Life Extension Magazine®

Issue: Nov 2018

Green Tea and Broccoli Reduce Breast Cancer Risk

Compounds in green tea and broccoli can reprogram genes in treatment-resistant malignant cells to make them more susceptible to eradication by conventional therapies. The combination of green tea and broccoli can reduce tumor size in difficult-to-treat cancers.

By Janet Seiken

Certain types of breast cancer cells are notoriously difficult to treat.

These cancers can undergo changes that make them impervious to some of the most effective treatments available.

Green tea and broccoli contain compounds that can restore treatment sensitivity to treatment-resistant breast cancer cells.

They accomplish this by reprogramming the genes of the malignant cells.

In a recent study, difficult-to-treat tumors from mice supplemented with both green tea and broccoli weighed only about a third as much as the same type of tumors from control mice.1 This indicated that the combination of green tea and broccoli could reduce tumor size in hard-to-treat cancers.

The ability to produce such changes makes these compounds promising against difficult-to-treat breast cancers—and may offer hope to the thousands of women impacted every year.

What you need to know

Some forms of breast cancer are more difficult to treat than others. Breast cancers that are estrogen receptor positive respond better to common treatment, however many of these cancers mutate and lose their estrogen receptors. Compounds found in broccoli and green tea utilize several mechanisms to reduce breast cancer severity and risk. New research shows that they can also create estrogen receptors on cancers cells.

Why Some Cancers are Difficult to Treat

Breast cancer is the most common malignancy in women, with a quarter of a million diagnosed every year. And it is the second leading cause of cancer death in women, killing more than 40,000.2

There are numerous types of breast cancer, some of which are more difficult to treat than others.

Estrogen receptor (ER) positive cancers are easier to treat because they have estrogen receptors on their surface. Tamoxifen can bind to the estrogen receptor and prevent estrogen from stimulating the growth of cancer cells.3-5

The problem is that some originally ER positive cells lose these receptors during cancer development, turning them into estrogen receptor (ER) negative cells.

Without estrogen receptors, hormone treatments like tamoxifen are not effective. This deprives its victims from an effective form of treatment—and condemns them to much higher risks of death.

New science has discovered that green tea and broccoli contain compounds that can restore the estrogen receptors in ER negative cells.

These findings may make these difficult-to-treat-cancers easier to destroy by anti-estrogen therapies.

Extracts Change Cancer Cell Genetics for the Better

Green tea  

Green tea and broccoli have a long list of anti-cancer actions.

Studies show that green tea contains polyphenols (particularly one called epigallocatechin-3-gallate, or EGCG) that have favorable effects against tumor cells of all kinds. This includes halting the cell reproductive cycle, triggering programmed cancer cell death, and preventing tumors from spreading (metastasis).1,6,7

Broccoli contains sulforaphane, a compound that shares some of EGCG’s anti-cancer properties, but in addition can prevent the liver from converting potential carcinogens into active ones.1,8-10

These compounds also have properties capable of reversing several cancer-related gene alterations. Both EGCG and sulforaphane have the ability to turn “on” genes that suppress tumors, while turning “off” genes that promote tumors (though they accomplish them by entirely different mechanisms).1,11-15

This ability to “turn genes on and off” — that is, to control their expression — is called epigenetics. This is an exciting area in medical science, as it is now understood that genes don’t need to be replaced, or have their structure altered, to determine whether or not they function. They can, in effect, be (epigenetically) reprogrammed.

In an effort to better understand how these two natural compounds can be therapeutically applied to breast cancer, researchers decided to test their specific epigenetic effects on breast cancer cells.1

In part one, researchers found that either compound alone significantly reduced survival of ER-negative breast cancer cells. When both compounds were used together, the result was further cancer cell death—showing that the combination is more potent than either phytonutrient on its own.1

The reason why the compounds were able to effectively sensitize the cells to the anti-breast cancer hormonal drug tamoxifen was because they reprogrammed the genes of the ER-negative cells to begin generating the missing estrogen receptors. Doing so abruptly restored the cells’ responsiveness to estrogen’s growth-promoting—and tamoxifen’s growth-inhibiting—effects.1

In other words, the botanicals produced an epigenetic change—causing undesirable ER-negative cells to alter their genetic expression and become ER-positive cells that are sensitive to being killed by tamoxifen.

Genetically Altering Breast Cancer Cells

Genetically Altering Breast Cancer Cells  

For part two of the study, the scientists implanted human ER-negative breast cancer cells into mice and allowed the tumors to grow.

Then they fed different groups of animals and tracked the growth of the tumors:1

  • A standard diet (control group), with and without the addition of tamoxifen.
  • Diets supplemented with either green tea polyphenols or with broccoli (separately), or
  • A combination of green tea and broccoli, with and without the addition of tamoxifen.

