c-fos and c-myc oncoprotein expression in human hepatocellular carcinomas.

Amounts of the proteins encoded by the two oncogenes c-myc and c-fos have been compared in seven specimens of hepatocellular carcinoma and two normal liver samples using a Western blot procedure. It was found that with the exception of one tumour, the amount of these proteins was markedly increased in the tumours when compared to the normal specimens. Furthermore, there appeared to be elevated c-myc and c-fos mRNA concentrations in the tumours which correlated with the protein levels.

Expression of c-erbA in human hepatocellular carcinomas.

The expression of the oncogene c-erbA was studied in six hepatocellular carcinoma specimens and normal hepatic tissue. Total RNA isolated from these samples was analysed by Northern as well as slot blot hybridisation to a radioactive c-erbA probe. When compared to normal tissue, expression in the tumour and tissue adjacent to tumour was markedly elevated.

Procollagen mRNA metabolism during the fibroblast cell cycle and its synthesis in transformed cells.

Procollagen mRNA was isolated from mouse embryos and used for the synthesis of a highly labelled cDNA probe complementary to collagen mRNA. This probe was used for the investigation of procollagen mRNA metabolism during the cell cycle of 3T6 mouse embryo fibroblasts in culture. Titration hybridization experiments revealed that procollagen mRNA was present throughout the cell cycle following stumulation of confluent monolayers.

Histone mRNA metabolism during the mouse fibroblast cell cycle.

The synthesis of histone mRNA in the nucleus and the eventual appearance of histone mRNA in the cytoplasm of 3T6 Swiss mouse embryo fibroblasts was investigated with a highly labelled cDNA probe complementary to histone mRNA. Very low levels of histone mRNA were found in G1 phase nuclei, with even lower levels in the cytoplasm. At the onset of DNA synthesis, there is a rapid increase in histone mRNA synthesis, with a concomitant increase of histone mRNA in the cytoplasm followed by its decline in both nucleus and cytoplasm on entering the G2 phase of the cell cycle.