[Characterization of ipriflavone structure by instrumental examination].

The elucidation of the chemical structure of lpriflavone was carried out by ultraviolet absorption spectrophotometric, infrared spectroscopic, 1H and 13C nuclear magnetic resonance spectroscopic, low and high resolution EI mass spectrometric, thermoanalytical, elemental analytical and X-ray diffraction methods. The results unambigously verify the structure of Ipriflavone.

Effect of dietary fat and monoclonal antibody therapy on the growth of human mammary adenocarcinoma MX-1 grafted in athymic mice.

A diet containing 11% per weight fish oils (Max-EPA) reduced the rate of growth of a transplantable human breast tumor (MX-1) grafted into immunodeficient mice (BALB/c, nu/nu) when compared to MX-1 tumors in mice fed polyunsaturated (corn oil) and saturated (lard) fatty acids; however, there was no difference between the corn oil and lard animal groups. Treatment with a cocktail of monoclonal antibodies (MoAbs) decreased the rat of growth of MX-1 in the corn oil fed animals but not in those fed lard or Max-EPA, but the rate of tumor growth of the Max-EPA treated group, either MoAb treated or not, was slower than that of the corn oil and lard groups.

Effect of dietary menhaden oil on tumor cell loss and the accumulation of mass of a transplantable mammary adenocarcinoma in BALB/c mice.

A reduction in the size of transplantable mammary adenocarcinoma IX was achieved when female BALB/c mice were fed isocaloric 10% fat diets containing either hydrogenated cottonseed oil (HCTO) or menhaden oil (MO) as opposed to those mice fed corn oil (CO). Indeed, CO increased the size of the neoplasms when fed alone at 5 or 1% of the diet, although such diets contained less fat calories than did the 10% fat diets containing the other two oils. At the 10% level of dietary fat, enhanced accumulation of tumor mass was observed even when 7.

Perturbations in cancer cell deformability and resistance to shear forces.

During hematogenous metastasis, circulating cancer cells appear to be killed in the microcirculation by a non-exclusive mechanism, involving the mechanical trauma consequent upon cancer cell interactions with the vessel wall. Various observations by others indicate that with increased cell deformability, there is decreased intravascular cell killing. We have therefore critically examined the effects of agents previously shown to modify cell deformability, on the susceptibility of Ehrlich ascites tumor and L1210 leukemia cells to mechanical damage on passage through polycarbonate membranes in vitro.