In mice treated with tamoxifen alone, the tumors were no smaller than those in untreated animals.1 This was expected since ER-negative cells cannot respond to tamoxifen because they lack the proper receptors.

But the combination of green tea and broccoli produced an entirely different effect.

Tumors from mice supplemented with both green tea and broccoli weighed only about a third as much as tumors from control mice.1 This indicated that the combination of green tea and broccoli could reduce tumor size in these hard-to-treat cancers.

This was an important finding on its own. But the interesting part of this work was that tumors from mice treated with the supplement combination— and also with tamoxifen—were smaller than any other tumors. They weighed only about 14% as much as tumors from untreated animals, and less than half as much as those from animals treated with the two supplements but not with tamoxifen.1

This finding validates that the combination of green tea and broccoli can alter the gene expression of treatment-resistant, ER-negative breast cancer cells, turning them into treatment-responsive, ER-positive cells.

The Bigger Picture

This finding is potentially good news for people with breast cancer, particularly ER-negative tumors that currently resist available therapy.

But its greater importance lies in its demonstration that a combination of botanicals can reprogram cells’ genes to make them function in a more normal, healthy fashion.

This finding has implications far beyond cancer treatment and prevention.

Imagine combinations that can switch on and off genes that contribute to Alzheimer’s and Parkinson’s diseases, those that generate over-active inflammation, or those that contribute to aging of our cells, tissues, and organs.

Summary

broccoli  

Researchers have shown that green tea and broccoli can change deadly, treatment-resistant breast cancer cells into treatment-sensitive cells by altering their genetic expression.

This is good news for cancer patients.

This study opens the door to future therapies using compounds to modify gene expression and restore nature’s own means of preventing disease.

If you have any questions on the scientific content of this article, please call a Life Extension® Wellness Specialist at 1-866-864-3027.

References

  1. Li Y, Meeran SM, Tollefsbol TO. Combinatorial bioactive botanicals re-sensitize tamoxifen treatment in ER-negative breast cancer via epigenetic reactivation of ERalpha expression. Sci Rep. 2017 Aug 24;7(1):9345.
  2. . Available at: http://www.nationalbreastcancer.org/breast-cancer-facts. Accessed August 20, 2018.
  3. Kerdivel G, Flouriot G, Pakdel F. Modulation of estrogen receptor alpha activity and expression during breast cancer progression. Vitam Horm. 2013;93:135-60.
  4. Rugo HS, Vidula N, Ma C. Improving Response to Hormone Therapy in Breast Cancer: New Targets, New Therapeutic Options. Am Soc Clin Oncol Educ Book. 2016;35:e40-54.
  5. Spears M, Bartlett J. The potential role of estrogen receptors and the SRC family as targets for the treatment of breast cancer. Expert Opin Ther Targets. 2009 Jun;13(6):665-74.
  6. Thangapazham RL, Singh AK, Sharma A, et al. Green tea polyphenols and its constituent epigallocatechin gallate inhibits proliferation of human breast cancer cells in vitro and in vivo. Cancer Lett. 2007 Jan 8;245(1-2):232-41.
  7. Yang CS, Landau JM, Huang MT, et al. Inhibition of carcinogenesis by dietary polyphenolic compounds. Annu Rev Nutr. 2001;21:381-406.
  8. Cheung KL, Kong AN. Molecular targets of dietary phenethyl isothiocyanate and sulforaphane for cancer chemoprevention. AAPS J. 2010 Mar;12(1):87-97.
  9. Higdon JV, Delage B, Williams DE, et al. Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacol Res. 2007 Mar;55(3):224-36.
  10. Pledgie-Tracy A, Sobolewski MD, Davidson NE. Sulforaphane induces cell type-specific apoptosis in human breast cancer cell lines. Mol Cancer Ther. 2007 Mar;6(3):1013-21.
  11. Meeran SM, Patel SN, Tollefsbol TO. Sulforaphane causes epigenetic repression of hTERT expression in human breast cancer cell lines. PLoS One. 2010 Jul 6;5(7):e11457.
  12. Fang M, Chen D, Yang CS. Dietary polyphenols may affect DNA methylation. J Nutr. 2007 Jan;137(1 Suppl):223S-8S.
  13. Meeran SM, Patel SN, Chan TH, et al. A novel prodrug of epigallocatechin-3-gallate: differential epigenetic hTERT repression in human breast cancer cells. Cancer Prev Res (Phila). 2011 Aug;4(8):1243-54.
  14. Fang MZ, Wang Y, Ai N, et al. Tea polyphenol (-)-epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylation-silenced genes in cancer cell lines. Cancer Res. 2003 Nov 15;63(22):7563-70.
  15. Ho E, Clarke JD, Dashwood RH. Dietary sulforaphane, a histone deacetylase inhibitor for cancer prevention. J Nutr. 2009 Dec;139(12):2393-6.

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