Author/Authors :
Bergamaschi، نويسنده , , Daniele and Gasco، نويسنده , , Milena and Hiller، نويسنده , , Louise and Sullivan، نويسنده , , Alexandra and Syed، نويسنده , , Nelofer and Trigiante، نويسنده , , Giuseppe and Yulug، نويسنده , , Isik and Merlano، نويسنده , , Marco and Numico، نويسنده , , Gianmauro and Comino، نويسنده , , Alberto and Attard، نويسنده , , Marlene and Reelfs، نويسنده , , Olivier and Gusterson، نويسنده , , Barry and Bell، نويسنده , , Alexandra K and Heath، نويسنده , , Victoria and Tavassoli، نويسنده , , Mahvash and Farrell، نويسنده , , Paul J and Smith، نويسنده , , Paul and Lu، نويسنده , , Xin and Crook، نويسنده , , Tim، نويسنده ,
Abstract :
Intact p73 function is shown to be an important determinant of cellular sensitivity to anticancer agents. Inhibition of p73 function by dominant-negative proteins or by mutant p53 abrogates apoptosis and cytotoxicity induced by these agents. A polymorphism encoding either arginine (72R) or proline (72P) at codon 72 of p53 influences inhibition of p73 by a range of p53 mutants identified in squamous cancers. Clinical response following cisplatin-based chemo-radiotherapy for advanced head and neck cancer is influenced by this polymorphism, cancers expressing 72R mutants having lower response rates than those expressing 72P mutants. Polymorphism in p53 may influence individual responsiveness to cancer therapy.
