PubMed:24023501
Annnotations
sentences
{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":59},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":60,"end":64},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":65,"end":275},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":276,"end":284},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":285,"end":474},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":475,"end":608},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":609,"end":761},"obj":"Sentence"},{"id":"TextSentencer_T8","span":{"begin":762,"end":770},"obj":"Sentence"},{"id":"TextSentencer_T9","span":{"begin":771,"end":1101},"obj":"Sentence"},{"id":"TextSentencer_T10","span":{"begin":1102,"end":1356},"obj":"Sentence"},{"id":"TextSentencer_T11","span":{"begin":1357,"end":1559},"obj":"Sentence"},{"id":"TextSentencer_T12","span":{"begin":1560,"end":1723},"obj":"Sentence"},{"id":"TextSentencer_T13","span":{"begin":1724,"end":1876},"obj":"Sentence"},{"id":"TextSentencer_T14","span":{"begin":1877,"end":1979},"obj":"Sentence"},{"id":"TextSentencer_T15","span":{"begin":1980,"end":1991},"obj":"Sentence"},{"id":"TextSentencer_T16","span":{"begin":1992,"end":2060},"obj":"Sentence"},{"id":"TextSentencer_T17","span":{"begin":2061,"end":2157},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":59},"obj":"Sentence"},{"id":"T2","span":{"begin":60,"end":64},"obj":"Sentence"},{"id":"T3","span":{"begin":65,"end":275},"obj":"Sentence"},{"id":"T4","span":{"begin":276,"end":284},"obj":"Sentence"},{"id":"T5","span":{"begin":285,"end":474},"obj":"Sentence"},{"id":"T6","span":{"begin":475,"end":608},"obj":"Sentence"},{"id":"T7","span":{"begin":609,"end":761},"obj":"Sentence"},{"id":"T8","span":{"begin":762,"end":770},"obj":"Sentence"},{"id":"T9","span":{"begin":771,"end":1101},"obj":"Sentence"},{"id":"T10","span":{"begin":1102,"end":1356},"obj":"Sentence"},{"id":"T11","span":{"begin":1357,"end":1559},"obj":"Sentence"},{"id":"T12","span":{"begin":1560,"end":1723},"obj":"Sentence"},{"id":"T13","span":{"begin":1724,"end":1876},"obj":"Sentence"},{"id":"T14","span":{"begin":1877,"end":1979},"obj":"Sentence"},{"id":"T15","span":{"begin":1980,"end":1991},"obj":"Sentence"},{"id":"T16","span":{"begin":1992,"end":2060},"obj":"Sentence"},{"id":"T17","span":{"begin":2061,"end":2157},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Hypermethylation of TGF-β1 gene promoter in gastric cancer.\nAIM: To examine transforming growth factor-β1 (TGF-β1) promoter methylation in gastric cancer and to determine if Helicobacter pylori (H. pylori) or interleukin (IL)-1β could induce TGF-β1 hypermethylation in vitro.\nMETHODS: We examined the frequency and extent of TGF-β1 promoter methylation using methylation-specific PCR in the gastric tissues from 47 gastric cancer patients and 39 non-gastric cancer subjects. H. pylori infection was confirmed by a positive result from either a serological test, histological analysis or C¹³ urea breath test. GES-1 and MKN-45 cells co-cultured with H. pylori or treated with IL-1β for 12, 24 and 48 h in vitro tested the effects of H. pylori or IL-1β on TGF-β1.\nRESULTS: Twenty-four/forty-seven (51%) cases of gastric cancer (GC) tissues showed TGF-β1 promoter methylation, 15/47 (31.9%) cases of matched non-cancerous gastric mucosa tissues from the GC patients, and 11/39 (28%) case of the normal gastric mucosa tissues from non-GC subjects showed TGF-β1 promoter methylation (51% vs 28%, P \u003c 0.05). Significantly higher levels of methylation of TGF-β1 were found in the tumor tissues than in non-tumor tissues from GC patients (0.24 ± 0.06 vs 0.17 ± 0.04, P \u003c 0.05) and normal gastric tissues from non-GC subjects (0.24 ± 0.06 vs 0.15 ± 0.03, P \u003c 0.05). TGF-β1 