THE FHCRC/NCI YEAST ANTICANCER DRUG SCREEN

摘要: Anticancer drug discovery has historically been done empirically, screening for compounds that inhibit the growth of tumor cells in culture, or are effective against implanted tumors mice. This approach is analogous to highly screens carried out 1950s and 1960s antimicrobial agents had its successes – indeed, many anticancer drugs currently clinical use were developed this fashion. However, as our understanding molecular mechanisms underlying development cancer improved, new approaches have begun build on knowledge. The recognition not all arising same tissue due defects calls treatments regimes will be tailored these alterations. screen described chapter was initiated with hypothesis single gene changes often associated particular hereditary sporadic forms may serve determinants sensitivity [27]. In principle, there two possible by which a can more toxic cell containing genetic alteration. First, mechanism damage caused normally repaired wild-type protein deleted altered mutant. An example mutants defective recombinational repair DNA double-strand breaks (DSBs) (e.g., yeast rad50 mutants) cause DSBs topoisomerase poison