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Korean Journal of Obstetrics & Gynecology 1999;42(10):2192-2198.
Published online January 1, 2001.
K-ras and p53 gene mutation in endometrial hyperplasia and adenocarcinoma.
Hye Ok Kim, Joo Han Lee, In Woo Lee, Sun Aee Han, Mee Ja Park, Hyun Deuk Cho, In Sun Kim, Chul Hwan Kim
Abstract
Endometrial adenocarcinoma is the third common malignancy of female genital tract and categorized as estrogen-dependent tumor (type I) or not (type II). Type II endometrial adenocarcinoma more frequently occurs in oriental, which may arise from genetic alterations such as K-ras and p53. To identify whether the K-ras and p53 mutational activation are occurred during endometrial carcinogenesis, we examined point mutations of K-ras codon 12, 13, 61 (PCR-RFLP) and p53 exon 5, 6, 7, 8 (PCR-SSCP) in the 19 samples of endometrial adenocarcinoma. The 9 samples of normal endometrium and 24 samples of endometrial hyperplasia were also examined. K-ras codon 12 mutations were found in one of 3 cases of atypical hyperplasia (33.3%) and three of 19 cases of endometrial adenocarcinoma (15.7%). The correlation with K-ras mutation and endometrial hyperplasia/adenocarcinoma was statistically insignificant(p=0.306). p53 mutation was found in only one case of endometrial adenocarcinoma which concomitantly occurred with K-ras mutation. It could not be determined that K-ras mutation was early or late event during endometrial carcinogenesis due to a few cases of atypical hyperplasia and no K-ras mutation in the benign endometrial hyperplasia. The endometrial adenocarcinoma with K-ras mutation was observed in postmenopausal old age groups, and revealed moderate to severe histologic grade, early clinical stage, and negative lymph node metastasis.
Key Words: K-ras, p53, endometrial hyperplasia, adenocarcinoma


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