PubMed:23928928 JSONTXT

{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":146},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":147,"end":158},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":159,"end":253},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":254,"end":388},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":389,"end":456},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":457,"end":461},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":462,"end":644},"obj":"Sentence"},{"id":"TextSentencer_T8","span":{"begin":645,"end":666},"obj":"Sentence"},{"id":"TextSentencer_T9","span":{"begin":667,"end":727},"obj":"Sentence"},{"id":"TextSentencer_T10","span":{"begin":728,"end":796},"obj":"Sentence"},{"id":"TextSentencer_T11","span":{"begin":797,"end":1002},"obj":"Sentence"},{"id":"TextSentencer_T12","span":{"begin":1003,"end":1078},"obj":"Sentence"},{"id":"TextSentencer_T13","span":{"begin":1079,"end":1142},"obj":"Sentence"},{"id":"TextSentencer_T14","span":{"begin":1143,"end":1329},"obj":"Sentence"},{"id":"TextSentencer_T15","span":{"begin":1330,"end":1462},"obj":"Sentence"},{"id":"TextSentencer_T16","span":{"begin":1463,"end":1732},"obj":"Sentence"},{"id":"TextSentencer_T17","span":{"begin":1733,"end":1745},"obj":"Sentence"},{"id":"TextSentencer_T18","span":{"begin":1746,"end":1873},"obj":"Sentence"},{"id":"TextSentencer_T19","span":{"begin":1874,"end":1961},"obj":"Sentence"},{"id":"TextSentencer_T20","span":{"begin":1962,"end":2045},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":146},"obj":"Sentence"},{"id":"T2","span":{"begin":147,"end":158},"obj":"Sentence"},{"id":"T3","span":{"begin":159,"end":253},"obj":"Sentence"},{"id":"T4","span":{"begin":254,"end":388},"obj":"Sentence"},{"id":"T5","span":{"begin":389,"end":456},"obj":"Sentence"},{"id":"T6","span":{"begin":457,"end":461},"obj":"Sentence"},{"id":"T7","span":{"begin":462,"end":644},"obj":"Sentence"},{"id":"T8","span":{"begin":645,"end":666},"obj":"Sentence"},{"id":"T9","span":{"begin":667,"end":727},"obj":"Sentence"},{"id":"T10","span":{"begin":728,"end":796},"obj":"Sentence"},{"id":"T11","span":{"begin":797,"end":1002},"obj":"Sentence"},{"id":"T12","span":{"begin":1003,"end":1078},"obj":"Sentence"},{"id":"T13","span":{"begin":1079,"end":1142},"obj":"Sentence"},{"id":"T14","span":{"begin":1143,"end":1329},"obj":"Sentence"},{"id":"T15","span":{"begin":1330,"end":1462},"obj":"Sentence"},{"id":"T16","span":{"begin":1463,"end":1732},"obj":"Sentence"},{"id":"T17","span":{"begin":1733,"end":1745},"obj":"Sentence"},{"id":"T18","span":{"begin":1746,"end":1873},"obj":"Sentence"},{"id":"T19","span":{"begin":1874,"end":1961},"obj":"Sentence"},{"id":"T20","span":{"begin":1962,"end":2045},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Association between environmental tobacco smoke exposure and lung cancer susceptibility: modification by antioxidant enzyme genetic polymorphisms.\nBACKGROUND: Environmental tobacco smoke (ETS) is the primary etiologic factor responsible for lung cancer. However, only 10-15 % of smokers develop lung cancer, suggesting a genetic role in modifying individual susceptibility to lung cancer. Antioxidant enzymes and genetic polymorphisms should be considered.\nAIM: The present study aimed to evaluate the role of antioxidant enzyme activity and genetic polymorphisms in modifying the susceptibility to lung cancer among individuals exposed to ETS.\nSUBJECTS AND METHODS: A total of 150 male subjects were divided into three groups: 50 lung cancer patients, 50 chronic smokers, and 50 passive smokers. Genotyping of microsomal epoxide hydrolase (mEH) exon 3 (Tyr(113)Hist) and exon 4 (Hist(139)Arg) polymorphisms were done by the polymerase chain reaction-restriction fragment length polymorphism technique. MnSOD (Val(16)Ala) polymorphism was detected by the real time-TaqMan assay. Erythrocyte MnSOD activity was measured spectrophotometrically.\nRESULTS: ETS-exposed individuals (both active and passive smokers) who carried the His allele of mEH exon3 have a 2.9-fold increased risk of lung cancer (odds ratio [OR] 2.9, P \u003c 0.001). In addition, ETS-exposed carriers of the Arg allele of mEH exon 4 have a 2.1-fold increased risk of lung cancer (OR 2.1, P = 0.024). However, no association between the MnSOD Val(16)Ala polymorphism and lung cancer was detected among ETS-exposed individuals (OR 1.6, P = 0.147), although the lung cancer group had significantly lower MnSOD activity than the chronic or passive smoker groups (P = 0.03).\nCONCLUSIONS: Exons 3 and 4 polymorphisms of the mEH gene may contribute to lung cancer susceptibility through disturbed antioxidant balance. However, this was not the case with the MnSOD Val(16)Ala single-nucleotid polymorphism. Antioxidant enzymes may modulate the influence of ETS exposure on lung cancer risk."}

