PubMed:10435586 JSONTXT

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":164,"end":186},"obj":"HP_0004808"},{"id":"T2","span":{"begin":170,"end":186},"obj":"HP_0012324"},{"id":"T3","span":{"begin":178,"end":186},"obj":"HP_0001909"}],"text":"Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2.\nThe chimeric gene, AML1/ETO (MTG8), generated in t(8;21) acute myeloid leukemia enhances the expression of Bcl-2. To evaluate whether this enhancement is the primary role of AML1/ETO in leukemogenesis, effects of over-expression of Bcl-2 in the murine myeloid precursor cell line, 32Dcl3, were examined. When 32Dcl3 cells expressing exogenous Bcl-2 were induced to differentiate, the onset of morphological differentiation was delayed. However, even the cells expressing very high levels of exogenous Bcl-2 eventually underwent differentiation without a significant decrease in the synthesis of Bcl-2. On the contrary, 32Dcl3 cells stably expressing AML1/ETO were completely resistant to differentiation and continued to grow in the presence of G-CSF. These results are consistent with the interpretation that stimulation of Bcl-2 expression is not the primary target of AML1/ETO."}

{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":41,"end":53},"obj":"cell_line"},{"id":"T2","span":{"begin":57,"end":71},"obj":"DNA"},{"id":"T3","span":{"begin":100,"end":105},"obj":"protein"},{"id":"T4","span":{"begin":111,"end":125},"obj":"DNA"},{"id":"T5","span":{"begin":126,"end":141},"obj":"DNA"},{"id":"T6","span":{"begin":156,"end":163},"obj":"DNA"},{"id":"T7","span":{"begin":214,"end":219},"obj":"protein"},{"id":"T8","span":{"begin":281,"end":289},"obj":"DNA"},{"id":"T9","span":{"begin":339,"end":344},"obj":"protein"},{"id":"T10","span":{"begin":352,"end":386},"obj":"cell_line"},{"id":"T11","span":{"begin":388,"end":394},"obj":"cell_line"},{"id":"T12","span":{"begin":416,"end":428},"obj":"cell_line"},{"id":"T13","span":{"begin":450,"end":455},"obj":"protein"},{"id":"T14","span":{"begin":608,"end":613},"obj":"protein"},{"id":"T15","span":{"begin":702,"end":707},"obj":"protein"},{"id":"T16","span":{"begin":726,"end":738},"obj":"cell_line"},{"id":"T17","span":{"begin":757,"end":765},"obj":"DNA"},{"id":"T18","span":{"begin":852,"end":857},"obj":"protein"},{"id":"T19","span":{"begin":932,"end":937},"obj":"protein"},{"id":"T20","span":{"begin":978,"end":986},"obj":"DNA"}],"text":"Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2.\nThe chimeric gene, AML1/ETO (MTG8), generated in t(8;21) acute myeloid leukemia enhances the expression of Bcl-2. To evaluate whether this enhancement is the primary role of AML1/ETO in leukemogenesis, effects of over-expression of Bcl-2 in the murine myeloid precursor cell line, 32Dcl3, were examined. When 32Dcl3 cells expressing exogenous Bcl-2 were induced to differentiate, the onset of morphological differentiation was delayed. However, even the cells expressing very high levels of exogenous Bcl-2 eventually underwent differentiation without a significant decrease in the synthesis of Bcl-2. On the contrary, 32Dcl3 cells stably expressing AML1/ETO were completely resistant to differentiation and continued to grow in the presence of G-CSF. These results are consistent with the interpretation that stimulation of Bcl-2 expression is not the primary target of AML1/ETO."}

