PubMed:11522623 JSONTXT

{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":135},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":136,"end":295},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":296,"end":516},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":517,"end":613},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":614,"end":855},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":856,"end":1062},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":1063,"end":1248},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":135},"obj":"Sentence"},{"id":"T2","span":{"begin":136,"end":295},"obj":"Sentence"},{"id":"T3","span":{"begin":296,"end":516},"obj":"Sentence"},{"id":"T4","span":{"begin":517,"end":613},"obj":"Sentence"},{"id":"T5","span":{"begin":614,"end":855},"obj":"Sentence"},{"id":"T6","span":{"begin":856,"end":1062},"obj":"Sentence"},{"id":"T7","span":{"begin":1063,"end":1248},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Identification of AF17 as a downstream gene of the beta-catenin/T-cell factor pathway and its involvement in colorectal carcinogenesis.\nTo elucidate the molecular mechanism of colorectal carcinogenesis, we have been attempting to isolate genes involved in the beta-catenin/T-cell factor pathway. In the experiments reported here, analysis by cDNA microarray indicated that AF17, a fusion partner of the MLL gene in acute leukemias with t(11;17)(q23;q21), was transactivated according to accumulation of beta-catenin. Expression of AF17 was significantly enhanced in 8 of the 12 colorectal cancer tissues examined. Introduction of a plasmid designed to express AF17 stimulated growth of NIH3T3 cells, and fluorescence-activated cell sorter analysis indicated that the AF17 regulation of cell-cycle progression was occurring mainly at the G(2)-M transition. Our results suggest that the AF17 gene product is likely to be involved in the beta-catenin-T-cell factor/lymphoid enhancer factor signaling pathway and to function as a growth-promoting, oncogenic protein. These findings should aid development of new strategies for diagnosis, treatment, and prevention of colon cancers and acute leukemias by clarifying the pathogenesis of these conditions."}

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"11522623-0#18#22#gene4302","span":{"begin":18,"end":22},"obj":"gene4302"},{"id":"11522623-0#120#134#diseaseC0596263","span":{"begin":120,"end":134},"obj":"diseaseC0596263"},{"id":"11522623-2#77#81#gene4302","span":{"begin":373,"end":377},"obj":"gene4302"},{"id":"11522623-2#107#110#gene4297","span":{"begin":403,"end":406},"obj":"gene4297"},{"id":"11522623-2#119#134#diseaseC0085669","span":{"begin":415,"end":430},"obj":"diseaseC0085669"},{"id":"11522623-3#14#18#gene4302","span":{"begin":531,"end":535},"obj":"gene4302"},{"id":"11522623-3#61#78#diseaseC0009402","span":{"begin":578,"end":595},"obj":"diseaseC0009402"},{"id":"11522623-3#61#78#diseaseC1527249","span":{"begin":578,"end":595},"obj":"diseaseC1527249"}],"relations":[{"id":"18#22#gene4302120#134#diseaseC0596263","pred":"associated_with","subj":"11522623-0#18#22#gene4302","obj":"11522623-0#120#134#diseaseC0596263"},{"id":"77#81#gene4302119#134#diseaseC0085669","pred":"associated_with","subj":"11522623-2#77#81#gene4302","obj":"11522623-2#119#134#diseaseC0085669"},{"id":"107#110#gene4297119#134#diseaseC0085669","pred":"associated_with","subj":"11522623-2#107#110#gene4297","obj":"11522623-2#119#134#diseaseC0085669"},{"id":"14#18#gene430261#78#diseaseC0009402","pred":"associated_with","subj":"11522623-3#14#18#gene4302","obj":"11522623-3#61#78#diseaseC0009402"},{"id":"14#18#gene430261#78#diseaseC1527249","pred":"associated_with","subj":"11522623-3#14#18#gene4302","obj":"11522623-3#61#78#diseaseC1527249"}],"text":"Identification of AF17 as a downstream gene of the beta-catenin/T-cell factor pathway and its involvement in colorectal carcinogenesis.\nTo elucidate the molecular mechanism of colorectal carcinogenesis, we have been attempting to isolate genes involved in the beta-catenin/T-cell factor pathway. In the experiments reported here, analysis by cDNA microarray indicated that AF17, a fusion partner of the MLL gene in acute leukemias with t(11;17)(q23;q21), was transactivated according to accumulation of beta-catenin. Expression of AF17 was significantly enhanced in 8 of the 12 colorectal cancer tissues examined. Introduction of a plasmid designed to express AF17 stimulated growth of NIH3T3 cells, and fluorescence-activated cell sorter analysis indicated that the AF17 regulation of cell-cycle progression was occurring mainly at the G(2)-M transition. Our results suggest that the AF17 gene product is likely to be involved in the beta-catenin-T-cell factor/lymphoid enhancer factor signaling pathway and to function as a growth-promoting, oncogenic protein. These findings should aid development of new strategies for diagnosis, treatment, and prevention of colon cancers and acute leukemias by clarifying the pathogenesis of these conditions."}

