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Acute and Chronic Transforming Retroviruses
Published in Pimentel Enrique, Oncogenes, 2020
The type of induced tumor would depend, at least partially, on the cellular oncogene that is activated by insertion of a viral promoter. For example, ALV, which is a chronic transforming retrovirus, induces lymphoid leukosis when the cellular oncogene c-myc is activated by insertion of the viral LTR but it induces erythroblastosis when a different oncogene, c-erbS, is activated by a similar mechanism.180
Vitamin E Effects on Avian Retrovirus-Induced Immune Dysfunctions
Published in Maryce M. Jacobs, Vitamins and Minerals in the Prevention and Treatment of Cancer, 2018
The avian immune dysfunction model systems investigated involve acute oncogenic avian retroviruses that induce a rapid, severe, generalized immune suppression and cause lethal cancers in a matter of weeks.8,35,36 Two avian retrovirus-induced immune disorder states were investigated: reticuloendotheliosis virus induced lymphoid leukosis with immunosuppression and avian erythroblastosis virus induced erythroleukemia with immunosuppression. These two avian retroviruses induce similar immune dysfunctions.8,36,37 The cascade of immunodeficiencies induced by the avian erythroblastosis virus is summarized in Figure 2.
Ia-Like Antigens of the Chicken
Published in Soldano Ferrone, Chella S. David, Ia Antigens: Man and Other Species, 1982
Donald L. Ewert, Max D. Cooper
In the chicken, Ia antigens have been demonstrated by immunofluorescence on B cells, macrophages, and an unidentified subpopulation of mononuclear cells in bone marrow, spleen, thymus, and bursa of Fabricius11 (Figure 3). Thrombocytes, thymocytes, erythrocytes, fibroblasts, spermatozoa, kidney cells, embryonic liver cells, and embryonic yolk sac cells were not stained. In addition to B cells of normal tissues, all lymphoid leukosis tumor cells examined express Ia antigens as well as surface lgM. Ia antigens have not been detected on normal unstimulated T cells or tumors of T cell origin.11,40
Fatty Acid Content and Tumor Growth Changes in Mice After Exposure to Extremely High-Frequency Electromagnetic Radiation and Consumption of N-3 Fatty Acids
Published in Nutrition and Cancer, 2019
Andrew B. Gapeyev, Alexander V. Aripovsky, Tatyana P. Kulagina
It is known that extremely high-frequency electromagnetic radiation (EHF EMR) with certain exposure parameters can have positive effects on many physiological and biochemical processes in the mammalian organism, without causing damaging effects (10,11). When studying the effects of EHF EMR on tumor growth, inhibitory effects on tumor cells was observed both in culture (12,13) and in experimental (14–17), and clinical oncology (18). It was found that EHF EMR is capable of inhibiting the tumor growth in different animal models, including sarcoma-45, nephritic cancer, intrahepatic cholangiocellular carcinoma, Zaidel's hepatoma, Lewis lung carcinoma, Walker carcinosarcoma, Pliss' lymphosarcoma, Shvetz's lymphoid leucosis, etc. (14,15). It was revealed that the exposure of mice with B16F10 melanoma to EHF EMR (61.22 GHz, 13.3 mW/cm2, 15 min daily for five consecutive days starting on the fifth day after injection) suppressed tumor growth (16). The decreased growth of solid Ehrlich carcinoma was found under the exposure of tumor-bearing mice to low-intensity EHF EMR with specific parameters (42.2 GHz, 0.1 mW/cm2, 20 min daily for five consecutive days beginning on the first day after inoculation) (17). However, the physiological and biochemical mechanisms underlying the antitumor effects of EHF EMR are practically unknown. The main hypothesis is that the EHF EMR is capable of modulating the immune system status thereby influencing the tumor growth (10,18). It was shown that the exposure of mice to EHF EMR (42.2 GHz, 36.5 mW/cm2, 30 min exposure duration) reduced the cyclophosphamide (CPA)-induced metastases of B16F10 melanoma cells and increased NK cell activity suppressed by CPA (19). It was demonstrated that exposure of mice to EHF EMR (61.22 GHz, 31 mW/cm2, 30 min daily for three consecutive days) caused upregulation in TNF-α production in peritoneal macrophages suppressed by CPA administration, increased IFN-γ production by splenocytes, and enhanced proliferative activity of T-cells (20). It was also found that exposure of CPA-treated mice to EHF EMR (42.2 GHz, 38 mW/cm2, 30 min daily for three consecutive days) upregulated the production of Th1 cytokines (TNF-α, IFN-γ, and IL-2, associated with antitumor responses) suppressed by CPA (21). The results obtained showed that the exposure to EHF EMR accelerates the recovery process selectively associated with T-cell-mediated immune response, tends to normalize Th1/Th2 balance, but has no significant effect on B-cell-mediated immunity. The exposure to EHF EMR can also cause free radical formation (22,23), which can in turn initiate signaling mechanisms leading to apoptosis of tumor cells (24,25).