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A transplantable tumor of inbred mice was obtained by inoculating BALB/c mice subcutaneously with SV40‐transformed mouse kidney (mKS‐A) cells. Tumors were produced by mKS‐A cells in the 71st cell culture passage, but not by cells in the 26th passage. The tumor line has been serially passed in BALB/c mice 14 times. In vitro cell culture lines were derived from tumors after 1, 2, 8, 10 and 12 passages in mice. The tumors, as well as the In vitro tumor cell lines, contained SV40 T‐antigen, and sera from the tumor‐bearing mice contained antibodies to the SV40 T‐antigen. SV40 was rescued from the In vitro tumor cell lines after fusion with green monkey kidney (CV‐1) cells in the presence of UV‐irradiated Sendai virus. The In vitro tumor cell lines derived from mouse passages 8, 10 and 12 were used as SV40 virus; 2) SV40‐transformed cell lines; 3) primary mouse (BALB/c or Yale Swiss) kidney cells, or 4) primary mouse (BALB/c or Yale Swiss) embryo cells. These results showed that the tumor line and the In vitro tumor cell lines have the transplantation antigen.

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Subcellular fractionation studies have shown that the thymidine (dT) kinases induced by vaccinia and herpes simplex type I ( H S V-I) viruses dT kinase-deficient HeLa (BU25) and L M ( TK-) cells. These analyses revealed that the sedimentation coefficients of the vaccinia and HSV-I induced dT kinases were similar to those of the HeLa S3 and L M cytosol enzymes, but the viralinduced dT kinases exhibited greater disc PAGE mobilities ( R m values) and lower p l values than the HeLa S3 and L M cytosol dT kinases. The vaccinia and HSV-I induced dT kinases were distinctly different. Both viral-induced enzymes also differed from L M ( T K -) mitochondrial dT kinase in sedimentation coefficient, R m and PI. Small differences were found between the H S V-I induced dT kinase and a human mitochondrialspecific isozyme. However, the HS V-1 induced dT kinase resembled the mitochondrialspecific human and mouse dT kinases in ability to

A resume has been presented of some recent investigations which show that DNA synthesis can be initiated in many types of quiescent animal cells by external stimuli, by introducing a quiescent nucleus into the cytoplasm of a proliferating cell, or by a virus infection. The components of the DNA replication apparatus are described. It is shown that deoxyribonucleoside triphosphate pools increase substantially in animal cells at the time DNA synthesis is initiated due to the enhanced activities of enzymes functioning in nucleotide synthesis. Especially striking is the increase of thymidine kinase activity, indicating that this enzyme may be a useful marker of the shift from the quiescent to the replicative state. The thymidine kinase isozymes of vertebrate cells have been characterized. Thymidine kinase F, which is found principally in the cytosol, is the isozyme that increases when G1 (Go) phase cells are stimulated or infected with oncogenic viruses. Chick cytosol thymidine kinase F can also be reactivated by introducing differentiated chick erythrocyte nuclei into the cytoplasm of enzyme-deficient LM (TK-) mouse cells. Furthermore, herpesviruses code for distinctive, virus-specific thymidine kinase isozymes, so that another way to transform thymidine kinase-deficient LM TK-) cells to kinase-positive cells is by infecting them with UV-irradiated herpes simplex viruses. The experiments on the activation of DNA synthesis and thymidine kinase F activity have been discussed in the context of the proliferative activity in vivo and the immortalization in culture of neoplastic cells. These experiments suggest that genes determining cell cycle proteins are readily accessible to transcription and translation in essentially all nucleated cells. The tendency of transformed cells to become multinucleated after cytochaliasin B treatment also suggests that one important difference between malignant cells and most normal cells may be the ability of malignant cells to 'stockpile' the proteins (and/or their messenger RNAs) of the DNA replicative apparatus and to maintain the 'stockpiles' in progeny cells.

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