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The accumulation of mutant p53 in human cancer cells : = Die Akkumulation von mutiertem p53 in humanen Krebszellen / vorgelegt von Monika Bug

The tumor suppressor p53 is mutated in more than 50% of all human solid tumors. This comprises mostly single residue missense point mutations that entail a loss of p53 tumor suppressor function. But at the same time, mutant p53 protein was shown to possess oncogenic activities, i.e. a gain of functi... Full description

PPN (Catalogue-ID): 684797305
Nebentitel: Die Akkumulation von mutiertem p53 in humanen Krebszellen
Personen: Bug, Monika
Format: eBook eBook
Language: English
Sprache der Zusammenfassung: Englisch
Published: 2010
Hochschule: Göttingen, Univ., Diss., 2010
Basisklassifikation: 42.15
Formangabe: Hochschulschrift
Physical Description: Online-Ressource (PDF-Datei: 357 S., 1.175 KB), Ill., graph. Darst.

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520 |a The tumor suppressor p53 is mutated in more than 50% of all human solid tumors. This comprises mostly single residue missense point mutations that entail a loss of p53 tumor suppressor function. But at the same time, mutant p53 protein was shown to possess oncogenic activities, i.e. a gain of function, promoting invasion and chemoresistance. Mutant p53 specifically accumulates in advanced tumors, but not in normal tissues, engineered to contain a mutant p53 gene. This means that tumor specific changes evoke the accumulation of mutant p53 during tumor progression. Within this study we observed that mutant p53 accumulates even further, when tumor cells are exposed to some, but not all chemotherapeutic drugs. While the anthracyclines doxorubicin, daunorubicin and epirubicin led to the accumulation of mutant p53, the highly similar compound idarubicin did not. We found the expression of mutant p53 to be regulated at different levels: First, treatment with the topoisomerase II inhibitors daunorubicin, doxorubicin, epirubicin, idarubicin, and etoposide, evokes a DNA damage response that results in the activation of E2F1 and its target gene TAp73. Our data suggest that, upon these genotoxic treatments, E2F1 contributes to the transcriptional activation of mutant p53 pre-mRNA synthesis, both directly and through induction of TAp73 ... 
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