methylation was found in 48.3% of H. pylori-positive gastric mucosal tissues whereas only 23.1% of H. pylori-negative gastric mucosal tissues showed TGF-β1 methylation (48.3% vs 23.1%, P \u003c 0.05). IL-1β appeared to induce a dose-dependent methylation of TGF-β1 and the strongest methylation was observed in GES-1 cells treated with 2.5 ng/mL of IL-1β for 48 h. Further studies showed that pre-treatment of GES-1 cells with 20 ng/mL IL-1RA for 1 h could partially abolish the effect of IL-1β on TGF-β1 methylation. Infection of GES-1 cells by H. pylori was not found to induce significant TGF-β1 promoter methylation.\nCONCLUSION: Our data revealed that TGF-β1 promoter is methylated in GC patients. IL-1β may be an important mediator for H. pylori induced gene methylation during GC development."}
DisGeNET
{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":2015,"end":2021},"obj":"gene:7040"},{"id":"T1","span":{"begin":2048,"end":2050},"obj":"disease:C0024623"},{"id":"T2","span":{"begin":2015,"end":2021},"obj":"gene:7040"},{"id":"T3","span":{"begin":2048,"end":2050},"obj":"disease:C0699791"},{"id":"T4","span":{"begin":2061,"end":2066},"obj":"gene:3553"},{"id":"T5","span":{"begin":2142,"end":2144},"obj":"disease:C0024623"},{"id":"T6","span":{"begin":2061,"end":2066},"obj":"gene:3553"},{"id":"T7","span":{"begin":2142,"end":2144},"obj":"disease:C0699791"}],"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":"Hypermethylation of TGF-β1 gene promoter in gastric cancer.\nAIM: To examine transforming growth factor-β1 (TGF-β1) promoter methylation in gastric cancer and to determine if Helicobacter pylori (H. pylori) or interleukin (IL)-1β could induce TGF-β1 hypermethylation in vitro.\nMETHODS: We examined the frequency and extent of TGF-β1 promoter methylation using methylation-specific PCR in the gastric tissues from 47 gastric cancer patients and 39 non-gastric cancer subjects. H. pylori infection was confirmed by a positive result from either a serological test, histological analysis or C¹³ urea breath test. GES-1 and MKN-45 cells co-cultured with H. pylori or treated with IL-1β for 12, 24 and 48 h in vitro tested the effects of H. pylori or IL-1β on TGF-β1.\nRESULTS: Twenty-four/forty-seven (51%) cases of gastric cancer (GC) tissues showed TGF-β1 promoter methylation, 15/47 (31.9%) cases of matched non-cancerous gastric mucosa tissues from the GC patients, and 11/39 (28%) case of the normal gastric mucosa tissues from non-GC subjects showed TGF-β1 promoter methylation (51% vs 28%, P \u003c 0.05). Significantly higher levels of methylation of TGF-β1 were found in the tumor tissues than in non-tumor tissues from GC patients (0.24 ± 0.06 vs 0.17 ± 0.04, P \u003c 0.05) and normal gastric tissues from non-GC subjects (0.24 ± 0.06 vs 0.15 ± 0.03, P \u003c 0.05). TGF-β1 methylation was found in 48.3% of H. pylori-positive gastric mucosal tissues whereas only 23.1% of H. pylori-negative gastric mucosal tissues showed TGF-β1 methylation (48.3% vs 23.1%, P \u003c 0.05). IL-1β appeared to induce a dose-dependent methylation of TGF-β1 and the strongest methylation was observed in GES-1 cells treated with 2.5 ng/mL of IL-1β for 48 h. Further studies showed that pre-treatment of GES-1 cells with 20 ng/mL IL-1RA for 1 h could partially abolish the effect of IL-1β on TGF-β1 methylation. Infection of GES-1 cells by H. pylori was not found to induce significant TGF-β1 promoter methylation.\nCONCLUSION: Our data revealed that TGF-β1 promoter is methylated in GC patients. IL-1β may be an important mediator for H. pylori induced gene methylation during GC development."}
PubmedHPO