{"project":"DisGeNet-2017-sample","denotations":[{"id":"T1002","span":{"begin":531,"end":535},"obj":"gene:4302"},{"id":"T1003","span":{"begin":578,"end":595},"obj":"disease:C0009402"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T1002","obj":"T1003"},{"id":"R2","pred":"associated_with","subj":"T1002","obj":"T1003"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Identification of AF17 as a downstream gene of the beta-catenin/T-cell factor pathway and its involvement in colorectal carcinogenesis.\nTo elucidate the molecular mechanism of colorectal carcinogenesis, we have been attempting to isolate genes involved in the beta-catenin/T-cell factor pathway. In the experiments reported here, analysis by cDNA microarray indicated that AF17, a fusion partner of the MLL gene in acute leukemias with t(11;17)(q23;q21), was transactivated according to accumulation of beta-catenin. Expression of AF17 was significantly enhanced in 8 of the 12 colorectal cancer tissues examined. Introduction of a plasmid designed to express AF17 stimulated growth of NIH3T3 cells, and fluorescence-activated cell sorter analysis indicated that the AF17 regulation of cell-cycle progression was occurring mainly at the G(2)-M transition. Our results suggest that the AF17 gene product is likely to be involved in the beta-catenin-T-cell factor/lymphoid enhancer factor signaling pathway and to function as a growth-promoting, oncogenic protein. These findings should aid development of new strategies for diagnosis, treatment, and prevention of colon cancers and acute leukemias by clarifying the pathogenesis of these conditions."}

{"project":"UBERON-AE","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":596,"end":603},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":1163,"end":1168},"obj":"http://purl.obolibrary.org/obo/UBERON_0001155"}],"text":"Identification of AF17 as a downstream gene of the beta-catenin/T-cell factor pathway and its involvement in colorectal carcinogenesis.\nTo elucidate the molecular mechanism of colorectal carcinogenesis, we have been attempting to isolate genes involved in the beta-catenin/T-cell factor pathway. In the experiments reported here, analysis by cDNA microarray indicated that AF17, a fusion partner of the MLL gene in acute leukemias with t(11;17)(q23;q21), was transactivated according to accumulation of beta-catenin. Expression of AF17 was significantly enhanced in 8 of the 12 colorectal cancer tissues examined. Introduction of a plasmid designed to express AF17 stimulated growth of NIH3T3 cells, and fluorescence-activated cell sorter analysis indicated that the AF17 regulation of cell-cycle progression was occurring mainly at the G(2)-M transition. Our results suggest that the AF17 gene product is likely to be involved in the beta-catenin-T-cell factor/lymphoid enhancer factor signaling pathway and to function as a growth-promoting, oncogenic protein. These findings should aid development of new strategies for diagnosis, treatment, and prevention of colon cancers and acute leukemias by clarifying the pathogenesis of these conditions."}

{"project":"performance-test","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":596,"end":603},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":1163,"end":1168},"obj":"http://purl.obolibrary.org/obo/UBERON_0001155"}],"text":"Identification of AF17 as a downstream gene of the beta-catenin/T-cell factor pathway and its involvement in colorectal carcinogenesis.\nTo elucidate the molecular mechanism of colorectal carcinogenesis, we have been attempting to isolate genes involved in the beta-catenin/T-cell factor pathway. In the experiments reported here, analysis by cDNA microarray indicated that AF17, a fusion partner of the MLL gene in acute leukemias with t(11;17)(q23;q21), was transactivated according to accumulation of beta-catenin. Expression of AF17 was significantly enhanced in 8 of the 12 colorectal cancer tissues examined. Introduction of a plasmid designed to express AF17 stimulated growth of NIH3T3 cells, and fluorescence-activated cell sorter analysis indicated that the AF17 regulation of cell-cycle progression was occurring mainly at the G(2)-M transition. Our results suggest that the AF17 gene product is likely to be involved in the beta-catenin-T-cell factor/lymphoid enhancer factor signaling pathway and to function as a growth-promoting, oncogenic protein. These findings should aid development of new strategies for diagnosis, treatment, and prevention of colon cancers and acute leukemias by clarifying the pathogenesis of these conditions."}

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":18,"end":22},"obj":"gene:4302"},{"id":"T1","span":{"begin":120,"end":134},"obj":"disease:C0596263"},{"id":"T2","span":{"begin":403,"end":406},"obj":"gene:4297"},{"id":"T3","span":{"begin":415,"end":430},"obj":"disease:C0085669"}],"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":"Identification of AF17 as a downstream gene of the beta-catenin/T-cell factor pathway and its involvement in colorectal carcinogenesis.\nTo elucidate the molecular mechanism of colorectal carcinogenesis, we have been attempting to isolate genes involved in the beta-catenin/T-cell factor pathway. In the experiments reported here, analysis by cDNA microarray indicated that AF17, a fusion partner of the MLL gene in acute leukemias with t(11;17)(q23;q21), was transactivated according to accumulation of beta-catenin. Expression of AF17 was significantly enhanced in 8 of the 12 colorectal cancer tissues examined. Introduction of a plasmid designed to express AF17 stimulated growth of NIH3T3 cells, and fluorescence-activated cell sorter analysis indicated that the AF17 regulation of cell-cycle progression was occurring mainly at the G(2)-M transition. Our results suggest that the AF17 gene product is likely to be involved in the beta-catenin-T-cell factor/lymphoid enhancer factor signaling pathway and to function as a growth-promoting, oncogenic protein. These findings should aid development of new strategies for diagnosis, treatment, and prevention of colon cancers and acute leukemias by clarifying the pathogenesis of these conditions."}