Oncogene and growth factor expression in ovarian cancer

The varying tumorbiological behavior of ovarian carcinomas probably influences both their operability and response to chemotherapy, which are the most relevant prognostic factors. The phenotype of different ovarian carcinomas is obviously associated with an activation of the EGF/TGF‐α signal pathway, including c‐myc and c‐jun expression. Analysis of EGF‐R, TGF‐α, c‐myc and c‐jun expression in 33 stage III/1V, and 2 stage I/II ovarian carcinomas with biochemical, molecular‐chemical and immunohistochemical methods showed a correlation between the mRNA and protein levels of EGF‐R and TGF‐α for tumors with low or high expressing rates. However, the concentration of measurable free EGF‐Rs seems to depend on the amount of TGF‐α expression by the tumors. The EGF‐R binding ligand TGF‐α is produced by epithelial tumor cells; stromal cells are usually TGF‐α‐negative, as shown by immunohistochemistry. High expression rates of EGF‐R, TGF‐α and c‐myc were detected in 6, 7, and 10 out of 35 ovarian carcinomas, respectively. C‐jun mRNA was detected in 18/19 cases studied. Non‐malignant tissues originating from myometrium or ovary expressed no (or only small amounts of) EGF‐R or TGF‐α mRNA, whereas a high c‐myc expression was found in 1/7 normal myometria, and in 2/5 normal ovaries. There was no strong correlation between EGF‐R/ TGF‐α and c‐myc/c‐jun expression. While an enhanced expression of EGF‐R, TGF‐α or c‐myc was found in 11/15 of ovarian carcinomas responding to chemotherapy, and in 3/11 carcinomas with tumor progression, 4/4 tumors exhibiting a ‘no change’ behavior were EGF‐R and TGF‐α mRNA negative. One of the latter 4 tumors was c‐myc positive, however.