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J Korean Cancer Assoc > Volume 31(3); 1999 > Article
Journal of the Korean Cancer Association 1999;31(3): 582-589.
p53 and bcl-2 Gene Expression in Gastational Trophoblastic Disease
Noh Hyun Park, Ju Won Roh, Jae Weom Kim, Yong Sang Song, In Ae Park, Soon Beom Kang, Hyo Pyo Lee
1Department of Obstetrics & Gynecology, College of Medicine, Seoul National University, Seoul, Korea.
2Department of Pathology, College of Medicine, Seoul National University, Seoul, Korea.
p53 and bcl-2 expressions are known as important cell survival factors and their levels of expression are related with patients prognosis in various human malignancies. But there are few data about p53 and bcl-2 expression and their role in the genesis of gestational trophoblastic disease (GTD). The aims of this study are to describe p53 and bcl-2 expression in normal trophoblast and hydatidifonn mole (HM), and to identify the role of p53 and bcl-2 in the genesis of gestational trophoblastic tumor (GlTI from HM.
Paraffin-embedded tissue sections from 32 cases of HM and 9 cases of normal early pregnancy placentas were obtained. Of 32 HM patients, 15 cases were cured after molar evacuation (group A), and 17 cases progressed to GT1' (group B). p53 and bcl-2 immunohistochemical stainings were done and their reactivity were graded. The positive rates of p53 and bcl-2 overexpression among normal placenta, group A, and group B were compared and analyzed.
p53 mutant gene overexpression was more frequently detected in HM (68%) than in normal placentas (22%)(p<0.05). bcl-2 was overexpressed in 31% of HM and 11% of normal placenta, but the difference was statistically insignificant (P > 0.05). The difference in bcl-2 and p53 expression between group A and group B was not observed (P>0.05). There was no inverse relationship between p53 and bcl-2 expression in group A, and group B (P>0.05).
p53 gene mutation may play a mle in the process of HM development, but p53 and bcl-2 were not associated with the genesis of GTI' from H-mole. More studies are needed to identify the molecular process in the progression of the GTD.
Key words: p53;bcl-2;Hydatidiform mole;Gestational trophoblastic disease;Gestational trophoblastic tumor
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