Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
EFFECT OF RADIATION AND CHEMOTHERAPY ON THE INTERFERON SYSTEM IN PATIENTS WITH NEOPLASTIC DISEASES (MEETING ABSTRACT)
Proc Annu Meet Am Soc Clin Oncol; 10:A210 1991. Unique Identifier : AIDSLINE ICDB/91671666 Ambrus J L; Chadha K; Stadler S; Halpern J; Khalil M; Piver S Hreschchyshyn MM; Ambrus CM; Roswell Park Cancer Inst., Buffalo, NY
Abstract:
In patients with cancer of the gastrointestinal tract, pancreas, uterus, cervix, AIDS-related and -unrelated Kaposi's sarcoma and lymphoma, measurable interferon levels were present in the circulation. The Sendai virus-stimulated white cells had decreased alpha interferon-producing activity. Non-antibody type interferon inhibitory activity was found in the plasma. In normal controls, measurable interferon or interferon inhibitor activity was never found in the circulation. Interferon-producing activity in normal individuals was high or low. This characteristic remained constant over a 3-yr observation period. The question arises whether individuals in the normal control group who are low producers are at higher risk of carcinogenesis and viral infections because of impaired immunosurveillance than high producers. Impairment of the interferon system in cancer patients may contribute to infectious complications. Preliminary results indicate that interferon production is cAMP-related. cAMP-increasing agents (eg, pentoxifylline) increased interferon synthesizing activity of low producer white cells in vitro. Surgical-chemotherapy and/or radiation therapy induced remission of neoplastic disease resulted in normalization of the interferon system.
Keywords: Antineoplastic Agents/*ADVERSE EFFECTS Cyclic AMP/PHYSIOLOGY Disease Susceptibility Female Human Interferons/ANTAGONISTS & INHIB/*BLOOD Male Neoplasms/DRUG THERAPY/*ETIOLOGY/RADIOTHERAPY/*THERAPY Pentoxifylline/PHARMACOLOGY Radiotherapy/*ADVERSE EFFECTS Reference Values Risk Factors Virus Diseases/ETIOLOGY ABSTRACT 911030
M91A1117
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