronide by UDP-glucuronosyltransferase (UGT) 1A1.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-153
16257834-2	2005	Irinotecan undergoes drug metabolism to form an active SN-38, which is further converted to its beta-glucuronide by UDP-glucuronosyltransferase (UGT) 1A1.	Irinotecan	55-60	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-153
16257834-3	2005	A variant in the promoter of UGT1A1 gene, UGT1A1*28 allele, has been extensively studied, and pharmacogenetic relationships between the variant and ADR to irinotecan have been reported.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
16257834-3	2005	A variant in the promoter of UGT1A1 gene, UGT1A1*28 allele, has been extensively studied, and pharmacogenetic relationships between the variant and ADR to irinotecan have been reported.	Irinotecan	155-165	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
16257834-4	2005	A case-control study of Japanese cancer patients demonstrated that the patients having UGT1A1*28 were at significantly increased risk of severe ADR to irinotecan.	Irinotecan	151-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	87-93
16257834-5	2005	To date, genetic variations of the UGT1A1 gene is the most important hereditary factor to predict severe ADR to irinotecan.	Irinotecan	112-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
16257834-7	2005	At present, irinotecan chemotherapy based on a patient"s UGT1A1 genetic status is scientifically reasonable.	Irinotecan	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-63
16399345-2	2005	In addition to bilirubin, UGT1A1 conjugates various endogenous and exogenous lipophilic compounds such as estrogens and the active metabolite of the anticancer drug irinotecan SN-38.	Irinotecan	165-175	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
16399345-2	2005	In addition to bilirubin, UGT1A1 conjugates various endogenous and exogenous lipophilic compounds such as estrogens and the active metabolite of the anticancer drug irinotecan SN-38.	Irinotecan	176-181	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
16399345-3	2005	Thus, activation by specific inducers of the UGT1A1 gene is critical in treating patients with unconjugated hyperbili-rubinemia and in preventing side effects of drug treatment such as SN-38-induced toxicity.	Irinotecan	185-190	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
16491956-0	2005	Irinotecan/5-fluorouracil combination induces alterations in mitochondrial membrane potential and caspases on colon cancer cell lines.	Irinotecan	0-10	caspase 8	Homo sapiens	98-106
16491956-5	2005	In this study, we verified whether the collapse in mitochondrial membrane and the activation of caspases is responsible for increased apoptosis observed with CPT-11/5-FU treatment.	Irinotecan	158-164	caspase 8	Homo sapiens	96-104
16491956-8	2005	In these cells, both caspase-3 and -9 were involved in the activation of apoptosis after CPT-11/5-FU treatment.	Irinotecan	89-95	caspase 3	Homo sapiens	21-37
16491956-12	2005	In spite of the differences among the cell lines, these results indicated that the increase in apoptosis in HT-29 cells observed with CPT-11 followed by 5-FU treatment could be explained by a disruption in mitochondria membrane potential that induced caspases activation.	Irinotecan	134-140	caspase 8	Homo sapiens	251-259
15604280-0	2004	Elimination of hepatic metastases of colon cancer cells via p53-independent cross-talk between irinotecan and Apo2 ligand/TRAIL.	Irinotecan	95-105	tumor protein p53	Homo sapiens	60-63
16020968-13	2005	CONCLUSIONS: Biweekly DTX/CPT-11 with G-CSF support is a well-tolerated and highly effective approach in anthracycline-/paclitaxel-pretreated patients.	Irinotecan	26-32	colony stimulating factor 3	Homo sapiens	38-43
15864124-0	2005	Genetic polymorphism in the phenobarbital-responsive enhancer module of the UDP-glucuronosyltransferase 1A1 gene and irinotecan toxicity.	Irinotecan	117-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-107
15864124-1	2005	Genetic polymorphism of the UDP-glucuronosyltransferase (UGT) 1A1 gene is associated with the decreased glucuronidation activity of an active metabolite of irinotecan, SN-38, and UGT1A1*28 has been shown as a predictive factor for irinotecan toxicity.	Irinotecan	156-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-65
15864124-1	2005	Genetic polymorphism of the UDP-glucuronosyltransferase (UGT) 1A1 gene is associated with the decreased glucuronidation activity of an active metabolite of irinotecan, SN-38, and UGT1A1*28 has been shown as a predictive factor for irinotecan toxicity.	Irinotecan	156-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	179-185
15864124-1	2005	Genetic polymorphism of the UDP-glucuronosyltransferase (UGT) 1A1 gene is associated with the decreased glucuronidation activity of an active metabolite of irinotecan, SN-38, and UGT1A1*28 has been shown as a predictive factor for irinotecan toxicity.	Irinotecan	168-173	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-65
15864124-1	2005	Genetic polymorphism of the UDP-glucuronosyltransferase (UGT) 1A1 gene is associated with the decreased glucuronidation activity of an active metabolite of irinotecan, SN-38, and UGT1A1*28 has been shown as a predictive factor for irinotecan toxicity.	Irinotecan	231-241	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	28-65
15864124-1	2005	Genetic polymorphism of the UDP-glucuronosyltransferase (UGT) 1A1 gene is associated with the decreased glucuronidation activity of an active metabolite of irinotecan, SN-38, and UGT1A1*28 has been shown as a predictive factor for irinotecan toxicity.	Irinotecan	231-241	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	179-185
15864124-12	2005	The determination of T-3279G and UGT1A1*28 genotypes might be clinically useful in predicting severe irinotecan toxicity in cancer patients.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
15604285-5	2004	Surprisingly, the RNase L-deficient cells were also highly resistant to apoptosis by combination treatments with a topoisomerase (Topo) I inhibitor (camptothecin, topotecan, or SN-38) and tumor necrosis factor-related apoptosis-inducing ligand [TRAIL (Apo2L)].	Irinotecan	177-182	ribonuclease L	Homo sapiens	18-25
15604280-3	2004	Whereas irinotecan-induced up-regulation of the proapoptotic proteins PUMA and Noxa requires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 and 5 (STAT3/5) signaling in both p53-proficient and p53-deficient tumor cells.	Irinotecan	111-121	tumor protein p53	Homo sapiens	238-241
15604280-4	2004	We show that irinotecan inhibits JAK2-STAT3/5-dependent expression of survival proteins (Bcl-x(L) and XIAP) and cooperates with Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL) to facilitate p53-independent apoptosis of colon cancer cells.	Irinotecan	13-23	Janus kinase 2	Homo sapiens	33-37
15604280-4	2004	We show that irinotecan inhibits JAK2-STAT3/5-dependent expression of survival proteins (Bcl-x(L) and XIAP) and cooperates with Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL) to facilitate p53-independent apoptosis of colon cancer cells.	Irinotecan	13-23	signal transducer and activator of transcription 3	Homo sapiens	38-45
15604280-2	2004	Using isogenic human colon cancer cells that differ only in their p53 status, we demonstrate that loss of p53 renders tumor cells relatively resistant to the topoisomerase I inhibitor, irinotecan.	Irinotecan	185-195	tumor protein p53	Homo sapiens	106-109
15604280-4	2004	We show that irinotecan inhibits JAK2-STAT3/5-dependent expression of survival proteins (Bcl-x(L) and XIAP) and cooperates with Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL) to facilitate p53-independent apoptosis of colon cancer cells.	Irinotecan	13-23	BCL2 like 1	Homo sapiens	89-97
15604280-3	2004	Whereas irinotecan-induced up-regulation of the proapoptotic proteins PUMA and Noxa requires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 and 5 (STAT3/5) signaling in both p53-proficient and p53-deficient tumor cells.	Irinotecan	8-18	tumor protein p53	Homo sapiens	93-96
15604280-4	2004	We show that irinotecan inhibits JAK2-STAT3/5-dependent expression of survival proteins (Bcl-x(L) and XIAP) and cooperates with Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL) to facilitate p53-independent apoptosis of colon cancer cells.	Irinotecan	13-23	X-linked inhibitor of apoptosis	Homo sapiens	102-106
15604280-4	2004	We show that irinotecan inhibits JAK2-STAT3/5-dependent expression of survival proteins (Bcl-x(L) and XIAP) and cooperates with Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL) to facilitate p53-independent apoptosis of colon cancer cells.	Irinotecan	13-23	TNF receptor superfamily member 10a	Homo sapiens	128-132
15604280-3	2004	Whereas irinotecan-induced up-regulation of the proapoptotic proteins PUMA and Noxa requires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 and 5 (STAT3/5) signaling in both p53-proficient and p53-deficient tumor cells.	Irinotecan	8-18	Janus kinase 2	Homo sapiens	147-151
15604280-4	2004	We show that irinotecan inhibits JAK2-STAT3/5-dependent expression of survival proteins (Bcl-x(L) and XIAP) and cooperates with Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL) to facilitate p53-independent apoptosis of colon cancer cells.	Irinotecan	13-23	TNF superfamily member 10	Homo sapiens	197-202
15604280-4	2004	We show that irinotecan inhibits JAK2-STAT3/5-dependent expression of survival proteins (Bcl-x(L) and XIAP) and cooperates with Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL) to facilitate p53-independent apoptosis of colon cancer cells.	Irinotecan	13-23	TNF superfamily member 10	Homo sapiens	203-208
15604280-4	2004	We show that irinotecan inhibits JAK2-STAT3/5-dependent expression of survival proteins (Bcl-x(L) and XIAP) and cooperates with Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL) to facilitate p53-independent apoptosis of colon cancer cells.	Irinotecan	13-23	tumor protein p53	Homo sapiens	224-227
15604280-5	2004	Whereas xenografts of p53-deficient colon cancer cells are relatively resistant to irinotecan compared with their p53-proficient counterparts, combined treatment with irinotecan and Apo2L/TRAIL eliminates hepatic metastases of both p53-proficient and p53-deficient cancer cells in vivo and significantly improves the survival of animals relative to treatment with either agent alone.	Irinotecan	83-93	tumor protein p53	Homo sapiens	22-25
15604280-5	2004	Whereas xenografts of p53-deficient colon cancer cells are relatively resistant to irinotecan compared with their p53-proficient counterparts, combined treatment with irinotecan and Apo2L/TRAIL eliminates hepatic metastases of both p53-proficient and p53-deficient cancer cells in vivo and significantly improves the survival of animals relative to treatment with either agent alone.	Irinotecan	83-93	TNF superfamily member 10	Homo sapiens	188-193
15604280-5	2004	Whereas xenografts of p53-deficient colon cancer cells are relatively resistant to irinotecan compared with their p53-proficient counterparts, combined treatment with irinotecan and Apo2L/TRAIL eliminates hepatic metastases of both p53-proficient and p53-deficient cancer cells in vivo and significantly improves the survival of animals relative to treatment with either agent alone.	Irinotecan	167-177	tumor protein p53	Homo sapiens	114-117
15604280-6	2004	Although the synergy between chemotherapy and Apo2L/TRAIL has been ascribed to p53, our data demonstrate that irinotecan enhances Apo2L/TRAIL-induced apoptosis of tumor cells via a distinct p53-independent mechanism involving inhibition of JAK2-STAT3/5 signaling.	Irinotecan	110-120	TNF superfamily member 10	Homo sapiens	130-135
15604280-6	2004	Although the synergy between chemotherapy and Apo2L/TRAIL has been ascribed to p53, our data demonstrate that irinotecan enhances Apo2L/TRAIL-induced apoptosis of tumor cells via a distinct p53-independent mechanism involving inhibition of JAK2-STAT3/5 signaling.	Irinotecan	110-120	TNF superfamily member 10	Homo sapiens	136-141
15604280-6	2004	Although the synergy between chemotherapy and Apo2L/TRAIL has been ascribed to p53, our data demonstrate that irinotecan enhances Apo2L/TRAIL-induced apoptosis of tumor cells via a distinct p53-independent mechanism involving inhibition of JAK2-STAT3/5 signaling.	Irinotecan	110-120	tumor protein p53	Homo sapiens	190-193
15604280-6	2004	Although the synergy between chemotherapy and Apo2L/TRAIL has been ascribed to p53, our data demonstrate that irinotecan enhances Apo2L/TRAIL-induced apoptosis of tumor cells via a distinct p53-independent mechanism involving inhibition of JAK2-STAT3/5 signaling.	Irinotecan	110-120	Janus kinase 2	Homo sapiens	240-244
15604280-6	2004	Although the synergy between chemotherapy and Apo2L/TRAIL has been ascribed to p53, our data demonstrate that irinotecan enhances Apo2L/TRAIL-induced apoptosis of tumor cells via a distinct p53-independent mechanism involving inhibition of JAK2-STAT3/5 signaling.	Irinotecan	110-120	signal transducer and activator of transcription 3	Homo sapiens	245-252
15604280-3	2004	Whereas irinotecan-induced up-regulation of the proapoptotic proteins PUMA and Noxa requires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 and 5 (STAT3/5) signaling in both p53-proficient and p53-deficient tumor cells.	Irinotecan	8-18	signal transducer and activator of transcription 3	Homo sapiens	211-218
15604280-7	2004	These findings identify a novel p53-independent channel of cross-talk between topoisomerase I inhibitors and Apo2L/TRAIL and suggest that the addition of Apo2L/TRAIL can improve the therapeutic index of irinotecan against both p53-proficient and p53-deficient colorectal cancers, including those that have metastasized to the liver.	Irinotecan	203-213	tumor protein p53	Homo sapiens	32-35
15604280-7	2004	These findings identify a novel p53-independent channel of cross-talk between topoisomerase I inhibitors and Apo2L/TRAIL and suggest that the addition of Apo2L/TRAIL can improve the therapeutic index of irinotecan against both p53-proficient and p53-deficient colorectal cancers, including those that have metastasized to the liver.	Irinotecan	203-213	TNF superfamily member 10	Homo sapiens	109-114
15604280-3	2004	Whereas irinotecan-induced up-regulation of the proapoptotic proteins PUMA and Noxa requires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 and 5 (STAT3/5) signaling in both p53-proficient and p53-deficient tumor cells.	Irinotecan	8-18	tumor protein p53	Homo sapiens	238-241
15604280-7	2004	These findings identify a novel p53-independent channel of cross-talk between topoisomerase I inhibitors and Apo2L/TRAIL and suggest that the addition of Apo2L/TRAIL can improve the therapeutic index of irinotecan against both p53-proficient and p53-deficient colorectal cancers, including those that have metastasized to the liver.	Irinotecan	203-213	TNF superfamily member 10	Homo sapiens	115-120
15604280-7	2004	These findings identify a novel p53-independent channel of cross-talk between topoisomerase I inhibitors and Apo2L/TRAIL and suggest that the addition of Apo2L/TRAIL can improve the therapeutic index of irinotecan against both p53-proficient and p53-deficient colorectal cancers, including those that have metastasized to the liver.	Irinotecan	203-213	TNF superfamily member 10	Homo sapiens	154-159
15604280-3	2004	Whereas irinotecan-induced up-regulation of the proapoptotic proteins PUMA and Noxa requires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 and 5 (STAT3/5) signaling in both p53-proficient and p53-deficient tumor cells.	Irinotecan	8-18	tumor protein p53	Homo sapiens	238-241
15604280-7	2004	These findings identify a novel p53-independent channel of cross-talk between topoisomerase I inhibitors and Apo2L/TRAIL and suggest that the addition of Apo2L/TRAIL can improve the therapeutic index of irinotecan against both p53-proficient and p53-deficient colorectal cancers, including those that have metastasized to the liver.	Irinotecan	203-213	TNF superfamily member 10	Homo sapiens	160-165
15604280-3	2004	Whereas irinotecan-induced up-regulation of the proapoptotic proteins PUMA and Noxa requires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 and 5 (STAT3/5) signaling in both p53-proficient and p53-deficient tumor cells.	Irinotecan	111-121	Janus kinase 2	Homo sapiens	147-151
15604280-7	2004	These findings identify a novel p53-independent channel of cross-talk between topoisomerase I inhibitors and Apo2L/TRAIL and suggest that the addition of Apo2L/TRAIL can improve the therapeutic index of irinotecan against both p53-proficient and p53-deficient colorectal cancers, including those that have metastasized to the liver.	Irinotecan	203-213	tumor protein p53	Homo sapiens	227-230
15604280-7	2004	These findings identify a novel p53-independent channel of cross-talk between topoisomerase I inhibitors and Apo2L/TRAIL and suggest that the addition of Apo2L/TRAIL can improve the therapeutic index of irinotecan against both p53-proficient and p53-deficient colorectal cancers, including those that have metastasized to the liver.	Irinotecan	203-213	tumor protein p53	Homo sapiens	227-230
15604280-3	2004	Whereas irinotecan-induced up-regulation of the proapoptotic proteins PUMA and Noxa requires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 and 5 (STAT3/5) signaling in both p53-proficient and p53-deficient tumor cells.	Irinotecan	111-121	signal transducer and activator of transcription 3	Homo sapiens	211-218
15604280-3	2004	Whereas irinotecan-induced up-regulation of the proapoptotic proteins PUMA and Noxa requires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 and 5 (STAT3/5) signaling in both p53-proficient and p53-deficient tumor cells.	Irinotecan	111-121	tumor protein p53	Homo sapiens	238-241
15634630-1	2004	BACKGROUND: To establish the recommended dose (RD) of the thymidylate-synthase inhibitor ZD9331 administered with irinotecan (CPT-11) in patients with pretreated metastatic colorectal cancer, and to assess toxicity profile, pharmacokinetics (PK), and anti-tumor activity in a phase I/II open, multicenter, intrapatient chemotherapy dose escalating trial.	Irinotecan	114-124	thymidylate synthetase	Homo sapiens	58-78
15634630-1	2004	BACKGROUND: To establish the recommended dose (RD) of the thymidylate-synthase inhibitor ZD9331 administered with irinotecan (CPT-11) in patients with pretreated metastatic colorectal cancer, and to assess toxicity profile, pharmacokinetics (PK), and anti-tumor activity in a phase I/II open, multicenter, intrapatient chemotherapy dose escalating trial.	Irinotecan	126-132	thymidylate synthetase	Homo sapiens	58-78
15574786-2	2004	Here we show for the first time that SN38, the potent active metabolite of irinotecan, induces c-Jun NH(2)-terminal kinase activation, Fas up-regulation, and caspase 8-mediated apoptosis in multiple myeloma (MM) cells.	Irinotecan	75-85	caspase 8	Homo sapiens	158-167
15592324-0	2004	Pharmacogenetics of human carboxylesterase 2, an enzyme involved in the activation of irinotecan into SN-38.	Irinotecan	86-96	carboxylesterase 2	Homo sapiens	26-44
20368829-0	2004	Responsiveness of CPT-11 in respect to hMLH1 and hMSH2 protein expression in the primary colorectal cancer.	Irinotecan	18-24	mutL homolog 1	Homo sapiens	39-44
20368829-0	2004	Responsiveness of CPT-11 in respect to hMLH1 and hMSH2 protein expression in the primary colorectal cancer.	Irinotecan	18-24	mutS homolog 2	Homo sapiens	49-54
20368829-1	2004	PURPOSE: The aim of this study was to evaluate the responsiveness to CPT-11 with respect to hMLH1 and hMSH2 protein expressions in primary colorectal tumors.	Irinotecan	69-75	mutL homolog 1	Homo sapiens	92-97
15592324-0	2004	Pharmacogenetics of human carboxylesterase 2, an enzyme involved in the activation of irinotecan into SN-38.	Irinotecan	102-107	carboxylesterase 2	Homo sapiens	26-44
20368829-1	2004	PURPOSE: The aim of this study was to evaluate the responsiveness to CPT-11 with respect to hMLH1 and hMSH2 protein expressions in primary colorectal tumors.	Irinotecan	69-75	mutS homolog 2	Homo sapiens	102-107
20368829-6	2004	Patients with tumors not expressing hMLH1 showed a significantly better response to CPT-11 (p=0.04).	Irinotecan	84-90	mutL homolog 1	Homo sapiens	36-41
15592324-1	2004	PURPOSE: Irinotecan, a drug widely used in the treatment of advanced colorectal cancers, is a prodrug requiring activation to 7-ethyl-10-hydroxycamptothecin (SN-38) by carboxylesterase 2 (hCE2).	Irinotecan	9-19	carboxylesterase 2	Homo sapiens	168-186
20368829-10	2004	CONCLUSION: The immunohistochemical determination of loss of hMLH1 and hMSH2 expressions may be used in determining the responsiveness to CPT-11-based chemotherapy.	Irinotecan	138-144	mutL homolog 1	Homo sapiens	61-66
20368829-10	2004	CONCLUSION: The immunohistochemical determination of loss of hMLH1 and hMSH2 expressions may be used in determining the responsiveness to CPT-11-based chemotherapy.	Irinotecan	138-144	mutS homolog 2	Homo sapiens	71-76
15592324-1	2004	PURPOSE: Irinotecan, a drug widely used in the treatment of advanced colorectal cancers, is a prodrug requiring activation to 7-ethyl-10-hydroxycamptothecin (SN-38) by carboxylesterase 2 (hCE2).	Irinotecan	9-19	carboxylesterase 2	Homo sapiens	188-192
15592324-1	2004	PURPOSE: Irinotecan, a drug widely used in the treatment of advanced colorectal cancers, is a prodrug requiring activation to 7-ethyl-10-hydroxycamptothecin (SN-38) by carboxylesterase 2 (hCE2).	Irinotecan	126-156	carboxylesterase 2	Homo sapiens	168-186
15592324-1	2004	PURPOSE: Irinotecan, a drug widely used in the treatment of advanced colorectal cancers, is a prodrug requiring activation to 7-ethyl-10-hydroxycamptothecin (SN-38) by carboxylesterase 2 (hCE2).	Irinotecan	126-156	carboxylesterase 2	Homo sapiens	188-192
15592324-1	2004	PURPOSE: Irinotecan, a drug widely used in the treatment of advanced colorectal cancers, is a prodrug requiring activation to 7-ethyl-10-hydroxycamptothecin (SN-38) by carboxylesterase 2 (hCE2).	Irinotecan	158-163	carboxylesterase 2	Homo sapiens	168-186
15592324-1	2004	PURPOSE: Irinotecan, a drug widely used in the treatment of advanced colorectal cancers, is a prodrug requiring activation to 7-ethyl-10-hydroxycamptothecin (SN-38) by carboxylesterase 2 (hCE2).	Irinotecan	158-163	carboxylesterase 2	Homo sapiens	188-192
15592324-10	2004	CONCLUSION: The hCE2 gene presents several polymorphisms, none of which seems to be involved in significant variations in protein activity and, therefore, in irinotecan activation.	Irinotecan	158-168	carboxylesterase 2	Homo sapiens	16-20
15536465-0	2004	Inhibition of acetylcholinesterase in patients receiving irinotecan (camptothecin-11).	Irinotecan	57-67	acetylcholinesterase (Cartwright blood group)	Homo sapiens	14-34
15523087-0	2004	Prediction of irinotecan pharmacokinetics by use of cytochrome P450 3A4 phenotyping probes.	Irinotecan	14-24	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	52-71
15523087-2	2004	The response to irinotecan is variable, possibly because of interindividual variation in the expression of the enzymes that metabolize irinotecan, including cytochrome P450 3A4 (CYP3A4) and uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	16-26	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	157-176
15523087-2	2004	The response to irinotecan is variable, possibly because of interindividual variation in the expression of the enzymes that metabolize irinotecan, including cytochrome P450 3A4 (CYP3A4) and uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	16-26	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	178-184
15523087-2	2004	The response to irinotecan is variable, possibly because of interindividual variation in the expression of the enzymes that metabolize irinotecan, including cytochrome P450 3A4 (CYP3A4) and uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	190-237
15523087-2	2004	The response to irinotecan is variable, possibly because of interindividual variation in the expression of the enzymes that metabolize irinotecan, including cytochrome P450 3A4 (CYP3A4) and uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	16-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	239-245
15523087-2	2004	The response to irinotecan is variable, possibly because of interindividual variation in the expression of the enzymes that metabolize irinotecan, including cytochrome P450 3A4 (CYP3A4) and uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	135-145	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	157-176
15523087-2	2004	The response to irinotecan is variable, possibly because of interindividual variation in the expression of the enzymes that metabolize irinotecan, including cytochrome P450 3A4 (CYP3A4) and uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	135-145	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	178-184
15523087-2	2004	The response to irinotecan is variable, possibly because of interindividual variation in the expression of the enzymes that metabolize irinotecan, including cytochrome P450 3A4 (CYP3A4) and uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	135-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	190-237
15523087-2	2004	The response to irinotecan is variable, possibly because of interindividual variation in the expression of the enzymes that metabolize irinotecan, including cytochrome P450 3A4 (CYP3A4) and uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1).	Irinotecan	135-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	239-245
15523087-12	2004	In addition, the presence of a UGT1A1 variant with a (TA)7 repeat in the promoter (UGT1A1*28) was associated with increased exposure to SN-38 (435 ng x h/mL, 95% confidence interval [CI] = 339 to 531 ng x h/mL in patients who are homozygous for wild-type UGT1A1; 631 ng x h/mL, 95% CI = 499 to 762 ng .	Irinotecan	136-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
15523087-12	2004	In addition, the presence of a UGT1A1 variant with a (TA)7 repeat in the promoter (UGT1A1*28) was associated with increased exposure to SN-38 (435 ng x h/mL, 95% confidence interval [CI] = 339 to 531 ng x h/mL in patients who are homozygous for wild-type UGT1A1; 631 ng x h/mL, 95% CI = 499 to 762 ng .	Irinotecan	136-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
15523087-12	2004	In addition, the presence of a UGT1A1 variant with a (TA)7 repeat in the promoter (UGT1A1*28) was associated with increased exposure to SN-38 (435 ng x h/mL, 95% confidence interval [CI] = 339 to 531 ng x h/mL in patients who are homozygous for wild-type UGT1A1; 631 ng x h/mL, 95% CI = 499 to 762 ng .	Irinotecan	136-141	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
15523087-14	2004	CONCLUSION: CYP3A4 phenotype, as assessed by midazolam clearance, is statistically significantly associated with irinotecan pharmacokinetics.	Irinotecan	113-123	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	12-18
15523087-15	2004	Evaluation of midazolam clearance combined with UGT1A1*28 genotyping may assist with optimization of irinotecan chemotherapy.	Irinotecan	101-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
15547701-8	2004	We identified two proto-oncogenes, nuclear receptor of T-cells (NOT) and c-fos, that were up-regulated in doxifluridine- and irinotecan-related regimens but unchanged in the 5-FU-related regimen.	Irinotecan	125-135	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	73-78
15547701-10	2004	These results suggest that doxifluridine has a synergistic impact on the therapeutic effect of irinotecan by up-regulating proto-oncogenes such as NOT and c-fos, and thus justify the use of one of the irinotecan and fluoropyrimidine combinations.	Irinotecan	95-105	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	155-160
15844664-1	2004	We conducted a phase II study of combination chemotherapy with nedaplatin (NP) with irinotecan (CPT) to determine the effects against unresectable non-small cell lung cancer (NSCLC) and to determine the qualitative and quantitative toxicities of this combination chemotherapy in 70 years or older patients.	Irinotecan	84-94	choline phosphotransferase 1	Homo sapiens	96-99
15736428-7	2004	Synergism was observed in ABC-1 and SBC-3 cells when cisplatin was given first, followed by SN-38 (7-ethyl-10-hydroxycamptothecin) and cisplatin.	Irinotecan	92-97	ATP binding cassette subfamily A member 1	Homo sapiens	26-31
15736428-7	2004	Synergism was observed in ABC-1 and SBC-3 cells when cisplatin was given first, followed by SN-38 (7-ethyl-10-hydroxycamptothecin) and cisplatin.	Irinotecan	99-129	ATP binding cassette subfamily A member 1	Homo sapiens	26-31
15536465-0	2004	Inhibition of acetylcholinesterase in patients receiving irinotecan (camptothecin-11).	Irinotecan	69-84	acetylcholinesterase (Cartwright blood group)	Homo sapiens	14-34
15492275-3	2004	Breast cancer resistance protein (ABCG2), a transporter that confers resistance to SN-38 (the active metabolite of irinotecan), was readily detected in six of nine xenograft models examined by immunohistochemistry.	Irinotecan	83-88	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	34-39
15688606-0	2004	Uridine diphosphoglucuronosyl transferase and methylenetetrahydrofolate reductase polymorphisms as genomic predictors of toxicity and response to irinotecan-, antifolate- and fluoropyrimidine-based chemotherapy.	Irinotecan	146-156	methylenetetrahydrofolate reductase	Homo sapiens	46-81
15688606-3	2004	In particular, uridine diphosphoglucuronosyl transferase 1A1 (UGT1A1) enzyme is responsible for detoxification of irinotecan active metabolite, SN38.	Irinotecan	114-124	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
15688606-4	2004	A polymorphic structure in the promoter region (UGT1A1*28) may affect irinotecan toxicity and SN38 plasma level.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
15492275-3	2004	Breast cancer resistance protein (ABCG2), a transporter that confers resistance to SN-38 (the active metabolite of irinotecan), was readily detected in six of nine xenograft models examined by immunohistochemistry.	Irinotecan	115-125	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	34-39
15492275-4	2004	In vitro gefitinib potently reversed resistance to SN-38 only in a cell line that overexpressed functional ABCG2.	Irinotecan	51-56	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	107-112
15492275-9	2004	It is concluded that gefitinib may modulate SN-38 activity at the cellular level to reverse tumor resistance mediated by ABCG2 through inhibiting drug efflux and may be used potentially in humans to modulate the oral bioavailability of a poorly absorbed camptothecin such as irinotecan.	Irinotecan	44-49	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	121-126
15354215-0	2004	Thymidylate synthase predictive power is overcome by irinotecan combination therapy with S-1 for gastric cancer.	Irinotecan	53-63	thymidylate synthetase	Homo sapiens	0-20
15354215-10	2004	TS predictive power was overcome by CPT-11 combination therapy with S-1.	Irinotecan	36-42	thymidylate synthetase	Homo sapiens	0-2
15374978-8	2004	Conversely, concurrent treatment with SN-38 and UCN-01 resulted in S-phase checkpoint override, an amplified DNA damage response including increased phosphorylation of the DNA double-strand breakage marker H2AX and augmentation of clonogenic inhibition, which was independent of p53.	Irinotecan	38-43	H2A.X variant histone	Homo sapiens	206-210
15553727-3	2004	Administration of CPT-11 (80 mg/body) by a hepatic arterial infusion inhibited the growth of metastatic liver tumor and decreased serum levels of CEA and CA19-9 for several months without a significant adverse side effect.	Irinotecan	18-24	CEA cell adhesion molecule 3	Homo sapiens	146-149
15341677-11	2004	EGFR inhibitors are still experimental in every GI malignancy with the notable exception of cetuximab that is approved for second or third-line therapy of metastatic colorectal cancer, used either alone or in combination with irinotecan (Camptosar, Kalamazoo, Mich).	Irinotecan	226-236	epidermal growth factor receptor	Homo sapiens	0-4
15469406-3	2004	Although multiple genes may play a role in irinotecan activity, the UDP glycuronosyltransferase 1 family, polypeptide A1 (UGT1A1) enzyme has been strongly associated with toxicity.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-128
15469406-4	2004	A common dinucleotide repeat polymorphism in the UGT1A1 promoter region (UGT1A1*28) has been correlated with severe toxicity in cancer patients receiving irinotecan-containing therapy.	Irinotecan	154-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
15469406-4	2004	A common dinucleotide repeat polymorphism in the UGT1A1 promoter region (UGT1A1*28) has been correlated with severe toxicity in cancer patients receiving irinotecan-containing therapy.	Irinotecan	154-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
15292932-1	2004	CPT-11 (irinotecan) is a DNA-topoisomerase I inhibitor with preclinical activity against neuroblastoma (NB) xenografts.	Irinotecan	0-6	topoisomerase (DNA) I	Mus musculus	25-44
15292932-1	2004	CPT-11 (irinotecan) is a DNA-topoisomerase I inhibitor with preclinical activity against neuroblastoma (NB) xenografts.	Irinotecan	8-18	topoisomerase (DNA) I	Mus musculus	25-44
15292932-3	2004	IGR-NB8 is an immature NB xenograft with MYCN amplification and 1p deletion, which is sensitive to CPT-11.	Irinotecan	99-105	v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived	Mus musculus	41-45
15292935-0	2004	Phase I-II study of irinotecan (CPT-11) plus nedaplatin (254-S) with recombinant human granulocyte colony-stimulating factor support in patients with advanced or recurrent cervical cancer.	Irinotecan	20-30	colony stimulating factor 3	Homo sapiens	87-124
15374978-8	2004	Conversely, concurrent treatment with SN-38 and UCN-01 resulted in S-phase checkpoint override, an amplified DNA damage response including increased phosphorylation of the DNA double-strand breakage marker H2AX and augmentation of clonogenic inhibition, which was independent of p53.	Irinotecan	38-43	tumor protein p53	Homo sapiens	279-282
15367706-9	2004	Furthermore, P388/BCRP-transplanted mice treated with combination of irinotecan and gefitinib survived significantly longer than those treated with irinotecan alone or gefitinib alone.	Irinotecan	69-79	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	18-22
15517893-0	2004	UGT1A10 is responsible for SN-38 glucuronidation and its expression in human lung cancers.	Irinotecan	27-32	UDP glucuronosyltransferase family 1 member A10	Homo sapiens	0-7
15517893-2	2004	In order to extend this result to the clinical setting, it is important to elucidate the role of SN-38 glucuronidation by UGT1A isoforms in CPT-11/SN-38 resistance in vivo.	Irinotecan	97-102	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	122-127
15517893-2	2004	In order to extend this result to the clinical setting, it is important to elucidate the role of SN-38 glucuronidation by UGT1A isoforms in CPT-11/SN-38 resistance in vivo.	Irinotecan	140-146	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	122-127
15517893-2	2004	In order to extend this result to the clinical setting, it is important to elucidate the role of SN-38 glucuronidation by UGT1A isoforms in CPT-11/SN-38 resistance in vivo.	Irinotecan	147-152	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	122-127
15517893-3	2004	MATERIALS AND METHODS: We examined SN-38 glucuronidation activity in COS-7 cells transfected with full-length cDNAs for human UGT isoforms (UGT1A1, UGT1A3, UGT1A6 and UGT1A10).	Irinotecan	35-40	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	126-129
15517893-5	2004	RESULTS: Our HPLC assay results showed that both UGT1A1 and UGT1A10 are responsible for SN-38 glucuronidation.	Irinotecan	88-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
15517893-5	2004	RESULTS: Our HPLC assay results showed that both UGT1A1 and UGT1A10 are responsible for SN-38 glucuronidation.	Irinotecan	88-93	UDP glucuronosyltransferase family 1 member A10	Homo sapiens	60-67
15517893-6	2004	The levels of UGT1A1 and UGT1A10 expression in a CPT-11/SN-38-resistant cell line were increased compared to levels in the parent cell line.	Irinotecan	49-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
15517893-6	2004	The levels of UGT1A1 and UGT1A10 expression in a CPT-11/SN-38-resistant cell line were increased compared to levels in the parent cell line.	Irinotecan	49-55	UDP glucuronosyltransferase family 1 member A10	Homo sapiens	25-32
15517893-6	2004	The levels of UGT1A1 and UGT1A10 expression in a CPT-11/SN-38-resistant cell line were increased compared to levels in the parent cell line.	Irinotecan	56-61	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	14-20
15517893-6	2004	The levels of UGT1A1 and UGT1A10 expression in a CPT-11/SN-38-resistant cell line were increased compared to levels in the parent cell line.	Irinotecan	56-61	UDP glucuronosyltransferase family 1 member A10	Homo sapiens	25-32
15517893-9	2004	Our results suggest that not only UGT 1A1, but also UGT 1A10, plays an important role in detoxifying CPT-11/SN-38, leading to resistance to CPT-11/SN-38 in lung cancer.	Irinotecan	101-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-41
15517893-9	2004	Our results suggest that not only UGT 1A1, but also UGT 1A10, plays an important role in detoxifying CPT-11/SN-38, leading to resistance to CPT-11/SN-38 in lung cancer.	Irinotecan	101-107	UDP glucuronosyltransferase family 1 member A10	Homo sapiens	52-60
15517893-9	2004	Our results suggest that not only UGT 1A1, but also UGT 1A10, plays an important role in detoxifying CPT-11/SN-38, leading to resistance to CPT-11/SN-38 in lung cancer.	Irinotecan	108-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-41
15517893-9	2004	Our results suggest that not only UGT 1A1, but also UGT 1A10, plays an important role in detoxifying CPT-11/SN-38, leading to resistance to CPT-11/SN-38 in lung cancer.	Irinotecan	108-113	UDP glucuronosyltransferase family 1 member A10	Homo sapiens	52-60
15517893-9	2004	Our results suggest that not only UGT 1A1, but also UGT 1A10, plays an important role in detoxifying CPT-11/SN-38, leading to resistance to CPT-11/SN-38 in lung cancer.	Irinotecan	140-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-41
15517893-9	2004	Our results suggest that not only UGT 1A1, but also UGT 1A10, plays an important role in detoxifying CPT-11/SN-38, leading to resistance to CPT-11/SN-38 in lung cancer.	Irinotecan	140-146	UDP glucuronosyltransferase family 1 member A10	Homo sapiens	52-60
15517893-9	2004	Our results suggest that not only UGT 1A1, but also UGT 1A10, plays an important role in detoxifying CPT-11/SN-38, leading to resistance to CPT-11/SN-38 in lung cancer.	Irinotecan	147-152	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-41
15517893-9	2004	Our results suggest that not only UGT 1A1, but also UGT 1A10, plays an important role in detoxifying CPT-11/SN-38, leading to resistance to CPT-11/SN-38 in lung cancer.	Irinotecan	147-152	UDP glucuronosyltransferase family 1 member A10	Homo sapiens	52-60
15355921-0	2004	ABCG2 pharmacogenetics: ethnic differences in allele frequency and assessment of influence on irinotecan disposition.	Irinotecan	94-104	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
15355921-1	2004	PURPOSE: The ATP-binding cassette transporter ABCG2 (breast cancer resistance protein) is an efflux protein that plays a role in host detoxification of various xenobiotic substrates, including the irinotecan metabolite 7- ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	197-207	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	46-51
15355921-1	2004	PURPOSE: The ATP-binding cassette transporter ABCG2 (breast cancer resistance protein) is an efflux protein that plays a role in host detoxification of various xenobiotic substrates, including the irinotecan metabolite 7- ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	197-207	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	53-85
15355921-1	2004	PURPOSE: The ATP-binding cassette transporter ABCG2 (breast cancer resistance protein) is an efflux protein that plays a role in host detoxification of various xenobiotic substrates, including the irinotecan metabolite 7- ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	219-250	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	46-51
15355921-1	2004	PURPOSE: The ATP-binding cassette transporter ABCG2 (breast cancer resistance protein) is an efflux protein that plays a role in host detoxification of various xenobiotic substrates, including the irinotecan metabolite 7- ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	219-250	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	53-85
15355921-1	2004	PURPOSE: The ATP-binding cassette transporter ABCG2 (breast cancer resistance protein) is an efflux protein that plays a role in host detoxification of various xenobiotic substrates, including the irinotecan metabolite 7- ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	252-257	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	46-51
15355921-1	2004	PURPOSE: The ATP-binding cassette transporter ABCG2 (breast cancer resistance protein) is an efflux protein that plays a role in host detoxification of various xenobiotic substrates, including the irinotecan metabolite 7- ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	252-257	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	53-85
15355921-3	2004	The aim of this study was to evaluate the ethnic distribution and potential functional consequence of the ABCG2 421C&gt;A genotype in cancer patients treated with irinotecan.	Irinotecan	163-173	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	106-111
15355921-4	2004	EXPERIMENTAL DESIGN: ABCG2 genotyping was performed using Pyrosequencing on DNA from 88 American Caucasians, 94 African Americans, 938 Africans, and 95 Han Chinese, as well as in 84 European Caucasian patients treated with irinotecan undergoing additional blood sampling for pharmacokinetic studies.	Irinotecan	223-233	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	21-26
15355921-9	2004	CONCLUSIONS: The ABCG2 421C&gt;A polymorphism appears to play a limited role in the disposition of irinotecan in European Caucasians.	Irinotecan	99-109	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	17-22
19780248-7	2004	Cetuximab (an epidermal growth factor receptor antibody) plus irinotecan yields an increased overall response in patients with irinotecan-refractory colorectal disease.	Irinotecan	127-137	epidermal growth factor receptor	Homo sapiens	14-46
15367706-1	2004	Breast cancer resistance protein (BCRP) is an ATP binding cassette transporter that confers resistance to a series of anticancer agents such as 7-ethyl-10-hydroxycamptothecin (SN-38), topotecan, and mitoxantrone.	Irinotecan	144-174	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
15367706-1	2004	Breast cancer resistance protein (BCRP) is an ATP binding cassette transporter that confers resistance to a series of anticancer agents such as 7-ethyl-10-hydroxycamptothecin (SN-38), topotecan, and mitoxantrone.	Irinotecan	144-174	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
15367706-1	2004	Breast cancer resistance protein (BCRP) is an ATP binding cassette transporter that confers resistance to a series of anticancer agents such as 7-ethyl-10-hydroxycamptothecin (SN-38), topotecan, and mitoxantrone.	Irinotecan	176-181	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
15367706-1	2004	Breast cancer resistance protein (BCRP) is an ATP binding cassette transporter that confers resistance to a series of anticancer agents such as 7-ethyl-10-hydroxycamptothecin (SN-38), topotecan, and mitoxantrone.	Irinotecan	176-181	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
15367706-5	2004	Gefitinib reversed SN-38 resistance in BCRP-transduced human myelogenous leukemia K562 (K562/BCRP) or BCRP-transduced murine lymphocytic leukemia P388 (P388/BCRP) cells but not in these parental cells.	Irinotecan	19-24	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	39-43
15367706-6	2004	In addition, gefitinib sensitized human colon cancer HT-29 cells, which endogenously express BCRP, to SN-38.	Irinotecan	102-107	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	93-97
15280927-1	2004	SN-38 is the active metabolite of irinotecan and it is metabolised through conjugation by uridine diphosphate glucuronosyl transferase (UGT1A1).	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	136-142
15280927-1	2004	SN-38 is the active metabolite of irinotecan and it is metabolised through conjugation by uridine diphosphate glucuronosyl transferase (UGT1A1).	Irinotecan	34-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	136-142
15280927-2	2004	The major toxicity of irinotecan therapy is diarrhoea, which has been related to the enzymatic activity of UGT1A1.	Irinotecan	22-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
15280927-13	2004	The role of the UGT1A1 genotype as a predictor of toxicity in cancer patients receiving irinotecan demands the performance of a randomized trial to ascertain whether genotype-adjusted dosages of the drug can help to establish safe and effective doses not only for patients with the UGT1A1(*)28 homozygous genotype but also for those with the most common UGT1A1 6/6 or 6/7 genotype.	Irinotecan	88-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
15286088-0	2004	Influence of genetic variants in UGT1A1 and UGT1A9 on the in vivo glucuronidation of SN-38.	Irinotecan	85-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
15297419-0	2004	Relevance of different UGT1A1 polymorphisms in irinotecan-induced toxicity: a molecular and clinical study of 75 patients.	Irinotecan	47-57	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
15297419-1	2004	PURPOSE: We wanted to assess polymorphisms in the uridine diphosphoglucuronosyl transferase 1A1 (UGT 1A1) gene: the TATA box polymorphism and UGT 1A1 G71R and Y486D mutations in the coding sequence, the main mutations characterizing Gilbert"s syndrome, as predictors of severe toxic event occurrence after irinotecan (CPT-11) administration.	Irinotecan	306-316	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-95
15297419-1	2004	PURPOSE: We wanted to assess polymorphisms in the uridine diphosphoglucuronosyl transferase 1A1 (UGT 1A1) gene: the TATA box polymorphism and UGT 1A1 G71R and Y486D mutations in the coding sequence, the main mutations characterizing Gilbert"s syndrome, as predictors of severe toxic event occurrence after irinotecan (CPT-11) administration.	Irinotecan	306-316	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-104
15297419-1	2004	PURPOSE: We wanted to assess polymorphisms in the uridine diphosphoglucuronosyl transferase 1A1 (UGT 1A1) gene: the TATA box polymorphism and UGT 1A1 G71R and Y486D mutations in the coding sequence, the main mutations characterizing Gilbert"s syndrome, as predictors of severe toxic event occurrence after irinotecan (CPT-11) administration.	Irinotecan	318-324	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-95
15297419-1	2004	PURPOSE: We wanted to assess polymorphisms in the uridine diphosphoglucuronosyl transferase 1A1 (UGT 1A1) gene: the TATA box polymorphism and UGT 1A1 G71R and Y486D mutations in the coding sequence, the main mutations characterizing Gilbert"s syndrome, as predictors of severe toxic event occurrence after irinotecan (CPT-11) administration.	Irinotecan	318-324	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	97-104
15275881-2	2004	Inhibition of NF-kappaB by adenoviral delivery of an IkappaBalpha superrepressor (Ad.IkappaBalpha-SR) should potentiate 5-fluorouracil (5-FU) and irinotecan chemotherapy in gastric cancer cells.	Irinotecan	146-156	nuclear factor kappa B subunit 1	Homo sapiens	14-23
15275881-2	2004	Inhibition of NF-kappaB by adenoviral delivery of an IkappaBalpha superrepressor (Ad.IkappaBalpha-SR) should potentiate 5-fluorouracil (5-FU) and irinotecan chemotherapy in gastric cancer cells.	Irinotecan	146-156	NFKB inhibitor alpha	Homo sapiens	53-65
15275881-2	2004	Inhibition of NF-kappaB by adenoviral delivery of an IkappaBalpha superrepressor (Ad.IkappaBalpha-SR) should potentiate 5-fluorouracil (5-FU) and irinotecan chemotherapy in gastric cancer cells.	Irinotecan	146-156	NFKB inhibitor alpha	Homo sapiens	85-97
15275881-8	2004	RESULTS: 5-FU and SN-38 significantly induced NF-kappaB activation as measured by luciferase reporter assay (p &lt; 0.001).	Irinotecan	18-23	nuclear factor kappa B subunit 1	Homo sapiens	46-55
15275881-10	2004	In AGS cells, pretreatment with Ad.IkappaBalpha-SR followed by 5-FU (0.005 mmol/L) or SN-38 (10 ng/mL) led to increased growth inhibition of 13% and 59%, respectively (p &lt; 0.001).	Irinotecan	86-91	NFKB inhibitor alpha	Homo sapiens	35-47
15286088-8	2004	The median AUC ratio of SN-38G to SN-38 was significantly reduced in carriers of the variant UGT1A1(*)28 allele (7.00 [Wt] vs. 6.26 [Het] vs. 2.51 [Var]; p =.022).	Irinotecan	24-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
15286088-8	2004	The median AUC ratio of SN-38G to SN-38 was significantly reduced in carriers of the variant UGT1A1(*)28 allele (7.00 [Wt] vs. 6.26 [Het] vs. 2.51 [Var]; p =.022).	Irinotecan	34-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	93-99
15286088-9	2004	It is concluded that UGT1A9 functional variants are rare in Caucasians and likely to be clinically insignificant in irinotecan regimens.	Irinotecan	116-126	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	21-27
15286088-10	2004	Screening for the UGT1A1(*)28 polymorphism may identify patients with altered SN-38 pharmacokinetics.	Irinotecan	78-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
15286088-0	2004	Influence of genetic variants in UGT1A1 and UGT1A9 on the in vivo glucuronidation of SN-38.	Irinotecan	85-90	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	44-50
15286088-1	2004	The uridine diphosphate glucuronosyltransferase (UGT) 1A1 and 1A9 isoforms are involved in the phase II biotransformation of the irinotecan metabolite, SN-38.	Irinotecan	129-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-65
15286088-1	2004	The uridine diphosphate glucuronosyltransferase (UGT) 1A1 and 1A9 isoforms are involved in the phase II biotransformation of the irinotecan metabolite, SN-38.	Irinotecan	152-157	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-65
15286088-3	2004	The aim of this study was to evaluate the functional consequence of the UGT1A1(TA)(7)TAA (UGT1A1(*)28), UGT1A9 766G&gt;A (D256N; UGT1A9(*)5), and UGT1A9 98T&gt;C (M33T; UGT1A9(*)3) variants in Caucasian patients treated with irinotecan.	Irinotecan	225-235	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	72-78
15286088-3	2004	The aim of this study was to evaluate the functional consequence of the UGT1A1(TA)(7)TAA (UGT1A1(*)28), UGT1A9 766G&gt;A (D256N; UGT1A9(*)5), and UGT1A9 98T&gt;C (M33T; UGT1A9(*)3) variants in Caucasian patients treated with irinotecan.	Irinotecan	225-235	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	104-110
15286088-3	2004	The aim of this study was to evaluate the functional consequence of the UGT1A1(TA)(7)TAA (UGT1A1(*)28), UGT1A9 766G&gt;A (D256N; UGT1A9(*)5), and UGT1A9 98T&gt;C (M33T; UGT1A9(*)3) variants in Caucasian patients treated with irinotecan.	Irinotecan	225-235	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	129-135
15286088-3	2004	The aim of this study was to evaluate the functional consequence of the UGT1A1(TA)(7)TAA (UGT1A1(*)28), UGT1A9 766G&gt;A (D256N; UGT1A9(*)5), and UGT1A9 98T&gt;C (M33T; UGT1A9(*)3) variants in Caucasian patients treated with irinotecan.	Irinotecan	225-235	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	129-135
15286088-3	2004	The aim of this study was to evaluate the functional consequence of the UGT1A1(TA)(7)TAA (UGT1A1(*)28), UGT1A9 766G&gt;A (D256N; UGT1A9(*)5), and UGT1A9 98T&gt;C (M33T; UGT1A9(*)3) variants in Caucasian patients treated with irinotecan.	Irinotecan	225-235	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	129-135
15075385-0	2004	ABCG2 mediates differential resistance to SN-38 (7-ethyl-10-hydroxycamptothecin) and homocamptothecins.	Irinotecan	42-47	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
15075385-0	2004	ABCG2 mediates differential resistance to SN-38 (7-ethyl-10-hydroxycamptothecin) and homocamptothecins.	Irinotecan	49-79	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
15075385-5	2004	However, the resistance of three selected cell lines overexpressing wild-type or mutant ABCG2 to homocamptothecin or BN80915 was less than resistance to SN-38 (7-ethyl-10-hydroxycamptothecin), indicating that both the seven-membered E-ring present in homocamptothecin and the A- and B-ring modifications present in SN-38 are involved in substrate recognition by ABCG2.	Irinotecan	315-320	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	88-93
15075385-6	2004	HEK-293 cells transfected with vectors encoding wild-type or mutant ABCG2 were found to be less resistant to both homocamptothecins than to SN-38.	Irinotecan	140-145	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	68-73
15075385-7	2004	However, transfectants overexpressing mutant ABCG2 had relative resistance values for homocamptothecin and BN80915 4- to 14-fold higher than cells expressing wild-type ABCG2, suggesting that the gain of function resulting from mutation at amino acid 482, although not affecting SN-38, extends to the homocamptothecins.	Irinotecan	278-283	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	45-50
15075385-8	2004	Resistance was reversed by the ABCG2 inhibitor fumitremorgin C. BN80915 was 17-fold more potent than SN-38 in wild-type ABCG2-transfected cells, suggesting that BN80915 has the potential to overcome ABCG2-related resistance to SN-38, the active metabolite of CPT-11 (irinotecan).	Irinotecan	101-106	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	31-36
15075385-8	2004	Resistance was reversed by the ABCG2 inhibitor fumitremorgin C. BN80915 was 17-fold more potent than SN-38 in wild-type ABCG2-transfected cells, suggesting that BN80915 has the potential to overcome ABCG2-related resistance to SN-38, the active metabolite of CPT-11 (irinotecan).	Irinotecan	227-232	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	31-36
15075385-8	2004	Resistance was reversed by the ABCG2 inhibitor fumitremorgin C. BN80915 was 17-fold more potent than SN-38 in wild-type ABCG2-transfected cells, suggesting that BN80915 has the potential to overcome ABCG2-related resistance to SN-38, the active metabolite of CPT-11 (irinotecan).	Irinotecan	259-265	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	31-36
15075385-8	2004	Resistance was reversed by the ABCG2 inhibitor fumitremorgin C. BN80915 was 17-fold more potent than SN-38 in wild-type ABCG2-transfected cells, suggesting that BN80915 has the potential to overcome ABCG2-related resistance to SN-38, the active metabolite of CPT-11 (irinotecan).	Irinotecan	267-277	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	31-36
15256434-4	2004	Compared with control cells, metallothionein 1X (MT1X)-transfected AGS cells showed a 1.4-fold higher irinotecan IC(50) by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and tended to form more colonies.	Irinotecan	102-112	metallothionein 1X	Homo sapiens	29-47
15254716-1	2004	(Uridino-diphosphate)glucuronosyl-transferase enzyme 1A1 isoform (UGT1A1) is involved in glucuronidation of antineoplastic drugs such as SN38, the active metabolite of irinotecan, as well as estrogens and their metabolites.	Irinotecan	168-178	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	66-72
15170677-1	2004	Irinotecan (7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothecin; CPT-11) is a widely used potent antitumor drug that inhibits mammalian DNA topoisomerase I (Topo I); however, overexpression of ABCG2 (BCRP/MXR/ABCP) can confer cancer cell resistance to SN-38, the active form of CPT-11.	Irinotecan	0-10	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	208-213
