Table 3.

Description of studies evaluating the anticancer potential of AX and AXOS, in vivo.

Type of cancer/animal model	Carcinogenic agent/cancer cells	Dosage/experimental time	Findings	Reference
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]
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]
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]
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]
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]
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]

bw: body weight; ip: intraperitoneal; AST: serum aspartate aminotransferase; ALT: alanine aminotransferase; ALP: alkaline phosphatase; gamma GT: gamma glutamyl transpeptidase.