Increased estrogen receptor and epidermal growth factor receptor gene product co-expression in surgically resected gastric adenocarcinomas

Background Evidence exists that estrogens influence the action of epidermal growth factor (EGF) and its receptor (EGF‐R) at multiple levels. Estrogen and antiestrogen action on gastric and other gastrointestinal malignancies has been evaluated by several groups with conflicting results, and EGF‐R has been implicated in the current growth factor‐mediated models for gastric cancer progression. Methods ERs and EGF‐Rs were detected immunohistochemically in a total of 53 advanced gastric carcinomas using monoclonal antibodies (mAbs) to human ERs and EGF‐Rs. Results ERs were expressed in 30 (56%) and EGF‐Rs in 20 (38%) of the gastric tumors. ER(+) gastric tumors were closely associated with the intestinal type (P < 0.01), whereas EGF‐R(+) tumors were significantly correlated with poor differentiation status and ER(+) expression (P < 0.01). Of EGF‐R(+) tumors, 85% were also ER(+). EGF‐R and ER co‐expression was demonstrated in 17 tumors (32% of the group). These cases were significantly corelated with poor differentiation and large tumor size upon resection (P < 0.05). Conclusions ER and EGF‐R co‐expression indicates that a functional interaction between estrogens and EGF may exist in gastric cancer and that when such an interaction becomes operative, it may lead to dedifferentiation and increased tumor growth. © 1996 Wiley‐Liss, Inc.