The surgical removal of the primary tumor has been the cornerstone of treatment for the great majority of cancers. The rationale for this approach is straightforward: if you can get rid of the cancer by simply removing it from the body, then a cure can likely be achieved. Unfortunately, this approach does not take into account that after surgery the cancer will frequently metastasize (spread to different organs). Quite often the metastatic recurrence is far more serious than the original tumor. In fact, for many cancers it is the metastatic recurrence—and not the primary tumor—that ultimately proves to be fatal.1
In a shocking irony, a growing body of scientific evidence has revealed that cancer surgery can increase the risk of metastasis.2 This would fly in the face of conventional medical thinking, but the facts are undeniable.
To gain a better understanding of how surgery can increase the risk of metastasis, let’s first discuss the actual process of cancer metastasis. A complicated sequence of events must occur in order for cancer to spread to another part of the body.2 Isolated cancer cells that break away from the primary tumor must first breach the connective tissue immediately surrounding the cancer. Once the cancer cell has broken free of the surrounding connective tissue, the next step is to enter a blood or lymphatic vessel. This is easier said than done, as entry into a blood vessel requires the cancer cell to secrete enzymes that degrade the basement membrane of the blood vessel.3 Entry into a blood vessel is vitally important for the aspiring metastatic cancer cell, since it uses the bloodstream as a highway for transportation to other vital organs of the body—such as the liver, brain, or lungs—where it can form a new deadly tumor.
Now that the lone cancer cell has finally entered the bloodstream, its problems have only just begun. Traveling within the bloodstream can be a hazardous journey for cancer cells. Turbulence from the fast moving blood can damage and destroy the cancer cell. Furthermore, cancer cells must avoid detection and destruction from white blood cells circulating in the blood stream.
To complete its voyage, the rogue cancer cell must adhere to the lining of the blood vessel, where it degrades through and exits the basement membrane of the blood vessel. Its final task is to burrow through the surrounding connective tissue to arrive at the organ that is its final destination. Now the cancer cell can multiply and form a growing colony that serves as the foundation for a new metastatic cancer. Time is working against these solitary cancer cells. This entire sequence of events must happen quickly, since these cells have a limited life span.1
We now see that cancer metastasis is a complicated and difficult process. Fraught with peril, very few free-standing cancer cells survive this arduous journey.2 The probability of cancer cells surviving this journey and forming new metastases can be increased by anything that serves to make this process easier.
In a groundbreaking study published in the medical journal Annals of Surgery in 2009, researchers reported that cancer surgery itself can create an environment in the body that greatly lessens the obstacles to metastasis that cancers cells must normally face.2
Just as concerning is the revelation that cancer surgery can produce an alternate route of metastasis that bypasses natural barriers. During cancer surgery, the removal of the tumor almost always disrupts the structural integrity of the tumor and/or the blood vessels feeding the tumor. This can lead to an unobstructed dispersal of cancer cells into the bloodstream, or seeding of these cancer cells directly into the chest or abdomen.4-7 This surgery-induced “alternate route” can greatly simplify the path to metastasis.
To illustrate, a study published in the British Journal of Cancer in 2001 compared the survival of women with breast cancer who had their tumors removed surgically, to the survival of women with breast cancer who did not have surgery. As expected, the findings established that surgery substantially improved survival in the early years.
However, further analysis of the data determined that women who had surgery had a spike in their risk of death at eight years that was not evident in the group who did not have surgery.8 In their interpretation of the results, the authors of the study stated: “A reasonable hypothesis to explain the observed patterns of the hazard functions [risk of cancer death] is to assume that…primary tumor removal may result in sudden acceleration of metastatic process…”
Another group of researchers commenting on a study examining the surgical treatment of colon cancer were far bolder in their conclusions: “This finding strongly supports that surgery alters the natural course of the disease by elongating life expectancy in the greater part of the patient population, but also by simultaneously shortening survival in a smaller subset of patients. Thus, both experimental and clinical evidence support that surgery, although greatly reducing tumor mass and potentially curative, paradoxically can also augment metastasis development.”2
Given these disturbing findings, what can individuals undergoing surgery for their cancers do to protect themselves against an increased risk of metastasis? A worthwhile strategy would be to examine all of the mechanisms by which surgery promotes metastasis, and then create a comprehensive plan that counteracts each and every one of these mechanisms.