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"10435586-1#107#112#gene596","span":{"begin":214,"end":219},"obj":"gene596"},{"id":"10435586-1#57#79#diseaseC0023467","span":{"begin":164,"end":186},"obj":"diseaseC0023467"},{"id":"10435586-2#65#68#gene862","span":{"begin":286,"end":289},"obj":"gene862"},{"id":"10435586-2#118#123#gene596","span":{"begin":339,"end":344},"obj":"gene596"},{"id":"10435586-2#72#86#diseaseC0598766","span":{"begin":293,"end":307},"obj":"diseaseC0598766"}],"relations":[{"id":"107#112#gene59657#79#diseaseC0023467","pred":"associated_with","subj":"10435586-1#107#112#gene596","obj":"10435586-1#57#79#diseaseC0023467"},{"id":"65#68#gene86272#86#diseaseC0598766","pred":"associated_with","subj":"10435586-2#65#68#gene862","obj":"10435586-2#72#86#diseaseC0598766"},{"id":"118#123#gene59672#86#diseaseC0598766","pred":"associated_with","subj":"10435586-2#118#123#gene596","obj":"10435586-2#72#86#diseaseC0598766"}],"text":"Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2.\nThe chimeric gene, AML1/ETO (MTG8), generated in t(8;21) acute myeloid leukemia enhances the expression of Bcl-2. To evaluate whether this enhancement is the primary role of AML1/ETO in leukemogenesis, effects of over-expression of Bcl-2 in the murine myeloid precursor cell line, 32Dcl3, were examined. When 32Dcl3 cells expressing exogenous Bcl-2 were induced to differentiate, the onset of morphological differentiation was delayed. However, even the cells expressing very high levels of exogenous Bcl-2 eventually underwent differentiation without a significant decrease in the synthesis of Bcl-2. On the contrary, 32Dcl3 cells stably expressing AML1/ETO were completely resistant to differentiation and continued to grow in the presence of G-CSF. These results are consistent with the interpretation that stimulation of Bcl-2 expression is not the primary target of AML1/ETO."}

{"project":"genia-medco-coref","denotations":[{"id":"C4","span":{"begin":57,"end":71},"obj":"NP"},{"id":"C1","span":{"begin":107,"end":124},"obj":"NP"},{"id":"C2","span":{"begin":126,"end":141},"obj":"NP"},{"id":"C3","span":{"begin":214,"end":219},"obj":"NP"},{"id":"C13","span":{"begin":196,"end":219},"obj":"NP"},{"id":"C5","span":{"begin":281,"end":289},"obj":"NP"},{"id":"C6","span":{"begin":339,"end":344},"obj":"NP"},{"id":"C7","span":{"begin":348,"end":386},"obj":"NP"},{"id":"C8","span":{"begin":388,"end":394},"obj":"NP"},{"id":"C9","span":{"begin":702,"end":707},"obj":"NP"},{"id":"C11","span":{"begin":893,"end":911},"obj":"NP"},{"id":"C12","span":{"begin":912,"end":916},"obj":"NP"},{"id":"C14","span":{"begin":932,"end":948},"obj":"NP"},{"id":"C15","span":{"begin":978,"end":986},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-appos","subj":"C2","obj":"C1"},{"id":"R2","pred":"coref-ident","subj":"C5","obj":"C4"},{"id":"R3","pred":"coref-ident","subj":"C6","obj":"C3"},{"id":"R4","pred":"coref-appos","subj":"C8","obj":"C7"},{"id":"R5","pred":"coref-ident","subj":"C9","obj":"C6"},{"id":"R6","pred":"coref-relat","subj":"C12","obj":"C11"},{"id":"R7","pred":"coref-ident","subj":"C14","obj":"C13"},{"id":"R8","pred":"coref-ident","subj":"C15","obj":"C5"}],"text":"Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2.\nThe chimeric gene, AML1/ETO (MTG8), generated in t(8;21) acute myeloid leukemia enhances the expression of Bcl-2. To evaluate whether this enhancement is the primary role of AML1/ETO in leukemogenesis, effects of over-expression of Bcl-2 in the murine myeloid precursor cell line, 32Dcl3, were examined. When 32Dcl3 cells expressing exogenous Bcl-2 were induced to differentiate, the onset of morphological differentiation was delayed. However, even the cells expressing very high levels of exogenous Bcl-2 eventually underwent differentiation without a significant decrease in the synthesis of Bcl-2. On the contrary, 32Dcl3 cells stably expressing AML1/ETO were completely resistant to differentiation and continued to grow in the presence of G-CSF. These results are consistent with the interpretation that stimulation of Bcl-2 expression is not the primary target of AML1/ETO."}

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":106},"obj":"Sentence"},{"id":"S2","span":{"begin":107,"end":220},"obj":"Sentence"},{"id":"S3","span":{"begin":221,"end":410},"obj":"Sentence"},{"id":"S4","span":{"begin":411,"end":542},"obj":"Sentence"},{"id":"S5","span":{"begin":543,"end":708},"obj":"Sentence"},{"id":"S6","span":{"begin":709,"end":858},"obj":"Sentence"},{"id":"S7","span":{"begin":859,"end":987},"obj":"Sentence"}],"text":"Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2.\nThe chimeric gene, AML1/ETO (MTG8), generated in t(8;21) acute myeloid leukemia enhances the expression of Bcl-2. To evaluate whether this enhancement is the primary role of AML1/ETO in leukemogenesis, effects of over-expression of Bcl-2 in the murine myeloid precursor cell line, 32Dcl3, were examined. When 32Dcl3 cells expressing exogenous Bcl-2 were induced to differentiate, the onset of morphological differentiation was delayed. However, even the cells expressing very high levels of exogenous Bcl-2 eventually underwent differentiation without a significant decrease in the synthesis of Bcl-2. On the contrary, 32Dcl3 cells stably expressing AML1/ETO were completely resistant to differentiation and continued to grow in the presence of G-CSF. These results are consistent with the interpretation that stimulation of Bcl-2 expression is not the primary target of AML1/ETO."}