15170677-1	2004	Irinotecan (7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothecin; CPT-11) is a widely used potent antitumor drug that inhibits mammalian DNA topoisomerase I (Topo I); however, overexpression of ABCG2 (BCRP/MXR/ABCP) can confer cancer cell resistance to SN-38, the active form of CPT-11.	Irinotecan	0-10	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	215-219
15170677-1	2004	Irinotecan (7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothecin; CPT-11) is a widely used potent antitumor drug that inhibits mammalian DNA topoisomerase I (Topo I); however, overexpression of ABCG2 (BCRP/MXR/ABCP) can confer cancer cell resistance to SN-38, the active form of CPT-11.	Irinotecan	0-10	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	220-223
15170677-1	2004	Irinotecan (7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothecin; CPT-11) is a widely used potent antitumor drug that inhibits mammalian DNA topoisomerase I (Topo I); however, overexpression of ABCG2 (BCRP/MXR/ABCP) can confer cancer cell resistance to SN-38, the active form of CPT-11.	Irinotecan	0-10	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	224-228
15170677-1	2004	Irinotecan (7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothecin; CPT-11) is a widely used potent antitumor drug that inhibits mammalian DNA topoisomerase I (Topo I); however, overexpression of ABCG2 (BCRP/MXR/ABCP) can confer cancer cell resistance to SN-38, the active form of CPT-11.	Irinotecan	80-86	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	208-213
15170677-1	2004	Irinotecan (7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothecin; CPT-11) is a widely used potent antitumor drug that inhibits mammalian DNA topoisomerase I (Topo I); however, overexpression of ABCG2 (BCRP/MXR/ABCP) can confer cancer cell resistance to SN-38, the active form of CPT-11.	Irinotecan	80-86	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	215-219
15170677-1	2004	Irinotecan (7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothecin; CPT-11) is a widely used potent antitumor drug that inhibits mammalian DNA topoisomerase I (Topo I); however, overexpression of ABCG2 (BCRP/MXR/ABCP) can confer cancer cell resistance to SN-38, the active form of CPT-11.	Irinotecan	80-86	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	220-223
15170677-1	2004	Irinotecan (7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothecin; CPT-11) is a widely used potent antitumor drug that inhibits mammalian DNA topoisomerase I (Topo I); however, overexpression of ABCG2 (BCRP/MXR/ABCP) can confer cancer cell resistance to SN-38, the active form of CPT-11.	Irinotecan	80-86	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	224-228
15170677-2	2004	We have recently demonstrated that plasma membrane vesicles prepared from ABCG2-overexpressing PC-6/SN2-5H cells transported SN-38 and its glucuronide conjugate in an ATP-dependent manner (Nakatomi et al., Biochem Biophys Res Commun 2001;288:827-32).	Irinotecan	125-130	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	74-79
15170677-2	2004	We have recently demonstrated that plasma membrane vesicles prepared from ABCG2-overexpressing PC-6/SN2-5H cells transported SN-38 and its glucuronide conjugate in an ATP-dependent manner (Nakatomi et al., Biochem Biophys Res Commun 2001;288:827-32).	Irinotecan	125-130	proprotein convertase subtilisin/kexin type 5	Homo sapiens	95-99
15170677-5	2004	Their antitumor activities in the SN-38-resistant PC-6/SN2-5H2 cell line greatly varied, however, being correlated with intracellular accumulation levels.	Irinotecan	34-39	proprotein convertase subtilisin/kexin type 5	Homo sapiens	50-54
15299073-5	2004	A secondary goal was to develop molecules that specifically inhibit activation of CPT-11 by a rabbit liver carboxylesterase (rCE).	Irinotecan	82-88	liver carboxylesterase 1	Oryctolagus cuniculus	101-123
15254685-0	2004	Cisplatin enhances the p53-independent apoptosis induced by a topoisomerase I inhibitor (CPT-11) in the lens epithelial tumors in transgenic mice.	Irinotecan	89-95	transformation related protein 53, pseudogene	Mus musculus	23-26
15254685-6	2004	In addition, it was found that Cisplatin augmented CPT-11-induced p53-independent apoptosis in p53-deficient alphaT3 mice.	Irinotecan	51-57	transformation related protein 53, pseudogene	Mus musculus	66-69
15254685-6	2004	In addition, it was found that Cisplatin augmented CPT-11-induced p53-independent apoptosis in p53-deficient alphaT3 mice.	Irinotecan	51-57	transformation related protein 53, pseudogene	Mus musculus	95-98
15256434-4	2004	Compared with control cells, metallothionein 1X (MT1X)-transfected AGS cells showed a 1.4-fold higher irinotecan IC(50) by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and tended to form more colonies.	Irinotecan	102-112	metallothionein 1X	Homo sapiens	49-53
15205350-4	2004	In this study, we show that phytoestrogens/flavonoids, such as genistein, naringenin, acacetin, and kaempferol, potentiated the cytotoxicity of SN-38 and mitoxantrone in BCRP-transduced K562 (K562/BCRP) cells.	Irinotecan	144-149	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	170-174
15160289-1	2004	PURPOSE: To evaluate the ability of D-saccharic acid 1.4-lactone (SAL), a beta-glucuronidase inhibitor, to prevent irinotecan hydrochloride (CPT-11) from inducing mucosal damage as a cause of diarrhea in rats.	Irinotecan	141-147	glucuronidase, beta	Rattus norvegicus	74-92
15160289-11	2004	CONCLUSIONS: The beta-glucuronidase inhibitor SAL is able to significantly reduce CPT-11-induced mucosal damage in the small intestine of rats.	Irinotecan	82-88	glucuronidase, beta	Rattus norvegicus	17-35
15213307-3	2004	Activated MSC increases chk2 phosphorylation at threonine-68 induced by SN-38, with no significant effect on chk1 phosphorylation.	Irinotecan	72-77	checkpoint kinase 2	Homo sapiens	24-28
15213307-10	2004	The observed down-regulation of DNA replication proteins cdc6, MCM2, and cdc25A after exposure to SN-38 with MSC further indicates a relationship between drug response and DNA damage.	Irinotecan	98-103	cell division cycle 6	Homo sapiens	57-61
15213307-10	2004	The observed down-regulation of DNA replication proteins cdc6, MCM2, and cdc25A after exposure to SN-38 with MSC further indicates a relationship between drug response and DNA damage.	Irinotecan	98-103	minichromosome maintenance complex component 2	Homo sapiens	63-67
15213307-10	2004	The observed down-regulation of DNA replication proteins cdc6, MCM2, and cdc25A after exposure to SN-38 with MSC further indicates a relationship between drug response and DNA damage.	Irinotecan	98-103	cell division cycle 25A	Homo sapiens	73-79
15213307-11	2004	Exposure to SN-38 with MSC resulted in a significant increase of poly(ADP-ribose) polymerasecleavage and caspase 3 activation.	Irinotecan	12-17	caspase 3	Homo sapiens	105-114
15183125-9	2004	Interestingly, SN-38 was able to activate EGFR and its signal transduction pathway.	Irinotecan	15-20	epidermal growth factor receptor	Homo sapiens	42-46
15213307-0	2004	Enhanced 7-ethyl-10-hydroxycamptothecin (SN-38) lethality by methylselenocysteine is associated with Chk2 phosphorylation at threonine-68 and down-regulation of Cdc6 expression.	Irinotecan	9-39	checkpoint kinase 2	Homo sapiens	101-105
15213307-0	2004	Enhanced 7-ethyl-10-hydroxycamptothecin (SN-38) lethality by methylselenocysteine is associated with Chk2 phosphorylation at threonine-68 and down-regulation of Cdc6 expression.	Irinotecan	9-39	cell division cycle 6	Homo sapiens	161-165
15213307-0	2004	Enhanced 7-ethyl-10-hydroxycamptothecin (SN-38) lethality by methylselenocysteine is associated with Chk2 phosphorylation at threonine-68 and down-regulation of Cdc6 expression.	Irinotecan	41-46	checkpoint kinase 2	Homo sapiens	101-105
15213307-0	2004	Enhanced 7-ethyl-10-hydroxycamptothecin (SN-38) lethality by methylselenocysteine is associated with Chk2 phosphorylation at threonine-68 and down-regulation of Cdc6 expression.	Irinotecan	41-46	cell division cycle 6	Homo sapiens	161-165
15213307-2	2004	We found that methioninase-activated MSC potentiates 7-ethyl-10-hydroxycamptothecin (SN-38)-induced cell lethality in vitro in the p53-defective human head and neck carcinoma A253 cells.	Irinotecan	53-83	tumor protein p53	Homo sapiens	131-134
15213307-2	2004	We found that methioninase-activated MSC potentiates 7-ethyl-10-hydroxycamptothecin (SN-38)-induced cell lethality in vitro in the p53-defective human head and neck carcinoma A253 cells.	Irinotecan	85-90	tumor protein p53	Homo sapiens	131-134
15205350-1	2004	Breast cancer resistance protein (BCRP), also called ABCG2, confers resistance to anticancer agents such as 7-ethyl-10-hydroxycamptothecin (SN-38), mitoxantrone, and topotecan.	Irinotecan	108-138	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
15205350-1	2004	Breast cancer resistance protein (BCRP), also called ABCG2, confers resistance to anticancer agents such as 7-ethyl-10-hydroxycamptothecin (SN-38), mitoxantrone, and topotecan.	Irinotecan	108-138	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
15205350-1	2004	Breast cancer resistance protein (BCRP), also called ABCG2, confers resistance to anticancer agents such as 7-ethyl-10-hydroxycamptothecin (SN-38), mitoxantrone, and topotecan.	Irinotecan	108-138	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	53-58
15205350-1	2004	Breast cancer resistance protein (BCRP), also called ABCG2, confers resistance to anticancer agents such as 7-ethyl-10-hydroxycamptothecin (SN-38), mitoxantrone, and topotecan.	Irinotecan	140-145	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
15205350-1	2004	Breast cancer resistance protein (BCRP), also called ABCG2, confers resistance to anticancer agents such as 7-ethyl-10-hydroxycamptothecin (SN-38), mitoxantrone, and topotecan.	Irinotecan	140-145	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
15205350-1	2004	Breast cancer resistance protein (BCRP), also called ABCG2, confers resistance to anticancer agents such as 7-ethyl-10-hydroxycamptothecin (SN-38), mitoxantrone, and topotecan.	Irinotecan	140-145	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	53-58
15205350-4	2004	In this study, we show that phytoestrogens/flavonoids, such as genistein, naringenin, acacetin, and kaempferol, potentiated the cytotoxicity of SN-38 and mitoxantrone in BCRP-transduced K562 (K562/BCRP) cells.	Irinotecan	144-149	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	197-201
15132777-0	2004	The expressions of p21 and pRB may be good indicators for the sensitivity of esophageal squamous cell cancers to CPT-11: Cell proliferation activity correlates with the effect of CPT-11.	Irinotecan	113-119	H3 histone pseudogene 16	Homo sapiens	19-22
15179405-0	2004	UGT1A1 haplotypes associated with reduced glucuronidation and increased serum bilirubin in irinotecan-administered Japanese patients with cancer.	Irinotecan	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
15027118-10	2004	Furthermore, we show, for the first time in clinical samples, that the ABCG2 mRNA content in hepatic metastases is higher after an irinotecan-based chemotherapy than in irinotecan-naive metastases.	Irinotecan	131-141	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	71-76
15027118-10	2004	Furthermore, we show, for the first time in clinical samples, that the ABCG2 mRNA content in hepatic metastases is higher after an irinotecan-based chemotherapy than in irinotecan-naive metastases.	Irinotecan	169-179	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	71-76
15027118-11	2004	In conclusion, this study supports the potential involvement of ABCG2 in the development of irinotecan resistance in vivo.	Irinotecan	92-102	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	64-69
14760509-2	2004	Given the high frequency of K-Ras mutations in malignancies commonly treated with irinotecan, the broad preclinical antiproliferative activity of R115777 and its largely non-overlapping toxicity profile with irinotecan, this phase I study of the combination of R115777 and irinotecan in patients with advanced cancer was undertaken.	Irinotecan	82-92	KRAS proto-oncogene, GTPase	Homo sapiens	28-33
15161687-0	2004	Enhanced chemosensitivity to irinotecan by RNA interference-mediated down-regulation of the nuclear factor-kappaB p65 subunit.	Irinotecan	29-39	RELA proto-oncogene, NF-kB subunit	Homo sapiens	114-117
15161687-2	2004	This is based on the fact that a variety of chemotherapy agents such as CPT-11 activate NF-kappaB to result in the expression of genes such as c-IAP1 and c-IAP2 that might be responsible for the inhibition of chemotherapy-induced apoptosis.	Irinotecan	72-78	baculoviral IAP repeat containing 2	Homo sapiens	143-149
15161687-2	2004	This is based on the fact that a variety of chemotherapy agents such as CPT-11 activate NF-kappaB to result in the expression of genes such as c-IAP1 and c-IAP2 that might be responsible for the inhibition of chemotherapy-induced apoptosis.	Irinotecan	72-78	baculoviral IAP repeat containing 3	Homo sapiens	154-160
15161687-4	2004	Reduction of endogenous p65 by siRNA treatment significantly impaired CPT-11-mediated NF-kappaB activation, enhanced apoptosis, and reduced colony formation in soft agar.	Irinotecan	70-76	RELA proto-oncogene, NF-kB subunit	Homo sapiens	24-27
15027118-0	2004	ABCG2 overexpression in colon cancer cells resistant to SN38 and in irinotecan-treated metastases.	Irinotecan	68-78	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
15027118-3	2004	The aim of the present study was to determine the involvement of ABCG2 in resistance to SN38 (the active metabolite of irinotecan) in colorectal cancer.	Irinotecan	119-129	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	65-70
15132777-0	2004	The expressions of p21 and pRB may be good indicators for the sensitivity of esophageal squamous cell cancers to CPT-11: Cell proliferation activity correlates with the effect of CPT-11.	Irinotecan	113-119	RB transcriptional corepressor 1	Homo sapiens	27-30
15132777-0	2004	The expressions of p21 and pRB may be good indicators for the sensitivity of esophageal squamous cell cancers to CPT-11: Cell proliferation activity correlates with the effect of CPT-11.	Irinotecan	179-185	H3 histone pseudogene 16	Homo sapiens	19-22
15132777-4	2004	Among these proteins, the expression levels of p21 and pRB showed significant differences that were associated with the IC50 values for CPT-11 (P = 0.0339 and P = 0.0109, respectively).	Irinotecan	136-142	H3 histone pseudogene 16	Homo sapiens	47-50
15132777-4	2004	Among these proteins, the expression levels of p21 and pRB showed significant differences that were associated with the IC50 values for CPT-11 (P = 0.0339 and P = 0.0109, respectively).	Irinotecan	136-142	RB transcriptional corepressor 1	Homo sapiens	55-58
15100172-0	2004	Hydrolysis of irinotecan and its oxidative metabolites, 7-ethyl-10-[4-N-(5-aminopentanoic acid)-1-piperidino] carbonyloxycamptothecin and 7-ethyl-10-[4-(1-piperidino)-1-amino]-carbonyloxycamptothecin, by human carboxylesterases CES1A1, CES2, and a newly expressed carboxylesterase isoenzyme, CES3.	Irinotecan	14-24	carboxylesterase 2	Homo sapiens	210-227
15100172-0	2004	Hydrolysis of irinotecan and its oxidative metabolites, 7-ethyl-10-[4-N-(5-aminopentanoic acid)-1-piperidino] carbonyloxycamptothecin and 7-ethyl-10-[4-(1-piperidino)-1-amino]-carbonyloxycamptothecin, by human carboxylesterases CES1A1, CES2, and a newly expressed carboxylesterase isoenzyme, CES3.	Irinotecan	14-24	carboxylesterase 2	Homo sapiens	236-240
15132777-5	2004	Namely, the expression of p21 or pRB independently could be a good indicator of CPT-11 efficacy in ESCC.	Irinotecan	80-86	H3 histone pseudogene 16	Homo sapiens	26-29
15132777-5	2004	Namely, the expression of p21 or pRB independently could be a good indicator of CPT-11 efficacy in ESCC.	Irinotecan	80-86	RB transcriptional corepressor 1	Homo sapiens	33-36
15100172-0	2004	Hydrolysis of irinotecan and its oxidative metabolites, 7-ethyl-10-[4-N-(5-aminopentanoic acid)-1-piperidino] carbonyloxycamptothecin and 7-ethyl-10-[4-(1-piperidino)-1-amino]-carbonyloxycamptothecin, by human carboxylesterases CES1A1, CES2, and a newly expressed carboxylesterase isoenzyme, CES3.	Irinotecan	14-24	carboxylesterase 3	Homo sapiens	292-296
15143945-0	2004	Effect of human noxa on irinotecan-induced apoptosis in human gastric carcinoma cell lines.	Irinotecan	24-34	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	16-20
15100172-6	2004	Carboxylesterases metabolize the carbamate prodrug 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11; irinotecan) to its active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38), a potent topoisomerase I inhibitor.	Irinotecan	51-117	carboxylesterase 2	Homo sapiens	0-17
15100172-6	2004	Carboxylesterases metabolize the carbamate prodrug 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11; irinotecan) to its active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38), a potent topoisomerase I inhibitor.	Irinotecan	127-137	carboxylesterase 2	Homo sapiens	0-17
15100172-6	2004	Carboxylesterases metabolize the carbamate prodrug 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11; irinotecan) to its active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38), a potent topoisomerase I inhibitor.	Irinotecan	164-194	carboxylesterase 2	Homo sapiens	0-17
15100172-6	2004	Carboxylesterases metabolize the carbamate prodrug 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11; irinotecan) to its active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38), a potent topoisomerase I inhibitor.	Irinotecan	196-201	carboxylesterase 2	Homo sapiens	0-17
15100172-8	2004	In this study, we investigate whether these oxidative metabolites, NPC and APC, can be metabolized to SN-38 by purified human carboxylesterases, CES1A1, CES2, and CES3.	Irinotecan	102-107	carboxylesterase 2	Homo sapiens	126-143
15100172-8	2004	In this study, we investigate whether these oxidative metabolites, NPC and APC, can be metabolized to SN-38 by purified human carboxylesterases, CES1A1, CES2, and CES3.	Irinotecan	102-107	carboxylesterase 2	Homo sapiens	153-157
15100172-8	2004	In this study, we investigate whether these oxidative metabolites, NPC and APC, can be metabolized to SN-38 by purified human carboxylesterases, CES1A1, CES2, and CES3.	Irinotecan	102-107	carboxylesterase 3	Homo sapiens	163-167
15100172-9	2004	We find that CPT-11, APC, and NPC can all be metabolized by carboxylesterases to SN-38.	Irinotecan	81-86	carboxylesterase 2	Homo sapiens	60-77
15143945-6	2004	MKN45 that has wild-type p53 showed severe inhibition by irinotecan compared with MKN28, which has mutated p53.	Irinotecan	57-67	tumor protein p53	Homo sapiens	25-28
15255290-0	2004	Transport of SN-38 by the wild type of human ABC transporter ABCG2 and its inhibition by quercetin, a natural flavonoid.	Irinotecan	13-18	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	61-66
15007088-0	2004	Genetic variants in the UDP-glucuronosyltransferase 1A1 gene predict the risk of severe neutropenia of irinotecan.	Irinotecan	103-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-55
15007088-2	2004	UDP-glucuronosyltransferase 1A1 (UGT1A1) catalyzes the glucuronidation of the active metabolite SN-38.	Irinotecan	96-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-31
15007088-2	2004	UDP-glucuronosyltransferase 1A1 (UGT1A1) catalyzes the glucuronidation of the active metabolite SN-38.	Irinotecan	96-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	33-39
15007088-14	2004	CONCLUSION: UGT1A1 genotype and total bilirubin levels are strongly associated with severe neutropenia, and could be used to identify cancer patients predisposed to the severe toxicity of irinotecan.	Irinotecan	188-198	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
15059881-3	2004	Previously, 4-anilinoquinazoline TKIs have been shown to inhibit the function of the breast cancer resistance-associated drug transporter (ABCG2), reversing resistance to camptothecin derivatives topotecan and SN-38.	Irinotecan	210-215	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	139-144
15059881-5	2004	Here, we show that imatinib mesylate potently reverses ABCG2-mediated resistance to topotecan and SN-38 and significantly increases accumulation of topotecan only in cells expressing functional ABCG2.	Irinotecan	98-103	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	55-60
15059881-0	2004	Imatinib mesylate is a potent inhibitor of the ABCG2 (BCRP) transporter and reverses resistance to topotecan and SN-38 in vitro.	Irinotecan	113-118	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	47-52
15059881-0	2004	Imatinib mesylate is a potent inhibitor of the ABCG2 (BCRP) transporter and reverses resistance to topotecan and SN-38 in vitro.	Irinotecan	113-118	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	54-58
15255290-1	2004	Irinotecan (CPT-11) is a widely-used potent anticancer drug that inhibits mammalian DNA topoisomerase I, however overexpression of the ATP-binding cassette transporter ABCG2 can confer cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	0-10	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	168-173
15255290-1	2004	Irinotecan (CPT-11) is a widely-used potent anticancer drug that inhibits mammalian DNA topoisomerase I, however overexpression of the ATP-binding cassette transporter ABCG2 can confer cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	12-18	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	168-173
15255290-1	2004	Irinotecan (CPT-11) is a widely-used potent anticancer drug that inhibits mammalian DNA topoisomerase I, however overexpression of the ATP-binding cassette transporter ABCG2 can confer cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	212-217	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	168-173
15255290-1	2004	Irinotecan (CPT-11) is a widely-used potent anticancer drug that inhibits mammalian DNA topoisomerase I, however overexpression of the ATP-binding cassette transporter ABCG2 can confer cancer cells resistance to SN-38, the active form of CPT-11.	Irinotecan	238-244	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	168-173
15255290-2	2004	In the present study, we have examined the contribution of three variant forms of ABCG2 to SN-38 resistance.	Irinotecan	91-96	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	82-87
15255290-3	2004	Exogenous expression of the Arg482 (wild type), Gly482, and Thr482 variants of ABCG2 conferred HEK293 cells resistance to SN-38 by 15.0-, 5.0-, and 5.3-fold, respectively.	Irinotecan	122-127	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	79-84
15255290-4	2004	In plasma membrane vesicles prepared from the ABCG2 variant cDNA-transfected HEK293 cells, [Arg482]ABCG2 transported SN-38 and its glucuronide conjugate in an ATP-dependent manner; however, only minimal transport activities were observed with the other variants (Gly482 and Thr482).	Irinotecan	117-122	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	46-51
15255290-4	2004	In plasma membrane vesicles prepared from the ABCG2 variant cDNA-transfected HEK293 cells, [Arg482]ABCG2 transported SN-38 and its glucuronide conjugate in an ATP-dependent manner; however, only minimal transport activities were observed with the other variants (Gly482 and Thr482).	Irinotecan	117-122	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	99-104
15255290-7	2004	When [Arg482]ABCG2-transfected HEK293 cells were incubated with SN-38 in the presence of 20 microM quercetin, cellular resistance to SN-38 was partly reversed.	Irinotecan	64-69	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	13-18
15255290-7	2004	When [Arg482]ABCG2-transfected HEK293 cells were incubated with SN-38 in the presence of 20 microM quercetin, cellular resistance to SN-38 was partly reversed.	Irinotecan	133-138	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	13-18
15001986-6	2004	Activated wt-p53 increased apoptosis and enhanced sensitivity to CPT-11.	Irinotecan	65-71	tumor protein p53	Homo sapiens	13-16
15134628-5	2004	CPT-11 was administered on days 1, 8, 15, and 22 at 225 mg/m2 for patients receiving CYP3A1- or CYP3A4-inducing anticonvulsants and at 125 mg/m2 for those not on these medications.	Irinotecan	0-6	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	96-102
15041737-0	2004	Characterization of p53 wild-type and null isogenic colorectal cancer cell lines resistant to 5-fluorouracil, oxaliplatin, and irinotecan.	Irinotecan	127-137	tumor protein p53	Homo sapiens	20-23
15001986-0	2004	Enhanced sensitivity to irinotecan by Cdk1 inhibition in the p53-deficient HT29 human colon cancer cell line.	Irinotecan	24-34	cyclin dependent kinase 1	Homo sapiens	38-42
15001986-0	2004	Enhanced sensitivity to irinotecan by Cdk1 inhibition in the p53-deficient HT29 human colon cancer cell line.	Irinotecan	24-34	tumor protein p53	Homo sapiens	61-64
15001986-9	2004	Cdk1 induction was exploited in vivo to improve the sensitivity to CPT-11 by additional treatment with the cdk-I CYC-202.	Irinotecan	67-73	cyclin dependent kinase 1	Homo sapiens	0-4
15001986-2	2004	Irinotecan (CPT-11), a DNA topoisomerase 1 inhibitor, has been recently incorporated to the adjuvant therapy.	Irinotecan	0-10	DNA topoisomerase I	Homo sapiens	23-42
15001986-2	2004	Irinotecan (CPT-11), a DNA topoisomerase 1 inhibitor, has been recently incorporated to the adjuvant therapy.	Irinotecan	12-18	DNA topoisomerase I	Homo sapiens	23-42
15001986-3	2004	Since the DNA-damage checkpoint depends on p53 activation, the status of p53 might critically influence the response to CPT-11.	Irinotecan	120-126	tumor protein p53	Homo sapiens	43-46
15001986-10	2004	We demonstrate a gain of sensitivity to CPT-11 in a p53-mutated colon cancer model either by restoring wild-type p53 function or by sequential treatment with cdk-Is.	Irinotecan	40-46	tumor protein p53	Homo sapiens	52-55
15001986-3	2004	Since the DNA-damage checkpoint depends on p53 activation, the status of p53 might critically influence the response to CPT-11.	Irinotecan	120-126	tumor protein p53	Homo sapiens	73-76
15001986-10	2004	We demonstrate a gain of sensitivity to CPT-11 in a p53-mutated colon cancer model either by restoring wild-type p53 function or by sequential treatment with cdk-Is.	Irinotecan	40-46	tumor protein p53	Homo sapiens	113-116
14618629-1	2004	Breast cancer resistance protein (BCRP/ABCG2) of an ATP-binding cassette half-transporter confers resistance against mitoxantrone and camptothecin derivatives of topotecan and irinotecan.	Irinotecan	176-186	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
14973080-9	2004	In 4-day cytotoxicity assays, ABCG2-mediated resistance to SN-38 and topotecan was abrogated in ABCG2-transfected HEK-293 cells treated with 1 micro M tariquidar, and ABCG2-transfected cells were 6-7-fold resistant to UCN-01.	Irinotecan	59-64	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	30-35
14973080-9	2004	In 4-day cytotoxicity assays, ABCG2-mediated resistance to SN-38 and topotecan was abrogated in ABCG2-transfected HEK-293 cells treated with 1 micro M tariquidar, and ABCG2-transfected cells were 6-7-fold resistant to UCN-01.	Irinotecan	59-64	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	96-101
14973080-9	2004	In 4-day cytotoxicity assays, ABCG2-mediated resistance to SN-38 and topotecan was abrogated in ABCG2-transfected HEK-293 cells treated with 1 micro M tariquidar, and ABCG2-transfected cells were 6-7-fold resistant to UCN-01.	Irinotecan	59-64	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	96-101
14973083-1	2004	The breast cancer resistance protein (BCRP) is an ATP-binding cassette half transporter that confers resistance to anticancer drugs such as mitoxantrone, anthracyclines, topotecan, and SN-38.	Irinotecan	185-190	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	4-36
14973083-1	2004	The breast cancer resistance protein (BCRP) is an ATP-binding cassette half transporter that confers resistance to anticancer drugs such as mitoxantrone, anthracyclines, topotecan, and SN-38.	Irinotecan	185-190	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	38-42
14973083-1	2004	The breast cancer resistance protein (BCRP) is an ATP-binding cassette half transporter that confers resistance to anticancer drugs such as mitoxantrone, anthracyclines, topotecan, and SN-38.	Irinotecan	185-190	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	50-87
15350151-5	2004	Drugs most prominently affected and contraindicated for concomitant use with St John"s wort are metabolised via both CYP3A4 and P-glycoprotein pathways, including HIV protease inhibitors, HIV non-nucleoside reverse transcriptase inhibitors (only CYP3A4), the immunosuppressants ciclosporin and tacrolimus, and the antineoplastic agents irinotecan and imatinib mesylate.	Irinotecan	336-346	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	117-123
14658007-7	2004	As expected, in vitro studies revealed that a 5-day exposure to TSP-1 at concentrations up to 130 microg/ml was not cytotoxic alone and did not affect the cytotoxicity of CPT-11, or of its active metabolite SN38, in HT-29 cells.	Irinotecan	207-211	thrombospondin 1	Homo sapiens	64-69
14962716-2	2004	In vitro studies have shown that irinotecan downregulates thymidylate synthase (TS) expression in tumour cells, leading to synergy between irinotecan and 5-FU that is maximal when irinotecan is given 24 h prior to 5-FU.	Irinotecan	33-43	thymidylate synthetase	Homo sapiens	58-78
14962716-2	2004	In vitro studies have shown that irinotecan downregulates thymidylate synthase (TS) expression in tumour cells, leading to synergy between irinotecan and 5-FU that is maximal when irinotecan is given 24 h prior to 5-FU.	Irinotecan	139-149	thymidylate synthetase	Homo sapiens	58-78
14962716-2	2004	In vitro studies have shown that irinotecan downregulates thymidylate synthase (TS) expression in tumour cells, leading to synergy between irinotecan and 5-FU that is maximal when irinotecan is given 24 h prior to 5-FU.	Irinotecan	139-149	thymidylate synthetase	Homo sapiens	58-78
15195891-7	2004	Favourable results were reported for the monoclonal antibody C225 (cetuximab) against the epidermal growth factor receptor in patients with ACC refractory to irinotecan.	Irinotecan	158-168	epidermal growth factor receptor	Homo sapiens	90-122
14967028-0	2004	Molecular modeling of CPT-11 metabolism by carboxylesterases (CEs): use of pnb CE as a model.	Irinotecan	22-28	carboxylesterase 1	Homo sapiens	43-60
14967028-1	2004	CPT-11 is a prodrug that is converted in vivo to the topoisomerase I poison SN-38 by carboxylesterases (CEs).	Irinotecan	0-6	carboxylesterase 1	Homo sapiens	85-102
14967028-1	2004	CPT-11 is a prodrug that is converted in vivo to the topoisomerase I poison SN-38 by carboxylesterases (CEs).	Irinotecan	76-81	carboxylesterase 1	Homo sapiens	85-102
14967028-3	2004	Despite extensive sequence homology, however, the human homologues of this protein, hCE1 and hiCE, metabolize CPT-11 with significantly lower efficiencies.	Irinotecan	110-116	carboxylesterase 1	Homo sapiens	84-88
14961077-4	2004	Using 19 glioblastoma cell lines, including 15 low-passage ex vivo cell lines derived from patients, as well as isogenic glioblastoma cells varying in p53 status, we show that clinically relevant levels of SN-38 potently induce cell cycle arrest and temporary senescence in glioblastoma cells with wild-type p53 while causing massive apoptosis in p53-deficient cells (P&lt;0.0002).	Irinotecan	206-211	tumor protein p53	Homo sapiens	151-154
14961077-4	2004	Using 19 glioblastoma cell lines, including 15 low-passage ex vivo cell lines derived from patients, as well as isogenic glioblastoma cells varying in p53 status, we show that clinically relevant levels of SN-38 potently induce cell cycle arrest and temporary senescence in glioblastoma cells with wild-type p53 while causing massive apoptosis in p53-deficient cells (P&lt;0.0002).	Irinotecan	206-211	tumor protein p53	Homo sapiens	308-311
14961077-4	2004	Using 19 glioblastoma cell lines, including 15 low-passage ex vivo cell lines derived from patients, as well as isogenic glioblastoma cells varying in p53 status, we show that clinically relevant levels of SN-38 potently induce cell cycle arrest and temporary senescence in glioblastoma cells with wild-type p53 while causing massive apoptosis in p53-deficient cells (P&lt;0.0002).	Irinotecan	206-211	tumor protein p53	Homo sapiens	308-311
15075664-10	2004	Furthermore, the combination of S-1 with cisplatin (CDDP), irinotecan or docetaxel for the treatment of gastric cancer and with CDDP for non-small cell and pancreatic cancer is feasible and active.	Irinotecan	59-69	proteasome 26S subunit, non-ATPase 1	Homo sapiens	32-35
15641483-0	2004	Low overexpression of HER-2/neu in advanced colorectal cancer limits the usefulness of trastuzumab (Herceptin) and irinotecan as therapy.	Irinotecan	115-125	erb-b2 receptor tyrosine kinase 2	Homo sapiens	22-31
15641483-2	2004	BACKGROUND: To determine the response rate of trastuzumab and irinotecan in HER-2/neu overexpressing advanced colorectal cancer (CRC), determine the frequency of HER-2/neu expression in CRC, and evaluate the pharmacokinetics of trastuzumab in a phase II study.	Irinotecan	62-72	erb-b2 receptor tyrosine kinase 2	Homo sapiens	76-85
14618629-1	2004	Breast cancer resistance protein (BCRP/ABCG2) of an ATP-binding cassette half-transporter confers resistance against mitoxantrone and camptothecin derivatives of topotecan and irinotecan.	Irinotecan	176-186	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
14618629-1	2004	Breast cancer resistance protein (BCRP/ABCG2) of an ATP-binding cassette half-transporter confers resistance against mitoxantrone and camptothecin derivatives of topotecan and irinotecan.	Irinotecan	176-186	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	39-44
14618629-1	2004	Breast cancer resistance protein (BCRP/ABCG2) of an ATP-binding cassette half-transporter confers resistance against mitoxantrone and camptothecin derivatives of topotecan and irinotecan.	Irinotecan	176-186	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	52-89
14618629-7	2004	Compared to the parental PC-6 cells, PC-6/SN2-5H2 cells were 141-, 173- and 57.2-fold resistant to topotecan, SN-38 and mitoxantrone, respectively.	Irinotecan	110-115	proprotein convertase subtilisin/kexin type 5	Homo sapiens	37-41
14645705-2	2003	Mismatch-repair-deficient colonic tumors evade TRAIL-induced apoptosis through mutational inactivation of Bax, but chemotherapeutics including Camptosar (CPT-11) restore TRAIL sensitivity.	Irinotecan	143-152	TNF superfamily member 10	Homo sapiens	170-175
15031593-9	2004	The monoclonal EGF receptor antibody cetuximab alone and in combination with irinotecan is active in second-line treatment.	Irinotecan	77-87	epidermal growth factor	Homo sapiens	15-18
15031593-10	2004	The VEGF antibody bevacizumab prolongs survival when given in combination with 5-FU/FA and irinotecan.	Irinotecan	91-101	vascular endothelial growth factor A	Homo sapiens	4-8
15655572-9	2004	The anti-VEGF bevacizumab increases the efficacy of first-line irinotecan therapy, while the addition of cetuximab restores irinotecan sensitivity in second line treatment of stage IV CRC.	Irinotecan	63-73	vascular endothelial growth factor A	Homo sapiens	9-13
14566825-2	2003	Expression of wild-type BCRP confers resistance to multiple chemotherapeutic agents such as mitoxantrone, SN-38 and topotecan, but not to doxorubicin.	Irinotecan	106-111	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	24-28
14566825-6	2003	Cells transfected with N557D-BCRP cDNA showed similar resistance to mitoxantrone but lower resistance to SN-38 than the wild-type BCRP-transfected cells.	Irinotecan	105-110	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	29-33
14566825-7	2003	Cells transfected with N557E-, H630E- or H630L-BCRP cDNA showed similar degrees of resistance to mitoxantrone and SN-38.	Irinotecan	114-119	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	47-51
14645705-2	2003	Mismatch-repair-deficient colonic tumors evade TRAIL-induced apoptosis through mutational inactivation of Bax, but chemotherapeutics including Camptosar (CPT-11) restore TRAIL sensitivity.	Irinotecan	154-160	TNF superfamily member 10	Homo sapiens	170-175
14645705-4	2003	Here, we imaged p53 transcriptional activity in Bax-/- carcinomas by using bioluminescence, in vivo, and find that p53 is required for sensitization to TRAIL by CPT-11.	Irinotecan	161-167	BCL2 associated X, apoptosis regulator	Homo sapiens	48-51
14645705-4	2003	Here, we imaged p53 transcriptional activity in Bax-/- carcinomas by using bioluminescence, in vivo, and find that p53 is required for sensitization to TRAIL by CPT-11.	Irinotecan	161-167	tumor protein p53	Homo sapiens	115-118
14645705-4	2003	Here, we imaged p53 transcriptional activity in Bax-/- carcinomas by using bioluminescence, in vivo, and find that p53 is required for sensitization to TRAIL by CPT-11.	Irinotecan	161-167	TNF superfamily member 10	Homo sapiens	152-157
14645705-6	2003	Caspase 8 inhibition protects both CPT-11 pretreated wild-type and Bax-/- HCT116 cells from TRAIL-induced apoptosis, whereas caspase 9 inhibition only rescued the wild-type HCT116 cells from death induced by TRAIL.	Irinotecan	35-41	caspase 8	Homo sapiens	0-9
14645705-6	2003	Caspase 8 inhibition protects both CPT-11 pretreated wild-type and Bax-/- HCT116 cells from TRAIL-induced apoptosis, whereas caspase 9 inhibition only rescued the wild-type HCT116 cells from death induced by TRAIL.	Irinotecan	35-41	TNF superfamily member 10	Homo sapiens	92-97
14645705-8	2003	In contrast to Bax-/- cells, Bak-deficient human cancers undergo apoptosis in response to TRAIL or CPT-11, implying that these proteins have nonoverlapping functions.	Irinotecan	99-105	BCL2 antagonist/killer 1	Homo sapiens	29-32
14679008-3	2003	Identification of the UGT responsible for glucuronidation of SN-38 and the anthraquinone NU/ICRF 505 was achieved by first using a panel of human cDNA-expressed isozymes to measure conjugating activity.	Irinotecan	61-66	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	22-25
14617791-1	2003	7-Ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (irinotecan, CPT-11) is a camptothecin prodrug that is metabolized by carboxylesterases (CE) to the active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38), a topoisomerase I inhibitor.	Irinotecan	0-65	carboxylesterase 1	Homo sapiens	136-153
14716146-4	2003	The monoclonal antibody cetuximab, targeted against EGFR, offers another new and very effective therapeutic option to patients with advanced irinotecan-refractory colorectal cancer--even those who are already pretreated with oxaliplatin.	Irinotecan	141-151	epidermal growth factor receptor	Homo sapiens	52-56
14612912-4	2003	In cytotoxicity assays, all ABCG2 proteins conferred high levels of resistance to mitoxantrone, SN-38, and topotecan, while mutant ABCG2 also exhibited a gain of function for mitoxantrone as they conferred a four-fold greater resistance compared to wild type.	Irinotecan	96-101	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	28-33
14646693-0	2003	Haplotype analysis of ABCB1/MDR1 blocks in a Japanese population reveals genotype-dependent renal clearance of irinotecan.	Irinotecan	111-121	ATP binding cassette subfamily B member 1	Homo sapiens	22-27
14646693-0	2003	Haplotype analysis of ABCB1/MDR1 blocks in a Japanese population reveals genotype-dependent renal clearance of irinotecan.	Irinotecan	111-121	ATP binding cassette subfamily B member 1	Homo sapiens	28-32
14763144-10	2003	Partial responses were observed with cetuximab either alone (RR: 10%) or in combination with CPT-11 (RR: 22%) in patients with CPT-11 refractory advanced CRC which expressed EGF-R.	Irinotecan	93-99	epidermal growth factor receptor	Homo sapiens	174-179
14763144-10	2003	Partial responses were observed with cetuximab either alone (RR: 10%) or in combination with CPT-11 (RR: 22%) in patients with CPT-11 refractory advanced CRC which expressed EGF-R.	Irinotecan	127-133	epidermal growth factor receptor	Homo sapiens	174-179
14586211-0	2003	Weekly regimen of irinotecan/docetaxel in previously treated non-small cell lung cancer patients and correlation with uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) polymorphism.	Irinotecan	18-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	118-165
14586211-0	2003	Weekly regimen of irinotecan/docetaxel in previously treated non-small cell lung cancer patients and correlation with uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) polymorphism.	Irinotecan	18-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-173
14617791-1	2003	7-Ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (irinotecan, CPT-11) is a camptothecin prodrug that is metabolized by carboxylesterases (CE) to the active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38), a topoisomerase I inhibitor.	Irinotecan	67-77	carboxylesterase 1	Homo sapiens	136-153
14617791-1	2003	7-Ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (irinotecan, CPT-11) is a camptothecin prodrug that is metabolized by carboxylesterases (CE) to the active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38), a topoisomerase I inhibitor.	Irinotecan	79-85	carboxylesterase 1	Homo sapiens	136-153
14617791-1	2003	7-Ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (irinotecan, CPT-11) is a camptothecin prodrug that is metabolized by carboxylesterases (CE) to the active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38), a topoisomerase I inhibitor.	Irinotecan	184-214	carboxylesterase 1	Homo sapiens	136-153
14617791-1	2003	7-Ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (irinotecan, CPT-11) is a camptothecin prodrug that is metabolized by carboxylesterases (CE) to the active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38), a topoisomerase I inhibitor.	Irinotecan	216-221	carboxylesterase 1	Homo sapiens	136-153
14584274-7	2003	The circulating TPO concentration remained almost constant in the irinotecan group, with no significant increases, while that in the docetaxel group was increased significantly on day 4 (p &lt; 0.05), day 8 (p &lt; 0.05), and day 15 (p &lt; 0.01) after therapy.	Irinotecan	66-76	thrombopoietin	Homo sapiens	16-19
14534729-0	2003	The relative contributions of carboxylesterase and beta-glucuronidase in the formation of SN-38 in human colorectal tumours.	Irinotecan	90-95	glucuronidase beta	Homo sapiens	51-69
14534729-3	2003	SN-38 is subsequently metabolised to its inactive glucuronide, SN-38G, which can however be reactivated to SN-38 by beta-glucuronidase.	Irinotecan	0-5	glucuronidase beta	Homo sapiens	116-134
14534729-3	2003	SN-38 is subsequently metabolised to its inactive glucuronide, SN-38G, which can however be reactivated to SN-38 by beta-glucuronidase.	Irinotecan	63-68	glucuronidase beta	Homo sapiens	116-134
14534729-3	2003	SN-38 is subsequently metabolised to its inactive glucuronide, SN-38G, which can however be reactivated to SN-38 by beta-glucuronidase.	Irinotecan	63-68	glucuronidase beta	Homo sapiens	116-134
14534729-4	2003	The purpose of this study was to examine the role of carboxylesterases and beta-glucuronidase in the in vitro production of SN-38 in human colorectal tumours.	Irinotecan	124-129	glucuronidase beta	Homo sapiens	75-93
14534729-8	2003	Therefore, tumour beta-glucuronidase may play a significant role in the exposure of tumours to SN-38 in vivo, particularly during prolonged infusions of CPT-11.	Irinotecan	95-100	glucuronidase beta	Homo sapiens	18-36
14534729-8	2003	Therefore, tumour beta-glucuronidase may play a significant role in the exposure of tumours to SN-38 in vivo, particularly during prolonged infusions of CPT-11.	Irinotecan	153-159	glucuronidase beta	Homo sapiens	18-36
14522368-7	2003	Cytochrome P450 3A4 inducing anti-epileptic drugs like phenytoin, carbamazepine and phenobarbital may significantly increase the metabolism of many chemotherapeutic agents like CPT11 and paclitaxel (but also of newer biological agents like many tyrosine kinase inhibitors).	Irinotecan	177-182	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-19
14581373-9	2003	Only CES2 gene expression correlated with the carboxylesterase activity assays (P &lt; 0.01) with CPT-11 and 4-methylumbelliferyl acetate as substrates.	Irinotecan	98-104	carboxylesterase 2	Homo sapiens	5-9
14581373-12	2003	CONCLUSIONS: We conclude that CES2 is the most abundant carboxylesterase in colon tumors that is responsible for CPT-11 hydrolysis.	Irinotecan	113-119	carboxylesterase 2	Homo sapiens	30-34
14581373-13	2003	This pilot study reinforces the hypothesis that there is a large interindividual variation in expression of carboxylesterases that may contribute to variation in therapeutic outcome and/or toxicity of CPT-11 therapy for colon cancer.	Irinotecan	201-207	carboxylesterase 2	Homo sapiens	108-125
14584274-8	2003	There was also a significant difference between the docetaxel group and irinotecan group with respect to circulating TPO concentration (p &lt; 0.05).	Irinotecan	72-82	thrombopoietin	Homo sapiens	117-120
12911669-12	2003	CONCLUSIONS: We conclude that irinotecan causes diarrhea by inducing apoptosis and hypoproliferation in both the small and large intestines, and causes colonic damage with changes in goblet cells and mucin secretion.	Irinotecan	30-40	solute carrier family 13 member 2	Rattus norvegicus	200-205
14522894-6	2003	A better response to irinotecan was observed in the patients whose tumors have lost BAX expression (P &lt; 0.001).	Irinotecan	21-31	BCL2 associated X, apoptosis regulator	Homo sapiens	84-87
12912956-1	2003	PURPOSE: Breast cancer resistance protein (BCRP/ABCG2), an ATP binding cassette half-transporter, confers resistance to mitoxantrone, doxorubicin, and topoisomerase I inhibitors of irinotecan and topotecan.	Irinotecan	181-191	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	9-41
12920197-1	2003	Breast cancer resistance protein (BCRP), an ATP-binding cassette transporter, confers resistance to a series of anticancer reagents such as mitoxantrone, 7-ethyl-10-hydroxycamptothecin, and topotecan.	Irinotecan	154-184	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
12920197-1	2003	Breast cancer resistance protein (BCRP), an ATP-binding cassette transporter, confers resistance to a series of anticancer reagents such as mitoxantrone, 7-ethyl-10-hydroxycamptothecin, and topotecan.	Irinotecan	154-184	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
12932648-5	2003	The SN-38 formulations were stable in human serum albumin and high lactone concentrations were observed even after 3 h. In vivo studies in nude mice showed prolonged half-life of the active (lactone form) drug in whole blood and increased efficacy compared to Camptosar in a mouse xenograft tumor model.	Irinotecan	4-9	albumin	Mus musculus	50-57
12960109-5	2003	The homozygous T allele of the ABCB1 1236C&gt;T polymorphism was associated with significantly increased exposure to irinotecan (P = 0.038) and its active metabolite SN-38 (P = 0.031).	Irinotecan	117-127	ATP binding cassette subfamily B member 1	Homo sapiens	31-36
12960109-5	2003	The homozygous T allele of the ABCB1 1236C&gt;T polymorphism was associated with significantly increased exposure to irinotecan (P = 0.038) and its active metabolite SN-38 (P = 0.031).	Irinotecan	166-171	ATP binding cassette subfamily B member 1	Homo sapiens	31-36
12960109-7	2003	The extent of SN-38 glucuronidation was slightly impaired in homozygous variants of UGT1A1*28, although differences were not statistically significant (P = 0.22).	Irinotecan	14-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	84-90
12960109-8	2003	CONCLUSIONS: It is concluded that genotyping for ABCB1 1236C&gt;T may be one of the factors assisting with dose optimization of irinotecan chemotherapy in cancer patients.	Irinotecan	128-138	ATP binding cassette subfamily B member 1	Homo sapiens	49-54
12907654-3	2003	When combined with the topoisomerase I inhibitor CPT-11 (irinotecan), Apo2L/TRAIL exhibits enhanced apoptotic activity in C4-2 cells cultured in vitro as well as xenografted as tumors in vivo.	Irinotecan	49-55	TNF superfamily member 10	Homo sapiens	70-75
12907654-3	2003	When combined with the topoisomerase I inhibitor CPT-11 (irinotecan), Apo2L/TRAIL exhibits enhanced apoptotic activity in C4-2 cells cultured in vitro as well as xenografted as tumors in vivo.	Irinotecan	49-55	TNF superfamily member 10	Homo sapiens	76-81
12907654-3	2003	When combined with the topoisomerase I inhibitor CPT-11 (irinotecan), Apo2L/TRAIL exhibits enhanced apoptotic activity in C4-2 cells cultured in vitro as well as xenografted as tumors in vivo.	Irinotecan	57-67	TNF superfamily member 10	Homo sapiens	70-75
12907654-3	2003	When combined with the topoisomerase I inhibitor CPT-11 (irinotecan), Apo2L/TRAIL exhibits enhanced apoptotic activity in C4-2 cells cultured in vitro as well as xenografted as tumors in vivo.	Irinotecan	57-67	TNF superfamily member 10	Homo sapiens	76-81
12907654-10	2003	Activation of multiple caspases and PARP cleavage were also observed in the C4-2 tumors treated with doses resulting in effective tumor control at 42 days after Apo2L/TRAIL plus CPT-11 treatment.	Irinotecan	178-184	caspase 8	Homo sapiens	23-31
12907654-10	2003	Activation of multiple caspases and PARP cleavage were also observed in the C4-2 tumors treated with doses resulting in effective tumor control at 42 days after Apo2L/TRAIL plus CPT-11 treatment.	Irinotecan	178-184	poly(ADP-ribose) polymerase 1	Homo sapiens	36-40
12907654-13	2003	Our data indicate that the combined treatment of Apo2L/TRAIL and CPT-11 achieves tumor control in prostate cancer tumors through regulation of Bcl-2 family proteins and potent activation of caspases.	Irinotecan	65-71	BCL2 apoptosis regulator	Homo sapiens	143-148
12907654-13	2003	Our data indicate that the combined treatment of Apo2L/TRAIL and CPT-11 achieves tumor control in prostate cancer tumors through regulation of Bcl-2 family proteins and potent activation of caspases.	Irinotecan	65-71	caspase 8	Homo sapiens	190-198
12914384-8	2003	UGT1A1 (uridine diphoshate-glucuronosyltransferase 1A1) is involved on irinotecan metabolism.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
12914384-8	2003	UGT1A1 (uridine diphoshate-glucuronosyltransferase 1A1) is involved on irinotecan metabolism.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-54
12914384-9	2003	MRP2 (multi-drug resistance associated protein) and MDR1 (multi-drug resistance gene) are involved in irinotecan as well as anthracyclines transport.	Irinotecan	102-112	ATP binding cassette subfamily C member 2	Homo sapiens	0-4
12914384-9	2003	MRP2 (multi-drug resistance associated protein) and MDR1 (multi-drug resistance gene) are involved in irinotecan as well as anthracyclines transport.	Irinotecan	102-112	ATP binding cassette subfamily B member 1	Homo sapiens	52-56
12912956-1	2003	PURPOSE: Breast cancer resistance protein (BCRP/ABCG2), an ATP binding cassette half-transporter, confers resistance to mitoxantrone, doxorubicin, and topoisomerase I inhibitors of irinotecan and topotecan.	Irinotecan	181-191	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	43-47
12912956-1	2003	PURPOSE: Breast cancer resistance protein (BCRP/ABCG2), an ATP binding cassette half-transporter, confers resistance to mitoxantrone, doxorubicin, and topoisomerase I inhibitors of irinotecan and topotecan.	Irinotecan	181-191	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	48-53
12912956-2	2003	Recently, we reported that BCRP efficiently transported SN-38 (the active metabolite of irinotecan) with a high affinity in lung cancer cells in vitro (K. Nakatomi et al., Biochem.	Irinotecan	56-61	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	27-31
12912956-2	2003	Recently, we reported that BCRP efficiently transported SN-38 (the active metabolite of irinotecan) with a high affinity in lung cancer cells in vitro (K. Nakatomi et al., Biochem.	Irinotecan	88-98	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	27-31
12912956-9	2003	RESULTS: The levels of BCRP mRNA expression in the cell lines were significantly correlated with the BCRP function and the sensitivity to SN-38 and topotecan.	Irinotecan	138-143	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	23-27
12869632-5	2003	The role of the ATP-dependent drug transporter ABCG2 in CPT-11 cytotoxicity is unclear because some ABCG2 mutants confer camptothecin resistance, whereas others do not.	Irinotecan	56-62	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	47-52
12871782-1	2003	The anticancer agent irinotecan (CPT-11) is a prodrug converted to its active form, SN-38, by human carboxylesterase (hCE) and the SN-38 is further metabolized to its inactive form, SN-38G.	Irinotecan	21-31	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	118-121
12871782-1	2003	The anticancer agent irinotecan (CPT-11) is a prodrug converted to its active form, SN-38, by human carboxylesterase (hCE) and the SN-38 is further metabolized to its inactive form, SN-38G.	Irinotecan	33-39	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	118-121
12871782-1	2003	The anticancer agent irinotecan (CPT-11) is a prodrug converted to its active form, SN-38, by human carboxylesterase (hCE) and the SN-38 is further metabolized to its inactive form, SN-38G.	Irinotecan	84-89	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	118-121
12871782-1	2003	The anticancer agent irinotecan (CPT-11) is a prodrug converted to its active form, SN-38, by human carboxylesterase (hCE) and the SN-38 is further metabolized to its inactive form, SN-38G.	Irinotecan	131-136	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	118-121
12871782-1	2003	The anticancer agent irinotecan (CPT-11) is a prodrug converted to its active form, SN-38, by human carboxylesterase (hCE) and the SN-38 is further metabolized to its inactive form, SN-38G.	Irinotecan	131-136	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	118-121
12730278-2	2003	Recent studies have revealed that other UGT1A isoforms, UGT1A7 and UGT1A9, also participate in SN-38 glucuronidation.	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	40-45
12730278-2	2003	Recent studies have revealed that other UGT1A isoforms, UGT1A7 and UGT1A9, also participate in SN-38 glucuronidation.	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	56-62
12730278-2	2003	Recent studies have revealed that other UGT1A isoforms, UGT1A7 and UGT1A9, also participate in SN-38 glucuronidation.	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	67-73
12730278-3	2003	Although several genetic polymorphisms are reported for UGT1A1 and UGT1A7 that affect the SN-38 glucuronidation activities, no such polymorphisms have been identified for UGT1A9.	Irinotecan	90-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
12730278-3	2003	Although several genetic polymorphisms are reported for UGT1A1 and UGT1A7 that affect the SN-38 glucuronidation activities, no such polymorphisms have been identified for UGT1A9.	Irinotecan	90-95	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	67-73
12730278-4	2003	In the present study, UGT1A9 exon 1 and its flanking regions were sequenced from 61 Japanese cancer patients who were all treated with irinotecan.	Irinotecan	135-145	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	22-28
12730278-8	2003	The SN-38 glucuronidation efficiency (normalized Vmax/Km) of D256N was less than 5% that of wild-type UGT1A9.	Irinotecan	4-9	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	102-108
12730278-10	2003	These findings highlight the importance of further studies into the potential influence of UGT1A9 D256N variant to irinotecan metabolism in vivo.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	91-97
