Human gastric choriocarcinoma serially transplanted in nude mice.

A gastric choriocarcinoma cell line capable of producing human chorionic gonadotropin (HCG) was studied by sc transplantation and serial passages into nude mice fed under specific pathogen-free (SPF) conditions. The tumor-take rate at the serial heterotransplantation in SPF mice was high (greater than 95%), in contrast with a low rate in coventional animals (35%). The restoration of morphology and function of the original neoplasm were exclusively verified in SPF mice. Multiple lung metastases were found in 2 animals. The production, storage, and excretion of HCG by tumor cells were confirmed by its high content in serum and cystic fluid in tumors and by its intracellular localization. The tumor cells also contained a specific placental alkaline phosphatase in their membranes. The cells were various trophoblastic types ranging from primitive cytotrophoblasts to typical syncytial cells. The hormone effects of the tumor on sex organs of tumor-bearing animals were evident.

Induction of supermelanin synthesis and morphological changes in interspecific reconstituted cells and its reversal by tumor promoter.

Chloramphenicol-resistant (CAPr) reconstituted cells and cybrids were isolated by fusion of karyoplasts (or intact cells) of mouse amelanotic melanoma B16 cells with cytoplasts of hypoxanthine-guanine phosphoribosyltransferase (HGPRT) -deficient, CAPr rat myoblastic cells, L6TG.CAPr, and double selection in HAT medium containing CAP. Reconstituted cells or cybrids exhibited unique cellular arrangement, and about one third of the isolated clones expressed high tyrosinase activity and marked melanin synthesis, although the parental mouse cells expressed low tyrosinase activity and the parental rat cells did not express tyrosinase activity. These phenotypic changes have been stable for more than a year. The phenotypic reversions of these clonal cells were induced by treatment with a tumor promoter. There were changes in the morphology of the treated cells to that of the mouse B16 cells and extinction of tyrosinase activity and melanin synthesis in pigmented clonal cells. These phenotypic changes and reversions induced by a promoter were repeatedly reversible.