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| Type of cancer/animal model | Carcinogenic agent/cancer cells | Dosage/experimental time | Findings | Reference |
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Solid Erlich carcinoma
Female albino mice | Erlich ascites, carcinoma cells, and intramuscular inoculation | MGN-3/Biobran (25 mg/kg bw) ip
Six times/week for 25 days at either day 4 or day 11 post-cancer cell inoculation. | MGN-3 suppressed the growth of tumors, normalized lipid peroxidation, and increased glutathione contents. Increased activity of endogenous antioxidant scavenging enzymes (superoxide dismutase, glutathione peroxidase, catalase, and glutathione-S-transferase) in blood, liver, and tumor tissue. | [19] |
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Colon carcinogenesis
Male F344 rats | 1,2,-Dimethylhydrazine (DMH), subcutaneous injection. | High-fat diet plus AXOS (48 g/kg).
10 days before receiving carcinogen and continued for 13 weeks. | Lower counts of preneoplastic lesions (mucin depleted foci (MDF)) in comparison to the control group. Fewer preneoplastic lesions (aberrant crypt foci (ACF)) in the distal part of the colon. | [17] |
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S180 tumor-bearing mice
ICR male mice | Mouse sarcoma S180 cells, intramuscular inoculation. | AX orally administered (100, 200, and 400 mg/kg bw). | Administration of AX significantly inhibited the growth of mouse transplantable tumors and promoted thymus and spleen indexes, splenocyte proliferation, NK cell and macrophage phagocytosis activity, and IL-2 production. Increased peripheral leukocyte count and bone marrow cellularity. | [16] |
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Neuroblastoma
NOD-scid
IL-2Rgnull mice | Injection of NB1691luc cells. | NK cells activated with 100 μg/mL MGN-3/Biobran injected intravenously.
7 days after injection of tumor cells and performed twice a week for 4 weeks. | Significant inhibition of neuroblastoma growth and improvement in survival in the group treated with Biobran.
Increase in the activation-associated receptors CD69 and CD25 on NK cells. | [93] |
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Glandular stomach carcinogenesis.
Male Wistar rats | Methylnitrosoguanidine (MNNG), via oral gavage. | MNNG plus Biobran (40 mg/kg bw) every other day via oral gavage.
8 months | Biobran reduced incidence of animals bearing gastric dysplasia and adenocarcinoma.
Decrease in expression of tumor marker Ki-67 and increase in the level of apoptotic gastric cancer cells via cell cycle arrest (sub-G1) and mitochondria-dependent pathway. Protection against lymphocytopenia. | [15] |
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Hepatocarcinogenesis.
Male albino rats | N-nitrosodiethylamine (NDEA) and carbon tetrachloride (CCl4). | MGN-3/Biobran (25 mg/kg bw), 5 times/week ip
2 weeks prior to receiving carcinogen and continued for 20 weeks. | Reduction in liver tumor incidence, decrease of preneoplastic foci in hepatic parenchyma, and inhibition of development of hepatocellular carcinoma. Regulation of AST, ALT, ALP, and gamma GT levels. Increase in cell cycle sub-G0/G1 population. Downregulation of expression of NF-κBp65 and Bcl2, upregulated p53, Bax, and caspase-3 and increased the Bax/Bcl-2 ratio. | [94] |
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