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Mutations in the p53 gene are associated with a wide variety of human tumors, including those of the breast. To assess functionally the role of the p53 gene in the development of human breast cancer, we introduced either wild-type or mutant p53 cDNA into three human breast cancer cell lines by DNA transfection. The cell lines MDA-MB 468 and T47 D contain only single mutated copies of the p53 gene, whereas the status of p53 in the breast cancer cell line MCF 7 remains equivocal. Following transfection, MCF 7 cells continued to grow unaffected both in vitro and in vivo in the presence of high levels of expression of the exogenous wild-type p53 gene. In contrast, however, the continued expression of an exogenous wild-type p53 gene was incompatible with cellular growth in both the MDA-MB 468 and T47 D cell lines. Elevated levels of expression of the exogenous mutant p53 gene did not alter the growth of the cell lines in vitro. These data strongly suggest that the wild-type p53 gene can function as a suppressor of cellular growth in breast cancer cells. That the wild-type p53 gene does not suppress the growth of MCF 7 cells indicates that at least some human breast tumors can arise without functional inactivation of the p53 gene by mutation. These tumors may represent a separate prognostic group.

Culture, characterization and sensitivity to laser and photosensitizers of bovine coronary artery endothelium is presented. Endothelial cells from bovine coronary artery specimens obtained after sacrifice were successfully cultured. Endothelial cells were obtained from the anterior descending coronary artery. Cells were grown in RPMI-1640 with 20% fetal bovine serum. Preconditioned medium was required to enhance the efficiency of the initial inoculum. The resulting cultures could be passed for up to 15 times and maintained a stable, normal karyotype throughout this period. The culture reached a stable confluency packing density by two to three weeks (5 x 10(5) to 10(6) cells/cm2). When cultures were maintained at the confluency packing density for three to four weeks, the cells had the unique tendency to assume capillary-like networks of cell cords around which neighboring cells showed polar orientation and migration towards the apparent tube-like structures without the need for added extracellular matrix. All cultured cells were stained positive with mouse anti-human factor VIII monoclonal antibody tagged with either Texas red-streptavidin or fluorescein isothiocyanate (FITC). All cultures were negative for staining with mouse monoclonal antibody to alpha actin tagged with FITC, suggesting absence of smooth muscle cells or fibroblasts. Cells were negligibly sensitive to argon laser irradiation at wave lengths 620 nm at 37 J/cm2. Cultured cells showed dose dependent sensitivity to both unactivated HPD and phycocyanin with minimal cytotoxicity (less than 20%) at concentrations below 0.5 and 50 micrograms/ml, respectively. Laser activation of the photosensitizers at these concentrations resulted in similar but significant cell death, 40% and 41% respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Monoclonal antibodies have been derived against a variety of antigens on human leukocytes. We describe a complement-fixing, IgG2a, murine monoclonal antibody that was derived against ARH-77, a human plasma cell line. In a Western blot of a lysate of ARH-77, anti-ARH-77 recognized a 155 kD protein. On normal B cells, the antibody co-capped with surface immunoglobulin. Analysis of blood and lymph nodes indicated that the determinant recognized by the antibody is expressed by most B cells, T cells, monocytes, and lymphomas with surface immunoglobulin. The determinant was not present on granulocytes, platelets, mantle zone lymphocytes, or serum immunoglobulin. We conclude that anti-ARH-77 is a cytotoxic monoclonal antibody that recognizes a determinant shared by human mononuclear leukocytes. The determinant may be an exposed part of a membrane anchor or bridging protein associated with receptors on mononuclear cells.