p73 is effective in p53-null pancreatic cancer cells resistant to wild-type TP53 gene replacement.

Cancer Res. 2003; 63:2737-2741.

Rödicker F, Pützer BM.

Novel therapies such as gene therapy are needed for the treatment of pancreatic carcinomas. Here we show that adenovirus-mediated p73 overexpression results in a strong induction of apoptosis, whereas the effect of p53 varies between different cell lines. In particular, p53-negative AsPC-1 cells are resistant to p53-mediated apoptosis. In these cells, only ectopically expressed p73 activates the proapoptotic p53 target P53AIP1, whereas phosphorylation of p53 at Ser-46, shown to regulate transcriptional activation of P53AIP1, is missing. Our findings support the use of p73 as an anticancer drug in p53-null pancreatic cancer cells that are resistant to wild-type TP53 gene replacement.

Pubmed

Vorheriger Beitrag

Gene therapeutic approaches for medullary thyroid carcinoma treatment.

Nächster Beitrag

Inactivation of the RB tumor suppressor gene by oncogenic isoforms of the p53 family member p73.

p73 is effective in p53-null pancreatic cancer cells resistant to wild-type TP53 gene replacement.

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Institut für Experimentelle Gentherapie und Tumorforschung

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