PubMed:22359319 JSONTXT

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":833,"end":839},"obj":"gene:1493"},{"id":"T1","span":{"begin":779,"end":796},"obj":"disease:C0346647"},{"id":"T2","span":{"begin":833,"end":839},"obj":"gene:1493"},{"id":"T3","span":{"begin":779,"end":796},"obj":"disease:C0235974"},{"id":"T4","span":{"begin":948,"end":954},"obj":"gene:1493"},{"id":"T5","span":{"begin":926,"end":943},"obj":"disease:C0346647"},{"id":"T6","span":{"begin":948,"end":954},"obj":"gene:1493"},{"id":"T7","span":{"begin":926,"end":943},"obj":"disease:C0235974"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"},{"id":"R2","pred":"associated_with","subj":"T2","obj":"T3"},{"id":"R3","pred":"associated_with","subj":"T4","obj":"T5"},{"id":"R4","pred":"associated_with","subj":"T6","obj":"T7"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"The functional cytotoxic T lymphocyte-associated Protein 4 49G-to-A genetic variant and risk of pancreatic cancer.\nBACKGROUND: Antitumor T lymphocytes play an essential part in immune surveillance of cancer cells. Cytotoxic T lymphocyte-associated Protein 4 (CTLA-4) is a negative regulator of T cell activation and proliferation and therefore influences immune surveillance of carcinogenesis of pancreas. Thus, this study examined the association between functional CTLA-4 49G-to-A (49G\u003eA) single-nucleotide polymorphism and pancreatic cancer risk.\nMETHODS: Genotypes were determined in 368 patients with pancreatic cancer and 926 controls, and odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by logistic regression.\nRESULTS: A significant increased risk of pancreatic cancer was found to be associated with the CTLA-4 49G\u003eA single-nucleotide polymorphism. Compared with noncarriers, the OR of developing pancreatic cancer for CTLA-4 49 GA or AA carriers was 1.75 (95% CI = 1.34-2.30, P = 4.83 × 10(-5) ) or 2.54 (95% CI = 1.67-3.87, P = 1.36 × 10(-5) ), respectively. In stratified analyses, the association was more pronounced in GA and AA carriers aged ≤60 years (OR = 3.10, 95% CI = 2.15-4.47, P(interaction) = .002), smokers with GA and AA genotypes (OR = 3.92, 95% CI = 2.39-6.43, P(interaction) = .037), and drinkers with GA and AA genotypes (OR = 4.55, 95% CI = 2.65-7.82, P(interaction) = .042), compared with GG carriers. Moreover, a supermultiplicative interaction between the CTLA-4 49AA genotype and smoking plus drinking was also evident in intensifying risk of pancreatic cancer (P(interaction) = 5.64 × 10(-12) ).\nCONCLUSIONS: These results suggest that CTLA-4 49G\u003eA polymorphism is involved in susceptibility to developing pancreatic cancer, alone and in a gene-environment interaction manner."}

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":200,"end":206},"obj":"HP_0002664"},{"id":"T2","span":{"begin":526,"end":543},"obj":"HP_0002894"},{"id":"T3","span":{"begin":537,"end":543},"obj":"HP_0002664"}],"text":"The functional cytotoxic T lymphocyte-associated Protein 4 49G-to-A genetic variant and risk of pancreatic cancer.\nBACKGROUND: Antitumor T lymphocytes play an essential part in immune surveillance of cancer cells. Cytotoxic T lymphocyte-associated Protein 4 (CTLA-4) is a negative regulator of T cell activation and proliferation and therefore influences immune surveillance of carcinogenesis of pancreas. Thus, this study examined the association between functional CTLA-4 49G-to-A (49G\u003eA) single-nucleotide polymorphism and pancreatic cancer risk.\nMETHODS: Genotypes were determined in 368 patients with pancreatic cancer and 926 controls, and odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by logistic regression.\nRESULTS: A significant increased risk of pancreatic cancer was found to be associated with the CTLA-4 49G\u003eA single-nucleotide polymorphism. Compared with noncarriers, the OR of developing pancreatic cancer for CTLA-4 49 GA or AA carriers was 1.75 (95% CI = 1.34-2.30, P = 4.83 × 10(-5) ) or 2.54 (95% CI = 1.67-3.87, P = 1.36 × 10(-5) ), respectively. In stratified analyses, the association was more pronounced in GA and AA carriers aged ≤60 years (OR = 3.10, 95% CI = 2.15-4.47, P(interaction) = .002), smokers with GA and AA genotypes (OR = 3.92, 95% CI = 2.39-6.43, P(interaction) = .037), and drinkers with GA and AA genotypes (OR = 4.55, 95% CI = 2.65-7.82, P(interaction) = .042), compared with GG carriers. Moreover, a supermultiplicative interaction between the CTLA-4 49AA genotype and smoking plus drinking was also evident in intensifying risk of pancreatic cancer (P(interaction) = 5.64 × 10(-12) ).\nCONCLUSIONS: These results suggest that CTLA-4 49G\u003eA polymorphism is involved in susceptibility to developing pancreatic cancer, alone and in a gene-environment interaction manner."}

