Background: In colon cancer, K-Ras oncogenes, which appear to be linked to chemoresistance and poor prognosis, are activated in more than 50 % of cases, whereas the tumor suppressor gene p53 is mutationally altered in about 70 % of all cases. The transcription factor p53, which is frequently mutated at codon 273, maintains wild-type configuration and possibly carries out residual functions. Although blocking of activated K-Ras may constitute a rational therapeutic concept for this treatmentresistant malignancy, a strategy influencing both oncogenic Ras and the tumor suppressor p53 may be even more promising. Materials and Methods: We evaluated the effects o
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