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食道癌発生の初期段階（Dysplasia）におけるCyclin D1の過剰発現について：SHAMMA Awad、土岐祐一郎、塩崎　均、山本　真、井上雅智、辻仲利政、矢野雅彦、門田守人（阪大・医・外）

Cyclin D1 overexpression in squamous dysplasia is an early event in esphageal carcinogenesis : Awad SHAMMA, Yuichiro DOKI, Hitoshi SHIOZAKI, Makoto YAMAMOTO, Masatoshi INOUE, Toshimasa TSUJINAKA, Masahiko YANO, Morito MONDEN ( Dept. of Surg. II, Osaka Univ., Med. School)

Many studies have discussed the clinical significance of dysplasia as a precancerous lesion of the esophagus. Since cell cycle dysregulation is one of the characteristics of cancer, we evaluated the status of cyclin D1, Rb, p16^INK4 and p27^KIP1 in 36 squamous dysplasias (23 MD and 13 SD) and 34 early cancers (15 CIS and 19 MIC) of the esophagus by immunohistochemistry. In comparison to normal tissue, their expressions were judged as strong (++), equivalent (+) and weak (-). Cyclin D1 overexpression (++) was as frequent in dysplasia as early cancer (dysplasia; 30%, early cancer; 35%). Losses of p16^INK4 and p27^KIP1 were less frequent in dysplasia than early cancer (p16^INK4; 20% vs. 45%, p<0.005, p27^KIP1; 16% vs. 42%, p<0.001). The PCNA index was gradually increasing from dysplasia to cancer, and significantly correlated with cyclin D1 status (dysplasia; p<0.03, early cancer; p<0.02). Thus cyclin D1 overexpression starts early in dysplasia while losses of p16^INK4 and p27^KIP1 are involved during transformation to cancer. This data showed that esophageal carcinogenesis is a multistep process and indicated that esophageal dysplasia should be treated as a precancerous lesion.