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":1240,"end":1243},"obj":"gene:2052"},{"id":"T1","span":{"begin":1284,"end":1295},"obj":"disease:C0242379"},{"id":"T2","span":{"begin":1240,"end":1243},"obj":"gene:2052"},{"id":"T3","span":{"begin":1284,"end":1295},"obj":"disease:C0684249"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"},{"id":"R2","pred":"associated_with","subj":"T2","obj":"T3"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Association between environmental tobacco smoke exposure and lung cancer susceptibility: modification by antioxidant enzyme genetic polymorphisms.\nBACKGROUND: Environmental tobacco smoke (ETS) is the primary etiologic factor responsible for lung cancer. However, only 10-15 % of smokers develop lung cancer, suggesting a genetic role in modifying individual susceptibility to lung cancer. Antioxidant enzymes and genetic polymorphisms should be considered.\nAIM: The present study aimed to evaluate the role of antioxidant enzyme activity and genetic polymorphisms in modifying the susceptibility to lung cancer among individuals exposed to ETS.\nSUBJECTS AND METHODS: A total of 150 male subjects were divided into three groups: 50 lung cancer patients, 50 chronic smokers, and 50 passive smokers. Genotyping of microsomal epoxide hydrolase (mEH) exon 3 (Tyr(113)Hist) and exon 4 (Hist(139)Arg) polymorphisms were done by the polymerase chain reaction-restriction fragment length polymorphism technique. MnSOD (Val(16)Ala) polymorphism was detected by the real time-TaqMan assay. Erythrocyte MnSOD activity was measured spectrophotometrically.\nRESULTS: ETS-exposed individuals (both active and passive smokers) who carried the His allele of mEH exon3 have a 2.9-fold increased risk of lung cancer (odds ratio [OR] 2.9, P \u003c 0.001). In addition, ETS-exposed carriers of the Arg allele of mEH exon 4 have a 2.1-fold increased risk of lung cancer (OR 2.1, P = 0.024). However, no association between the MnSOD Val(16)Ala polymorphism and lung cancer was detected among ETS-exposed individuals (OR 1.6, P = 0.147), although the lung cancer group had significantly lower MnSOD activity than the chronic or passive smoker groups (P = 0.03).\nCONCLUSIONS: Exons 3 and 4 polymorphisms of the mEH gene may contribute to lung cancer susceptibility through disturbed antioxidant balance. However, this was not the case with the MnSOD Val(16)Ala single-nucleotid polymorphism. Antioxidant enzymes may modulate the influence of ETS exposure on lung cancer risk."}

{"project":"Allie","denotations":[{"id":"SS1_23928928_2_0","span":{"begin":159,"end":186},"obj":"expanded"},{"id":"SS2_23928928_2_0","span":{"begin":188,"end":191},"obj":"abbr"},{"id":"SS1_23928928_9_0","span":{"begin":811,"end":839},"obj":"expanded"},{"id":"SS2_23928928_9_0","span":{"begin":841,"end":844},"obj":"abbr"},{"id":"SS1_23928928_13_0","span":{"begin":1297,"end":1307},"obj":"expanded"},{"id":"SS2_23928928_13_0","span":{"begin":1309,"end":1311},"obj":"abbr"}],"relations":[{"id":"AE1_23928928_2_0","pred":"abbreviatedTo","subj":"SS1_23928928_2_0","obj":"SS2_23928928_2_0"},{"id":"AE1_23928928_9_0","pred":"abbreviatedTo","subj":"SS1_23928928_9_0","obj":"SS2_23928928_9_0"},{"id":"AE1_23928928_13_0","pred":"abbreviatedTo","subj":"SS1_23928928_13_0","obj":"SS2_23928928_13_0"}],"text":"Association between environmental tobacco smoke exposure and lung cancer susceptibility: modification by antioxidant enzyme genetic polymorphisms.\nBACKGROUND: Environmental tobacco smoke (ETS) is the primary etiologic factor responsible for lung cancer. However, only 10-15 % of smokers develop lung cancer, suggesting a genetic role in modifying individual susceptibility to lung cancer. Antioxidant enzymes and genetic polymorphisms should be considered.\nAIM: The present study aimed to evaluate the role of antioxidant enzyme activity and genetic polymorphisms in modifying the susceptibility to lung cancer among individuals exposed to ETS.\nSUBJECTS AND METHODS: A total of 150 male subjects were divided into three groups: 50 lung cancer patients, 50 chronic smokers, and 50 passive smokers. Genotyping of microsomal epoxide hydrolase (mEH) exon 3 (Tyr(113)Hist) and exon 4 (Hist(139)Arg) polymorphisms were done by the polymerase chain reaction-restriction fragment length polymorphism technique. MnSOD (Val(16)Ala) polymorphism was detected by the real time-TaqMan assay. Erythrocyte MnSOD activity was measured spectrophotometrically.