What is Modified Citrus Pectin,MCP,an inhibitor of cancer metastasis and its wide uses?

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Mechanism of Action and Research Updated.

Modified Citrus Pectin MCP photo picture image Research indicates that in order for metastasis to occur, cancerous cells must first clump together; galectins on their surface are thought to be responsible for much of this metastatic potential. Galactose-rich, modified citrus pectin has a binding affinity for galectins on the surface of cancer cells, resulting in an inhibition, or blocking, of cancer cell aggregation, adhesion, and metastasis. Due to the life-threatening nature of metastatic cancer, most research on anti-metastatic therapies has either been in in vitro cell cultures or in animal studies. Although it is still unclear exactly how these study results translate to humans, MCP studies are promising.

 Modified citrus pectin, when administered orally to rats, was found to inhibit spontaneous prostate carcinoma metastasis. It had no effect on the growth of the primary tumor. Injected modified citrus pectin was found to inhibit metastasis of melanoma cells in mice. The mechanism of these anticarcinogenic effects is not clear.

 Galectins comprise a family of galactoside-binding mammalian lectins. Lectins themselves comprise a group of hemagglutinating proteins found in plant seeds, which bind the branching carbohydrate molecules of glycoproteins and glycolipids on cell surfaces, resulting in agglutination or proliferation, among other things. Galectins are proteins that can bind to carbohydrates via carbohydrate recognition domains (CRDs). At present, the galactin family includes 10 members. Apparently, galectins are secreted from cells via nonclassical secretory pathways. Galectin-3, one of the members of the family, is thought to be involved in mitosis and proliferation. On the cell surface, galectin-3 mediates cell-cell adhesion and cell-matrix interaction via binding to its complementary glycoconjugates, such as laminin and fibronectin, and thereby is thought to play an important role in the pathogenesis of cancer metastasis.

 Some metastic events may involve cellular interactions that are mediated by cell surface components, including galectins. The galactose-containing carbohydrate side chains of modified citrus pectin may interfere with these cellular interactions by competing with the natural ligands of the galectins and by doing so, inhibit the metastatic process. It is thought that galectins may play a role in human prostate cancer, and in particular, human prostate cancer metastasis.

 Actions and Pharmacology:

 Actions: Modified citrus pectin has putative anticarcinogenic activity.

 Pharmacology: There is little on the pharmacokinetics of modified citrus pectin in humans. Based on rat studies, modified citrus pectin is probably absorbed to some degree following ingestion. However, research is necessary to determine its absorption efficiency, as well as its distribution, metabolism and excretion.

 Spreading Metastases:

 Conventional cancer treatment involves surgery to remove primary tumors, followed by chemotherapy, radiation, or a combination of treatments designed to eradicate all remaining traces of cancer. This follow-up therapy is critical for addressing the biggest threat from cancer:the formation of secondary cancers, or metastases. Metastases are not new or different cancers, but new cancer colonies started from cells that have migrated to new sites. Sites where metastases commonly occur include the bones, lungs, prostate, kidney, liver, thyroid and brain. Left unchecked, metastases can quickly overwhelm the body defenses. In fact, it is metastases, not primary tumors that are responsible for most cancer deaths.

 Halting Metastases:

 Over the last two decades, research into controlling or halting cancer metastases has led to two promising new strategies. The first, antiangiogenesis, targets the growth of new blood vessels (angiogenesis) that are required for tumor growth. Originally pioneered by noted cancer researcher Dr. Judah Folkman, antiangiogenesis grew from his observation that tumors cannot grow without access to a constant supply of new blood vessels. Folkman theorized that cancer cells actively communicate with surrounding tissues to trigger the growth of new blood vessels (neovascularization) needed to supply nutrients and remove waste products. Once neovascularization is initiated, hundreds of new capillaries converge on the tumor site and are quickly coated with new layers of rapidly dividing tumor cells.

 Folkman also theorized that, just as certain chemical messengers can initiate new capillary formation, other signals could inhibit neovascularization. This insight led to the development of antiangiogenic therapy, which, in contrast to other cancer treatments, does not directly destroy tumors, but aims to limit their blood supply, causing tumors to shrink. By 1997 researchers were excited by promising results from several antiangiogenic drugs. Speaking of one early angiogenesis inhibitor called TNP470, in 1997 Folkman commented on the results of early clinical human trials, stating, 'We have not seen a tumor that we cannot regress (shrink).' Currently TNP470 and several other angiogenesis inhibitors are in clinical trials, and other promising compounds are under study in university laboratories and in some 30 pharmaceutical and biotechnology companies around the world. For more information on nutritional compounds that have been shown to help inhibit new capillary growth and reduce angiogenesis refer to 'Nutritional Support for Cellular Mutagenic Concerns,' in the June 2003 issue of Vitamin Research News.

 Intercepting Cancer Cells:

 The second strategy for controlling metastases works by intercepting migrating cancer cells before they have a chance to establish new tumors. This approach targets a family of carbohydrate binding proteins called lectins. Lectins are attracted to sugar molecules found on the surface of almost all cells. Lectins help cancer cells stick together to form multi-celled clusters that are believed to be necessary for metastases formation. Lectins also enable cancer cells to communicate with each other, as well as with other types of cells (cell-to-cell communication) to trigger cellular transformations that assist the spread of cancer. One class of lectin,called galectins (for galactoside-binding lectins),possesses an especially strong affinity for galactose, a simple sugar located on the surface of cells lining blood vessels.

 A number of cancer researchers have focused on a particular galectin: galectin-3, that has been found to be directly involved in the progression and spread of several types of cancers, including breast, prostate and colon cancer. Serum levels of galectin-3 correlate closely with the spread of cancer, and may serve as a biological marker to help physicians and patients monitor the efficacy of anti-cancer therapies.

 The Protein-Sugar Connection:

 The powerful attraction between galectins and galactose plays a pivotal role in how cancers spread in the body. After a cancer cell has broken free from its primary tumor (or is accidentally dislodged during surgery) it floats freely through the blood and lymph systems until it eventually becomes trapped in a small blood vessel (microcapillary). Firmly lodged in the microcapillary, galectins on the surface of the cancer cell start to bind to galactose receptors on endothelial cells (the cells that form the inside lining of blood vessels). After securely attaching to the endothelium the cancer cells penetrate through the blood vessel walls. The final step after invading the vessel involves the release of chemical signals that trigger new blood vessel growth (angiogenesis), and a new tumor colony is firmly established.

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last edit date:22th,June.2009.