Effect of Prostaglandin E in Multiple Experimental Models. VIII. Effect on Host Response to Metastatic Tumor,
Abstract
Prostaglandin E (PGE) is produced by certain tumors and is reported to decrease primary tumor growth. We evaluated its effect in multiple tumor models utilizing a 1 week course of the long acting PGE derivative dimethyl-PGE (dPGE) at a dosage of 100 g/kg/day vs. a lactated Ringers control. For all tumor models, a suspension of 1 x 10 to the sixth power colon carcinoma cells were injected into Wistar-Furth rats. When the suspension was injected subcutaneously and the drug was begun at the time of tumor challenge, there was no effect on survival. When the tumor was injected intraperitoneally or intravenously and the drug begun at the time of tumor challenge, dPGE decreased survival time. When the tumor was administered intravenously but dPGE was delayed for 5 days, there was no effect on survival time. When rats were given a l week course of dPGE or saline, dPGE was found not to alter natural killer (NK) cell cytotoxicity, macrophage cytotoxicity, spontaneous lymphocyte blastogenesis, or mitogen stimulated blastogenesis. DPGE failed to alter lymphocyte metabolism of glucose in nonstimulated lymphocytes, but decreased the rate of glucose metabolism and adenosine deaminase activity in mitogen stimulated lated lymphocytes. In conclusion Immunology, Lymphocytes, NK Cells, Carcinoma.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jan 01, 1991
- Accession Number
- ADA251651
Entities
People
- Eliezer Flescher
- Gabriel Fernandes
- J. P. Waymack
- Jaya Venkatraman
- Rey F. Guzman
Organizations
- United States Army Institute of Surgical Research