\nRESULTS: ETS-exposed individuals (both active and passive smokers) who carried the His allele of mEH exon3 have a 2.9-fold increased risk of lung cancer (odds ratio [OR] 2.9, P \u003c 0.001). In addition, ETS-exposed carriers of the Arg allele of mEH exon 4 have a 2.1-fold increased risk of lung cancer (OR 2.1, P = 0.024). However, no association between the MnSOD Val(16)Ala polymorphism and lung cancer was detected among ETS-exposed individuals (OR 1.6, P = 0.147), although the lung cancer group had significantly lower MnSOD activity than the chronic or passive smoker groups (P = 0.03).\nCONCLUSIONS: Exons 3 and 4 polymorphisms of the mEH gene may contribute to lung cancer susceptibility through disturbed antioxidant balance. However, this was not the case with the MnSOD Val(16)Ala single-nucleotid polymorphism. Antioxidant enzymes may modulate the influence of ETS exposure on lung cancer risk."}

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":241,"end":252},"obj":"HP_0100526"},{"id":"T2","span":{"begin":246,"end":252},"obj":"HP_0002664"},{"id":"T3","span":{"begin":295,"end":306},"obj":"HP_0100526"},{"id":"T4","span":{"begin":300,"end":306},"obj":"HP_0002664"},{"id":"T5","span":{"begin":376,"end":387},"obj":"HP_0100526"},{"id":"T6","span":{"begin":381,"end":387},"obj":"HP_0002664"}],"text":"Association between environmental tobacco smoke exposure and lung cancer susceptibility: modification by antioxidant enzyme genetic polymorphisms.\nBACKGROUND: Environmental tobacco smoke (ETS) is the primary etiologic factor responsible for lung cancer. However, only 10-15 % of smokers develop lung cancer, suggesting a genetic role in modifying individual susceptibility to lung cancer. Antioxidant enzymes and genetic polymorphisms should be considered.\nAIM: The present study aimed to evaluate the role of antioxidant enzyme activity and genetic polymorphisms in modifying the susceptibility to lung cancer among individuals exposed to ETS.\nSUBJECTS AND METHODS: A total of 150 male subjects were divided into three groups: 50 lung cancer patients, 50 chronic smokers, and 50 passive smokers. Genotyping of microsomal epoxide hydrolase (mEH) exon 3 (Tyr(113)Hist) and exon 4 (Hist(139)Arg) polymorphisms were done by the polymerase chain reaction-restriction fragment length polymorphism technique. MnSOD (Val(16)Ala) polymorphism was detected by the real time-TaqMan assay. Erythrocyte MnSOD activity was measured spectrophotometrically.\nRESULTS: ETS-exposed individuals (both active and passive smokers) who carried the His allele of mEH exon3 have a 2.9-fold increased risk of lung cancer (odds ratio [OR] 2.9, P \u003c 0.001). In addition, ETS-exposed carriers of the Arg allele of mEH exon 4 have a 2.1-fold increased risk of lung cancer (OR 2.1, P = 0.024). However, no association between the MnSOD Val(16)Ala polymorphism and lung cancer was detected among ETS-exposed individuals (OR 1.6, P = 0.147), although the lung cancer group had significantly lower MnSOD activity than the chronic or passive smoker groups (P = 0.03).\nCONCLUSIONS: Exons 3 and 4 polymorphisms of the mEH gene may contribute to lung cancer susceptibility through disturbed antioxidant balance. However, this was not the case with the MnSOD Val(16)Ala single-nucleotid polymorphism. Antioxidant enzymes may modulate the influence of ETS exposure on lung cancer risk."}

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"23928928-11#36#41#gene6648","span":{"begin":1499,"end":1504},"obj":"gene6648"},{"id":"23928928-11#42#52#gene6648","span":{"begin":1505,"end":1515},"obj":"gene6648"},{"id":"23928928-11#201#206#gene6648","span":{"begin":1664,"end":1669},"obj":"gene6648"},{"id":"23928928-11#70#81#diseaseC0242379","span":{"begin":1533,"end":1544},"obj":"diseaseC0242379"},{"id":"23928928-11#70#81#diseaseC0684249","span":{"begin":1533,"end":1544},"obj":"diseaseC0684249"},{"id":"23928928-11#70#81#diseaseC1306460","span":{"begin":1533,"end":1544},"obj":"diseaseC1306460"},{"id":"23928928-11#70#81#diseaseC0242379","span":{"begin":1533,"end":1544},"obj":"diseaseC0242379"},{"id":"23928928-11#70#81#diseaseC0684249","span":{"begin":1533,"end":1544},"obj":"diseaseC0684249"},{"id":"23928928-11#70#81#diseaseC1306460","span":{"begin":1533,"end":1544},"obj":"diseaseC1306460"},{"id":"23928928-11#159#170#diseaseC0242379","span":{"begin":1622,"end":1633},"obj":"diseaseC0242379"},{"id":"23928928-11#159#170#diseaseC0684249","span":{"begin":1622,"end":1633},"obj":"diseaseC0684249"},{"id":"23928928-11#159#170#diseaseC1306460","span":{"begin":1622