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Human health riskassessments, of course, deal with only one species. These differences in the clinical signi?cance of Pin1overexpression may be rationalized considering the provocative hypothesis that inbreast cancer the mutant p53 network may be the major determinant of aggressive-ness among the oncogenic mechanisms ampli?ed by Pin1, while in other tumortypes, other mutant p53-independent mechanisms may take over

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