{"project":"Allie","denotations":[{"id":"SS1_22359319_3_0","span":{"begin":214,"end":257},"obj":"expanded"},{"id":"SS2_22359319_3_0","span":{"begin":259,"end":265},"obj":"abbr"},{"id":"SS1_22359319_6_0","span":{"begin":646,"end":657},"obj":"expanded"},{"id":"SS2_22359319_6_0","span":{"begin":659,"end":662},"obj":"abbr"},{"id":"SS1_22359319_6_1","span":{"begin":672,"end":692},"obj":"expanded"},{"id":"SS2_22359319_6_1","span":{"begin":694,"end":697},"obj":"abbr"}],"relations":[{"id":"AE1_22359319_3_0","pred":"abbreviatedTo","subj":"SS1_22359319_3_0","obj":"SS2_22359319_3_0"},{"id":"AE1_22359319_6_0","pred":"abbreviatedTo","subj":"SS1_22359319_6_0","obj":"SS2_22359319_6_0"},{"id":"AE1_22359319_6_1","pred":"abbreviatedTo","subj":"SS1_22359319_6_1","obj":"SS2_22359319_6_1"}],"text":"The functional cytotoxic T lymphocyte-associated Protein 4 49G-to-A genetic variant and risk of pancreatic cancer.\nBACKGROUND: Antitumor T lymphocytes play an essential part in immune surveillance of cancer cells. Cytotoxic T lymphocyte-associated Protein 4 (CTLA-4) is a negative regulator of T cell activation and proliferation and therefore influences immune surveillance of carcinogenesis of pancreas. Thus, this study examined the association between functional CTLA-4 49G-to-A (49G\u003eA) single-nucleotide polymorphism and pancreatic cancer risk.\nMETHODS: Genotypes were determined in 368 patients with pancreatic cancer and 926 controls, and odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by logistic regression.\nRESULTS: A significant increased risk of pancreatic cancer was found to be associated with the CTLA-4 49G\u003eA single-nucleotide polymorphism. Compared with noncarriers, the OR of developing pancreatic cancer for CTLA-4 49 GA or AA carriers was 1.75 (95% CI = 1.34-2.30, P = 4.83 × 10(-5) ) or 2.54 (95% CI = 1.67-3.87, P = 1.36 × 10(-5) ), respectively. In stratified analyses, the association was more pronounced in GA and AA carriers aged ≤60 years (OR = 3.10, 95% CI = 2.15-4.47, P(interaction) = .002), smokers with GA and AA genotypes (OR = 3.92, 95% CI = 2.39-6.43, P(interaction) = .037), and drinkers with GA and AA genotypes (OR = 4.55, 95% CI = 2.65-7.82, P(interaction) = .042), compared with GG carriers. Moreover, a supermultiplicative interaction between the CTLA-4 49AA genotype and smoking plus drinking was also evident in intensifying risk of pancreatic cancer (P(interaction) = 5.64 × 10(-12) ).\nCONCLUSIONS: These results suggest that CTLA-4 49G\u003eA polymorphism is involved in susceptibility to developing pancreatic cancer, alone and in a gene-environment interaction manner."}

{"project":"DisGeNET5_variant_disease","denotations":[{"id":"22359319-9#34#39#geners231775","span":{"begin":1698,"end":1703},"obj":"geners231775"},{"id":"22359319-9#97#114#diseaseC0235974","span":{"begin":1761,"end":1778},"obj":"diseaseC0235974"},{"id":"22359319-9#97#114#diseaseC0346647","span":{"begin":1761,"end":1778},"obj":"diseaseC0346647"}],"relations":[{"id":"34#39#geners23177597#114#diseaseC0235974","pred":"associated_with","subj":"22359319-9#34#39#geners231775","obj":"22359319-9#97#114#diseaseC0235974"},{"id":"34#39#geners23177597#114#diseaseC0346647","pred":"associated_with","subj":"22359319-9#34#39#geners231775","obj":"22359319-9#97#114#diseaseC0346647"}],"text":"The functional cytotoxic T lymphocyte-associated Protein 4 49G-to-A genetic variant and risk of pancreatic cancer.\nBACKGROUND: Antitumor T lymphocytes play an essential part in immune surveillance of cancer cells. Cytotoxic T lymphocyte-associated Protein 4 (CTLA-4) is a negative regulator of T cell activation and proliferation and therefore influences immune surveillance of carcinogenesis of pancreas. Thus, this study examined the association between functional CTLA-4 49G-to-A (49G\u003eA) single-nucleotide polymorphism and pancreatic cancer risk.\nMETHODS: Genotypes were determined in 368 patients with pancreatic cancer and 926 controls, and odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by logistic regression.\nRESULTS: A significant increased risk of pancreatic cancer was found to be associated with the CTLA-4 49G\u003eA single-nucleotide polymorphism. Compared with noncarriers, the OR of developing pancreatic cancer for CTLA-4 49 GA or AA carriers was 1.75 (95% CI = 1.34-2.30, P = 4.83 × 10(-5) ) or 2.54 (95% CI = 1.67-3.87, P = 1.36 × 10(-5) ), respectively. In stratified analyses, the association was more pronounced in GA and AA carriers aged ≤60 years (OR = 3.10, 95% CI = 2.15-4.47, P(interaction) = .002), smokers with GA and AA genotypes (OR = 3.92, 95% CI = 2.39-6.43, P(interaction) = .037), and drinkers with GA and AA genotypes (OR = 4.55, 95% CI = 2.65-7.82, P(interaction) = .042), compared with GG carriers. Moreover, a supermultiplicative interaction between the CTLA-4 49AA genotype and smoking plus drinking was also evident in intensifying risk of pancreatic cancer (P(interaction) = 5.64 × 10(-12) ).\nCONCLUSIONS: These results suggest that CTLA-4 49G\u003eA polymorphism is involved in susceptibility to developing pancreatic cancer, alone and in a gene-environment interaction manner."}

