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Biomedical subjects

W F Piessens

Publications and source records attributed to W F Piessens.

At least 91 records · Page 5Linked to original sources
PubMed1977

Inhibition or enhancement of rat mammary tumors dependent on dose BCG.

The effect of BCG on the growth of transplantable rat mammary tumors in W/Fu rats was studied. Admixture of mycobacteria to tumor cells in vitro prior to their injection in vivo either had no effect on or resulted in inhibition of or enhancement of the growth of the tumor transplants. Inhibition occurred at high and enhancement at low mycobacteria:tumor cell ratios. However, following suppression of local tumor growth with high doses of BCG, the growth of a second tumor graft was enhanced. Pretreatment of rats with BCG alone also enhanced the growth of a subsequent tumor graft. These results suggest an inverse relationship between the optimal dose of BCG for suppression of local tumor and that required to induced systemic immunity.

Animals↗
PubMed1977

Transplantable mammary tumors in Wistar/Furth rats: development, antigenicity, and effect of hormone manipulations.

Transplantable tumor lines were developed from 7,12-dimethylbenz[a]anthracene-induced mammary tumors in inbred WF rats. Although the primary tumors regressed following oophorectomy, the growth of late generations of the transplantable lines was not affected by castration or by treatment with estrogens, androgens, and progesterone. This result coincided with a change in the morphology of the tumors from well-differentiated to poorly differentiated anaplastic tumors. The transplantable mammary tumors were antigenic in vitro as evidenced by stimulation of syngeneic lymphocytes in mixed lymphocyte-tumor cell cultures. However, prior sensitization by excision of a first tumor graft failed to protect the animals against a second challenge with cells from the same tumor line.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1977

Increased binding and killing of neuraminidase-galactose oxidase-treated tumor cells by normal macrophages.

The binding of Line 10 hepatoma cells to normal syngeneic guinea pig macrophages is increased when the tumor cells are treated with neuraminidase and galactose oxidase (NAGO) before they are added to the macrophage monolayers. The effect is abolished by exposure of the NAGO-treated tumor cells to sodium borohydride. Line 1 hepatoma cells treated with NAGO or with sodium periodate are killed to a greater extent than untreated tumor cells. This effect can also be reversed by sodium borohydride. Further, periodate-treated macrophages become cytotoxic for unmodified tumor cells. These results demonstrate that increased tumor cell killing occurs when artificial contacts (presumably via Schiff bases) are established between normal macrophages and tumor cells. They are consistent with the hypothesis that close cell to cell contact is necessary for macrophage-mediated cytotoxicity.

Alcohol Oxidoreductases↗
PubMed1977

Increased responsiveness to macrophage-activating factor (MAF) after alteration of macrophage membranes.

Guinea pig macrophages pretreated with the esterase inhibitor, antithrombin III (AT III) show increased responsiveness to macrophage-activating factor (MAF) as demonstrated by their enhanced cytotoxicity for tumor cells. Other proteins that are not esterase inhibitors did not enhance the effect of MAF on the macrophage. Enhancement of MAF activity was also obtained when macrophages were preincubated with the cell surface reactant, diazotized sulfanilic acid (DSA). These studies indicate that the effect of MAF can be enhanced by chemical modifications of the macrophage membrane. They also provide further evidence to support the hypothesis that an esterase on the macrophage membrane modulates this cell's responsiveness to lymphocyte mediators.

Animals↗
PubMed1975

Multiple in vitro mechanisms of tumor cytotoxicity demonstrated in the line-1 guinea pig hepatoma model.

The line-1 guinea pig hepatoma was used to study in vitro tumor cytotoxicity. Cytotoxicity was determined by measurement of the loss of tritiated thymidine-labeled target cells from culture vessels. With this technique, we demonstrated that significant tumor cytotoxicity was caused by lymphoid cells from tumor-immune guinea pigs, by cells from guinea pigs immunized against an antigen urelated to the tumor target, and by cell-free supernatants rich in lymphocyte mediators. Addition of normal peritoneal exudate cells enhanced the cytotoxic potential of a small number of highly purified immune lymphocytes, which suggested that recruitment of normal cells is an additional mechanism of tumor cell death in this system.

Animals↗
PubMed1975

Macrophages activated in vitro with lymphocyte mediators kill neoplastic but not normal cells.

Normal guinea pig macrophages incubated for 3 days in vitro with mediator-rich lymphocyte supernatants become cytotoxic for the syngeneic tumors, line 1 hepatoma and MCA-25 fibrosarcoma. Under identical experimental conditions the survival of two normal syngeneic cell types, fibroblasts and kidney cells, was not affected. The activating supernatants were prepared by stimulating sensitized lymphocyte cultures with an antigen unrelated to the target cells. Therefore, this type of macrophage-mediated cytotoxicity appears to be nonspecific but restricted to cells with malignant growth capacities.

Ascitic Fluid↗
PubMed1975

Macrophages activated as suspension cultures with lymphocyte mediators devoid of antigen become cytotoxic for tumor cells.

Normal peritoneal exudate cells (PEC) were activated as suspension cultures either in mediator-rich supernatants from o-chlorobenzoyl-bovine gamma-globulin (OCB-BGG) stimulated lymphocytes or in antigen-free Sephadex fractions from these supernants. After 24 hr incubation thration. The adherent cell fractions of PEC, recovered by trypsinization from monolayers and activated by this technique, were as cytotoxic as unfractionated PEC. Lymphocyte supernatants and antigen-free fractions of the supernatants induced comparable macrophage-mediated tumor cytotoxicity. Treatment of activated macrophages with trypsin did not alter their cytotoxic capacity.

Animals↗