임신성 융모성 질환과 정상 태반 조직에서의 p53 단백의 과발현 = The Overxpression of p53 in gestational Trophoblastic Disease and Normal Human Placenta

다국어 초록 (Multilingual Abstract)

Mutations in the tumor suppressor p53 gene are the most frequently observed genetic lesions in human cancers. It seems that wild type p53 does significant role on growth and differentiation of normal cells. Mutations and allelic loss of the p53 gene are thought to be a cause of tumor development and to be correlated with the prognostic factors in various human cancers such as breast, ovary and lung cancer.
Mutant p53 proteins have a prolonged half-life and can be detected by immunohistochemistry. In case of GTD(gestational trophoblastic disease), although the mutation of p53 gene mutation was revealed to be very rare, the overexpression of p53 in immunohistochemical staining has been reported in wide range of discrepancy and its role or prognostic significance in GTD is uncertain.
This study is performed to define the status of p53 overexpression in GTD and to evaluate the correlations between p53 overexpression and prognostic factors of GTD.
The results are as follows
1. p53 overexpression was detected in none of normal placental tissue, in 58.3%(14/24) of hydatidiform mole, in 75%(6/8) of invasive mole, in 75%(3/4) of choriocarcinoma, and in 100%(1/1) of placental site trophoblastic tumor, and showed significant difference of the p53 overexpression between normal placenta and GTD. We could not find any difference of the p53 overexpression between benign group(H-mole) of GTD and malignant one(invasive mole, choriocarcinoma, and placental site trophoblastic tumor)
2. In H-mole, low-risk group showed significantly higher prevalence of p53 overexpression than high-risk group did. In malignant group, there is no difference in the prevalence of p53 overexpression between early(FIGO stage I) and late(II-IV) stage-diseases, but the prevalence of p53 overexpression of low-risk group is slightly higher than that of high-risk group although we failed to find statistical significance.
In conclusion, the high prevalence of p53 overexpression in GTD suggests that p53 may have a certain role in the pathogenesis of GTD or at least represent generalized DNA demage or genotic instability of GTD. And the hither prevalence of p53 overexpression in low-risk group suggests that accumulation of wild-type p53 may be related with favorable prognosis in GTD.