What You Need to Know: Cancer Surgery
Surgery Increases Cancer Cell AdhesionOne mechanism by which surgery increases the risk of metastasis is by enhancing cancer cell adhesion.9 Cancer cells that have broken 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, just as one person is unlikely to form a thriving community. Cancer cells use adhesion molecules—such as galectin-3—to facilitate their ability to clump together. Present on the surface of cancer cells, these molecules act like velcro by allowing free-standing cancer cells to adhere to each other.10 Cancer cells circulating in the bloodstream also make use of galectin-3 surface adhesion molecules to latch onto the lining of blood vessels.11 The adherence of circulating tumor cells (CTC) to the blood vessel walls is an essential step for the process of metastasis. Just like a person sliding down an icy hill has no hope of stopping if they cannot grab onto something, a cancer cell that cannot adhere to the blood vessel wall will just continue to wander through the blood stream incapable of forming metastases. Unable to latch onto the wall of the blood vessel, these circulating tumor cells become like “ships without a port” and are unable to dock. Eventually, white blood cells circulating in the bloodstream will target and destroy the CTC. If the CTC 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.10
Combating Cancer Cell AdhesionRegrettably, 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.12 Therefore, it is critically important for the person undergoing cancer surgery to take measures that can help to neutralize the surgery-induced increase in cancer cell adhesion. Fortunately, a natural supplement called modified citrus pectin (MCP) can do just that. Citrus pectin—a type of dietary fiber—is not absorbed from the intestine. However, modified citrus pectin has been altered so that it can be absorbed into the blood and exert its anti-cancer effects. The mechanism by which modified citrus pectin inhibits cancer cell adhesion is by binding to galectin-3 adhesion molecules on the surface of cancer cells, thereby preventing cancer cells from sticking together and forming a cluster.13 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 an astounding 95%. Modified citrus pectin also substantially decreased the adhesion of breast cancer cells to the blood vessel walls.13
Impressive research has documented the power of modified citrus pectin to directly inhibit cancer metastasis. In a study published in the Journal of the National Cancer Institute, modified citrus pectin was administered to rats that were injected with prostate cancer cells, while rats not receiving modified citrus pectin served as the control group. Lung metastasis was noted in 93% of the control group, whereas only 50% of the modified citrus pectin group experienced lung metastasis. Even more noteworthy was the finding that the modified citrus pectin group had an 89% reduction in the size of the metastatic colonies, compared to the control group.14 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.15
After these exciting findings in animal research, modified citrus pectin was then put to the test in men with prostate cancer. In this trial, 10 men with recurrent prostate cancer received modified citrus pectin (14.4 g per day). After one year, a considerable improvement in cancer progression was noted, as determined by a reduction of the rate at which the prostate-specific antigen (PSA) level increased.16 This was followed by a study in which 49 men with prostate cancer of various types were given modified citrus pectin for a four-week cycle. After two cycles of treatment with modified citrus pectin, 22% of the men experienced a stabilization of their disease or improved quality of life; 12% had stable disease for more than 24 weeks. The authors of the study concluded that “MCP (modified citrus pectin) seems to have positive impacts especially regarding clinical benefit and life quality for patients with far advanced solid tumor.”17
Please remember that these prostate cancer study subjects already suffered from advanced disease. It would appear more logical if these patients had initiated modified citrus pectin supplementation before surgical procedures to prevent metastatic colonies from being established, as was done in the successful laboratory studies.
In addition to modified citrus pectin, a well-known over-the-counter medication can also play a pivotal role in reducing cancer cell adhesion. 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 molecule—called E-selectin—on the surface of cells lining blood vessels.15 Cancers cells latch onto E-selectin in order to adhere to the lining of blood vessels.18 By preventing the expression of E-selectin, cimetidine significantly limits the ability of cancer cell adherence to the blood vessel walls. This effect is analogous to removing the velcro from the blood vessels walls that would normally enable circulating tumor cells to bind.
Cimetidine’s potent anti-cancer effects were clearly displayed in a report published in the British Journal of Cancer in 2002. In this study, 64 colon cancer patients received chemotherapy with or without cimetidine (800 mg per day) for one year. The 10-year survival for the cimetidine group was almost 90%. This is in stark contrast to the control group, which had a 10-year survival of only 49.8%. Remarkably, for those patients with a more aggressive form of colon cancer, the 10-year survival was 85% in those treated with cimetidine compared to a dismal 23% in the control group.19 The authors of the study concluded, “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 from 59% to 93%!20
This data provides a compelling case for cancer patients, at least five days prior to surgery, to ingest at least 14 grams of modified citrus pectin and 800 mg of cimetidine daily. This combination regimen may be followed for a year or longer to reduce metastatic risk.
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