Molecularly targeted therapies for p53-mutant cancers

摘要: The tumor suppressor p53 is lost or mutated in approximately half of human cancers. Mutant not only loses its anti-tumor transcriptional activity, but also often acquires oncogenic functions to promote proliferation, invasion, and drug resistance. Traditional strategies have been taken directly target mutants through identifying small molecular compounds deplete mutant p53, restore suppressive function. Accumulating evidence suggest that cancer cells with exhibit specific functional dependencies on secondary genes pathways survive, providing alternative targets indirectly treat p53-mutant Targeting these pathways, critical for survival the presence mutations, holds great promise treatment. In addition, exhibits novel gain-of-functions growth metastasis. Here, we review discuss targeting focus protein directly, progress required cells.