The whole relationship between prostaglandins and cancer has not received the attention it should from experimental oncologists. This may be because the whole area of prostaglandins is immensely confusing, with different cyclo-oxygenase metabolites having completely opposite results. Thus when one adds a cyclo-oxygenase inhibitor to a system, any result is possible. It is not even settled whether PGE has a physiologic role or is merely a metabolite of an unstable intermediate compound that is the 'real' PG, or whether the effects of cyclo-oxygenase inhibitors are because of inhibition of production of the classic prostaglandins (PGE and PGF) or by inhibition of production of thromboxanes, prostacyclin, etc. This lack of precise definition of the system tends to discourage precision in experimentation, which in turn tends to keep careful investigators out of the area. The investigator studying the effects of PG synthetase inhibitors on cancer growth must accept these limitations.
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