PubMed:7504687 JSONTXT

{"project":"bionlp-st-cg-2013-training","denotations":[{"id":"T1","span":{"begin":5,"end":42},"obj":"Gene_or_gene_product"},{"id":"T2","span":{"begin":62,"end":80},"obj":"Cell"},{"id":"T3","span":{"begin":109,"end":114},"obj":"Organism"},{"id":"T4","span":{"begin":115,"end":141},"obj":"Cell"},{"id":"T5","span":{"begin":188,"end":198},"obj":"Cell"},{"id":"T6","span":{"begin":199,"end":203},"obj":"Cell"},{"id":"T7","span":{"begin":204,"end":212},"obj":"Gene_or_gene_product"},{"id":"T8","span":{"begin":229,"end":234},"obj":"Organism"},{"id":"T9","span":{"begin":235,"end":248},"obj":"Cancer"},{"id":"T10","span":{"begin":262,"end":270},"obj":"Gene_or_gene_product"},{"id":"T11","span":{"begin":296,"end":302},"obj":"Tissue"},{"id":"T12","span":{"begin":370,"end":375},"obj":"Cancer"},{"id":"T13","span":{"begin":430,"end":435},"obj":"Gene_or_gene_product"},{"id":"T14","span":{"begin":455,"end":465},"obj":"Gene_or_gene_product"},{"id":"T15","span":{"begin":467,"end":474},"obj":"Gene_or_gene_product"},{"id":"T16","span":{"begin":480,"end":487},"obj":"Gene_or_gene_product"},{"id":"T17","span":{"begin":497,"end":504},"obj":"Cell"},{"id":"T18","span":{"begin":505,"end":510},"obj":"Organism"},{"id":"T19","span":{"begin":511,"end":534},"obj":"Cell"},{"id":"T20","span":{"begin":557,"end":562},"obj":"Cell"},{"id":"T21","span":{"begin":566,"end":578},"obj":"Organism"},{"id":"T22","span":{"begin":589,"end":594},"obj":"Organism"},{"id":"T23","span":{"begin":595,"end":626},"obj":"Cell"},{"id":"T24","span":{"begin":637,"end":652},"obj":"Immaterial_anatomical_entity"},{"id":"T25","span":{"begin":690,"end":705},"obj":"Immaterial_anatomical_entity"},{"id":"T26","span":{"begin":721,"end":732},"obj":"Cell"},{"id":"T27","span":{"begin":744,"end":764},"obj":"Cancer"},{"id":"T28","span":{"begin":769,"end":773},"obj":"Organ"},{"id":"T29","span":{"begin":819,"end":827},"obj":"Gene_or_gene_product"},{"id":"T30","span":{"begin":902,"end":929},"obj":"Cancer"},{"id":"T31","span":{"begin":976,"end":982},"obj":"Cancer"},{"id":"T32","span":{"begin":999,"end":1014},"obj":"Immaterial_anatomical_entity"},{"id":"T33","span":{"begin":1070,"end":1075},"obj":"Organism"},{"id":"T34","span":{"begin":1076,"end":1090},"obj":"Cell"},{"id":"T35","span":{"begin":1121,"end":1142},"obj":"Cancer"},{"id":"T36","span":{"begin":1146,"end":1156},"obj":"Cancer"},{"id":"T37","span":{"begin":1189,"end":1196},"obj":"Cell"},{"id":"T38","span":{"begin":1222,"end":1250},"obj":"Organism"},{"id":"T39","span":{"begin":1261,"end":1266},"obj":"Organism_substance"},{"id":"T40","span":{"begin":1296,"end":1309},"obj":"Cell"},{"id":"T41","span":{"begin":1324,"end":1331},"obj":"Cell"},{"id":"T42","span":{"begin":1344,"end":1349},"obj":"Organism"},{"id":"T43","span":{"begin":1350,"end":1367},"obj":"Cell"},{"id":"T44","span":{"begin":1422,"end":1430},"obj":"Gene_or_gene_product"},{"id":"T45","span":{"begin":1469,"end":1473},"obj":"Gene_or_gene_product"},{"id":"T46","span":{"begin":1514,"end":1524},"obj":"Cell"},{"id":"T47","span":{"begin":1525,"end":1533},"obj":"Gene_or_gene_product"},{"id":"T48","span":{"begin":1556,"end":1574},"obj":"Cancer"}],"text":"Anti-transforming growth factor (TGF)-beta antibodies inhibit breast cancer cell tumorigenicity and increase mouse spleen natural killer cell activity. Implications for a possible role of tumor cell/host TGF-beta interactions in human breast cancer progression.\nTGF-beta effects on angiogenesis, stroma formation, and immune function suggest its possible involvement in tumor progression. This hypothesis was tested using the 2G7 IgG2b, which neutralizes TGF-beta 1, -beta 2, and -beta 3, and the MDA-231 human breast cancer cell line. Inoculation of these cells in athymic mice decreases mouse spleen natural killer (NK) cell activity. Intraperitoneal injections of 2G7 starting 1 d after intraperitoneal inoculation of tumor cells suppressed intraabdominal tumor and lung metastases, whereas the nonneutralizing anti-TGF-beta 12H5 IgG2a had no effect. 