{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":139,"end":153},"obj":"HP_0012126"},{"id":"T2","span":{"begin":147,"end":153},"obj":"HP_0002664"}],"text":"Hypermethylation of TGF-β1 gene promoter in gastric cancer.\nAIM: To examine transforming growth factor-β1 (TGF-β1) promoter methylation in gastric cancer and to determine if Helicobacter pylori (H. pylori) or interleukin (IL)-1β could induce TGF-β1 hypermethylation in vitro.\nMETHODS: We examined the frequency and extent of TGF-β1 promoter methylation using methylation-specific PCR in the gastric tissues from 47 gastric cancer patients and 39 non-gastric cancer subjects. H. pylori infection was confirmed by a positive result from either a serological test, histological analysis or C¹³ urea breath test. GES-1 and MKN-45 cells co-cultured with H. pylori or treated with IL-1β for 12, 24 and 48 h in vitro tested the effects of H. pylori or IL-1β on TGF-β1.\nRESULTS: Twenty-four/forty-seven (51%) cases of gastric cancer (GC) tissues showed TGF-β1 promoter methylation, 15/47 (31.9%) cases of matched non-cancerous gastric mucosa tissues from the GC patients, and 11/39 (28%) case of the normal gastric mucosa tissues from non-GC subjects showed TGF-β1 promoter methylation (51% vs 28%, P \u003c 0.05). Significantly higher levels of methylation of TGF-β1 were found in the tumor tissues than in non-tumor tissues from GC patients (0.24 ± 0.06 vs 0.17 ± 0.04, P \u003c 0.05) and normal gastric tissues from non-GC subjects (0.24 ± 0.06 vs 0.15 ± 0.03, P \u003c 0.05). TGF-β1 methylation was found in 48.3% of H. pylori-positive gastric mucosal tissues whereas only 23.1% of H. pylori-negative gastric mucosal tissues showed TGF-β1 methylation (48.3% vs 23.1%, P \u003c 0.05). IL-1β appeared to induce a dose-dependent methylation of TGF-β1 and the strongest methylation was observed in GES-1 cells treated with 2.5 ng/mL of IL-1β for 48 h. Further studies showed that pre-treatment of GES-1 cells with 20 ng/mL IL-1RA for 1 h could partially abolish the effect of IL-1β on TGF-β1 methylation. Infection of GES-1 cells by H. pylori was not found to induce significant TGF-β1 promoter methylation.\nCONCLUSION: Our data revealed that TGF-β1 promoter is methylated in GC patients. IL-1β may be an important mediator for H. pylori induced gene methylation during GC development."}
Allie
{"project":"Allie","denotations":[{"id":"SS1_24023501_2_0","span":{"begin":76,"end":105},"obj":"expanded"},{"id":"SS2_24023501_2_0","span":{"begin":107,"end":113},"obj":"abbr"},{"id":"SS1_24023501_2_1","span":{"begin":174,"end":193},"obj":"expanded"},{"id":"SS2_24023501_2_1","span":{"begin":195,"end":204},"obj":"abbr"},{"id":"SS1_24023501_2_2","span":{"begin":209,"end":220},"obj":"expanded"},{"id":"SS2_24023501_2_2","span":{"begin":222,"end":224},"obj":"abbr"},{"id":"SS1_24023501_8_0","span":{"begin":810,"end":824},"obj":"expanded"},{"id":"SS2_24023501_8_0","span":{"begin":826,"end":828},"obj":"abbr"}],"relations":[{"id":"AE1_24023501_2_0","pred":"abbreviatedTo","subj":"SS1_24023501_2_0","obj":"SS2_24023501_2_0"},{"id":"AE1_24023501_2_1","pred":"abbreviatedTo","subj":"SS1_24023501_2_1","obj":"SS2_24023501_2_1"},{"id":"AE1_24023501_2_2","pred":"abbreviatedTo","subj":"SS1_24023501_2_2","obj":"SS2_24023501_2_2"},{"id":"AE1_24023501_8_0","pred":"abbreviatedTo","subj":"SS1_24023501_8_0","obj":"SS2_24023501_8_0"}],"text":"Hypermethylation of TGF-β1 gene promoter in gastric cancer.\nAIM: To examine transforming growth factor-β1 (TGF-β1) promoter methylation in gastric cancer and to determine if Helicobacter pylori (H. pylori) or interleukin (IL)-1β could induce TGF-β1 hypermethylation in vitro.