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Example sentences for: suppressive
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COX-2 is an inducible enzyme upregulated in inflammatory states [ 20 21 ] . Notably, many NSCLC and what have been characterized as "premalignant" lung lesions have been shown to constitutively express the COX-2 enzyme and produce prostaglandin E-2 (PGE-2), the primary product of the COX-2 pathway [ 22 23 24 25 26 ] . Importantly, PGE-2 production by tumor cells has been linked to tumor-induced immunosuppression in NSCLC [ 2 3 4 5 ] . PGE-2 has been shown to directly suppress T cell mediated immunity, the primary effector against tumor cells, at a variety of levels [ 2 3 4 5 6 7 ] . Further, PGE-2 has been shown to induce the IL10 in mononuclear cells [ 4 5 ] . IL10 is a prominent immunosuppressive cytokine that may have a dominant role in preventing innate antitumor responses in the NSCLC environment [ 2 3 4 5 ] , [ 8 9 10 11 12 13 14 15 16 17 18 19 ] . Among myriad suppressive effects on T cells and antigen presenting cells, IL10 is known to inhibit IL12 production [ 14 15 16 17 18 ] . IL12 plays a key role in the initiation and potentiation of cellular immune responses and alteration of the IL12 producing function in circulating mononuclear phagocytes may be a critical factor in suppressed T cell immunity to NSCLC [ 27 28 ] .
All 11 of 12 patients in Table 3 who reinitiated therapy retained suppressive ability of their respective regimens, as did all other patients who did not show resistance mutations in phase II.
However, no impact on cell growth in culture was found in clones with high constitutive Syk activity, nor was the growth suppressive effect of anti-IgM treatment enhanced (Figure 7A).
In regards to immunological outcomes, a concern associated with interruption of suppressive therapy is the potential for irreversible, viral-mediated CD4 T cell loss leading to disease progression [6,22].
Study-defined criteria for therapy failure of a previously suppressive regimen were met by 4/21 patients in the continuous therapy/single interruption arm (patients S37, S47, S52, and S59) in association with self-reported nonadherence to therapy and detection of resistance mutations in phase I, as listed in Table 2. One patient in the repeated interruptions arm (1/21; patient S56) failed therapy after 20 wk following the third TI by maintaining a viral load between 50 and 999 copies/ml in the presence of previously undetected resistance mutations.
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