TP53 and nasopharyngeal carcinoma: Maestro et al (1999)reported that the expression of Twist was associated with p53-induced growth arrest and that this effect was correlated with the ability of Twist to interfere with the activation of a p53-dependent reporter and to impair the induction of p53 target genes in response to DNA damage. In addition, Wang et al (2004) demonstrated that increased Twist was responsible for the development of acquired Paclitaxel resistance in nasopharyngeal carcinoma cells and ectopic expression of Twist conferred resistance to microtubule-disrupting agents, including paclitaxel.