Dr. Nobuto Yamamoto

Very Interesting.  Thanks for posting.

Now lets hope some greedy pharmaceutical company buys the rights, studies it extensively and gets it to market soon.

I would love for this to be true, but if its sounds too good to be true..........

Typically, 10 years or more for a promising lab result to become a product.

Very interesting.  Here is some discussion on it from a UK website.  It seems to shed some light on interpreting the results.  The metastatic part may not be exactly what we would call metastatic, there was no observation of metastatic tumour themselves, but rather a measure of a blood indicator of micrometastasis believed by Yamamoto to be indicative of disease vs cure.  More like patients in remission being speculatively "cured".  Still sounds promising.

 http://scienceblog.cancerresearchuk.org/2008/12/03/cancer-cured-for-good-gc-maf-and-the-miracle-cure/

Thanks, Timothy!

Yamamoto is clearly a controversial figure. I am going to follow up and contact him. Philadelphia is not so far away that I couldn't go meet with him and see what his future clinical trial plans are, perhaps when my chemo is over and I'm in better shape physically.

This thread is exactly the kind of interesting and civl discussion that I would love to see more of on this board. I really appreciate when someone actually takes the time to look into a subject and bring the results into our conversation, as opposed to posting brief, snarky comments that add zero enlightenment to the discussion, only adding hostility and flames, and derailing the discussion. I personally would love to see both conventional and alt/comp treatments receive respectful discussion, as both likely have their place.

The last nurse who administered my chemo at the cancer center where I am receiving treatment has been doing oncology for 12 years, and she was the first to say that there is no interest in finding a cure for cancer, because the entire field is based on constant treatment provision. Her job, and everyone else's,depends on prolonged treatment of cancer patients, and a tremendous amount of revenue is at stake for medical institutions. They often base provision of care for less well remunerative conditions, and treatment of the poor and uninsured on the more lucrative specialties, such as cancer care. The oncologists themselves often don't make much more than other physicians, but the radiology scans and infusion procedures are very well reimbursed. All the incentives are perverse in this system of care.

Perhaps if primary care were more respected and properly reimbursed there wouldn't be such a need to offset expenses by promoting noncurative procedure based care in the other specialties.

It is such a complex and chaotic web we weave, in healthcare. 

Effects of Vitamin D₃-Binding Protein-Derived Macrophage Activating Factor (GcMAF) on Angiogenesis

Shigeru Kanda, Yasushi Mochizuki, Yasuyoshi Miyata, Hiroshi Kanetake, Nobuto Yamamoto

Affiliations of authors: S. Kanda, Department of Molecular Microbiology and Immunology, Division of Endothelial Cell Biology, and Department of Urology, Nagasaki University Graduate School of Medicine, Nagasaki, Japan; Y. Mochizuki, Y. Miyata, H. Kanetake, Department of Urology, Nagasaki University Graduate School of Medicine; N. Yamamoto, Socrates Institute for Therapeutic Immunology, Philadelphia, PA.

Correspondence to: Shigeru Kanda, M.D., Ph.D., Department of Molecular Microbiology and Immunology, Division of Endothelial Cell Biology, Nagasaki University Graduate School of Medicine, 1-7-1, Sakamoto, Nagasaki 852-8501, Japan (e-mail: shigeruk@net.nagasaki-u.ac.jp ).

Background: The vitamin D₃-binding protein (Gc protein)-derivedmacrophage activating factor (GcMAF) activates tumoricidal macrophagesagainst a variety of cancers indiscriminately. We investigatedwhether GcMAF also acts as an antiangiogenic factor on endothelialcells. Methods: The effects of GcMAF on angiogenic growth factor-inducedcell proliferation, chemotaxis, and tube formation were examinedin vitro by using cultured endothelial cells (murine IBE cells,porcine PAE cells, and human umbilical vein endothelial cells[HUVECs]) and in vivo by using a mouse cornea micropocket assay.Blocking monoclonal antibodies to CD36, a receptor for the antiangiogenicfactor thrombospondin-1, which is also a possible receptor forGcMAF, were used to investigate the mechanism of GcMAF action.Results: GcMAF inhibited the endothelial cell proliferation,chemotaxis, and tube formation that were all stimulated by fibroblastgrowth factor-2 (FGF-2), vascular endothelial growth factor-A,or angiopoietin 2. FGF-2-induced neovascularization in murinecornea was also inhibited by GcMAF. Monoclonal antibodies againstmurine and human CD36 receptor blocked the antiangiogenic actionof GcMAF on the angiogenic factor stimulation of endothelialcell chemotaxis. Conclusions: In addition to its ability toactivate tumoricidal macrophages, GcMAF has direct antiangiogeniceffects on endothelial cells independent of tissue origin. Theantiangiogenic effects of GcMAF may be mediated through theCD36 receptor

Any one taking gcmaf. ?

Ok,thank u