,"end":1633},"obj":"diseaseC1306460"},{"id":"23928928-11#70#81#diseaseC0242379","span":{"begin":1533,"end":1544},"obj":"diseaseC0242379"},{"id":"23928928-11#70#81#diseaseC0684249","span":{"begin":1533,"end":1544},"obj":"diseaseC0684249"},{"id":"23928928-11#70#81#diseaseC1306460","span":{"begin":1533,"end":1544},"obj":"diseaseC1306460"},{"id":"23928928-11#159#170#diseaseC0242379","span":{"begin":1622,"end":1633},"obj":"diseaseC0242379"},{"id":"23928928-11#159#170#diseaseC0684249","span":{"begin":1622,"end":1633},"obj":"diseaseC0684249"},{"id":"23928928-11#159#170#diseaseC1306460","span":{"begin":1622,"end":1633},"obj":"diseaseC1306460"},{"id":"23928928-12#35#38#gene2052","span":{"begin":1781,"end":1784},"obj":"gene2052"},{"id":"23928928-12#62#73#diseaseC0242379","span":{"begin":1808,"end":1819},"obj":"diseaseC0242379"},{"id":"23928928-12#62#73#diseaseC0684249","span":{"begin":1808,"end":1819},"obj":"diseaseC0684249"},{"id":"23928928-12#62#73#diseaseC1306460","span":{"begin":1808,"end":1819},"obj":"diseaseC1306460"}],"relations":[{"id":"36#41#gene664870#81#diseaseC0242379","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#70#81#diseaseC0242379"},{"id":"36#41#gene664870#81#diseaseC0684249","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#70#81#diseaseC0684249"},{"id":"36#41#gene664870#81#diseaseC1306460","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#70#81#diseaseC1306460"},{"id":"36#41#gene664870#81#diseaseC0242379","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#70#81#diseaseC0242379"},{"id":"36#41#gene664870#81#diseaseC0684249","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#70#81#diseaseC0684249"},{"id":"36#41#gene664870#81#diseaseC1306460","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#70#81#diseaseC1306460"},{"id":"36#41#gene6648159#170#diseaseC0242379","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#159#170#diseaseC0242379"},{"id":"36#41#gene6648159#170#diseaseC0684249","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#159#170#diseaseC0684249"},{"id":"36#41#gene6648159#170#diseaseC1306460","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#159#170#diseaseC1306460"},{"id":"36#41#gene664870#81#diseaseC0242379","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#70#81#diseaseC0242379"},{"id":"36#41#gene664870#81#diseaseC0684249","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#70#81#diseaseC0684249"},{"id":"36#41#gene664870#81#diseaseC1306460","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#70#81#diseaseC1306460"},{"id":"36#41#gene6648159#170#diseaseC0242379","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#159#170#diseaseC0242379"},{"id":"36#41#gene6648159#170#diseaseC0684249","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#159#170#diseaseC0684249"},{"id":"36#41#gene6648159#170#diseaseC1306460","pred":"associated_with","subj":"23928928-11#36#41#gene6648","obj":"23928928-11#159#170#diseaseC1306460"},{"id":"42#52#gene664870#81#diseaseC0242379","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#70#81#diseaseC0242379"},{"id":"42#52#gene664870#81#diseaseC0684249","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#70#81#diseaseC0684249"},{"id":"42#52#gene664870#81#diseaseC1306460","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#70#81#diseaseC1306460"},{"id":"42#52#gene664870#81#diseaseC0242379","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#70#81#diseaseC0242379"},{"id":"42#52#gene664870#81#diseaseC0684249","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#70#81#diseaseC0684249"},{"id":"42#52#gene664870#81#diseaseC1306460","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#70#81#diseaseC1306460"},{"id":"42#52#gene6648159#170#diseaseC0242379","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#159#170#diseaseC0242379"},{"id":"42#52#gene6648159#170#diseaseC0684249","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#159#170#diseaseC0684249"},{"id":"42#52#gene6648159#170#diseaseC1306460","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#159#170#diseaseC1306460"},{"id":"42#52#gene664870#81#diseaseC0242379","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#70#81#diseaseC0242379"},{"id":"42#52#gene664870#81#diseaseC0684249","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#70#81#diseaseC0684249"},{"id":"42#52#gene664870#81#diseaseC1306460","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#70#81#diseaseC1306460"},{"id":"42#52#gene6648159#170#diseaseC0242379","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#159#170#diseaseC0242379"},{"id":"42#52#gene6648159#170#diseaseC0684249","