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Effect of prostaglandin E in multiple experimental models. VIII. effect on host response to metastatic tumor
Author(s) -
Waymack J. Paul,
Flescher Eliezer,
Venkatraman Jaya,
Fernandes Gabriel,
Guzman Rey F.,
Yurt Roger W.,
Mason Arthur D.,
Pruitt Basil A.
Publication year - 1991
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.2930480406
Subject(s) - prostaglandin e , medicine , primary tumor , lymphocyte , endocrinology , prostaglandin e2 , prostaglandin , metastasis , cancer research , immunology , pharmacology , cancer
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 μg/kg/day vs. a lactated Ringers control. For all tumor models, a suspension of 1 × 10 6 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 1 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 lymphocytes. In conclusion, PGE appears to enhance metastatic growth of tumor lines where it does not alter primary tumor growth. This effect does not appear immunologically mediated.