Loss of heterozygosity on chromosome 16q, expression of her2/neu and p53 mutations in endometrial cancer. 1995

G Massenkeil, and R Caduff, and H Oberhuber, and I Schwartewaldhoff, and P Diener, and F Bannwart, and H Walt, and R Schafer
UNIV ZURICH HOSP,INST CLIN PATHOL,DEPT PATHOL,DIV CANC RES,CH-8091 ZURICH,SWITZERLAND. KANTONSSPITAL,INST PATHOL,CH-9000 ST GALLEN,SWITZERLAND. CITY HOSP TRIEMLI,INST PATHOL,CH-8047 ZURICH,SWITZERLAND. UNIV ZURICH HOSP,DEPT OBSTET & GYNECOL,RES DIV GYNECOL,CH-8091 ZURICH,SWITZERLAND.

We analyzed endometrial adenocarcinomas for mutations of the p53 anti-oncogene, expression of the HER2/neu oncogene and for loss of heterozygosity on chromosome 16q. p53 mutations were found in 3 of 25 tumors. Elevated expression of HER2/neu found in 7 of 24 tumors involves a mechanism other than gene amplification. LOH on chromosome 16q22-24 was observed in 4 of 13 informative tumors. Four of 25 endometrial tumors exhibited two or more alterations. Tumors with the highest HER2/neu protein level exhibited a negative progesterone receptor status. Accumulation of these changes may determine the biological behaviour of a subset of endometrial tumors.

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