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#159#170#diseaseC0684249"},{"id":"42#52#gene6648159#170#diseaseC1306460","pred":"associated_with","subj":"23928928-11#42#52#gene6648","obj":"23928928-11#159#170#diseaseC1306460"},{"id":"201#206#gene664870#81#diseaseC0242379","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#70#81#diseaseC0242379"},{"id":"201#206#gene664870#81#diseaseC0684249","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#70#81#diseaseC0684249"},{"id":"201#206#gene664870#81#diseaseC1306460","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#70#81#diseaseC1306460"},{"id":"201#206#gene664870#81#diseaseC0242379","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#70#81#diseaseC0242379"},{"id":"201#206#gene664870#81#diseaseC0684249","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#70#81#diseaseC0684249"},{"id":"201#206#gene664870#81#diseaseC1306460","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#70#81#diseaseC1306460"},{"id":"201#206#gene6648159#170#diseaseC0242379","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#159#170#diseaseC0242379"},{"id":"201#206#gene6648159#170#diseaseC0684249","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#159#170#diseaseC0684249"},{"id":"201#206#gene6648159#170#diseaseC1306460","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#159#170#diseaseC1306460"},{"id":"201#206#gene664870#81#diseaseC0242379","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#70#81#diseaseC0242379"},{"id":"201#206#gene664870#81#diseaseC0684249","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#70#81#diseaseC0684249"},{"id":"201#206#gene664870#81#diseaseC1306460","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#70#81#diseaseC1306460"},{"id":"201#206#gene6648159#170#diseaseC0242379","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#159#170#diseaseC0242379"},{"id":"201#206#gene6648159#170#diseaseC0684249","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#159#170#diseaseC0684249"},{"id":"201#206#gene6648159#170#diseaseC1306460","pred":"associated_with","subj":"23928928-11#201#206#gene6648","obj":"23928928-11#159#170#diseaseC1306460"},{"id":"35#38#gene205262#73#diseaseC0242379","pred":"associated_with","subj":"23928928-12#35#38#gene2052","obj":"23928928-12#62#73#diseaseC0242379"},{"id":"35#38#gene205262#73#diseaseC0684249","pred":"associated_with","subj":"23928928-12#35#38#gene2052","obj":"23928928-12#62#73#diseaseC0684249"},{"id":"35#38#gene205262#73#diseaseC1306460","pred":"associated_with","subj":"23928928-12#35#38#gene2052","obj":"23928928-12#62#73#diseaseC1306460"}],"text":"Association between environmental tobacco smoke exposure and lung cancer susceptibility: modification by antioxidant enzyme genetic polymorphisms.\nBACKGROUND: Environmental tobacco smoke (ETS) is the primary etiologic factor responsible for lung cancer. However, only 10-15 % of smokers develop lung cancer, suggesting a genetic role in modifying individual susceptibility to lung cancer. Antioxidant enzymes and genetic polymorphisms should be considered.\nAIM: The present study aimed to evaluate the role of antioxidant enzyme activity and genetic polymorphisms in modifying the susceptibility to lung cancer among individuals exposed to ETS.\nSUBJECTS AND METHODS: A total of 150 male subjects were divided into three groups: 50 lung cancer patients, 50 chronic smokers, and 50 passive smokers. Genotyping of microsomal epoxide hydrolase (mEH) exon 3 (Tyr(113)Hist) and exon 4 (Hist(139)Arg) polymorphisms were done by the polymerase chain reaction-restriction fragment length polymorphism technique. MnSOD (Val(16)Ala) polymorphism was detected by the real time-TaqMan assay. Erythrocyte MnSOD activity was measured spectrophotometrically.\nRESULTS: ETS-exposed individuals (both active and passive smokers) who carried the His allele of mEH exon3 have a 2.9-fold increased risk of lung cancer (odds ratio [OR] 2.9, P \u003c 0.001). In addition, ETS-exposed carriers of the Arg allele of mEH exon 4 have a 2.1-fold increased risk of lung cancer (OR 2.1, P = 0.024). However, no association between the MnSOD Val(16)Ala polymorphism and lung cancer was detected among ETS-exposed individuals (OR 1.6, P = 0.147), although the lung cancer group had significantly lower MnSOD activity than the chronic or passive smoker groups (P = 0.03).\nCONCLUSIONS: Exons 3 and 4 polymorphisms of the mEH gene may contribute to lung cancer susceptibility through disturbed antioxidant balance. However, this was not the case with the MnSOD Val(16)Ala single-nucleotid polymorphism. Antioxidant enzymes may modulate the influence of ETS exposure on lung cancer risk."}