\nMETHODS: We examined the frequency and extent of TGF-β1 promoter methylation using methylation-specific PCR in the gastric tissues from 47 gastric cancer patients and 39 non-gastric cancer subjects. H. pylori infection was confirmed by a positive result from either a serological test, histological analysis or C¹³ urea breath test. GES-1 and MKN-45 cells co-cultured with H. pylori or treated with IL-1β for 12, 24 and 48 h in vitro tested the effects of H. pylori or IL-1β on TGF-β1.\nRESULTS: Twenty-four/forty-seven (51%) cases of gastric cancer (GC) tissues showed TGF-β1 promoter methylation, 15/47 (31.9%) cases of matched non-cancerous gastric mucosa tissues from the GC patients, and 11/39 (28%) case of the normal gastric mucosa tissues from non-GC subjects showed TGF-β1 promoter methylation (51% vs 28%, P \u003c 0.05). Significantly higher levels of methylation of TGF-β1 were found in the tumor tissues than in non-tumor tissues from GC patients (0.24 ± 0.06 vs 0.17 ± 0.04, P \u003c 0.05) and normal gastric tissues from non-GC subjects (0.24 ± 0.06 vs 0.15 ± 0.03, P \u003c 0.05). TGF-β1 methylation was found in 48.3% of H. pylori-positive gastric mucosal tissues whereas only 23.1% of H. pylori-negative gastric mucosal tissues showed TGF-β1 methylation (48.3% vs 23.1%, P \u003c 0.05). IL-1β appeared to induce a dose-dependent methylation of TGF-β1 and the strongest methylation was observed in GES-1 cells treated with 2.5 ng/mL of IL-1β for 48 h. Further studies showed that pre-treatment of GES-1 cells with 20 ng/mL IL-1RA for 1 h could partially abolish the effect of IL-1β on TGF-β1 methylation. Infection of GES-1 cells by H. pylori was not found to induce significant TGF-β1 promoter methylation.\nCONCLUSION: Our data revealed that TGF-β1 promoter is methylated in GC patients. IL-1β may be an important mediator for H. pylori induced gene methylation during GC development."}
DisGeNET5_gene_disease
{"project":"DisGeNET5_gene_disease","denotations":[{"id":"24023501-0#20#26#gene7040","span":{"begin":1050,"end":1056},"obj":"gene7040"},{"id":"24023501-0#44#58#diseaseC0024623","span":{"begin":1475,"end":1635},"obj":"diseaseC0024623"},{"id":"24023501-0#44#58#diseaseC0699791","span":{"begin":1475,"end":1635},"obj":"diseaseC0699791"},{"id":"24023501-1#11#40#gene7040","span":{"begin":76,"end":105},"obj":"gene7040"},{"id":"24023501-1#42#48#gene7040","span":{"begin":107,"end":113},"obj":"gene7040"},{"id":"24023501-1#177#183#gene7040","span":{"begin":242,"end":248},"obj":"gene7040"},{"id":"24023501-1#109#139#diseaseC0374997","span":{"begin":174,"end":204},"obj":"diseaseC0374997"},{"id":"24023501-11#0#5#gene3553","span":{"begin":2061,"end":2066},"obj":"gene3553"},{"id":"24023501-11#81#83#diseaseC0024623","span":{"begin":2142,"end":2144},"obj":"diseaseC0024623"},{"id":"24023501-11#81#83#diseaseC0699791","span":{"begin":2142,"end":2144},"obj":"diseaseC0699791"}],"relations":[{"id":"20#26#gene704044#58#diseaseC0024623","pred":"associated_with","subj":"24023501-0#20#26#gene7040","obj":"24023501-0#44#58#diseaseC0024623"},{"id":"20#26#gene704044#58#diseaseC0699791","pred":"associated_with","subj":"24023501-0#20#26#gene7040","obj":"24023501-0#44#58#diseaseC0699791"},{"id":"11#40#gene7040109#139#diseaseC0374997","pred":"associated_with","subj":"24023501-1#11#40#gene7040","obj":"24023501-1#109#139#diseaseC0374997"},{"id":"42#48#gene7040109#139#diseaseC0374997","pred":"associated_with","subj":"24023501-1#42#48#gene7040","obj":"24023501-1#109#139#diseaseC0374997"},{"id":"177#183#gene7040109#139#diseaseC0374997","pred":"associated_with","subj":"24023501-1#177#183#gene7040","obj":"24023501-1#109#139#diseaseC0374997"},{"id":"0#5#gene355381#83#diseaseC0024623","pred":"associated_with","subj":"24023501-11#0#5#gene3553","obj":"24023501-11#81#83#diseaseC0024623"},{"id":"0#5#gene355381#83#diseaseC0699791","pred":"associated_with","subj":"24023501-11#0#5#gene3553","obj":"24023501-11#81#83#diseaseC0699791"}],"text":"Hypermethylation of TGF-β1 gene promoter in gastric cancer.