PubMed:10416957 JSONTXT

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":168,"end":173},"obj":"HP_0002664"},{"id":"T2","span":{"begin":219,"end":224},"obj":"HP_0002664"},{"id":"T3","span":{"begin":280,"end":285},"obj":"HP_0002664"},{"id":"T4","span":{"begin":797,"end":802},"obj":"HP_0002664"},{"id":"T5","span":{"begin":944,"end":949},"obj":"HP_0002664"}],"text":"The p53 paradox in the pathogenesis of tumor progression.\nRecent evidence suggests that the p53 molecule appears in two different forms: the mutant p53 that stimulates tumor progression, and wild type p53 that inhibits tumor progression. In addition, it has been established that tumor necrosis factor-alpha (TNF-alpha) can activate the expression of wild type p53 in concert with the nuclear transcription factor, NF-kappa B. Both TNF-alpha and NF-kappa B are also involved in the stimulation of the pathway that leads to the expression of major histocompatibility complex (MHC) class I molecules and, hence, antigen presentation to the T cells. In this paper we shall advance the hypothesis that: (i) TNF-alpha indirectly controls immune surveillance; and (ii) TNF-alpha controls DNA repair and tumor suppression through the regulation of wild type p53. Thus, it is hypothesized that elevated TNF-alpha is primarily responsible for promoting tumor progression."}

{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":4,"end":7},"obj":"protein"},{"id":"T2","span":{"begin":92,"end":104},"obj":"protein"},{"id":"T3","span":{"begin":141,"end":151},"obj":"protein"},{"id":"T4","span":{"begin":191,"end":204},"obj":"protein"},{"id":"T5","span":{"begin":280,"end":307},"obj":"protein"},{"id":"T6","span":{"begin":309,"end":318},"obj":"protein"},{"id":"T7","span":{"begin":351,"end":364},"obj":"protein"},{"id":"T8","span":{"begin":385,"end":413},"obj":"protein"},{"id":"T9","span":{"begin":415,"end":425},"obj":"protein"},{"id":"T10","span":{"begin":432,"end":441},"obj":"protein"},{"id":"T11","span":{"begin":446,"end":456},"obj":"protein"},{"id":"T12","span":{"begin":541,"end":597},"obj":"protein"},{"id":"T13","span":{"begin":638,"end":645},"obj":"cell_type"},{"id":"T14","span":{"begin":703,"end":712},"obj":"protein"},{"id":"T15","span":{"begin":763,"end":772},"obj":"protein"},{"id":"T16","span":{"begin":841,"end":854},"obj":"protein"},{"id":"T17","span":{"begin":895,"end":904},"obj":"protein"}],"text":"The p53 paradox in the pathogenesis of tumor progression.\nRecent evidence suggests that the p53 molecule appears in two different forms: the mutant p53 that stimulates tumor progression, and wild type p53 that inhibits tumor progression. In addition, it has been established that tumor necrosis factor-alpha (TNF-alpha) can activate the expression of wild type p53 in concert with the nuclear transcription factor, NF-kappa B. Both TNF-alpha and NF-kappa B are also involved in the stimulation of the pathway that leads to the expression of major histocompatibility complex (MHC) class I molecules and, hence, antigen presentation to the T cells. In this paper we shall advance the hypothesis that: (i) TNF-alpha indirectly controls immune surveillance; and (ii) TNF-alpha controls DNA repair and tumor suppression through the regulation of wild type p53. Thus, it is hypothesized that elevated TNF-alpha is primarily responsible for promoting tumor progression."}

