Transplantation of a human ovarian cystadenocarcinoma into severe combined immunodeficient (SCID) mice--formation of metastases without significant alteration of the tumour cell phenotype.

Human ovarian papillary cystadenocarcinoma cells were injected intraperitoneally into severe combined immunodeficient (SCID) mice. After intraperitoneal application the cells, designated SoTü, grew well in vivo, lodged on to the peritoneum, formed local metastatic deposits, led to the development of ascites in the mice and formed distant metastases in the lungs. If lodged in the ovary, the morphology of the SoTü tumour remarkably resembled that of the primary tumour in the patient. In contrast, several attempts failed to maintain the SoTü cells in vitro. If SCID mouse ascites derived SoTü were transplanted subcutaneously in SCID mice, they formed cystic tumours which also metastasized into the lungs. Immunophenotypical analysis of cell adhesion molecule expression, cell proliferation markers, various oncoproteins, keratin, vimentin, and lectin binding site expression all showed striking similarity between the primary tumour and the SCID mouse explants. In particular, expression of binding sites for the lectin Helix pomatia agglutinin (HPA), which has been shown to be an index of metastatic potential in several human carcinomas, was found on the primary tumour as well as on tumour cells grown in SCID mice, indicating that HPA might be a prognostic indicator in ovarian carcinoma as well. Our results demonstrate that the human/SCID mouse system can mimic growth and distant metastasis formation of human ovarian carcinoma. Although the formation of distant metastases is a relatively rare event in patients, this model system might help to elucidate mechanisms of metastasis formation in ovarian cancer.