Green Tea, The Best Functional Food In Reduced Risk and Treatment of Breast Cancer

Green tea may be the next generation of inexpensive herbal medicine for reduced risk and treatment of breast cancer, a renowned institute study suggested

Breast cancer (malignant breast neoplasm) is cancer that starts in the tissues of the breast either from the inner lining of milk ducts (Ductal carcinoma) or the lobules (Lobular carcinoma) that supply the ducts with milk. there are also rare cases that breast cancer starts in other areas of the breast.

Green tea, a precious drink processes numbers of health benefit known to almost everyone in Asia and the Western world. However, as yin in nature herbal medicine or food, long term injection of large amounts may obstruct the balance of yin-yang, induced "yin excessive syndrome" or "yang vacuity syndrome" including weaken immunity and painful case of GERD,... according to traditional Chinese medicine's Yin-Yang theory.

According to the joint study lead by the Xinyang Normal UniversityHenan, Epigallocatechin-3-gallate (EGCG), a bioactive compound in green tea inhibited the risk of breast cancer through many mechanisms involving primarily in cell death and survival.

The study also insisted on the efficacy of Epigallocatechin-3-gallate (EGCG) in reduced risk of breast cancer probably due to the main function in induced cancer cell cycle arrest in interference of cell division.

In MDA-MB-231 breast cancer cell line, Epigallocatechin gallate isolated from green tea-induced apoptosis and inhibited tumorigenesis through the expression of multiple signaling pathways in breast cancer cells.


Also, EGCG decreased MDA-MB-231 cell viability and significantly downregulated the expression of β-catenin in regulated the coordination of cell-cell adhesion and gene transcription, according to Western blot analysis as patients with breast cancer is found to associate to high levels of β-catenin in breast cancer tissue than in normal tissue.

Dr. Hong OY, the lead author said, "EGCG inhibits the growth of MDA-MB-231 cells through the inactivation of the β-catenin signaling pathway. Based on these promising results, EGCG may be a potential treatment for triple negative breast cancer patients.".


In polychlorinated biphenyls (PCBs) accumulated in human breast cancer tissue induced the growth of estrogen-sensitive tumors, EGCG inhibited the early onset of breast cancer through modifying estrogenic activity against cell proliferation in a dose-dependent manner.


Furthermore, at a dose of at 25 μM, EGCG also exerted antiproliferative and pro-apoptotic action in the activation of the ERβ receptor.

With all the information collected above, green tea, containing rich sources of anti malignant and nonmalignant tumors phytochemicals, may be considered as a functional food in reduced risk and treatment of breast cancer.


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Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bioscience, ISSN 0975-6299.

Sources
(1) Bioinformatic Prediction of Possible Targets and Mechanisms of Action of the Green TeaCompound Epigallocatechin-3-Gallate Against Breast Cancer by Song X1,2, Zhang M3, Chen L1, Lin Q2.(PubMed)
(2) Epigallocatechin gallate inhibits the growth of MDA-MB-231 breast cancer cells via inactivation of the β-catenin signaling pathway by Hong OY1, Noh EM2, Jang HY1, Lee YR2, Lee BK3, Jung SH3, Kim JS1, Youn HJ3.(PubMed)
(3) Green Tea Catechin, EGCG, Suppresses PCB 102-Induced Proliferation in Estrogen-Sensitive Breast Cancer Cells by Baker KM1, Bauer AC2.(PubMed)