{"project":"GENIAcorpus","denotations":[{"id":"T1","span":{"begin":9,"end":37},"obj":"other_name"},{"id":"T2","span":{"begin":41,"end":53},"obj":"cell_line"},{"id":"T3","span":{"begin":57,"end":71},"obj":"DNA_domain_or_region"},{"id":"T4","span":{"begin":100,"end":105},"obj":"protein_molecule"},{"id":"T5","span":{"begin":111,"end":125},"obj":"DNA_family_or_group"},{"id":"T6","span":{"begin":126,"end":141},"obj":"DNA_domain_or_region"},{"id":"T7","span":{"begin":156,"end":163},"obj":"DNA_domain_or_region"},{"id":"T8","span":{"begin":164,"end":186},"obj":"other_name"},{"id":"T9","span":{"begin":214,"end":219},"obj":"protein_molecule"},{"id":"T10","span":{"begin":281,"end":289},"obj":"DNA_domain_or_region"},{"id":"T11","span":{"begin":293,"end":307},"obj":"other_name"},{"id":"T12","span":{"begin":339,"end":344},"obj":"protein_molecule"},{"id":"T13","span":{"begin":352,"end":386},"obj":"cell_line"},{"id":"T14","span":{"begin":388,"end":394},"obj":"cell_line"},{"id":"T15","span":{"begin":416,"end":428},"obj":"cell_line"},{"id":"T16","span":{"begin":450,"end":455},"obj":"protein_molecule"},{"id":"T17","span":{"begin":500,"end":529},"obj":"other_name"},{"id":"T18","span":{"begin":608,"end":613},"obj":"protein_molecule"},{"id":"T19","span":{"begin":702,"end":707},"obj":"protein_molecule"},{"id":"T20","span":{"begin":726,"end":738},"obj":"cell_line"},{"id":"T21","span":{"begin":757,"end":765},"obj":"DNA_domain_or_region"},{"id":"T22","span":{"begin":852,"end":857},"obj":"protein_molecule"},{"id":"T23","span":{"begin":932,"end":937},"obj":"protein_molecule"},{"id":"T24","span":{"begin":978,"end":986},"obj":"DNA_domain_or_region"}],"text":"Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2.\nThe chimeric gene, AML1/ETO (MTG8), generated in t(8;21) acute myeloid leukemia enhances the expression of Bcl-2. To evaluate whether this enhancement is the primary role of AML1/ETO in leukemogenesis, effects of over-expression of Bcl-2 in the murine myeloid precursor cell line, 32Dcl3, were examined. When 32Dcl3 cells expressing exogenous Bcl-2 were induced to differentiate, the onset of morphological differentiation was delayed. However, even the cells expressing very high levels of exogenous Bcl-2 eventually underwent differentiation without a significant decrease in the synthesis of Bcl-2. On the contrary, 32Dcl3 cells stably expressing AML1/ETO were completely resistant to differentiation and continued to grow in the presence of G-CSF. These results are consistent with the interpretation that stimulation of Bcl-2 expression is not the primary target of AML1/ETO."}

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":214,"end":219},"obj":"gene:596"},{"id":"T1","span":{"begin":164,"end":186},"obj":"disease:C0023467"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2.\nThe chimeric gene, AML1/ETO (MTG8), generated in t(8;21) acute myeloid leukemia enhances the expression of Bcl-2. To evaluate whether this enhancement is the primary role of AML1/ETO in leukemogenesis, effects of over-expression of Bcl-2 in the murine myeloid precursor cell line, 32Dcl3, were examined. When 32Dcl3 cells expressing exogenous Bcl-2 were induced to differentiate, the onset of morphological differentiation was delayed. However, even the cells expressing very high levels of exogenous Bcl-2 eventually underwent differentiation without a significant decrease in the synthesis of Bcl-2. On the contrary, 32Dcl3 cells stably expressing AML1/ETO were completely resistant to differentiation and continued to grow in the presence of G-CSF. These results are consistent with the interpretation that stimulation of Bcl-2 expression is not the primary target of AML1/ETO."}