12869632-7	2003	Our results indicate that the expression of ABCG2 protects cells from CPT-11 toxicity, even in the presence of high levels of a rabbit liver carboxylesterase (rCE), which can efficiently activate the drug.	Irinotecan	70-76	ATP-binding cassette sub-family G member 2	Oryctolagus cuniculus	44-49
12939466-0	2003	Gene-directed enzyme prodrug therapy for osteosarcoma: sensitization to CPT-11 in vitro and in vivo by adenoviral delivery of a gene encoding secreted carboxylesterase-2.	Irinotecan	72-78	carboxylesterase 2	Homo sapiens	151-169
12682043-4	2003	The ABCG2-mediated transport of [3H]E1S was potently inhibited by SN-38 and many sulfate conjugates but not by glucuronide and glutathione conjugates or other anionic compounds.	Irinotecan	66-71	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	4-9
12939466-5	2003	GDEPT aims at high production of CE2 at the tumor site, resulting in efficient local conversion of CPT-11 into SN-38.	Irinotecan	99-105	carboxylesterase 2	Homo sapiens	33-36
12939466-5	2003	GDEPT aims at high production of CE2 at the tumor site, resulting in efficient local conversion of CPT-11 into SN-38.	Irinotecan	111-116	carboxylesterase 2	Homo sapiens	33-36
12855666-1	2003	PURPOSE: To identify determinants of the effect of antisense-mediated Bcl-xl down-regulation (Bcl-xl knockdown) on the response of colorectal cancer cells to SN38, the active metabolite of irinotecan, a topoisomerase I inhibitor licensed for colorectal cancer chemotherapy.	Irinotecan	189-199	BCL2 like 1	Homo sapiens	70-76
12855666-1	2003	PURPOSE: To identify determinants of the effect of antisense-mediated Bcl-xl down-regulation (Bcl-xl knockdown) on the response of colorectal cancer cells to SN38, the active metabolite of irinotecan, a topoisomerase I inhibitor licensed for colorectal cancer chemotherapy.	Irinotecan	189-199	BCL2 like 1	Homo sapiens	94-100
12886870-3	2003	Inhibition of the cyclooxygenase-2 (COX-2) enzyme, which is active in tumorigenesis, may augment efficacy and reduce toxicity of platinum/irinotecan combinations.	Irinotecan	138-148	prostaglandin-endoperoxide synthase 2	Homo sapiens	18-34
12886870-3	2003	Inhibition of the cyclooxygenase-2 (COX-2) enzyme, which is active in tumorigenesis, may augment efficacy and reduce toxicity of platinum/irinotecan combinations.	Irinotecan	138-148	prostaglandin-endoperoxide synthase 2	Homo sapiens	36-41
12817897-0	2003	Effect of P-glycoprotein modulator, cyclosporin A, on the gastrointestinal excretion of irinotecan and its metabolite SN-38 in rats.	Irinotecan	88-98	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	10-24
12810652-8	2003	In addition, immunoblotting studies indicate that whereas increased BCRP expression is evident in cells selected for resistance to irinotecan, BCRP expression is not detectable in two different cell lines selected for resistance to 9-NC.	Irinotecan	131-141	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	68-72
12817897-0	2003	Effect of P-glycoprotein modulator, cyclosporin A, on the gastrointestinal excretion of irinotecan and its metabolite SN-38 in rats.	Irinotecan	118-123	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	10-24
12817897-1	2003	PURPOSE: The purpose of this work was to investigate the role of the hepatic and intestinal P-glycoprotein (P-gp) and canalicular multispecific organic anion transporter/multidrug resistance-associated protein 2 (cMOAT/MRP2) on both biliary excretion and intestinal exsorption of irinotecan hydrochloride (CPT-11) and its metabolite, SN-38, in the lactone and carboxylate forms.	Irinotecan	280-304	ATP binding cassette subfamily C member 2	Rattus norvegicus	213-218
12817897-1	2003	PURPOSE: The purpose of this work was to investigate the role of the hepatic and intestinal P-glycoprotein (P-gp) and canalicular multispecific organic anion transporter/multidrug resistance-associated protein 2 (cMOAT/MRP2) on both biliary excretion and intestinal exsorption of irinotecan hydrochloride (CPT-11) and its metabolite, SN-38, in the lactone and carboxylate forms.	Irinotecan	306-312	ATP binding cassette subfamily C member 2	Rattus norvegicus	213-218
12817897-1	2003	PURPOSE: The purpose of this work was to investigate the role of the hepatic and intestinal P-glycoprotein (P-gp) and canalicular multispecific organic anion transporter/multidrug resistance-associated protein 2 (cMOAT/MRP2) on both biliary excretion and intestinal exsorption of irinotecan hydrochloride (CPT-11) and its metabolite, SN-38, in the lactone and carboxylate forms.	Irinotecan	334-339	ATP binding cassette subfamily C member 2	Rattus norvegicus	213-218
12817897-8	2003	CONCLUSIONS: The transports of CPT-11 and SN-38 via the biliary route seem to be essentially related with cMOAT/MRP2, whereas those of both compounds via the intestinal membrane seem to be related with P-gp.	Irinotecan	31-37	ATP binding cassette subfamily C member 2	Rattus norvegicus	106-111
12817897-8	2003	CONCLUSIONS: The transports of CPT-11 and SN-38 via the biliary route seem to be essentially related with cMOAT/MRP2, whereas those of both compounds via the intestinal membrane seem to be related with P-gp.	Irinotecan	31-37	ATP binding cassette subfamily C member 2	Rattus norvegicus	112-116
12817897-8	2003	CONCLUSIONS: The transports of CPT-11 and SN-38 via the biliary route seem to be essentially related with cMOAT/MRP2, whereas those of both compounds via the intestinal membrane seem to be related with P-gp.	Irinotecan	31-37	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	202-206
12817897-8	2003	CONCLUSIONS: The transports of CPT-11 and SN-38 via the biliary route seem to be essentially related with cMOAT/MRP2, whereas those of both compounds via the intestinal membrane seem to be related with P-gp.	Irinotecan	42-47	ATP binding cassette subfamily C member 2	Rattus norvegicus	106-111
12817897-8	2003	CONCLUSIONS: The transports of CPT-11 and SN-38 via the biliary route seem to be essentially related with cMOAT/MRP2, whereas those of both compounds via the intestinal membrane seem to be related with P-gp.	Irinotecan	42-47	ATP binding cassette subfamily C member 2	Rattus norvegicus	112-116
12817897-8	2003	CONCLUSIONS: The transports of CPT-11 and SN-38 via the biliary route seem to be essentially related with cMOAT/MRP2, whereas those of both compounds via the intestinal membrane seem to be related with P-gp.	Irinotecan	42-47	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	202-206
12712458-11	2003	The combination of a PKC inhibitor with CPT-11 or SN-38 led to decreased expression of the antiapoptotic protein bcl-2, and increased expression of the proapoptotic protein bax.	Irinotecan	40-46	BCL2 apoptosis regulator	Homo sapiens	113-118
12712458-11	2003	The combination of a PKC inhibitor with CPT-11 or SN-38 led to decreased expression of the antiapoptotic protein bcl-2, and increased expression of the proapoptotic protein bax.	Irinotecan	40-46	BCL2 associated X, apoptosis regulator	Homo sapiens	173-176
12712458-11	2003	The combination of a PKC inhibitor with CPT-11 or SN-38 led to decreased expression of the antiapoptotic protein bcl-2, and increased expression of the proapoptotic protein bax.	Irinotecan	50-55	BCL2 apoptosis regulator	Homo sapiens	113-118
12712458-11	2003	The combination of a PKC inhibitor with CPT-11 or SN-38 led to decreased expression of the antiapoptotic protein bcl-2, and increased expression of the proapoptotic protein bax.	Irinotecan	50-55	BCL2 associated X, apoptosis regulator	Homo sapiens	173-176
12847914-5	2003	Moreover, inhibition of FAK gene expression by a phosphorothioated antisense oligodeoxynucleotide targeting the portion of the gene encoding amino acids 262-268, increased the sensitivity of ZR-75-1, MDA-MB-231 and MCF7 breast cancer cells to treatment with TPT or CPT-11.	Irinotecan	265-271	protein tyrosine kinase 2	Homo sapiens	24-27
12800608-6	2003	Two recent pharmacogenetic trials (one performed in the United States and the other in Japan) investigated the clinical significance of UGT1A1 gene mutations for both the pharmacokinetics of irinotecan metabolites and the toxicity profile.	Irinotecan	191-201	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	136-142
12769780-8	2003	In particular, the UGT1A1*28 allele has been associated with an increased toxicity after irinotecan chemotherapy.	Irinotecan	89-99	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	19-25
12800601-13	2003	COX-2 inhibitors also improve tumor response to chemotherapeutic agents, including irinotecan.	Irinotecan	83-93	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-5
12800601-14	2003	Additional therapeutic benefit was observed for celecoxib (Celebrex), a selective COX-2 inhibitor, consisting of a strong reduction in irinotecan-induced diarrhea.	Irinotecan	135-145	prostaglandin-endoperoxide synthase 2	Homo sapiens	82-87
12800606-15	2003	The recommended phase II doses of irinotecan and temozolomide on treatment arms 1 and 3 remain to be determined as patient accrual is currently ongoing.	Irinotecan	34-44	ADRM1 26S proteasome ubiquitin receptor	Homo sapiens	75-87
12800608-0	2003	Irinotecan treatment in cancer patients with UGT1A1 polymorphisms.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
12800608-1	2003	At the present time, pharmacogenetic investigation of irinotecan (CPT-11, Camptosar) therapy is mainly focused on the clinical relevance of genetic variation in the UDP-glucuronosyltransferase (UGT1A1) gene.	Irinotecan	54-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
12800608-1	2003	At the present time, pharmacogenetic investigation of irinotecan (CPT-11, Camptosar) therapy is mainly focused on the clinical relevance of genetic variation in the UDP-glucuronosyltransferase (UGT1A1) gene.	Irinotecan	66-72	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
12800608-1	2003	At the present time, pharmacogenetic investigation of irinotecan (CPT-11, Camptosar) therapy is mainly focused on the clinical relevance of genetic variation in the UDP-glucuronosyltransferase (UGT1A1) gene.	Irinotecan	74-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	194-200
12800608-3	2003	UGT1A1 genotypes associated with Gilbert"s syndrome (a mild intermittent hyperbilirubinemia) are characterized by reduced glucuronidation of SN-38.	Irinotecan	141-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
12704006-4	2003	The BCRP-overexpressing tumor cells are resistant to mitoxantrone, adriamycin, daunorubicin, etoposide, topotecan and irinotecan, but lack resistance to paclitaxel and vincristine.	Irinotecan	118-128	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	4-8
12617927-2	2003	Since this prodrug is significantly less cytotoxic than SN-38 itself and efficiently releases the drug in vitro in the presence of beta-D-glucuronidase, it can be considered as an appropriate candidate for cancer treatment by a PMT strategy.	Irinotecan	56-61	glucuronidase beta	Homo sapiens	131-151
12485949-9	2003	M-LK transfected cells manifested more severe cytotoxicity than TGH transfected cells upon being exposed to irinotecan.	Irinotecan	108-118	carboxylesterase 1D	Mus musculus	64-67
12538824-0	2003	p53-mediated regulation of expression of a rabbit liver carboxylesterase confers sensitivity to 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11).	Irinotecan	96-161	tumor protein p53	Homo sapiens	0-3
12538824-0	2003	p53-mediated regulation of expression of a rabbit liver carboxylesterase confers sensitivity to 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11).	Irinotecan	96-161	liver carboxylesterase 1	Oryctolagus cuniculus	50-72
12538824-0	2003	p53-mediated regulation of expression of a rabbit liver carboxylesterase confers sensitivity to 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11).	Irinotecan	163-169	tumor protein p53	Homo sapiens	0-3
12538824-0	2003	p53-mediated regulation of expression of a rabbit liver carboxylesterase confers sensitivity to 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11).	Irinotecan	163-169	liver carboxylesterase 1	Oryctolagus cuniculus	50-72
12538824-3	2003	Upon transfection of these plasmids into cells expressing either wt or mutant p53, differential expression of the CE has been observed, resulting in sensitization of the cells expressing the latter protein to the anticancer prodrug irinotecan, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carb- onyloxycamptothecin (CPT-11).	Irinotecan	232-242	tumor protein p53	Homo sapiens	78-81
12538824-3	2003	Upon transfection of these plasmids into cells expressing either wt or mutant p53, differential expression of the CE has been observed, resulting in sensitization of the cells expressing the latter protein to the anticancer prodrug irinotecan, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carb- onyloxycamptothecin (CPT-11).	Irinotecan	244-312	tumor protein p53	Homo sapiens	78-81
12538824-3	2003	Upon transfection of these plasmids into cells expressing either wt or mutant p53, differential expression of the CE has been observed, resulting in sensitization of the cells expressing the latter protein to the anticancer prodrug irinotecan, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carb- onyloxycamptothecin (CPT-11).	Irinotecan	314-320	tumor protein p53	Homo sapiens	78-81
12538824-5	2003	These studies indicate that the inactivation of wtp53 by mutant p53 in human tumor cells may be sufficient enough to generate a therapeutic window for enhanced cytotoxicity with CPT-11.	Irinotecan	178-184	tumor protein p53	Homo sapiens	50-53
12569373-1	2003	To determine a standard combination chemotherapy for patients with advanced non-small-cell lung cancer (NSCLC), we conducted a phase III trial of irinotecan (CPT-11) to test the hypotheses that CPT-11+cisplatin is superior to cisplatin+vindesine and that CPT-11 monotherapy is not inferior to cisplatin+vindesine.	Irinotecan	146-156	choline phosphotransferase 1	Homo sapiens	158-161
12570720-6	2003	Irinotecan is subjected to be shunted between CYP3A4 mediated oxidative metabolism to form two inactive metabolites APC or NPC and tissue carboxylesterase mediated hydrolysis to form SN-38 which is eventually detoxified via glucuronidation by UGT1A1 to form SN-38G.	Irinotecan	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	46-52
12570720-6	2003	Irinotecan is subjected to be shunted between CYP3A4 mediated oxidative metabolism to form two inactive metabolites APC or NPC and tissue carboxylesterase mediated hydrolysis to form SN-38 which is eventually detoxified via glucuronidation by UGT1A1 to form SN-38G.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	243-249
12570720-6	2003	Irinotecan is subjected to be shunted between CYP3A4 mediated oxidative metabolism to form two inactive metabolites APC or NPC and tissue carboxylesterase mediated hydrolysis to form SN-38 which is eventually detoxified via glucuronidation by UGT1A1 to form SN-38G.	Irinotecan	183-188	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	243-249
12570720-6	2003	Irinotecan is subjected to be shunted between CYP3A4 mediated oxidative metabolism to form two inactive metabolites APC or NPC and tissue carboxylesterase mediated hydrolysis to form SN-38 which is eventually detoxified via glucuronidation by UGT1A1 to form SN-38G.	Irinotecan	258-263	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	46-52
12570720-7	2003	The pharmacology of this compound is further complicated by the existence of genetic inter-individual differences in activation and deactivation enzymes of irinotecan (e.g., CYP3A4, CYP3A5, UGT1A1) and sharing competitive elimination pathways with many concomitant medications, such as anticonvulsants, St. John"s Wort, and ketoconazole.	Irinotecan	156-166	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	174-180
12570720-7	2003	The pharmacology of this compound is further complicated by the existence of genetic inter-individual differences in activation and deactivation enzymes of irinotecan (e.g., CYP3A4, CYP3A5, UGT1A1) and sharing competitive elimination pathways with many concomitant medications, such as anticonvulsants, St. John"s Wort, and ketoconazole.	Irinotecan	156-166	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	182-188
12570720-9	2003	This review highlights the latest findings in drug activation, transport mechanisms, glucuronidation, and CYP3A-mediated drug-drug interactions of irinotecan in order to unlock some of its complicated pharmacology and to provide ideas for relevant future studies into optimization of this promising agent.	Irinotecan	147-157	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	106-111
15618737-1	2003	Eight novel single nucleotide polymorphisms (SNPs) were found in the gene encoding the ATP-binding cassette transporter, ABCG2/BCRP, from 60 Japanese individuals administered the anti-cancer drug irinotecan.	Irinotecan	196-206	ATP binding cassette subfamily A member 4	Homo sapiens	87-119
12775012-11	2003	Several preliminary results of combination phase I/II studies of S-1 with CDDP or CPT-11 have recently been obtained, and phase II studies are in progress.	Irinotecan	82-88	proteasome 26S subunit, non-ATPase 1	Homo sapiens	65-68
15618737-1	2003	Eight novel single nucleotide polymorphisms (SNPs) were found in the gene encoding the ATP-binding cassette transporter, ABCG2/BCRP, from 60 Japanese individuals administered the anti-cancer drug irinotecan.	Irinotecan	196-206	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	121-126
15618737-1	2003	Eight novel single nucleotide polymorphisms (SNPs) were found in the gene encoding the ATP-binding cassette transporter, ABCG2/BCRP, from 60 Japanese individuals administered the anti-cancer drug irinotecan.	Irinotecan	196-206	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	127-131
15618752-1	2003	Twelve novel single nucleotide polymorphisms (SNPs) were found in the CES2 gene from 153 Japanese individuals, who were administered irinotecan or steroidal drugs.	Irinotecan	133-143	carboxylesterase 2	Homo sapiens	70-74
12607608-3	2002	Carboxylesterase-2 has been identified as the key enzyme in the metabolic activation of the irinotecan, a topoisomerase I inhibitor commonly used in the treatment of many solid tumors.	Irinotecan	92-102	carboxylesterase 2	Homo sapiens	0-18
12485959-0	2003	Glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan (CPT-11), by human UGT1A1 variants, G71R, P229Q, and Y486D.	Irinotecan	19-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
12485959-0	2003	Glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan (CPT-11), by human UGT1A1 variants, G71R, P229Q, and Y486D.	Irinotecan	51-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
12485959-0	2003	Glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan (CPT-11), by human UGT1A1 variants, G71R, P229Q, and Y486D.	Irinotecan	83-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
12485959-0	2003	Glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan (CPT-11), by human UGT1A1 variants, G71R, P229Q, and Y486D.	Irinotecan	95-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
12485959-1	2003	7-Ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of antitumor agent irinotecan (CPT-11), is conjugated and detoxified to SN-38-glucuronide by UDP-glucuronosyltransferase (UGT) 1A1.	Irinotecan	0-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-191
12485959-1	2003	7-Ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of antitumor agent irinotecan (CPT-11), is conjugated and detoxified to SN-38-glucuronide by UDP-glucuronosyltransferase (UGT) 1A1.	Irinotecan	32-37	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-191
12485959-1	2003	7-Ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of antitumor agent irinotecan (CPT-11), is conjugated and detoxified to SN-38-glucuronide by UDP-glucuronosyltransferase (UGT) 1A1.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-191
12485959-1	2003	7-Ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of antitumor agent irinotecan (CPT-11), is conjugated and detoxified to SN-38-glucuronide by UDP-glucuronosyltransferase (UGT) 1A1.	Irinotecan	92-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	154-191
12485959-2	2003	Genetic polymorphisms in UGT1A1 are thought to contribute to severe diarrhea and/or leukopenia caused by CPT-11.	Irinotecan	105-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
12485959-4	2003	However, little information is available on the influence of UGT1A1 polymorphisms in the coding region on the SN-38 glucuronidation activity.	Irinotecan	110-115	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
12485959-7	2003	WT UGT1A1 catalyzed SN-38 glucuronidation with an apparent K(m) value of 11.5 microM, whereas those of G71R, P229Q, and Y486D were 14.0, 18.0, and 63.5 microM, respectively.	Irinotecan	20-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	3-9
12485959-10	2003	The decreased SN-38 glucuronidation efficiency ratio of G71R and P229Q could be critical in combination with other polymorphisms in the UGT1A1 gene.	Irinotecan	14-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	136-142
12533678-1	2003	Breast cancer resistance protein (BCRP), an ATP-binding cassette transporter, confers resistance to a series of anticancer agents such as SN-38, mitoxantrone, and topotecan.	Irinotecan	138-143	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
12533678-1	2003	Breast cancer resistance protein (BCRP), an ATP-binding cassette transporter, confers resistance to a series of anticancer agents such as SN-38, mitoxantrone, and topotecan.	Irinotecan	138-143	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
12533678-13	2003	Reversal of SN-38 and mitoxantrone resistance in K562/BCRP cells by TAG-139 was 5-fold stronger than that by estrone.	Irinotecan	12-17	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	54-58
12607608-8	2002	The results suggest that liver and gastrointestinal tract with carboxylesterase-2 are likely the most important sites of conversion of irinotecan to the active metabolite SN-38, but carboxylesterase-2 within the other tissues may be contributive to this process.	Irinotecan	135-145	carboxylesterase 2	Homo sapiens	63-81
12607608-8	2002	The results suggest that liver and gastrointestinal tract with carboxylesterase-2 are likely the most important sites of conversion of irinotecan to the active metabolite SN-38, but carboxylesterase-2 within the other tissues may be contributive to this process.	Irinotecan	171-176	carboxylesterase 2	Homo sapiens	63-81
12384538-0	2002	Cyclooxygenase-2 inhibition with celecoxib enhances antitumor efficacy and reduces diarrhea side effect of CPT-11.	Irinotecan	107-113	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-16
12464801-4	2002	We also investigated the relationship between PBREM-(TA)n haplotypes and the glucuronidation rate of the UGT1A1 substrate SN-38.	Irinotecan	122-127	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	105-111
12218061-3	2002	Here we demonstrate that the first 4-8 N-terminal amino acids of Smac/DIABLO fused to the Drosophila antennapaedia penetratin sequence, a carrier peptide, enhance the induction of apoptosis and long term antiproliferative effects of diverse antineoplastic agents including paclitaxel, etoposide, 7-ethyl-10-hydroxycamptothecin (SN-38), and doxorubicin in MCF-7 breast cancer cells.	Irinotecan	296-326	diablo	Drosophila melanogaster	65-69
12218061-3	2002	Here we demonstrate that the first 4-8 N-terminal amino acids of Smac/DIABLO fused to the Drosophila antennapaedia penetratin sequence, a carrier peptide, enhance the induction of apoptosis and long term antiproliferative effects of diverse antineoplastic agents including paclitaxel, etoposide, 7-ethyl-10-hydroxycamptothecin (SN-38), and doxorubicin in MCF-7 breast cancer cells.	Irinotecan	296-326	diablo	Drosophila melanogaster	70-76
12218061-3	2002	Here we demonstrate that the first 4-8 N-terminal amino acids of Smac/DIABLO fused to the Drosophila antennapaedia penetratin sequence, a carrier peptide, enhance the induction of apoptosis and long term antiproliferative effects of diverse antineoplastic agents including paclitaxel, etoposide, 7-ethyl-10-hydroxycamptothecin (SN-38), and doxorubicin in MCF-7 breast cancer cells.	Irinotecan	328-333	diablo	Drosophila melanogaster	65-69
12218061-3	2002	Here we demonstrate that the first 4-8 N-terminal amino acids of Smac/DIABLO fused to the Drosophila antennapaedia penetratin sequence, a carrier peptide, enhance the induction of apoptosis and long term antiproliferative effects of diverse antineoplastic agents including paclitaxel, etoposide, 7-ethyl-10-hydroxycamptothecin (SN-38), and doxorubicin in MCF-7 breast cancer cells.	Irinotecan	328-333	diablo	Drosophila melanogaster	70-76
12482336-0	2002	Combination of 5-fluorouracil and irinotecan on modulation of thymidylate synthase and topoisomerase I expression and cell cycle regulation in human colon cancer LoVo cells: clinical relevance.	Irinotecan	34-44	thymidylate synthetase	Homo sapiens	62-82
12465401-0	2002	[A case of AFP-producing gastric cancer with multiple liver metastases responding to CPT-11 and cisplatin combination chemotherapy].	Irinotecan	85-91	alpha fetoprotein	Homo sapiens	11-14
12465401-1	2002	A case of AFP-producing gastric cancer successfully treated with CPT-11 and cisplatin combined therapy is reported together with a review of the literature.	Irinotecan	65-71	alpha fetoprotein	Homo sapiens	10-13
12465401-8	2002	This result suggests that combination chemotherapy consisting of CPT-11 and cisplatin may be effective and safe for patients with AFP-producing gastric cancer with multiple liver metastases.	Irinotecan	65-71	alpha fetoprotein	Homo sapiens	130-133
12484020-0	2002	[A case of postoperative liver metastasis of alpha-fetoprotein producing gastric cancer successfully treated with intrahepatic chemotherapy (adriamycin, cisplatin, irinotecan hydrochloride)].	Irinotecan	164-188	alpha fetoprotein	Homo sapiens	45-62
12484020-5	2002	Twenty cycles of intrahepatic arterial infusion with adriamycin, cisplatin, and irinotecan hydrochloride resulted in a 93% decrease in the liver metastases along with normalization of the serum AFP level.	Irinotecan	80-104	alpha fetoprotein	Homo sapiens	194-197
12370755-0	2002	Phosphorylation of chk1 at serine-345 affected by topoisomerase I poison SN-38.	Irinotecan	73-78	checkpoint kinase 1	Homo sapiens	19-23
12370755-6	2002	Increased chk1 phosphorylation at Ser345 induced by SN-38 was accompanied by the observed G2 phase arrest in the A253 cell line, while significant downregulation of chk1 and cdc25C phosphorylation, which resulted in the abrogation of G2/M checkpoint arrest, was noted in FaDu cells at this timepoint.	Irinotecan	52-57	checkpoint kinase 1	Homo sapiens	10-14
12370755-7	2002	These results suggest that alterations of chk1 signaling are associated with the response to topoisomerase I poison SN-38.	Irinotecan	116-121	checkpoint kinase 1	Homo sapiens	42-46
12370755-9	2002	A deficiency in G2 arrest was observed in FaDu cells, suggesting endogenous hMLH1 protein expression is associated with the abrogation of G2/M arrest, subsequently with the response to topoisomerase I poison SN-38.	Irinotecan	208-213	mutL homolog 1	Homo sapiens	76-81
12440157-3	2002	To increase the clinical usefulness of theanine, we examined its effects on the antitumor activity of cisplatin and irinotecan (CPT-11), which a known to be transported by the efflux system related to MRP.	Irinotecan	116-126	ATP-binding cassette, sub-family C (CFTR/MRP), member 1	Mus musculus	201-204
12440157-3	2002	To increase the clinical usefulness of theanine, we examined its effects on the antitumor activity of cisplatin and irinotecan (CPT-11), which a known to be transported by the efflux system related to MRP.	Irinotecan	128-134	ATP-binding cassette, sub-family C (CFTR/MRP), member 1	Mus musculus	201-204
12384538-6	2002	We also assessed the involvement of COX-2 in the pathogenesis of CPT-11-induced late diarrhea using a rat model.	Irinotecan	65-71	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	36-41
12384541-5	2002	Combining TRAIL with either 5-fluorouracil (5-FU) or CPT-11 (irinotecan hydrochloride) produced a greatly enhanced antitumor effect over that of either agent alone, with 50% of the animals achieving complete tumor regression with a combination of TRAIL and CPT-11.	Irinotecan	53-59	TNF superfamily member 10	Homo sapiens	247-252
12384541-5	2002	Combining TRAIL with either 5-fluorouracil (5-FU) or CPT-11 (irinotecan hydrochloride) produced a greatly enhanced antitumor effect over that of either agent alone, with 50% of the animals achieving complete tumor regression with a combination of TRAIL and CPT-11.	Irinotecan	61-85	TNF superfamily member 10	Homo sapiens	10-15
12384541-5	2002	Combining TRAIL with either 5-fluorouracil (5-FU) or CPT-11 (irinotecan hydrochloride) produced a greatly enhanced antitumor effect over that of either agent alone, with 50% of the animals achieving complete tumor regression with a combination of TRAIL and CPT-11.	Irinotecan	61-85	TNF superfamily member 10	Homo sapiens	247-252
12384541-5	2002	Combining TRAIL with either 5-fluorouracil (5-FU) or CPT-11 (irinotecan hydrochloride) produced a greatly enhanced antitumor effect over that of either agent alone, with 50% of the animals achieving complete tumor regression with a combination of TRAIL and CPT-11.	Irinotecan	257-263	TNF superfamily member 10	Homo sapiens	10-15
12384541-9	2002	Tumors treated with CPT-11 showed increased membrane expression of DR5, suggesting that CPT-11 may increase sensitivity to TRAIL by up-regulation of DR5.	Irinotecan	20-26	TNF receptor superfamily member 10b	Homo sapiens	67-70
12384541-9	2002	Tumors treated with CPT-11 showed increased membrane expression of DR5, suggesting that CPT-11 may increase sensitivity to TRAIL by up-regulation of DR5.	Irinotecan	20-26	TNF superfamily member 10	Homo sapiens	123-128
12384541-9	2002	Tumors treated with CPT-11 showed increased membrane expression of DR5, suggesting that CPT-11 may increase sensitivity to TRAIL by up-regulation of DR5.	Irinotecan	20-26	TNF receptor superfamily member 10b	Homo sapiens	149-152
12384541-9	2002	Tumors treated with CPT-11 showed increased membrane expression of DR5, suggesting that CPT-11 may increase sensitivity to TRAIL by up-regulation of DR5.	Irinotecan	88-94	TNF receptor superfamily member 10b	Homo sapiens	67-70
12384541-9	2002	Tumors treated with CPT-11 showed increased membrane expression of DR5, suggesting that CPT-11 may increase sensitivity to TRAIL by up-regulation of DR5.	Irinotecan	88-94	TNF superfamily member 10	Homo sapiens	123-128
12384541-9	2002	Tumors treated with CPT-11 showed increased membrane expression of DR5, suggesting that CPT-11 may increase sensitivity to TRAIL by up-regulation of DR5.	Irinotecan	88-94	TNF receptor superfamily member 10b	Homo sapiens	149-152
12369998-3	2002	When overexpressed in cell lines, ABCG2 has the ability to confer high levels of resistance to anthracyclines, mitoxantrone, bisantrene, and the camptothecins topotecan and SN-38.	Irinotecan	173-178	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-39
12209584-0	2002	Cellular effects of CPT-11 on colon carcinoma cells: dependence on p53 and hMLH1 status.	Irinotecan	20-26	tumor protein p53	Homo sapiens	67-70
12237777-3	2002	An approach to achieve tumour specific activation of CPT-11 is to transduce the cDNA encoding carboxylesterase into tumour cells.	Irinotecan	53-59	carboxylesterase 2	Homo sapiens	94-110
12237777-11	2002	Importantly, in combination with CPT-11 both recombinant carboxylesterase proteins exerted strong antiproliferative effects on human colon cancer cells.	Irinotecan	33-39	carboxylesterase 2	Homo sapiens	57-73
12237778-8	2002	In vivo experiments in well-established 2780DX8 human tumour xenografts demonstrated that the growth inhibition induced by CPT-11 was more affected by breast cancer resistance protein expression than that of DX-8951f.	Irinotecan	123-129	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	151-183
12209584-0	2002	Cellular effects of CPT-11 on colon carcinoma cells: dependence on p53 and hMLH1 status.	Irinotecan	20-26	mutL homolog 1	Homo sapiens	75-80
12181297-8	2002	PAF-induced (10 microM) Cl- secretion was inhibited by carboxy-PTIO (200 microM) and ODQ (10 microM), whereas irinotecan-induced (500 microM) Cl- secretion was not significantly inhibited by these drugs.	Irinotecan	110-120	PCNA clamp associated factor	Rattus norvegicus	0-3
12359059-6	2002	(2) An inhibitor of the nuclear transport of GSTpi, edible mushroom lectin (Agaricus bisporus lectin, ABL), increased the sensitivity of the cancer cells to DOX and CDDP, and partially to CPT-11.	Irinotecan	188-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
12181437-0	2002	Common human UGT1A polymorphisms and the altered metabolism of irinotecan active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	92-122	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	13-18
12181437-0	2002	Common human UGT1A polymorphisms and the altered metabolism of irinotecan active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38).	Irinotecan	124-129	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	13-18
12181437-3	2002	The purpose of this study was to determine whether common polymorphic UDP-glucuronosyltransferase (UGT) affects SN-38 glucuronidation.	Irinotecan	112-117	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	70-97
12181437-3	2002	The purpose of this study was to determine whether common polymorphic UDP-glucuronosyltransferase (UGT) affects SN-38 glucuronidation.	Irinotecan	112-117	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	99-102
12181437-5	2002	To assess the relative activity of UGT isoenzymes for SN-38, rates of formation of SN-38-G were monitored by liquid chromatography/mass spectrometry analysis and normalized by level of UGT cellular expression.	Irinotecan	54-59	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	35-38
12181437-6	2002	Determination of intrinsic clearances predicts that hepatic UGT1A1 and UGT1A9 and the extrahepatic UGT1A7 are major components in SN-38-G formation, whereas a minor role is suggested for UGT1A6, UGT1A8, and UGT1A10.	Irinotecan	130-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
12181437-6	2002	Determination of intrinsic clearances predicts that hepatic UGT1A1 and UGT1A9 and the extrahepatic UGT1A7 are major components in SN-38-G formation, whereas a minor role is suggested for UGT1A6, UGT1A8, and UGT1A10.	Irinotecan	130-135	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	71-77
12181437-6	2002	Determination of intrinsic clearances predicts that hepatic UGT1A1 and UGT1A9 and the extrahepatic UGT1A7 are major components in SN-38-G formation, whereas a minor role is suggested for UGT1A6, UGT1A8, and UGT1A10.	Irinotecan	130-135	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	99-105
12181437-7	2002	In support of the involvement of UGT1A9, a strong coefficient of correlation was observed in the glucuronidation of SN-38 and a substrate, mainly glucuronidate, by UGT1A9 (flavopiridol) by human liver microsomes (coefficient of correlation, 0.905; p = 0.002).	Irinotecan	116-121	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	33-39
12181437-7	2002	In support of the involvement of UGT1A9, a strong coefficient of correlation was observed in the glucuronidation of SN-38 and a substrate, mainly glucuronidate, by UGT1A9 (flavopiridol) by human liver microsomes (coefficient of correlation, 0.905; p = 0.002).	Irinotecan	116-121	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	164-170
12181437-11	2002	Taken together, these data provide the evidence that molecular determinants of irinotecan response may include the UGT1A polymorphisms studied herein and common genetic variants of the hepatic UGT1A9 isoenzyme yet to be described.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	115-120
12181437-11	2002	Taken together, these data provide the evidence that molecular determinants of irinotecan response may include the UGT1A polymorphisms studied herein and common genetic variants of the hepatic UGT1A9 isoenzyme yet to be described.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	193-199
12380945-4	2002	Irinotecan (CPT-II, Camptosar) has demonstrated efficacy in the treatment of small-cell lung cancer (SCLC).	Irinotecan	0-10	carnitine palmitoyltransferase 2	Homo sapiens	12-18
12189228-2	2002	In this study, we determined the effect of SJW on the metabolism of irinotecan, a pro-drug of SN-38 and a known substrate for CYP3A4.	Irinotecan	68-78	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	126-132
12171891-5	2002	This scenario raises the possibility that local conversion of irinotecan to SN-38 by CES2 in tumor tissues might occur.	Irinotecan	62-72	carboxylesterase 2	Homo sapiens	85-89
12171891-0	2002	Human carboxylesterase 2 is commonly expressed in tumor tissue and is correlated with activation of irinotecan.	Irinotecan	100-110	carboxylesterase 2	Homo sapiens	6-24
12171891-5	2002	This scenario raises the possibility that local conversion of irinotecan to SN-38 by CES2 in tumor tissues might occur.	Irinotecan	76-81	carboxylesterase 2	Homo sapiens	85-89
12171891-10	2002	Liver microsomal CES2 protein expression was significantly correlated with irinotecan activation to SN-38 (R(s) = 0.70; P = 0.007).	Irinotecan	75-85	carboxylesterase 2	Homo sapiens	17-21
12171891-10	2002	Liver microsomal CES2 protein expression was significantly correlated with irinotecan activation to SN-38 (R(s) = 0.70; P = 0.007).	Irinotecan	100-105	carboxylesterase 2	Homo sapiens	17-21
12171891-11	2002	This study confirms that CES2 is a key enzyme for irinotecan activation.	Irinotecan	50-60	carboxylesterase 2	Homo sapiens	25-29
12171891-12	2002	Tumor CES2 expression may contribute to variable response to irinotecan chemotherapy for solid tumors.	Irinotecan	61-71	carboxylesterase 2	Homo sapiens	6-10
12171903-0	2002	Irinotecan activation by human carboxylesterases in colorectal adenocarcinoma cells.	Irinotecan	0-10	carboxylesterase 1	Homo sapiens	31-48
12171903-1	2002	Carboxylesterases play a critical role in the bioactivation of the anticancer prodrug irinotecan [7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxy-camptothecin; CPT-11] into its active metabolite SN-38 (ethyl-10-hydroxy-camptothecin).	Irinotecan	86-96	carboxylesterase 1	Homo sapiens	0-17
12171903-1	2002	Carboxylesterases play a critical role in the bioactivation of the anticancer prodrug irinotecan [7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxy-camptothecin; CPT-11] into its active metabolite SN-38 (ethyl-10-hydroxy-camptothecin).	Irinotecan	98-164	carboxylesterase 1	Homo sapiens	0-17
12171903-1	2002	Carboxylesterases play a critical role in the bioactivation of the anticancer prodrug irinotecan [7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxy-camptothecin; CPT-11] into its active metabolite SN-38 (ethyl-10-hydroxy-camptothecin).	Irinotecan	166-172	carboxylesterase 1	Homo sapiens	0-17
12171903-1	2002	Carboxylesterases play a critical role in the bioactivation of the anticancer prodrug irinotecan [7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxy-camptothecin; CPT-11] into its active metabolite SN-38 (ethyl-10-hydroxy-camptothecin).	Irinotecan	201-206	carboxylesterase 1	Homo sapiens	0-17
12171903-2	2002	We reported recently that human carboxylesterase-2 (hCE-2) is a higher-affinity, higher-velocity enzyme for irinotecan hydrolysis when compared with hCE-1.	Irinotecan	108-118	carboxylesterase 2	Homo sapiens	32-50
12171903-2	2002	We reported recently that human carboxylesterase-2 (hCE-2) is a higher-affinity, higher-velocity enzyme for irinotecan hydrolysis when compared with hCE-1.	Irinotecan	108-118	carboxylesterase 2	Homo sapiens	52-57
12171903-4	2002	Extracts of HT29 cells transfected with hCE-2 exhibited significantly higher irinotecan hydrolysis (5.2 pmol/mg protein/hr) than hCE-1 (1.0 pmol/mg protein/hr).	Irinotecan	77-87	carboxylesterase 2	Homo sapiens	40-45
12171903-5	2002	HT29 cells over-expressing hCE-2 were more sensitive to the toxic effects of irinotecan than cells expressing hCE-1 (EC50 = 0.3 micro M and 6.8 micro M, respectively).	Irinotecan	77-87	carboxylesterase 2	Homo sapiens	27-32
12171903-6	2002	Our data further support the notion that hCE-2 plays a substantial role in irinotecan activation in human tissue at relevant pharmacologic concentrations.	Irinotecan	75-85	carboxylesterase 2	Homo sapiens	41-46
12199631-2	2002	The hepatic metabolism and biliary secretion of irinotecan (CPT-11, Camptosar) and metabolites is complex and involves cytochrome P450 isoenzymes, carboxylesterases, glucuronosyltransferase, and the ATP-dependent export pumps MRP-2 and MXR.	Irinotecan	48-58	ATP binding cassette subfamily C member 2	Homo sapiens	226-231
12199631-2	2002	The hepatic metabolism and biliary secretion of irinotecan (CPT-11, Camptosar) and metabolites is complex and involves cytochrome P450 isoenzymes, carboxylesterases, glucuronosyltransferase, and the ATP-dependent export pumps MRP-2 and MXR.	Irinotecan	48-58	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	236-239
12199631-2	2002	The hepatic metabolism and biliary secretion of irinotecan (CPT-11, Camptosar) and metabolites is complex and involves cytochrome P450 isoenzymes, carboxylesterases, glucuronosyltransferase, and the ATP-dependent export pumps MRP-2 and MXR.	Irinotecan	60-66	ATP binding cassette subfamily C member 2	Homo sapiens	226-231
12199631-2	2002	The hepatic metabolism and biliary secretion of irinotecan (CPT-11, Camptosar) and metabolites is complex and involves cytochrome P450 isoenzymes, carboxylesterases, glucuronosyltransferase, and the ATP-dependent export pumps MRP-2 and MXR.	Irinotecan	60-66	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	236-239
12199631-2	2002	The hepatic metabolism and biliary secretion of irinotecan (CPT-11, Camptosar) and metabolites is complex and involves cytochrome P450 isoenzymes, carboxylesterases, glucuronosyltransferase, and the ATP-dependent export pumps MRP-2 and MXR.	Irinotecan	68-77	ATP binding cassette subfamily C member 2	Homo sapiens	226-231
12199631-2	2002	The hepatic metabolism and biliary secretion of irinotecan (CPT-11, Camptosar) and metabolites is complex and involves cytochrome P450 isoenzymes, carboxylesterases, glucuronosyltransferase, and the ATP-dependent export pumps MRP-2 and MXR.	Irinotecan	68-77	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	236-239
12479221-1	2002	Breast cancer resistance protein (BCRP) confers multidrug resistance to cancer cells against agents such as SN-38 (an active metabolite of irinotecan), mitoxantrone, and topotecan.	Irinotecan	108-113	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
12124325-3	2002	One of the genes markedly up-regulated during cell cycle arrest by SN-38 and suppressed during apoptosis by SN-38 followed by flavopiridol in Hct116 cells is Drg1.	Irinotecan	67-72	developmentally regulated GTP binding protein 1	Homo sapiens	158-162
12124325-3	2002	One of the genes markedly up-regulated during cell cycle arrest by SN-38 and suppressed during apoptosis by SN-38 followed by flavopiridol in Hct116 cells is Drg1.	Irinotecan	108-113	developmentally regulated GTP binding protein 1	Homo sapiens	158-162
12124325-4	2002	We found that Drg1 had profound effects on SN-38 sensitivity.	Irinotecan	43-48	developmentally regulated GTP binding protein 1	Homo sapiens	14-18
12124325-5	2002	Inhibition of endogenous Drg1 expression in Hct116 cells by stable expression of an antisense (AS) Drg1 cDNA increased the sensitivity of cells to undergo apoptosis by SN-38.	Irinotecan	168-173	developmentally regulated GTP binding protein 1	Homo sapiens	25-29
12124325-5	2002	Inhibition of endogenous Drg1 expression in Hct116 cells by stable expression of an antisense (AS) Drg1 cDNA increased the sensitivity of cells to undergo apoptosis by SN-38.	Irinotecan	168-173	developmentally regulated GTP binding protein 1	Homo sapiens	99-103
12124325-6	2002	Clonogenic and apoptosis assays with AS Drg1-expressing cells showed a 2-fold decrease in the IC50 and a 4-5-fold increase in induction of apoptosis with SN-38.	Irinotecan	154-159	developmentally regulated GTP binding protein 1	Homo sapiens	40-44
12124325-7	2002	Conversely, the forced expression of Drg1 in SW620 cells increased the resistance of these cells to SN-38-induced apoptosis by 2-5-fold.	Irinotecan	100-105	developmentally regulated GTP binding protein 1	Homo sapiens	37-41
12124325-8	2002	Moreover, when xenografted in mice, AS Drg1-expressing Hct116 cells were 3-fold more sensitive to CPT-11 as compared with vector transfected Hct116 cells.	Irinotecan	98-104	developmentally regulated GTP binding protein 1	Mus musculus	39-43
12124325-9	2002	Similarly, tumors established from Drg1 overexpressing SW620 cells were more resistant to CPT-11 as compared with tumors established from vector-transfected SW620 cells in mice.	Irinotecan	90-96	developmentally regulated GTP binding protein 1	Homo sapiens	35-39
12124325-10	2002	Taken together, our data suggest that Drg1 is a novel gene that plays a direct role in resistance to CPT-11.	Irinotecan	101-107	developmentally regulated GTP binding protein 1	Homo sapiens	38-42
12124325-11	2002	Inhibition of Drg1 may provide a new means to increase the sensitivity of colon cancer cells to CPT-11.	Irinotecan	96-102	developmentally regulated GTP binding protein 1	Homo sapiens	14-18
12065434-0	2002	Intestinal transport of irinotecan in Caco-2 cells and MDCK II cells overexpressing efflux transporters Pgp, cMOAT, and MRP1.	Irinotecan	24-34	PGP	Canis lupus familiaris	104-107
12065434-0	2002	Intestinal transport of irinotecan in Caco-2 cells and MDCK II cells overexpressing efflux transporters Pgp, cMOAT, and MRP1.	Irinotecan	24-34	ATP binding cassette subfamily C member 1	Canis lupus familiaris	120-124
12143255-5	2002	After 2-4 months of CPT-11-based chemotherapy, significant increase in CD3+CD4+ cell numbers was observed in 8 patients who had initial CD3+CD4+ counts of less than 600 per microL (358 +/- 154 vs. 652 +/- 319 cells per microL, Wilcoxon test, P &lt; 0.01), while in patients with higher initial CD3+CD4+ counts a trend for decrease was observed during therapy.	Irinotecan	20-26	CD4 molecule	Homo sapiens	75-78
12143255-5	2002	After 2-4 months of CPT-11-based chemotherapy, significant increase in CD3+CD4+ cell numbers was observed in 8 patients who had initial CD3+CD4+ counts of less than 600 per microL (358 +/- 154 vs. 652 +/- 319 cells per microL, Wilcoxon test, P &lt; 0.01), while in patients with higher initial CD3+CD4+ counts a trend for decrease was observed during therapy.	Irinotecan	20-26	CD4 molecule	Homo sapiens	140-143
12143255-5	2002	After 2-4 months of CPT-11-based chemotherapy, significant increase in CD3+CD4+ cell numbers was observed in 8 patients who had initial CD3+CD4+ counts of less than 600 per microL (358 +/- 154 vs. 652 +/- 319 cells per microL, Wilcoxon test, P &lt; 0.01), while in patients with higher initial CD3+CD4+ counts a trend for decrease was observed during therapy.	Irinotecan	20-26	CD4 molecule	Homo sapiens	140-143
12143255-8	2002	CPT-11-based therapy seems to ameliorate CD3+CD4+ lymphocytopenia, possibly by neutralizing the immunosuppressive effects of uncontrolled tumor growth.	Irinotecan	0-6	CD4 molecule	Homo sapiens	45-48
12118026-8	2002	CONCLUSION: Inhibition of CYP3A4 in cancer patients treated with irinotecan leads to significantly increased formation of SN-38.	Irinotecan	65-75	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	26-32
12118026-8	2002	CONCLUSION: Inhibition of CYP3A4 in cancer patients treated with irinotecan leads to significantly increased formation of SN-38.	Irinotecan	122-127	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	26-32
12065434-9	2002	Furthermore, the secretory efflux P(eff) of CPT-11 was significantly decreased by Pgp inhibitors, elacridar (GF120918) (IC50 = 0.38 +/- 0.06 microM) and verapamil (IC(50) = 234 +/- 48 microM) in MDCK II/Pgp cells and by cMOAT inhibitor 3-([(3-(2-[7-chloro-2-quinolinyl]ethyl)phenyl]-[(3-dimethylamino-3-oxoprphyl)-thio)-methyl]-thio) propanoic acid (MK571) (IC50) = 469 +/- 60 micro;M) in MDCK II/cMOAT cells.	Irinotecan	44-50	PGP	Canis lupus familiaris	82-85
12065434-9	2002	Furthermore, the secretory efflux P(eff) of CPT-11 was significantly decreased by Pgp inhibitors, elacridar (GF120918) (IC50 = 0.38 +/- 0.06 microM) and verapamil (IC(50) = 234 +/- 48 microM) in MDCK II/Pgp cells and by cMOAT inhibitor 3-([(3-(2-[7-chloro-2-quinolinyl]ethyl)phenyl]-[(3-dimethylamino-3-oxoprphyl)-thio)-methyl]-thio) propanoic acid (MK571) (IC50) = 469 +/- 60 micro;M) in MDCK II/cMOAT cells.	Irinotecan	44-50	PGP	Canis lupus familiaris	203-206
12065434-10	2002	Overall, the current study suggests that Pgp and cMOAT are capable of mediating the efflux of CPT-11 in vitro.	Irinotecan	94-100	PGP	Canis lupus familiaris	41-44
12063551-2	2002	The combination treatment of GEM 231 and irinotecan produced enhanced and prolonged tumor-growth inhibition, compared with irinotecan monotherapy, against human colon (HCT-116), pancreas (Panc-1), prostate (PC3) and lung (SKMES) tumors in mice.	Irinotecan	41-51	proprotein convertase subtilisin/kexin type 1	Homo sapiens	207-210
12094251-8	2002	After a 7-day exposure to anti-CD32, the recovery of ALL cells cocultured with stroma was reduced to 5.5% +/- 2.8% of control values in 380 cells (n = 14), 19.4% +/- 6.1% (n = 8) in RS4;11, and 4.0% +/- 1.3% (n = 6) in KOPN55bi.	Irinotecan	182-185	Fc gamma receptor IIa	Homo sapiens	31-35
12019202-9	2002	In conclusion, potential clinical interactions with the metabolism of irinotecan are likely to be important for vinorelbine, which strongly inhibits irinotecan catabolism by CYP3A4 at clinically relevant concentrations, but not for the other drugs, which exert an effect at concentrations not achievable in patients.	Irinotecan	70-80	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	174-180
12019202-9	2002	In conclusion, potential clinical interactions with the metabolism of irinotecan are likely to be important for vinorelbine, which strongly inhibits irinotecan catabolism by CYP3A4 at clinically relevant concentrations, but not for the other drugs, which exert an effect at concentrations not achievable in patients.	Irinotecan	149-159	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	174-180
12479221-1	2002	Breast cancer resistance protein (BCRP) confers multidrug resistance to cancer cells against agents such as SN-38 (an active metabolite of irinotecan), mitoxantrone, and topotecan.	Irinotecan	108-113	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
12479221-1	2002	Breast cancer resistance protein (BCRP) confers multidrug resistance to cancer cells against agents such as SN-38 (an active metabolite of irinotecan), mitoxantrone, and topotecan.	Irinotecan	139-149	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
12479221-1	2002	Breast cancer resistance protein (BCRP) confers multidrug resistance to cancer cells against agents such as SN-38 (an active metabolite of irinotecan), mitoxantrone, and topotecan.	Irinotecan	139-149	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
12479221-11	2002	Therefore, people with C376T and/or C421A polymorphisms may express low amounts of BCRP, and this low BCRP expression might result in hypersensitivity of normal cells to such anticancer drugs as irinotecan and mitoxantrone.	Irinotecan	195-205	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	83-87
12479221-11	2002	Therefore, people with C376T and/or C421A polymorphisms may express low amounts of BCRP, and this low BCRP expression might result in hypersensitivity of normal cells to such anticancer drugs as irinotecan and mitoxantrone.	Irinotecan	195-205	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	102-106
11888671-0	2002	Loss of one allele of the p53 gene in the lens epithelial tumor in transgenic mice suppresses apoptosis induced by a topoisomerase I inhibitor (CPT-11).	Irinotecan	144-150	transformation related protein 53, pseudogene	Mus musculus	26-29
11888671-6	2002	In addition, it was found that CPT-11 could also induce apoptosis via a p53-independent pathway.	Irinotecan	31-37	transformation related protein 53, pseudogene	Mus musculus	72-75
12032863-0	2002	Enhanced tumor killing by Apo2L/TRAIL and CPT-11 co-treatment is associated with p21 cleavage and differential regulation of Apo2L/TRAIL ligand and its receptors.	Irinotecan	42-48	H3 histone pseudogene 16	Homo sapiens	81-84
12032863-0	2002	Enhanced tumor killing by Apo2L/TRAIL and CPT-11 co-treatment is associated with p21 cleavage and differential regulation of Apo2L/TRAIL ligand and its receptors.	Irinotecan	42-48	TNF superfamily member 10	Homo sapiens	125-130
12032863-0	2002	Enhanced tumor killing by Apo2L/TRAIL and CPT-11 co-treatment is associated with p21 cleavage and differential regulation of Apo2L/TRAIL ligand and its receptors.	Irinotecan	42-48	TNF superfamily member 10	Homo sapiens	131-136
12032863-1	2002	Apo2L/TRAIL exhibits enhanced apoptotic activity in tumor xenograft models when used in combination with the topoisomerase 1 inhibitor CPT-11.	Irinotecan	135-141	TNF superfamily member 10	Homo sapiens	0-5
12032863-1	2002	Apo2L/TRAIL exhibits enhanced apoptotic activity in tumor xenograft models when used in combination with the topoisomerase 1 inhibitor CPT-11.	Irinotecan	135-141	TNF superfamily member 10	Homo sapiens	6-11
12032863-4	2002	Upregulation of decoy receptors by CPT-11 was partially inhibited by co-administration of Apo2L/TRAIL.	Irinotecan	35-41	TNF superfamily member 10	Homo sapiens	90-95
12032863-4	2002	Upregulation of decoy receptors by CPT-11 was partially inhibited by co-administration of Apo2L/TRAIL.	Irinotecan	35-41	TNF superfamily member 10	Homo sapiens	96-101
12032863-5	2002	CPT-11 treatment resulted in accumulation of cells at G(2)M-phase and correlated with a substantial increase in the protein levels of the cyclin-dependent kinase inhibitor p21.	Irinotecan	0-6	H3 histone pseudogene 16	Homo sapiens	172-175
12032863-6	2002	However, cells co-treated with CPT-11 and Apo2L/TRAIL, or pretreated with CPT-11 for up to 24 h followed by 2 h Apo2L/TRAIL, resulted in a caspase-dependent degradation of p21, reversal of G(2)-M phase arrest with a concomitant increase in apoptosis.	Irinotecan	31-37	TNF superfamily member 10	Homo sapiens	112-117
12032863-6	2002	However, cells co-treated with CPT-11 and Apo2L/TRAIL, or pretreated with CPT-11 for up to 24 h followed by 2 h Apo2L/TRAIL, resulted in a caspase-dependent degradation of p21, reversal of G(2)-M phase arrest with a concomitant increase in apoptosis.	Irinotecan	31-37	TNF superfamily member 10	Homo sapiens	118-123
12032863-6	2002	However, cells co-treated with CPT-11 and Apo2L/TRAIL, or pretreated with CPT-11 for up to 24 h followed by 2 h Apo2L/TRAIL, resulted in a caspase-dependent degradation of p21, reversal of G(2)-M phase arrest with a concomitant increase in apoptosis.	Irinotecan	31-37	H3 histone pseudogene 16	Homo sapiens	172-175
12032863-6	2002	However, cells co-treated with CPT-11 and Apo2L/TRAIL, or pretreated with CPT-11 for up to 24 h followed by 2 h Apo2L/TRAIL, resulted in a caspase-dependent degradation of p21, reversal of G(2)-M phase arrest with a concomitant increase in apoptosis.	Irinotecan	74-80	TNF superfamily member 10	Homo sapiens	118-123
12032863-6	2002	However, cells co-treated with CPT-11 and Apo2L/TRAIL, or pretreated with CPT-11 for up to 24 h followed by 2 h Apo2L/TRAIL, resulted in a caspase-dependent degradation of p21, reversal of G(2)-M phase arrest with a concomitant increase in apoptosis.	Irinotecan	74-80	H3 histone pseudogene 16	Homo sapiens	172-175
12032863-8	2002	These data indicate that the up-regulation of Apo2L/TRAIL ligand and its death receptors as well as cleavage of p21 protein in the Apo2L/TRAIL plus CPT-11 treatment contributes to the positive cooperation between these agents in enhancing tumor cell apoptosis.	Irinotecan	148-154	TNF superfamily member 10	Homo sapiens	46-51
