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PubMed:15674201 JSONTXT

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DisGeNET

Id Subject Object Predicate Lexical cue
T0 1662-1666 gene:7422 denotes VEGF
T1 1644-1651 disease:C1559271 denotes ascites
T2 2011-2015 gene:7422 denotes VEGF
T3 2030-2047 disease:C0346647 denotes pancreatic cancer
T4 2011-2015 gene:7422 denotes VEGF
T5 2030-2047 disease:C0235974 denotes pancreatic cancer
R1 T0 T1 associated_with VEGF,ascites
R2 T2 T3 associated_with VEGF,pancreatic cancer
R3 T4 T5 associated_with VEGF,pancreatic cancer

DisGeNET5_gene_disease

Id Subject Object Predicate Lexical cue
15674201-0#0#4#gene7422 0-4 gene7422 denotes VEGF
15674201-0#83#100#diseaseC0235974 83-100 diseaseC0235974 denotes pancreatic cancer
15674201-0#83#100#diseaseC0346647 83-100 diseaseC0346647 denotes pancreatic cancer
15674201-15#31#35#gene7422 1808-1812 gene7422 denotes VEGF
15674201-15#101#111#diseaseC0027627 1878-1888 diseaseC0027627 denotes metastasis
0#4#gene742283#100#diseaseC0235974 15674201-0#0#4#gene7422 15674201-0#83#100#diseaseC0235974 associated_with VEGF,pancreatic cancer
0#4#gene742283#100#diseaseC0346647 15674201-0#0#4#gene7422 15674201-0#83#100#diseaseC0346647 associated_with VEGF,pancreatic cancer
31#35#gene7422101#111#diseaseC0027627 15674201-15#31#35#gene7422 15674201-15#101#111#diseaseC0027627 associated_with VEGF,metastasis

PubMed_Structured_Abstracts

Id Subject Object Predicate Lexical cue
T1 114-401 BACKGROUND denotes Vascular endothelial growth factor (VEGF), a key mediator of angiogenesis, is overexpressed in pancreatic cancer. This study evaluated VEGF production in pancreatic cancer cells and the effect of VEGF antisense on growth and angiogenesis of human pancreatic cancer in a nude mouse model.
T2 411-1005 METHODS denotes In vitro: VEGF in cell culture supernatant of pancreatic cancer cells (AsPC-1, poorly differentiated; HPAF-2, moderately differentiated) was assessed by enzyme-linked immunosorbent assay. In vivo: A VEGF antisense oligonucleotide (AS-3) was synthesized. One-mm(3) fragments of subcutaneous pancreatic cancer donor tumors were implanted into the pancreas of nude mice also receiving AS-3 (10 mg/kg/day) or vehicle intraperitoneally for 14 weeks. Primary tumor volume, metastasis, and VEGF in plasma and ascites were determined at autopsy. Microvessel density was analyzed in CD31-stained tumors.
T3 1015-1682 RESULTS denotes In vitro: Both pancreatic cancer cell lines secreted VEGF protein (AsPC-1, 4200 +/- 40 pg/10(6) cells; HPAF-2, 8120 +/- 60 pg/10(6) cells). In vivo: AS-3 reduced tumor volume in the HPAF-2 group (860 +/- 140 vs 3830 +/- 590 mm(3)) and metastatic spread in both groups (AsPC-1, 6.5 +/- 0.8 vs 16.7 +/- 0.9 points; HPAF-2, 2.5 +/- 0.2 vs 8.3 +/- 1.5 points). Tumor volume was not different in the AsPC-1 group (1050 +/- 80 vs 1400 +/- 150 mm(3)). Survival was increased in the AsPC-1 group. Plasma levels of VEGF and microvessel density in tumors were significantly reduced in treated animals. Only control animals (50%) developed ascites with high VEGF concentrations.
T4 1696-2054 CONCLUSIONS denotes Human pancreatic cancer cells secrete VEGF at biologically relevant high levels. AS-3 therapy normalizes plasma VEGF and decreases neoangiogenesis, thereby reducing tumor growth and metastasis and improving survival. AS-3-treated animals developed no ascites, suggesting decreased vascular permeability by reducing VEGF expression in pancreatic cancer cells.