PubMed:10416957
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/10416957","sourcedb":"PubMed","sourceid":"10416957","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/10416957","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 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