RESUMEN
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.
