Studies on ras oncogene activation in endometrial carcinoma.

Fujimoto I, Shimizu Y, Hirai Y, Chen JT, Teshima H, Hasumi K, Masubuchi K, Takahashi M

Gynecologic oncology

Feb 1, 1993

Sources

1 min read

0:00 / 0:00

Sign in to access this feature

Create a free account or sign in to use AI summaries, listen to articles, download PDFs, and save to your library.

1 view

Abstract

The frequency of K-ras point mutation(PM) at codon 12 was studied in 45 patients with endometrial carcinoma. In vitro amplification of target sequences of DNA extracted from endometrial cancer tissues by polymerase chain reaction and dot blotting with oligonucleotide hybridization were performed. Ten of 45 endometrial carcinomas disclosed K-ras PM at codon 12 (22.2%). Transition from GGT to GAT was most frequent in PM(41.7%). Simultaneously, double PM (GAT/GCT) were also detected in 2 cases. No relationship appeared to be present between PM and clinical prognosis such as clinical stage, histological type, histological grade of differentiation, depth of myometrial invasion, and ascitic cytology. The positive rates of lymph node metastasis tended to be higher in the group with positive PM than in the group without PM. K-ras and C-myc gene amplifications were found in 2 (5.1%) and 3 (7.7%) of 39 cases, respectively. No PM of H-ras at codons 12 and 61 was detected. Our results showed that the PM of K-ras gene at codon 12 was a fairly common event in genetic abnormality and suggested it would have some role in the progression of carcinogenesis in endometrial carcinoma.