In a study done at Fukuoka University, Japan, researchers discovered that fucoidan inhibited the invasion of cancer cells.  They discovered that fucoidan specifically inhibited the attachement of cancer cells to laminin.  (Soeda S. et al. “Aminated fucoidan promotes the invasion of 3 LL cells through reconstituted basement membrane: its possible mechanism of action,” Cancer Letter, 1994 Sep: 85(1):133-8.)

At the National Institute of Lung Disease and Tuberculoses, in Warsaw, Poland, researchers discovered that lectin-like adhesion molecules situated on pulmonary cell surfaces are at least partially responsible for the adhesion of sarcoma cells.  By adding fucoidan to the incubated cells, the sarcoma cells were inhibited from adhering to the healthy cells.  In vivo, it was discovered that administering fucoidan significantly inhibited the settling of metastatic sarcoma cells in the lungs of mice.  Basically, when lectin-like adhesion sights are blocked by glycoconjugates, like fucoidan, tumor cell colonization can be significantly inhibited.  (Roszkowski W et al.  “Blocking of lectin-like adhesion molecules on pulmonary cells inhibits lung sarcomaL-1 colonization in BALB/c-mice,” Experientia, 1989 Jun:45(6:584-8.)

In another study done at Fukuoka University, by the Faculty of Pharmeceutical Sciences, researches found that fucoidan is a “potent inhibitor of tumor cell invasion.”  Specifically, fucoidan inhibited the ability of the tumor cells to bind with laminin.  Researchers further speculated that fucoidan blocked the adhesion by inhibiting the actual physical interaction between tumor cells and laminin.  (Soeda S et al. “Inhibitory effect of oversulfated fucoidan on invasion thgrough reconstituted basement membrane by murine Lewis lung carcinoma,” Jpn J Cancer Research, 1994 Nov:85(11)44-50.)

At Mie University, in Tsu, Japan, researchers experimented with lung metastasis induced by Lewis lung carcinoma.  By injecting fucoidan after the removal of the primary tumor, metastasis was inhibited.  The results of this study show that fucoidan may have clinical value in the prevention of cancer metastasis.  (Itoh, H. et al.  “Immunological analysis of inhibition of lung metastases by fucoidan (GIV-A) prepared from brown seaweed Sargassum thunbergii,” Anticancer Research, 1995 Sep-Oct: 15(5B):1937-47.)

In a study done at the Saint Louis Hospital, in Paris, France, researchers discovered that thrombospondin is an adhesive glycoprotein that promotes breast cancer adhesion to vascular endothelial cells.  Once again, fucoidan was shown to be able to block the binding of thrombospondin to these cells by more than 60 percent. (Incardona F. et al.  “Heparin-binding domain, type 1 and type 2 repeats of thrombospondin mediate its interaction with human breast cancer cells,” J Cell Biochem, 1996 Sep: 62(4):431-42.)

Researchers at Gifu University in Japan extracted 31 fractions of neutral and acidic polysaccharides from brown sea plant.  They then tested these fractions for anti-tumor activity in mice with Ehrlich carcinoma.  Two ot the fractions had such activity.  On the basis of chemical and spectral analyses these compounds were found to be fucoidan.  (Zhang C. et al. “Antitumor active fucoidan from the brown seaweed, umitoranoo (Sargassum thunbergii), Biosci Biotechnol Biochem, 1995 Apr:59(4):563-7.)

A similar study done at the Kitasato Universtiy in Japan showed the same results with sarcoma-180 implanted in rats.  (Yamamoto, Ichiro et al.  “Antitumor Effect of Seaweed,” Japan, J. Esp. Med 1997, Vol. 47, 3, Pl 133-40.)
 

In the Laboratoire de Pharmacologie Marine, in Nantes, France, researchers studied the anti-tumor and anti-proliferative properties of fucoidan extracts from brown sea plant.  They discovered that fucoidan exerts a reversible antiproliferative activity in the GI p[hase of the cell cycle.  Their study also showed anti-tumor activity in mice bearing non-small-cell bronchopulmonary carcinoma cancer.  Their study indicates that fucoidan exhibits inhibitory effects both in vitro and in vivo as a potent anti-tumor agent. (Riou D. et al.  “Antitumor and antiproliferative effects of fucan extracted from ascophyllum nodosum against a non-small-cell bronchopulmonary carcinoma line,” Anticancer Research, 1996 May-Jun: 16(3A):1213-8.)
 

The department of Hematology at Philipps University in Marburg, Germany, discovered that the addition of fucoidan to adrenal cancer cells, inhibited angiogenesis binding, thereby stopping the vasculation of tumor growths.  (Zugmaier G. et al.  “Polysulfated heparinoids selectively inactive heparin-binding angiogenesis factors,” Ann N Y Academy of Science, 1999:886:243-8.) 

In a study done at Mie University in Japan, researchers discovered that fucoidan acted as an activator for the reticuloendothelial system (the phagocytic system of the body, including the fixed macrophages of tissues, liver and spleen).  Fucoidan enhanced the phagocytosis of macrophages.  This study suggests that the antitumor activity of  fucoidan is related to the enhancement of the body’s immune system.  (Itoh H. et al.  “Antitumor activity and immunological properties of marine algal polysaccharides, especially fucoidan, prepared from Sargassum thunbergii of Phaeophyceae,” Anticancer Research 1993 Nov-Dec:13(6A):2045-52.)
 

At the Harvard medical School, researchers introduced mammary tumors into female rats.  The study showed that rats treated with fucoidan took a longer time to tumor than did the control rats. (Teas, Jan et al. “Dietary Seaweed (Laminaria) and Mammary Carcinogenesis in Rats.) Cancer Research Vol. 44, July, 1984, 2758-2761.)

Doctors at the Department of Medicine at the University of Washingtom, Seattle, discovered that by administering fucoidan to mice and primates they were able to increase the level of white blood cells.  White blood cells are macrophages responsible for phagocytosis of viruses and damaged cells.  (Sweeney EA, et al.  “Sulfated polysaccarides increase plasma levels of SDF-1 in monkeys and mice: involvement in mobilization of stem/progenitor cells,” Blood, 2002 Jan: 99(1):44-51.)
 

According to researchers, fucoidan acts as a second signal for activation of macrophages.  This second signal incites the body to respond to threats and act against them.  Fucoidan also triggered cytolysis of aged macrophages.  (Somers SD et al.  “Maleyated bovine serum albumin triggers cytolytic function in selected populations of primed murine macrophages,” J Immunol, 1987 Aug: 139(4):1361-8.) 

Fucoidan has been shown to play an important role in the immune response.  One study showed that fucoidan blocked macrophage activation during the inductive phase, but enhanced macrophage activation during the effector phase.  (Sugawara I et al.  “Fucoidan blocks macrophage activation in an inductive phase but promotes macrophage activation in an effector phase,” Microbiol Immunol, 1984:28(3):371-7.)

The Department of Biology at the Chinese University of Hong Kong reported a study that suggests that fucoidan fights cancer by enhancing cell-mediated immune responses.  This enhancement may result in the activation of many kinds of immune cells that are vitally important to the maintenance of homeostasis.  (Ooi, Vincent and Fang Liu. “Immunomodulation and Anti-Cancer Activity of Polysaccaride-Protein Complexes.: Current Medicinal Chemistry, 2000, 7, 715-729.)