12032863-8	2002	These data indicate that the up-regulation of Apo2L/TRAIL ligand and its death receptors as well as cleavage of p21 protein in the Apo2L/TRAIL plus CPT-11 treatment contributes to the positive cooperation between these agents in enhancing tumor cell apoptosis.	Irinotecan	148-154	TNF superfamily member 10	Homo sapiens	52-57
12032863-8	2002	These data indicate that the up-regulation of Apo2L/TRAIL ligand and its death receptors as well as cleavage of p21 protein in the Apo2L/TRAIL plus CPT-11 treatment contributes to the positive cooperation between these agents in enhancing tumor cell apoptosis.	Irinotecan	148-154	H3 histone pseudogene 16	Homo sapiens	112-115
12032863-8	2002	These data indicate that the up-regulation of Apo2L/TRAIL ligand and its death receptors as well as cleavage of p21 protein in the Apo2L/TRAIL plus CPT-11 treatment contributes to the positive cooperation between these agents in enhancing tumor cell apoptosis.	Irinotecan	148-154	TNF superfamily member 10	Homo sapiens	131-136
12032863-8	2002	These data indicate that the up-regulation of Apo2L/TRAIL ligand and its death receptors as well as cleavage of p21 protein in the Apo2L/TRAIL plus CPT-11 treatment contributes to the positive cooperation between these agents in enhancing tumor cell apoptosis.	Irinotecan	148-154	TNF superfamily member 10	Homo sapiens	137-142
12006545-0	2002	Overexpression of PTEN increases sensitivity to SN-38, an active metabolite of the topoisomerase I inhibitor irinotecan, in ovarian cancer cells.	Irinotecan	48-53	phosphatase and tensin homolog	Homo sapiens	18-22
12006545-0	2002	Overexpression of PTEN increases sensitivity to SN-38, an active metabolite of the topoisomerase I inhibitor irinotecan, in ovarian cancer cells.	Irinotecan	109-119	phosphatase and tensin homolog	Homo sapiens	18-22
12006545-7	2002	In vitro examination of sensitivity to anticancer agents showed that the 50% growth-inhibitory concentration value for irinotecan metabolite (SN-38) in SHIN-3/PTEN was 800 nM, a 6.6-fold higher sensitivity compared with that of the control (5300 nM).	Irinotecan	119-129	phosphatase and tensin homolog	Homo sapiens	159-163
12006545-7	2002	In vitro examination of sensitivity to anticancer agents showed that the 50% growth-inhibitory concentration value for irinotecan metabolite (SN-38) in SHIN-3/PTEN was 800 nM, a 6.6-fold higher sensitivity compared with that of the control (5300 nM).	Irinotecan	142-147	phosphatase and tensin homolog	Homo sapiens	159-163
12006545-9	2002	The percentage of apoptotic cells in SHIN-3/PTEN was 16.6 +/- 0.7% 24 h after addition of SN-38, a significant increase over controls (8.6 +/- 0.9%; P &lt; 0.01).	Irinotecan	90-95	phosphatase and tensin homolog	Homo sapiens	44-48
12006545-11	2002	CONCLUSIONS: These results indicate that high PTEN expression enhances the sensitivity of ovarian cancer cells to irinotecan and the induction of apoptosis and the suppression of topoisomerase I activity in cancer cells are suggested as possible mechanisms attributable to high PTEN expression.	Irinotecan	114-124	phosphatase and tensin homolog	Homo sapiens	46-50
11956509-0	2002	Cholinergic toxic syndrome by the anticancer drug irinotecan: acetylcholinesterase does not play a major role.	Irinotecan	50-60	acetylcholinesterase (Cartwright blood group)	Homo sapiens	62-82
12036456-2	2002	It is converted by carboxyesterase to an active metabolite, SN-38, which is further conjugated and detoxified to SN-38-glucuronide by UDP-glucuronosyltransferase (UGT).	Irinotecan	60-65	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	134-161
12036456-2	2002	It is converted by carboxyesterase to an active metabolite, SN-38, which is further conjugated and detoxified to SN-38-glucuronide by UDP-glucuronosyltransferase (UGT).	Irinotecan	60-65	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	163-166
12036456-4	2002	All the patients had received irinotecan-containing chemotherapy and were evaluated to see whether the variant UGT1A7 genotype would increase the likelihood of severe toxicity of irinotecan consisting of grade 4 leukopenia and/or grade 3 or more diarrhea.	Irinotecan	179-189	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	111-117
11914914-2	2002	We studied the role of P-glycoprotein (P-gp) in in vivo biliary excretion of CPT-11, SN-38 and SN-38G in mice lacking mdr1-type P-gp [ mdr1a/1b(-/-)] in the presence of the multidrug resistance (MDR) reversal agent, PSC833.	Irinotecan	77-83	phosphoglycolate phosphatase	Mus musculus	39-43
11914914-2	2002	We studied the role of P-glycoprotein (P-gp) in in vivo biliary excretion of CPT-11, SN-38 and SN-38G in mice lacking mdr1-type P-gp [ mdr1a/1b(-/-)] in the presence of the multidrug resistance (MDR) reversal agent, PSC833.	Irinotecan	95-100	phosphoglycolate phosphatase	Mus musculus	39-43
11914914-6	2002	This also implied a major role of other undetermined non-P-gp-mediated mechanism(s) for hepatic transport of CPT-11, which was inhibited by PSC833 (1.8+/-0.8% with PSC833, 6.6+/-0.6% without PSC833) in mdr1a/1b(-/-) mice.	Irinotecan	109-115	phosphoglycolate phosphatase	Mus musculus	57-61
11914914-6	2002	This also implied a major role of other undetermined non-P-gp-mediated mechanism(s) for hepatic transport of CPT-11, which was inhibited by PSC833 (1.8+/-0.8% with PSC833, 6.6+/-0.6% without PSC833) in mdr1a/1b(-/-) mice.	Irinotecan	109-115	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	202-207
11967565-2	2002	We present the 2.5 A crystal structure of rabbit liver carboxylesterase (rCE), the most efficient enzyme known to activate CPT-11 in this manner, in complex with the leaving group 4PP.	Irinotecan	123-129	liver carboxylesterase 1	Oryctolagus cuniculus	49-71
11914914-0	2002	Biliary transport of irinotecan and metabolites in normal and P-glycoprotein-deficient mice.	Irinotecan	21-31	phosphoglycolate phosphatase	Mus musculus	62-76
11956509-2	2002	This study investigated (1) the pattern of acetylcholinesterase activity in patients receiving treatment with irinotecan and (2) the relationship between acetylcholinesterase activity and plasma concentrations of irinotecan, 7-ethyl-10-hydroxycamptothecin (SN-38), and SN-38 glucuronide (SN-38G).	Irinotecan	213-223	acetylcholinesterase (Cartwright blood group)	Homo sapiens	154-174
11956509-9	2002	In vitro, the activity of acetylcholinesterase was inhibited by 100-micromol/L irinotecan (-24.8%) and markedly reduced by 1-micromol/L physostigmine (-86.7%), whereas neither SN-38 nor camptothecin had an effect.	Irinotecan	79-89	acetylcholinesterase (Cartwright blood group)	Homo sapiens	26-46
11956509-9	2002	In vitro, the activity of acetylcholinesterase was inhibited by 100-micromol/L irinotecan (-24.8%) and markedly reduced by 1-micromol/L physostigmine (-86.7%), whereas neither SN-38 nor camptothecin had an effect.	Irinotecan	176-181	acetylcholinesterase (Cartwright blood group)	Homo sapiens	26-46
11956509-1	2002	BACKGROUND: The anticancer drug irinotecan induces cholinergic side effects that are currently ascribed to the blockade of acetylcholinesterase.	Irinotecan	32-42	acetylcholinesterase (Cartwright blood group)	Homo sapiens	123-143
11956509-2	2002	This study investigated (1) the pattern of acetylcholinesterase activity in patients receiving treatment with irinotecan and (2) the relationship between acetylcholinesterase activity and plasma concentrations of irinotecan, 7-ethyl-10-hydroxycamptothecin (SN-38), and SN-38 glucuronide (SN-38G).	Irinotecan	110-120	acetylcholinesterase (Cartwright blood group)	Homo sapiens	43-63
11990699-2	2002	Recent studies have shown that irinotecan also undergoes oxidative metabolism by the P450 isozyme CYP3A4, leading to the formation of a minor inactive metabolite, 7-ethyl-10-[4-N-[(5-aminopentanoic acid)-1-piperidino]-carbonyloxy-camptothecin (APC).	Irinotecan	31-41	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	98-104
11901092-6	2002	Furthermore, CPT-11 and SN-38 were suggested to be mechanism-based inactivators of CYP3A4.	Irinotecan	13-19	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	83-89
11901092-6	2002	Furthermore, CPT-11 and SN-38 were suggested to be mechanism-based inactivators of CYP3A4.	Irinotecan	24-29	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	83-89
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	24-30	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	84-90
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	24-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	24-30	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	104-110
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	24-30	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	238-244
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	35-40	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	84-90
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	35-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	35-40	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	104-110
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	35-40	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	238-244
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	180-186	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	84-90
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	180-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	180-186	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	104-110
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	180-186	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	238-244
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	248-253	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	84-90
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	248-253	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	104-110
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	180-186	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	84-90
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	180-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	180-186	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	104-110
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	180-186	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	238-244
11927002-1	2002	Breast cancer resistance protein (BCRP), an adenosine triphosphate-binding cassette transporter, confers resistance to a series of anticancer reagents, including mitoxantrone, SN-38 and topotecan.	Irinotecan	176-181	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
11927002-1	2002	Breast cancer resistance protein (BCRP), an adenosine triphosphate-binding cassette transporter, confers resistance to a series of anticancer reagents, including mitoxantrone, SN-38 and topotecan.	Irinotecan	176-181	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
11927002-2	2002	In the present study, we found that estrone and 17beta-estradiol potentiated the cytotoxicity of mitoxantrone, SN-38 and topotecan in BCRP-transduced K562 cells (K562 / BCRP).	Irinotecan	111-116	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	134-138
11901092-1	2002	The inhibition and mechanism-based inactivation potencies of irinotecan (7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin; CPT-11) and its active metabolite (7-ethyl-10-hydroxycamptothecin; SN-38) for human cytochrome P450 (P450) enzymes were investigated to evaluate the potential for drug interactions involving CPT-11 using microsomes from insect cells expressing specific human P450 isoforms.	Irinotecan	73-138	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	224-245
11901092-3	2002	CPT-11 and SN-38 competitively inhibited CYP3A4 (testosterone 6 beta-hydroxylation) activity with K(i) values of 129 and 121 microM, respectively.	Irinotecan	0-6	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	41-47
11901092-3	2002	CPT-11 and SN-38 competitively inhibited CYP3A4 (testosterone 6 beta-hydroxylation) activity with K(i) values of 129 and 121 microM, respectively.	Irinotecan	11-16	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	41-47
11901092-4	2002	CYP2A6 (coumarin 7-hydroxylation) and CYP2C9 (diclofenac 4"-hydroxylation) activities exhibited a mixed type of inhibition comprising competitive and noncompetitive components in response to SN-38, the K(i) values being 181 and 156 microM, respectively.	Irinotecan	191-196	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	0-6
11901092-4	2002	CYP2A6 (coumarin 7-hydroxylation) and CYP2C9 (diclofenac 4"-hydroxylation) activities exhibited a mixed type of inhibition comprising competitive and noncompetitive components in response to SN-38, the K(i) values being 181 and 156 microM, respectively.	Irinotecan	191-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
11894120-0	2002	Antisense anti-MDM2 mixed-backbone oligonucleotides enhance therapeutic efficacy of topoisomerase I inhibitor irinotecan in nude mice bearing human cancer xenografts: In vivo activity and mechanisms.	Irinotecan	110-120	transformed mouse 3T3 cell double minute 2	Mus musculus	15-19
11894120-5	2002	In LS174T cells, the antisense oligonucleotide, but not the mismatch oligonucleotide, specifically inhibited MDM2 expression, resulting in a significant increase in irinotecan-associated p53 activation and p21 induction.	Irinotecan	165-175	tumor protein p53	Homo sapiens	187-190
11894120-6	2002	In DLD-1 cells, the antisense oligonucleotide specifically inhibited MDM2 expression, resulting in a significant increase in irinotecan-associated p21 induction although mutant p53 levels remained unchanged.	Irinotecan	125-135	MDM2 proto-oncogene	Homo sapiens	69-73
11894120-6	2002	In DLD-1 cells, the antisense oligonucleotide specifically inhibited MDM2 expression, resulting in a significant increase in irinotecan-associated p21 induction although mutant p53 levels remained unchanged.	Irinotecan	125-135	H3 histone pseudogene 16	Homo sapiens	147-150
11990699-2	2002	Recent studies have shown that irinotecan also undergoes oxidative metabolism by the P450 isozyme CYP3A4, leading to the formation of a minor inactive metabolite, 7-ethyl-10-[4-N-[(5-aminopentanoic acid)-1-piperidino]-carbonyloxy-camptothecin (APC).	Irinotecan	31-41	APC regulator of WNT signaling pathway	Homo sapiens	244-247
11990699-3	2002	The elucidation of this metabolic pathway suggests the potential for drug interactions when irinotecan is administered with other inducers or substrates of CYP3A4.	Irinotecan	92-102	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	156-162
11805731-0	2002	Polymorphisms of UDP-glucuronosyltransferase and pharmacokinetics of irinotecan.	Irinotecan	69-79	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	17-44
11805731-2	2002	SN-38 is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) to yield its beta-glucuronide (SN-38G).	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	46-73
11805731-2	2002	SN-38 is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) to yield its beta-glucuronide (SN-38G).	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	75-78
11805731-2	2002	SN-38 is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) to yield its beta-glucuronide (SN-38G).	Irinotecan	111-116	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	46-73
11805731-2	2002	SN-38 is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) to yield its beta-glucuronide (SN-38G).	Irinotecan	111-116	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	75-78
11805731-4	2002	Interindividual variation of sensitivity to irinotecan is related to large variations of biotransformation of the active metabolite SN-38, some of which would be caused by genetic polymorphism of UGT1A1, an isozyme responsible for the SN-38 glucuronidation.	Irinotecan	44-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
11805731-4	2002	Interindividual variation of sensitivity to irinotecan is related to large variations of biotransformation of the active metabolite SN-38, some of which would be caused by genetic polymorphism of UGT1A1, an isozyme responsible for the SN-38 glucuronidation.	Irinotecan	132-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
11805731-4	2002	Interindividual variation of sensitivity to irinotecan is related to large variations of biotransformation of the active metabolite SN-38, some of which would be caused by genetic polymorphism of UGT1A1, an isozyme responsible for the SN-38 glucuronidation.	Irinotecan	235-240	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	196-202
11805731-9	2002	The 4 subjects carrying UGT1A1*28 allele had values of the AUC(SN-38)/AUC(SN-38G) above the 75th percentile of the total population, suggesting a potential pharmacogenetic/pharmacokinetic relationship.	Irinotecan	63-68	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
11805731-9	2002	The 4 subjects carrying UGT1A1*28 allele had values of the AUC(SN-38)/AUC(SN-38G) above the 75th percentile of the total population, suggesting a potential pharmacogenetic/pharmacokinetic relationship.	Irinotecan	74-79	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
11805731-11	2002	The large variation in the UGT activity being related to the genetic status would warrant pharmacogenetic-guided dosing of irinotecan.	Irinotecan	123-133	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	27-30
12017271-2	2002	In this study we determined the therapeutic effects of an antisense anti-MDM2 oligonucleotide administered alone or in combination with the clinically used chemotherapeutic agents Paclitaxel and Irinotecan.	Irinotecan	195-205	MDM2 proto-oncogene	Homo sapiens	73-77
11700302-8	2002	The loss of ATR-dependent checkpoint function sensitized GM847 human fibroblasts to the cytotoxic effects of the topoisomerase I poisons TPT and 7-ethyl-10-hydroxycamptothecin, as assessed by inhibition of colony formation, increased trypan blue uptake, and development of apoptotic morphological changes.	Irinotecan	145-175	ATR serine/threonine kinase	Homo sapiens	12-15
15618702-1	2002	Three novel single nucleotide polymorphisms (SNPs) were found in the UDP-glucuronosyltransferase (UGT) 1A10 gene from 24 Japanese patients with various cancers who were administered the anti-tumor drug, irinotecan (CPT-11).	Irinotecan	203-213	UDP glucuronosyltransferase family 1 member A10	Homo sapiens	69-107
15618649-2	2002	Since the biliary excretion of its active metabolite (SN-38) and SN-38 glucuronide (SN38-Glu), which are mediated by the multidrug resistance associated protein-2 (MRP2/ABCC2), has been proposed to be related to this gastrointestinal toxicity, we have attempted here to examine the potential of various therapeutic agents to interact with the biliary excretion in order to identify MRP2 inhibitors to prevent this toxicity.	Irinotecan	54-59	ATP binding cassette subfamily C member 2	Homo sapiens	121-162
15618649-2	2002	Since the biliary excretion of its active metabolite (SN-38) and SN-38 glucuronide (SN38-Glu), which are mediated by the multidrug resistance associated protein-2 (MRP2/ABCC2), has been proposed to be related to this gastrointestinal toxicity, we have attempted here to examine the potential of various therapeutic agents to interact with the biliary excretion in order to identify MRP2 inhibitors to prevent this toxicity.	Irinotecan	54-59	ATP binding cassette subfamily C member 2	Homo sapiens	164-168
15618661-3	2002	SN-38-selected PC-6/SN2-5H human lung carcinoma cells were shown to overexpress ABCG2 with the reduced intracellular accumulation of SN-38, the active metabolite of irinotecan.	Irinotecan	0-5	proprotein convertase subtilisin/kexin type 5	Homo sapiens	15-19
15618661-3	2002	SN-38-selected PC-6/SN2-5H human lung carcinoma cells were shown to overexpress ABCG2 with the reduced intracellular accumulation of SN-38, the active metabolite of irinotecan.	Irinotecan	0-5	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	80-85
15618661-3	2002	SN-38-selected PC-6/SN2-5H human lung carcinoma cells were shown to overexpress ABCG2 with the reduced intracellular accumulation of SN-38, the active metabolite of irinotecan.	Irinotecan	133-138	proprotein convertase subtilisin/kexin type 5	Homo sapiens	15-19
15618661-3	2002	SN-38-selected PC-6/SN2-5H human lung carcinoma cells were shown to overexpress ABCG2 with the reduced intracellular accumulation of SN-38, the active metabolite of irinotecan.	Irinotecan	133-138	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	80-85
15618649-2	2002	Since the biliary excretion of its active metabolite (SN-38) and SN-38 glucuronide (SN38-Glu), which are mediated by the multidrug resistance associated protein-2 (MRP2/ABCC2), has been proposed to be related to this gastrointestinal toxicity, we have attempted here to examine the potential of various therapeutic agents to interact with the biliary excretion in order to identify MRP2 inhibitors to prevent this toxicity.	Irinotecan	54-59	ATP binding cassette subfamily C member 2	Homo sapiens	169-174
15618649-2	2002	Since the biliary excretion of its active metabolite (SN-38) and SN-38 glucuronide (SN38-Glu), which are mediated by the multidrug resistance associated protein-2 (MRP2/ABCC2), has been proposed to be related to this gastrointestinal toxicity, we have attempted here to examine the potential of various therapeutic agents to interact with the biliary excretion in order to identify MRP2 inhibitors to prevent this toxicity.	Irinotecan	54-59	ATP binding cassette subfamily C member 2	Homo sapiens	382-386
15618661-3	2002	SN-38-selected PC-6/SN2-5H human lung carcinoma cells were shown to overexpress ABCG2 with the reduced intracellular accumulation of SN-38, the active metabolite of irinotecan.	Irinotecan	165-175	proprotein convertase subtilisin/kexin type 5	Homo sapiens	15-19
15618702-1	2002	Three novel single nucleotide polymorphisms (SNPs) were found in the UDP-glucuronosyltransferase (UGT) 1A10 gene from 24 Japanese patients with various cancers who were administered the anti-tumor drug, irinotecan (CPT-11).	Irinotecan	215-221	UDP glucuronosyltransferase family 1 member A10	Homo sapiens	69-107
15618661-3	2002	SN-38-selected PC-6/SN2-5H human lung carcinoma cells were shown to overexpress ABCG2 with the reduced intracellular accumulation of SN-38, the active metabolite of irinotecan.	Irinotecan	165-175	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	80-85
15618661-4	2002	We have recently demonstrated that plasma membrane vesicles prepared from those cells transported SN-38 in an ATP-dependent manner, and it was suggested that ABCG2 is involved in the active extrusion of SN-38 from cancer cells.	Irinotecan	98-103	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	158-163
15618661-4	2002	We have recently demonstrated that plasma membrane vesicles prepared from those cells transported SN-38 in an ATP-dependent manner, and it was suggested that ABCG2 is involved in the active extrusion of SN-38 from cancer cells.	Irinotecan	203-208	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	158-163
15618661-8	2002	Contrary to our expectation, however, ATPase activity in the cell membranes expressing ABCG2 was stimulated by neither SN-38 nor rhodamine 123.	Irinotecan	119-124	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	87-92
15618661-9	2002	It is suggested that there is a partner protein of ABCG2 required for heterodimer formation to exhibit transport activity toward SN-38.	Irinotecan	129-134	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	51-56
11802813-2	2002	We found that a DNA repair protein, O(6)-methylguanine-DNA methyltransferase (MGMT), participated in resistance to irinotecan hydrochloride (CPT-11), its active metabolite SN-38, and a novel CPT derivative, DX-8951f.	Irinotecan	115-139	O-6-methylguanine-DNA methyltransferase	Homo sapiens	36-76
11773147-0	2002	Irinotecan dosing: does the CPT in CPT-11 stand for "Can"t Predict Toxicity"?	Irinotecan	0-10	choline phosphotransferase 1	Homo sapiens	28-31
11773147-0	2002	Irinotecan dosing: does the CPT in CPT-11 stand for "Can"t Predict Toxicity"?	Irinotecan	0-10	choline phosphotransferase 1	Homo sapiens	35-38
11802813-2	2002	We found that a DNA repair protein, O(6)-methylguanine-DNA methyltransferase (MGMT), participated in resistance to irinotecan hydrochloride (CPT-11), its active metabolite SN-38, and a novel CPT derivative, DX-8951f.	Irinotecan	115-139	O-6-methylguanine-DNA methyltransferase	Homo sapiens	78-82
11802813-2	2002	We found that a DNA repair protein, O(6)-methylguanine-DNA methyltransferase (MGMT), participated in resistance to irinotecan hydrochloride (CPT-11), its active metabolite SN-38, and a novel CPT derivative, DX-8951f.	Irinotecan	141-147	O-6-methylguanine-DNA methyltransferase	Homo sapiens	36-76
11802813-2	2002	We found that a DNA repair protein, O(6)-methylguanine-DNA methyltransferase (MGMT), participated in resistance to irinotecan hydrochloride (CPT-11), its active metabolite SN-38, and a novel CPT derivative, DX-8951f.	Irinotecan	141-147	O-6-methylguanine-DNA methyltransferase	Homo sapiens	78-82
11802813-2	2002	We found that a DNA repair protein, O(6)-methylguanine-DNA methyltransferase (MGMT), participated in resistance to irinotecan hydrochloride (CPT-11), its active metabolite SN-38, and a novel CPT derivative, DX-8951f.	Irinotecan	172-177	O-6-methylguanine-DNA methyltransferase	Homo sapiens	36-76
11802813-2	2002	We found that a DNA repair protein, O(6)-methylguanine-DNA methyltransferase (MGMT), participated in resistance to irinotecan hydrochloride (CPT-11), its active metabolite SN-38, and a novel CPT derivative, DX-8951f.	Irinotecan	172-177	O-6-methylguanine-DNA methyltransferase	Homo sapiens	78-82
12541026-0	2002	Irinotecan plus low-dose cisplatin for alpha-fetoprotein-producing gastric carcinoma with multiple liver metastases: report of two cases.	Irinotecan	0-10	alpha fetoprotein	Homo sapiens	39-56
11990381-2	2002	We have previously demonstrated the role of UGT1A1 enzyme in the glucuronidation of SN-38 and a significant correlation between in vitro glucuronidation of SN-38 and UGT1A1 gene promoter polymorphism.	Irinotecan	156-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	166-172
11990381-4	2002	Here we report the results from a prospective clinical pharmacogenetic study to determine the significance of UGT1A1*28 polymorphism on irinotecan disposition and toxicity in patients with cancer.	Irinotecan	136-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
11990381-10	2002	The results suggest that screening for UGT1A1*28 polymorphism may identify patients with lower SN-38 glucuronidation rates and greater susceptibility to irinotecan induced gastrointestinal and bone marrow toxicity.	Irinotecan	95-100	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
11990381-10	2002	The results suggest that screening for UGT1A1*28 polymorphism may identify patients with lower SN-38 glucuronidation rates and greater susceptibility to irinotecan induced gastrointestinal and bone marrow toxicity.	Irinotecan	153-163	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
11990381-0	2002	UGT1A1*28 polymorphism as a determinant of irinotecan disposition and toxicity.	Irinotecan	43-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
11990381-2	2002	We have previously demonstrated the role of UGT1A1 enzyme in the glucuronidation of SN-38 and a significant correlation between in vitro glucuronidation of SN-38 and UGT1A1 gene promoter polymorphism.	Irinotecan	84-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
11990381-2	2002	We have previously demonstrated the role of UGT1A1 enzyme in the glucuronidation of SN-38 and a significant correlation between in vitro glucuronidation of SN-38 and UGT1A1 gene promoter polymorphism.	Irinotecan	84-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	166-172
11990381-2	2002	We have previously demonstrated the role of UGT1A1 enzyme in the glucuronidation of SN-38 and a significant correlation between in vitro glucuronidation of SN-38 and UGT1A1 gene promoter polymorphism.	Irinotecan	156-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	44-50
11688982-1	2001	Overexpression of breast cancer resistance protein (BCRP) ABCG2 reportedly confers cancer cell resistance to camptothecin-based anticancer drugs, such as topotecan and 7-ethyl-10-hydroxycamptothecin (SN-38: the active metabolite of irinotecan).	Irinotecan	168-198	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	18-50
11751522-4	2001	Exposure of parental Hct116 cells to clinically achievable concentrations of SN-38 (the active metabolite of CPT-11) induces p21 and a G(2) arrest.	Irinotecan	77-82	H3 histone pseudogene 16	Homo sapiens	125-128
11751522-4	2001	Exposure of parental Hct116 cells to clinically achievable concentrations of SN-38 (the active metabolite of CPT-11) induces p21 and a G(2) arrest.	Irinotecan	109-115	H3 histone pseudogene 16	Homo sapiens	125-128
11751522-6	2001	In contrast, Hct116 cells that are p21 deficient (p21-/- Hct116) readily undergo apoptosis after treatment with SN-38.	Irinotecan	112-117	H3 histone pseudogene 16	Homo sapiens	35-38
11751522-6	2001	In contrast, Hct116 cells that are p21 deficient (p21-/- Hct116) readily undergo apoptosis after treatment with SN-38.	Irinotecan	112-117	H3 histone pseudogene 16	Homo sapiens	50-53
11751522-10	2001	Sequential treatment with SN-38 followed by flavopiridol was associated with higher activation of caspase-3 and greater cleavage of both p21 and XIAP, an inhibitor of apoptosis, compared with other treatment schedules.	Irinotecan	26-31	caspase 3	Homo sapiens	98-107
11751522-10	2001	Sequential treatment with SN-38 followed by flavopiridol was associated with higher activation of caspase-3 and greater cleavage of both p21 and XIAP, an inhibitor of apoptosis, compared with other treatment schedules.	Irinotecan	26-31	H3 histone pseudogene 16	Homo sapiens	137-140
11751522-10	2001	Sequential treatment with SN-38 followed by flavopiridol was associated with higher activation of caspase-3 and greater cleavage of both p21 and XIAP, an inhibitor of apoptosis, compared with other treatment schedules.	Irinotecan	26-31	X-linked inhibitor of apoptosis	Homo sapiens	145-149
11742701-1	2001	In the last years, the main topoisomerase I inhibitors (TP1-I) (i.e. topotecan and irinotecan) have been used in combination chemotherapy in non-small cell lung cancer.	Irinotecan	83-93	transition protein 1	Homo sapiens	56-59
11740913-10	2001	The in vitro activity of human erythrocyte acetylcholinesterase was significantly inhibited by irinotecan (-21.5% at 100 microM) or physostigmine (-84.8% at 1 microM), whereas SN-38 or camptothecin had no effect.	Irinotecan	95-105	acetylcholinesterase	Rattus norvegicus	43-63
11740913-10	2001	The in vitro activity of human erythrocyte acetylcholinesterase was significantly inhibited by irinotecan (-21.5% at 100 microM) or physostigmine (-84.8% at 1 microM), whereas SN-38 or camptothecin had no effect.	Irinotecan	176-181	acetylcholinesterase	Rattus norvegicus	43-63
11740913-11	2001	Rat atrial acetylcholinesterase was also significantly inhibited in vitro by irinotecan (-16.9% at 100 microM).	Irinotecan	77-87	acetylcholinesterase	Rattus norvegicus	11-31
11740913-13	2001	A direct activation of cholinergic receptors or an interaction with central nervous sites does not appear to account for these inhibitory actions, whereas a blockade of acetylcholinesterase seems to occur at concentrations of irinotecan that may not be relevant in clinical settings.	Irinotecan	226-236	acetylcholinesterase	Rattus norvegicus	169-189
11688982-0	2001	Transport of 7-ethyl-10-hydroxycamptothecin (SN-38) by breast cancer resistance protein ABCG2 in human lung cancer cells.	Irinotecan	13-43	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	55-87
11688982-0	2001	Transport of 7-ethyl-10-hydroxycamptothecin (SN-38) by breast cancer resistance protein ABCG2 in human lung cancer cells.	Irinotecan	13-43	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	88-93
11688982-0	2001	Transport of 7-ethyl-10-hydroxycamptothecin (SN-38) by breast cancer resistance protein ABCG2 in human lung cancer cells.	Irinotecan	45-50	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	55-87
11688982-0	2001	Transport of 7-ethyl-10-hydroxycamptothecin (SN-38) by breast cancer resistance protein ABCG2 in human lung cancer cells.	Irinotecan	45-50	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	88-93
11688982-1	2001	Overexpression of breast cancer resistance protein (BCRP) ABCG2 reportedly confers cancer cell resistance to camptothecin-based anticancer drugs, such as topotecan and 7-ethyl-10-hydroxycamptothecin (SN-38: the active metabolite of irinotecan).	Irinotecan	168-198	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	52-56
11688982-1	2001	Overexpression of breast cancer resistance protein (BCRP) ABCG2 reportedly confers cancer cell resistance to camptothecin-based anticancer drugs, such as topotecan and 7-ethyl-10-hydroxycamptothecin (SN-38: the active metabolite of irinotecan).	Irinotecan	168-198	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	58-63
11688982-1	2001	Overexpression of breast cancer resistance protein (BCRP) ABCG2 reportedly confers cancer cell resistance to camptothecin-based anticancer drugs, such as topotecan and 7-ethyl-10-hydroxycamptothecin (SN-38: the active metabolite of irinotecan).	Irinotecan	200-205	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	18-50
11688982-1	2001	Overexpression of breast cancer resistance protein (BCRP) ABCG2 reportedly confers cancer cell resistance to camptothecin-based anticancer drugs, such as topotecan and 7-ethyl-10-hydroxycamptothecin (SN-38: the active metabolite of irinotecan).	Irinotecan	200-205	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	52-56
11688982-1	2001	Overexpression of breast cancer resistance protein (BCRP) ABCG2 reportedly confers cancer cell resistance to camptothecin-based anticancer drugs, such as topotecan and 7-ethyl-10-hydroxycamptothecin (SN-38: the active metabolite of irinotecan).	Irinotecan	200-205	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	58-63
11688982-1	2001	Overexpression of breast cancer resistance protein (BCRP) ABCG2 reportedly confers cancer cell resistance to camptothecin-based anticancer drugs, such as topotecan and 7-ethyl-10-hydroxycamptothecin (SN-38: the active metabolite of irinotecan).	Irinotecan	232-242	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	18-50
11688982-1	2001	Overexpression of breast cancer resistance protein (BCRP) ABCG2 reportedly confers cancer cell resistance to camptothecin-based anticancer drugs, such as topotecan and 7-ethyl-10-hydroxycamptothecin (SN-38: the active metabolite of irinotecan).	Irinotecan	232-242	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	52-56
11688982-1	2001	Overexpression of breast cancer resistance protein (BCRP) ABCG2 reportedly confers cancer cell resistance to camptothecin-based anticancer drugs, such as topotecan and 7-ethyl-10-hydroxycamptothecin (SN-38: the active metabolite of irinotecan).	Irinotecan	232-242	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	58-63
11688982-2	2001	We have recently shown that SN-38-selected PC-6/SN2-5H human lung carcinoma cells overexpressed BCRP with the reduced intracellular accumulation of SN-38 and SN-38-glucuronide (S. Kawabata et al., Biochem.	Irinotecan	28-33	proprotein convertase subtilisin/kexin type 5	Homo sapiens	43-47
11688982-2	2001	We have recently shown that SN-38-selected PC-6/SN2-5H human lung carcinoma cells overexpressed BCRP with the reduced intracellular accumulation of SN-38 and SN-38-glucuronide (S. Kawabata et al., Biochem.	Irinotecan	28-33	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	96-100
11688982-2	2001	We have recently shown that SN-38-selected PC-6/SN2-5H human lung carcinoma cells overexpressed BCRP with the reduced intracellular accumulation of SN-38 and SN-38-glucuronide (S. Kawabata et al., Biochem.	Irinotecan	148-153	proprotein convertase subtilisin/kexin type 5	Homo sapiens	43-47
11688982-2	2001	We have recently shown that SN-38-selected PC-6/SN2-5H human lung carcinoma cells overexpressed BCRP with the reduced intracellular accumulation of SN-38 and SN-38-glucuronide (S. Kawabata et al., Biochem.	Irinotecan	148-153	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	96-100
11688982-7	2001	In the present study, we have examined whether BCRP transports SN-38 and/or SN-38-glucuronide in vitro, by using plasma membrane vesicles from the parental PC-6 and resistant PC-6/SN2-5H cells, where SN-38 and SN-38-glucuronide accumulation in membrane vesicles was measured by HPLC.	Irinotecan	63-68	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	47-51
11688982-8	2001	Both SN-38 and SN-38-glucuronide were ATP-dependently transported into membrane vesicles prepared from PC-6/SN2-5H cells, whereas no transport activity was observed in membrane vesicles from PC-6 cells.	Irinotecan	5-10	proprotein convertase subtilisin/kexin type 5	Homo sapiens	103-107
11688982-9	2001	The kinetic parameters of the transport observed in PC-6/SN2-5H vesicles were K(m) = 4.0 microM, V(max) = 714 pmol/mg/min for SN-38 and K(m) = 26 microM, V(max) = 833 pmol/mg/min for SN-38-glucuronide.	Irinotecan	126-131	proprotein convertase subtilisin/kexin type 5	Homo sapiens	52-56
11688982-10	2001	These findings suggest that BCRP expressed in PC-6/SN2-5H cells transports both SN-38 and SN-38-glucuronide with a higher affinity toward SN-38.	Irinotecan	80-85	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	28-32
11688982-10	2001	These findings suggest that BCRP expressed in PC-6/SN2-5H cells transports both SN-38 and SN-38-glucuronide with a higher affinity toward SN-38.	Irinotecan	80-85	proprotein convertase subtilisin/kexin type 5	Homo sapiens	46-50
11688982-10	2001	These findings suggest that BCRP expressed in PC-6/SN2-5H cells transports both SN-38 and SN-38-glucuronide with a higher affinity toward SN-38.	Irinotecan	90-95	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	28-32
11688982-10	2001	These findings suggest that BCRP expressed in PC-6/SN2-5H cells transports both SN-38 and SN-38-glucuronide with a higher affinity toward SN-38.	Irinotecan	90-95	proprotein convertase subtilisin/kexin type 5	Homo sapiens	46-50
11822765-6	2001	When G-CSF was added, dose escalation beyond 350 mg/m2 could not be achieved due to grade 2-3 toxicities that prevented on-time retreatment with CPT-11.	Irinotecan	145-151	colony stimulating factor 3	Homo sapiens	5-10
11691793-3	2001	We have studied the effects on NFkappaB activation of two topoisomerase poisons and DNA damaging agents that are used in chemotherapy: SN38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of CPT11, and doxorubicin.	Irinotecan	135-139	nuclear factor kappa B subunit 1	Homo sapiens	31-39
11691793-3	2001	We have studied the effects on NFkappaB activation of two topoisomerase poisons and DNA damaging agents that are used in chemotherapy: SN38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of CPT11, and doxorubicin.	Irinotecan	141-171	nuclear factor kappa B subunit 1	Homo sapiens	31-39
11602529-10	2001	These findings indicate that this newly detected metabolite is a CYP3A4-generated product that may be produced in hepatic microsomes of patients treated with CPT-11.	Irinotecan	158-164	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	65-71
11716702-0	2001	Identification and activities of human carboxylesterases for the activation of CPT-11, a clinically approved anticancer drug.	Irinotecan	79-85	carboxylesterase 1	Homo sapiens	39-56
11716702-7	2001	hCE-2 was 26-fold more active than human carboxylesterase 1 and was 65% as active as rabbit liver carboxylesterase, the most active CPT-11 hydrolyzing enzyme known.	Irinotecan	132-138	carboxylesterase 2	Homo sapiens	0-5
11716702-7	2001	hCE-2 was 26-fold more active than human carboxylesterase 1 and was 65% as active as rabbit liver carboxylesterase, the most active CPT-11 hydrolyzing enzyme known.	Irinotecan	132-138	liver carboxylesterase 1	Oryctolagus cuniculus	92-114
11716702-8	2001	The anti-p97 mAb 96.5 was linked to hCE-2, forming a conjugate that could bind to antigen-positive cancer cells and convert CPT-11 to SN-38.	Irinotecan	124-130	carboxylesterase 2	Homo sapiens	36-41
11716702-8	2001	The anti-p97 mAb 96.5 was linked to hCE-2, forming a conjugate that could bind to antigen-positive cancer cells and convert CPT-11 to SN-38.	Irinotecan	134-139	carboxylesterase 2	Homo sapiens	36-41
11761438-5	2001	Pretreatment of the SW480 primary colon carcinoma cell line with IFN-gamma, 5-FU, CPT-11 or CDDP enhanced ICAM-1 and Fas expression, resulting in Ag-specific CTL-mediated lysis involving Fas-dependent and -independent mechanisms.	Irinotecan	82-88	intercellular adhesion molecule 1	Homo sapiens	106-112
11761438-6	2001	In contrast, pretreatment of the SW620 metastatic isolate, derived from the same patient, with IFN-gamma, CPT-11 or CDDP, but not 5-FU, enhanced ICAM-1 expression, resulting in Ag-specific CTL-mediated lysis via Fas-independent mechanisms only.	Irinotecan	106-112	intercellular adhesion molecule 1	Homo sapiens	145-151
11705873-9	2001	Moreover, CPT-11, cisplatin, oxaliplatin, and Taxol remain highly cytotoxic in cells that overexpress TS.	Irinotecan	10-16	thymidylate synthetase	Homo sapiens	102-104
11602529-0	2001	A new metabolite of irinotecan in which formation is mediated by human hepatic cytochrome P-450 3A4.	Irinotecan	20-30	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	79-99
11602529-3	2001	Several oxidative metabolites of CPT-11 have been identified in humans, including 7-ethyl-10-[4-N-(5-aminopentanoic acid)-1-piperidino]carbonyloxycamptothecin (APC) and 7-ethyl-10-(4-amino-1-piperidino)carbonyloxycamptothecin (NPC), generated by cytochrome P-450 3A4 (CYP3A4).	Irinotecan	33-39	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	246-266
11602529-3	2001	Several oxidative metabolites of CPT-11 have been identified in humans, including 7-ethyl-10-[4-N-(5-aminopentanoic acid)-1-piperidino]carbonyloxycamptothecin (APC) and 7-ethyl-10-(4-amino-1-piperidino)carbonyloxycamptothecin (NPC), generated by cytochrome P-450 3A4 (CYP3A4).	Irinotecan	33-39	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	268-274
11822765-11	2001	CONCLUSIONS: When administered every two weeks, the recommended phase II starting dose of CPT-11 is 250 mg/m2 when given alone and 300 mg/m2 when supported by G-CSF.	Irinotecan	90-96	colony stimulating factor 3	Homo sapiens	159-164
11593056-7	2001	Irinotecan induced apoptosis with an increase of poly(ADP-ribose) polymerase (PARP) cleavage in SW-620 cells (60 versus 7% basal level).	Irinotecan	0-10	poly(ADP-ribose) polymerase 1	Homo sapiens	49-76
11714450-9	2001	When we assessed the mRNA levels of the multidrug resistance-associated protein (MRP), which may be an efflux pump for DDP, the combination of paclitaxel or SN-38 with DDP down-regulated these levels, which are up-regulated by DDP alone.	Irinotecan	157-162	ATP binding cassette subfamily C member 3	Homo sapiens	40-79
11714450-9	2001	When we assessed the mRNA levels of the multidrug resistance-associated protein (MRP), which may be an efflux pump for DDP, the combination of paclitaxel or SN-38 with DDP down-regulated these levels, which are up-regulated by DDP alone.	Irinotecan	157-162	ATP binding cassette subfamily C member 3	Homo sapiens	81-84
11593056-7	2001	Irinotecan induced apoptosis with an increase of poly(ADP-ribose) polymerase (PARP) cleavage in SW-620 cells (60 versus 7% basal level).	Irinotecan	0-10	poly(ADP-ribose) polymerase 1	Homo sapiens	78-82
11593056-8	2001	Pretreatment of these cells with oxaliplatin abolished the increase in PARP cleavage induced by irinotecan (29%).	Irinotecan	96-106	poly(ADP-ribose) polymerase 1	Homo sapiens	71-75
11507714-8	2001	The intra- and inter-day precision of enzyme assay for UDP-glucuronosyltransferase (UGT) activity toward SN-38 in human liver microsomes was less than 4%.	Irinotecan	105-110	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	55-82
12049482-0	2001	The inhibition of acetylcholinesterase by irinotecan and related camptothecins: key structural properties and experimental variables.	Irinotecan	42-52	acetylcholinesterase (Cartwright blood group)	Homo sapiens	18-38
11695848-0	2001	Human liver UDP-glucuronosyltransferase isoforms involved in the glucuronidation of 7-ethyl-10-hydroxycamptothecin.	Irinotecan	84-114	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	12-39
11695848-2	2001	The human liver UDP-glucuronosyltransferase (UGT) isoforms involved in the glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan (CPT-11), have been studied using microsomes from human liver and insect cells expressing human UGTs (1A1, 1A3, 1A4, 1A6, 1A9, 2B7, 2B15).	Irinotecan	94-124	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	16-43
11695848-2	2001	The human liver UDP-glucuronosyltransferase (UGT) isoforms involved in the glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan (CPT-11), have been studied using microsomes from human liver and insect cells expressing human UGTs (1A1, 1A3, 1A4, 1A6, 1A9, 2B7, 2B15).	Irinotecan	94-124	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	45-48
11695848-2	2001	The human liver UDP-glucuronosyltransferase (UGT) isoforms involved in the glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan (CPT-11), have been studied using microsomes from human liver and insect cells expressing human UGTs (1A1, 1A3, 1A4, 1A6, 1A9, 2B7, 2B15).	Irinotecan	126-131	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	16-43
11695848-2	2001	The human liver UDP-glucuronosyltransferase (UGT) isoforms involved in the glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan (CPT-11), have been studied using microsomes from human liver and insect cells expressing human UGTs (1A1, 1A3, 1A4, 1A6, 1A9, 2B7, 2B15).	Irinotecan	126-131	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	45-48
11695848-2	2001	The human liver UDP-glucuronosyltransferase (UGT) isoforms involved in the glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan (CPT-11), have been studied using microsomes from human liver and insect cells expressing human UGTs (1A1, 1A3, 1A4, 1A6, 1A9, 2B7, 2B15).	Irinotecan	159-169	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	16-43
11695848-2	2001	The human liver UDP-glucuronosyltransferase (UGT) isoforms involved in the glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan (CPT-11), have been studied using microsomes from human liver and insect cells expressing human UGTs (1A1, 1A3, 1A4, 1A6, 1A9, 2B7, 2B15).	Irinotecan	159-169	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	45-48
11695848-2	2001	The human liver UDP-glucuronosyltransferase (UGT) isoforms involved in the glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan (CPT-11), have been studied using microsomes from human liver and insect cells expressing human UGTs (1A1, 1A3, 1A4, 1A6, 1A9, 2B7, 2B15).	Irinotecan	171-177	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	16-43
11695848-2	2001	The human liver UDP-glucuronosyltransferase (UGT) isoforms involved in the glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan (CPT-11), have been studied using microsomes from human liver and insect cells expressing human UGTs (1A1, 1A3, 1A4, 1A6, 1A9, 2B7, 2B15).	Irinotecan	171-177	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	45-48
11695848-4	2001	The glucuronidation of SN-38 was catalysed by UGT1A1, UGT1A3, UGT1A6 and UGT1A9 as well as by liver microsomes.	Irinotecan	23-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
11695848-4	2001	The glucuronidation of SN-38 was catalysed by UGT1A1, UGT1A3, UGT1A6 and UGT1A9 as well as by liver microsomes.	Irinotecan	23-28	UDP glucuronosyltransferase family 1 member A3	Homo sapiens	54-60
11695848-4	2001	The glucuronidation of SN-38 was catalysed by UGT1A1, UGT1A3, UGT1A6 and UGT1A9 as well as by liver microsomes.	Irinotecan	23-28	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	62-68
11695848-4	2001	The glucuronidation of SN-38 was catalysed by UGT1A1, UGT1A3, UGT1A6 and UGT1A9 as well as by liver microsomes.	Irinotecan	23-28	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	73-79
11695848-5	2001	Among these UGT isoforms, UGT1A1 showed the highest activity of SN-38 glucuronidation at both low (1 microM) and high (200 microM) substrate concentrations.	Irinotecan	64-69	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	12-15
11695848-5	2001	Among these UGT isoforms, UGT1A1 showed the highest activity of SN-38 glucuronidation at both low (1 microM) and high (200 microM) substrate concentrations.	Irinotecan	64-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	26-32
11695848-10	2001	The UGT isoforms involved in SN-38 glucuronidation could be classified into two types: low-Km types such as UGT1A1 and UGT1A9, and high-Km types such as UGT1A3 and UGT1A6, in terms of affinity toward substrate.	Irinotecan	29-34	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	4-7
11695848-10	2001	The UGT isoforms involved in SN-38 glucuronidation could be classified into two types: low-Km types such as UGT1A1 and UGT1A9, and high-Km types such as UGT1A3 and UGT1A6, in terms of affinity toward substrate.	Irinotecan	29-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
11695848-10	2001	The UGT isoforms involved in SN-38 glucuronidation could be classified into two types: low-Km types such as UGT1A1 and UGT1A9, and high-Km types such as UGT1A3 and UGT1A6, in terms of affinity toward substrate.	Irinotecan	29-34	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	119-125
11695848-10	2001	The UGT isoforms involved in SN-38 glucuronidation could be classified into two types: low-Km types such as UGT1A1 and UGT1A9, and high-Km types such as UGT1A3 and UGT1A6, in terms of affinity toward substrate.	Irinotecan	29-34	UDP glucuronosyltransferase family 1 member A3	Homo sapiens	153-159
11695848-10	2001	The UGT isoforms involved in SN-38 glucuronidation could be classified into two types: low-Km types such as UGT1A1 and UGT1A9, and high-Km types such as UGT1A3 and UGT1A6, in terms of affinity toward substrate.	Irinotecan	29-34	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	164-170
11695848-14	2001	The activity of SN-38 glucuronidation by liver microsomes and UGT1A1 was effectively inhibited by bilirubin.	Irinotecan	16-21	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	62-68
11695848-16	2001	Although cholic acid derivatives strongly inhibited the activity of SN-38 glucuronidation by UGT1A3, the inhibition profile did not parallel that in liver microsomes.	Irinotecan	68-73	UDP glucuronosyltransferase family 1 member A3	Homo sapiens	93-99
11695848-18	2001	These results demonstrate that at least four UGT1A isoforms are responsible for SN-38 glucuronidation in human livers, and suggest that the role and contribution of each differ substantially.	Irinotecan	80-85	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	45-50
11559526-6	2001	Cross-resistance studies suggest that, compared with wild-type MXR/BCRP/ABCP, cells having an R482T mutation have higher anthracycline resistance, whereas an R482G mutation seems to confer relatively less resistance to SN-38 and topotecan.	Irinotecan	219-224	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	63-66
11559526-6	2001	Cross-resistance studies suggest that, compared with wild-type MXR/BCRP/ABCP, cells having an R482T mutation have higher anthracycline resistance, whereas an R482G mutation seems to confer relatively less resistance to SN-38 and topotecan.	Irinotecan	219-224	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	67-71
11559526-6	2001	Cross-resistance studies suggest that, compared with wild-type MXR/BCRP/ABCP, cells having an R482T mutation have higher anthracycline resistance, whereas an R482G mutation seems to confer relatively less resistance to SN-38 and topotecan.	Irinotecan	219-224	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	72-76
11474256-8	2001	Maximum tolerated dosage (MTD) for the topotecan and irinotecan combination was defined as that which permitted 4 weeks of topotecan and irinotecan administration with G-CSF at or near the dose intensity reported for each single agent.	Irinotecan	53-63	colony stimulating factor 2	Homo sapiens	168-173
12049482-2	2001	Recently, we demonstrated that CPT-11 (lactone) is also a potent inhibitor of human acetylcholinesterase (AChE) at clinically relevant concentrations.	Irinotecan	31-37	acetylcholinesterase (Cartwright blood group)	Homo sapiens	84-104
12049482-2	2001	Recently, we demonstrated that CPT-11 (lactone) is also a potent inhibitor of human acetylcholinesterase (AChE) at clinically relevant concentrations.	Irinotecan	31-37	acetylcholinesterase (Cartwright blood group)	Homo sapiens	106-110
12049482-5	2001	Those compounds possessing N-substitutions at C-10 were all found to inhibit AChE in a similar kinetic manner to CPT-11, but with a broad range of potencies.	Irinotecan	113-119	acetylcholinesterase (Cartwright blood group)	Homo sapiens	77-81
11507714-8	2001	The intra- and inter-day precision of enzyme assay for UDP-glucuronosyltransferase (UGT) activity toward SN-38 in human liver microsomes was less than 4%.	Irinotecan	105-110	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	84-87
11376565-0	2001	CPT-11 alters the circadian rhythm of dihydropyrimidine dehydrogenase mRNA in mouse liver.	Irinotecan	0-6	dihydropyrimidine dehydrogenase	Mus musculus	38-69
11455023-2	2001	We identified a rabbit liver carboxylesterase (CE) that was very efficient at CPT-11 metabolism; however, a human homolog that was more than 81% identical to this protein activated the drug poorly.	Irinotecan	78-84	liver carboxylesterase 1	Oryctolagus cuniculus	23-45
11724314-0	2001	Streptococcal preparation OK-432 enhances the antitumor activity of CPT-11 by increasing Th1-cytokine production in mice.	Irinotecan	68-74	negative elongation factor complex member C/D, Th1l	Mus musculus	89-92
11724314-4	2001	RESULTS: SN-38, the active metabolite of CPT-11, exerted dose-dependent inhibition of interferon (IFN)-gamma production induced by OK-432 in mouse splenocytes.	Irinotecan	9-14	interferon gamma	Mus musculus	86-108
11724314-4	2001	RESULTS: SN-38, the active metabolite of CPT-11, exerted dose-dependent inhibition of interferon (IFN)-gamma production induced by OK-432 in mouse splenocytes.	Irinotecan	41-47	interferon gamma	Mus musculus	86-108
11724314-5	2001	In contrast, the optimum concentration of SN-38 increased interleukin (IL)-6 and IL-12 production by OK-432-activated splenocytes.	Irinotecan	42-47	interleukin 6	Mus musculus	58-76
11724314-7	2001	Investigation of cytokine production showed that CPT-11 treatment principally inhibited IL-12 and IFN-gamma production, which was improved by the combined administration with OK-432.	Irinotecan	49-55	interferon gamma	Mus musculus	98-107
11724314-8	2001	CONCLUSION: These results indicate that CPT-11 inhibits type-1 T helper (Th1) cells despite its potential to stimulate macrophages and that OK-432 enhances the antitumor activity of CPT-11 by increasing Th1-cytokine production.	Irinotecan	40-46	negative elongation factor complex member C/D, Th1l	Mus musculus	73-76
11724314-8	2001	CONCLUSION: These results indicate that CPT-11 inhibits type-1 T helper (Th1) cells despite its potential to stimulate macrophages and that OK-432 enhances the antitumor activity of CPT-11 by increasing Th1-cytokine production.	Irinotecan	182-188	negative elongation factor complex member C/D, Th1l	Mus musculus	203-206
11431344-0	2001	Sensitization of human tumor cells to CPT-11 via adenoviral-mediated delivery of a rabbit liver carboxylesterase.	Irinotecan	38-44	liver carboxylesterase 1	Oryctolagus cuniculus	90-112
11351255-5	2001	Cotreatment of N-acetyl-Asp-Glu-Val-Asp aldehyde (AC-DEVD-CHO), a caspase 3 inhibitor prevented cytotoxic effect of VP-16 and SN-38 (p&lt;0.01).	Irinotecan	126-131	caspase 3	Homo sapiens	66-75
