Background: Hydatidiform moles are gestational trophoblastic neoplasms that include both partial and complete moles. Apoptosis plays important roles in the normal placental morphogenesis and in the pathogenesis of the gestational trophoblastic neoplasia. TP53 is a tumor suppressor gene (pro-apoptotic molecule) that maintains genomic stability either by inducing cell-cycle arrest or apoptosis. BCL-2 is a proto-oncogene (a pro-survival molecule) that enhances growth and survival of cells. Epidermal growth factor receptor (EGF-R) is a transmembrane glycoprotein, which can bind and be activated by various ligands. It stimulates cell division and differentiation.
Objectives: The study examined the expression pattern of p53, BCL-2 and EGF-R proteins in the hydatidiform moles.
Materials and methods: Immunoperoxidase-staining methods and specific monoclonal antibodies were used to examine the expression of p53, BCL-2 and EGF-R in partial and complete moles (10 cases each). Trophoblastic tissue from first trimester terminations of pregnancy (non-molar tissue, 20 specimens) served as a control group. The data were evaluated to determine variations in the expression pattern among the molar and non-molar tissues.
Results: The expression patterns of these proteins varied between first trimester pregnancy terminations and molar placentas. Chorionic villi from first trimester pregnancy terminations showed strong expression of BCL-2 and EGF-R protein. In molar chorionic villi, there was a moderate expression of BCL-2 and EGF-R proteins. p53 protein expression was absent in first trimester pregnancy terminations and a partial mole whereas moderate nuclear positivity was found in the complete mole. There was a significant positive correlation between BCL-2 and EGF-R protein expression whereas inverse correlation exists between p53 and BCL-2/EGF-R protein expression.
Conclusions: The prominent expression of both EGF-R and BCL-2 (indicators of cell proliferation/survival) in the molar trophoblast suggests their involvement in the development of these tumors. The lack of significant p53 protein overexpression suggests the lack of underlying p53 mutations in hydatidiform moles.