作者: S Pilotti , M I Colnaghi , G Spatti , S C Righetti , F Zunino
DOI:
关键词:
摘要: The p53 protein is a multifunctional transcriptional regulator involved in cellular response to DNA damage and has been implicated as putative determinant of sensitivity tumor cells cytotoxic agents. Since the gene becomes inactivated over one-half advanced ovarian carcinoma, this study we have examined relationships between alterations, immunoreactivity, cisplatin-based chemotherapy cancer patients. All patients had (FIGO stage III or IV) carcinoma and, with one exception, were untreated at time collection specimens. After initial debulking surgery, received high-dose cisplatin therapy. Tumor samples analyzed for mutations accumulation, findings correlated responsiveness. Of 33 tumors examined, found 20 cases, including 15 missense mutations, 2 deletions, nonsense base substitution splice site. Twenty showed positive immunostaining p53. Only associated immunostaining. In addition, overexpression was detected five absence mutations. Most (12 14) stabilization refractory therapy, well overexpressing wild-type (4 5). A significant correlation type mutation (i.e., mutations), pathological conclusion, present results are consistent role chemosensitivity carcinoma.