11419031-8	2001	Furthermore, a recent randomized trial showed that the combination of a newer agent (irinotecan) with cisplatin was superior to a standard etoposide and cisplatin regimen in patients with newly diagnosed extensive-stage SCLC.	Irinotecan	85-95	SCLC1	Homo sapiens	220-224
11489791-5	2001	CPT-11 is subject to extensive metabolic conversion by various enzyme systems, including esterases to form SN-38, UGT1A1 mediating glucuronidation of SN-38, as well as CYP3A4, which forms several pharmacologically inactive oxidation products.	Irinotecan	0-6	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
11489791-5	2001	CPT-11 is subject to extensive metabolic conversion by various enzyme systems, including esterases to form SN-38, UGT1A1 mediating glucuronidation of SN-38, as well as CYP3A4, which forms several pharmacologically inactive oxidation products.	Irinotecan	150-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	114-120
11395570-4	2001	Both the lactone and carboxylate forms of CPT-11 and SN-38 were actively transported across the cell monolayers, mainly by the apical-localized P-gp pump.	Irinotecan	42-48	ATP binding cassette subfamily B member 1	Homo sapiens	144-148
11395570-4	2001	Both the lactone and carboxylate forms of CPT-11 and SN-38 were actively transported across the cell monolayers, mainly by the apical-localized P-gp pump.	Irinotecan	53-58	ATP binding cassette subfamily B member 1	Homo sapiens	144-148
11395570-8	2001	In contrast, SN-38 efficacy decreased in the presence of P-gp inhibitors due to active transport toward the basolateral side, thereby reducing drug accumulation.	Irinotecan	13-18	ATP binding cassette subfamily B member 1	Homo sapiens	57-61
11350876-7	2001	Our findings indicate that bacterial beta-glucuronidase plays a crucial role in CPT-11-induced diarrhea without affecting enterocycling and systemic SN-38 levels.	Irinotecan	80-86	glucuronidase beta	Homo sapiens	37-55
11376565-3	2001	To optimize the schedule of the CPT-11 plus 5-FU combination, we investigated the effect of CPT-11 on the circadian rhythm of DPD in vivo.	Irinotecan	92-98	dihydropyrimidine dehydrogenase	Mus musculus	126-129
11376565-5	2001	After intravenous administration of CPT-11 (30 mg / kg) at 20:00, the circadian rhythm of the DPD mRNA level in the liver was no longer observed 18 h later (14:00), but it was unaffected 6 and 18 h later (at 14:00 and 02:00) when CPT-11 was given at 08:00.	Irinotecan	36-42	dihydropyrimidine dehydrogenase	Mus musculus	94-97
11376565-5	2001	After intravenous administration of CPT-11 (30 mg / kg) at 20:00, the circadian rhythm of the DPD mRNA level in the liver was no longer observed 18 h later (14:00), but it was unaffected 6 and 18 h later (at 14:00 and 02:00) when CPT-11 was given at 08:00.	Irinotecan	230-236	dihydropyrimidine dehydrogenase	Mus musculus	94-97
11376565-6	2001	In addition, a dose-dependent lengthening of the period of the circadian rhythm of DPD was observed for 42 h after intravenous injection of CPT-11 at 20:00.	Irinotecan	140-146	dihydropyrimidine dehydrogenase	Mus musculus	83-86
11376565-7	2001	The levels of DPD protein and activity at 21 h after administration of CPT-11 (at 17:00) were significantly higher than at 9 h (at 05:00).	Irinotecan	71-77	dihydropyrimidine dehydrogenase	Mus musculus	14-17
11376565-8	2001	These results suggest that CPT-11 may influence the circadian rhythm of DPD at the transcriptional level.	Irinotecan	27-33	dihydropyrimidine dehydrogenase	Mus musculus	72-75
11376565-9	2001	Modulation of the circadian rhythm of DPD by CPT-11 may be a factor in optimizing the combination of 5-FU and CPT-11.	Irinotecan	45-51	dihydropyrimidine dehydrogenase	Mus musculus	38-41
11376565-9	2001	Modulation of the circadian rhythm of DPD by CPT-11 may be a factor in optimizing the combination of 5-FU and CPT-11.	Irinotecan	110-116	dihydropyrimidine dehydrogenase	Mus musculus	38-41
11309308-16	2001	delivered BCRP substrates, e.g., topotecan or irinotecan, by using a BCRP inhibitor.	Irinotecan	46-56	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	10-14
11309308-16	2001	delivered BCRP substrates, e.g., topotecan or irinotecan, by using a BCRP inhibitor.	Irinotecan	46-56	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	69-73
11309344-7	2001	From the combined data, we conclude that the affinities of topoisomerase I drugs for BCRP are, in decreasing order: SN-38 &gt; topotecan &gt; 9-aminocamptothecin approximately CPT-11 &gt; NX211 &gt; DX8951f &gt; BNP1350.	Irinotecan	116-121	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	85-89
11309344-7	2001	From the combined data, we conclude that the affinities of topoisomerase I drugs for BCRP are, in decreasing order: SN-38 &gt; topotecan &gt; 9-aminocamptothecin approximately CPT-11 &gt; NX211 &gt; DX8951f &gt; BNP1350.	Irinotecan	176-182	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	85-89
11280753-3	2001	The RC0.1 and RC1 cells have high cross-resistance to CPT derivatives including SN-38 and topotecan, but are not cross-resistant to the non-top1 inhibitors etoposide, doxorubicin, and vincristine.	Irinotecan	80-85	chromobox 8	Homo sapiens	14-17
11259359-1	2001	Amonafide and irinotecan are anticancer drugs representative of the clinical relevance of N-acetyltransferase (NAT) and uridine diphosphate glucuronosyltransferase (UGT) polymorphisms in cancer chemotherapy, respectively.	Irinotecan	14-24	bromodomain containing 2	Homo sapiens	90-109
11259359-1	2001	Amonafide and irinotecan are anticancer drugs representative of the clinical relevance of N-acetyltransferase (NAT) and uridine diphosphate glucuronosyltransferase (UGT) polymorphisms in cancer chemotherapy, respectively.	Irinotecan	14-24	bromodomain containing 2	Homo sapiens	111-114
11259359-1	2001	Amonafide and irinotecan are anticancer drugs representative of the clinical relevance of N-acetyltransferase (NAT) and uridine diphosphate glucuronosyltransferase (UGT) polymorphisms in cancer chemotherapy, respectively.	Irinotecan	14-24	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	120-163
11259359-1	2001	Amonafide and irinotecan are anticancer drugs representative of the clinical relevance of N-acetyltransferase (NAT) and uridine diphosphate glucuronosyltransferase (UGT) polymorphisms in cancer chemotherapy, respectively.	Irinotecan	14-24	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	165-168
11259359-7	2001	SN-38, the active metabolite of irinotecan, is glucuronidated to the inactive SN-38 glucuronide by UGT1A1, the isoform catalyzing bilirubin glucuronidation.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
11259359-7	2001	SN-38, the active metabolite of irinotecan, is glucuronidated to the inactive SN-38 glucuronide by UGT1A1, the isoform catalyzing bilirubin glucuronidation.	Irinotecan	32-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
11259359-13	2001	A phenotyping procedure for UGT1A1 has not been identified and genotyping of the UGT1A1 promoter in patients receiving irinotecan may identify patients at increased risk of toxicity.	Irinotecan	119-129	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	81-87
11259359-14	2001	A clinical trial at the University of Chicago is ongoing to demonstrate the predictive significance of UGT1A1 genotyping for irinotecan pharmacodynamics.	Irinotecan	125-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	103-109
11115510-3	2001	Inhibiting the degradation of IkappaBalpha by pretreatment with the proteasome inhibitor MG-132 significantly inhibited NF-kappaB activation and apoptosis but not DNA damage induced by SN-38 or VP-16.	Irinotecan	185-190	NFKB inhibitor alpha	Homo sapiens	30-42
11115510-4	2001	Transfection of NSCLC-3 or NSCLC-5 cells with dominant negative mutant IkappaBalpha (mIkappaBalpha) inhibited SN-38 or VP-16 induced transcription and DNA binding activity of NF-kappaB without altering drug-induced apoptosis.	Irinotecan	110-115	NFKB inhibitor alpha	Homo sapiens	71-83
11177741-4	2001	Preliminary data suggest that gene expression levels of topoisomerase I, p21, bcl-2, and ICE may be predictive of response to therapy with CPT-11.	Irinotecan	139-145	H3 histone pseudogene 16	Homo sapiens	73-76
11265410-0	2001	[A case of AFP-producing gastric cancer responding to low-dose CPT-11 and low-dose cisplatin combination chemotherapy].	Irinotecan	63-69	alpha fetoprotein	Homo sapiens	11-14
11177741-4	2001	Preliminary data suggest that gene expression levels of topoisomerase I, p21, bcl-2, and ICE may be predictive of response to therapy with CPT-11.	Irinotecan	139-145	BCL2 apoptosis regulator	Homo sapiens	78-83
11177741-4	2001	Preliminary data suggest that gene expression levels of topoisomerase I, p21, bcl-2, and ICE may be predictive of response to therapy with CPT-11.	Irinotecan	139-145	carboxylesterase 2	Homo sapiens	89-92
11177741-5	2001	Increased toxicity seen in patients treated with CPT-11 may be explained by polymorphism in the UGT1A1 gene, which is responsible for glucuronidation of the active metabolite of CPT-11.	Irinotecan	49-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
11177741-5	2001	Increased toxicity seen in patients treated with CPT-11 may be explained by polymorphism in the UGT1A1 gene, which is responsible for glucuronidation of the active metabolite of CPT-11.	Irinotecan	178-184	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
11265410-2	2001	We report an AFP-producing gastric cancer that showed a partial response to low-dose CPT-11 and low-dose cisplatin combination chemotherapy.	Irinotecan	85-91	alpha fetoprotein	Homo sapiens	13-16
11265410-3	2001	AFP-producing gastric cancers successfully treated with chemotherapy have been reported, but to our knowledge this is the first report of successful treatment with low-dose CPT-11 and low-dose cisplatin combination chemotherapy.	Irinotecan	173-179	alpha fetoprotein	Homo sapiens	0-3
11162657-0	2001	Breast cancer resistance protein directly confers SN-38 resistance of lung cancer cells.	Irinotecan	50-55	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
11230497-2	2001	With the recognition that topoisomerase-I (TOP-I) is an important therapeutic target in cancer therapy, irinotecan, a semisynthetic TOP-I-interactive camptothecin derivative, has been clinically established in the treatment of colorectal cancer.	Irinotecan	104-114	DNA topoisomerase I	Homo sapiens	26-41
11230497-2	2001	With the recognition that topoisomerase-I (TOP-I) is an important therapeutic target in cancer therapy, irinotecan, a semisynthetic TOP-I-interactive camptothecin derivative, has been clinically established in the treatment of colorectal cancer.	Irinotecan	104-114	DNA topoisomerase I	Homo sapiens	43-48
11230497-2	2001	With the recognition that topoisomerase-I (TOP-I) is an important therapeutic target in cancer therapy, irinotecan, a semisynthetic TOP-I-interactive camptothecin derivative, has been clinically established in the treatment of colorectal cancer.	Irinotecan	104-114	DNA topoisomerase I	Homo sapiens	132-137
11162657-2	2001	BCRP-overexpressing cells show cross-resistance to camptothecin derivatives such as irinotecan, SN-38 (the active metabolite of irinotecan), and topotecan.	Irinotecan	84-94	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-4
11162657-2	2001	BCRP-overexpressing cells show cross-resistance to camptothecin derivatives such as irinotecan, SN-38 (the active metabolite of irinotecan), and topotecan.	Irinotecan	96-101	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-4
11162657-2	2001	BCRP-overexpressing cells show cross-resistance to camptothecin derivatives such as irinotecan, SN-38 (the active metabolite of irinotecan), and topotecan.	Irinotecan	128-138	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-4
11162657-5	2001	The intracellular SN-38 accumulation was reduced in the sublines, and BCRP mRNA was overexpressed in proportion to the degree of SN-38 resistance.	Irinotecan	129-134	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	70-74
11162657-6	2001	These findings suggest that BCRP confers SN-38 resistance in the sublines.	Irinotecan	41-46	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	28-32
11162657-9	2001	These data indicate that BCRP is directly involved with SN-38 resistance, by efflux transport of SN-38.	Irinotecan	56-61	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	25-29
11162657-9	2001	These data indicate that BCRP is directly involved with SN-38 resistance, by efflux transport of SN-38.	Irinotecan	97-102	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	25-29
11142689-0	2000	Phase I study of carboplatin, docetaxel and irinotecan with recombinant human granulocyte colony stimulating factor support in patients with advanced non-small cell lung cancer.	Irinotecan	44-54	colony stimulating factor 3	Homo sapiens	78-115
11162602-4	2001	The reduction in cyclin B1 expression and G2 arrest were also seen after treatment with etoposide and irinotecan.	Irinotecan	102-112	cyclin B1	Homo sapiens	17-26
11212269-4	2001	We report here that a human degradation-resistant GLP-2 analogue, h[Gly2]-GLP-2 significantly improves survival, reduces bacteremia, attenuates epithelial injury, and inhibits crypt apoptosis in the murine gastrointestinal tract after administration of topoisomerase I inhibitor irinotecan hydrochloride or the antimetabolite 5-fluorouracil.	Irinotecan	279-303	glucagon	Homo sapiens	74-79
11212277-0	2001	The HER tyrosine kinase inhibitor CI1033 enhances cytotoxicity of 7-ethyl-10-hydroxycamptothecin and topotecan by inhibiting breast cancer resistance protein-mediated drug efflux.	Irinotecan	66-96	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	125-157
11212277-10	2001	Moreover, CI1033 enhanced the uptake and cytotoxicity of SN-38 and TPT in cells transfected with BCRP but not empty vector.	Irinotecan	57-62	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	97-101
11783425-0	2001	UGT1A1 polymorphism predicts irinotecan toxicity: evolving proof.	Irinotecan	29-39	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
11212269-4	2001	We report here that a human degradation-resistant GLP-2 analogue, h[Gly2]-GLP-2 significantly improves survival, reduces bacteremia, attenuates epithelial injury, and inhibits crypt apoptosis in the murine gastrointestinal tract after administration of topoisomerase I inhibitor irinotecan hydrochloride or the antimetabolite 5-fluorouracil.	Irinotecan	279-303	glucagon	Homo sapiens	50-55
11156391-2	2000	Irinotecan is metabolized to form active SN-38, which is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) 1A1 enzyme.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-131
11156391-2	2000	Irinotecan is metabolized to form active SN-38, which is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) 1A1 enzyme.	Irinotecan	41-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-131
11156391-3	2000	Genetic polymorphisms of the UGT1A1 would affect an interindividual variation of the toxicity by irinotecan via the alternation of bioavailability of SN-38.	Irinotecan	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
11156391-3	2000	Genetic polymorphisms of the UGT1A1 would affect an interindividual variation of the toxicity by irinotecan via the alternation of bioavailability of SN-38.	Irinotecan	150-155	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
11156391-4	2000	In this case-control study, retrospective review of clinical records and determination of UGT1A1 polymorphisms were performed to investigate whether a patient with the variant UGT1A1 genotypes would be at higher risk for severe toxicity by irinotecan.	Irinotecan	240-250	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	176-182
11156391-9	2000	Multivariate analysis suggested that the genotype either heterozygous or homozygous for UGT1A1*28 would be a significant risk factor for severe toxicity by irinotecan (P &lt; 0.001; odds ratio, 7.23; 95% confidence interval, 2.52-22.3).	Irinotecan	156-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
11156391-13	2000	We suggest that determination of the UGT1A1 genotypes might be clinically useful for predicting severe toxicity by irinotecan in cancer patients.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
11156391-14	2000	This research warrants a prospective trial to corroborate the usefulness of gene diagnosis of UGT1A1 polymorphisms prior tb irinotecan chemotherapy.	Irinotecan	124-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
11137204-7	2000	RESULTS: At the dose of CPT-11 120 mg/m2, three out of four enrolled patients presented DLTs (grade 4 neutropenia, febrile neutropenia and delayed diarrhea); the addition of G-CSF at this level did not permit further dose-escalation.	Irinotecan	24-30	colony stimulating factor 3	Homo sapiens	174-179
11142689-1	2000	A phase I study was conducted in patients with stage IIIB or IV non-small cell lung cancer to determine the maximum tolerated dose (MTD) of irinotecan combined with a fixed schedule of docetaxel and carboplatin with recombinant human granulocyte colony stimulating factor (rhG-CSF) (nartograstim) support.	Irinotecan	140-150	colony stimulating factor 3	Homo sapiens	234-271
11084429-6	2000	We found a good correlation between inactivation of TGFB-RII, BAX or hMSH3 genes and tumor response to CPT-11 (P =0.002).	Irinotecan	103-109	transforming growth factor beta 1	Homo sapiens	52-56
11108431-6	2000	With regard to irinotecan, patients with Gilbert"s syndrome phenotype have reduced inactivation of the active topoisomerase I inhibitor 7-ethyl-10-hydroxycamptothecin (SN-38) caused by a mutation in the UDP-glucuronosyltransferase 1A1 gene promoter.	Irinotecan	15-25	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	203-234
11108431-6	2000	With regard to irinotecan, patients with Gilbert"s syndrome phenotype have reduced inactivation of the active topoisomerase I inhibitor 7-ethyl-10-hydroxycamptothecin (SN-38) caused by a mutation in the UDP-glucuronosyltransferase 1A1 gene promoter.	Irinotecan	136-166	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	203-234
11108431-6	2000	With regard to irinotecan, patients with Gilbert"s syndrome phenotype have reduced inactivation of the active topoisomerase I inhibitor 7-ethyl-10-hydroxycamptothecin (SN-38) caused by a mutation in the UDP-glucuronosyltransferase 1A1 gene promoter.	Irinotecan	168-173	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	203-234
11084429-6	2000	We found a good correlation between inactivation of TGFB-RII, BAX or hMSH3 genes and tumor response to CPT-11 (P =0.002).	Irinotecan	103-109	BCL2 associated X, apoptosis regulator	Homo sapiens	62-65
11084429-6	2000	We found a good correlation between inactivation of TGFB-RII, BAX or hMSH3 genes and tumor response to CPT-11 (P =0.002).	Irinotecan	103-109	mutS homolog 3	Homo sapiens	69-74
10912951-4	2000	The etoposide-resistant line with the highest P-gp level was cross-resistant also to SN-38, CPT-11 and topotecan (TPT), but not to 9-aminocamptothecin (9-AC), CPT and DX-8951f.	Irinotecan	85-90	ATP binding cassette subfamily B member 1	Homo sapiens	46-50
11081458-8	2000	A 48-year-old patient with a HCC that had developed within a normal liver but of very poor prognosis because of a multifocal primary tumor with a large nodule measuring 10 cm of diameter, associated with a portal thrombosis, could tolerate very intensive treatment with irinotecan using doses up to 700 mg/m2 every 2 weeks and was responsive to treatment as measured by alpha-fetoprotein levels.	Irinotecan	270-280	alpha fetoprotein	Homo sapiens	370-387
10999728-2	2000	In the liver, SN-38 is glucuronidated (SN-38G) by UGT1A1, which also conjugates bilirubin.	Irinotecan	14-19	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
10999728-2	2000	In the liver, SN-38 is glucuronidated (SN-38G) by UGT1A1, which also conjugates bilirubin.	Irinotecan	39-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
10999728-8	2000	Interestingly, individual levels of fecal beta-glucuronidase, which is known to mediate SN-38G hydrolysis, were not related to any of the SN-38 kinetic parameters (r = 0.09; P = 0.26), suggesting that interindividual variation in this enzyme is unimportant in explaining SN-38 pharmacokinetic variability.	Irinotecan	88-93	glucuronidase beta	Homo sapiens	42-60
10971167-1	2000	OBJECTIVE: This study was conducted in refractory or relapsed small-cell lung cancer to determine activity and toxicity of the combination of cisplatin, ifosfamide, and irinotecan with rhG-CSF support.	Irinotecan	169-179	colony stimulating factor 2	Homo sapiens	189-192
10912947-7	2000	Sample pretreatment procedures of the CPT analogs topotecan, irinotecan, 9-aminocamptothecin and lurtotecan are summarized and discussed in this review.	Irinotecan	61-71	choline phosphotransferase 1	Homo sapiens	38-41
10912951-4	2000	The etoposide-resistant line with the highest P-gp level was cross-resistant also to SN-38, CPT-11 and topotecan (TPT), but not to 9-aminocamptothecin (9-AC), CPT and DX-8951f.	Irinotecan	92-98	ATP binding cassette subfamily B member 1	Homo sapiens	46-50
10811101-4	2000	We show that the topoisomerase I inhibitor 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11) activates NF-kappaB in most colorectal cancer cell lines.	Irinotecan	110-116	nuclear factor kappa B subunit 1	Homo sapiens	128-137
10811101-4	2000	We show that the topoisomerase I inhibitor 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11) activates NF-kappaB in most colorectal cancer cell lines.	Irinotecan	43-108	nuclear factor kappa B subunit 1	Homo sapiens	128-137
10811101-6	2000	These data demonstrate that the protection from apoptosis induced in response to CPT-11 treatment is effectively inhibited by the transient inhibition of NF-kappaB in a variety of human colon cancer cell lines and in a tumor xenograft model, resulting in a significantly enhanced tumoricidal response to CPT-11 via increased induction of apoptosis.	Irinotecan	81-87	nuclear factor kappa B subunit 1	Homo sapiens	154-163
10811101-6	2000	These data demonstrate that the protection from apoptosis induced in response to CPT-11 treatment is effectively inhibited by the transient inhibition of NF-kappaB in a variety of human colon cancer cell lines and in a tumor xenograft model, resulting in a significantly enhanced tumoricidal response to CPT-11 via increased induction of apoptosis.	Irinotecan	304-310	nuclear factor kappa B subunit 1	Homo sapiens	154-163
10738246-2	2000	We have found that ectopic p16(INK4) expression increased cellular sensitivity of human non-small-cell-lung-cancer (NSCLC) A549 cells to a selective growth-inhibitory effect induced by the topoisomerase-I inhibitor 11, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxy camptothecin (CPT-11) in vitro.	Irinotecan	288-294	cyclin dependent kinase inhibitor 2A	Homo sapiens	31-35
10815927-0	2000	Metabolism of irinotecan (CPT-11) by CYP3A4 and CYP3A5 in humans.	Irinotecan	14-24	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	37-43
10815927-0	2000	Metabolism of irinotecan (CPT-11) by CYP3A4 and CYP3A5 in humans.	Irinotecan	14-24	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	48-54
10815927-0	2000	Metabolism of irinotecan (CPT-11) by CYP3A4 and CYP3A5 in humans.	Irinotecan	26-32	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	37-43
10815927-0	2000	Metabolism of irinotecan (CPT-11) by CYP3A4 and CYP3A5 in humans.	Irinotecan	26-32	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	48-54
10815927-2	2000	The objective of this study was to determine the oxidative metabolites of CPT-11 recovered in human urine samples and to identify cytochrome P450 (CYP) involved in their formation.	Irinotecan	74-80	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	147-150
10815927-7	2000	Only CYP3A4 produced both APC and NPC, resulting from the oxidation of the piperidinylpiperidine side chain of CPT-11 along with metabolite M2.	Irinotecan	111-117	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	5-11
10815927-8	2000	The metabolism of CPT-11 by CYP3A5 was markedly different because neither APC or NPC nor M2 was produced, whereas only one new metabolite, M4 (molecular weight, 558), was generated by de-ethylation of the CPT moiety.	Irinotecan	18-24	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	28-34
10815927-11	2000	The parameters of CPT-11 biotransformation into M2 and M4 were examined using cell lines expressing, respectively, with CYP3A4 and CYP3A5, indicating that CPT-11 is preferentially metabolized by CYP3A4.	Irinotecan	18-24	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	120-126
10815927-11	2000	The parameters of CPT-11 biotransformation into M2 and M4 were examined using cell lines expressing, respectively, with CYP3A4 and CYP3A5, indicating that CPT-11 is preferentially metabolized by CYP3A4.	Irinotecan	18-24	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	131-137
10815927-11	2000	The parameters of CPT-11 biotransformation into M2 and M4 were examined using cell lines expressing, respectively, with CYP3A4 and CYP3A5, indicating that CPT-11 is preferentially metabolized by CYP3A4.	Irinotecan	18-24	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	195-201
10815927-11	2000	The parameters of CPT-11 biotransformation into M2 and M4 were examined using cell lines expressing, respectively, with CYP3A4 and CYP3A5, indicating that CPT-11 is preferentially metabolized by CYP3A4.	Irinotecan	155-161	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	131-137
10815927-11	2000	The parameters of CPT-11 biotransformation into M2 and M4 were examined using cell lines expressing, respectively, with CYP3A4 and CYP3A5, indicating that CPT-11 is preferentially metabolized by CYP3A4.	Irinotecan	155-161	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	195-201
10815927-12	2000	In conclusion, CYP3A plays a major role in the metabolism of CPT-11, with some differences of the metabolic profile exhibited by 3A4 and 3A5.	Irinotecan	61-67	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	15-20
10838661-10	2000	Collectively, the results suggest that augmentation of the therapeutic efficacy of irinotecan against colon cancer liver metastases by immunomodulation with JBT 3002 may be associated with elevated inducible nitric oxide synthase and endogenous interleukin-15 in tumor-infiltrating macrophages.	Irinotecan	83-93	nitric oxide synthase 2, inducible	Mus musculus	198-229
10838661-10	2000	Collectively, the results suggest that augmentation of the therapeutic efficacy of irinotecan against colon cancer liver metastases by immunomodulation with JBT 3002 may be associated with elevated inducible nitric oxide synthase and endogenous interleukin-15 in tumor-infiltrating macrophages.	Irinotecan	83-93	interleukin 15	Mus musculus	245-259
10933967-6	2000	Specifically, IMR32.ODC.CE cells expressed approximately eightfold more CE activity than IMR32.CMV.neo cells; and 5 microM CPT-11 reduced the clonogenic potential of IMR32.ODC.CE cells to zero, while 50 microM CPT-11 was required to produce the same effect with IMR32.CMV.neo cells.	Irinotecan	123-129	ornithine decarboxylase 1	Homo sapiens	20-23
10933967-6	2000	Specifically, IMR32.ODC.CE cells expressed approximately eightfold more CE activity than IMR32.CMV.neo cells; and 5 microM CPT-11 reduced the clonogenic potential of IMR32.ODC.CE cells to zero, while 50 microM CPT-11 was required to produce the same effect with IMR32.CMV.neo cells.	Irinotecan	123-129	ornithine decarboxylase 1	Homo sapiens	172-175
10738246-0	2000	Ectopic p16(ink4) expression enhances CPT-11-induced apoptosis through increased delay in S-phase progression in human non-small-cell-lung-cancer cells.	Irinotecan	38-44	cyclin dependent kinase inhibitor 2A	Homo sapiens	8-11
10738246-0	2000	Ectopic p16(ink4) expression enhances CPT-11-induced apoptosis through increased delay in S-phase progression in human non-small-cell-lung-cancer cells.	Irinotecan	38-44	cyclin dependent kinase inhibitor 2A	Homo sapiens	12-16
10738246-2	2000	We have found that ectopic p16(INK4) expression increased cellular sensitivity of human non-small-cell-lung-cancer (NSCLC) A549 cells to a selective growth-inhibitory effect induced by the topoisomerase-I inhibitor 11, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxy camptothecin (CPT-11) in vitro.	Irinotecan	288-294	cyclin dependent kinase inhibitor 2A	Homo sapiens	27-30
10738246-3	2000	In this study, we observed enhanced apoptosis characterized by DNA fragmentation in A549 cells transfected with p16(INK4) cDNA (A549/p16-1) and treated with CPT-11.	Irinotecan	157-163	cyclin dependent kinase inhibitor 2A	Homo sapiens	112-115
10738246-3	2000	In this study, we observed enhanced apoptosis characterized by DNA fragmentation in A549 cells transfected with p16(INK4) cDNA (A549/p16-1) and treated with CPT-11.	Irinotecan	157-163	cyclin dependent kinase inhibitor 2A	Homo sapiens	116-120
10738246-3	2000	In this study, we observed enhanced apoptosis characterized by DNA fragmentation in A549 cells transfected with p16(INK4) cDNA (A549/p16-1) and treated with CPT-11.	Irinotecan	157-163	cyclin dependent kinase inhibitor 2A	Homo sapiens	133-136
10738246-5	2000	In A549/p16-1 cells, cytosolic peptidase activities that cleaved Z-DEVD-7-amino-4-trifluoromethylcoumarin increased during CPT-11-induced apoptosis and were suppressed by a highly specific caspase-3 and caspase-3-like inhibitor, Z-DEVD-fluoromethylketone.	Irinotecan	123-129	cyclin dependent kinase inhibitor 2A	Homo sapiens	8-11
10738246-5	2000	In A549/p16-1 cells, cytosolic peptidase activities that cleaved Z-DEVD-7-amino-4-trifluoromethylcoumarin increased during CPT-11-induced apoptosis and were suppressed by a highly specific caspase-3 and caspase-3-like inhibitor, Z-DEVD-fluoromethylketone.	Irinotecan	123-129	caspase 3	Sus scrofa	189-198
10738246-5	2000	In A549/p16-1 cells, cytosolic peptidase activities that cleaved Z-DEVD-7-amino-4-trifluoromethylcoumarin increased during CPT-11-induced apoptosis and were suppressed by a highly specific caspase-3 and caspase-3-like inhibitor, Z-DEVD-fluoromethylketone.	Irinotecan	123-129	caspase 3	Homo sapiens	203-212
10738246-6	2000	These findings indicate that p16(INK) is positively involved in the activation pathway of the caspase-3 induced by CPT-11.	Irinotecan	115-121	cyclin dependent kinase inhibitor 2A	Homo sapiens	29-32
10738246-6	2000	These findings indicate that p16(INK) is positively involved in the activation pathway of the caspase-3 induced by CPT-11.	Irinotecan	115-121	caspase 3	Homo sapiens	94-103
10738246-7	2000	The increased delay in S-phase progression and subsequent induction of apoptosis were observed in CPT-11-treated A549/p16-1 cells on the basis of DNA histograms.	Irinotecan	98-104	cyclin dependent kinase inhibitor 2A	Homo sapiens	118-121
10738246-8	2000	Specific down-regulation of the cyclin-A protein level in A549/p16-1 cells was observed after CPT-11-treatment, whereas cyclin B, cdk2, and cdc2 protein levels were unaffected.	Irinotecan	94-100	proliferating cell nuclear antigen	Homo sapiens	32-38
10738246-9	2000	These results suggest that ectopic p16(INK4) expression inappropriately decreases cyclin A and thereby terminates CPT-11-induced G(2)/M accumulation, which is followed by increased apoptosis in p16(INK4)-expressing A549 cells.	Irinotecan	114-120	cyclin dependent kinase inhibitor 2A	Homo sapiens	35-38
10738246-9	2000	These results suggest that ectopic p16(INK4) expression inappropriately decreases cyclin A and thereby terminates CPT-11-induced G(2)/M accumulation, which is followed by increased apoptosis in p16(INK4)-expressing A549 cells.	Irinotecan	114-120	cyclin dependent kinase inhibitor 2A	Homo sapiens	39-43
10738246-9	2000	These results suggest that ectopic p16(INK4) expression inappropriately decreases cyclin A and thereby terminates CPT-11-induced G(2)/M accumulation, which is followed by increased apoptosis in p16(INK4)-expressing A549 cells.	Irinotecan	114-120	cyclin dependent kinase inhibitor 2A	Homo sapiens	198-202
10728672-4	2000	hCE-2 has a 12.5-fold higher affinity for CPT-11 and a 5-fold higher maximal rate of CPT-11 hydrolysis when compared with hCE-1.	Irinotecan	42-48	carboxylesterase 2	Homo sapiens	0-5
10728672-4	2000	hCE-2 has a 12.5-fold higher affinity for CPT-11 and a 5-fold higher maximal rate of CPT-11 hydrolysis when compared with hCE-1.	Irinotecan	85-91	carboxylesterase 2	Homo sapiens	0-5
10728672-5	2000	In cytotoxicity assays, incubation of 1 microM CPT-11 with hCE-2 (3.6 microg/ml) resulted in a 60% reduction in survival of SQ20b cells.	Irinotecan	47-53	carboxylesterase 2	Homo sapiens	59-64
10728672-6	2000	No significant reduction in cell survival was observed after incubation of CPT-11 with hCE-1.	Irinotecan	75-81	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	87-92
10728672-8	2000	hCE-2 likely plays a substantial role in CPT-11 activation in human liver at relevant pharmacological concentrations.	Irinotecan	41-47	carboxylesterase 2	Homo sapiens	0-5
10690558-5	2000	Compared to A253/Vec, A253/Bax cells exhibited 9.5- and 13.5-fold increases in sensitivity to raltitrexed and SN-38, respectively.	Irinotecan	110-115	BCL2 associated X, apoptosis regulator	Homo sapiens	27-30
10741701-0	2000	Pharmacokinetics of irinotecan and its metabolites SN-38 and APC in children with recurrent solid tumors after protracted low-dose irinotecan.	Irinotecan	20-30	APC regulator of WNT signaling pathway	Homo sapiens	61-64
10741701-0	2000	Pharmacokinetics of irinotecan and its metabolites SN-38 and APC in children with recurrent solid tumors after protracted low-dose irinotecan.	Irinotecan	131-141	APC regulator of WNT signaling pathway	Homo sapiens	61-64
10732766-0	2000	Sensitivity to CPT-11 of xenografted human colorectal cancers as a function of microsatellite instability and p53 status.	Irinotecan	15-21	tumor protein p53	Homo sapiens	110-113
10732766-16	2000	Taken together, these observations indicate that MSI and p53 alterations could be associated with different CPT-11 sensitivities; MSI phenotype moderately influences the CPT-11 sensitivity, MSI+ being more sensitive than MSI(-)CRC freshly obtained from patients, mutp53 status being associated with a poor response to CPT-11.	Irinotecan	108-114	RB binding protein 4, chromatin remodeling factor	Homo sapiens	49-52
10732766-16	2000	Taken together, these observations indicate that MSI and p53 alterations could be associated with different CPT-11 sensitivities; MSI phenotype moderately influences the CPT-11 sensitivity, MSI+ being more sensitive than MSI(-)CRC freshly obtained from patients, mutp53 status being associated with a poor response to CPT-11.	Irinotecan	108-114	tumor protein p53	Homo sapiens	57-60
10732766-16	2000	Taken together, these observations indicate that MSI and p53 alterations could be associated with different CPT-11 sensitivities; MSI phenotype moderately influences the CPT-11 sensitivity, MSI+ being more sensitive than MSI(-)CRC freshly obtained from patients, mutp53 status being associated with a poor response to CPT-11.	Irinotecan	170-176	RB binding protein 4, chromatin remodeling factor	Homo sapiens	130-133
10732766-16	2000	Taken together, these observations indicate that MSI and p53 alterations could be associated with different CPT-11 sensitivities; MSI phenotype moderately influences the CPT-11 sensitivity, MSI+ being more sensitive than MSI(-)CRC freshly obtained from patients, mutp53 status being associated with a poor response to CPT-11.	Irinotecan	170-176	RB binding protein 4, chromatin remodeling factor	Homo sapiens	130-133
10732766-16	2000	Taken together, these observations indicate that MSI and p53 alterations could be associated with different CPT-11 sensitivities; MSI phenotype moderately influences the CPT-11 sensitivity, MSI+ being more sensitive than MSI(-)CRC freshly obtained from patients, mutp53 status being associated with a poor response to CPT-11.	Irinotecan	170-176	RB binding protein 4, chromatin remodeling factor	Homo sapiens	130-133
10732775-4	2000	In this report, we demonstrated that apoptosis induced by 7-ethyl-10-hydroxycamptothecin, tumour necrosis factor-alpha (TNF-alpha) or interleukin (IL)-2-activated natural killer (NK) cells was significantly inhibited in tumour cells transduced with the SCC Ag-1 cDNA, as compared to control cells in vitro.	Irinotecan	58-88	serpin family B member 3	Homo sapiens	253-256
10770640-11	2000	These findings suggest that CPT-11 and 5-FU may thus be useful as possible anticancer agents for use in a combination therapy regimen using wt p53 gene transfer.	Irinotecan	28-34	tumor protein p53	Homo sapiens	143-146
10690558-12	2000	In contrast, both raltitrexed and irinotecan were significantly more active against A253/Bax xenografts than against A253/Vec xenografts; the yield for complete tumor regression (cure) was 40% and 100% with raltitrexed and irinotecan, respectively, with no significant toxicity.	Irinotecan	34-44	BCL2 associated X, apoptosis regulator	Homo sapiens	89-92
10646841-0	2000	Therapy of human pancreatic carcinoma implants by irinotecan and the oral immunomodulator JBT 3002 is associated with enhanced expression of inducible nitric oxide synthase in tumor-infiltrating macrophages.	Irinotecan	50-60	nitric oxide synthase 2	Homo sapiens	141-172
10639573-6	2000	Differing from MMC, MGMT was shown to participate in the resistance of Topo I inhibitors (CPT-11, SN-38 and DX-8951f), while GSTpi and MDR1 were involved in docetaxel (TXT) resistance.	Irinotecan	90-96	O-6-methylguanine-DNA methyltransferase	Homo sapiens	20-24
10639573-6	2000	Differing from MMC, MGMT was shown to participate in the resistance of Topo I inhibitors (CPT-11, SN-38 and DX-8951f), while GSTpi and MDR1 were involved in docetaxel (TXT) resistance.	Irinotecan	98-103	O-6-methylguanine-DNA methyltransferase	Homo sapiens	20-24
10646841-11	2000	injection of CPT-11 can decrease the growth of human pancreatic carcinoma and the incidence of metastasis in nude mice by both a direct antitumor effect and the activation of iNOS in infiltrating macrophages.	Irinotecan	13-19	nitric oxide synthase 2, inducible	Mus musculus	175-179
10854139-5	2000	Gemcitabine and to a lesser extent irinotecan inhibited the secretion of the proinflammatory cytokine IL-6 at concentrations of each drug that produced only small decreases in cell viability.	Irinotecan	35-45	interleukin 6	Homo sapiens	102-106
10803918-10	2000	The combined treatment of irradiation and SN-38 showed supraadditive effects in all four cell lines independent of their p53 status.	Irinotecan	42-47	transformation related protein 53, pseudogene	Mus musculus	121-124
10803925-1	2000	PURPOSE: To investigate the effects of several camptothecin analogs including 9-aminocamptothecin (9-AC), SN38, topotecan, and irinotecan (CPT-11) on the enzymes involved in the pyrimidine salvage pathway including thymidylate synthase (TS).	Irinotecan	139-145	thymidylate synthetase	Homo sapiens	215-235
10803925-1	2000	PURPOSE: To investigate the effects of several camptothecin analogs including 9-aminocamptothecin (9-AC), SN38, topotecan, and irinotecan (CPT-11) on the enzymes involved in the pyrimidine salvage pathway including thymidylate synthase (TS).	Irinotecan	139-145	thymidylate synthetase	Homo sapiens	237-239
10854139-7	2000	Higher doses of gemcitabine and irinotecan caused a surge in IL-6 release and this was not due to release of intracellular stores of IL-6 through lysis of the cells.	Irinotecan	32-42	interleukin 6	Homo sapiens	61-65
10854139-8	2000	CONCLUSIONS: These results suggest that irinotecan and gemcitabine are not only more likely to be active against mesothelioma than other new chemotherapy agents but may also produce a palliative effect in nonresponders to these agents by decreasing the secretion of IL-6.	Irinotecan	40-50	interleukin 6	Homo sapiens	266-270
10626806-0	1999	Tumor necrosis factor-related apoptosis-inducing ligand"s antitumor activity in vivo is enhanced by the chemotherapeutic agent CPT-11.	Irinotecan	127-133	TNF superfamily member 10	Homo sapiens	0-55
10626806-6	1999	Moreover, the combination of TRAIL and CPT-11, a water-soluble analogue of camptothecin, greatly enhanced the antitumor activity of TRAIL in vivo.	Irinotecan	39-45	TNF superfamily member 10	Homo sapiens	132-137
10626806-7	1999	TRAIL plus CPT-11 treatment of both 3- and 10-day established TRAIL-sensitive tumors resulted in both a significant inhibition of tumor growth and a high proportion of complete tumor regressions.	Irinotecan	11-17	TNF superfamily member 10	Homo sapiens	62-67
10626806-8	1999	Treatment of TRAIL-resistant tumors with TRAIL and CPT-11 dramatically slowed tumor growth and induced a transient tumor regression.	Irinotecan	51-57	TNF superfamily member 10	Homo sapiens	13-18
10626806-9	1999	These data demonstrate that TRAIL alone is a potent antitumor agent in vivo, and its activity can be significantly enhanced in combination with the chemotherapeutic agent CPT-11.	Irinotecan	171-177	TNF superfamily member 10	Homo sapiens	28-33
10570064-11	1999	Also, preliminary molecular modeling of the interaction between AChE and CPT-11 indicated that the latter does not bind at the same site as tacrine.	Irinotecan	73-79	acetylcholinesterase (Cartwright blood group)	Homo sapiens	64-68
10604724-0	1999	Schedule-dependent cytotoxicity of SN-38 in p53 wild-type and mutant colon adenocarcinoma cell lines.	Irinotecan	35-40	tumor protein p53	Homo sapiens	44-47
10604724-10	1999	Dose-dependent p53-associated G1 arrest, in the absence of DNA synthesis indicates an additional cytotoxic mechanism for SN-38, which requires higher concentrations than the S phase mechanism, and detection of which seems to involve p53.	Irinotecan	121-126	tumor protein p53	Homo sapiens	15-18
10604724-12	1999	Although expression of wild-type p53 leads to a more rapid induction of apoptosis, SN-38 cytotoxicity was generally greater in cells with mutant p53, as wild-type cells escaped apoptosis by p53 associated prolonged cell cycle arrest.	Irinotecan	83-88	tumor protein p53	Homo sapiens	145-148
10604724-12	1999	Although expression of wild-type p53 leads to a more rapid induction of apoptosis, SN-38 cytotoxicity was generally greater in cells with mutant p53, as wild-type cells escaped apoptosis by p53 associated prolonged cell cycle arrest.	Irinotecan	83-88	tumor protein p53	Homo sapiens	145-148
10570064-13	1999	The rapid reversibility of the inhibition of AChE by CPT-11 and the lower activity of the carboxylate form are likely reasons for the transient nature of the cholinergic toxicity observed clinically.	Irinotecan	53-59	acetylcholinesterase (Cartwright blood group)	Homo sapiens	45-49
10411544-10	1999	Apo2L cooperated synergistically with the chemotherapeutic drugs 5-fluorouracil or CPT-11, causing substantial tumor regression or complete tumor ablation.	Irinotecan	83-89	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	0-5
10569939-1	1999	Homocamptothecin (hCPT) contains a seven-membered beta-hydroxylactone in place of the conventional six-membered alpha-hydroxylactone ring found in camptothecin and its tumor active analogues, including topotecan and irinotecan.	Irinotecan	216-226	choline phosphotransferase 1	Homo sapiens	18-22
10493507-4	1999	Furthermore, BCRP/MXR/ABCP expression levels in various partially revertant T8 cells correlated with the levels of resistance to topotecan, SN-38, and mitoxantrone, strongly suggesting BCRP/MXR/ABCP to be the transporter responsible for the enhanced efflux.	Irinotecan	140-145	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	13-17
10493507-4	1999	Furthermore, BCRP/MXR/ABCP expression levels in various partially revertant T8 cells correlated with the levels of resistance to topotecan, SN-38, and mitoxantrone, strongly suggesting BCRP/MXR/ABCP to be the transporter responsible for the enhanced efflux.	Irinotecan	140-145	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	18-21
10493507-4	1999	Furthermore, BCRP/MXR/ABCP expression levels in various partially revertant T8 cells correlated with the levels of resistance to topotecan, SN-38, and mitoxantrone, strongly suggesting BCRP/MXR/ABCP to be the transporter responsible for the enhanced efflux.	Irinotecan	140-145	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	22-26
10493507-4	1999	Furthermore, BCRP/MXR/ABCP expression levels in various partially revertant T8 cells correlated with the levels of resistance to topotecan, SN-38, and mitoxantrone, strongly suggesting BCRP/MXR/ABCP to be the transporter responsible for the enhanced efflux.	Irinotecan	140-145	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	185-189
10493507-4	1999	Furthermore, BCRP/MXR/ABCP expression levels in various partially revertant T8 cells correlated with the levels of resistance to topotecan, SN-38, and mitoxantrone, strongly suggesting BCRP/MXR/ABCP to be the transporter responsible for the enhanced efflux.	Irinotecan	140-145	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	190-193
10493507-4	1999	Furthermore, BCRP/MXR/ABCP expression levels in various partially revertant T8 cells correlated with the levels of resistance to topotecan, SN-38, and mitoxantrone, strongly suggesting BCRP/MXR/ABCP to be the transporter responsible for the enhanced efflux.	Irinotecan	140-145	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	194-198
10416605-5	1999	The glycinate esters are also 20-40-fold less potent than CPT-11 in inhibiting human acetylcholinesterase.	Irinotecan	58-64	acetylcholinesterase (Cartwright blood group)	Homo sapiens	85-105
10606256-2	1999	The most extensively studied of these has been irinotecan (CPT-II).	Irinotecan	47-57	carnitine palmitoyltransferase 2	Homo sapiens	59-65
10695015-5	1999	Human cMOAT cDNA transfected LLC-PK1 cells, LLC/cMOAT-1, have increased resistance to vincristine (VCR), 7-ethyl-10-hydroxycamptothecin (SN-38), and cisplatin.	Irinotecan	105-135	ATP binding cassette subfamily C member 2	Homo sapiens	6-11
10695015-5	1999	Human cMOAT cDNA transfected LLC-PK1 cells, LLC/cMOAT-1, have increased resistance to vincristine (VCR), 7-ethyl-10-hydroxycamptothecin (SN-38), and cisplatin.	Irinotecan	137-142	ATP binding cassette subfamily C member 2	Homo sapiens	6-11
10695015-6	1999	The multidrug resistance (MDR)-reversing agents, cyclosporin A (CsA) and PAK-104P, almost completely reversed the resistance to VCR, SN-38 and cisplatin of LLC/cMOAT-1 cells by interacting with the substrate binding site of cMOAT.	Irinotecan	133-138	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	160-165
10473099-0	1999	Oral administration of the immunomodulator JBT-3002 induces endogenous interleukin 15 in intestinal macrophages for protection against irinotecan-mediated destruction of intestinal epithelium.	Irinotecan	135-145	interleukin 15	Mus musculus	71-85
10473099-10	1999	Immunohistochemical analyses of the intestines of mice treated with JBT-3002 and CPT-11 demonstrated an increase in the number of dividing cells in the crypts and enhanced expression of IL-15 in lamina propria cells; the increase correlated with increased expression of the IL-15 gene as determined by semiquantitative reverse transcriptase-PCR.	Irinotecan	81-87	interleukin 15	Mus musculus	186-191
10473099-10	1999	Immunohistochemical analyses of the intestines of mice treated with JBT-3002 and CPT-11 demonstrated an increase in the number of dividing cells in the crypts and enhanced expression of IL-15 in lamina propria cells; the increase correlated with increased expression of the IL-15 gene as determined by semiquantitative reverse transcriptase-PCR.	Irinotecan	81-87	interleukin 15	Mus musculus	274-279
10473099-12	1999	Moreover, the presence of IL-15 decreased irinotecan-mediated cytotoxicity of IEC-6 epithelial cells.	Irinotecan	42-52	interleukin 15	Rattus norvegicus	26-31
10473099-14	1999	administration of JBT-3002 induces expression of IL-15 by macrophages in the lamina propria, which can prevent irinotecan-induced injury to the intestinal mucosa.	Irinotecan	111-121	interleukin 15	Mus musculus	49-54
10381366-0	1999	Glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38) by the human UDP-glucuronosyltransferases encoded at the UGT1 locus.	Irinotecan	19-49	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-119
10381366-0	1999	Glucuronidation of 7-ethyl-10-hydroxycamptothecin (SN-38) by the human UDP-glucuronosyltransferases encoded at the UGT1 locus.	Irinotecan	51-56	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	115-119
10381366-3	1999	In this study, we examined the potential for each of the UGT1-encoded isoforms (UGT1A1 and UGT1A3 through UGT1A10) to glucuronidate SN-38.	Irinotecan	132-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	57-61
10381366-3	1999	In this study, we examined the potential for each of the UGT1-encoded isoforms (UGT1A1 and UGT1A3 through UGT1A10) to glucuronidate SN-38.	Irinotecan	132-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
10381366-3	1999	In this study, we examined the potential for each of the UGT1-encoded isoforms (UGT1A1 and UGT1A3 through UGT1A10) to glucuronidate SN-38.	Irinotecan	132-137	UDP glucuronosyltransferase family 1 member A3	Homo sapiens	91-97
10381366-3	1999	In this study, we examined the potential for each of the UGT1-encoded isoforms (UGT1A1 and UGT1A3 through UGT1A10) to glucuronidate SN-38.	Irinotecan	132-137	UDP glucuronosyltransferase family 1 member A10	Homo sapiens	106-113
10381366-8	1999	UGT1A7 glucuronidates SN-38 with an apparent Km of 5 microM.	Irinotecan	22-27	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	0-6
10340924-0	1999	Phenotype-genotype correlation of in vitro SN-38 (active metabolite of irinotecan) and bilirubin glucuronidation in human liver tissue with UGT1A1 promoter polymorphism.	Irinotecan	43-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
10340924-0	1999	Phenotype-genotype correlation of in vitro SN-38 (active metabolite of irinotecan) and bilirubin glucuronidation in human liver tissue with UGT1A1 promoter polymorphism.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-146
10340924-1	1999	BACKGROUND: Hepatic uridine diphosphate glucuronosyltransferase (UGT) isoform 1A1 (UGT1A1) is primarily responsible for the glucuronidation of SN-38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of the anticancer agent irinotecan.	Irinotecan	143-148	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
10340924-1	1999	BACKGROUND: Hepatic uridine diphosphate glucuronosyltransferase (UGT) isoform 1A1 (UGT1A1) is primarily responsible for the glucuronidation of SN-38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of the anticancer agent irinotecan.	Irinotecan	150-180	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
10340924-1	1999	BACKGROUND: Hepatic uridine diphosphate glucuronosyltransferase (UGT) isoform 1A1 (UGT1A1) is primarily responsible for the glucuronidation of SN-38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of the anticancer agent irinotecan.	Irinotecan	229-239	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
10220571-0	1999	ATP-Dependent efflux of CPT-11 and SN-38 by the multidrug resistance protein (MRP) and its inhibition by PAK-104P.	Irinotecan	24-30	ATP binding cassette subfamily C member 1	Homo sapiens	48-76
10410150-1	1999	Two phase I studies (CIC-therapy) were conducted in advanced non-small cell lung cancer (NSCLC) to determine the maximum tolerable dose (MTD) of CPT-11 combined with cisplatin and ifosfamide, and MTD of cisplatin combined with CPT-11 and ifosfamide with G-CSF support, respectively.	Irinotecan	145-151	colony stimulating factor 3	Homo sapiens	254-259
10220571-0	1999	ATP-Dependent efflux of CPT-11 and SN-38 by the multidrug resistance protein (MRP) and its inhibition by PAK-104P.	Irinotecan	24-30	ATP binding cassette subfamily C member 1	Homo sapiens	78-81
10220571-0	1999	ATP-Dependent efflux of CPT-11 and SN-38 by the multidrug resistance protein (MRP) and its inhibition by PAK-104P.	Irinotecan	35-40	ATP binding cassette subfamily C member 1	Homo sapiens	48-76
10220571-0	1999	ATP-Dependent efflux of CPT-11 and SN-38 by the multidrug resistance protein (MRP) and its inhibition by PAK-104P.	Irinotecan	35-40	ATP binding cassette subfamily C member 1	Homo sapiens	78-81
10220571-3	1999	To see whether MRP is involved in CPT-11 and SN-38 resistance, MRP cDNA was transfected into KB-3-1 cells.	Irinotecan	45-50	ATP binding cassette subfamily C member 1	Homo sapiens	15-18
10220571-4	1999	The transfectant, KB/MRP, which overexpressed MRP, was resistant to both CPT-11 and SN-38.	Irinotecan	73-79	ATP binding cassette subfamily C member 1	Homo sapiens	21-24
10220571-4	1999	The transfectant, KB/MRP, which overexpressed MRP, was resistant to both CPT-11 and SN-38.	Irinotecan	73-79	ATP binding cassette subfamily C member 1	Homo sapiens	46-49
10220571-4	1999	The transfectant, KB/MRP, which overexpressed MRP, was resistant to both CPT-11 and SN-38.	Irinotecan	84-89	ATP binding cassette subfamily C member 1	Homo sapiens	21-24
10220571-4	1999	The transfectant, KB/MRP, which overexpressed MRP, was resistant to both CPT-11 and SN-38.	Irinotecan	84-89	ATP binding cassette subfamily C member 1	Homo sapiens	46-49
10220571-6	1999	The accumulation of both CPT-11 and SN-38 in C-A120 and KB/MRP cells was lower than that in KB-3-1 cells.	Irinotecan	25-31	ATP binding cassette subfamily C member 1	Homo sapiens	59-62
10220571-6	1999	The accumulation of both CPT-11 and SN-38 in C-A120 and KB/MRP cells was lower than that in KB-3-1 cells.	Irinotecan	36-41	ATP binding cassette subfamily C member 1	Homo sapiens	59-62
10220571-7	1999	The treatment with 10 microM PAK-104P increased the accumulation of CPT-11 and SN-38 in C-A120 and KB/MRP cells to a level similar to that found in KB-3-1 cells.	Irinotecan	68-74	ATP binding cassette subfamily C member 1	Homo sapiens	102-105
10220571-7	1999	The treatment with 10 microM PAK-104P increased the accumulation of CPT-11 and SN-38 in C-A120 and KB/MRP cells to a level similar to that found in KB-3-1 cells.	Irinotecan	79-84	ATP binding cassette subfamily C member 1	Homo sapiens	102-105
10220571-8	1999	The ATP-dependent efflux of CPT-11 and SN-38 from C-A120 and KB/MRP cells was inhibited by PAK-104P.	Irinotecan	28-34	ATP binding cassette subfamily C member 1	Homo sapiens	64-67
10220571-8	1999	The ATP-dependent efflux of CPT-11 and SN-38 from C-A120 and KB/MRP cells was inhibited by PAK-104P.	Irinotecan	39-44	ATP binding cassette subfamily C member 1	Homo sapiens	64-67
10220571-11	1999	These findings suggest that MRP transports CPT-11 and SN-38 and is involved in resistance to CPT-11 and SN-38 and that PAK-104P reverses the resistance to CPT-11 and SN-38 in tumors that overexpress MRP.	Irinotecan	43-49	ATP binding cassette subfamily C member 1	Homo sapiens	28-31
10220571-11	1999	These findings suggest that MRP transports CPT-11 and SN-38 and is involved in resistance to CPT-11 and SN-38 and that PAK-104P reverses the resistance to CPT-11 and SN-38 in tumors that overexpress MRP.	Irinotecan	43-49	ATP binding cassette subfamily C member 1	Homo sapiens	199-202
10220571-11	1999	These findings suggest that MRP transports CPT-11 and SN-38 and is involved in resistance to CPT-11 and SN-38 and that PAK-104P reverses the resistance to CPT-11 and SN-38 in tumors that overexpress MRP.	Irinotecan	54-59	ATP binding cassette subfamily C member 1	Homo sapiens	28-31
10220571-11	1999	These findings suggest that MRP transports CPT-11 and SN-38 and is involved in resistance to CPT-11 and SN-38 and that PAK-104P reverses the resistance to CPT-11 and SN-38 in tumors that overexpress MRP.	Irinotecan	54-59	ATP binding cassette subfamily C member 1	Homo sapiens	199-202
10220571-11	1999	These findings suggest that MRP transports CPT-11 and SN-38 and is involved in resistance to CPT-11 and SN-38 and that PAK-104P reverses the resistance to CPT-11 and SN-38 in tumors that overexpress MRP.	Irinotecan	93-99	ATP binding cassette subfamily C member 1	Homo sapiens	28-31
10220571-11	1999	These findings suggest that MRP transports CPT-11 and SN-38 and is involved in resistance to CPT-11 and SN-38 and that PAK-104P reverses the resistance to CPT-11 and SN-38 in tumors that overexpress MRP.	Irinotecan	104-109	ATP binding cassette subfamily C member 1	Homo sapiens	28-31
