A component in celery and celery fights bc

Very interesting.

The ingredients for LOTS and LOTS of medications (Big Pharma) and supplements (Big Herba) are found in nature.  

The argument that nobody wants to pursue xyz because it can't be patented is just not true.

Profit-driven motives aren't exclusive to "Big Pharma," and neither is the ability to patent/manufacture/market natural-based or completely synthetic substances.

I, recently, read in a local newspaper archive (an article dated May 2010) that - one of the reasons it's taken so long to get to the human clinical trial stage for Metformin as a potential breast cancer drug - is that the company that makes the drug would have had to take it "off patent" in order to do the clinical trial.  And, since taking it "off patent" would have meant that any pharmaceutical company could, then, have manufactured the drug, the company holding Metformin's patent wouldn't participate in a clinical trial because they would lose too much money.  And no other pharmaceutical company would fund a clinical trial because - with no high-cost, patent-protected drug to sell after the trial was completed - it wasn't worth their while.  So funding for the trial had to come from other sources: the NCIC clinical trials group funded by the Canadian Cancer Society; the National Cancer Institute in the USA; and the Breast Cancer Research Foundation in New York.

Shameful, huh?  Sometimes I wonder if we're never going to see a prevention/cure in our lifetime ...

Apigenin - Why Fruits And Vegetables Improve Patient Response To Chemotherapy
By News Staff | October 22nd 2008

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Apigenin is also found in the Chinese and Japanese herb Platycodon grandiflorum (Chinese bellflower root) used against cancer.

J Med Food. 2010 Apr;13(2):298-305.
Platycodin D induces apoptosis in MCF-7 human breast cancer cells.
Yu JS, Kim AK.
Source

College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
Abstract

Platycodin D (PD), a major constituent isolated from the root of Platycodon grandiflorum, has been suggested to possess anticancer activities, as indicated by its capabilities to induce mitotic arrest and apoptosis in several cancer cells. However, little is known of the underlying action mechanism. This study is the first to investigate the anticancer effect of PD in the human breast cancer cell, MCF-7. Our data showed that PD exhibited marked cell growth inhibition by inducing apoptosis. This induction was associated with activation of caspase-8 and -9 activities and poly(ADP-ribose) polymerase. PD triggered the mitochondrial apoptotic pathway, as indicated by up-regulation of levels of cellular Bax and down-regulation of levels of Bcl-2 and caspase-9 activation. We found that PD induced proteolytic activation of Bid, a member of the proapoptotic Bcl-2 family, implicating PD-induced apoptosis as possibly being functionally linked to a death receptor-mediated pathway. The PD treatment also was accompanied by an increase in cellular generation of reactive oxygen species, indicating that PD-induced apoptosis is likely to be mediated through mitochondrial dysfunction. In addition, we revealed that the mitogen-activated protein kinases, including extracellular signal-regulated kinase 1/2, c-Jun NH(2)-terminal kinase 1/2, and p38, which play important roles in apoptosis, were activated by treatment with PD. These results provide a basic mechanism for the anticancer properties of PD and suggest that PD is a promising candidate for chemotherapy and chemoprevention of breast cancer.

PMID: 20412017 [PubMed - indexed for MEDLINE]