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Antineoplastons

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877
Anybody ever thought about if Antineoplastons would work for ME/CFS? Sounds like Dr Burzynski is using cell methylation to some extent if I'm understanding correctly?

Are these defective genes in cancer common to the defective genes in CFS?

Be great if this were a turn key solution for HGRV disease's.



http://www.burzynskiclinic.com/what-are-antineoplastons.html

Antineoplastons (ANP) are peptides and amino acid derivatives, discovered by Dr. S. Burzynski, M.D., Ph.D. in 1967.

Dr. Burzynski first identified naturally occurring peptides in the human body that control cancer growth. He observed that cancer patients typically had deficiency of certain peptides in their blood as compared to healthy individuals. According to Dr. Burzynski, Antineoplastons are components of a biochemical defense system that controls cancer without destroying normal cells.

Chemically, the Antineoplastons include peptides, amino acid derivatives and organic acids. They occur naturally in blood and urine and they are reproduced synthetically for medicinal use. The name of Antineoplastons comes from their functions in controlling neoplastic, or cancerous, cells (anti-neoplastic cells agents).

Antineoplastons act as molecular switches, which turn off life processes in abnormal cells and force them to die through apoptosis (programmed death of a cell). While they trigger the death of cancer cells, they do not inhibit normal cell growth. They specifically target cancer cells without harming healthy cells.

It is generally known that the cancerous process results from increased activity of oncogenes and decreased expression of tumor suppressor genes. Antineoplastons "turn on" tumor suppressor genes and "turn off" oncogenes restoring the proper balance in gene expression.


http://www.burzynskiclinic.com/images/stories/ANP_mechamism_of_activity.pdf

Phenylacetic acid (PN; the active ingredient of Antineoplaston AS2-1) inhibits farnesylation of protein p21 of the
RAS oncogene, inhibits RAS and BCL-2, and activates the tumor suppressor genes TP53 and p21 through
demethylation of their promoters.
Phenylacetylglutamine (PG; the main ingredient of Antineoplaston A10 I) restores global methylation of DNA,
inhibits the oncogenes AKT2 and MYCC, activates the tumor suppressor genes PTEN and MAD, and restores
activity of the mutated INI1 protein through normalization of nuclear transport.
Both PN and PG promote apoptosis: PN through inhibition of BCL-2 and PG through deamidation of the BCL-XL
protein.