Battista P, Pizzicannella G, Vitullo P, Palmirotta R, Mariani-Costantini R
Istituto di Patologia Umana e Medicina Sociale, Università Gabriele D'Annunzio, Chieti, Italy.
Mod Pathol. 1993 Mar;6(2):162-6.
Autocrine neoplastic growth circuits are based on excess synthesis of growth factors and/or cognate membrane receptors. We analyzed by immunohistochemistry 19 typical lung carcinoids for the expression of the epidermal growth factor (EGF), transforming growth factor alpha (TGF alpha), EGF receptor (EGFr), and EGFr-related c-erbB-2 protein (p185). Thirteen tumors (68%) were positive for TGF alpha, 11 for EGFr (58%), three for EGF (16%), and four for p185 (21%). Six carcinoids (32%) were consistently negative for these gene products. The following patterns of coexpression could be documented: TGF alpha, EGFr, EGF, and p185: two cases (11%); TGF alpha, EGFr, and EGF: one case (5%); TGF alpha, EGFr, and p185: two cases (11%); TGF alpha and EGFr: six cases (32%); TGF alpha by itself: two cases (11%). Thus, EGFr was coexpressed with its ligands, TGF alpha and EGF, and the receptor encoded by c-erbB-2 was detected in carcinoids positive for EGFr and TGF alpha. Therefore, alterations of EGF/EGFr-related growth control pathways may be implicated in the pathogenesis of pulmonary carcinoids via the establishment of autocrine growth promoting circuits, as documented in adenocarcinomas and squamous cell carcinomas of the lung.
自分泌肿瘤生长回路基于生长因子和/或同源膜受体的过度合成。我们通过免疫组织化学分析了19例典型肺类癌中表皮生长因子（EGF）、转化生长因子α（TGFα）、EGF受体（EGFr）和EGFr相关的c-erbB-2蛋白（p185）的表达情况。13例肿瘤（68%）TGFα呈阳性，11例（58%）EGFr呈阳性，3例（16%）EGF呈阳性，4例（21%）p185呈阳性。6例类癌（32%）这些基因产物始终呈阴性。可记录到以下共表达模式：TGFα、EGFr、EGF和p185：2例（11%）；TGFα、EGFr和EGF：1例（5%）；TGFα、EGFr和p185：2例（11%）；TGFα和EGFr：6例（32%）；单独的TGFα：2例（11%）。因此，EGFr与其配体TGFα和EGF共表达，并且在EGFr和TGFα呈阳性的类癌中检测到了由c-erbB-2编码的受体。因此，EGF/EGFr相关生长控制途径的改变可能通过建立自分泌生长促进回路而参与肺类癌的发病机制，正如在肺腺癌和鳞状细胞癌中所记录的那样。