\nAIM: To examine transforming growth factor-β1 (TGF-β1) promoter methylation in gastric cancer and to determine if Helicobacter pylori (H. pylori) or interleukin (IL)-1β could induce TGF-β1 hypermethylation in vitro.\nMETHODS: We examined the frequency and extent of TGF-β1 promoter methylation using methylation-specific PCR in the gastric tissues from 47 gastric cancer patients and 39 non-gastric cancer subjects. H. pylori infection was confirmed by a positive result from either a serological test, histological analysis or C¹³ urea breath test. GES-1 and MKN-45 cells co-cultured with H. pylori or treated with IL-1β for 12, 24 and 48 h in vitro tested the effects of H. pylori or IL-1β on TGF-β1.\nRESULTS: Twenty-four/forty-seven (51%) cases of gastric cancer (GC) tissues showed TGF-β1 promoter methylation, 15/47 (31.9%) cases of matched non-cancerous gastric mucosa tissues from the GC patients, and 11/39 (28%) case of the normal gastric mucosa tissues from non-GC subjects showed TGF-β1 promoter methylation (51% vs 28%, P \u003c 0.05). Significantly higher levels of methylation of TGF-β1 were found in the tumor tissues than in non-tumor tissues from GC patients (0.24 ± 0.06 vs 0.17 ± 0.04, P \u003c 0.05) and normal gastric tissues from non-GC subjects (0.24 ± 0.06 vs 0.15 ± 0.03, P \u003c 0.05). TGF-β1 methylation was found in 48.3% of H. pylori-positive gastric mucosal tissues whereas only 23.1% of H. pylori-negative gastric mucosal tissues showed TGF-β1 methylation (48.3% vs 23.1%, P \u003c 0.05). IL-1β appeared to induce a dose-dependent methylation of TGF-β1 and the strongest methylation was observed in GES-1 cells treated with 2.5 ng/mL of IL-1β for 48 h. Further studies showed that pre-treatment of GES-1 cells with 20 ng/mL IL-1RA for 1 h could partially abolish the effect of IL-1β on TGF-β1 methylation. Infection of GES-1 cells by H. pylori was not found to induce significant TGF-β1 promoter methylation.\nCONCLUSION: Our data revealed that TGF-β1 promoter is methylated in GC patients. IL-1β may be an important mediator for H. pylori induced gene methylation during GC development."}
DisGeNet-2017-sample
{"project":"DisGeNet-2017-sample","denotations":[{"id":"T756","span":{"begin":1050,"end":1056},"obj":"gene:7040"},{"id":"T757","span":{"begin":1475,"end":1635},"obj":"disease:C0024623"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T756","obj":"T757"},{"id":"R2","pred":"associated_with","subj":"T756","obj":"T757"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Hypermethylation of TGF-β1 gene promoter in gastric cancer.\nAIM: To examine transforming growth factor-β1 (TGF-β1) promoter methylation in gastric cancer and to determine if Helicobacter pylori (H. pylori) or interleukin (IL)-1β could induce TGF-β1 hypermethylation in vitro.\nMETHODS: We examined the frequency and extent of TGF-β1 promoter methylation using methylation-specific PCR in the gastric tissues from 47 gastric cancer patients and 39 non-gastric cancer subjects. H. pylori infection was confirmed by a positive result from either a serological test, histological analysis or C¹³ urea breath test. GES-1 and MKN-45 cells co-cultured with H. pylori or treated with IL-1β for 12, 24 and 48 h in vitro tested the effects of H. pylori or IL-1β on TGF-β1.