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Depressed mononuclear cell function in advanced neoplastic disease

J A Stratton, P J DiSaia

    American Journal of Reproductive Immunology : AJRI : Official Journal of the American Society for the Immunology of Reproduction and the International Coordination Committee for Immunology of Reproduction
    |April 1, 1982
    PubMed
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    Patients with invasive gynecologic neoplasms showed impaired immune cell function. Malnutrition associated with advanced cancer likely causes these depressed immune responses, not suppressor cells.

    Area of Science:

    • Immunology
    • Oncology
    • Gynecologic Oncology

    Background:

    • Patients with invasive gynecologic neoplasms often exhibit altered immune function.
    • Ascitic fluid and associated cells are crucial in understanding the tumor microenvironment's impact on immunity.

    Purpose of the Study:

    • To assess the immunocompetence of mononuclear ascites cells.
    • To investigate the immunoregulatory properties of cell-free ascitic fluid.
    • To compare immune responses in cancer patients to normal subjects.

    Main Methods:

    • Analysis of ascites fluids and blood mononuclear cells from 9 gynecologic cancer patients.
    • Stimulation of mononuclear cells with polyclonal mitogens like phytohemagglutinin, concanavalin-A, and pokeweed mitogen.
    • Assessment of immune cell responses in the presence of autologous serum or cell-free ascitic fluid.

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    Main Results:

    • Mononuclear cells from cancer patients demonstrated poor response to polyclonal mitogens.
    • Autologous serum and ascitic fluid enhanced responses to phytohemagglutinin and pokeweed mitogen but not concanavalin-A.
    • A significant depression in response to succinyl-concanavalin-A was observed.
    • No evidence of suppressor cells within the ascites cell populations was found.

    Conclusions:

    • Depressed immune responses in gynecologic cancer patients are likely linked to malnutrition.
    • The findings suggest malnutrition, rather than suppressor cells, is a key factor in immune dysfunction in advanced malignancy.