@entity3352 has been shown clinically to inhibit growth of SCCHN (Panje, 1981). This inhibition appears to be due to augmentation of cellular immunity. The inhibitory effect of @entity3352 may act by limiting @entity5 associated @entity1421 production, thereby allowing return of costimulatory cytokines by antigen presenting cells. This would have the net result of relief from host unresponsiveness and promotion of B-cell and CTL differentiation, allowing the individual to mount an effective response. The enhancement of @entity5 infiltrating lymphocytes in SCCHN seen with @entity3352 administration could presumably be further augmented when given in combination with cytokine therapy. Future investigation may allow the biochemical staging of an individuals' @entity5 to determine the optimal combination of cytokine therapy and @entity3009 inhibition through selective use of NSAID's. The effect of NSAID manipulation of @entity3009 and @entity4352 metabolism on prevention of @entity3 in SCCHN has yet to be studied. Given that a preselected, potentially responsive subset of immunocytes exists within the @entity5 tissue and lymph nodes, the development of the @entity10086 phenomenon in TIL's and @entity5 draining lymph nodes from surgical specimens is a viable and exceedingly interesting area for future investigations in autologous @entity10086 immunotherapy. The potential exists to harvest a preselected population of @entity5 infiltrating (Boscia, 1988) or @entity5 draining immunocytes (McKinnon, 1990). These can then potentially be returned to a state of antigen responsiveness with a combination of cytokine exposure (e.g. @entity5041 ) and systemic cytokine therapy. With subsequent inhibition of @entity5 associated @entity3009 synthesis by the systemic administration of @entity3009 synthesis inhibitors, it may be possible to successfully alter the host response to @entity5 .

Tumor infiltrating lymphocytes in squamous cell carcinoma of the head and neck: mechanisms of enhancement using XXXX synthetase inhibitors.

@entity5 :: ('MESH:D009369', 'Disease') :: ['tumor'] @entity1421 :: ('MESH:D015232', 'Chemical') :: ['prostaglandin E2'] @entity3009 :: ('CHEBI:26333', 'Chemical') :: ['prostaglandin'] @entity4352 :: ('CHEBI:25029', 'Chemical') :: ['leukotriene'] @entity5041 :: ('116562(Tax:10116)', 'Gene') :: ['rIL-2'] @entity3 :: ('MESH:D009362', 'Disease') :: ['metastatic disease'] @entity3352 :: ('MESH:D007213', 'Chemical') :: ['Indomethacin', 'indomethacin'] @entity10086 :: ('80216', 'Gene') :: ['LAK']
@entity3009 :: (CHEBI:26333,Chemical) :: ['prostaglandin']
