Curcumin helps prevent breast cancer metastasis in mice

October 15, 2005

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In this issue
	Life Extension Update Exclusive
		Curcumin helps prevent breast cancer metastasis in mice
	Protocol
		Breast Cancer
	Featured Products
		Super Curcumin
		DNA Protection Formula

Life Extension Update Exclusive

Curcumin helps prevent breast cancer metastasis in mice

A study published in the October 15 2005 issue of the American Association for Cancer Research journal Clinical Cancer Research http://clincancerres.aacrjournals.org found that c urcumin, which occurs in the spice turmeric, prevents breast cancer from spreading to the lungs of mice given the compound.

Researchers at the University of Texas M. D. Anderson Cancer Center injected 60 mice with human metastatic breast cancer cells. When the tumors reached the size of 10 millimeters they were surgically removed. Five days later half the mice were provided with diets enhanced with curcumin, while the remainder received standard diets until the study’s conclusion. Fifteen of the mice in each of these groups were injected with paclitaxel at days 10, 17 and 24 following tumor removal. Although paclitaxel is effective in its ability to treat breast cancer, it also encourages metastasis when used for a long period of time and is therefore not effective to treat the advanced form of the disease.

Upon examination of the animals’ lungs five weeks after the tumors were removed, 96 percent of the mice who received neither curcumin nor paclitaxel had visible metastases. While paclitaxel alone elicited a modest reduction in visible metastases, curcumin provided significant reduction, and the combination of curcumin and paclitaxel prevented these macrometastases entirely. Microscopic metastases were found in only 28 percent of the mice receiving the curcumin/drug combination, and these consisted of only a few cells, suggesting that the treatment prevented the growth of tumor cells present in the lungs before the primary tumors were removed.

The toxicity of paclitaxel activates an inflammatory protein, (nuclear factor kappa B) that induces metastasis, but curcumin inhibits this response. The finding that the addition of curcumin to paclitaxel resulted in reduced could enable a lower dose of the potentially toxic drug to be administered.

Lead researcher and professor of cancer medicine at M. D. Anderson's Department of Experimental Therapeutics, Bharat Aggarwal, PhD, commented, "We are excited about the results of the study and the possible implications for taking the findings into the clinic in the next several years. At this time, advanced breast cancer is a difficult foe to fight with few proven treatments available after surgery, chemotherapy and radiation therapy."

Protocol

Breast cancer

Curcumin has a number of biological effects in the body. However, one of the most important functions is curcumin's ability to inhibit growth signals emitted by tumor cells that elicit angiogenesis (growth and development of new blood vessels into the tumor).

Curcumin inhibits the epidermal growth factor receptor and is up to 90% effective in a dose-dependent manner. It is important to note that while curcumin has been shown to be up to 90% effective in inhibiting the expression of the epidermal growth factor receptor on cancer cell membranes, this does not mean it will be effective in 90% of cancer patients or reduce tumor volume by 90%. However, because two-thirds of all cancers overexpress the epidermal growth factor receptor and such overexpression frequently fuels the metastatic spread of the cancer throughout the body, suppression of this receptor is desirable. Other anticancer mechanisms of curcumin include:

Inhibition of the induction of basic fibroblast growth factor (bFGF). bFGF is both a potent growth signal (mitogen) for many cancers and an important signaling factor in angiogenesis (Arbiser et al. 1998).
Antioxidant activity. In vitro it has been shown to be stronger than vitamin E in prevention of lipid peroxidation (Sharma 1976; Toda et al. 1985).
Inhibition of the expression of COX-2 (cyclooxygenase 2), the enzyme involved in the production of prostaglandin E2 (PGE-2), a tumor-promoting hormone-like agent (Zhang et al. 1999).
Inhibition of a transcription factor in cancer cells known as nuclear factor-kappa B (NF-KB). Many cancers overexpress NF-KB and use this as a growth vehicle to escape regulatory control (Bierhaus et al. 1997; Plummer et al. 1999).
Increased expression of nuclear p53 protein in human basal cell carcinomas, hepatomas, and leukemia cell lines. This increases apoptosis (cell death) (Jee et al. 1998).
Increases production of transforming growth factor-beta (TGF-beta), a potent growth inhibitor, producing apoptosis (Park et al. 2003; Sporn et al. 1989).
TGF-beta is known to enhance wound healing and may play an important role in the enhancement of wound healing by curcumin (Mani H et al. 2002; Sidhu et al. 1998).
Inhibits PTK (protein tyrosine kinases) and PKC (protein kinase C). PTK and PKC both help relay chemical signals through the cell. Abnormally high levels of these substances are often required for cancer cell signal transduction messages. These include proliferation, cell migration, metastasis, angiogenesis, avoidance of apoptosis, and differentiation (Reddy et al. 1994; Davidson et al. 1996).
Inhibits AP-1 (activator protein-1) through a non-antioxidant pathway. While curcumin is an antioxidant (Kuo et al. 1996), it appears to inhibit signal-transduction via protein phosphorylation thereby decreasing cancer-cell activity, regulation, and proliferation (Huang et al. 1991).

Based on the favorable, multiple mechanisms listed above, higher-dose curcumin would appear to be useful for cancer patients to take. However, as far as curcumin being taken at the same time as chemotherapy drugs, there are contradictions in the scientific literature. Therefore, caution is advised.

https://www.lifeextension.com/protocols/cancer/breast-cancer

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