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Cancer Surgery

Surgery Increases Cancer Cell Adhesion

One mechanism by which surgery increases the risk of metastasis is by enhancing cancer cell adhesion (Dowdall 2002). Cancer cells that break away from the primary tumor utilize adhesion to boost their ability to form metastases in distant organs. These cancer cells must be able to clump together and form colonies that can expand and grow. It is unlikely that a single cancer cell will form a metastatic tumor. Cancer cells use adhesion molecules (which are present on the surface of cancer cells), such as galectin-3, to facilitate their ability to clump together (Raz 1987). Cancer cells circulating in the bloodstream also make use of galectin-3 surface adhesion molecules to latch onto the lining of blood vessels (Yu 2007). The adherence of circulating tumor cells (CTCs) to the blood vessel walls is an essential step for the process of metastasis. A cancer cell that cannot adhere to the blood vessel wall will just continue to wander through the blood stream incapable of forming metastases. Eventually, white blood cells circulating in the bloodstream will target and destroy the CTCs. If the CTCs successfully bind to the blood vessel wall and burrow their way through the basement membrane, they will then utilize galectin-3 adhesion molecules to adhere to the organ to form a new metastatic cancer (Raz 1987).

Combating Cancer Cell Adhesion

Research has shown that cancer surgery increases tumor cell adhesion. In one experiment that mimicked surgical conditions, scientists reported that the binding of cancer cells to the blood vessel walls was increased by 250%, compared to cancer cells not exposed to surgical conditions (ten Kate 2004). A natural supplement called modified citrus pectin (MCP) can help neutralize the surgery-induced increase in cancer cell adhesion. Citrus pectin—a type of dietary fiber—is not absorbed into the intestine. However, modified citrus pectin has been altered so that it can be absorbed into the blood and exert its anti-cancer effects. Modified citrus pectin inhibits cancer cell adhesion by binding to galectin-3 adhesion molecules on the surface of cancer cells, thereby preventing cancer cells from sticking together and forming a cluster (Nangia-Makker 2002). Modified citrus pectin can also inhibit circulating tumor cells from latching onto the lining of blood vessels. This was demonstrated by an experiment in which modified citrus pectin blocked the adhesion of galectin-3 to the lining of blood vessels by 95%. Modified citrus pectin also substantially decreased the adhesion of breast cancer cells to the blood vessel walls (Nangia-Makker 2002).

In one study, rats were injected with prostate cancer cells. One group received the modified citrus pectin while the other (control group) did not. Lung metastasis was noted in 50% of the modified citrus pectin group versus 93% in the control group. Even more noteworthy was that the modified citrus pectin group had an 89% reduction in the size of the metastatic colonies compared to the control group (Pienta 1995). In a similar experiment, mice injected with melanoma cancer cells that were fed modified citrus pectin experienced a greater than 90% reduction in lung metastasis compared to the control group (Platt 1992).

In a human trial, 10 men with recurrent prostate cancer received 14.4 g daily of modified citrus pectin. After one year, a considerable improvement in cancer progression was noted as determined by a rate reduction in the prostate-specific antigen (PSA) level (Guess 2003). This was followed by a study in which 49 men with various types of prostate cancer were given modified citrus pectin for a four-week cycle. After two treatment cycles, 22% of the men experienced a stabilization of their disease or improved quality of life; 12% remained stable for more than 24 weeks. The authors of the study concluded that “MCP seems to have positive impacts especially regarding clinical benefit and life quality for patients with far advanced solid tumor” (Azemar 2007).

Cimetidine, commonly known as Tagamet®, is a drug historically used to alleviate heartburn. A growing body of scientific evidence has revealed that cimetidine also possesses potent anti-cancer activity. Cimetidine inhibits cancer cell adhesion by blocking the expression of an adhesive (cancer cells latch on) molecule called E-selectin on the surface of cells lining blood vessels (Platt 1992). By preventing the expression of E-selectin, cimetidine significantly limits the ability of cancer cell adherence to the blood vessel walls.

In a study supporting the potential anti-cancer effects of cimetidine, 64 colon cancer patients received chemotherapy with or without cimetidine (800 mg per day) for one year. The 10-year survival rate for the cimetidine group was almost 90% versus 49.8% for the control group. For those patients with a more aggressive form of colon cancer, the 10-year survival was 85% in those treated with cimetidine compared to 23% in the control group (Matsumoto 2002). The authors of the study concluded that “taken together, these results suggested a mechanism underlying the beneficial effect of cimetidine on colorectal cancer patients, presumably by blocking the expression of E-selectin on vascular endothelial [lining of blood vessels] cells and inhibiting the adhesion of cancer cells.” These findings were supported by another study with colorectal cancer patients wherein cimetidine given for just seven days at the time of surgery increased three-year survival rate from 59% to 93% (Adams 1994).

This combination regimen of 14g of modified citrus pectin and 800mg of cimetidine, taken at least five days before surgery, may be followed for a year or longer to reduce metastatic risk.