Gene expressions and cellular adhesion in experimental carcinogenesis of rat submandibular gland

在大鼠亚人类凝胶（SMG）中的钙生成过程，跟踪含有2%的DMBA海绵颗粒插入，已研究了几种历史化学标记和RT-PCR的用途。K8.12细胞因子、表皮生长因子、内皮素-3和S-100蛋白被用于肠道淀粉样体的免疫化学标记物。Calponin曾被用于肌表皮细胞的免疫化学标记物。Proliferating cell nuclear antigen imunohistochem #和D13-D1H-thymidine auto-radiograph were used to obtain proliferating potential。基础纤维块生长因子（bFGF）及其受体（FGFr），以及c-erbB-2作为oncogene产品被研究。在碳水化合物发生期间，在几种类型的半导体细胞中找到了促进细胞，包括神经元部分在内的肌表皮细胞显示没有或最小的促进保护。在大鼠SMG中的碳水化合物瘤的历史模式、经修改的肌上皮细胞的差异和/或结构可能会加深影响形成腺癌细胞中的管结构结构。没有钙蛋白阳性的经修改的肌表皮细胞在块状细胞内发现，通过在腺体内发现，它们被安排在生长和降解的微管-导电结构的基础层中。在癌基因产品的变化中， bFGF和FGFr在同一肿瘤细胞内增强了他们的免疫化学表达中的肿瘤巢和共存。这些结果可能会建议， bFGF可能通过自动蛋白和/或副蛋白途径刺激碳水化合物发生。Furthermore，一个生长过程导致了c-erbB-2 mRNA水平的增加。RT-PCR产品的c-erbB-2在正常SMG中缺失，在3周内发生骨质疏松症，但在6周内显示出一半和所有病例，在12周内标本中，尊重。Excessive c-erbB-2 prot-oncogene产品可能是SMG癌症生成遵循DMBA管理的课程之一。

A process of carcinogenesis in rat submandibular gland (SMG), following the 2%DMBA containing sponge pellet insertion, was studied by the use of several histochemical markers and RT-PCR. K8.12 cytokeratin, epidermal growth factor, endothelin-3 and S-100 protein were used for the imunohistochemical markers of salivary gland duct. Calponin was used for the imunohistochemical marker of mioepithelial cells. Proliferating cell nuclear antigen imunohistochemistry and ィイD13ィエD1H-thymidine auto-radiograph were used to obtain proliferating potential. Basis fibroblast growth factor (bFGF) and its receptor (FGFr), and c-erbB-2 were studied as oncogene products.During the carcinogenesis, proliferating cells were found in several kinds of ductal cells, though acinar compartment including myoepithelial cells showed no or minimal proliferating protential. In the histological patterns of carcinoma in rat SMG, the differentiation and/or conduction of modified myoepithelial cells may deeply influenced to form tubro-ductal structures in adenocarcinoma. There were no calponin positive modified myoepithelial cells found in squamous cell carcinoma, through in the adenomacarcinoma, they were arranged in the basal layer of the proliferating and dysplastic tubro-ductal structures.In the variation of oncogene products during carinogenesis, bFGF and FGFr were enhanced their immunohistochemical expression in the tumor nest and coexisted in the same tumor cells. These result may suggest that, bFGF may stimulate carcinogenesis by autocrin and/or paracrin pathway. Furthermore, a progression of carcinogenesis brought to increase of c-erbB-2 mRNA level. RT-PCR product of c-erbB-2 was absent in normal SMG and 3 weeks of carnogenesis but showed harlf and all cases in 6 weeks and in 12 weeks specimens, respectively. Excessive c-erbB-2 prot-oncogene product may be one of a course for SMG carcinogenesis following DMBA administration.