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dc.contributor.authorSchultz, R. M.en
dc.contributor.authorPavlidis, Nicholasen
dc.contributor.authorStylos, W. A.en
dc.contributor.authorChirigos, M. A.en
dc.creatorSchultz, R. M.en
dc.creatorPavlidis, Nicholasen
dc.creatorStylos, W. A.en
dc.creatorChirigos, M. A.en
dc.date.accessioned2018-06-22T09:53:12Z
dc.date.available2018-06-22T09:53:12Z
dc.date.issued1978
dc.identifier.urihttps://gnosis.library.ucy.ac.cy/handle/7/41714
dc.description.abstractThe ability of interferon-treated macrophages to kill or inhibit the growth of tumor cells is markedly influenced by the local environment. The macrophage cytotoxic effector system is regulated by serum and other environmental factors that suppress tumor killing. Prostaglandins E1 and E2, but not F2alpha reversibly inhibited the tumoricidal state of interferon-treated macrophages. Hydrocortisone was similarly active at suppressing macrophage function. Such nonimmunologically derived factors could prevent the final triggering step for macrophage-mediated tumor killing in the local environment of the tumor and may be important in the pathogenesis of progressive tumor growth.en
dc.language.isoengen
dc.sourceCancer treatment reportsen
dc.subjectMaleen
dc.subjectAnimalsen
dc.subjectHydrocortisoneen
dc.subjectMiceen
dc.subjectImmunologicen
dc.subjectLeukemiaen
dc.subjectCytotoxicityen
dc.subjectExperimentalen
dc.subjectInterferonsen
dc.subjectMacrophagesen
dc.subjectProstaglandins een
dc.subjectSyntheticen
dc.titleCytotoxic activity of interferon-treated macrophages studied by various inhibitorsen
dc.typeinfo:eu-repo/semantics/article
dc.description.volume62
dc.description.issue11
dc.description.startingpage1889
dc.description.endingpage1892
dc.author.facultyΙατρική Σχολή / Medical School
dc.type.uhtypeArticleen


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