Objective
P53 gene mutations are common in cancer. Human tumors accumulate abundant mutant p53 protein. Wild type (wt) p53 is a potent tumor supressor. In addition to loosing the inhibitory functions of wt p53, cancer-associated mutant p53 may gain new oncogenic functions to actively promote cancer. Wt p53 is studied extensively, but little is known about gain of function of mutant p53 and its relevance to cancer. Based on recent findings by the partners, we will explore biological effects of tumor-derived p53 mutants and their biochemical basis. We will use cell-free assays, cultured cells and mouse models. Different mutants will be compared. A special database will address correlations between mutant p53 status and patient outcome. Using a novel assay, chemical libraries will be screened for p53-inhibitory drugs. This should advance understanding of cancer etiology and define new therapy taegets.
Fields of science (EuroSciVoc)
CORDIS classifies projects with EuroSciVoc, a multilingual taxonomy of fields of science, through a semi-automatic process based on NLP techniques.
CORDIS classifies projects with EuroSciVoc, a multilingual taxonomy of fields of science, through a semi-automatic process based on NLP techniques.
- natural sciencescomputer and information sciencesdatabases
- natural sciencesbiological sciencesbiochemistrybiomoleculesproteins
- natural sciencesbiological sciencesgeneticsmutation
- medical and health sciencesclinical medicineoncology
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Call for proposal
Data not availableFunding Scheme
CSC - Cost-sharing contractsCoordinator
HAMBURG
Germany