{"project":"DisGeNET5_variant_disease","denotations":[{"id":"23928928-11#42#52#geners4880","span":{"begin":1505,"end":1515},"obj":"geners4880"},{"id":"23928928-11#70#81#diseaseC0242379","span":{"begin":1533,"end":1544},"obj":"diseaseC0242379"},{"id":"23928928-11#70#81#diseaseC0684249","span":{"begin":1533,"end":1544},"obj":"diseaseC0684249"},{"id":"23928928-11#70#81#diseaseC1306460","span":{"begin":1533,"end":1544},"obj":"diseaseC1306460"},{"id":"23928928-11#159#170#diseaseC0242379","span":{"begin":1622,"end":1633},"obj":"diseaseC0242379"},{"id":"23928928-11#159#170#diseaseC0684249","span":{"begin":1622,"end":1633},"obj":"diseaseC0684249"},{"id":"23928928-11#159#170#diseaseC1306460","span":{"begin":1622,"end":1633},"obj":"diseaseC1306460"}],"relations":[{"id":"42#52#geners488070#81#diseaseC0242379","pred":"associated_with","subj":"23928928-11#42#52#geners4880","obj":"23928928-11#70#81#diseaseC0242379"},{"id":"42#52#geners488070#81#diseaseC0684249","pred":"associated_with","subj":"23928928-11#42#52#geners4880","obj":"23928928-11#70#81#diseaseC0684249"},{"id":"42#52#geners488070#81#diseaseC1306460","pred":"associated_with","subj":"23928928-11#42#52#geners4880","obj":"23928928-11#70#81#diseaseC1306460"},{"id":"42#52#geners4880159#170#diseaseC0242379","pred":"associated_with","subj":"23928928-11#42#52#geners4880","obj":"23928928-11#159#170#diseaseC0242379"},{"id":"42#52#geners4880159#170#diseaseC0684249","pred":"associated_with","subj":"23928928-11#42#52#geners4880","obj":"23928928-11#159#170#diseaseC0684249"},{"id":"42#52#geners4880159#170#diseaseC1306460","pred":"associated_with","subj":"23928928-11#42#52#geners4880","obj":"23928928-11#159#170#diseaseC1306460"}],"text":"Association between environmental tobacco smoke exposure and lung cancer susceptibility: modification by antioxidant enzyme genetic polymorphisms.\nBACKGROUND: Environmental tobacco smoke (ETS) is the primary etiologic factor responsible for lung cancer. However, only 10-15 % of smokers develop lung cancer, suggesting a genetic role in modifying individual susceptibility to lung cancer. Antioxidant enzymes and genetic polymorphisms should be considered.\nAIM: The present study aimed to evaluate the role of antioxidant enzyme activity and genetic polymorphisms in modifying the susceptibility to lung cancer among individuals exposed to ETS.\nSUBJECTS AND METHODS: A total of 150 male subjects were divided into three groups: 50 lung cancer patients, 50 chronic smokers, and 50 passive smokers. Genotyping of microsomal epoxide hydrolase (mEH) exon 3 (Tyr(113)Hist) and exon 4 (Hist(139)Arg) polymorphisms were done by the polymerase chain reaction-restriction fragment length polymorphism technique. MnSOD (Val(16)Ala) polymorphism was detected by the real time-TaqMan assay. Erythrocyte MnSOD activity was measured spectrophotometrically.\nRESULTS: ETS-exposed individuals (both active and passive smokers) who carried the His allele of mEH exon3 have a 2.9-fold increased risk of lung cancer (odds ratio [OR] 2.9, P \u003c 0.001). In addition, ETS-exposed carriers of the Arg allele of mEH exon 4 have a 2.1-fold increased risk of lung cancer (OR 2.1, P = 0.024). However, no association between the MnSOD Val(16)Ala polymorphism and lung cancer was detected among ETS-exposed individuals (OR 1.6, P = 0.147), although the lung cancer group had significantly lower MnSOD activity than the chronic or passive smoker groups (P = 0.03).\nCONCLUSIONS: Exons 3 and 4 polymorphisms of the mEH gene may contribute to lung cancer susceptibility through disturbed antioxidant balance. However, this was not the case with the MnSOD Val(16)Ala single-nucleotid polymorphism. Antioxidant enzymes may modulate the influence of ETS exposure on lung cancer risk."}

{"project":"DisGeNet-2017-sample","denotations":[{"id":"T923","span":{"begin":1499,"end":1504},"obj":"gene:6648"},{"id":"T924","span":{"begin":1533,"end":1544},"obj":"disease:C0242379"},{"id":"T925","span":{"begin":1505,"end":1515},"obj":"gene:6648"},{"id":"T926","span":{"begin":1622,"end":1633},"obj":"disease:C0242379"},{"id":"T927","span":{"begin":1664,"end":1669},"obj":"gene:6648"},{"id":"T928","span":{"begin":1781,"end":1784},"obj":"gene:2052"},{"id":"T929","span":{"begin":1808,"end":1819},"obj":"disease:C0242379"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T923","obj":"T924"},{"id":"R2","pred":"associated_with","subj":"T923","obj":"T924"},{"id":"R3","pred":"associated_with","subj":"T923","obj":"T924"},{"id":"R4","pred":"associated_with","subj":"T925","obj":"T924"},{"id":"R5","pred":"associated_with","subj":"T925","obj":"T924"},{"id":"R6","pred":"associated_with","subj":"T925","obj":"T924"},{"id":"R7","pred":"associated_with","subj":"T925","obj":"T926"},{"id":"R8","pred":"associated_with","subj":"T925","obj":"T926"},{"id":"R9","pred":"associated_with","subj":"T925","obj":"T926"},{"id":"R10","pred":"associated_with","subj":"T927","obj":"T924"},{"id":"R11","pred":"associated_with","subj":"T927","obj":"T924"},{"id":"R12","pred":"associated_with","subj":"T927","obj":"T924"},{"id":"R13","pred":"associated_with","subj":"T927","obj":"T926"},{"id":"R14","pred":"associated_with","subj":"T927","obj":"T926"},{"id":"R15","pred":"associated_with","subj":"T927","obj":"T926"},{"id":"R16","pred":"associated_with","subj":"T928","obj":"T929"},{"id":"R17","pred":"associated_with","subj":"T928","obj":"T929"},{"id":"R18","pred":"associated_with","subj":"T928","obj":"T929"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Association between environmental tobacco smoke exposure and lung cancer susceptibility: modification by antioxidant enzyme genetic polymorphisms.\nBACKGROUND: Environmental tobacco smoke (ETS) is the primary etiologic factor responsible for lung cancer. However, only 10-15 % of smokers develop lung cancer, suggesting a genetic role in modifying individual susceptibility to lung cancer. Antioxidant enzymes and genetic polymorphisms should be considered.\nAIM: The present study aimed to evaluate the role of antioxidant enzyme activity and genetic polymorphisms in modifying the susceptibility to lung cancer among individuals exposed to ETS.\nSUBJECTS AND METHODS: A total of 150 male subjects were divided into three groups: 50 lung cancer patients, 50 chronic smokers, and 50 passive smokers. Genotyping of microsomal epoxide hydrolase (mEH) exon 3 (Tyr(113)Hist) and exon 4 (Hist(139)Arg) polymorphisms were done by the polymerase chain reaction-restriction fragment length polymorphism technique. MnSOD (Val(16)Ala) polymorphism was detected by the real time-TaqMan assay. Erythrocyte MnSOD activity was measured spectrophotometrically.\nRESULTS: ETS-exposed individuals (both active and passive smokers) who carried the His allele of mEH exon3 have a 2.9-fold increased risk of lung cancer (odds ratio [OR] 2.9, P \u003c 0.001). In addition, ETS-exposed carriers of the Arg allele of mEH exon 4 have a 2.1-fold increased risk of lung cancer (OR 2.1, P = 0.024). However, no association between the MnSOD Val(16)Ala polymorphism and lung cancer was detected among ETS-exposed individuals (OR 1.6, P = 0.147), although the lung cancer group had significantly lower MnSOD activity than the chronic or passive smoker groups (P = 0.03).\nCONCLUSIONS: Exons 3 and 4 polymorphisms of the mEH gene may contribute to lung cancer susceptibility through disturbed antioxidant balance. However, this was not the case with the MnSOD Val(16)Ala single-nucleotid polymorphism. Antioxidant enzymes may modulate the influence of ETS exposure on lung cancer risk."}

{"project":"UBERON-AE","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":61,"end":65},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":241,"end":245},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":295,"end":299},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":376,"end":380},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":599,"end":603},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T6","span":{"begin":731,"end":735},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T7","span":{"begin":1284,"end":1288},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T8","span":{"begin":1430,"end":1434},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T9","span":{"begin":1533,"end":1537},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T10","span":{"begin":1622,"end":1626},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T11","span":{"begin":1808,"end":1812},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T12","span":{"begin":2028,"end":2032},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"}],"text":"Association between environmental tobacco smoke exposure and lung cancer susceptibility: modification by antioxidant enzyme genetic polymorphisms.\nBACKGROUND: Environmental tobacco smoke (ETS) is the primary etiologic factor responsible for lung cancer. However, only 10-15 % of smokers develop lung cancer, suggesting a genetic role in modifying individual susceptibility to lung cancer. Antioxidant enzymes and genetic polymorphisms should be considered.\nAIM: The present study aimed to evaluate the role of antioxidant enzyme activity and genetic polymorphisms in modifying the susceptibility to lung cancer among individuals exposed to ETS.