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"22359319-0#15#58#gene1493","span":{"begin":15,"end":58},"obj":"gene1493"},{"id":"22359319-0#96#113#diseaseC0235974","span":{"begin":96,"end":113},"obj":"diseaseC0235974"},{"id":"22359319-0#96#113#diseaseC0346647","span":{"begin":96,"end":113},"obj":"diseaseC0346647"},{"id":"22359319-2#0#43#gene1493","span":{"begin":214,"end":257},"obj":"gene1493"},{"id":"22359319-2#45#51#gene1493","span":{"begin":259,"end":265},"obj":"gene1493"},{"id":"22359319-2#164#178#diseaseC0596263","span":{"begin":378,"end":392},"obj":"diseaseC0596263"}],"relations":[{"id":"15#58#gene149396#113#diseaseC0235974","pred":"associated_with","subj":"22359319-0#15#58#gene1493","obj":"22359319-0#96#113#diseaseC0235974"},{"id":"15#58#gene149396#113#diseaseC0346647","pred":"associated_with","subj":"22359319-0#15#58#gene1493","obj":"22359319-0#96#113#diseaseC0346647"},{"id":"0#43#gene1493164#178#diseaseC0596263","pred":"associated_with","subj":"22359319-2#0#43#gene1493","obj":"22359319-2#164#178#diseaseC0596263"},{"id":"45#51#gene1493164#178#diseaseC0596263","pred":"associated_with","subj":"22359319-2#45#51#gene1493","obj":"22359319-2#164#178#diseaseC0596263"}],"text":"The functional cytotoxic T lymphocyte-associated Protein 4 49G-to-A genetic variant and risk of pancreatic cancer.\nBACKGROUND: Antitumor T lymphocytes play an essential part in immune surveillance of cancer cells. Cytotoxic T lymphocyte-associated Protein 4 (CTLA-4) is a negative regulator of T cell activation and proliferation and therefore influences immune surveillance of carcinogenesis of pancreas. Thus, this study examined the association between functional CTLA-4 49G-to-A (49G\u003eA) single-nucleotide polymorphism and pancreatic cancer risk.\nMETHODS: Genotypes were determined in 368 patients with pancreatic cancer and 926 controls, and odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by logistic regression.\nRESULTS: A significant increased risk of pancreatic cancer was found to be associated with the CTLA-4 49G\u003eA single-nucleotide polymorphism. Compared with noncarriers, the OR of developing pancreatic cancer for CTLA-4 49 GA or AA carriers was 1.75 (95% CI = 1.34-2.30, P = 4.83 × 10(-5) ) or 2.54 (95% CI = 1.67-3.87, P = 1.36 × 10(-5) ), respectively. In stratified analyses, the association was more pronounced in GA and AA carriers aged ≤60 years (OR = 3.10, 95% CI = 2.15-4.47, P(interaction) = .002), smokers with GA and AA genotypes (OR = 3.92, 95% CI = 2.39-6.43, P(interaction) = .037), and drinkers with GA and AA genotypes (OR = 4.55, 95% CI = 2.65-7.82, P(interaction) = .042), compared with GG carriers. Moreover, a supermultiplicative interaction between the CTLA-4 49AA genotype and smoking plus drinking was also evident in intensifying risk of pancreatic cancer (P(interaction) = 5.64 × 10(-12) ).\nCONCLUSIONS: These results suggest that CTLA-4 49G\u003eA polymorphism is involved in susceptibility to developing pancreatic cancer, alone and in a gene-environment interaction manner."}