\nRESULTS: Twenty-four/forty-seven (51%) cases of gastric cancer (GC) tissues showed TGF-β1 promoter methylation, 15/47 (31.9%) cases of matched non-cancerous gastric mucosa tissues from the GC patients, and 11/39 (28%) case of the normal gastric mucosa tissues from non-GC subjects showed TGF-β1 promoter methylation (51% vs 28%, P \u003c 0.05). Significantly higher levels of methylation of TGF-β1 were found in the tumor tissues than in non-tumor tissues from GC patients (0.24 ± 0.06 vs 0.17 ± 0.04, P \u003c 0.05) and normal gastric tissues from non-GC subjects (0.24 ± 0.06 vs 0.15 ± 0.03, P \u003c 0.05). TGF-β1 methylation was found in 48.3% of H. pylori-positive gastric mucosal tissues whereas only 23.1% of H. pylori-negative gastric mucosal tissues showed TGF-β1 methylation (48.3% vs 23.1%, P \u003c 0.05). IL-1β appeared to induce a dose-dependent methylation of TGF-β1 and the strongest methylation was observed in GES-1 cells treated with 2.5 ng/mL of IL-1β for 48 h. Further studies showed that pre-treatment of GES-1 cells with 20 ng/mL IL-1RA for 1 h could partially abolish the effect of IL-1β on TGF-β1 methylation. Infection of GES-1 cells by H. pylori was not found to induce significant TGF-β1 promoter methylation.\nCONCLUSION: Our data revealed that TGF-β1 promoter is methylated in GC patients. IL-1β may be an important mediator for H. pylori induced gene methylation during GC development."}
UBERON-AE
{"project":"UBERON-AE","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":399,"end":406},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":830,"end":837},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":934,"end":941},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":1014,"end":1021},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":1179,"end":1186},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T6","span":{"begin":1205,"end":1212},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T7","span":{"begin":1288,"end":1295},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T8","span":{"begin":1433,"end":1440},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T9","span":{"begin":1498,"end":1505},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T10","span":{"begin":927,"end":933},"obj":"http://purl.obolibrary.org/obo/UBERON_0000344"},{"id":"PD-UBERON-AE-B_T11","span":{"begin":1007,"end":1013},"obj":"http://purl.obolibrary.org/obo/UBERON_0000344"}],"text":"Hypermethylation of TGF-β1 gene promoter in gastric cancer.\nAIM: To examine transforming growth factor-β1 (TGF-β1) promoter methylation in gastric cancer and to determine if Helicobacter pylori (H. pylori) or interleukin (IL)-1β could induce TGF-β1 hypermethylation in vitro.\nMETHODS: We examined the frequency and extent of TGF-β1 promoter methylation using methylation-specific PCR in the gastric tissues from 47 gastric cancer patients and 39 non-gastric cancer subjects. H. pylori infection was confirmed by a positive result from either a serological test, histological analysis or C¹³ urea breath test. GES-1 and MKN-45 cells co-cultured with H. pylori or treated with IL-1β for 12, 24 and 48 h in vitro tested the effects of H. pylori or IL-1β on TGF-β1.\nRESULTS: Twenty-four/forty-seven (51%) cases of gastric cancer (GC) tissues showed TGF-β1 promoter methylation, 15/47 (31.9%) cases of matched non-cancerous gastric mucosa tissues from the GC patients, and 11/39 (28%) case of the normal gastric mucosa tissues from non-GC subjects showed TGF-β1 promoter methylation (51% vs 28%, P \u003c 0.05). Significantly higher levels of methylation of TGF-β1 were found in the tumor tissues than in non-tumor tissues from GC patients (0.24 ± 0.06 vs 0.17 ± 0.04, P \u003c 0.05) and normal gastric tissues from non-GC subjects (0.24 ± 0.06 vs 0.15 ± 0.03, P \u003c 0.05). TGF-β1 methylation was found in 48.3% of H. pylori-positive gastric mucosal tissues whereas only 23.1% of H. pylori-negative gastric mucosal tissues showed TGF-β1 methylation (48.3% vs 23.1%, P \u003c 0.05). IL-1β appeared to induce a dose-dependent methylation of TGF-β1 and the strongest methylation was observed in GES-1 cells treated with 2.5 ng/mL of IL-1β for 48 h. Further studies showed that pre-treatment of GES-1 cells with 20 ng/mL IL-1RA for 1 h could partially abolish the effect of IL-1β on TGF-β1 methylation. Infection of GES-1 cells by H. pylori was not found to induce significant TGF-β1 promoter methylation.\nCONCLUSION: Our data revealed that TGF-β1 promoter is methylated in GC patients. IL-1β may be an important mediator for H. pylori induced gene methylation during GC development."}
