AOR PHYTO C ...IP6 90'S
Shrinking Tumors In a study of human liver cancer cells transplanted into mice that were subsequently treated with IP6, the researchers found that IP6 slowed or stopped the growth of liver cancer cells and shrank existing tumors three to four fold. In one human liver cell study, Shamsuddin's team treated human hepato-carcinoma cells with varying doses of pure IP6. The result was partial to complete inhibition of cell growth and proliferation. Treated cells transplanted into mice produced no tumors over the 41 days of the experiment, while 71% of control mice developed tumors. When these control mice were treated with IP6 for 12 days, their tumors weighed 3-4 fold less than before IP6 treatment, suggesting that IP6 is useful as a preventative and as a treatment. Shamsuddin has tested IP6 on colon, lung, breast, prostate, leukemia, fibrosarcomas, and muscle cell cancer in test tubes and in experimental animals, including human cancers transplanted into animals. In all types, whether IP6 is administered before, during, or after exposure to a carcinogen or the development of tumors, treated animals have shown fewer, smaller tumors with reduced growth rates. Cellular Differentiation Restored Histological studies have shown that IP6-treated human cancer cells (including the colon cancer cell line HT-29, rhabdomyosarcomas, HepG2 human liver cancer, and erhythmoleukemias) show signs of differentiation, returning them to normal appearance and function (phenotype). As Shamsuddin has remarked, "IP6 does not kill cancer cells; it tames them and makes them behave like normal cells." Human Studies Finally, at least two human studies have been conducted. In 2002, a 6-14 month follow-up pilot study was done on 6 patients with colorectal cancer. The patients had undergone chemotherapy and surgery to remove the tumours. Daily IP6 and inositol supplementation reduced their chemotherapy side effects. After 14 months, one patient opted out of a second round of chemo because the rate of tumour growth had significantly decreased. In 2010, a small randomized placebo controlled trial 6 months in length evaluated supplementing breast cancer patients with 3 g twice daily of IP6 + inositol. Compared to the placebo group, the treatment group did not experience cytopenia or drops in leukocyte and platelet counts, and they had a better quality of life and functional status. Mechanisms of Action There are several probable ways that IP6 exerts its effects: (1) Antioxidant Protection through Chelation:Antioxidants are believed to fight cancer because they prevent free radical damage to DNA. Unbound iron (ferritin), though not a free radical itself, can be the catalyst for the deadly Fenton Reaction, in which iron reacts with the relatively harmless hydrogen peroxide (H2O2) and forms the highly reactive hydroxyl radical (OH.). IP6 chelates free iron, thereby preventing the hydroxyl radical production before it starts. (2) Immune Function: Animal experiments conducted by Dr. Shamsuddin have clearly shown dramatic increases in the activity of Natural Killer Cells (NK) in animals treated with IP6. This increase corresponds neatly with decreased tumor incidence in treated animals, as one would expect, since NK cells' main function in the body is to seek out and destroy cancerous and virus-infected cells. (3) Cellular Signaling: The inositol phosphates (IPs) are involved in cellular signaling, regulating calcium balance within the cell and thus the rate of cell division. Dr. Shamsuddin has shown that IP6 administration both elevates the levels of several IPs within the cell and slows cell division. This may in part explain IP6's anti-cancer activity. (4) Gene Expression: IP6 appears to be a competitive inhibitor for the enzyme phosphatidylinositol-3 kinase (PI3K), which is the enzyme that activates activator protein 1 (AP-1). AP-1 is a protein transcription factor induced by asbestos and other cancer promoters, which binds to, and activates, known cancer genes such as c-FOS and c-JUN. IP6 has also been reported to up regulate expression of the tumor-suppression gene p-53, an exciting development indeed.Research by AOR
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