10220571-11	1999	These findings suggest that MRP transports CPT-11 and SN-38 and is involved in resistance to CPT-11 and SN-38 and that PAK-104P reverses the resistance to CPT-11 and SN-38 in tumors that overexpress MRP.	Irinotecan	93-99	ATP binding cassette subfamily C member 1	Homo sapiens	28-31
10220571-11	1999	These findings suggest that MRP transports CPT-11 and SN-38 and is involved in resistance to CPT-11 and SN-38 and that PAK-104P reverses the resistance to CPT-11 and SN-38 in tumors that overexpress MRP.	Irinotecan	104-109	ATP binding cassette subfamily C member 1	Homo sapiens	28-31
10197614-0	1999	The anticancer prodrug CPT-11 is a potent inhibitor of acetylcholinesterase but is rapidly catalyzed to SN-38 by butyrylcholinesterase.	Irinotecan	23-29	acetylcholinesterase (Cartwright blood group)	Homo sapiens	55-75
10378768-13	1999	These findings suggested that an unknown transporter distinct from P-gp, MRP or cMOAT is expressed in KCP-4 cells and transports CPT-11 and SN-38.	Irinotecan	129-135	ATP binding cassette subfamily B member 1	Homo sapiens	67-71
10378768-13	1999	These findings suggested that an unknown transporter distinct from P-gp, MRP or cMOAT is expressed in KCP-4 cells and transports CPT-11 and SN-38.	Irinotecan	129-135	ATP binding cassette subfamily C member 1	Homo sapiens	73-76
10378768-13	1999	These findings suggested that an unknown transporter distinct from P-gp, MRP or cMOAT is expressed in KCP-4 cells and transports CPT-11 and SN-38.	Irinotecan	129-135	ATP binding cassette subfamily C member 2	Homo sapiens	80-85
10378768-13	1999	These findings suggested that an unknown transporter distinct from P-gp, MRP or cMOAT is expressed in KCP-4 cells and transports CPT-11 and SN-38.	Irinotecan	140-145	ATP binding cassette subfamily B member 1	Homo sapiens	67-71
10378768-13	1999	These findings suggested that an unknown transporter distinct from P-gp, MRP or cMOAT is expressed in KCP-4 cells and transports CPT-11 and SN-38.	Irinotecan	140-145	ATP binding cassette subfamily C member 1	Homo sapiens	73-76
10378768-13	1999	These findings suggested that an unknown transporter distinct from P-gp, MRP or cMOAT is expressed in KCP-4 cells and transports CPT-11 and SN-38.	Irinotecan	140-145	ATP binding cassette subfamily C member 2	Homo sapiens	80-85
10197614-2	1999	Although CPT-11 was not a substrate for acetylcholinesterase (AcChE), in vitro assays confirmed that CPT-11 inhibited both human and electric eel AcChE with apparent K(i)s of 415 and 194 nM, respectively.	Irinotecan	101-107	acetylcholinesterase (Cartwright blood group)	Homo sapiens	146-151
10197614-3	1999	In contrast, human or equine butyryl-cholinesterase (BuChE) converted CPT-11 to SN-38 with K(m)s of 42.4 and 44.2 microM for the human and horse BuChE, respectively.	Irinotecan	70-76	butyrylcholinesterase	Equus caballus	29-51
10197614-3	1999	In contrast, human or equine butyryl-cholinesterase (BuChE) converted CPT-11 to SN-38 with K(m)s of 42.4 and 44.2 microM for the human and horse BuChE, respectively.	Irinotecan	70-76	butyrylcholinesterase	Equus caballus	53-58
10197614-3	1999	In contrast, human or equine butyryl-cholinesterase (BuChE) converted CPT-11 to SN-38 with K(m)s of 42.4 and 44.2 microM for the human and horse BuChE, respectively.	Irinotecan	70-76	butyrylcholinesterase	Equus caballus	145-150
10197614-3	1999	In contrast, human or equine butyryl-cholinesterase (BuChE) converted CPT-11 to SN-38 with K(m)s of 42.4 and 44.2 microM for the human and horse BuChE, respectively.	Irinotecan	80-85	butyrylcholinesterase	Equus caballus	29-51
10197614-3	1999	In contrast, human or equine butyryl-cholinesterase (BuChE) converted CPT-11 to SN-38 with K(m)s of 42.4 and 44.2 microM for the human and horse BuChE, respectively.	Irinotecan	80-85	butyrylcholinesterase	Equus caballus	53-58
10101137-0	1999	Possible involvement of P-glycoprotein in biliary excretion of CPT-11 in rats.	Irinotecan	63-69	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	24-38
10197614-3	1999	In contrast, human or equine butyryl-cholinesterase (BuChE) converted CPT-11 to SN-38 with K(m)s of 42.4 and 44.2 microM for the human and horse BuChE, respectively.	Irinotecan	80-85	butyrylcholinesterase	Equus caballus	145-150
10101137-1	1999	In our previous work, we found that the biliary excretion of the carboxylate form of irinotecan, CPT-11, on rat bile canalicular membrane consists of two components, the low-affinity one being canalicular multispecific organic anion transporter (cMOAT).	Irinotecan	85-95	ATP binding cassette subfamily C member 2	Rattus norvegicus	193-244
10101137-1	1999	In our previous work, we found that the biliary excretion of the carboxylate form of irinotecan, CPT-11, on rat bile canalicular membrane consists of two components, the low-affinity one being canalicular multispecific organic anion transporter (cMOAT).	Irinotecan	85-95	ATP binding cassette subfamily C member 2	Rattus norvegicus	246-251
10101137-1	1999	In our previous work, we found that the biliary excretion of the carboxylate form of irinotecan, CPT-11, on rat bile canalicular membrane consists of two components, the low-affinity one being canalicular multispecific organic anion transporter (cMOAT).	Irinotecan	97-103	ATP binding cassette subfamily C member 2	Rattus norvegicus	193-244
10197614-4	1999	Modeling of CPT-11 within the predicted active site of AcChE and BuChE corroborated experimental results indicating that, although the drug was oriented correctly for activation, the constraints dictated by the active site gorge were such that CPT-11 would be unlikely to be activated by AcChE.	Irinotecan	12-18	acetylcholinesterase (Cartwright blood group)	Homo sapiens	55-60
10101137-1	1999	In our previous work, we found that the biliary excretion of the carboxylate form of irinotecan, CPT-11, on rat bile canalicular membrane consists of two components, the low-affinity one being canalicular multispecific organic anion transporter (cMOAT).	Irinotecan	97-103	ATP binding cassette subfamily C member 2	Rattus norvegicus	246-251
10197614-4	1999	Modeling of CPT-11 within the predicted active site of AcChE and BuChE corroborated experimental results indicating that, although the drug was oriented correctly for activation, the constraints dictated by the active site gorge were such that CPT-11 would be unlikely to be activated by AcChE.	Irinotecan	12-18	acetylcholinesterase (Cartwright blood group)	Homo sapiens	288-293
10101137-3	1999	The ATP-dependent uptake of the carboxylate form of CPT-11 was inhibited significantly by several substrates and/or modulators of P-glycoprotein, including PSC-833, verapamil, and cyclosporin A, at a substrate concentration of 5 microM, at which the high-affinity component is involved predominantly in CPT-11 transport.	Irinotecan	52-58	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	130-144
10101137-3	1999	The ATP-dependent uptake of the carboxylate form of CPT-11 was inhibited significantly by several substrates and/or modulators of P-glycoprotein, including PSC-833, verapamil, and cyclosporin A, at a substrate concentration of 5 microM, at which the high-affinity component is involved predominantly in CPT-11 transport.	Irinotecan	303-309	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	130-144
10197614-4	1999	Modeling of CPT-11 within the predicted active site of AcChE and BuChE corroborated experimental results indicating that, although the drug was oriented correctly for activation, the constraints dictated by the active site gorge were such that CPT-11 would be unlikely to be activated by AcChE.	Irinotecan	244-250	acetylcholinesterase (Cartwright blood group)	Homo sapiens	55-60
10101137-4	1999	When the concentration of the carboxylate form of CPT-11 was 250 microM, at which the low-affinity component (cMOAT) is involved predominantly in its transport, the inhibitory effect of the above compounds was reduced greatly.	Irinotecan	50-56	ATP binding cassette subfamily C member 2	Rattus norvegicus	110-115
10101137-7	1999	These results suggest that P-glycoprotein may act as the high-affinity component in the biliary excretion of the carboxylate form of CPT-11 in rats.	Irinotecan	133-139	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	27-41
10197614-4	1999	Modeling of CPT-11 within the predicted active site of AcChE and BuChE corroborated experimental results indicating that, although the drug was oriented correctly for activation, the constraints dictated by the active site gorge were such that CPT-11 would be unlikely to be activated by AcChE.	Irinotecan	244-250	butyrylcholinesterase	Equus caballus	65-70
10197614-4	1999	Modeling of CPT-11 within the predicted active site of AcChE and BuChE corroborated experimental results indicating that, although the drug was oriented correctly for activation, the constraints dictated by the active site gorge were such that CPT-11 would be unlikely to be activated by AcChE.	Irinotecan	244-250	acetylcholinesterase (Cartwright blood group)	Homo sapiens	288-293
10100720-5	1999	Results from experiments performed on colon cancer xenografts also show an association between PARP cleavage and response to treatment with TPT or CPT-11.	Irinotecan	147-153	poly(ADP-ribose) polymerase 1	Homo sapiens	95-99
10202930-5	1999	We show here that inhibition of NF-kappaB through the adenoviral delivery of a modified form of IkappaBalpha, the inhibitor of NF-kappaB, sensitizes chemoresistant tumors to the apoptotic potential of TNFalpha and of the chemotherapeutic compound CPT-11, resulting in tumor regression.	Irinotecan	247-253	nuclear factor kappa B subunit 1	Homo sapiens	32-41
10202930-5	1999	We show here that inhibition of NF-kappaB through the adenoviral delivery of a modified form of IkappaBalpha, the inhibitor of NF-kappaB, sensitizes chemoresistant tumors to the apoptotic potential of TNFalpha and of the chemotherapeutic compound CPT-11, resulting in tumor regression.	Irinotecan	247-253	NFKB inhibitor alpha	Homo sapiens	96-108
10202930-5	1999	We show here that inhibition of NF-kappaB through the adenoviral delivery of a modified form of IkappaBalpha, the inhibitor of NF-kappaB, sensitizes chemoresistant tumors to the apoptotic potential of TNFalpha and of the chemotherapeutic compound CPT-11, resulting in tumor regression.	Irinotecan	247-253	nuclear factor kappa B subunit 1	Homo sapiens	127-136
10202930-5	1999	We show here that inhibition of NF-kappaB through the adenoviral delivery of a modified form of IkappaBalpha, the inhibitor of NF-kappaB, sensitizes chemoresistant tumors to the apoptotic potential of TNFalpha and of the chemotherapeutic compound CPT-11, resulting in tumor regression.	Irinotecan	247-253	tumor necrosis factor	Homo sapiens	201-209
9918583-7	1999	These results suggest that MRP and P-gp are involved in the active efflux of SN-38 and CPT-11, respectively, from human KB-derived cells.	Irinotecan	77-82	ATP binding cassette subfamily C member 3	Homo sapiens	27-30
9918583-7	1999	These results suggest that MRP and P-gp are involved in the active efflux of SN-38 and CPT-11, respectively, from human KB-derived cells.	Irinotecan	77-82	ATP binding cassette subfamily B member 1	Homo sapiens	35-39
9918583-7	1999	These results suggest that MRP and P-gp are involved in the active efflux of SN-38 and CPT-11, respectively, from human KB-derived cells.	Irinotecan	87-93	ATP binding cassette subfamily C member 3	Homo sapiens	27-30
9918583-7	1999	These results suggest that MRP and P-gp are involved in the active efflux of SN-38 and CPT-11, respectively, from human KB-derived cells.	Irinotecan	87-93	ATP binding cassette subfamily B member 1	Homo sapiens	35-39
10500811-6	1999	Moreover CPT and SN-38 induced a strong decrease of mdr1 mRNA in MDR treated cells.	Irinotecan	17-22	ATP binding cassette subfamily B member 1	Homo sapiens	52-56
10321506-0	1999	A phase II study of irinotecan and infusional cisplatin with recombinant human granulocyte colony-stimulating factor support for advanced non-small-cell lung cancer.	Irinotecan	20-30	colony stimulating factor 3	Homo sapiens	79-116
9786315-1	1998	In six published phase II trials, irinotecan (CPT-II; Camptosar; Pharmacia &amp; Upjohn Co, Kalamazoo, MI) has demonstrated consistent activity with response rates of approximately 13% to 27% in patients with advanced colorectal cancer (CRC) refractory to 5-fluorouracil (5-FU) therapy.	Irinotecan	34-44	carnitine palmitoyltransferase 2	Homo sapiens	46-52
9865925-0	1998	Conversion of the CPT-11 metabolite APC to SN-38 by rabbit liver carboxylesterase.	Irinotecan	18-24	liver carboxylesterase 1	Oryctolagus cuniculus	59-81
9865925-0	1998	Conversion of the CPT-11 metabolite APC to SN-38 by rabbit liver carboxylesterase.	Irinotecan	43-48	liver carboxylesterase 1	Oryctolagus cuniculus	59-81
9865925-2	1998	We report here the conversion of APC (7-ethyl-[4-N-(5-aminopentanoic acid)-1-piperidino] carbonyloxycamptothecin), an inactive metabolite of CPT-11, to SN-38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of CPT-11, by a rabbit liver carboxylesterase.	Irinotecan	152-157	liver carboxylesterase 1	Oryctolagus cuniculus	237-259
9766655-5	1998	These E2F-1 transfectants, although resistant to fluoropyrimidines and serum deprivation, were more sensitive to etoposide, doxorubicin, and SN38 (the active metabolite of irinotecan) but not to Taxol.	Irinotecan	141-145	E2F transcription factor 1	Homo sapiens	6-11
9766655-5	1998	These E2F-1 transfectants, although resistant to fluoropyrimidines and serum deprivation, were more sensitive to etoposide, doxorubicin, and SN38 (the active metabolite of irinotecan) but not to Taxol.	Irinotecan	172-182	E2F transcription factor 1	Homo sapiens	6-11
10489165-3	1999	A253/Bax cells exhibited a significant increase in in vitro sensitivity to various anticancer drugs, including tomudex (9.5-fold), SN-38 (13.8-fold), doxorubicin (7.9-fold), taxol (3.1-fold), 5-FU (2.7-fold), and 5-FU/LV (4.5-fold).	Irinotecan	131-136	BCL2 associated X, apoptosis regulator	Homo sapiens	5-8
9781601-6	1998	Characteristics of patient subgroups were not different, however, the median survival of patients with elevated c-fos expression from the time of treatment with CPT-11 was 436 days, whereas patients with no detectable c-fos expression had a median survival of 365 days (p = 0.045).	Irinotecan	161-167	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	112-117
9786315-1	1998	In six published phase II trials, irinotecan (CPT-II; Camptosar; Pharmacia &amp; Upjohn Co, Kalamazoo, MI) has demonstrated consistent activity with response rates of approximately 13% to 27% in patients with advanced colorectal cancer (CRC) refractory to 5-fluorouracil (5-FU) therapy.	Irinotecan	54-63	carnitine palmitoyltransferase 2	Homo sapiens	46-52
9615866-12	1998	Irinotecan undergoes a complex in vivo biotransformation involving several enzyme systems, such as carboxylesterase, UDPGT and cytochrome P450, in children as well as in adults.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	117-122
9699654-0	1998	Interleukin 15 offers selective protection from irinotecan-induced intestinal toxicity in a preclinical animal model.	Irinotecan	48-58	interleukin 15	Rattus norvegicus	0-14
9699654-3	1998	A rat model with dose-limiting toxicity profiles that are similar to those observed in patients treated with CPT-11 was developed and used to evaluate the role of interleukin 15 (IL-15) in the modulation of the therapeutic selectivity of CPT-11 in normal rats and rats bearing advanced colorectal cancer.	Irinotecan	238-244	interleukin 15	Homo sapiens	163-177
9699654-3	1998	A rat model with dose-limiting toxicity profiles that are similar to those observed in patients treated with CPT-11 was developed and used to evaluate the role of interleukin 15 (IL-15) in the modulation of the therapeutic selectivity of CPT-11 in normal rats and rats bearing advanced colorectal cancer.	Irinotecan	238-244	interleukin 15	Homo sapiens	179-184
9699654-9	1998	IL-15 offered complete and sustained selective protection against CPT-11-induced delayed diarrhea and lethality.	Irinotecan	66-72	interleukin 15	Rattus norvegicus	0-5
9699654-13	1998	The results clearly demonstrated the ability of IL-15 to provide significant protection from CPT-11-induced intestinal toxicity with maintenance of antitumor activity, resulting in an increase in the therapeutic index of CPT-11.	Irinotecan	93-99	interleukin 15	Rattus norvegicus	48-53
9699654-13	1998	The results clearly demonstrated the ability of IL-15 to provide significant protection from CPT-11-induced intestinal toxicity with maintenance of antitumor activity, resulting in an increase in the therapeutic index of CPT-11.	Irinotecan	221-227	interleukin 15	Rattus norvegicus	48-53
9726087-7	1998	In this model, CPT-11 at a dose 50 mg/kg, daily x5 (MTD) achieved 100% complete tumor regression.	Irinotecan	15-21	metallothionein 1E	Homo sapiens	52-55
9726089-9	1998	SN-38 is eliminated mainly through conjugation by hepatic uridine glucuronosyltransferase (UGT*1.1), the same isoezyme responsible for glucuronidation of bilirubin.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-98
9726089-10	1998	Grade 4 irinotecan-related toxicity (ie, neutropenia, diarrhea) has recently been reported in two patients with deficient UGT*1.1 activity.	Irinotecan	8-18	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	122-129
9726089-12	1998	Deconjugation of SN-38G to SN-38 by beta-glucuronidase produced by the intestinal flora may contribute to enterohepatic recirculation of SN-38 and delayed intestinal toxicity.	Irinotecan	17-22	glucuronidase beta	Homo sapiens	36-54
9726089-12	1998	Deconjugation of SN-38G to SN-38 by beta-glucuronidase produced by the intestinal flora may contribute to enterohepatic recirculation of SN-38 and delayed intestinal toxicity.	Irinotecan	27-32	glucuronidase beta	Homo sapiens	36-54
9726089-12	1998	Deconjugation of SN-38G to SN-38 by beta-glucuronidase produced by the intestinal flora may contribute to enterohepatic recirculation of SN-38 and delayed intestinal toxicity.	Irinotecan	27-32	glucuronidase beta	Homo sapiens	36-54
9726096-3	1998	A cholinergic syndrome resulting from the inhibition of acetylcholinesterase activity by irinotecan is frequently seen within the first 24 hours after irinotecan administration but is easily controlled with atropine.	Irinotecan	89-99	acetylcholinesterase (Cartwright blood group)	Homo sapiens	56-76
9726096-3	1998	A cholinergic syndrome resulting from the inhibition of acetylcholinesterase activity by irinotecan is frequently seen within the first 24 hours after irinotecan administration but is easily controlled with atropine.	Irinotecan	151-161	acetylcholinesterase (Cartwright blood group)	Homo sapiens	56-76
9635592-0	1998	Isolation and partial characterization of a cDNA encoding a rabbit liver carboxylesterase that activates the prodrug irinotecan (CPT-11).	Irinotecan	117-127	liver carboxylesterase 1	Oryctolagus cuniculus	67-89
9635592-0	1998	Isolation and partial characterization of a cDNA encoding a rabbit liver carboxylesterase that activates the prodrug irinotecan (CPT-11).	Irinotecan	129-135	liver carboxylesterase 1	Oryctolagus cuniculus	67-89
9619871-6	1998	These results suggest that upregulation of bcl-2 in 4-pp-R cells is related to the resistance to CPT-11 as well as to A23187 or dexamethasone.	Irinotecan	97-103	BCL2 apoptosis regulator	Homo sapiens	43-48
9506540-3	1998	When p53 was expressed at sublethal levels, it sensitized cells to the DNA-damaging drugs Adriamycin, mitomycin C, actinomycin D, etoposide (VP16), cisplatin and CPT11.	Irinotecan	162-167	tumor protein p53	Homo sapiens	5-8
9515577-8	1998	When cells were first incubated with CPT-11, the decrease in thymidylate synthase (TS) activity was identical to that obtained after 5FU exposure (1.09 to 0.023 pmol/min/mg protein), but this decrease persisted for 24 hr (0.014 pmol/min/mg protein) (p = 0.035).	Irinotecan	37-43	thymidylate synthetase	Homo sapiens	61-81
9743293-8	1998	Thus, although p53-dependent apoptosis is induced by camptothecin, topotecan and SN-38 in this human ovarian carcinoma cell line, these drugs induce p53-independent death, as measured by clonogenic assay.	Irinotecan	81-86	tumor protein p53	Homo sapiens	15-18
9748119-1	1998	The induction of severe diarrhea limits the usefulness of the DNA topoisomerase I inhibitor irinotecan (CPT-11) in the treatment of advanced colon cancer.	Irinotecan	92-102	topoisomerase (DNA) I	Mus musculus	62-81
9748119-1	1998	The induction of severe diarrhea limits the usefulness of the DNA topoisomerase I inhibitor irinotecan (CPT-11) in the treatment of advanced colon cancer.	Irinotecan	104-110	topoisomerase (DNA) I	Mus musculus	62-81
9789606-0	1998	UGT1A1 genotypes and glucuronidation of SN-38, the active metabolite of irinotecan.	Irinotecan	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
9789606-1	1998	BACKGROUND: Irinotecan (CPT-11) is metabolized by esterase to form a SN-38, which is further conjugated by UGT1A1.	Irinotecan	12-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
9789606-1	1998	BACKGROUND: Irinotecan (CPT-11) is metabolized by esterase to form a SN-38, which is further conjugated by UGT1A1.	Irinotecan	24-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
9789606-1	1998	BACKGROUND: Irinotecan (CPT-11) is metabolized by esterase to form a SN-38, which is further conjugated by UGT1A1.	Irinotecan	69-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
9789606-3	1998	We investigated whether there might be an inter-individual difference in pharmacokinetics of SN-38 and its glucuronide, depending on the genotypes of UGT1A1.	Irinotecan	93-98	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	150-156
9569026-9	1998	Bax-K562 cells showed significantly higher fractions of apoptotic cells than pCI-neo-K562 cells when treated with ara-C, doxorubicin or SN-38.	Irinotecan	136-141	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
9472629-0	1998	CPT-11 sensitivity in relation to the expression of P170-glycoprotein and multidrug resistance-associated protein.	Irinotecan	0-6	phosphoglycolate phosphatase	Homo sapiens	52-69
9466980-5	1998	The purpose of this study was to identify the specific isoform of UGT involved in SN-38 glucuronidation.	Irinotecan	82-87	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	66-69
9466980-8	1998	Gunn rats and CN-I patients lacked SN-38 glucuronidating activity, indicating the role of UGT1 isoform in SN-38 glucuronidation.	Irinotecan	106-111	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-94
9466980-10	1998	Intact SN-38 glucuronidation was observed only in HK293 cells transfected with the UGT1A1 isozyme.	Irinotecan	7-12	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	83-89
9466980-11	1998	These results demonstrate that UGT1A1 is the isoform responsible for SN-38 glucuronidation.	Irinotecan	69-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
9466980-12	1998	These findings indicate a genetic predisposition to the metabolism of irinotecan, suggesting that patients with low UGT1A1 activity, such as those with Gilbert"s syndrome, may be at an increased risk for irinotecan toxicity.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-122
9466980-12	1998	These findings indicate a genetic predisposition to the metabolism of irinotecan, suggesting that patients with low UGT1A1 activity, such as those with Gilbert"s syndrome, may be at an increased risk for irinotecan toxicity.	Irinotecan	204-214	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	116-122
9533544-7	1998	In addition, we evaluated the effect of a sensitive (HC1) and resistant (ELC2) human colon adenocarcinoma xenograft on irinotecan and SN-38 lactone disposition after administration of irinotecan 10 mg/kg i.v.	Irinotecan	119-129	CYCS pseudogene 39	Homo sapiens	53-56
9533544-7	1998	In addition, we evaluated the effect of a sensitive (HC1) and resistant (ELC2) human colon adenocarcinoma xenograft on irinotecan and SN-38 lactone disposition after administration of irinotecan 10 mg/kg i.v.	Irinotecan	119-129	elaC ribonuclease Z 2	Homo sapiens	73-77
9533544-15	1998	administration, mice bearing HC1 xenografts had 43% greater SN-38 lactone systemic exposure compared to those with ELC2 xenografts and non-tumor-bearing mice.	Irinotecan	60-73	heterochromatin, Chr 1	Mus musculus	29-32
9533544-18	1998	SN-38 systemic exposure associated with the lowest oral dose (25 mg/kg) achieving complete response for HC1 was 942.6 ng/ml x h. These results emphasize the importance of pharmacokinetic studies as part of tumor response studies in xenograft models.	Irinotecan	0-5	CYCS pseudogene 39	Homo sapiens	104-107
9472629-0	1998	CPT-11 sensitivity in relation to the expression of P170-glycoprotein and multidrug resistance-associated protein.	Irinotecan	0-6	ATP binding cassette subfamily C member 3	Homo sapiens	74-113
9472629-1	1998	The relevance of P170-glycoprotein (P-gp) and multidrug resistance-associated protein (MRP) for the sensitivity to CPT-11 was investigated in human malignant cell lines as well as in human tumour xenografts.	Irinotecan	115-121	phosphoglycolate phosphatase	Homo sapiens	17-34
9472629-1	1998	The relevance of P170-glycoprotein (P-gp) and multidrug resistance-associated protein (MRP) for the sensitivity to CPT-11 was investigated in human malignant cell lines as well as in human tumour xenografts.	Irinotecan	115-121	phosphoglycolate phosphatase	Homo sapiens	36-40
9472629-1	1998	The relevance of P170-glycoprotein (P-gp) and multidrug resistance-associated protein (MRP) for the sensitivity to CPT-11 was investigated in human malignant cell lines as well as in human tumour xenografts.	Irinotecan	115-121	ATP binding cassette subfamily C member 3	Homo sapiens	46-85
9472629-1	1998	The relevance of P170-glycoprotein (P-gp) and multidrug resistance-associated protein (MRP) for the sensitivity to CPT-11 was investigated in human malignant cell lines as well as in human tumour xenografts.	Irinotecan	115-121	ATP binding cassette subfamily C member 3	Homo sapiens	87-90
9472629-4	1998	The P-gp modulators BIBW22BS, verapamil and dexniguldipine partly reversed the resistance against CPT-11 in the P-gp-positive sublines.	Irinotecan	98-104	phosphoglycolate phosphatase	Homo sapiens	4-8
9472629-4	1998	The P-gp modulators BIBW22BS, verapamil and dexniguldipine partly reversed the resistance against CPT-11 in the P-gp-positive sublines.	Irinotecan	98-104	phosphoglycolate phosphatase	Homo sapiens	112-116
9472629-6	1998	In contrast to doxorubicin and vincristine, the BRO/mdr1.1 xenografts were at least as sensitive to CPT-11 as the BRO xenografts.	Irinotecan	100-106	ATP binding cassette subfamily B member 1	Homo sapiens	52-56
9472629-9	1998	The MRP-positive subline GLC4/ADR was cross-resistant against carboxylesterase-activated CPT-11 and SN-38.	Irinotecan	89-95	ATP binding cassette subfamily C member 3	Homo sapiens	4-7
9472629-9	1998	The MRP-positive subline GLC4/ADR was cross-resistant against carboxylesterase-activated CPT-11 and SN-38.	Irinotecan	89-95	aldo-keto reductase family 1 member B	Homo sapiens	30-33
9426050-0	1998	Overexpression of a rabbit liver carboxylesterase sensitizes human tumor cells to CPT-11.	Irinotecan	82-88	liver carboxylesterase 1	Oryctolagus cuniculus	27-49
9472629-9	1998	The MRP-positive subline GLC4/ADR was cross-resistant against carboxylesterase-activated CPT-11 and SN-38.	Irinotecan	100-105	ATP binding cassette subfamily C member 3	Homo sapiens	4-7
9426050-3	1998	Data in this study show metabolism of CPT-11 to SN-38 (7-ethyl-10-hydroxycamptothecin) by a rabbit liver carboxylesterase in vitro and growth-inhibitory activity of the products of the reaction.	Irinotecan	38-44	liver carboxylesterase 1	Oryctolagus cuniculus	99-121
9426050-3	1998	Data in this study show metabolism of CPT-11 to SN-38 (7-ethyl-10-hydroxycamptothecin) by a rabbit liver carboxylesterase in vitro and growth-inhibitory activity of the products of the reaction.	Irinotecan	48-53	liver carboxylesterase 1	Oryctolagus cuniculus	99-121
9426050-3	1998	Data in this study show metabolism of CPT-11 to SN-38 (7-ethyl-10-hydroxycamptothecin) by a rabbit liver carboxylesterase in vitro and growth-inhibitory activity of the products of the reaction.	Irinotecan	55-85	liver carboxylesterase 1	Oryctolagus cuniculus	99-121
9744772-0	1998	Inhibition of intestinal microflora beta-glucuronidase modifies the distribution of the active metabolite of the antitumor agent, irinotecan hydrochloride (CPT-11) in rats.	Irinotecan	130-154	glucuronidase, beta	Rattus norvegicus	36-54
9472629-9	1998	The MRP-positive subline GLC4/ADR was cross-resistant against carboxylesterase-activated CPT-11 and SN-38.	Irinotecan	100-105	aldo-keto reductase family 1 member B	Homo sapiens	30-33
9744772-0	1998	Inhibition of intestinal microflora beta-glucuronidase modifies the distribution of the active metabolite of the antitumor agent, irinotecan hydrochloride (CPT-11) in rats.	Irinotecan	156-162	glucuronidase, beta	Rattus norvegicus	36-54
9393754-0	1997	Intravenous administration of irinotecan elevates the blood beta-glucuronidase activity in rats.	Irinotecan	30-40	glucuronidase, beta	Rattus norvegicus	60-78
9744772-2	1998	We have previously found that the inhibition of beta-glucuronidase, which hydrolyzes detoxified SN-38 (SN-38 glucuronide) to reform SN-38, in the lumen by eliminating the intestinal microflora with antibiotics, markedly ameliorates the intestinal toxicity of CPT-11 in rats.	Irinotecan	96-101	glucuronidase, beta	Rattus norvegicus	48-66
9744772-2	1998	We have previously found that the inhibition of beta-glucuronidase, which hydrolyzes detoxified SN-38 (SN-38 glucuronide) to reform SN-38, in the lumen by eliminating the intestinal microflora with antibiotics, markedly ameliorates the intestinal toxicity of CPT-11 in rats.	Irinotecan	103-108	glucuronidase, beta	Rattus norvegicus	48-66
9744772-2	1998	We have previously found that the inhibition of beta-glucuronidase, which hydrolyzes detoxified SN-38 (SN-38 glucuronide) to reform SN-38, in the lumen by eliminating the intestinal microflora with antibiotics, markedly ameliorates the intestinal toxicity of CPT-11 in rats.	Irinotecan	259-265	glucuronidase, beta	Rattus norvegicus	48-66
9744772-9	1998	CONCLUSIONS: These results suggest that SN-38, which results from the hydrolysis of SN-38 glucuronide by beta-glucuronidase in the intestinal microflora, contributes considerably to the distribution of SN-38 in the large intestine tissue, and that inhibition of the beta-glucuronidase activity by antibiotics results in decreased accumulation of SN-38 in the large intestine.	Irinotecan	40-45	glucuronidase, beta	Rattus norvegicus	105-123
9744772-9	1998	CONCLUSIONS: These results suggest that SN-38, which results from the hydrolysis of SN-38 glucuronide by beta-glucuronidase in the intestinal microflora, contributes considerably to the distribution of SN-38 in the large intestine tissue, and that inhibition of the beta-glucuronidase activity by antibiotics results in decreased accumulation of SN-38 in the large intestine.	Irinotecan	40-45	glucuronidase, beta	Rattus norvegicus	266-284
9744772-9	1998	CONCLUSIONS: These results suggest that SN-38, which results from the hydrolysis of SN-38 glucuronide by beta-glucuronidase in the intestinal microflora, contributes considerably to the distribution of SN-38 in the large intestine tissue, and that inhibition of the beta-glucuronidase activity by antibiotics results in decreased accumulation of SN-38 in the large intestine.	Irinotecan	84-89	glucuronidase, beta	Rattus norvegicus	105-123
9744772-9	1998	CONCLUSIONS: These results suggest that SN-38, which results from the hydrolysis of SN-38 glucuronide by beta-glucuronidase in the intestinal microflora, contributes considerably to the distribution of SN-38 in the large intestine tissue, and that inhibition of the beta-glucuronidase activity by antibiotics results in decreased accumulation of SN-38 in the large intestine.	Irinotecan	84-89	glucuronidase, beta	Rattus norvegicus	266-284
9744772-9	1998	CONCLUSIONS: These results suggest that SN-38, which results from the hydrolysis of SN-38 glucuronide by beta-glucuronidase in the intestinal microflora, contributes considerably to the distribution of SN-38 in the large intestine tissue, and that inhibition of the beta-glucuronidase activity by antibiotics results in decreased accumulation of SN-38 in the large intestine.	Irinotecan	84-89	glucuronidase, beta	Rattus norvegicus	105-123
9744772-9	1998	CONCLUSIONS: These results suggest that SN-38, which results from the hydrolysis of SN-38 glucuronide by beta-glucuronidase in the intestinal microflora, contributes considerably to the distribution of SN-38 in the large intestine tissue, and that inhibition of the beta-glucuronidase activity by antibiotics results in decreased accumulation of SN-38 in the large intestine.	Irinotecan	84-89	glucuronidase, beta	Rattus norvegicus	266-284
9750028-3	1998	In vivo pharmacokinetic studies revealed that the biliary excretion of the four anionic forms of CPT-11 and its metabolites was reduced in Eisai hyperbilirubinemic rats, which carry a mutation of the hepatic canalicular multispecific organic anion transporter (cMOAT) gene.	Irinotecan	97-103	ATP binding cassette subfamily C member 2	Rattus norvegicus	208-259
9750028-3	1998	In vivo pharmacokinetic studies revealed that the biliary excretion of the four anionic forms of CPT-11 and its metabolites was reduced in Eisai hyperbilirubinemic rats, which carry a mutation of the hepatic canalicular multispecific organic anion transporter (cMOAT) gene.	Irinotecan	97-103	ATP binding cassette subfamily C member 2	Rattus norvegicus	261-266
9750028-5	1998	Detailed analysis using isolated liver bile canalicular membrane vesicles to identify transport systems showed that cMOAT is responsible for biliary excretion of the low-affinity component of the carboxylate form of CPT-11 and the high-affinity component of both the lactone and carboxylate forms of SN-38 glucuronide.	Irinotecan	216-222	ATP binding cassette subfamily C member 2	Rattus norvegicus	116-121
9750028-6	1998	The carboxylate form of SN-38 is transported by cMOAT alone.	Irinotecan	24-29	ATP binding cassette subfamily C member 2	Rattus norvegicus	48-53
9750028-8	1998	In addition, ATP dependence in the uptake of CPT-11 by membrane vesicles obtained from a P-glycoprotein (P-gp)-overexpressing cell line was observed.	Irinotecan	45-51	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	89-103
9750028-8	1998	In addition, ATP dependence in the uptake of CPT-11 by membrane vesicles obtained from a P-glycoprotein (P-gp)-overexpressing cell line was observed.	Irinotecan	45-51	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	105-109
9750028-9	1998	Thus P-gp may be responsible for transport of the high-affinity component of the carboxylate form of CPT-11.	Irinotecan	101-107	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	5-9
9654107-6	1998	Simultaneous exposure to paclitaxel and SN-38 for 24 h produced antagonistic (subadditive and protective) effects in the human lung cancer cell line A549, the breast cancer cell line MCF7, and the colon cancer cell line WiDr, and produced additive effects in the ovarian cancer cell line PA1.	Irinotecan	40-45	PAXIP1 associated glutamate rich protein 1	Homo sapiens	288-291
9393754-4	1997	Prompted by the enzymological and structural similarity of CPT-11 to organophosphorus and carbamate insecticides, we studied the effect of CPT-11 on blood beta-GL activity in rats.	Irinotecan	139-145	glucuronidase, beta	Rattus norvegicus	155-162
9393754-6	1997	injection of CPT-11 in rats significantly elevated their plasma beta-GL activity (with phenolphthalein glucuronide as a substrate) at doses of 10 and 40 mg/kg, with peak activity observed 2-3 h after administration.	Irinotecan	13-19	glucuronidase, beta	Rattus norvegicus	64-71
9157988-1	1997	We have reported previously that a canalicular multispecific organic anion transporter (cMOAT) is responsible for the biliary excretion of carboxylate forms of irinotecan, 7-ethyl-10-[4-(1-piperidino)-1 piperidino] carbonyloxy camptothecin (CPT-11), its active metabolite SN-38, and glucuronide conjugate (SN38-Glu) and the lactone form of SN38-Glu in rats.	Irinotecan	160-170	ATP binding cassette subfamily C member 2	Rattus norvegicus	35-86
9402181-2	1997	Preclinical studies showed that UGT*1.1 is the isozyme responsible for SN-38 glucuronidation.	Irinotecan	71-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	32-39
9402181-3	1997	Patients with Gilbert"s syndrome have deficient UGT*1.1 activity, therefore may have an increased risk for related CPT-11 toxicity.	Irinotecan	115-121	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-55
9334824-1	1997	The anti-tumor activity of irinotecan (CPT-11), a DNA-topoisomerase 1 inhibitor, was evaluated in 5 advanced stage subcutaneous medulloblastoma xenografts in nude mice, using different schedules of administration.	Irinotecan	27-37	topoisomerase (DNA) I	Mus musculus	50-69
9334824-1	1997	The anti-tumor activity of irinotecan (CPT-11), a DNA-topoisomerase 1 inhibitor, was evaluated in 5 advanced stage subcutaneous medulloblastoma xenografts in nude mice, using different schedules of administration.	Irinotecan	39-45	topoisomerase (DNA) I	Mus musculus	50-69
9473740-4	1997	Furthermore, sensitivity of PC-7/CPT cells to SN-38 was improved by inhibiting UGT activity.	Irinotecan	46-51	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	79-82
9473740-6	1997	These results not only imply that upregulation of UGT activity in PC-7/CPT cells may contribute in part to SN-38 resistance, but also illustrate the important of drug metabolism within malignant cells themselves, as a cause of drug resistance.	Irinotecan	107-112	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	50-53
9345343-0	1997	Irinotecan hydrochloride (CPT-11) resistance identified by K-ras mutation in patients with progressive colon cancer after treatment with 5-fluorouracil (5-FU).	Irinotecan	0-24	KRAS proto-oncogene, GTPase	Homo sapiens	59-64
9345343-0	1997	Irinotecan hydrochloride (CPT-11) resistance identified by K-ras mutation in patients with progressive colon cancer after treatment with 5-fluorouracil (5-FU).	Irinotecan	26-32	KRAS proto-oncogene, GTPase	Homo sapiens	59-64
9345343-1	1997	OBJECTIVE: To determine the prognostic role of a K-ras mutation in tumor tissue of patients with refractory colon cancer who received irinotecan hydrochloride (CPT-11).	Irinotecan	134-158	KRAS proto-oncogene, GTPase	Homo sapiens	49-54
9345343-1	1997	OBJECTIVE: To determine the prognostic role of a K-ras mutation in tumor tissue of patients with refractory colon cancer who received irinotecan hydrochloride (CPT-11).	Irinotecan	160-166	KRAS proto-oncogene, GTPase	Homo sapiens	49-54
9345343-9	1997	CONCLUSION: Determination of the presence of a K-ras mutation may predict survival in patients with progressive colon cancer after treatment with 5-fluorouracil who receive CPT-11.	Irinotecan	173-179	KRAS proto-oncogene, GTPase	Homo sapiens	47-52
9414664-4	1997	Ectopic p16INK4-expressing cells also showed approximately 4.0-fold increase in sensitivity to SN-38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of CPT-11, compared to the parent cells.	Irinotecan	95-100	cyclin dependent kinase inhibitor 2A	Homo sapiens	8-15
9414664-4	1997	Ectopic p16INK4-expressing cells also showed approximately 4.0-fold increase in sensitivity to SN-38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of CPT-11, compared to the parent cells.	Irinotecan	102-132	cyclin dependent kinase inhibitor 2A	Homo sapiens	8-15
9414664-4	1997	Ectopic p16INK4-expressing cells also showed approximately 4.0-fold increase in sensitivity to SN-38 (7-ethyl-10-hydroxycamptothecin), the active metabolite of CPT-11, compared to the parent cells.	Irinotecan	160-166	cyclin dependent kinase inhibitor 2A	Homo sapiens	8-15
9259410-3	1997	In this study, we established an SN-38-resistant cell line, PC-6/SN2-5, from the human oat cell carcinoma PC-6 cell line by a stepwise selection system, investigated the mechanism of resistance of this cell line and then compared the antitumor activity of camptothecin analogs against the cell line.	Irinotecan	33-38	proprotein convertase subtilisin/kexin type 5	Homo sapiens	60-64
9259410-3	1997	In this study, we established an SN-38-resistant cell line, PC-6/SN2-5, from the human oat cell carcinoma PC-6 cell line by a stepwise selection system, investigated the mechanism of resistance of this cell line and then compared the antitumor activity of camptothecin analogs against the cell line.	Irinotecan	33-38	proprotein convertase subtilisin/kexin type 5	Homo sapiens	106-110
9259410-4	1997	PC-6/SN2-5 cells were resistant to SN-38 (32-fold) and SK&amp;F 104864 (topotecan; 14-fold), but barely resistant to CPT-11 (3-fold) and DX-8951f (2-fold).	Irinotecan	35-40	proprotein convertase subtilisin/kexin type 5	Homo sapiens	0-4
9259410-4	1997	PC-6/SN2-5 cells were resistant to SN-38 (32-fold) and SK&amp;F 104864 (topotecan; 14-fold), but barely resistant to CPT-11 (3-fold) and DX-8951f (2-fold).	Irinotecan	117-123	proprotein convertase subtilisin/kexin type 5	Homo sapiens	0-4
9259410-6	1997	Determination of the cellular drug concentration by either flow cytometric analysis or the high-performance liquid chromatography method confirmed that the cellular accumulation of SN-38 and topotecan was significantly reduced in PC-6/SN2-5 cells, whereas that of DX-8951f was only slightly reduced.	Irinotecan	181-186	proprotein convertase subtilisin/kexin type 5	Homo sapiens	230-234
9184074-0	1997	Sequential operation of ceramide synthesis and ICE cascade in CPT-11-initiated apoptotic death signaling.	Irinotecan	62-68	caspase 1	Mus musculus	47-50
9184074-3	1997	CPT-11-initiated cytolytic activity was prevented by both caspase inhibitors YVAD-CHO and DEVD-CHO, or ceramide synthesis inhibitor fumonisin B1, and accelerated by sphingomyelin, suggesting the direct involvement of ceramide synthesis and the interleukin 1-beta converting enzyme (ICE) cascade.	Irinotecan	0-6	caspase 1	Mus musculus	58-65
9184074-3	1997	CPT-11-initiated cytolytic activity was prevented by both caspase inhibitors YVAD-CHO and DEVD-CHO, or ceramide synthesis inhibitor fumonisin B1, and accelerated by sphingomyelin, suggesting the direct involvement of ceramide synthesis and the interleukin 1-beta converting enzyme (ICE) cascade.	Irinotecan	0-6	caspase 1	Mus musculus	244-280
9184074-3	1997	CPT-11-initiated cytolytic activity was prevented by both caspase inhibitors YVAD-CHO and DEVD-CHO, or ceramide synthesis inhibitor fumonisin B1, and accelerated by sphingomyelin, suggesting the direct involvement of ceramide synthesis and the interleukin 1-beta converting enzyme (ICE) cascade.	Irinotecan	0-6	caspase 1	Mus musculus	282-285
9157988-1	1997	We have reported previously that a canalicular multispecific organic anion transporter (cMOAT) is responsible for the biliary excretion of carboxylate forms of irinotecan, 7-ethyl-10-[4-(1-piperidino)-1 piperidino] carbonyloxy camptothecin (CPT-11), its active metabolite SN-38, and glucuronide conjugate (SN38-Glu) and the lactone form of SN38-Glu in rats.	Irinotecan	241-247	ATP binding cassette subfamily C member 2	Rattus norvegicus	35-86
9157988-1	1997	We have reported previously that a canalicular multispecific organic anion transporter (cMOAT) is responsible for the biliary excretion of carboxylate forms of irinotecan, 7-ethyl-10-[4-(1-piperidino)-1 piperidino] carbonyloxy camptothecin (CPT-11), its active metabolite SN-38, and glucuronide conjugate (SN38-Glu) and the lactone form of SN38-Glu in rats.	Irinotecan	241-247	ATP binding cassette subfamily C member 2	Rattus norvegicus	88-93
9157988-1	1997	We have reported previously that a canalicular multispecific organic anion transporter (cMOAT) is responsible for the biliary excretion of carboxylate forms of irinotecan, 7-ethyl-10-[4-(1-piperidino)-1 piperidino] carbonyloxy camptothecin (CPT-11), its active metabolite SN-38, and glucuronide conjugate (SN38-Glu) and the lactone form of SN38-Glu in rats.	Irinotecan	272-277	ATP binding cassette subfamily C member 2	Rattus norvegicus	35-86
9157988-1	1997	We have reported previously that a canalicular multispecific organic anion transporter (cMOAT) is responsible for the biliary excretion of carboxylate forms of irinotecan, 7-ethyl-10-[4-(1-piperidino)-1 piperidino] carbonyloxy camptothecin (CPT-11), its active metabolite SN-38, and glucuronide conjugate (SN38-Glu) and the lactone form of SN38-Glu in rats.	Irinotecan	272-277	ATP binding cassette subfamily C member 2	Rattus norvegicus	88-93
9157988-5	1997	The carboxylate form of SN-38 was found to be transported by cMOAT alone.	Irinotecan	24-29	ATP binding cassette subfamily C member 2	Rattus norvegicus	61-66
9157988-6	1997	We conclude that multiple transporters, including cMOAT, are responsible for the biliary excretion of CPT-11 and its metabolites (anionic forms), and the contribution of each transporter differs greatly, depending on the substrates.	Irinotecan	102-108	ATP binding cassette subfamily C member 2	Rattus norvegicus	50-55
9157988-1	1997	We have reported previously that a canalicular multispecific organic anion transporter (cMOAT) is responsible for the biliary excretion of carboxylate forms of irinotecan, 7-ethyl-10-[4-(1-piperidino)-1 piperidino] carbonyloxy camptothecin (CPT-11), its active metabolite SN-38, and glucuronide conjugate (SN38-Glu) and the lactone form of SN38-Glu in rats.	Irinotecan	160-170	ATP binding cassette subfamily C member 2	Rattus norvegicus	88-93
8891470-2	1996	Irinotecan (CPT-II) is a semisynthetic derivative of camptothecin.	Irinotecan	0-10	carnitine palmitoyltransferase 2	Homo sapiens	12-18
9095327-3	1997	In the SCLC cell line, supra-additive effect was observed for SN-38 in combination with cisplatin, etoposide (VP-16) and paclitaxel (Taxol).	Irinotecan	62-67	host cell factor C1	Homo sapiens	110-115
20650253-0	1996	Involvement of CPP32/Yama-like protease in CPT-11-induced death signal transduction pathway.	Irinotecan	43-49	caspase 3	Homo sapiens	15-20
20650253-0	1996	Involvement of CPP32/Yama-like protease in CPT-11-induced death signal transduction pathway.	Irinotecan	43-49	caspase 3	Homo sapiens	21-25
20650253-1	1996	CPT-11, a derivative of camptothecin (CPT) that interacts with type-I DNA topoisomerase, induced apoptosis in HL60 and Daudi cells in vitro.	Irinotecan	0-6	DNA topoisomerase I	Homo sapiens	63-87
8922198-1	1996	BACKGROUND: CPT-11 (irinotecan), a camptothecin-derived anticancer agent with DNA topoisomerase 1 inhibitory activity, has demonstrated a broad spectrum of in vitro and in vivo activity in solid tumour models including multidrug-resistant tumours.	Irinotecan	12-18	DNA topoisomerase I	Homo sapiens	78-97
8922198-1	1996	BACKGROUND: CPT-11 (irinotecan), a camptothecin-derived anticancer agent with DNA topoisomerase 1 inhibitory activity, has demonstrated a broad spectrum of in vitro and in vivo activity in solid tumour models including multidrug-resistant tumours.	Irinotecan	20-30	DNA topoisomerase I	Homo sapiens	78-97
9095327-9	1997	These results suggest that all the drugs we selected can be used with SN-38 simultaneously for NSCLC, while for SCLC, cisplatin, VP-16 and Taxol are the most suitable for combination with SN-38.	Irinotecan	188-193	host cell factor C1	Homo sapiens	129-134
9155540-0	1997	A phase I study of irinotecan and infusional cisplatin with recombinant human granulocyte colony-stimulating factor support in the treatment of advanced non-small cell lung cancer.	Irinotecan	19-29	colony stimulating factor 3	Homo sapiens	78-115
9155540-1	1997	We conducted a phase I study to examine whether support with recombinant human granulocyte colony-stimulating factor (rG-CSF) would permit dose intensification of irinotecan (CPT-11) in combination with cisplatin (20 mg/m2 x 5 days) in non-small cell lung cancer (NSCLC) patients.	Irinotecan	163-173	colony stimulating factor 3	Homo sapiens	79-116
9155540-1	1997	We conducted a phase I study to examine whether support with recombinant human granulocyte colony-stimulating factor (rG-CSF) would permit dose intensification of irinotecan (CPT-11) in combination with cisplatin (20 mg/m2 x 5 days) in non-small cell lung cancer (NSCLC) patients.	Irinotecan	163-173	colony stimulating factor 3	Rattus norvegicus	118-124
9155540-1	1997	We conducted a phase I study to examine whether support with recombinant human granulocyte colony-stimulating factor (rG-CSF) would permit dose intensification of irinotecan (CPT-11) in combination with cisplatin (20 mg/m2 x 5 days) in non-small cell lung cancer (NSCLC) patients.	Irinotecan	175-181	colony stimulating factor 3	Homo sapiens	79-116
9155540-1	1997	We conducted a phase I study to examine whether support with recombinant human granulocyte colony-stimulating factor (rG-CSF) would permit dose intensification of irinotecan (CPT-11) in combination with cisplatin (20 mg/m2 x 5 days) in non-small cell lung cancer (NSCLC) patients.	Irinotecan	175-181	colony stimulating factor 3	Rattus norvegicus	118-124
9033637-10	1997	We observed a positive relationship between the DNA topoisomerase-1 activity and the cellular sensitivity to carboxylesterase-activated CPT-11 (r = 0.75, p &lt; 0.1) as well as to SN-38 (r = 0.89, p &lt; 0.05).	Irinotecan	136-142	DNA topoisomerase I	Homo sapiens	48-67
9033637-10	1997	We observed a positive relationship between the DNA topoisomerase-1 activity and the cellular sensitivity to carboxylesterase-activated CPT-11 (r = 0.75, p &lt; 0.1) as well as to SN-38 (r = 0.89, p &lt; 0.05).	Irinotecan	180-185	DNA topoisomerase I	Homo sapiens	48-67
9033637-12	1997	In conclusion, the DNA topoisomerase-1 activity was the best determinant for CPT-11/SN-38 sensitivity in this panel of unselected human colon-cancer cell lines.	Irinotecan	77-83	DNA topoisomerase I	Homo sapiens	19-38
9033637-12	1997	In conclusion, the DNA topoisomerase-1 activity was the best determinant for CPT-11/SN-38 sensitivity in this panel of unselected human colon-cancer cell lines.	Irinotecan	84-89	DNA topoisomerase I	Homo sapiens	19-38
9054958-1	1997	PURPOSE: Irinotecan (CPT-11) is hydrolyzed to its active metabolite SN-38 which is subsequently conjugated by uridine diphosphate glucuronosyl transferase (UDP-GT) to the glucuronide (SN-38G).	Irinotecan	9-19	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	110-154
9054958-1	1997	PURPOSE: Irinotecan (CPT-11) is hydrolyzed to its active metabolite SN-38 which is subsequently conjugated by uridine diphosphate glucuronosyl transferase (UDP-GT) to the glucuronide (SN-38G).	Irinotecan	9-19	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	156-162
9054958-1	1997	PURPOSE: Irinotecan (CPT-11) is hydrolyzed to its active metabolite SN-38 which is subsequently conjugated by uridine diphosphate glucuronosyl transferase (UDP-GT) to the glucuronide (SN-38G).	Irinotecan	21-27	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	110-154
9054958-1	1997	PURPOSE: Irinotecan (CPT-11) is hydrolyzed to its active metabolite SN-38 which is subsequently conjugated by uridine diphosphate glucuronosyl transferase (UDP-GT) to the glucuronide (SN-38G).	Irinotecan	21-27	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	156-162
9054958-1	1997	PURPOSE: Irinotecan (CPT-11) is hydrolyzed to its active metabolite SN-38 which is subsequently conjugated by uridine diphosphate glucuronosyl transferase (UDP-GT) to the glucuronide (SN-38G).	Irinotecan	68-73	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	110-154
9054958-1	1997	PURPOSE: Irinotecan (CPT-11) is hydrolyzed to its active metabolite SN-38 which is subsequently conjugated by uridine diphosphate glucuronosyl transferase (UDP-GT) to the glucuronide (SN-38G).	Irinotecan	68-73	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	156-162
9054958-1	1997	PURPOSE: Irinotecan (CPT-11) is hydrolyzed to its active metabolite SN-38 which is subsequently conjugated by uridine diphosphate glucuronosyl transferase (UDP-GT) to the glucuronide (SN-38G).	Irinotecan	184-189	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	110-154
9054958-1	1997	PURPOSE: Irinotecan (CPT-11) is hydrolyzed to its active metabolite SN-38 which is subsequently conjugated by uridine diphosphate glucuronosyl transferase (UDP-GT) to the glucuronide (SN-38G).	Irinotecan	184-189	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	156-162
9030234-4	1997	Introduction of bcl 2 gene into human small cell lung cancer cells conferred resistance to mitomycin C and irinotecan.	Irinotecan	107-117	BCL2 apoptosis regulator	Homo sapiens	16-21
9121221-0	1996	Antitumor effect of CPT-11, a new derivative of camptothecin, against human prostate cancer (PC-3) in vitro and prostate rat tumor (AT-3) in vivo.	Irinotecan	20-26	chromobox 8	Homo sapiens	76-97
9121221-4	1996	CPT-11 at concentrations between 10 ng/ml and 50 micrograms/ml inhibited the growth of the PC-3 prostate human cancer cell line up &lt; 0.001).	Irinotecan	0-6	chromobox 8	Homo sapiens	91-95
20650253-8	1996	These results indicate the direct involvement of CPP32/Yama-like protease in the CPT-11-induced death signal transduction pathway, and no involvement of Fas antigen in the pathway.	Irinotecan	81-87	caspase 3	Homo sapiens	49-54
20650253-8	1996	These results indicate the direct involvement of CPP32/Yama-like protease in the CPT-11-induced death signal transduction pathway, and no involvement of Fas antigen in the pathway.	Irinotecan	81-87	caspase 3	Homo sapiens	55-59
8917343-0	1996	Induction of tumor necrosis factor by a camptothecin derivative, irinotecan, in mice and human mononuclear cells.	Irinotecan	65-75	tumor necrosis factor	Mus musculus	13-34
8917343-1	1996	Irinotecan (CPT-11) has been reported to be cytotoxic to tumor cells through its inhibitory activity on type I DNA topoisomerase.	Irinotecan	0-10	DNA topoisomerase I	Homo sapiens	104-128
8917343-1	1996	Irinotecan (CPT-11) has been reported to be cytotoxic to tumor cells through its inhibitory activity on type I DNA topoisomerase.	Irinotecan	12-18	DNA topoisomerase I	Homo sapiens	104-128
8917343-3	1996	We investigated the ability of CPT-11 to induce tumor necrosis factor (TNF) production.	Irinotecan	31-37	tumor necrosis factor	Homo sapiens	48-69
8917343-3	1996	We investigated the ability of CPT-11 to induce tumor necrosis factor (TNF) production.	Irinotecan	31-37	tumor necrosis factor	Homo sapiens	71-74
8917343-5	1996	The priming effect of CPT-11 on endogenous production of TNF was examined by injecting the drug intravenously into mice, followed 3 hours by the injection of OK432.	Irinotecan	22-28	tumor necrosis factor	Mus musculus	57-60
8917343-7	1996	A significant amount of TNF was released when MNCs were incubated with 100-300 microM of CPT-11 for more than 4 hours, but not with vinblastin sulfate, indicating a triggering effect of TNF production on MNCs in vitro.	Irinotecan	89-95	tumor necrosis factor	Homo sapiens	24-27
8917343-7	1996	A significant amount of TNF was released when MNCs were incubated with 100-300 microM of CPT-11 for more than 4 hours, but not with vinblastin sulfate, indicating a triggering effect of TNF production on MNCs in vitro.	Irinotecan	89-95	tumor necrosis factor	Homo sapiens	186-189
8706020-0	1996	Involvement of beta-glucuronidase in intestinal microflora in the intestinal toxicity of the antitumor camptothecin derivative irinotecan hydrochloride (CPT-11) in rats.	Irinotecan	127-151	glucuronidase, beta	Rattus norvegicus	15-33
8841050-16	1996	In conclusion, adverse reactions caused by the combination therapy with CPT-11 and CDDP (CPT-11: 50-60 mg/m2 on days 1, 8 and 15, CDDP: 50-60 mg/m2 on day 1) can be relieved by short term administration of G-CSF and it is suggested that the combination therapy may be effective in treating ovarian carcinoma.	Irinotecan	72-78	colony stimulating factor 3	Homo sapiens	206-211
