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A Slungaard

Publications and source records attributed to A Slungaard.

22 records · Page 2Linked to original sources
PubMed1983

Antineoplastic effects of Bordetella pertussis adenylate cyclase.

Urea extracts of B. pertussis, but not B. bronchiseptica, cause large and sustained intracellular cAMP elevation in several neoplastic cell lines. These cAMP elevations are associated with growth inhibition (HL-60, Friend erythroleukemia) and a phenotypic change/differentiation (HL-60, L1210). B. pertussis extract injections prolong survival of L1210 tumor-bearing mice. Pretreatment of L1210 cells with B. pertussis extract both delays mortality and induces growth of solid tumors instead of ascites in subsequently inoculated mice. We conclude that B. pertussis adenylate cyclase is capable of invading a variety of neoplastic cells to catalyze the intracellular formation of large amounts of cAMP. These cAMP elevations are durable and promote growth arrest, differentiation, or phenotypic alterations reflected in altered biologic behavior. B. pertussis adenylate cyclase should prove to be a useful tool for manipulating cAMP levels in neoplastic cells to elucidate the role of cAMP in malignant transformation.

Adenylyl Cyclases↗
PubMed1982

Tumor-induced eosinophilia and endocardial fibrosis: evidence for ectopic eosinophilopoietin production and toxic O2 metabolite-mediated endothelial damage.

We have described a patient with the clinical triad of anaplastic pulmonary carcinoma, extreme eosinophilia, and endocardial damage, with resulting fibrosis and mural "thrombosis." Since the "thrombi" consisted mainly of masses of aggregated eosinophils in close approximation to areas of fibrotic cardiac endothelium, it was hypothesized that eosinophils might provoke endothelial damage. Indeed, eosinophils generated large amounts of toxic oxygen species and were highly toxic to cultured endothelial cells in vitro; moreover, high concentrations of corticosteroids inhibited in tandem these phenomena. In addition, from the patient's tumor a 45,000-dalton "eosinophilopoietin" was extracted which stimulated eosinophil colonies without help from T-lymphocytes. We believe our results help explain both the hypereosinophilia which accompanies certain anaplastic carcinomas and the endocardial damage with thrombosis and embolization which may occur in any patient with excessive eosinophils. In this latter regard, our studies suggest that very high doses of corticosteroids--since they decrease generation of toxic oxygen products by, and the numbers of, eosinophils--may be rational therapy in hypereosinophilic syndromes.

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