performance-test
{"project":"performance-test","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":927,"end":933},"obj":"http://purl.obolibrary.org/obo/UBERON_0000344"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":1007,"end":1013},"obj":"http://purl.obolibrary.org/obo/UBERON_0000344"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":399,"end":406},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":830,"end":837},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":934,"end":941},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T6","span":{"begin":1014,"end":1021},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T7","span":{"begin":1179,"end":1186},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T8","span":{"begin":1205,"end":1212},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T9","span":{"begin":1288,"end":1295},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T10","span":{"begin":1433,"end":1440},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T11","span":{"begin":1498,"end":1505},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"}],"text":"Hypermethylation of TGF-β1 gene promoter in gastric cancer.\nAIM: To examine transforming growth factor-β1 (TGF-β1) promoter methylation in gastric cancer and to determine if Helicobacter pylori (H. pylori) or interleukin (IL)-1β could induce TGF-β1 hypermethylation in vitro.\nMETHODS: We examined the frequency and extent of TGF-β1 promoter methylation using methylation-specific PCR in the gastric tissues from 47 gastric cancer patients and 39 non-gastric cancer subjects. H. pylori infection was confirmed by a positive result from either a serological test, histological analysis or C¹³ urea breath test. GES-1 and MKN-45 cells co-cultured with H. pylori or treated with IL-1β for 12, 24 and 48 h in vitro tested the effects of H. pylori or IL-1β on TGF-β1.\nRESULTS: Twenty-four/forty-seven (51%) cases of gastric cancer (GC) tissues showed TGF-β1 promoter methylation, 15/47 (31.9%) cases of matched non-cancerous gastric mucosa tissues from the GC patients, and 11/39 (28%) case of the normal gastric mucosa tissues from non-GC subjects showed TGF-β1 promoter methylation (51% vs 28%, P \u003c 0.05). Significantly higher levels of methylation of TGF-β1 were found in the tumor tissues than in non-tumor tissues from GC patients (0.24 ± 0.06 vs 0.17 ± 0.04, P \u003c 0.05) and normal gastric tissues from non-GC subjects (0.24 ± 0.06 vs 0.15 ± 0.03, P \u003c 0.05). TGF-β1 methylation was found in 48.3% of H. pylori-positive gastric mucosal tissues whereas only 23.1% of H. pylori-negative gastric mucosal tissues showed TGF-β1 methylation (48.3% vs 23.1%, P \u003c 0.05). IL-1β appeared to induce a dose-dependent methylation of TGF-β1 and the strongest methylation was observed in GES-1 cells treated with 2.5 ng/mL of IL-1β for 48 h. Further studies showed that pre-treatment of GES-1 cells with 20 ng/mL IL-1RA for 1 h could partially abolish the effect of IL-1β on TGF-β1 methylation. Infection of GES-1 cells by H. pylori was not found to induce significant TGF-β1 promoter methylation.\nCONCLUSION: Our data revealed that TGF-β1 promoter is methylated in GC patients. IL-1β may be an important mediator for H. pylori induced gene methylation during GC development."}