8841050-16	1996	In conclusion, adverse reactions caused by the combination therapy with CPT-11 and CDDP (CPT-11: 50-60 mg/m2 on days 1, 8 and 15, CDDP: 50-60 mg/m2 on day 1) can be relieved by short term administration of G-CSF and it is suggested that the combination therapy may be effective in treating ovarian carcinoma.	Irinotecan	89-95	colony stimulating factor 3	Homo sapiens	206-211
8706020-0	1996	Involvement of beta-glucuronidase in intestinal microflora in the intestinal toxicity of the antitumor camptothecin derivative irinotecan hydrochloride (CPT-11) in rats.	Irinotecan	153-159	glucuronidase, beta	Rattus norvegicus	15-33
8706020-8	1996	Analysis of CPT-11 and its metabolites in the feces indicated that antibiotics completely inhibited the deconjugation of the glucuronic conjugate of 7-ethyl-10-hydroxycamptothecin by beta-glucuronidase.	Irinotecan	12-18	glucuronidase, beta	Rattus norvegicus	183-201
8706020-8	1996	Analysis of CPT-11 and its metabolites in the feces indicated that antibiotics completely inhibited the deconjugation of the glucuronic conjugate of 7-ethyl-10-hydroxycamptothecin by beta-glucuronidase.	Irinotecan	149-179	glucuronidase, beta	Rattus norvegicus	183-201
8706020-9	1996	It is suggested that CPT-11-induced diarrhea would be attributable to the damage to the cecum, and that the inhibition of the beta-glucuronidase activity in the intestinal microflora is a major protective effect of antibiotics.	Irinotecan	21-27	glucuronidase, beta	Rattus norvegicus	126-144
8625310-11	1996	Treatment with CPT-11 or SN-38 also induced a markedly greater and more persistent reduction in topo I mRNA abundance in KB/STP-2 cells than in KB cells.	Irinotecan	15-21	sulfotransferase family 1A member 2	Homo sapiens	124-129
8683231-2	1996	MATERIALS AND METHODS: The recommended phase II dose of weekly CPT-11 administered as a 90-minute infusion is 145 mg/m2 with granulocyte colony-stimulating factor (G-CSF) and maximal antidiarrheal support.	Irinotecan	63-69	colony stimulating factor 3	Homo sapiens	125-162
8683231-2	1996	MATERIALS AND METHODS: The recommended phase II dose of weekly CPT-11 administered as a 90-minute infusion is 145 mg/m2 with granulocyte colony-stimulating factor (G-CSF) and maximal antidiarrheal support.	Irinotecan	63-69	colony stimulating factor 3	Homo sapiens	164-169
8625310-11	1996	Treatment with CPT-11 or SN-38 also induced a markedly greater and more persistent reduction in topo I mRNA abundance in KB/STP-2 cells than in KB cells.	Irinotecan	25-30	sulfotransferase family 1A member 2	Homo sapiens	124-129
8625310-14	1996	This novel regulation of topo I mRNA by topo I-targeting agents could be associated with acquirement of drug resistance to saintopin or SN-38/CPT-11 in KB/STP-2 cells.	Irinotecan	136-141	sulfotransferase family 1A member 2	Homo sapiens	155-160
8625310-14	1996	This novel regulation of topo I mRNA by topo I-targeting agents could be associated with acquirement of drug resistance to saintopin or SN-38/CPT-11 in KB/STP-2 cells.	Irinotecan	142-148	sulfotransferase family 1A member 2	Homo sapiens	155-160
8633248-3	1996	The antitumor effects of CPT-11 and SN-38 are exerted through a novel mechanism of action; inhibition of DNA topoisomerase I.	Irinotecan	25-31	topoisomerase (DNA) I	Mus musculus	105-124
8812723-0	1996	Stimulation of interleukin-1beta-converting enzyme activity during growth inhibition by CPT-11 in the human myeloid leukemia cell line K562.	Irinotecan	88-94	caspase 1	Homo sapiens	15-50
8812723-6	1996	To determine how CPT-11 brings about cell death by apoptosis, we investigated the effects of CPT-11 on the expression of ICE activity in K562 cells, which represent human myeloid leukemia cells.	Irinotecan	93-99	caspase 1	Homo sapiens	121-124
8812723-8	1996	We also found that the levels of mRNA for ICE in the cells were increased in the presence of CPT-11.	Irinotecan	93-99	caspase 1	Homo sapiens	42-45
8812723-10	1996	These features suggested that CPT-11 enhances the apoptotic cell death in K562 cells and that a part of induction of apoptosis by CPT-11 may be correlated with the stimulation of the ICE activity.	Irinotecan	30-36	caspase 1	Homo sapiens	183-186
8812723-10	1996	These features suggested that CPT-11 enhances the apoptotic cell death in K562 cells and that a part of induction of apoptosis by CPT-11 may be correlated with the stimulation of the ICE activity.	Irinotecan	130-136	caspase 1	Homo sapiens	183-186
8633248-3	1996	The antitumor effects of CPT-11 and SN-38 are exerted through a novel mechanism of action; inhibition of DNA topoisomerase I.	Irinotecan	36-41	topoisomerase (DNA) I	Mus musculus	105-124
7733646-1	1995	The interaction between hyperthermia and a DNA topoisomerase I inhibitor, 7-ethyl-10-(4-(1-piperidyl)-1-piperidyl)-carbonyloxy- camptothecin (CPT-11), was studied in the mouse mammary carcinoma FM3A cells.	Irinotecan	142-148	topoisomerase (DNA) I	Mus musculus	43-62
7494232-1	1995	BACKGROUND: Irinotecan--or CPT-11; 7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxy-camptotheci n--is an inhibitor of DNA topoisomerase I and is clinically effective against several cancers.	Irinotecan	12-22	topoisomerase (DNA) I	Mus musculus	124-143
7494232-1	1995	BACKGROUND: Irinotecan--or CPT-11; 7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxy-camptotheci n--is an inhibitor of DNA topoisomerase I and is clinically effective against several cancers.	Irinotecan	27-33	topoisomerase (DNA) I	Mus musculus	124-143
7494232-1	1995	BACKGROUND: Irinotecan--or CPT-11; 7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxy-camptotheci n--is an inhibitor of DNA topoisomerase I and is clinically effective against several cancers.	Irinotecan	35-105	topoisomerase (DNA) I	Mus musculus	124-143
8664184-4	1995	Of those currently under investigation, CPT-11 seems to represent the most promising, since its mode of action is something other than inhibition of thymidylate synthase.	Irinotecan	40-46	thymidylate synthetase	Homo sapiens	149-169
7493918-2	1995	We investigated whether baicalin, an inhibitor of beta-glucuronidase, which deconjugates the glucuronide of the active metabolite of CPT-11, SN-38 (7-ethyl-10-hydorxycamptothecin), and Japanese herbal medicines (Kampo medicines) which contain baicalin can ameliorate CPT-11-induced intestinal toxicity in rats.	Irinotecan	133-139	glucuronidase, beta	Rattus norvegicus	50-68
7493918-2	1995	We investigated whether baicalin, an inhibitor of beta-glucuronidase, which deconjugates the glucuronide of the active metabolite of CPT-11, SN-38 (7-ethyl-10-hydorxycamptothecin), and Japanese herbal medicines (Kampo medicines) which contain baicalin can ameliorate CPT-11-induced intestinal toxicity in rats.	Irinotecan	141-146	glucuronidase, beta	Rattus norvegicus	50-68
7493918-2	1995	We investigated whether baicalin, an inhibitor of beta-glucuronidase, which deconjugates the glucuronide of the active metabolite of CPT-11, SN-38 (7-ethyl-10-hydorxycamptothecin), and Japanese herbal medicines (Kampo medicines) which contain baicalin can ameliorate CPT-11-induced intestinal toxicity in rats.	Irinotecan	267-273	glucuronidase, beta	Rattus norvegicus	50-68
7493919-0	1995	Inhibition of UDP-glucuronosyltransferase by aglycons of natural glucuronides in kampo medicines using SN-38 as a substrate.	Irinotecan	103-108	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	14-41
7493919-1	1995	7-Ethyl-10-[4-(piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11), a potent anticancer agent for lung and gynecological cancers, is metabolized in vivo to the active compound, 7-ethyl-10-hydroxycamptothecin (SN-38), which is subsequently conjugated to SN-38-glucuronide by UDP-glucuronosyltransferase (UDP-GT).	Irinotecan	65-71	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	280-307
7493919-1	1995	7-Ethyl-10-[4-(piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11), a potent anticancer agent for lung and gynecological cancers, is metabolized in vivo to the active compound, 7-ethyl-10-hydroxycamptothecin (SN-38), which is subsequently conjugated to SN-38-glucuronide by UDP-glucuronosyltransferase (UDP-GT).	Irinotecan	65-71	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	309-315
7493919-2	1995	Three purified aglycons of natural glucuronides, baicalein, luteolin and glycyrrhetic acid, inhibited UDP-GT activity towards SN-38 as a substrate.	Irinotecan	126-131	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	102-108
7766631-10	1995	The stability of 10-hydroxycamptothecin-induced cleavable complexes was intermediate to those of CPT and SN-38, indicating that both the 10-hydroxy and the 7-ethyl group of SN-38 probably interact with the drug binding site of top1-cleavable complexes.	Irinotecan	173-178	choline phosphotransferase 1	Homo sapiens	97-100
7763013-0	1995	Sequence-dependent modulation of anticancer drug activities by 7-ethyl-10-hydroxycamptothecin in an HST-1 human squamous carcinoma cell line.	Irinotecan	63-93	fibroblast growth factor 4	Homo sapiens	100-105
7763013-3	1995	RESULTS: SN-38 potentiated the antitumor activity of CDDP in all schedules with a maximal effect observed with a simultaneous administration, while SN-38 enhanced the cytotoxicity of MMC, 5-FU, or VP-16 only in certain schedules.	Irinotecan	148-153	host cell factor C1	Homo sapiens	197-202
7763013-5	1995	CONCLUSIONS: These results demonstrate that SN-38 may have the advantage of augmenting the anticancer activity in combination with CDDP, MMC, 5-FU, and VP-16, depending on the schedule of administration, and should thus be incorporated into the design of a clinical trial for obtaining maximal therapeutic synergy.	Irinotecan	44-49	host cell factor C1	Homo sapiens	152-157
7623066-6	1995	Total glutathione S-transferase (GST) and GST-p activities were similar in CPT-11-sensitive and -resistant cells.	Irinotecan	75-81	glutathione S-transferase kappa 1	Homo sapiens	6-31
7623066-6	1995	Total glutathione S-transferase (GST) and GST-p activities were similar in CPT-11-sensitive and -resistant cells.	Irinotecan	75-81	glutathione S-transferase kappa 1	Homo sapiens	33-36
7623066-6	1995	Total glutathione S-transferase (GST) and GST-p activities were similar in CPT-11-sensitive and -resistant cells.	Irinotecan	75-81	glutathione S-transferase pi 1	Homo sapiens	42-47
7521905-0	1994	Phase I and pharmacologic study of irinotecan and etoposide with recombinant human granulocyte colony-stimulating factor support for advanced lung cancer.	Irinotecan	35-45	colony stimulating factor 3	Homo sapiens	83-120
7737904-3	1995	However, HAC2/0.1, a CDDP-resistant human ovarian cancer cell line which is also resistant to CPT-11 because of decreased intracellular activation of CPT-11, was about 12.8-fold more resistant to KW-2189.	Irinotecan	94-100	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	9-17
7737904-3	1995	However, HAC2/0.1, a CDDP-resistant human ovarian cancer cell line which is also resistant to CPT-11 because of decreased intracellular activation of CPT-11, was about 12.8-fold more resistant to KW-2189.	Irinotecan	150-156	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	9-17
7737904-12	1995	The decreased conversion of CPT-11 to SN-38 in HAC2/0.1 cells might be explained by decreased carboxyl esterase activity.	Irinotecan	28-34	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	47-51
7737904-12	1995	The decreased conversion of CPT-11 to SN-38 in HAC2/0.1 cells might be explained by decreased carboxyl esterase activity.	Irinotecan	38-43	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	47-51
8074481-3	1994	An in vitro drug sensitivity assay revealed that HAC2/CPT was 9.7 and 4.7 times as resistant as HAC2 to CPT-11 and 7-ethyl-10-hydroxy-CPT-11 (SN-38), an active metabolite of CPT-11, respectively.	Irinotecan	142-147	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	49-53
8060137-1	1994	In order to select a suitable combination chemotherapy with BOF-A2 from the view of both anti-tumor effect (IR) and decrease of side effect, we studied a combination significance of BOF-A2 with CPT-11 that promised for a new anticancer drug, CDDP or mitomycin C (MMC) that used widely to many cancer patients and interferon-alpha (IFN-alpha) against colon, stomach and renal cancer, respectively, by using xenografted nude mice.	Irinotecan	194-200	interferon alpha 1	Homo sapiens	331-340
8089365-2	1994	In the present experiment, the possible modifying effects of Peplomycin (PEP, 30 mg/kg body weight) and Camptothecin-11, an inhibitor of DNA topoisomerase I (CPT-11, 15 and 50 mg/kg body weight), on radiation skin injury were studied.	Irinotecan	104-119	topoisomerase (DNA) I	Mus musculus	137-156
8074481-3	1994	An in vitro drug sensitivity assay revealed that HAC2/CPT was 9.7 and 4.7 times as resistant as HAC2 to CPT-11 and 7-ethyl-10-hydroxy-CPT-11 (SN-38), an active metabolite of CPT-11, respectively.	Irinotecan	142-147	choline phosphotransferase 1	Homo sapiens	54-57
7920428-5	1994	In studies on the kinetic parameters of the hydrolysis of CPT-11 by the purified carboxylesterase isozymes the highest Vmax value of the isozymes was found in human HU1 and the smallest was seen in rat RL1.	Irinotecan	58-64	homeobox B5	Homo sapiens	165-168
8074481-3	1994	An in vitro drug sensitivity assay revealed that HAC2/CPT was 9.7 and 4.7 times as resistant as HAC2 to CPT-11 and 7-ethyl-10-hydroxy-CPT-11 (SN-38), an active metabolite of CPT-11, respectively.	Irinotecan	142-147	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	96-100
7920428-5	1994	In studies on the kinetic parameters of the hydrolysis of CPT-11 by the purified carboxylesterase isozymes the highest Vmax value of the isozymes was found in human HU1 and the smallest was seen in rat RL1.	Irinotecan	58-64	ribonuclease A family member 1, pancreatic	Rattus norvegicus	202-205
7505810-0	1994	Phase I study of irinotecan and cisplatin with granulocyte colony-stimulating factor support for advanced non-small-cell lung cancer.	Irinotecan	17-27	colony stimulating factor 3	Homo sapiens	47-84
21566972-0	1994	Bcl-2 gene prevents induction of apoptosis in l1210 murine leukemia-cells by sn-38, a metabolite of the camptothecin derivative cpt-11.	Irinotecan	77-82	B cell leukemia/lymphoma 2	Mus musculus	0-5
21566972-0	1994	Bcl-2 gene prevents induction of apoptosis in l1210 murine leukemia-cells by sn-38, a metabolite of the camptothecin derivative cpt-11.	Irinotecan	128-134	B cell leukemia/lymphoma 2	Mus musculus	0-5
21566972-5	1994	We demonstrated in addition that enforced expression of the bcl-2 gene in L1210 cells by MPZenNeo (bcl-2) retroviral gene transfer increased resistance to the apoptosis induced by SN-38 and CPT.	Irinotecan	180-185	B cell leukemia/lymphoma 2	Mus musculus	60-65
21566972-5	1994	We demonstrated in addition that enforced expression of the bcl-2 gene in L1210 cells by MPZenNeo (bcl-2) retroviral gene transfer increased resistance to the apoptosis induced by SN-38 and CPT.	Irinotecan	180-185	B cell leukemia/lymphoma 2	Mus musculus	99-104
21566972-6	1994	These findings suggest the possibility that the bcl-2 gene impedes the activity of a common pathway for apoptosis induced by SN-38 and CPT.	Irinotecan	125-130	B cell leukemia/lymphoma 2	Mus musculus	48-53
8070019-1	1994	The camptothecin derivative 7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxy camptothecin (CPT-11) has attracted the attention of clinicians because of its high antitumor activity against refractory solid cancers.	Irinotecan	28-95	choline phosphotransferase 1	Homo sapiens	97-100
8070019-3	1994	The mechanisms of resistance to CPT-11 in PC-7/CPT-11 cells were reduced conversion of CPT-11 to its active metabolite SN-38 and point mutation topoisomerase I.	Irinotecan	119-124	choline phosphotransferase 1	Homo sapiens	32-35
8070019-3	1994	The mechanisms of resistance to CPT-11 in PC-7/CPT-11 cells were reduced conversion of CPT-11 to its active metabolite SN-38 and point mutation topoisomerase I.	Irinotecan	119-124	choline phosphotransferase 1	Homo sapiens	47-50
8070019-3	1994	The mechanisms of resistance to CPT-11 in PC-7/CPT-11 cells were reduced conversion of CPT-11 to its active metabolite SN-38 and point mutation topoisomerase I.	Irinotecan	119-124	choline phosphotransferase 1	Homo sapiens	47-50
7505810-11	1994	With the use of rhG-CSF, the CPT-11 dose can be increased 33% above that in the original regimen (60 mg/m2 of CPT-11 and 80 mg/m2 of cisplatin).	Irinotecan	29-35	colony stimulating factor 2	Homo sapiens	20-23
7505810-11	1994	With the use of rhG-CSF, the CPT-11 dose can be increased 33% above that in the original regimen (60 mg/m2 of CPT-11 and 80 mg/m2 of cisplatin).	Irinotecan	110-116	colony stimulating factor 2	Homo sapiens	20-23
8476431-0	1993	Apoptosis of lung cancer cells caused by some anti-cancer agents (MMC, CPT-11, ADM) is inhibited by bcl-2.	Irinotecan	71-77	BCL2 apoptosis regulator	Homo sapiens	100-105
21584513-5	1992	Northern blot analysis showed about 5-fold increase in CAT mRNA levels in Kst-6 cells treated with CPT-11 or VP-16, but not with novobiocin.	Irinotecan	99-105	catalase	Homo sapiens	55-58
11578320-4	1993	In both cell lines, IFN-gamma at clinically achievable concentrations (10 and 100 U ml-1 enhanced the anti-proliferative activity of CPT-11 in the range of concentrations where CPT-11 showed more than 10% cell growth inhibition.	Irinotecan	133-139	interferon gamma	Homo sapiens	20-29
11578320-4	1993	In both cell lines, IFN-gamma at clinically achievable concentrations (10 and 100 U ml-1 enhanced the anti-proliferative activity of CPT-11 in the range of concentrations where CPT-11 showed more than 10% cell growth inhibition.	Irinotecan	177-183	interferon gamma	Homo sapiens	20-29
1332623-1	1992	CPT-11 and Topotecan are a new semisynthetic derivative of CPT, and have been shown to inhibit DNA topoisomerase I and to have a strong antitumor activity with low toxicity against murine tumor.	Irinotecan	0-6	topoisomerase (DNA) I	Mus musculus	95-114
21584513-3	1992	Exposure to inhibitors of DNA topoisomerase I (camptothecin: CPT-11) and II (etoposide: VP-16 and teniposide: VM-26) could efficiently induce CAT activities in both time- and dose-dependent manners.	Irinotecan	61-67	host cell factor C1	Homo sapiens	88-93
21584513-6	1992	Proximal MDR1 promoter-binding activities of transacting factor were augmented in nuclear extracts from KB cells treated with CPT-11, VM-26, and VP-16.	Irinotecan	126-132	ATP binding cassette subfamily B member 1	Homo sapiens	9-13
21584513-3	1992	Exposure to inhibitors of DNA topoisomerase I (camptothecin: CPT-11) and II (etoposide: VP-16 and teniposide: VM-26) could efficiently induce CAT activities in both time- and dose-dependent manners.	Irinotecan	61-67	catalase	Homo sapiens	142-145
1345810-7	1992	On the other hand, the conversion of CPT-11 to SN-38 in HAC2/0.1 was about 3-fold less than in HAC2/P.	Irinotecan	37-43	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	56-64
1345810-7	1992	On the other hand, the conversion of CPT-11 to SN-38 in HAC2/0.1 was about 3-fold less than in HAC2/P.	Irinotecan	37-43	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	56-60
1345810-9	1992	The accumulation of CPT-11 in HAC2/0.1 but not in HAC2/P was increased by BSO treatment.	Irinotecan	20-26	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	30-38
1345810-7	1992	On the other hand, the conversion of CPT-11 to SN-38 in HAC2/0.1 was about 3-fold less than in HAC2/P.	Irinotecan	47-52	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	56-64
1345810-9	1992	The accumulation of CPT-11 in HAC2/0.1 but not in HAC2/P was increased by BSO treatment.	Irinotecan	20-26	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	30-34
1345810-10	1992	On the other hand, in HAC2/P the 50% inhibitory concentrations of SN-38 and CPT-11 were not influenced by BSO treatment.	Irinotecan	66-71	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	22-26
1345810-10	1992	On the other hand, in HAC2/P the 50% inhibitory concentrations of SN-38 and CPT-11 were not influenced by BSO treatment.	Irinotecan	76-82	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	22-26
1345810-11	1992	The 50% inhibitory concentration of CPT-11 for HAC2/0.1 was not reduced by BSO treatment to the level for HAC2/P, even though the GSH content had been reduced more than in HAC2/P.	Irinotecan	36-42	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	47-55
1345810-11	1992	The 50% inhibitory concentration of CPT-11 for HAC2/0.1 was not reduced by BSO treatment to the level for HAC2/P, even though the GSH content had been reduced more than in HAC2/P.	Irinotecan	36-42	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	47-51
1345810-7	1992	On the other hand, the conversion of CPT-11 to SN-38 in HAC2/0.1 was about 3-fold less than in HAC2/P.	Irinotecan	47-52	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	56-60
1804390-0	1991	Augmentation of antiproliferative activity of CPT-11, a new derivative of camptothecin, by tumor necrosis factor against proliferation of gynecologic tumor cell lines.	Irinotecan	46-52	tumor necrosis factor	Homo sapiens	91-112
1309380-1	1992	PURPOSE: Camptothecin-11 (CPT-11) is a new semisynthetic derivative of CPT, and has been shown to inhibit DNA topoisomerase I and to have a strong antitumor activity with low toxicity in murine tumors.	Irinotecan	9-24	topoisomerase (DNA) I	Mus musculus	106-125
1309380-1	1992	PURPOSE: Camptothecin-11 (CPT-11) is a new semisynthetic derivative of CPT, and has been shown to inhibit DNA topoisomerase I and to have a strong antitumor activity with low toxicity in murine tumors.	Irinotecan	26-32	topoisomerase (DNA) I	Mus musculus	106-125
1804390-4	1991	In all four cell lines, rH-TNF at clinically achievable concentrations exhibited synergy with CPT-11.	Irinotecan	94-100	tumor necrosis factor	Homo sapiens	27-30
33805415-3	2021	We summarized meta-analyses, genome-wide association studies, clinical trials, drug labels, and guidelines relating to the impact of UGT1A1 polymorphisms on irinotecan, belinostat, pazopanib, or nilotinib toxicities.	Irinotecan	157-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	133-139
33805415-4	2021	For irinotecan, UGT1A1*28 was significantly associated with neutropenia and diarrhea, particularly with doses >= 180 mg/m2, supporting the use of UGT1A1 to guide irinotecan prescribing.	Irinotecan	162-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	16-22
33805415-4	2021	For irinotecan, UGT1A1*28 was significantly associated with neutropenia and diarrhea, particularly with doses >= 180 mg/m2, supporting the use of UGT1A1 to guide irinotecan prescribing.	Irinotecan	162-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	146-152
33033581-11	2020	Knockdown of NeuroD1 enhanced the sensitivity to irinotecan of GNEC cell lines.	Irinotecan	49-59	neuronal differentiation 1	Homo sapiens	13-20
33941341-0	2021	A four-component combination derived from Huang-Qin Decoction significantly enhances anticancer activity of irinotecan.	Irinotecan	108-118	forkhead box G1	Homo sapiens	48-51
33941341-11	2021	In vitro assessment indicated that HB4 could enhance the effect of CPT-11 on inhibiting cell proliferation and inducing apoptosis in HCT116.	Irinotecan	67-73	keratin 84	Homo sapiens	35-38
33941341-12	2021	Furthermore, the in vivo study confirmed that HB4 and HQD have similar pharmacological activity and could both enhance the antitumor effect of CPT-11 in HCT116 xenograft model.	Irinotecan	143-149	keratin 84	Homo sapiens	46-49
33941341-13	2021	Meanwhile, HB4 could also reduce the CPT-11 induced GI toxicity.	Irinotecan	37-43	keratin 84	Homo sapiens	11-14
33777142-13	2021	Conclusions: The oncological outcomes of patients with BRAF-mutated mCRC treated using FOLFIRI plus bevacizumab with irinotecan dose escalation as a first-line therapy are acceptable with tolerable AEs; this may be a feasible treatment option in such patients.	Irinotecan	117-127	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	55-59
33235468-0	2020	Tumor Response to Irinotecan is Associated with IL-10 Expression Level in Metastatic Colorectal Cancer-Results from mCRC Biomarker Study.	Irinotecan	18-28	interleukin 10	Homo sapiens	48-53
33235468-11	2020	By utilizing univariate and multivariate Cox proportional hazard analyses, we found that low IL-10 level in plasma was significantly associated with improved overall survival (OS) of mCRC patients treated with irinotecan-containing regimen-with optimal cutoff value of 5.525pg/mL, respectively (p =0.002).	Irinotecan	210-220	interleukin 10	Homo sapiens	93-98
33235468-12	2020	In addition, the low IL-10 expression level in tumor tissue was significantly associated with the improved OS for the irinotecan-containing regimen (p = 0.023).	Irinotecan	118-128	interleukin 10	Homo sapiens	21-26
33235468-13	2020	Conclusion: Our study demonstrated that IL-10 could act as a prognostic biomarker for mCRC patients undergoing irinotecan-containing chemotherapy.	Irinotecan	111-121	interleukin 10	Homo sapiens	40-45
33235483-7	2020	Prevalent UGT1A1 gene [TA]7TAA promoter allelic variant UGT1A1*28, characterized by an extra TA repeat, is associated with low transcriptional and reduced enzymatic effectiveness, decreased SN38 active irinotecan metabolite glucuronidation, vs wild-type UGT1A1*1 [A(TA)6TAA].	Irinotecan	202-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
33235483-7	2020	Prevalent UGT1A1 gene [TA]7TAA promoter allelic variant UGT1A1*28, characterized by an extra TA repeat, is associated with low transcriptional and reduced enzymatic effectiveness, decreased SN38 active irinotecan metabolite glucuronidation, vs wild-type UGT1A1*1 [A(TA)6TAA].	Irinotecan	202-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
33235483-7	2020	Prevalent UGT1A1 gene [TA]7TAA promoter allelic variant UGT1A1*28, characterized by an extra TA repeat, is associated with low transcriptional and reduced enzymatic effectiveness, decreased SN38 active irinotecan metabolite glucuronidation, vs wild-type UGT1A1*1 [A(TA)6TAA].	Irinotecan	202-212	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	56-62
33235483-11	2020	Implementation of up-front evaluation of the five validated DPYD variants and UGT1A1*28 in the multidisciplinary molecular tumor board, also including CRC genetic characterization, addresses potential treatments with fluoropyrimidines and irinotecan associations at proper doses and schedules, particularly for early CRC, MCRC patients fit for intensive regimens or unfit for conventional regimens, requiring treatment modulations, and also for patients who experience severe, unexpected toxicities.	Irinotecan	239-249	dihydropyrimidine dehydrogenase	Homo sapiens	60-64
33235483-11	2020	Implementation of up-front evaluation of the five validated DPYD variants and UGT1A1*28 in the multidisciplinary molecular tumor board, also including CRC genetic characterization, addresses potential treatments with fluoropyrimidines and irinotecan associations at proper doses and schedules, particularly for early CRC, MCRC patients fit for intensive regimens or unfit for conventional regimens, requiring treatment modulations, and also for patients who experience severe, unexpected toxicities.	Irinotecan	239-249	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	78-84
33777142-0	2021	UGT1A1 Polymorphism for Irinotecan Dose Escalation in Patients with BRAF-Mutated Metastatic Colorectal Cancer Treated with First-Line Bevacizumab and FOLFIRI.	Irinotecan	24-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
33777142-0	2021	UGT1A1 Polymorphism for Irinotecan Dose Escalation in Patients with BRAF-Mutated Metastatic Colorectal Cancer Treated with First-Line Bevacizumab and FOLFIRI.	Irinotecan	24-34	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	68-72
33777142-3	2021	In this study, we explored the effects and oncological outcomes of UGT1A1 polymorphism for irinotecan escalation in patients with BRAF-mutated mCRC.	Irinotecan	91-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	67-73
33777142-3	2021	In this study, we explored the effects and oncological outcomes of UGT1A1 polymorphism for irinotecan escalation in patients with BRAF-mutated mCRC.	Irinotecan	91-101	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	130-134
33793796-0	2021	Possible roles of intestinal P-glycoprotein and cytochrome P450 3A on the limited oral absorption of irinotecan.	Irinotecan	101-111	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	29-43
33793796-0	2021	Possible roles of intestinal P-glycoprotein and cytochrome P450 3A on the limited oral absorption of irinotecan.	Irinotecan	101-111	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	48-66
33793796-6	2021	The pharmacokinetics of irinotecan was investigated when verapamil, an inhibitor of the P-glycoprotein (P-gp) and cytochrome P450 3A (CYP3A) was pre-administered.	Irinotecan	24-34	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	88-102
33793796-6	2021	The pharmacokinetics of irinotecan was investigated when verapamil, an inhibitor of the P-glycoprotein (P-gp) and cytochrome P450 3A (CYP3A) was pre-administered.	Irinotecan	24-34	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	104-108
33793796-6	2021	The pharmacokinetics of irinotecan was investigated when verapamil, an inhibitor of the P-glycoprotein (P-gp) and cytochrome P450 3A (CYP3A) was pre-administered.	Irinotecan	24-34	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	114-132
33793796-6	2021	The pharmacokinetics of irinotecan was investigated when verapamil, an inhibitor of the P-glycoprotein (P-gp) and cytochrome P450 3A (CYP3A) was pre-administered.	Irinotecan	24-34	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	134-139
33793796-7	2021	KEY FINDINGS: The intestinal absorption of irinotecan was enhanced in the presence of verapamil, indicating that efflux by intestinal P-gp contributes to its limited oral absorption.	Irinotecan	43-53	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	134-138
33793796-10	2021	CONCLUSION: The findings presented herein suggest that intestinal efflux by P-gp is mainly and intestinal metabolism by CYP3A is partially responsible for the limited oral absorption of irinotecan.	Irinotecan	186-196	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	76-80
33793796-10	2021	CONCLUSION: The findings presented herein suggest that intestinal efflux by P-gp is mainly and intestinal metabolism by CYP3A is partially responsible for the limited oral absorption of irinotecan.	Irinotecan	186-196	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	120-125
33790151-0	2021	[The Efficacy of topo I-pS10 Expression in Gastric Cancer as a Predictive Biomarker for Irinotecan Use].	Irinotecan	88-98	taste 2 receptor member 12 pseudogene	Homo sapiens	24-28
33790151-3	2021	We have developed an immunohistochemical staining-based biomarker; topo I-pS10, for predicting irinotecan efficacy.	Irinotecan	95-105	taste 2 receptor member 12 pseudogene	Homo sapiens	74-78
33790151-13	2021	CONCLUSION: topo I-pS10 staining can be used as a predictive biomarker for irinotecan for gastric cancer patients.	Irinotecan	75-85	taste 2 receptor member 12 pseudogene	Homo sapiens	19-23
34718178-6	2022	Impressively, BI@PEG-SN38 nanoparticles effectively reverse chemoresistance to CPT-11 (resistance index dropping from ~274.00-456.00 to ~1.70-4.68) and PEG-S-S-SN38 (resistance index dropping from ~5.83-14.00 to ~1.70-4.68) in three BCRP-overexpressing cancer cell lines.	Irinotecan	79-85	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	233-237
26386386-3	2015	Overexpression of a multidrug resistance (MDR) transporter ABCG2 in vitro has been shown to cause resistance to 5-fluorouracil (5-FU) and irinotecan, components of the most commonly adopted regimens for treating CRC.	Irinotecan	138-148	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	59-64
34854953-15	2022	CONCLUSION: Tlr4DeltaIEC and WT had no baseline compositional microbiome differences, but functional differences at baseline and following irinotecan.	Irinotecan	139-149	toll-like receptor 4	Mus musculus	12-24
34699766-0	2022	The PPARgamma-dependent effect of flavonoid luteolin against damage induced by the chemotherapeutic irinotecan in human intestinal cells.	Irinotecan	100-110	peroxisome proliferator activated receptor gamma	Homo sapiens	4-13
34699766-5	2022	Irinotecan downregulated PPARgamma expression and upregulated inflammatory and oxidative genes, while luteolin upregulated PPARgamma, HO-1, SOD and decreased expression of IL-1beta and iNOS.	Irinotecan	0-10	peroxisome proliferator activated receptor gamma	Homo sapiens	25-34
34699766-8	2022	The present study showed that the protective effect of luteolin against irinotecan is PPARgamma dependent.	Irinotecan	72-82	peroxisome proliferator activated receptor gamma	Homo sapiens	86-95
34968866-0	2022	Phospho-Aspirin (MDC-22) inhibits pancreatic cancer growth in patient-derived tumor xenografts and KPC mice by targeting EGFR: Enhanced efficacy in combination with irinotecan.	Irinotecan	165-175	C-C motif chemokine ligand 22	Homo sapiens	17-20
34968866-8	2022	In human pancreatic cancer cell lines, MDC-22 enhanced the growth inhibitory effect of irinotecan, and to a lesser degree those of gemcitabine and nab-paclitaxel.	Irinotecan	87-97	C-C motif chemokine ligand 22	Homo sapiens	39-42
34968866-10	2022	Furthermore, MDC-22 enhanced irinotecan"s effect on cell migration, in part, by inhibiting EGFR/FAK signaling.	Irinotecan	29-39	epidermal growth factor receptor	Homo sapiens	91-95
34968866-10	2022	Furthermore, MDC-22 enhanced irinotecan"s effect on cell migration, in part, by inhibiting EGFR/FAK signaling.	Irinotecan	29-39	protein tyrosine kinase 2	Homo sapiens	96-99
34718178-7	2022	More importantly, reversal of BCRP-mediated chemoresistance to CPT-11 (P values lower than 0.001-0.0001) and PEG-S-S-SN38 (P values lower than 0.01-0.001) by BI@PEG-SN38 nanoparticles are further confirmed with two panels of colorectal cancer xenograft models in vivo.	Irinotecan	63-69	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	30-34
34718178-10	2022	By generating panels of colorectal cancer models, we demonstrate that BI@PEG-SN38 nanoparticles effectively and selectively reversed BCRP-mediated tumor resistance to SN38/CPT-11 in vitro and in vivo.	Irinotecan	172-178	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	133-137
34689170-10	2022	CONCLUSIONS: TIMELESS rs2291739 might have different effects on therapeutic efficacy between oxaliplatin- and irinotecan-based chemotherapies.	Irinotecan	110-120	timeless circadian regulator	Homo sapiens	13-21
34700030-3	2022	METHODS: We performed next generation sequencing to study the evolution of KRAS wild-type CRC organoids during adaptation to irinotecan-based chemotherapy combined with EGFR-inhibition.	Irinotecan	125-135	KRAS proto-oncogene, GTPase	Homo sapiens	75-79
34667024-9	2022	SN-38 had the lowest IC50 (approximately 10 nM), and its pro-apoptotic effects were countered by knockdown of CEBPA but not of TP53 Irinotecan significantly inhibited tumor growth at well tolerated doses, induced nuclear expression of C/EBPalpha, and inhibited HIF1a expression in DDLS patient-derived and cancer cell line xenograft models.	Irinotecan	0-5	CCAAT enhancer binding protein alpha	Homo sapiens	110-115
34667024-9	2022	SN-38 had the lowest IC50 (approximately 10 nM), and its pro-apoptotic effects were countered by knockdown of CEBPA but not of TP53 Irinotecan significantly inhibited tumor growth at well tolerated doses, induced nuclear expression of C/EBPalpha, and inhibited HIF1a expression in DDLS patient-derived and cancer cell line xenograft models.	Irinotecan	0-5	CCAAT enhancer binding protein alpha	Homo sapiens	235-245
34667024-9	2022	SN-38 had the lowest IC50 (approximately 10 nM), and its pro-apoptotic effects were countered by knockdown of CEBPA but not of TP53 Irinotecan significantly inhibited tumor growth at well tolerated doses, induced nuclear expression of C/EBPalpha, and inhibited HIF1a expression in DDLS patient-derived and cancer cell line xenograft models.	Irinotecan	0-5	hypoxia inducible factor 1 subunit alpha	Homo sapiens	261-266
34667024-9	2022	SN-38 had the lowest IC50 (approximately 10 nM), and its pro-apoptotic effects were countered by knockdown of CEBPA but not of TP53 Irinotecan significantly inhibited tumor growth at well tolerated doses, induced nuclear expression of C/EBPalpha, and inhibited HIF1a expression in DDLS patient-derived and cancer cell line xenograft models.	Irinotecan	132-142	CCAAT enhancer binding protein alpha	Homo sapiens	235-245
34667024-9	2022	SN-38 had the lowest IC50 (approximately 10 nM), and its pro-apoptotic effects were countered by knockdown of CEBPA but not of TP53 Irinotecan significantly inhibited tumor growth at well tolerated doses, induced nuclear expression of C/EBPalpha, and inhibited HIF1a expression in DDLS patient-derived and cancer cell line xenograft models.	Irinotecan	132-142	hypoxia inducible factor 1 subunit alpha	Homo sapiens	261-266
34667024-12	2022	These include irinotecan, which induces apoptosis of DDLS cells in a C/EBPalpha-dependent, p53-independent manner and should be clinically evaluated in patients with advanced DDLS.	Irinotecan	14-24	CCAAT enhancer binding protein alpha	Homo sapiens	69-79
34667024-12	2022	These include irinotecan, which induces apoptosis of DDLS cells in a C/EBPalpha-dependent, p53-independent manner and should be clinically evaluated in patients with advanced DDLS.	Irinotecan	14-24	tumor protein p53	Homo sapiens	91-94
34860573-0	2022	All You Need to Know About UGT1A1 Genetic Testing for Patients Treated With Irinotecan: A Practitioner-Friendly Guide.	Irinotecan	76-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-33
34697081-12	2022	The use of tissue-specific humanized models expressing UGT1A1 in liver or intestine has confirmed the relevance of the intestinal tract in the detoxification of irinotecan.	Irinotecan	161-171	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	55-61
34911343-18	2022	NAT2 590G>A appears to be a potential prognostic factor for OS of SCLC patients after irinotecan therapy and 481C>T came out to be significant factor using CART.	Irinotecan	86-96	N-acetyltransferase 2	Homo sapiens	0-4
34941047-1	2021	BACKGROUND: Combined treatment with anlotinib, irinotecan, as well as vincristine for advanced Ewing sarcoma (EWS) has been verified been effective in the prospective trial of Peking University People"s Hospital EWS trial-02.	Irinotecan	47-57	EWS RNA binding protein 1	Homo sapiens	212-215
34941047-11	2021	CONCLUSION: QoL exhibited a trend towards improvement in accordance with high objective response in this trial with the receipt of combination therapy of anlotinib, vinsristine, and irinotecan for advanced EWS.	Irinotecan	182-192	EWS RNA binding protein 1	Homo sapiens	206-209
34697081-5	2022	Mice were challenged with irinotecan (CPT-11), a prodrug hydrolyzed by carboxylesterases to form the active metabolite SN-38 and detoxified by UGT1A1.	Irinotecan	26-36	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	143-149
34697081-5	2022	Mice were challenged with irinotecan (CPT-11), a prodrug hydrolyzed by carboxylesterases to form the active metabolite SN-38 and detoxified by UGT1A1.	Irinotecan	38-44	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	143-149
34697081-7	2022	When exposed to a low dose of CPT-11 (10 mg/kg), hUGT1A1HEP mice displayed greater intestinal inflammatory (IL-1beta and IL-6) insult in addition to p53-triggered apoptotic responses.	Irinotecan	30-36	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-56
34697081-7	2022	When exposed to a low dose of CPT-11 (10 mg/kg), hUGT1A1HEP mice displayed greater intestinal inflammatory (IL-1beta and IL-6) insult in addition to p53-triggered apoptotic responses.	Irinotecan	30-36	interleukin 1 alpha	Mus musculus	108-116
34697081-7	2022	When exposed to a low dose of CPT-11 (10 mg/kg), hUGT1A1HEP mice displayed greater intestinal inflammatory (IL-1beta and IL-6) insult in addition to p53-triggered apoptotic responses.	Irinotecan	30-36	interleukin 6	Mus musculus	121-125
34697081-7	2022	When exposed to a low dose of CPT-11 (10 mg/kg), hUGT1A1HEP mice displayed greater intestinal inflammatory (IL-1beta and IL-6) insult in addition to p53-triggered apoptotic responses.	Irinotecan	30-36	transformation related protein 53, pseudogene	Mus musculus	149-152
34725191-0	2022	Combination therapy of hepatocellular carcinoma by GPC3-targeted bispecific antibody and Irinotecan is potent in suppressing tumor growth in mice.	Irinotecan	89-99	glypican 3	Mus musculus	51-55
34971802-1	2022	OBJECTIVE: Intra-tumoral expression of the serine hydrolase carboxylesterase 2 (CES2) contributes to the activation of the pro-drug irinotecan in pancreatic ductal adenocarcinoma (PDAC).	Irinotecan	132-142	carboxylesterase 2H	Mus musculus	60-78
34971802-1	2022	OBJECTIVE: Intra-tumoral expression of the serine hydrolase carboxylesterase 2 (CES2) contributes to the activation of the pro-drug irinotecan in pancreatic ductal adenocarcinoma (PDAC).	Irinotecan	132-142	carboxylesterase 2H	Mus musculus	80-84
34860573-2	2022	Severe neutropenia and diarrhea are common dose-limiting toxicities of irinotecan-based therapy, and UGT1A1 polymorphisms are one of the major risk factors of these toxicities.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
34860573-3	2022	In 2005, the US Food and Drug Administration revised the drug label to indicate that patients with UGT1A1*28 homozygous genotype should receive a decreased dose of irinotecan.	Irinotecan	164-174	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
34811961-10	2021	Alkaline phosphatase (ALP), SA, and WBC counts were important predictors of survival among patients treated with second-line liposomal irinotecan.	Irinotecan	135-145	alkaline phosphatase, placental	Homo sapiens	0-20
34811961-10	2021	Alkaline phosphatase (ALP), SA, and WBC counts were important predictors of survival among patients treated with second-line liposomal irinotecan.	Irinotecan	135-145	alkaline phosphatase, placental	Homo sapiens	22-25
34894942-3	2021	Herein, we reported a novel strategy to construct highly releasable and structurally stable SN-38-conjugates, in which CTSB linkers directly connected to the 10-OH group through ether bond, not to the common 20-OH group of lactones of SN-38.	Irinotecan	92-97	cathepsin B	Homo sapiens	119-123
34651524-3	2021	Sacituzumab govitecan (IMMU-132) is an antibody drug conjugate (ADC) comprised of an active metabolite of irinotecan, SN-38, bound to a humanized monoclonal antibody which targets trophoblastic cell-surface antigen 2 (Trop-2).	Irinotecan	106-116	tumor associated calcium signal transducer 2	Homo sapiens	218-224
34075792-0	2021	Silencing of E-cadherin expression leads to increased chemosensitivity to irinotecan and oxaliplatin in colorectal cancer cell lines.	Irinotecan	74-84	cadherin 1	Homo sapiens	13-23
34651524-3	2021	Sacituzumab govitecan (IMMU-132) is an antibody drug conjugate (ADC) comprised of an active metabolite of irinotecan, SN-38, bound to a humanized monoclonal antibody which targets trophoblastic cell-surface antigen 2 (Trop-2).	Irinotecan	118-123	tumor associated calcium signal transducer 2	Homo sapiens	218-224
34887262-7	2021	We determined the efficacy of low-dose SN-38 or metformin in sensitizing unresponsive tumors to respond to anti-PD-1 therapy in a syngeneic tumor system.	Irinotecan	39-44	programmed cell death 1	Homo sapiens	112-116
34258881-0	2021	Mechanistic insights into p53-regulated cytotoxicity of combined entinostat and irinotecan against colorectal cancer cells.	Irinotecan	80-90	tumor protein p53	Homo sapiens	26-29
34887262-8	2021	We deciphered novel therapeutic mechanisms underlying the SN-38 and anti-PD-1 therapy-mediated engagement of natural killer (NK) or CD8+ T cells to infiltrate tumors and boost antitumor immunity.	Irinotecan	58-63	CD8a molecule	Homo sapiens	132-135
34887262-10	2021	Low-dose SN-38 or metformin abrogated PD-L1 protein expression, promoted FOXO3 protein level, and significantly increased the animal survival rate in syngeneic mouse tumor models.	Irinotecan	9-14	CD274 antigen	Mus musculus	38-43
34887262-10	2021	Low-dose SN-38 or metformin abrogated PD-L1 protein expression, promoted FOXO3 protein level, and significantly increased the animal survival rate in syngeneic mouse tumor models.	Irinotecan	9-14	forkhead box O3	Mus musculus	73-78
34887262-11	2021	SN-38 or metformin sensitized unresponsive tumors responding to anti-PD-1 therapy by engaging NK or CD8+ T cells to infiltrate the tumor microenvironment (TME) and secret interferon-gamma and granzyme B to kill tumors.	Irinotecan	0-5	programmed cell death 1	Mus musculus	69-73
34887262-11	2021	SN-38 or metformin sensitized unresponsive tumors responding to anti-PD-1 therapy by engaging NK or CD8+ T cells to infiltrate the tumor microenvironment (TME) and secret interferon-gamma and granzyme B to kill tumors.	Irinotecan	0-5	CD8a molecule	Homo sapiens	100-103
34887262-11	2021	SN-38 or metformin sensitized unresponsive tumors responding to anti-PD-1 therapy by engaging NK or CD8+ T cells to infiltrate the tumor microenvironment (TME) and secret interferon-gamma and granzyme B to kill tumors.	Irinotecan	0-5	interferon gamma	Homo sapiens	171-187
34887262-11	2021	SN-38 or metformin sensitized unresponsive tumors responding to anti-PD-1 therapy by engaging NK or CD8+ T cells to infiltrate the tumor microenvironment (TME) and secret interferon-gamma and granzyme B to kill tumors.	Irinotecan	0-5	granzyme B	Homo sapiens	192-202
34887262-12	2021	SN-38 suppressed the levels of c-Myc and STAT3 proteins, which controlled PD-L1 expression.	Irinotecan	0-5	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	31-36
34887262-12	2021	SN-38 suppressed the levels of c-Myc and STAT3 proteins, which controlled PD-L1 expression.	Irinotecan	0-5	signal transducer and activator of transcription 3	Mus musculus	41-46
34887262-12	2021	SN-38 suppressed the levels of c-Myc and STAT3 proteins, which controlled PD-L1 expression.	Irinotecan	0-5	CD274 antigen	Mus musculus	74-79
34887262-15	2021	CONCLUSION: We show that SN-38 or metformin can boost antitumor immunity in the TME by inhibiting c-Myc and STAT3 through FOXO3 activation.	Irinotecan	25-30	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	98-103
34887262-15	2021	CONCLUSION: We show that SN-38 or metformin can boost antitumor immunity in the TME by inhibiting c-Myc and STAT3 through FOXO3 activation.	Irinotecan	25-30	signal transducer and activator of transcription 3	Homo sapiens	108-113
34887262-15	2021	CONCLUSION: We show that SN-38 or metformin can boost antitumor immunity in the TME by inhibiting c-Myc and STAT3 through FOXO3 activation.	Irinotecan	25-30	forkhead box O3	Homo sapiens	122-127
34258881-5	2021	The topoisomerase-1 inhibitor irinotecan induces acetylation of several lysine residues within p53.	Irinotecan	30-40	transformation related protein 53, pseudogene	Mus musculus	95-98
34258881-6	2021	Inhibition of histone deacetylaces (HDACs) with the class I HDAC inhibitor entinostat synergistically triggers mitochondrial damage and apoptosis in irinotecan-treated p53-positive CRC cells.	Irinotecan	149-159	transformation related protein 53, pseudogene	Mus musculus	168-171
34847314-4	2021	Additional, well-planned trials of the UGT1A1 genotype-based approach to irinotecan therapy are predicted to reduce adverse drug events in people with the UGT1A1*28/*28 genotypes and improve treatment efficacy in the rest of the patients, which might be cost-effective.	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	39-45
34676875-0	2021	Knockdown of TRIM9 attenuates irinotecan-induced intestinal mucositis in IEC-6 cells by regulating DUSP6 expression via the P38 pathway.	Irinotecan	30-40	tripartite motif-containing 9	Rattus norvegicus	13-18
34676875-0	2021	Knockdown of TRIM9 attenuates irinotecan-induced intestinal mucositis in IEC-6 cells by regulating DUSP6 expression via the P38 pathway.	Irinotecan	30-40	dual specificity phosphatase 6	Rattus norvegicus	99-104
34676875-0	2021	Knockdown of TRIM9 attenuates irinotecan-induced intestinal mucositis in IEC-6 cells by regulating DUSP6 expression via the P38 pathway.	Irinotecan	30-40	mitogen activated protein kinase 14	Rattus norvegicus	124-127
34676875-3	2021	The present study aimed to investigate the effect of TRIM9 on irinotecan-induced intestinal mucositis in the rat intestinal epithelial cell line IEC-6.	Irinotecan	62-72	tripartite motif-containing 9	Rattus norvegicus	53-58
34676875-6	2021	Treatment with irinotecan significantly inhibited cell proliferation and induced cell apoptosis, TRIM9 expression, intestinal mucosal barrier impairment, the levels of inflammatory cytokines and P38 phosphorylation in IEC-6 cells, while the expression levels of epithelial barrier tight-junction protein ZO-1 and Claudin-4 were decreased.	Irinotecan	15-25	tripartite motif-containing 9	Rattus norvegicus	97-102
34676875-6	2021	Treatment with irinotecan significantly inhibited cell proliferation and induced cell apoptosis, TRIM9 expression, intestinal mucosal barrier impairment, the levels of inflammatory cytokines and P38 phosphorylation in IEC-6 cells, while the expression levels of epithelial barrier tight-junction protein ZO-1 and Claudin-4 were decreased.	Irinotecan	15-25	mitogen activated protein kinase 14	Rattus norvegicus	195-198
34676875-6	2021	Treatment with irinotecan significantly inhibited cell proliferation and induced cell apoptosis, TRIM9 expression, intestinal mucosal barrier impairment, the levels of inflammatory cytokines and P38 phosphorylation in IEC-6 cells, while the expression levels of epithelial barrier tight-junction protein ZO-1 and Claudin-4 were decreased.	Irinotecan	15-25	tight junction protein 1	Rattus norvegicus	304-308
34676875-6	2021	Treatment with irinotecan significantly inhibited cell proliferation and induced cell apoptosis, TRIM9 expression, intestinal mucosal barrier impairment, the levels of inflammatory cytokines and P38 phosphorylation in IEC-6 cells, while the expression levels of epithelial barrier tight-junction protein ZO-1 and Claudin-4 were decreased.	Irinotecan	15-25	claudin 4	Rattus norvegicus	313-322
34676875-7	2021	Knockdown of TRIM9 partly counteracted the effect of irinotecan treatment, and inhibition of P38 potently reversed the effect of TRIM9 overexpression in IEC-6 cells.	Irinotecan	53-63	tripartite motif-containing 9	Rattus norvegicus	13-18
34847314-4	2021	Additional, well-planned trials of the UGT1A1 genotype-based approach to irinotecan therapy are predicted to reduce adverse drug events in people with the UGT1A1*28/*28 genotypes and improve treatment efficacy in the rest of the patients, which might be cost-effective.	Irinotecan	73-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	155-161
34917992-7	2021	Conclusions: EGFR tyrosine inhibitors plus irinotecan plus cisplatin chemotherapy might be a potential treatment option for advanced pulmonary neuroendocrine neoplasms harboring EGFR mutations.	Irinotecan	43-53	epidermal growth factor receptor	Homo sapiens	178-182
34815254-8	2022	The small molecule exportin-1 inhibitor selinexor in combination with cisplatin or irinotecan dramatically inhibited tumor growth in chemonaive and chemorelapsed SCLC patient-derived xenografts, respectively.	Irinotecan	83-93	exportin 1	Homo sapiens	19-29
34794220-1	2021	Objective: To investigate the correlation between UGT1A1 polymorphisms and the irinotecan plus S-1 regimen-induced toxicities in Chinese advanced esophageal squamous cell carcinoma (ESCC) patients.	Irinotecan	79-89	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-56
34794220-5	2021	Irinotecan plus S-1 regimen-induced toxicities of patients with different UGT1A1 polymorphisms were observed.	Irinotecan	0-10	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
34830383-8	2021	We found that the phenylfurocoumarin derivative (R)-9-(3,4-dimethoxyphenyl)-4-((3,3-dimethyloxiran-2-yl)methoxy)-7H-furo (3,2-g)chromen-7-one (PFC) significantly decreased the IC50 of SN-38 in HCT-116/BCRP colon cancer cells.	Irinotecan	184-189	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	201-205
34830244-9	2021	p130Cas was inducible by 5-fluorouracil (5-FU) and FOLFIRI (folinic acid, 5-FU, irinotecan), and p130Cas and EREG were upregulated in distant metastases (GSE121418).	Irinotecan	80-90	BCAR1 scaffold protein, Cas family member	Homo sapiens	0-7
34795594-0	2021	Berberine Improves Irinotecan-Induced Intestinal Mucositis Without Impairing the Anti-colorectal Cancer Efficacy of Irinotecan by Inhibiting Bacterial beta-glucuronidase.	Irinotecan	116-126	glucuronidase beta	Homo sapiens	151-169
34474344-0	2021	LEF1 silencing sensitizes colorectal cancer cells to oxaliplatin, 5-FU, and irinotecan.	Irinotecan	76-86	lymphoid enhancer binding factor 1	Homo sapiens	0-4
34327766-0	2021	Impact of UGT1A1 Genotype on the Efficacy and Safety of Irinotecan-based Chemotherapy in Metastatic Colorectal Cancer.	Irinotecan	56-66	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	10-16
34327766-2	2021	We evaluated the associations between the UGT1A1 genotype linked to adverse events - caused by irinotecan - and the efficacy and safety of mXELIRI and FOLFIRI.	Irinotecan	95-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-48
34536357-6	2021	CES2 mRNA level was significantly increased by double knockdown of METTL3 and METTL14 but was decreased by knockdown of FTO or ALKBH5 in HepaRG and HepG2 cells, leading to changes in its protein level and hydrolase activity for 7-ethyl-10-(4-(1-piperidino)-1-piperidino)carbonyloxycamptothecin (CPT-11), suggesting that m6A modification negatively regulates CES2 expression.	Irinotecan	228-293	carboxylesterase 2	Homo sapiens	0-4
34536357-6	2021	CES2 mRNA level was significantly increased by double knockdown of METTL3 and METTL14 but was decreased by knockdown of FTO or ALKBH5 in HepaRG and HepG2 cells, leading to changes in its protein level and hydrolase activity for 7-ethyl-10-(4-(1-piperidino)-1-piperidino)carbonyloxycamptothecin (CPT-11), suggesting that m6A modification negatively regulates CES2 expression.	Irinotecan	228-293	methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit	Homo sapiens	67-73
34536357-6	2021	CES2 mRNA level was significantly increased by double knockdown of METTL3 and METTL14 but was decreased by knockdown of FTO or ALKBH5 in HepaRG and HepG2 cells, leading to changes in its protein level and hydrolase activity for 7-ethyl-10-(4-(1-piperidino)-1-piperidino)carbonyloxycamptothecin (CPT-11), suggesting that m6A modification negatively regulates CES2 expression.	Irinotecan	228-293	methyltransferase 14, N6-adenosine-methyltransferase subunit	Homo sapiens	78-85
34536357-6	2021	CES2 mRNA level was significantly increased by double knockdown of METTL3 and METTL14 but was decreased by knockdown of FTO or ALKBH5 in HepaRG and HepG2 cells, leading to changes in its protein level and hydrolase activity for 7-ethyl-10-(4-(1-piperidino)-1-piperidino)carbonyloxycamptothecin (CPT-11), suggesting that m6A modification negatively regulates CES2 expression.	Irinotecan	228-293	FTO alpha-ketoglutarate dependent dioxygenase	Homo sapiens	120-123
34536357-6	2021	CES2 mRNA level was significantly increased by double knockdown of METTL3 and METTL14 but was decreased by knockdown of FTO or ALKBH5 in HepaRG and HepG2 cells, leading to changes in its protein level and hydrolase activity for 7-ethyl-10-(4-(1-piperidino)-1-piperidino)carbonyloxycamptothecin (CPT-11), suggesting that m6A modification negatively regulates CES2 expression.	Irinotecan	228-293	alkB homolog 5, RNA demethylase	Homo sapiens	127-133
34536357-6	2021	CES2 mRNA level was significantly increased by double knockdown of METTL3 and METTL14 but was decreased by knockdown of FTO or ALKBH5 in HepaRG and HepG2 cells, leading to changes in its protein level and hydrolase activity for 7-ethyl-10-(4-(1-piperidino)-1-piperidino)carbonyloxycamptothecin (CPT-11), suggesting that m6A modification negatively regulates CES2 expression.	Irinotecan	295-301	carboxylesterase 2	Homo sapiens	0-4
