title: Decreased expression of epidermal growth factor and its receptor in the malignant transformation of trophoblasts.
abstract: BACKGROUND
  Gestational trophoblastic neoplasms comprise the neoplastic spectrum of nonmalignant hydatidiform mole, invasive hydatidiform mole, and truly malignant choriocarcinoma. Increasing evidence indicates that epidermal growth factor (EGF) acts as an enhancer of trophoblast function to produce human chorionic gonadotropin and that EGF and its receptor may provide a growth advantage to certain carcinoma cells. The current study was undertaken to evaluate a possible link between malignant transformation of trophoblast and expression of EGF and EGF receptor.
  
  
  METHODS
  Cytologic localization and cellular levels of expression of EGF and EGF receptor in hydatidiform mole, invasive hydatidiform mole, and choriocarcinoma tissue specimens were examined by the avidin-biotin immunoperoxidase techniques with monoclonal antibodies against EGF and EGF receptor.
  
  
  RESULTS
  EGF in hydatidiform mole and invasive mole was localized in syncytiotrophoblasts, whereas cytologic localization of EGF receptor in hydatidiform mole and invasive mole was observed in both cytotrophoblasts and syncytiotrophoblasts. By contrast, EGF and EGF receptor in choriocarcinoma were exhibited in cytotrophoblastic and syncytiotrophoblastic elements. Most (72%) hydatidiform moles immunostained intensely for EGF and EGF receptor, whereas most (78%) choriocarcinomas immunostained slightly for EGF and EGF receptor. Invasive mole occupied the middle position in the staining intensity for EGF and EGF receptor, between hydatidiform mole and choriocarcinoma, with 50% of the cases exhibiting moderate staining.
  
  
  CONCLUSIONS
  The simultaneous expression of EGF and EGF receptor in the neoplastic trophoblasts implies that EGF may act in an autocrine-paracrine manner in trophoblastic neoplasms. Furthermore, the results obtained suggest that cytologic expression of EGF and EGF receptor in trophoblastic neoplasms decreases in the malignant transformation of trophoblast.
authors.affiliation: Department of Obstetrics and Gynecology, Kobe University School of Medicine, Japan.
authors.forename: C A
authors.initials: CA
authors.lastname: Ladines-Llave
authors.forename: T
authors.initials: T
authors.lastname: Maruo
authors.forename: A M
authors.initials: AM
authors.lastname: Manalo
authors.forename: M
authors.initials: M
authors.lastname: Mochizuki
mesh_terms: D002471:Cell Transformation, Neoplastic / Q000737:chemistry / Q000235:genetics / Q000473:pathology; D004815:Epidermal Growth Factor / Q000032:analysis / Q000235:genetics*; D066246:ErbB Receptors / Q000032:analysis / Q000235:genetics*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D006828:Hydatidiform Mole / Q000737:chemistry / Q000235:genetics* / Q000473:pathology; D002820:Hydatidiform Mole, Invasive / Q000737:chemistry / Q000235:genetics* / Q000473:pathology; D007124:Immunoenzyme Techniques; D011247:Pregnancy; D013194:Staining and Labeling; D014327:Trophoblasts / Q000737:chemistry / Q000473:pathology; D014594:Uterine Neoplasms / Q000737:chemistry / Q000235:genetics* / Q000473:pathology
chemical_list: D004815:Epidermal Growth Factor; D066246:ErbB Receptors