{"project":"genia-medco-coref","denotations":[{"id":"C1","span":{"begin":39,"end":56},"obj":"NP"},{"id":"C2","span":{"begin":116,"end":135},"obj":"NP"},{"id":"C4","span":{"begin":137,"end":151},"obj":"NP"},{"id":"C5","span":{"begin":152,"end":156},"obj":"NP"},{"id":"C6","span":{"begin":168,"end":185},"obj":"NP"},{"id":"C8","span":{"begin":191,"end":204},"obj":"NP"},{"id":"C9","span":{"begin":205,"end":209},"obj":"NP"},{"id":"C10","span":{"begin":219,"end":236},"obj":"NP"},{"id":"C7","span":{"begin":191,"end":236},"obj":"NP"},{"id":"C3","span":{"begin":137,"end":236},"obj":"NP"},{"id":"C11","span":{"begin":280,"end":319},"obj":"NP"},{"id":"C12","span":{"begin":351,"end":364},"obj":"NP"},{"id":"C13","span":{"begin":381,"end":413},"obj":"NP"},{"id":"C14","span":{"begin":415,"end":425},"obj":"NP"},{"id":"C15","span":{"begin":497,"end":508},"obj":"NP"},{"id":"C16","span":{"begin":509,"end":513},"obj":"NP"},{"id":"C17","span":{"begin":678,"end":692},"obj":"NP"},{"id":"C18","span":{"begin":693,"end":697},"obj":"NP"},{"id":"C19","span":{"begin":703,"end":712},"obj":"NP"},{"id":"C20","span":{"begin":763,"end":772},"obj":"NP"},{"id":"C21","span":{"begin":841,"end":854},"obj":"NP"},{"id":"C22","span":{"begin":944,"end":961},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-relat","subj":"C5","obj":"C4"},{"id":"R2","pred":"coref-ident","subj":"C6","obj":"C1"},{"id":"R3","pred":"coref-relat","subj":"C9","obj":"C8"},{"id":"R4","pred":"coref-ident","subj":"C10","obj":"C6"},{"id":"R5","pred":"coref-appos","subj":"C3","obj":"C2"},{"id":"R6","pred":"coref-ident","subj":"C12","obj":"C7"},{"id":"R7","pred":"coref-appos","subj":"C14","obj":"C13"},{"id":"R8","pred":"coref-relat","subj":"C16","obj":"C15"},{"id":"R9","pred":"coref-relat","subj":"C18","obj":"C17"},{"id":"R10","pred":"coref-ident","subj":"C19","obj":"C11"},{"id":"R11","pred":"coref-ident","subj":"C20","obj":"C19"},{"id":"R12","pred":"coref-ident","subj":"C21","obj":"C12"},{"id":"R13","pred":"coref-ident","subj":"C22","obj":"C10"}],"text":"The p53 paradox in the pathogenesis of tumor progression.\nRecent evidence suggests that the p53 molecule appears in two different forms: the mutant p53 that stimulates tumor progression, and wild type p53 that inhibits tumor progression. In addition, it has been established that tumor necrosis factor-alpha (TNF-alpha) can activate the expression of wild type p53 in concert with the nuclear transcription factor, NF-kappa B. Both TNF-alpha and NF-kappa B are also involved in the stimulation of the pathway that leads to the expression of major histocompatibility complex (MHC) class I molecules and, hence, antigen presentation to the T cells. In this paper we shall advance the hypothesis that: (i) TNF-alpha indirectly controls immune surveillance; and (ii) TNF-alpha controls DNA repair and tumor suppression through the regulation of wild type p53. Thus, it is hypothesized that elevated TNF-alpha is primarily responsible for promoting tumor progression."}

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":57},"obj":"Sentence"},{"id":"S2","span":{"begin":58,"end":237},"obj":"Sentence"},{"id":"S3","span":{"begin":238,"end":426},"obj":"Sentence"},{"id":"S4","span":{"begin":427,"end":646},"obj":"Sentence"},{"id":"S5","span":{"begin":647,"end":855},"obj":"Sentence"},{"id":"S6","span":{"begin":856,"end":962},"obj":"Sentence"}],"text":"The p53 paradox in the pathogenesis of tumor progression.\nRecent evidence suggests that the p53 molecule appears in two different forms: the mutant p53 that stimulates tumor progression, and wild type p53 that inhibits tumor progression. In addition, it has been established that tumor necrosis factor-alpha (TNF-alpha) can activate the expression of wild type p53 in concert with the nuclear transcription factor, NF-kappa B. Both TNF-alpha and NF-kappa B are also involved in the stimulation of the pathway that leads to the expression of major histocompatibility complex (MHC) class I molecules and, hence, antigen presentation to the T cells. In this paper we shall advance the hypothesis that: (i) TNF-alpha indirectly controls immune surveillance; and (ii) TNF-alpha controls DNA repair and tumor suppression through the regulation of wild type p53. Thus, it is hypothesized that elevated TNF-alpha is primarily responsible for promoting tumor progression."}