34536357-6	2021	CES2 mRNA level was significantly increased by double knockdown of METTL3 and METTL14 but was decreased by knockdown of FTO or ALKBH5 in HepaRG and HepG2 cells, leading to changes in its protein level and hydrolase activity for 7-ethyl-10-(4-(1-piperidino)-1-piperidino)carbonyloxycamptothecin (CPT-11), suggesting that m6A modification negatively regulates CES2 expression.	Irinotecan	295-301	methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit	Homo sapiens	67-73
34536357-6	2021	CES2 mRNA level was significantly increased by double knockdown of METTL3 and METTL14 but was decreased by knockdown of FTO or ALKBH5 in HepaRG and HepG2 cells, leading to changes in its protein level and hydrolase activity for 7-ethyl-10-(4-(1-piperidino)-1-piperidino)carbonyloxycamptothecin (CPT-11), suggesting that m6A modification negatively regulates CES2 expression.	Irinotecan	295-301	methyltransferase 14, N6-adenosine-methyltransferase subunit	Homo sapiens	78-85
34536357-6	2021	CES2 mRNA level was significantly increased by double knockdown of METTL3 and METTL14 but was decreased by knockdown of FTO or ALKBH5 in HepaRG and HepG2 cells, leading to changes in its protein level and hydrolase activity for 7-ethyl-10-(4-(1-piperidino)-1-piperidino)carbonyloxycamptothecin (CPT-11), suggesting that m6A modification negatively regulates CES2 expression.	Irinotecan	295-301	FTO alpha-ketoglutarate dependent dioxygenase	Homo sapiens	120-123
34536357-6	2021	CES2 mRNA level was significantly increased by double knockdown of METTL3 and METTL14 but was decreased by knockdown of FTO or ALKBH5 in HepaRG and HepG2 cells, leading to changes in its protein level and hydrolase activity for 7-ethyl-10-(4-(1-piperidino)-1-piperidino)carbonyloxycamptothecin (CPT-11), suggesting that m6A modification negatively regulates CES2 expression.	Irinotecan	295-301	alkB homolog 5, RNA demethylase	Homo sapiens	127-133
34536357-6	2021	CES2 mRNA level was significantly increased by double knockdown of METTL3 and METTL14 but was decreased by knockdown of FTO or ALKBH5 in HepaRG and HepG2 cells, leading to changes in its protein level and hydrolase activity for 7-ethyl-10-(4-(1-piperidino)-1-piperidino)carbonyloxycamptothecin (CPT-11), suggesting that m6A modification negatively regulates CES2 expression.	Irinotecan	295-301	carboxylesterase 2	Homo sapiens	358-362
34474344-10	2021	In summary, we showed the role of LEF1 in chemo-resistance of colorectal cancer cells to Oxaliplatin, Irinotecan and 5-FU.	Irinotecan	102-112	lymphoid enhancer binding factor 1	Homo sapiens	34-38
34703007-5	2022	RESULTS: Irinotecan clearance was influenced by rs4149057 in SLCO1B1, body surface area, and co-administration of 5-fluorouracil/leucovorin/bevacizumab.	Irinotecan	9-19	solute carrier organic anion transporter family member 1B1	Homo sapiens	61-68
34365218-5	2021	Further, majority of the non-platinum drugs except irinotecan increased ERK1/2 activation in platinum-taxol resistant cells as observed by live-cell BRET assessment which were associated with p90RSK1/2 and BAD activation along with upregulation of multidrug transporter gene ABCC1 and cell survival genes like cyclin D1 and Bcl2.	Irinotecan	51-61	mitogen-activated protein kinase 3	Homo sapiens	72-78
34365218-5	2021	Further, majority of the non-platinum drugs except irinotecan increased ERK1/2 activation in platinum-taxol resistant cells as observed by live-cell BRET assessment which were associated with p90RSK1/2 and BAD activation along with upregulation of multidrug transporter gene ABCC1 and cell survival genes like cyclin D1 and Bcl2.	Irinotecan	51-61	ribosomal protein S6 kinase A1	Homo sapiens	192-201
34365218-5	2021	Further, majority of the non-platinum drugs except irinotecan increased ERK1/2 activation in platinum-taxol resistant cells as observed by live-cell BRET assessment which were associated with p90RSK1/2 and BAD activation along with upregulation of multidrug transporter gene ABCC1 and cell survival genes like cyclin D1 and Bcl2.	Irinotecan	51-61	ATP binding cassette subfamily C member 1	Homo sapiens	275-280
34365218-5	2021	Further, majority of the non-platinum drugs except irinotecan increased ERK1/2 activation in platinum-taxol resistant cells as observed by live-cell BRET assessment which were associated with p90RSK1/2 and BAD activation along with upregulation of multidrug transporter gene ABCC1 and cell survival genes like cyclin D1 and Bcl2.	Irinotecan	51-61	cyclin D1	Homo sapiens	310-319
34365218-5	2021	Further, majority of the non-platinum drugs except irinotecan increased ERK1/2 activation in platinum-taxol resistant cells as observed by live-cell BRET assessment which were associated with p90RSK1/2 and BAD activation along with upregulation of multidrug transporter gene ABCC1 and cell survival genes like cyclin D1 and Bcl2.	Irinotecan	51-61	BCL2 apoptosis regulator	Homo sapiens	324-328
34703007-6	2022	SN-38 clearance was influenced by rs887829 in UGT1A1, pre-treatment total bilirubin, and EGFR rare variant burden.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	46-52
34703007-6	2022	SN-38 clearance was influenced by rs887829 in UGT1A1, pre-treatment total bilirubin, and EGFR rare variant burden.	Irinotecan	0-5	epidermal growth factor receptor	Homo sapiens	89-93
34703007-7	2022	Within each UGT1A1 genotype group, elevated pre-treatment total bilirubin and/or presence of at least one rare variant in EGFR resulted in significantly lower SN-38 clearance.	Irinotecan	159-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
34703007-7	2022	Within each UGT1A1 genotype group, elevated pre-treatment total bilirubin and/or presence of at least one rare variant in EGFR resulted in significantly lower SN-38 clearance.	Irinotecan	159-164	epidermal growth factor receptor	Homo sapiens	122-126
34216140-9	2021	Mice injected with irinotecan presented systemic bacterial translocation and increased TLR4 immunostaining in the intestine.	Irinotecan	19-29	toll-like receptor 4	Mus musculus	87-91
34680166-4	2021	The major constituent in this fraction was isolated and found to be 5,3",5"-trihydroxy-3,6,7,4"-tetramethoxyflavone (2), which at a concentration of 25 mug/mL potentiated the growth-inhibitory activity of SN-38 to a degree comparable to that of the known BCRP inhibitor Ko143 at 1 muM.	Irinotecan	205-210	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	255-259
34680166-5	2021	A dye accumulation experiment suggested that 2 inhibits BCRP, and docking studies showed that 2 binds to the same BCRP site as SN-38.	Irinotecan	127-132	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	56-60
34680166-5	2021	A dye accumulation experiment suggested that 2 inhibits BCRP, and docking studies showed that 2 binds to the same BCRP site as SN-38.	Irinotecan	127-132	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	114-118
34680166-6	2021	These results indicate that 2 acts synergistically with SN-38, with 2 being a BCRP efflux pump inhibitor while SN-38 inhibits topoisomerase-1.	Irinotecan	56-61	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	78-82
34216140-10	2021	In line with the clinical findings, Tlr4 gene deficiency enhanced irinotecan-related diarrhea and TLR9 expression in mice.	Irinotecan	66-76	toll-like receptor 4	Mus musculus	36-40
34216140-11	2021	An increased myeloperoxidase activity and Il-18 expression (2.5-fold change) along with IL-10 decreased production in Tlr4-/- mice (P<0.05 vs. irinotecan-treated WT group) indicated boosted intestinal damage and inflammatory response.	Irinotecan	143-153	myeloperoxidase	Mus musculus	13-28
34216140-11	2021	An increased myeloperoxidase activity and Il-18 expression (2.5-fold change) along with IL-10 decreased production in Tlr4-/- mice (P<0.05 vs. irinotecan-treated WT group) indicated boosted intestinal damage and inflammatory response.	Irinotecan	143-153	interleukin 18	Mus musculus	42-47
34216140-11	2021	An increased myeloperoxidase activity and Il-18 expression (2.5-fold change) along with IL-10 decreased production in Tlr4-/- mice (P<0.05 vs. irinotecan-treated WT group) indicated boosted intestinal damage and inflammatory response.	Irinotecan	143-153	interleukin 10	Mus musculus	88-93
34486919-4	2021	Furthermore, prospective trials have shown that patients harboring the UGT1A1 *1/*1 and *1/*28 genotypes can tolerate higher doses of irinotecan, which may in turn impact on a better outcome.	Irinotecan	134-144	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	71-77
34486919-5	2021	Upfront UGT1A1 genotyping could therefore be a usefulness strategy in order to individualize irinotecan dosing, but consensus on the recommended dose based on the UGT1A1 genotype is still lacking.	Irinotecan	93-103	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	8-14
34486919-8	2021	EXPERT OPINION: Implementation of UGT1A1*28 and UGT1A1*6 genotyping in clinical practice is a first step toward personalizing irinotecan therapy.	Irinotecan	126-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	34-40
34486919-8	2021	EXPERT OPINION: Implementation of UGT1A1*28 and UGT1A1*6 genotyping in clinical practice is a first step toward personalizing irinotecan therapy.	Irinotecan	126-136	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
34176192-8	2021	IMPLICATIONS FOR PRACTICE: Sacituzumab govitecan (TRODELVY) is a novel antibody-drug conjugate composed of the active metabolite of irinotecan (SN-38) conjugated to a monoclonal antibody targeting Trop-2, an epithelial cell surface antigen overexpressed in many cancers.	Irinotecan	144-149	tumor associated calcium signal transducer 2	Homo sapiens	197-203
34641401-5	2021	When synergy was observed, for example with curcumin and irinotecan, this was unrelated to MET induction, as assessed by changes in E-cadherin and vimentin expression.	Irinotecan	57-67	cadherin 1	Homo sapiens	132-142
34176192-2	2021	Sacituzumab govitecan (IMMU-132) is an antibody-drug conjugate that contains the irinotecan active metabolite, SN-38, linked to a humanized monoclonal antibody targeting trophoblast cell surface antigen 2 (Trop-2), which is overexpressed in many solid tumors.	Irinotecan	111-116	tumor associated calcium signal transducer 2	Homo sapiens	206-212
34176192-8	2021	IMPLICATIONS FOR PRACTICE: Sacituzumab govitecan (TRODELVY) is a novel antibody-drug conjugate composed of the active metabolite of irinotecan (SN-38) conjugated to a monoclonal antibody targeting Trop-2, an epithelial cell surface antigen overexpressed in many cancers.	Irinotecan	132-142	tumor associated calcium signal transducer 2	Homo sapiens	197-203
34528449-3	2021	Results: A novel cis-eQTL, rs28967009, was identified for UGT1A1, which is predicted to upregulate UGT1A1 expression thereby potentially affecting the metabolism of dolutegravir and irinotecan, which are extensively prescribed in SA for HIV and colorectal cancer treatment, respectively.	Irinotecan	182-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
34528449-3	2021	Results: A novel cis-eQTL, rs28967009, was identified for UGT1A1, which is predicted to upregulate UGT1A1 expression thereby potentially affecting the metabolism of dolutegravir and irinotecan, which are extensively prescribed in SA for HIV and colorectal cancer treatment, respectively.	Irinotecan	182-192	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
34528449-4	2021	Conclusion: As increased UGT1A1 expression could affect the clinical outcome of dolutegravir and irinotecan treatment by increasing drug clearance, patients with the rs28967009A variant may require increased drug doses to reach therapeutic levels or should be prescribed alternative drugs.	Irinotecan	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
34641401-5	2021	When synergy was observed, for example with curcumin and irinotecan, this was unrelated to MET induction, as assessed by changes in E-cadherin and vimentin expression.	Irinotecan	57-67	vimentin	Homo sapiens	147-155
34504265-9	2021	Both irinotecan and SN38 led to a global downregulation of genes involved in fibrosis such as COL1A1, COL1A2, MMP1 and ACTA2 in dermal fibroblasts from SSc patients (respectively - 27; - 20.5; - 30.2 and - 30% for irinotecan and - 61; - 55; - 50 and - 54% for SN38).	Irinotecan	5-15	collagen type I alpha 1 chain	Homo sapiens	94-100
34572902-5	2021	VKNG-1, at 6 microM, selectively inhibited ABCG2 transporter and sensitized ABCG2-overexpressing drug-resistant cancer cells to the ABCG2 substrate anticancer drugs mitoxantrone, SN-38, and doxorubicin in ABCG2-overexpressing colon cancers.	Irinotecan	179-184	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	76-81
34572902-5	2021	VKNG-1, at 6 microM, selectively inhibited ABCG2 transporter and sensitized ABCG2-overexpressing drug-resistant cancer cells to the ABCG2 substrate anticancer drugs mitoxantrone, SN-38, and doxorubicin in ABCG2-overexpressing colon cancers.	Irinotecan	179-184	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	132-137
34572902-9	2021	In addition, VKNG-1 enhanced the anticancer efficacy of irinotecan in ABCG2- overexpressing mouse tumor xenografts.	Irinotecan	56-66	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	70-75
34504265-9	2021	Both irinotecan and SN38 led to a global downregulation of genes involved in fibrosis such as COL1A1, COL1A2, MMP1 and ACTA2 in dermal fibroblasts from SSc patients (respectively - 27; - 20.5; - 30.2 and - 30% for irinotecan and - 61; - 55; - 50 and - 54% for SN38).	Irinotecan	5-15	collagen type I alpha 2 chain	Homo sapiens	102-108
34504265-9	2021	Both irinotecan and SN38 led to a global downregulation of genes involved in fibrosis such as COL1A1, COL1A2, MMP1 and ACTA2 in dermal fibroblasts from SSc patients (respectively - 27; - 20.5; - 30.2 and - 30% for irinotecan and - 61; - 55; - 50 and - 54% for SN38).	Irinotecan	5-15	matrix metallopeptidase 1	Homo sapiens	110-114
34504265-9	2021	Both irinotecan and SN38 led to a global downregulation of genes involved in fibrosis such as COL1A1, COL1A2, MMP1 and ACTA2 in dermal fibroblasts from SSc patients (respectively - 27; - 20.5; - 30.2 and - 30% for irinotecan and - 61; - 55; - 50 and - 54% for SN38).	Irinotecan	5-15	actin alpha 2, smooth muscle	Homo sapiens	119-124
34572750-9	2021	Nine patients with toxicity-associated pharmacogenomic variants were treated with a relevant medication: seven UGT1A1 intermediate metabolizers were treated with irinotecan, one intermediate DPYD metabolizer was treated with 5-fluorouracil, and one TPMT poor metabolizer was treated with mercaptopurine.	Irinotecan	162-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	111-117
34572750-11	2021	One UGT1A1 heterozygote died after a single dose of irinotecan due to irinotecan-related adverse effects.	Irinotecan	52-62	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
34337875-8	2021	The level of AURKA was significantly associated with the resistance to SB 505124, NU-7441, and irinotecan drugs (p < 0.01).	Irinotecan	95-105	aurora kinase A	Homo sapiens	13-18
34572750-11	2021	One UGT1A1 heterozygote died after a single dose of irinotecan due to irinotecan-related adverse effects.	Irinotecan	70-80	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	4-10
34116144-1	2021	BACKGROUND: The pivotal phase III ASCENT trial demonstrated improved survival outcomes associated with sacituzumab govitecan (SG), an anti-Trop-2 antibody-drug conjugate linked with the topoisomerase-inhibitor SN-38, over single-agent chemotherapy of physician"s choice (TPC) in previously-treated metastatic triple-negative breast cancer (mTNBC).	Irinotecan	210-215	tumor associated calcium signal transducer 2	Homo sapiens	139-145
34117512-1	2021	PURPOSE: SN-38, a pharmacologically active metabolite of irinotecan, is taken up into hepatocytes by organic anion transporting polypeptide (OATP) 1B1.	Irinotecan	9-14	solute carrier organic anion transporter family member 1B1	Homo sapiens	101-150
34117512-1	2021	PURPOSE: SN-38, a pharmacologically active metabolite of irinotecan, is taken up into hepatocytes by organic anion transporting polypeptide (OATP) 1B1.	Irinotecan	57-67	solute carrier organic anion transporter family member 1B1	Homo sapiens	101-150
34117512-2	2021	The effects of functional OATP1B1 521T>C on the pharmacokinetics of SN-38 remain controversial.	Irinotecan	68-73	solute carrier organic anion transporter family member 1B1	Homo sapiens	26-33
34117512-3	2021	Here, we prospectively examined the effects of OATP1B1 function on the area under the plasma total or unbound concentration-time curve (tAUC or uAUC) of SN-38 by assessing OATP1B1 521T>C and the plasma levels of endogenous OATP1B1 substrates, coproporphyrin (CP)-I and III, in cancer patients treated with irinotecan.	Irinotecan	153-158	solute carrier organic anion transporter family member 1B1	Homo sapiens	47-54
34117512-3	2021	Here, we prospectively examined the effects of OATP1B1 function on the area under the plasma total or unbound concentration-time curve (tAUC or uAUC) of SN-38 by assessing OATP1B1 521T>C and the plasma levels of endogenous OATP1B1 substrates, coproporphyrin (CP)-I and III, in cancer patients treated with irinotecan.	Irinotecan	153-158	solute carrier organic anion transporter family member 1B1	Homo sapiens	172-179
34117512-12	2021	CONCLUSION: The contribution of OATP1B1 activity to inter-patient variability in the systemic exposure to SN-38 is likely minimal in patients without severe renal failure.	Irinotecan	106-111	solute carrier organic anion transporter family member 1B1	Homo sapiens	32-39
34502348-4	2021	In this study, we discovered that by attenuating the drug transport function of ABCG2, TP-3654 resensitizes ABCG2-overexpressing multidrug-resistant cancer cells to cytotoxic ABCG2 substrate drugs topotecan, SN-38 and mitoxantrone.	Irinotecan	208-213	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	80-85
34502348-4	2021	In this study, we discovered that by attenuating the drug transport function of ABCG2, TP-3654 resensitizes ABCG2-overexpressing multidrug-resistant cancer cells to cytotoxic ABCG2 substrate drugs topotecan, SN-38 and mitoxantrone.	Irinotecan	208-213	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	108-113
34526906-0	2021	Corrigendum: 7-Ethyl-10-Hydroxycamptothecin, A DNA Topoisomerase I Inhibitor, Performs BRD4 Inhibitory Activity and Inhibits Human Leukemic Cell Growth.	Irinotecan	13-43	bromodomain containing 4	Homo sapiens	87-91
34502348-4	2021	In this study, we discovered that by attenuating the drug transport function of ABCG2, TP-3654 resensitizes ABCG2-overexpressing multidrug-resistant cancer cells to cytotoxic ABCG2 substrate drugs topotecan, SN-38 and mitoxantrone.	Irinotecan	208-213	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	175-180
34408079-6	2021	We demonstrated that induction of telomere dysfunction resulted in ATM activation that, in turn, conferred resistance to temozolomide + SN-38 (4.2-fold change in IC50, P < 0.001).	Irinotecan	136-141	ataxia telangiectasia mutated	Mus musculus	67-70
34408079-7	2021	ATM knockdown (shRNA) or inhibition using a clinical-stage small-molecule inhibitor (AZD0156) reversed resistance to temozolomide + irinotecan in ALT neuroblastoma cell lines in vitro (P < 0.001) and in four ALT xenografts in vivo (EFS, P < 0.0001).	Irinotecan	132-142	ataxia telangiectasia mutated	Mus musculus	0-3
34281853-3	2021	PATIENTS AND METHODS: We retrospectively collected the clinical data of KRAS exon 2 wild type (WT) mCRC patients treated with EGFR inhibitor monotherapy or EGFR inhibitor plus irinotecan as third-line chemotherapy.	Irinotecan	176-186	KRAS proto-oncogene, GTPase	Homo sapiens	72-76
34300575-6	2021	All three TDP1 inhibitors had no effect on TOP1 activity and acted synergistically with the TOP1 poison SN-38 to increase the amount of TOP1 cleavage-induced DNA damage.	Irinotecan	104-109	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	10-14
34300575-6	2021	All three TDP1 inhibitors had no effect on TOP1 activity and acted synergistically with the TOP1 poison SN-38 to increase the amount of TOP1 cleavage-induced DNA damage.	Irinotecan	104-109	DNA topoisomerase I	Homo sapiens	92-96
34300575-6	2021	All three TDP1 inhibitors had no effect on TOP1 activity and acted synergistically with the TOP1 poison SN-38 to increase the amount of TOP1 cleavage-induced DNA damage.	Irinotecan	104-109	DNA topoisomerase I	Homo sapiens	136-140
34300575-7	2021	Further, they promoted cell death even with low dose SN-38, thereby establishing two new classes of TDP1 inhibitors with clinical potential.	Irinotecan	53-58	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	100-104
34201500-8	2021	Interestingly, shortly after engraftment, Irinotecan completely blocked leukemia expansion in mouse xenografts of a pediatric MLL-rearranged ALL cell line, as well as in two patient-derived xenograft (PDX) models of MLL-rearranged infant ALL.	Irinotecan	42-52	lysine (K)-specific methyltransferase 2A	Mus musculus	126-129
34193275-2	2021	Recently, we have reported that CPT-11-induced gastrointestinal damage is associated with the upregulation of intestinal P-glycoprotein (P-gp) expression and decreased absorption of its substrate, dabigatran etexilate (DABE), using a rat model.	Irinotecan	32-38	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	121-135
34193275-2	2021	Recently, we have reported that CPT-11-induced gastrointestinal damage is associated with the upregulation of intestinal P-glycoprotein (P-gp) expression and decreased absorption of its substrate, dabigatran etexilate (DABE), using a rat model.	Irinotecan	32-38	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	137-141
34193275-4	2021	The aim of this study was to quantitatively evaluate how P-gp activity changes in rats with CPT-11-induced gastrointestinal damage, as assessed by the absorption of digoxin (DGX), a typical P-gp substrate.	Irinotecan	92-98	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	57-61
34193275-4	2021	The aim of this study was to quantitatively evaluate how P-gp activity changes in rats with CPT-11-induced gastrointestinal damage, as assessed by the absorption of digoxin (DGX), a typical P-gp substrate.	Irinotecan	92-98	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	190-194
34193275-11	2021	CONCLUSIONS: Increased P-gp expression in rats with CPT-11-induced gastrointestinal damage is not necessarily associated with increased P-gp activity or contribution to the drug absorption in vivo.	Irinotecan	52-58	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	23-27
34201500-9	2021	Also, from a more clinically relevant perspective, Irinotecan monotherapy was able to induce sustainable disease remissions in MLL-rearranged ALL xenotransplanted mice burdened with advanced leukemia.	Irinotecan	51-61	lysine (K)-specific methyltransferase 2A	Mus musculus	127-130
34201500-10	2021	Taken together, our data demonstrate that Irinotecan exerts highly potent anti-leukemia effects against pediatric MLL-rearranged ALL, and likely against other, more favorable subtypes of childhood ALL as well.	Irinotecan	42-52	lysine (K)-specific methyltransferase 2A	Mus musculus	114-117
34212047-10	2021	Results: FXYD6 was downregulated in CRC resistant patients and irinotecan- (Iri-) resistant SW620 cells (SW620/Iri).	Irinotecan	63-73	FXYD domain containing ion transport regulator 6	Homo sapiens	9-14
34212047-11	2021	FXYD6 silence inhibited cell apoptosis and enhanced prosurvival autophagy, whereas FXYD6 overexpression produced the opposite effect which alleviated the drug resistance to irinotecan and oxaliplatin of CRC cells.	Irinotecan	173-183	FXYD domain containing ion transport regulator 6	Homo sapiens	0-5
34212047-11	2021	FXYD6 silence inhibited cell apoptosis and enhanced prosurvival autophagy, whereas FXYD6 overexpression produced the opposite effect which alleviated the drug resistance to irinotecan and oxaliplatin of CRC cells.	Irinotecan	173-183	FXYD domain containing ion transport regulator 6	Homo sapiens	83-88
34201243-3	2021	The aim of this study was to evaluate the repositioning of the anti-cancer molecule irinotecan as a potential modulator of the antiviral and inflammatory responses of primary human synovial fibroblasts (HSF), the main stromal cells of the joint synovium.	Irinotecan	84-94	interleukin 6	Homo sapiens	203-206
34201243-6	2021	Quantitative RT-PCR analysis revealed that irinotecan at 15 microM was able to amplify the antiviral response (i.e., interferon-stimulated gene expression) of HSF exposed to PIC and reduce the expression of pro-inflammatory genes (CXCL8, IL-6 and COX-2) upon IL-1beta treatment.	Irinotecan	43-53	interleukin 6	Homo sapiens	159-162
34201243-6	2021	Quantitative RT-PCR analysis revealed that irinotecan at 15 microM was able to amplify the antiviral response (i.e., interferon-stimulated gene expression) of HSF exposed to PIC and reduce the expression of pro-inflammatory genes (CXCL8, IL-6 and COX-2) upon IL-1beta treatment.	Irinotecan	43-53	C-X-C motif chemokine ligand 8	Homo sapiens	231-236
34201243-6	2021	Quantitative RT-PCR analysis revealed that irinotecan at 15 microM was able to amplify the antiviral response (i.e., interferon-stimulated gene expression) of HSF exposed to PIC and reduce the expression of pro-inflammatory genes (CXCL8, IL-6 and COX-2) upon IL-1beta treatment.	Irinotecan	43-53	interleukin 6	Homo sapiens	238-242
34201243-6	2021	Quantitative RT-PCR analysis revealed that irinotecan at 15 microM was able to amplify the antiviral response (i.e., interferon-stimulated gene expression) of HSF exposed to PIC and reduce the expression of pro-inflammatory genes (CXCL8, IL-6 and COX-2) upon IL-1beta treatment.	Irinotecan	43-53	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	247-252
34201243-6	2021	Quantitative RT-PCR analysis revealed that irinotecan at 15 microM was able to amplify the antiviral response (i.e., interferon-stimulated gene expression) of HSF exposed to PIC and reduce the expression of pro-inflammatory genes (CXCL8, IL-6 and COX-2) upon IL-1beta treatment.	Irinotecan	43-53	interleukin 1 alpha	Homo sapiens	259-267
34268956-1	2021	PURPOSE: The purpose of this study was to compare the clinical efficacy and safety of S-1 + oxaliplatin (SOX) chemotherapy regimen combined with trastuzumab and irinotecan + cisplatin (IP) chemotherapy regimen combined with trastuzumab in treating human epidermal growth factor receptor 2 (HER-2)-positive advanced gastric cancer.	Irinotecan	161-171	erb-b2 receptor tyrosine kinase 2	Homo sapiens	254-288
34084136-1	2021	Human carboxylesterase 2 (CES2), one of the most abundant hydrolases distributed in the small intestine, has been validated as a key therapeutic target to ameliorate the intestinal toxicity caused by irinotecan.	Irinotecan	200-210	carboxylesterase 2	Homo sapiens	6-24
34268956-1	2021	PURPOSE: The purpose of this study was to compare the clinical efficacy and safety of S-1 + oxaliplatin (SOX) chemotherapy regimen combined with trastuzumab and irinotecan + cisplatin (IP) chemotherapy regimen combined with trastuzumab in treating human epidermal growth factor receptor 2 (HER-2)-positive advanced gastric cancer.	Irinotecan	161-171	erb-b2 receptor tyrosine kinase 2	Homo sapiens	290-295
35415893-2	2022	The aim of this clinical study was to evaluate the safety, efficacy and pharmacokinetics of a novel regimen comprised of metronomic oxaliplatin (O), chronomodulated capecitabine (X) and UGT1A1 genotype-guided dosing of irinotecan (IRI) (OXIRI) as well as its immunomodulatory effects.	Irinotecan	219-229	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	186-192
35415893-7	2022	UGT1A1-genotype directed dosing resulted in similar exposure levels of irinotecan, SN-38 and SN-38G in all patients.	Irinotecan	71-81	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
35415893-7	2022	UGT1A1-genotype directed dosing resulted in similar exposure levels of irinotecan, SN-38 and SN-38G in all patients.	Irinotecan	83-88	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
35579261-0	2022	Targeted delivery of irinotecan and SLP2 shRNA with GRP-conjugated magnetic graphene oxide for glioblastoma treatment.	Irinotecan	21-31	gastrin releasing peptide	Homo sapiens	52-55
35624189-4	2022	In this research, MMAE, SN-38, and DXd were selected as candidates for payloads of the anti-Trop-2 mAb SY02.	Irinotecan	24-29	tumor associated calcium signal transducer 2	Homo sapiens	92-98
35430260-9	2022	We identified that bile excretion and UDP-glucuronosyltransferases (UGT) played more important roles than fecal excretion and renal clearance in SN-38 pharmacokinetics.	Irinotecan	145-150	beta-1,3-glucuronyltransferase 2 (glucuronosyltransferase S)	Mus musculus	38-66
35430260-9	2022	We identified that bile excretion and UDP-glucuronosyltransferases (UGT) played more important roles than fecal excretion and renal clearance in SN-38 pharmacokinetics.	Irinotecan	145-150	beta-1,3-glucuronyltransferase 2 (glucuronosyltransferase S)	Mus musculus	68-71
35637361-1	2022	BACKGROUND: UGT1A1 polymorphisms should be considered when using irinotecan-containing regimens, especially in patients with a double-variant-type (DV), including homozygous for UGT1A1*28 and UGT1A1*6 and heterozygous for both UGT1A1*28 and UGT1A1*6.	Irinotecan	65-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
35545724-1	2022	PURPOSE: Sacituzumab govitecan (SG) is an antibody-drug conjugate composed of an anti-Trop-2 antibody coupled to SN-38 via a proprietary hydrolyzable linker.	Irinotecan	113-118	tumor associated calcium signal transducer 2	Homo sapiens	86-92
35506159-0	2022	Association of UGT1A1*6,*28 or ABCC2 c.3972C>T genetic polymorphisms with irinotecan induced toxicity in Asian cancer patients: Meta-analysis.	Irinotecan	74-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
35177165-1	2022	Uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) polymorphism plays a crucial role in the increased susceptibility and toxicity of patients to irinotecan.	Irinotecan	151-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-47
35177165-1	2022	Uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) polymorphism plays a crucial role in the increased susceptibility and toxicity of patients to irinotecan.	Irinotecan	151-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	49-55
35177165-2	2022	This retrospective, observational study compared the clinical outcomes and adverse events (AEs) in RAS wild-type metastatic colorectal cancer (mCRC) patients treated with cetuximab or bevacizumab plus FOLFIRI with UGT1A1 genotyping and irinotecan dose escalation as the first-line therapy.	Irinotecan	236-246	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	214-220
35177165-5	2022	All patients received irinotecan dose escalation based on UGT1A1 genotyping.	Irinotecan	22-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64
35177165-10	2022	Our results revealed that patients with wild-type RAS mCRC, regardless of biologics, with UGT1A1 genotyping can tolerate escalated doses of irinotecan and potentially achieve a more favorable clinical outcome without significantly increased toxicity.	Irinotecan	140-150	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	90-96
35628140-5	2022	Using a unique transgenic mouse (FAT-1) model combined with dietary supplementation experiments, we demonstrate that an elevated tissue n-3 PUFA status with a decreased n-6/n-3 PUFA ratio significantly reduces CPT-11-induced weight loss, bloody diarrhea, gut pathological changes, and mortality.	Irinotecan	210-216	FAT atypical cadherin 1	Mus musculus	33-38
35506159-0	2022	Association of UGT1A1*6,*28 or ABCC2 c.3972C>T genetic polymorphisms with irinotecan induced toxicity in Asian cancer patients: Meta-analysis.	Irinotecan	74-84	ATP binding cassette subfamily C member 2	Homo sapiens	31-36
35506159-2	2022	Also, ABCC2 c.3972C>T may affect toxicity of irinotecan.	Irinotecan	45-55	ATP binding cassette subfamily C member 2	Homo sapiens	6-11
35592314-16	2022	Finally, specific inhibitors, like irinotecan and puromycin, which correlate with SPA17 expression in different cancer types, were also screened using Connectivity Map (CMap).	Irinotecan	35-45	sperm autoantigenic protein 17	Homo sapiens	82-87
35506159-3	2022	It was aimed to assess the aggregated risk of neutropenia or diarrhea in Asian cancer patients taking irinotecan and inherited UGT1A1*6, UGT1A1*28 or ABCC2 c.3972C>T genetic variants.	Irinotecan	102-112	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143
35506159-3	2022	It was aimed to assess the aggregated risk of neutropenia or diarrhea in Asian cancer patients taking irinotecan and inherited UGT1A1*6, UGT1A1*28 or ABCC2 c.3972C>T genetic variants.	Irinotecan	102-112	ATP binding cassette subfamily C member 2	Homo sapiens	150-155
35506159-9	2022	Both UGT1A1*6 and UGT1A1*28 genetic variants should be screened in Asian cancer patients to reduce substantially irinotecan induced severe toxicities.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	5-11
35506159-9	2022	Both UGT1A1*6 and UGT1A1*28 genetic variants should be screened in Asian cancer patients to reduce substantially irinotecan induced severe toxicities.	Irinotecan	113-123	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	18-24
35530278-4	2022	SG consists of an anti-trophoblast cell-surface antigen 2 (Trop2) antibody conjugated with a topoisomerase I inhibitor, SN-38, which is diffused out of the targeted Trop2 positive cancer cells and induces the bystander killing effect on surrounding cells regardless of their Trop2 expression status.	Irinotecan	120-125	tumor associated calcium signal transducer 2	Homo sapiens	59-64
35489740-2	2022	Therefore, we conducted a phase II study to verify the efficacy and safety of the combination of S-1 and irinotecan plus bevacizumab (SIRB regimen) as second-line treatment for patients with oxaliplatin and cetuximab-refractory KRAS wild-type mCRC.	Irinotecan	105-115	KRAS proto-oncogene, GTPase	Homo sapiens	228-232
35233973-5	2022	We also assessed the impact of UGT1A1 gene polymorphisms, which are involved in irinotecan metabolism, on outcomes and toxicity.	Irinotecan	80-90	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	31-37
35147853-0	2022	Prediction of Drug-Drug Interaction Between Dabrafenib and Irinotecan via UGT1A1-Mediated Glucuronidation.	Irinotecan	59-69	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
35147853-4	2022	METHODS: Recombinant human uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and human liver microsomes (HLMs) were employed to catalyze the glucuronidation of SN-38 in vitro.	Irinotecan	167-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-74
35147853-4	2022	METHODS: Recombinant human uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) and human liver microsomes (HLMs) were employed to catalyze the glucuronidation of SN-38 in vitro.	Irinotecan	167-172	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-82
35147853-6	2022	RESULTS: Dabrafenib noncompetitively inhibited SN-38 glucuronidation in pooled HLMs and recombinant UGT1A1 with unbound inhibitor constant (Ki,u) values of 12.43 +- 0.28 and 3.89 +- 0.40 muM, respectively.	Irinotecan	47-52	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106
35147853-9	2022	CONCLUSION: Dabrafenib is a potent noncompetitive inhibitor of UGT1A1 and may bring potential risk of DDI when combined with irinotecan.	Irinotecan	125-135	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
35498511-8	2022	All patients with PC-only CRC were treated with first-line bevacizumab and FOLFIRI, and the irinotecan dose escalation depended on UGT1A1 polymorphism.	Irinotecan	92-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	131-137
35498511-13	2022	Conclusion: Our study revealed that in patients with PC-only mCRC treatment of first-line bevacizumab and FOLFIRI through irinotecan dose escalation according to UGT1A1 polymorphism could confer such patients with comparable outcomes to that of patients with LiM-only and LuM-only mCRC.	Irinotecan	122-132	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	162-168
35354375-8	2022	G-CSF use was observed among 63.6%, 34.9%, 33.9%, and 44.9% of patients treated with FOLFIRINOX, FOLFOX, FOLFIRI, and liposomal irinotecan-based regimens, respectively.	Irinotecan	128-138	colony stimulating factor 3	Homo sapiens	0-5
35445479-6	2022	SN-38 is inactivated by UGT1A1 enzymes.	Irinotecan	0-5	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30
35530278-4	2022	SG consists of an anti-trophoblast cell-surface antigen 2 (Trop2) antibody conjugated with a topoisomerase I inhibitor, SN-38, which is diffused out of the targeted Trop2 positive cancer cells and induces the bystander killing effect on surrounding cells regardless of their Trop2 expression status.	Irinotecan	120-125	tumor associated calcium signal transducer 2	Homo sapiens	165-170
35530278-4	2022	SG consists of an anti-trophoblast cell-surface antigen 2 (Trop2) antibody conjugated with a topoisomerase I inhibitor, SN-38, which is diffused out of the targeted Trop2 positive cancer cells and induces the bystander killing effect on surrounding cells regardless of their Trop2 expression status.	Irinotecan	120-125	tumor associated calcium signal transducer 2	Homo sapiens	275-280
35231830-5	2022	Moreover, we firstly proved that ATM inhibitors could sensitize Irinotecan and Etoposide in a time-dependent manner on MCF-7 and SW480 cells, antagonism in a short period treatment while synergy at a long-term treatment and ATM agonist worked in an opposite way of ATM inhibitors.	Irinotecan	64-74	ATM serine/threonine kinase	Homo sapiens	33-36
35412430-3	2022	Research suggests an association between methylated DCR1 (mDCR1) and lack of benefit with irinotecan (IFL) treatment.	Irinotecan	90-100	dicer 1, ribonuclease III	Homo sapiens	52-56
35396702-9	2022	The findings of this study suggest that irinotecan-induced hepatotoxicity is not directly associated with genetic variables but is mostly related to concomitant use of CYP3A inducers and platinum, as well as the presence of liver metastasis and CVD.	Irinotecan	40-50	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	168-173
35231830-5	2022	Moreover, we firstly proved that ATM inhibitors could sensitize Irinotecan and Etoposide in a time-dependent manner on MCF-7 and SW480 cells, antagonism in a short period treatment while synergy at a long-term treatment and ATM agonist worked in an opposite way of ATM inhibitors.	Irinotecan	64-74	ATM serine/threonine kinase	Homo sapiens	224-227
35231830-5	2022	Moreover, we firstly proved that ATM inhibitors could sensitize Irinotecan and Etoposide in a time-dependent manner on MCF-7 and SW480 cells, antagonism in a short period treatment while synergy at a long-term treatment and ATM agonist worked in an opposite way of ATM inhibitors.	Irinotecan	64-74	ATM serine/threonine kinase	Homo sapiens	265-268
35240418-6	2022	Co-treatment by CPT-11 and 10o significantly diminished the tumor volume, indicating the great potential of 10o as a candidate of Chk1/2 inhibitor.	Irinotecan	16-22	checkpoint kinase 1	Mus musculus	130-136
35187743-0	2022	eIF3a-PPP2R5A-mediated ATM/ATR dephosphorylation is essential for irinotecan-induced DNA damage response.	Irinotecan	66-76	eukaryotic translation initiation factor 3 subunit J	Homo sapiens	0-5
35187743-0	2022	eIF3a-PPP2R5A-mediated ATM/ATR dephosphorylation is essential for irinotecan-induced DNA damage response.	Irinotecan	66-76	protein phosphatase 2 regulatory subunit B'alpha	Homo sapiens	6-13
35187743-0	2022	eIF3a-PPP2R5A-mediated ATM/ATR dephosphorylation is essential for irinotecan-induced DNA damage response.	Irinotecan	66-76	ATM serine/threonine kinase	Homo sapiens	23-26
35187743-0	2022	eIF3a-PPP2R5A-mediated ATM/ATR dephosphorylation is essential for irinotecan-induced DNA damage response.	Irinotecan	66-76	ATR serine/threonine kinase	Homo sapiens	27-30
35187743-3	2022	This study focused on the role of eIF3a in irinotecan-induced DNA damage response.	Irinotecan	43-53	eukaryotic translation initiation factor 3 subunit J	Homo sapiens	34-39
35187743-4	2022	MATERIALS AND METHODS: The cck8 cell viability and clone survival analyses were used to test the regulatory role of eIF3a on irinotecan sensitivity in HT29 and CACO2 cell lines in vitro.	Irinotecan	125-135	eukaryotic translation initiation factor 3 subunit J	Homo sapiens	116-121
35187743-9	2022	Suppression of PPP2R5A resulted in chronic ATM/ATR phosphorylation and activation, impairing DNA repair and enhancing irinotecan sensitivity.	Irinotecan	118-128	protein phosphatase 2 regulatory subunit B'alpha	Homo sapiens	15-22
35187743-10	2022	CONCLUSIONS: Our study suggested eIF3a with a high potential to influence phenotypic functions, which may contribute substantially to the early identification of susceptible individuals and the provision of personalized medication to irinotecan-treated patients.	Irinotecan	234-244	eukaryotic translation initiation factor 3 subunit J	Homo sapiens	33-38
35456602-7	2022	As demonstrated by the results of inhibition on multi-receptors by Sunitinib, we confirmed that SN-38/Sunitinib co-loaded micelles to be a treatment modality that could inhibit VEGF and PDGF receptors and enhance the antitumor effect of SN-38 (p < 0.05).	Irinotecan	96-101	vascular endothelial growth factor A	Homo sapiens	177-181
35061524-0	2022	Precision Medicine: UGT1A1 Genotyping to Better Manage Irinotecan-Induced Toxicity.	Irinotecan	55-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	20-26
35190308-7	2022	We further found that bile acid mixture (BA mix) could inhibit hOAT2-mediated uptake of cGMP, 5-fluorouracil, irinotecan and paclitaxel.	Irinotecan	110-120	solute carrier family 22 member 7	Homo sapiens	63-68
35481414-1	2022	OBJECTIVE: To undertake a meta-analysis of the treatment effects of different second-line chemotherapy regimens compared with FOLFIRINOX (FOL (folinic acid), F (fluorouracil), IRIN (irinotecan), OX (oxaliplatin)) after failure of gemcitabine-based first-line therapy in patients with pancreatic cancer.	Irinotecan	176-180	hypocretin neuropeptide precursor	Homo sapiens	195-197
35361811-6	2022	Using isogenic HCT116 clones, we showed that this mutation of ATR sensitizes the cells to several drugs, including SN-38 (topoisomerase I inhibitor) and VE-822 (ATR inhibitor) and exacerbates their synergistic effects.	Irinotecan	115-120	ATR serine/threonine kinase	Homo sapiens	62-65
35059735-0	2022	Targeting MUCL1 protein inhibits cell proliferation and EMT by deregulating beta-catenin and increases irinotecan sensitivity in colorectal cancer.	Irinotecan	103-113	mucin like 1	Homo sapiens	10-15
35192728-4	2022	Together with extended tumor exposure to therapeutically effective drug levels via reversible conjugation to Pluronic F-108 (PF108), these features translated into rapid tumor regression and long-term survival in models of both ABCG2-overexpressing and p53-mutant high-risk neuroblastomas, in contrast to a marginal effect of the clinically used camptothecin derivative, irinotecan.	Irinotecan	371-381	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	228-233
35192728-4	2022	Together with extended tumor exposure to therapeutically effective drug levels via reversible conjugation to Pluronic F-108 (PF108), these features translated into rapid tumor regression and long-term survival in models of both ABCG2-overexpressing and p53-mutant high-risk neuroblastomas, in contrast to a marginal effect of the clinically used camptothecin derivative, irinotecan.	Irinotecan	371-381	tumor protein p53	Homo sapiens	253-256
35059735-14	2022	Targeting MUCL1 increases the drug sensitivity of CRC cells towards irinotecan.	Irinotecan	68-78	mucin like 1	Homo sapiens	10-15
35226656-2	2022	Mutations in the UGT1A1 gene can be associated with increased toxicity from irinotecan-based chemotherapy.	Irinotecan	76-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	17-23
35197630-7	2022	Our results show that irinotecan and CHEK1 inhibition have synergistic effects in microsatellite-stable or KRAS-TP53 double-mutant colon cancer cells, leading to apoptosis and suppression of tumour xenograft growth.	Irinotecan	22-32	KRAS proto-oncogene, GTPase	Homo sapiens	107-111
35197630-7	2022	Our results show that irinotecan and CHEK1 inhibition have synergistic effects in microsatellite-stable or KRAS-TP53 double-mutant colon cancer cells, leading to apoptosis and suppression of tumour xenograft growth.	Irinotecan	22-32	tumor protein p53	Homo sapiens	112-116
35226656-5	2022	Genetic testing identified a mutation in the UGT1A1 gene associated with increased toxicity to irinotecan, and the EIA tests performed for evaluation of C. difficile toxins A and B showed repeatedly negative results.	Irinotecan	95-105	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
35207692-1	2022	Current guidelines recommend pre-therapeutic UGT1A1 genotyping to guide irinotecan dosing, but the usefulness of this approach remains to be clarified.	Irinotecan	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	45-51
35152824-0	2022	Mitochondrial DNA as a Possible Ligand for TLR9 in Irinotecan-induced Small Intestinal Mucositis.	Irinotecan	51-61	toll-like receptor 9	Mus musculus	43-47
35152824-5	2022	WT mice injected with irinotecan presented a progressive increase in mtDNA in the serum along with increased hematocrit, shortening of small intestine length, reduction of intestinal villus:crypt ratio and increased influx of neutrophils, which were followed by higher expression of Nlrp3 and Casp1 mRNA and increased IL-1beta levels in the ileum when compared to vehicle-injected mice.	Irinotecan	22-32	NLR family, pyrin domain containing 3	Mus musculus	283-288
35152824-5	2022	WT mice injected with irinotecan presented a progressive increase in mtDNA in the serum along with increased hematocrit, shortening of small intestine length, reduction of intestinal villus:crypt ratio and increased influx of neutrophils, which were followed by higher expression of Nlrp3 and Casp1 mRNA and increased IL-1beta levels in the ileum when compared to vehicle-injected mice.	Irinotecan	22-32	caspase 1	Mus musculus	293-298
35152824-5	2022	WT mice injected with irinotecan presented a progressive increase in mtDNA in the serum along with increased hematocrit, shortening of small intestine length, reduction of intestinal villus:crypt ratio and increased influx of neutrophils, which were followed by higher expression of Nlrp3 and Casp1 mRNA and increased IL-1beta levels in the ileum when compared to vehicle-injected mice.	Irinotecan	22-32	interleukin 1 alpha	Mus musculus	318-326
35152824-8	2022	Overall, our findings show that the amount of circulating free CpG-DNA is increased upon chemotherapy and that TLR9 activation is important for NLRP3 inflammasome transcription and further IL-1beta release, playing a central role in the development of irinotecan-induced intestinal mucositis.	Irinotecan	252-262	toll-like receptor 9	Mus musculus	111-115
35152824-8	2022	Overall, our findings show that the amount of circulating free CpG-DNA is increased upon chemotherapy and that TLR9 activation is important for NLRP3 inflammasome transcription and further IL-1beta release, playing a central role in the development of irinotecan-induced intestinal mucositis.	Irinotecan	252-262	NLR family, pyrin domain containing 3	Mus musculus	144-149
35152824-8	2022	Overall, our findings show that the amount of circulating free CpG-DNA is increased upon chemotherapy and that TLR9 activation is important for NLRP3 inflammasome transcription and further IL-1beta release, playing a central role in the development of irinotecan-induced intestinal mucositis.	Irinotecan	252-262	interleukin 1 alpha	Mus musculus	189-197
35152824-9	2022	We suggest that TLR9 antagonism may be a new therapeutic strategy for limiting irinotecan-induced intestinal inflammation.	Irinotecan	79-89	toll-like receptor 9	Mus musculus	16-20
35131032-4	2022	Our results also reveal that cells depleted of KChIP3 are four times more resistant (measured as cell viability and DNA damage) to chemotherapeutics 5-Fluorouracil plus Irinotecan (5-FU+iri.)	Irinotecan	169-179	potassium voltage-gated channel interacting protein 3	Homo sapiens	47-53
34654938-3	2022	Patients with genotype UGT1A1*6 (exon 1, 211G > A) treated with the antineoplastic drug SN-38 have been reported to exhibit decreased glucuronide conjugation and increased incidence of intestinal toxicity and its severe side effects, including severe diarrhea.	Irinotecan	88-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	23-29
34998046-0	2022	UGT1A1 genotype-guided dosing of irinotecan: A prospective safety and cost analysis in poor metaboliser patients.	Irinotecan	33-43	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
34998046-1	2022	AIM: To determine the safety, feasibility, pharmacokinetics, and cost of UGT1A1 genotype-guided dosing of irinotecan.	Irinotecan	106-116	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79
34998046-2	2022	PATIENTS AND METHODS: In this prospective, multicentre, non-randomised study, patients intended for treatment with irinotecan were pre-therapeutically genotyped for UGT1A1*28 and UGT1A1*93.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	165-171
34998046-2	2022	PATIENTS AND METHODS: In this prospective, multicentre, non-randomised study, patients intended for treatment with irinotecan were pre-therapeutically genotyped for UGT1A1*28 and UGT1A1*93.	Irinotecan	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	179-185
34998046-9	2022	Systemic exposure of SN-38 of reduced dosing in UGT1A1 PMs was still slightly higher compared to a standard-dosed irinotecan patient cohort (difference: +32%).	Irinotecan	21-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	48-54
34998046-11	2022	CONCLUSION: UGT1A1 genotype-guided dosing significantly reduces the incidence of febrile neutropenia in UGT1A1 PM patients treated with irinotecan, results in a therapeutically effective systemic drug exposure, and is cost-saving.	Irinotecan	136-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	12-18
34998046-11	2022	CONCLUSION: UGT1A1 genotype-guided dosing significantly reduces the incidence of febrile neutropenia in UGT1A1 PM patients treated with irinotecan, results in a therapeutically effective systemic drug exposure, and is cost-saving.	Irinotecan	136-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
34998046-12	2022	Therefore, UGT1A1 genotype-guided dosing of irinotecan should be considered standard of care in order to improve individual patient safety.	Irinotecan	44-54	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	11-17
34654938-7	2022	The CYP3A4 POR UGT1A1*6 KI-Caco-2 cells were sensitive to SN-38-induced intestinal toxicity.	Irinotecan	58-63	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	4-10
34654938-7	2022	The CYP3A4 POR UGT1A1*6 KI-Caco-2 cells were sensitive to SN-38-induced intestinal toxicity.	Irinotecan	58-63	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
35127582-6	2022	Conclusion: Gemcitabine and L-OHP + EPI + irinotecan + 5-FU, L-OHP + EPI, and L-OHP + irinotecan + EPI were more effective against AFP-positive compared with AFP-negative liver cancer cells according to in vitro high-throughput drug sensitivity screening.	Irinotecan	42-52	alpha fetoprotein	Homo sapiens	158-161
35127582-6	2022	Conclusion: Gemcitabine and L-OHP + EPI + irinotecan + 5-FU, L-OHP + EPI, and L-OHP + irinotecan + EPI were more effective against AFP-positive compared with AFP-negative liver cancer cells according to in vitro high-throughput drug sensitivity screening.	Irinotecan	86-96	alpha fetoprotein	Homo sapiens	158-161
35049694-1	2022	The aim of this study was to examine the safety and efficacy of 40 microm and 75 microm calibrated irinotecan-eluting beads (DEBIRI-TACE) for the treatment of colorectal cancer metastases.	Irinotecan	99-109	ADAM metallopeptidase domain 17	Homo sapiens	132-136
35070248-6	2022	A 44-year-old BRCA1-mutated ovarian cancer patient was treated in sixth line with lurbinectedin and irinotecan with a time to further progression (TTFP) equal to 8 months.	Irinotecan	100-110	BRCA1 DNA repair associated	Homo sapiens	14-19
35070248-0	2022	Exceptional response to lurbinectedin and irinotecan in BRCA-mutated platinum-resistant ovarian cancer patient: a case report.	Irinotecan	42-52	BRCA1 DNA repair associated	Homo sapiens	56-60
35070248-5	2022	This article describes an exceptional response to lurbinectedin alone followed by the association with irinotecan in a BRCA-mutated platinum-resistant ovarian cancer patient.	Irinotecan	103-113	BRCA1 DNA repair associated	Homo sapiens	119-123
35127384-4	2022	CPT-11 causes DNA damage and the release of double-stranded DNA (dsDNA) from the intestine, leading to cyclic-GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING)-mediated colitis, which was significantly decreased by andrographolide both in vivo and in vitro.	Irinotecan	0-6	cyclic GMP-AMP synthase	Mus musculus	103-126
35127384-4	2022	CPT-11 causes DNA damage and the release of double-stranded DNA (dsDNA) from the intestine, leading to cyclic-GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING)-mediated colitis, which was significantly decreased by andrographolide both in vivo and in vitro.	Irinotecan	0-6	cyclic GMP-AMP synthase	Mus musculus	128-132
35491733-4	2022	PC3 cells co-cultured with ADSC.CE.TRAIL showed higher cytotoxicity than did CPT-11 monotherapy, ADSC.CE, or ADSC.sTRAIL under CPT-11 treatment.	Irinotecan	77-83	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	35-40
34996412-1	2022	BACKGROUND: Pharmacogenetic (PGx) testing for germline variants in the DPYD and UGT1A1 genes can be used to guide fluoropyrimidine and irinotecan dosing, respectively.	Irinotecan	135-145	dihydropyrimidine dehydrogenase	Homo sapiens	71-75
34996412-1	2022	BACKGROUND: Pharmacogenetic (PGx) testing for germline variants in the DPYD and UGT1A1 genes can be used to guide fluoropyrimidine and irinotecan dosing, respectively.	Irinotecan	135-145	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	80-86
35356222-0	2022	UGT1A1 Allele Test Not Only Minimizes the Toxicity But Also Maximizes the Therapeutic Effect of Irinotecan in the Treatment of Colorectal Cancer: A Narrative Review.	Irinotecan	96-106	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
35356222-2	2022	Adjusting the dose of irinotecan according to the uridine diphosphate glucuronosyltransferase (UGT) 1A1 genotype reflects the principle of individualized and precision medicine, and may improve the chemotherapy response and survival of CRC.	Irinotecan	22-32	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	50-103
35356222-3	2022	Methods: To summarize the feasibility, efficacy and safety of high dose irinotecan in CRC patients with UGT1A1 wild-type or heterozygous alleles, PubMed, EMBASE, MEDLINE and the Cochrane Central Register of Controlled Trials online databases were searched from the date of creation to October 22, 2021.	Irinotecan	72-82	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	104-110
35356222-5	2022	The results indicated that the maximum tolerated dose of irinotecan in CRC patients with UGT1A1 wild-type or heterozygous variant was significantly higher than the conventional recommended dose.	Irinotecan	57-67	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	89-95
35356222-6	2022	Chemotherapy based on high dose irinotecan improved the clinical efficacy in mCRC patients with UGT1A1*28 wild-type and heterozygous variant, and the toxicity was tolerated, as reflected in most studies.	Irinotecan	32-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	96-102
35356222-7	2022	Conclusions: We are optimistic about the application of high dose irinotecan for mCRC patients with UGT1A1*28 wild-type or heterozygous variant, which will provide a relatively clear direction for future research and certain norms for clinical practice.	Irinotecan	66-76	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	100-106