P53 Activation Therapy


P53 cancer gene activated by certain plant based food.

March 28, 2013 Staff 0 Comments bread crust, chemotherapy drug, cigarette smoke, cocoa powder, coffee bread, dna damage, flavorings, gallic acid, green teas, human cells, johns hopkins university, johns hopkins university school, johns hopkins university school of medicine, kimmel cancer center, liquid smoke flavoring, p53 cancer, p53 gene, repair proteins, scott kern, smoked foods

Biologists at John Hopkins Kimmel Cancer Center tested the potential harmful effect of food and flavorings on the cell DNA and released their findings in a study published in February 2013.

It was found that liquid smoke flavoring, black and green teas and coffee activated the highest levels of the p53 cancer linked gene.

The p53 gene is activated when DNA is damaged and expresses repair proteins that mend the damaged DNA. The activation and expression of p53 is directly linked to the level of DNA damage.

“We don’t know much about the foods we eat and how they affect cells in our bodies,” says Scott Kern, M.D., the Kovler Professor of Oncology and Pathology at the Johns Hopkins University School of Medicine. “But it’s clear that plants contain many compounds that are meant to deter humans and animals from eating them, like cellulose in stems and bitter-tasting tannins in leaves and beans we use to make teas and coffees, and their impact needs to be assessed.”

A test was developed for p53 activity, by using a fluorescent compound that “glows” when p53 is activated. Researchers mixed dilutions of food products and flavorings with human cells and grew them in laboratory dishes for 18 hours.

A baseline p53 activity was obtained and the scientists found that liquid smoke flavoring, black and green teas and coffee revealed a 30-fold increases in p53 activity, which was on par with their tests of p53 activity caused by a chemotherapy drug called etoposide.

Prior studies have shown that liquid smoke flavoring damages DNA in animal models, and Kern’s team analyzed p53 activity triggered by the chemicals found in liquid smoke. The chemicals with the highest level of p53 activity include: pyrogallol and gallic acid. Pyrogallol, commonly found in smoked foods, is also found in cigarette smoke, hair dye, tea, coffee, bread crust, roasted malt and cocoa powder and Gallic acid, a variant of pyrogallol, is found in teas and coffees. Liquid smoke is often used to add flavor to sausages, meat and other vegan based products.

Other flavorings like fish and oyster sauces, tabasco and soy sauces, and black bean sauces showed minimal p53 effects, as did soybean paste, kim chee, wasabi powder, hickory smoke powders and smoked paprika.

The researchers cautioned that more research is needed to confirm the laboratory based study.


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A major consequence of mutant p53 degradation in tumor cells after glucose deprivation is the loss of a critical check on the autophagic process that results in increased autophagy and leads to cell death (Fig. 1). Importantly, wild type p53 has been previously demonstrated to protect cells from glucose deprivation through induction of a reversible G1/S phase cell cycle arrest, suggesting that normal tissues will respond to glucose shortage differently than tumors harboring mutant p53.1

fig ft0fig mode=article f1

Taken together, these findings strongly indicate that some tumor-promoting forms of mutant p53 can be targeted for autophagic degradation through glucose restriction. These exciting results could be tested in the clinic by randomizing patients with tumors that harbor similar p53 mutations to a glucose-restrictive, low-carbohydrate diet compared with a normal diet. The expectation of such studies would be that the tumors of patients on a glucose-restrictive diet would see their tumors regress or grow more slowly than those on an unrestrictive glucose diet. However, the next step in this saga will be to see what combinations of chemotherapy or targeted therapy will be more effective against mutant p53 tumors that are glucose-restrictive.

Cell Cycle. 2013 Mar 1; 12(5): 718–719.

doi:  10.4161/cc.23948

PMCID: PMC3610718

PMID: 23422857

A low-carb diet kills tumor cells with a mutant p53 tumor suppressor gene

The Atkins diet suppresses tumor growth

Edward L. LaGory and Amato J. Giaccia*

Author information ► Copyright and License information ► Disclaimer

See the article “Dietary downregulation of mutant p53 levels via glucose restriction” in volume 11 on page 4436.

The Good News

What is really exciting is that this repair gene, p53, which protects cells from becoming cancerous, can be highly activated by many natural substances—substances that do not have the negative side effects of drug therapies. The ability to activate p53 within cells may halt cell proliferation, or even cause cancer cell death.


For example, cruciferous vegetables (especially watercress with its high content of PEITC) have been found to support p53. PEITC (phenethylisothyanate) decreases the levels of mutated p53 and helps to restore the normal activity of this protein.

Vitamin C is another promoter of P53, which is one of the reasons intravenous Vitamin C (IVC) and high-dose oral C therapies are so effective against cancer.

The resveratrol in red grapes and red wine (organic please, and research shows dark, red wines are best) also activates the P53 gene

. IP6

has been shown to alter the expression of p53. Zinc helps protect the p53 gene against cancer-forming mutations. Selenium can activate p53 in response to genetic damage, helping the cell to repair its DNA. Herbs such as sage, rosemary, ginger, curcumin, and ashwaganda support p53. Thymoquinone extracted from black seed triggers apoptotic cell death in colorectal and other cancers cells via the p53- dependent mechanism. Anthocyanins, abundant in red  onions, inhibit the damage that impaired p53 can cause on cells and tissue. Anthocyanins are also found in blackberries, blueberries, purple grapes, eggplant, and avocado.

P53 Supporters:

• Cruciferous vegetables, especially watercress



• Herbs such as sage, rosemary, ginger, curcumin, and ashwaganda

• EFA’s from omega 3 fatty acids (please use caution with fish oil supplements as they can be toxic). For a plant based formula, you could take BodyBio Balance Oil.

• Licorice

• Mistletoe

Vitamin D


• Vitamin C


Black Seed

Clinoptilolite (a special form of Zeolite)

On the other hand, processed foods, refined flours, and sugars will impair P53. Smokey flavoring and smoked foods can also damage DNA. Chemicals such as benzene and perchloroethylene, two volatile organic compounds, negatively affect p53, possibly causing them to stimulate rather than suppress cell proliferation.

The late Integrative Oncologist Dr Mitchell Gaynor, MD was famous for his passion for explaining that we can change the way our genes behave by making good dietary choices. For more gene-changing foods and lifestyle habits read Dr. Gaynor’s book, The Gene Therapy Plan, Taking Control of Your Genetic Destiny with Diet and Lifestyle.

P53 and BRCA are not the only genetic mutations that increase cancer risk. For example, mutations in th e CHEK2 gene are associated with an increased risk of developing many types of cancer, including breast, colon, prostate, and other cancers — sometimes at young ages. If you have a history of hereditary cancer you might benefit from genetic testing for CHEK2 and others.


You can request to be tested for the p53 mutation. The test is called the p53 Gene Mutation Analysis, Cell Based, offered by labs such as Quest Diagnostics. If your insurance company does not accept Quest or another lab that offers this test, you can petition your carrier for a Network Gap Exception.

You may need to consult a genetic counselor if your oncologist does not routinely check for mutations as these tests are not part of your typical pathology report.

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