{"project":"GENIAcorpus","denotations":[{"id":"T1","span":{"begin":4,"end":7},"obj":"protein_molecule"},{"id":"T2","span":{"begin":39,"end":56},"obj":"other_name"},{"id":"T3","span":{"begin":92,"end":104},"obj":"protein_molecule"},{"id":"T4","span":{"begin":141,"end":151},"obj":"protein_molecule"},{"id":"T5","span":{"begin":168,"end":185},"obj":"other_name"},{"id":"T6","span":{"begin":191,"end":204},"obj":"protein_molecule"},{"id":"T7","span":{"begin":219,"end":236},"obj":"other_name"},{"id":"T8","span":{"begin":280,"end":307},"obj":"protein_molecule"},{"id":"T9","span":{"begin":309,"end":318},"obj":"protein_molecule"},{"id":"T10","span":{"begin":351,"end":364},"obj":"protein_molecule"},{"id":"T11","span":{"begin":385,"end":413},"obj":"protein_family_or_group"},{"id":"T12","span":{"begin":415,"end":425},"obj":"protein_complex"},{"id":"T13","span":{"begin":432,"end":441},"obj":"protein_molecule"},{"id":"T14","span":{"begin":446,"end":456},"obj":"protein_complex"},{"id":"T15","span":{"begin":541,"end":597},"obj":"protein_family_or_group"},{"id":"T16","span":{"begin":638,"end":645},"obj":"cell_type"},{"id":"T17","span":{"begin":703,"end":712},"obj":"protein_molecule"},{"id":"T18","span":{"begin":733,"end":752},"obj":"other_name"},{"id":"T19","span":{"begin":763,"end":772},"obj":"protein_molecule"},{"id":"T20","span":{"begin":782,"end":792},"obj":"other_name"},{"id":"T21","span":{"begin":797,"end":814},"obj":"other_name"},{"id":"T22","span":{"begin":841,"end":854},"obj":"protein_molecule"},{"id":"T23","span":{"begin":895,"end":904},"obj":"protein_molecule"},{"id":"T24","span":{"begin":944,"end":961},"obj":"other_name"}],"text":"The p53 paradox in the pathogenesis of tumor progression.\nRecent evidence suggests that the p53 molecule appears in two different forms: the mutant p53 that stimulates tumor progression, and wild type p53 that inhibits tumor progression. In addition, it has been established that tumor necrosis factor-alpha (TNF-alpha) can activate the expression of wild type p53 in concert with the nuclear transcription factor, NF-kappa B. Both TNF-alpha and NF-kappa B are also involved in the stimulation of the pathway that leads to the expression of major histocompatibility complex (MHC) class I molecules and, hence, antigen presentation to the T cells. In this paper we shall advance the hypothesis that: (i) TNF-alpha indirectly controls immune surveillance; and (ii) TNF-alpha controls DNA repair and tumor suppression through the regulation of wild type p53. Thus, it is hypothesized that elevated TNF-alpha is primarily responsible for promoting tumor progression."}

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":895,"end":904},"obj":"gene:7124"},{"id":"T1","span":{"begin":944,"end":961},"obj":"disease:C0178874"}],"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":"The p53 paradox in the pathogenesis of tumor progression.\nRecent evidence suggests that the p53 molecule appears in two different forms: the mutant p53 that stimulates tumor progression, and wild type p53 that inhibits tumor progression. In addition, it has been established that tumor necrosis factor-alpha (TNF-alpha) can activate the expression of wild type p53 in concert with the nuclear transcription factor, NF-kappa B. Both TNF-alpha and NF-kappa B are also involved in the stimulation of the pathway that leads to the expression of major histocompatibility complex (MHC) class I molecules and, hence, antigen presentation to the T cells. In this paper we shall advance the hypothesis that: (i) TNF-alpha indirectly controls immune surveillance; and (ii) TNF-alpha controls DNA repair and tumor suppression through the regulation of wild type p53. Thus, it is hypothesized that elevated TNF-alpha is primarily responsible for promoting tumor progression."}