\nSUBJECTS AND METHODS: A total of 150 male subjects were divided into three groups: 50 lung cancer patients, 50 chronic smokers, and 50 passive smokers. Genotyping of microsomal epoxide hydrolase (mEH) exon 3 (Tyr(113)Hist) and exon 4 (Hist(139)Arg) polymorphisms were done by the polymerase chain reaction-restriction fragment length polymorphism technique. MnSOD (Val(16)Ala) polymorphism was detected by the real time-TaqMan assay. Erythrocyte MnSOD activity was measured spectrophotometrically.\nRESULTS: ETS-exposed individuals (both active and passive smokers) who carried the His allele of mEH exon3 have a 2.9-fold increased risk of lung cancer (odds ratio [OR] 2.9, P \u003c 0.001). In addition, ETS-exposed carriers of the Arg allele of mEH exon 4 have a 2.1-fold increased risk of lung cancer (OR 2.1, P = 0.024). However, no association between the MnSOD Val(16)Ala polymorphism and lung cancer was detected among ETS-exposed individuals (OR 1.6, P = 0.147), although the lung cancer group had significantly lower MnSOD activity than the chronic or passive smoker groups (P = 0.03).\nCONCLUSIONS: Exons 3 and 4 polymorphisms of the mEH gene may contribute to lung cancer susceptibility through disturbed antioxidant balance. However, this was not the case with the MnSOD Val(16)Ala single-nucleotid polymorphism. Antioxidant enzymes may modulate the influence of ETS exposure on lung cancer risk."}

{"project":"performance-test","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":61,"end":65},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":241,"end":245},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":295,"end":299},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":376,"end":380},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":599,"end":603},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T6","span":{"begin":731,"end":735},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T7","span":{"begin":1284,"end":1288},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T8","span":{"begin":1430,"end":1434},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T9","span":{"begin":1533,"end":1537},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T10","span":{"begin":1622,"end":1626},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T11","span":{"begin":1808,"end":1812},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE-B_T12","span":{"begin":2028,"end":2032},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"}],"text":"Association between environmental tobacco smoke exposure and lung cancer susceptibility: modification by antioxidant enzyme genetic polymorphisms.\nBACKGROUND: Environmental tobacco smoke (ETS) is the primary etiologic factor responsible for lung cancer. However, only 10-15 % of smokers develop lung cancer, suggesting a genetic role in modifying individual susceptibility to lung cancer. Antioxidant enzymes and genetic polymorphisms should be considered.\nAIM: The present study aimed to evaluate the role of antioxidant enzyme activity and genetic polymorphisms in modifying the susceptibility to lung cancer among individuals exposed to ETS.\nSUBJECTS AND METHODS: A total of 150 male subjects were divided into three groups: 50 lung cancer patients, 50 chronic smokers, and 50 passive smokers. Genotyping of microsomal epoxide hydrolase (mEH) exon 3 (Tyr(113)Hist) and exon 4 (Hist(139)Arg) polymorphisms were done by the polymerase chain reaction-restriction fragment length polymorphism technique. MnSOD (Val(16)Ala) polymorphism was detected by the real time-TaqMan assay. Erythrocyte MnSOD activity was measured spectrophotometrically.\nRESULTS: ETS-exposed individuals (both active and passive smokers) who carried the His allele of mEH exon3 have a 2.9-fold increased risk of lung cancer (odds ratio [OR] 2.9, P \u003c 0.001). In addition, ETS-exposed carriers of the Arg allele of mEH exon 4 have a 2.1-fold increased risk of lung cancer (OR 2.1, P = 0.024). However, no association between the MnSOD Val(16)Ala polymorphism and lung cancer was detected among ETS-exposed individuals (OR 1.6, P = 0.147), although the lung cancer group had significantly lower MnSOD activity than the chronic or passive smoker groups (P = 0.03).\nCONCLUSIONS: Exons 3 and 4 polymorphisms of the mEH gene may contribute to lung cancer susceptibility through disturbed antioxidant balance. However, this was not the case with the MnSOD Val(16)Ala single-nucleotid polymorphism. Antioxidant enzymes may modulate the influence of ETS exposure on lung cancer risk."}