The tumor suppressor genetp53is mutated, deleted, or rearranged in more than 50% of human tumors (1 ). Wild-type (wt)tp53stops growth and/or induces apoptosis in most transformed cells into which it is introduced, thus restricting research of such cells. One means of studying the effects of both wt and mutanttp53is to generate cells in whichtp53activity can be experimentally manipulated using inducible transcriptional control elements to drive wttp53expression (2 -4 ). Alternatively, temperature-sensitive (ts)tp53mutants may be used. Such mutants were first analyzed by Oren (5 ) and possess wttp53activity at 32�C, but behave like other mutantstp53molecules at 37�C.
