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Old 10-16-2007, 09:56 AM   #1
Lani
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Join Date: Mar 2006
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16 metastatic bc patients treated with new immunotherapy wtumorresoln,4yrsrcrrncefree

from the Socrates Institute of Tumor immunology in Philadelphia(???)

Int J Cancer. 2007 Oct 12; [Epub ahead of print]
Immunotherapy of metastatic breast cancer patients with vitamin D-binding protein-derived macrophage activating factor (GcMAF).

Yamamoto N, Suyama H, Yamamoto N, Ushijima N.
Division of Cancer Immunology and Molecular Biology, Socrates Institute for Therapeutic Immunology, Philadelphia, PA 19126?3305.
Serum vitamin D(3)-binding protein (Gc protein) is the precursor for the principal macrophage activating factor (MAF). The MAF precursor activity of serum Gc protein of breast cancer patients was lost or reduced because Gc protein was deglycosylated by serum alpha-N-acetylgalactosaminidase (Nagalase) secreted from cancerous cells. Patient serum Nagalase activity is proportional to tumor burden. The deglycosylated Gc protein cannot be converted to MAF, resulting in no macrophage activation and immunosuppression. Stepwise incubation of purified Gc protein with immobilized beta-galactosidase and sialidase generated probably the most potent macrophage activating factor (termed GcMAF) ever discovered, which produces no adverse effect in humans. Macrophages treated in vitro with GcMAF (100 pg/ml) are highly tumoricidal to mammary adenocarcinomas. Efficacy of GcMAF for treatment of metastatic breast cancer was investigated with 16 nonanemic patients who received weekly administration of GcMAF (100 ng). As GcMAF therapy progresses, the MAF precursor activity of patient Gc protein increased with a concomitant decrease in serum Nagalase. Because of proportionality of serum Nagalase activity to tumor burden, the time course progress of GcMAF therapy was assessed by serum Nagalase activity as a prognostic index. These patients had the initial Nagalase activities ranging from 2.32 to 6.28 nmole/min/mg protein. After about 16-22 administrations (approximately 3.5-5 months) of GcMAF, these patients had insignificantly low serum enzyme levels equivalent to healthy control enzyme levels, ranging from 0.38 to 0.63 nmole/min/mg protein, indicating eradication of the tumors. This therapeutic procedure resulted in no recurrence for more than 4 years. (c) 2007 Wiley-Liss, Inc.
PMID: 17935130 [PubMed - as supplied by publisher]
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Old 10-16-2007, 02:25 PM   #2
fullofbeans
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Join Date: Jan 2007
Location: UK
Posts: 617
Thanks for bring up this study. This is results that exite me along with the previous blocking of the Her pathways (Trastuzumab, pertuzumab Gefitinib) study that you also brought up..please continue.

Anyhow, here is a full version of a earlier paper that explain what the GcMAF is.
http://jnci.oxfordjournals.org/cgi/reprint/94/17/1311

The thing is GcMAF is completly non toxic to mice or human..so what are they waiting for?
__________________

35 y/o
June 06: BC stage I
Grade 3; ER/PR neg
Her-2+++; lumpectomies

Aug 06: Stage IV
liver mets: 6 tumours
July 06 to Jan 07: 2*FEC+6*Taxotere; 3*TACE; LITT
March 07- Sept 07: Vaccination trial (phase 2, peptide based) at the UW (Seattle).
Herceptin since 2006
NED til Oct 09
Recurrence Oct 2009: to internal mammary gland since October 2009 missed on Oct and March 2010 scan.. palpable nodes in May 2010 when I realised..
Nov 2011:7 mets to lungs progressing fast failed hercp/tykerb/xeloda combo..

superior vena cava blocked: stent but face remains puffy

April 2012: Teresa Trial, randomised to TDM1
Nov 2012 progressing on TDM1
Dec 2012 blockage of my airways by tumours, obliteration of these blocking tumours breathing better but hoping for more- at mo too many tumours to count in the lungs and nodes.

Dec 2012 Starting new trial S-222611 phase 1b dual egfr her2+ inhibitor.



'Under no circumstances should you lose hope..' Dalai Lama
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Old 10-16-2007, 05:48 PM   #3
AlaskaAngel
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more questions....

I wonder if their ending statement means that any of them did recur at 4 years? And since none of them were anemic, I wonder if that screened out a lot of those with mets who were less likely to survive?

A.A.
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