臺灣博碩士論文加值系統

本實驗目的是以致癌物(DMBA)誘發倉鼠頰囊袋鱗狀上皮細胞癌成癌過程
中GST-P(麩胱甘肱一硫一轉移鋂,胚胎型)共價鋂之現表變化.倉鼠頰囊袋
於十五週DMBA處理過程中,其上皮中GST-P表現,藉由免疫組織化學染色法
及免疫墨點分析法偵測,並比較兩者所得之結果.在對照組中,並無GST-P陽
性反應之細胞出現,而在實驗組,始自第一週(僅經三次DMBA處理)的上皮即
可發現GST-P陽性反應之細胞.在前十二週的實驗過程中,GST-P陽性反應之
細胞聚落,在數量及大小上,均呈逐漸增加, 但於十二週後, 其上昇變化漸
趨平緩.早期陽性反應,主要是以單細胞或細胞聚落分佈於基底層及偶而單
獨出現於表皮中層,故可推論為具有同源本質之"假設起始細胞";於實驗後
期,陽性反應區域變大,並且隨機散布在發育不良及無發育不良黏膜之各層
中或整層上.前十二週的實驗現,於角化層少見有GST-P陽性反應,唯實驗後
期之角化層呈陽性反應.無論外生性或向下侵襲之鱗狀上皮細胞癌均呈
GST-P蛋白帶出現,而在所有實驗組之組織粹取物中,均可發現分子量約26
kd之GST-P蛋白肱,其結果符合免疫組織化學染色法之發現,以上所得結果,
支持GST-P在倉鼠頰囊袋癌化過程中可能參與某種重要的改變步驟,並且對
於被致癌物影響之上皮細胞而細胞而言,是持續且穩定的標誌.因此藉由免
疫組織化學染色法偵測之上皮中GST-P在口腔化學性癌化過程中,可能是具
有潛力之口腔腫瘤標誌.然而其需要進一步證明在早期出現之GST-P陽性細
胞,的確會繼續展為倉鼠頰囊袋上皮細胞癌.

To date, GST isoenzymes appear to be potential markers in oral
mucosa.In the first part of our study(1992), assessments of the
expression and locallization of the GST isoenzymes in biopsies
from the normal oral mucosa,
benign fibroma, potentially premalignant(leukoplakia, submucous
fibrosis,verrucous hyperplasia and malignant(squamous cell
carcinoma and verrucouscarcinoma) oral lesions were made
immunohistochemically with specific polyclomal antibodies
raised against GST isoenzymes(alpha, mu and pi)in order to
evaluate the possible clinical application in the earlier
diagnosis of (pre)malignant oral lesions. The first part of our
study demonstrated that GST pi was expressed in oral
premalignant cells and almost absent in normal and benign
tissues. Incrers expression of GST pi was found in more than 75%
of oral cancers(verrucous carcinomas and squamous cell
carcinomas) examined but absent in omrmal or benign tissues.
This suggests that GST pimay prove to be another useful marker
of potentially malignant cells. Moreover, in the second part of
our study(1993), the tissue activity of GST isoenzymes in
various human premalignant and malignant intraoral lesions
using method of enzymatic activity with CDNB and electrophoresis
were investigated. The preliminary data revealed a strong GST pi
activity in oral (pre)malignant tissues.tatistically significant
differences were found whenthe expression of GST pi in
premalignant and malignant tissue was compared to normal oral
mucosa. This finding conformed to the first part of our
immunohistochemical study. In the third part of our study, the
sequential expression of GST P (a placental form of GST in
rodents and immunolgically related to human GST pi) during DMBA-
induced hamster cheek pouch squamous cell carcinogenesis was
investigated with the aim of increasing the understanding of
this enzyme in oral carcinogenesis.