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A study from the Division of Molecular Medicine and Genetics, Department of Internal Medicine, The Life Sciences Institute, University of Michigan, Ann Arbor, Michigan 48109, USA shows that “Snail1-dependent p53 repression regulates expansion and activity of tumour-initiating cells in breast cancer” This study was published in the 17 October 2016 issue of the journal “Nature Cell Biology” [the number 1 journal in Cell Biology with an I.F of 18.699] by Prof. Stephen J. Weiss, Ting Ne, and others.

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Natural product therapy for Breast Cancer: Amla extract (Emblica officinalis) extract increases the levels of tumor suppressor p53, inhibits the proliferation of tumor-initiating cells in breast cancer, suppresses the progression of metastatic breast cancer, and supports tumor relapse-free survival in breast cancer patients


Significance:

Given that: (1) cancer causes the highest economic loss compared to all the known causes of death worldwide; (2) in 2008, breast cancer has caused more than 400000 deaths; (3) in 2011, 17 lakhs new cases of breast cancer diagnosed; (4) breast cancer is the most common invasive cancer in women; and (5) in 2008, breast cancer has caused economic loss of 88 billion US dollars worldwide, there is an urgent need to find: (i) a cheaper alternative to the existing expensive drugs; (ii) a side-effect-free natural product-based drug; and (iii) a way to effectively treat and stall metastatic progression and relapse of breast cancer.

Breast cancer is the most common women cancer. Interestingly, compared to other women cancers, breast cancer not only metastasizes frequently but also relapses. However, the mechanistic basis of which remains largely unclear.


What we infer from what they say:

Stephen’s research team has recently shown that increased expression of the EMT (Epithelial-to-mesenchymal transition) regulator Snail1 promotes: (1) degradation of tumor suppressor p53 in breast cancer cells; and (2) expansion and activity of tumor-initiating cells that aid in relapse of breast cancer, suggesting that inhibition of metastatic promoter Snail1 expression in breast cancer cells will not only inhibit the progression of metastatic breast cancer, but also prevent relapse.


What we say

This study suggests, for the first time, a natural product-based therapy for metastatic breast cancer. Amla extract (Emblica officinalis), by increasing the expression of its target gene, it may increase the expression of tumor suppressor p53. Thereby, it may inhibit metastasis and relapse of breast cancer.

Figure 1 Emblica Officianalis (amla or generally known as Goose berry) extract inhibits the expansion and activity of tumor-initiating cells in metastatic breast cancer via up-regulation of its target gene

Figure 1 Emblica Officianalis (Amla, also known as Goose berry) extract inhibits the expansion and activity of tumor-initiating cells in metastatic breast cancer via up-regulation of its target gene

Thus, pharmacological formulations encompassing “Amla extract (Emblica officinalis)  or an active compound isolated from it” may be used to treat metastatic breast cancer.


Idea Proposed/Formulated by: Dr L Boominathan Ph.D.

Web: http://genomediscovery.org or http://newbioideas.com

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Citation: Boominathan, Natural product therapy for Breast Cancer: Amla extract (Emblica officinalis) increases the levels of tumor suppressor p53, inhibits the proliferation of tumor-initiating cells in breast cancer, suppresses the progression of metastatic breast cancer, and supports tumor relapse-free survival in breast cancer patients, 31/October/2015, 6.45 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org


Undisclosed information: How Amla extract (Emblica officinalis) increases the expression of tumor suppressor p53, and inhibits the proliferation of tumor-initiating cells in metastatic breast cancers?

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