The tumor suppressor p53 is a multifunctional protein whose main duty is to 
preserve the integrity of the genome. This function of wild-type p53 as 
"guardian of the genome" is achieved at different levels, as a cell cycle 
checkpoint protein, halting the cell cycle upon DNA damage, and via a direct 
involvement in processes of DNA repair. Alternatively, p53 can induce apoptosis. 
Mutations in the p53 gene occur in about 50% of all human tumors and eliminate 
the tumor suppressor functions of p53. However, many mutant p53 proteins have 
not simply lost tumor suppressor functions but have gained oncogenic properties 
which contribute to the progression of tumor cells to a more malignant 
phenotype. The molecular basis for this gain of function of mutant p53 is still 
unknown. However, mutant (mut) p53 specifically binds to nuclear matrix 
attachment region (MAR) DNA elements. MAR elements constitute important higher 
order regulatory elements of chromatin structure and function. By binding to 
these elements, mut p53 could modulate important cellular processes, like gene 
expression, replication, and recombination, resulting in phenotypic alterations 
of the tumor cells. Mut p53 thus could be the first representative of a new 
class of oncogenes, which exert their functions via long-range alterations or 
perturbation of chromatin structure and function.