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 I week course of the long acting PGE derivative dimethyl-PGE (dPGE) at a dosage of 100 Jg/kg/day vs. a lactated Ringers control. For all tumor models, a suspension of I X 106 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 1 on survival time. When rats were given a I 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 glucost. ;-nonstimulated lymphocytes, but decreased the rate of INTRODUCTIONThis belief is based primarily on in vitro studies where Oncology patients have been demonstrated to have leukocytes were cultured in the presence of PGE and elevated levels of prostaglandin E (PGE) in their primary were then assayed for various immune functions. These tumor tissue and systemic circulation Il]. The PGE has studies demonstrated that, in in vitro models, PGE also been reported to exert autocrine, paracrine, and impairs lymphocyte blastogenesis, natural killer (NK) endocrine effects on both the tumor, and the host cell cytotoxicity, macrophage cytotoxicity, and granuloresponse to the tumor [2]. The majority of effects of PGE cyte chemotaxis [5][6][7]. There have, however, been very on tumor cells appear to be directed towards inducing few studies evaluating the effect of PGE on immune differentiation of the tumor cell and to decreasing the rate

Tramadol use is associated with enhanced postoperative outcomes in breast cancer patients: a retrospective clinical study with in vitro confirmation

“…Ketorolac was reported to have a weaker immunosuppressive effect than intravenous morphine or tramadol in patients who underwent modified radical mastectomy. 33 Moreover, several studies have helped to identify the role of prostaglandins in immunity and inflammation 34,35 and the positive effect of NSAIDs on progression of cancer. 36e38 However, all these studies have had the limitation of focusing only on the immune response and not the clinical outcomes in patients with cancer.…”

Neutrophil‐lymphocyte and platelet‐lymphocyte ratio in patients after resection for hepato‐pancreatico‐biliary malignancies

“…Hence, a high peripheral neutrophil level may indicate cancer‐related inflammation. Tumor‐associated neutrophils produce vascular endothelial growth factor (VEGF), reactive oxygen species (ROS), basic fibroblast growth factor (bGF), and Prostaglandin E2 (PGE2), which promote angiogenesis, encourage tumor development and inhibit the function of cytotoxic lymphocytes, leading potentially to more aggressive tumors . Thrombocytosis is induced by the excessive stimulation of megakaryocytes differentiation by VEGF and cytokines (mainly IL‐1 and IL‐6) secreted by tumor cells .…”