2G7 transiently inhibited growth of established MDA-231 subcutaneous tumors. Histologically, both 2G7-treated and control tumors were identical. Intraperitoneal administration of 2G7 resulted in a marked increase in mouse spleen NK cell activity. 2G7 did not inhibit MDA-231 primary tumor or metastases formation, nor did it stimulate NK cell-mediated cytotoxicity in beige NK-deficient nude mice. Finally, serum-free conditioned medium from MDA-231 cells inhibited the NK cell activity of human blood lymphocytes. This inhibition was blocked by the neutralizing anti-TGF-beta 2G7 antibody but not by a nonspecific IgG2. These data support a possible role for tumor cell TGF-beta in the progression of mammary carcinomas by suppressing host immune surveillance."}

{"project":"DocumentLevelAnnotationSample","denotations":[{"id":"PD-UBERON-AE_T1","span":{"begin":62,"end":68},"obj":"http://purl.obolibrary.org/obo/UBERON_0000310"},{"id":"PD-UBERON-AE_T2","span":{"begin":235,"end":241},"obj":"http://purl.obolibrary.org/obo/UBERON_0000310"},{"id":"PD-UBERON-AE_T3","span":{"begin":511,"end":517},"obj":"http://purl.obolibrary.org/obo/UBERON_0000310"},{"id":"PD-UBERON-AE_T4","span":{"begin":115,"end":121},"obj":"http://purl.obolibrary.org/obo/UBERON_0002106"},{"id":"PD-UBERON-AE_T5","span":{"begin":595,"end":601},"obj":"http://purl.obolibrary.org/obo/UBERON_0002106"},{"id":"PD-UBERON-AE_T6","span":{"begin":1076,"end":1082},"obj":"http://purl.obolibrary.org/obo/UBERON_0002106"},{"id":"PD-UBERON-AE_T7","span":{"begin":296,"end":302},"obj":"http://purl.obolibrary.org/obo/UBERON_0003891"},{"id":"PD-UBERON-AE_T8","span":{"begin":769,"end":773},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"PD-UBERON-AE_T9","span":{"begin":1261,"end":1266},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE_T10","span":{"begin":1350,"end":1355},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"}],"text":"Anti-transforming growth factor (TGF)-beta antibodies inhibit breast cancer cell tumorigenicity and increase mouse spleen natural killer cell activity. Implications for a possible role of tumor cell/host TGF-beta interactions in human breast cancer progression.\nTGF-beta effects on angiogenesis, stroma formation, and immune function suggest its possible involvement in tumor progression. This hypothesis was tested using the 2G7 IgG2b, which neutralizes TGF-beta 1, -beta 2, and -beta 3, and the MDA-231 human breast cancer cell line. Inoculation of these cells in athymic mice decreases mouse spleen natural killer (NK) cell activity. Intraperitoneal injections of 2G7 starting 1 d after intraperitoneal inoculation of tumor cells suppressed intraabdominal tumor and lung metastases, whereas the nonneutralizing anti-TGF-beta 12H5 IgG2a had no effect. 2G7 transiently inhibited growth of established MDA-231 subcutaneous tumors. Histologically, both 2G7-treated and control tumors were identical. Intraperitoneal administration of 2G7 resulted in a marked increase in mouse spleen NK cell activity. 2G7 did not inhibit MDA-231 primary tumor or metastases formation, nor did it stimulate NK cell-mediated cytotoxicity in beige NK-deficient nude mice. Finally, serum-free conditioned medium from MDA-231 cells inhibited the NK cell activity of human blood lymphocytes. This inhibition was blocked by the neutralizing anti-TGF-beta 2G7 antibody but not by a nonspecific IgG2. These data support a possible role for tumor cell TGF-beta in the progression of mammary carcinomas by suppressing host immune surveillance."}