What is GcMAF?
Gc-MAF is a human protein, found in all healthy humans. GcMAF can be provided as a replacement therapy for those whose own immune system is depleted. Taking GcMAF replaces the missing part of the immune system. GcMAF can be beneficial in over 50 different diseases and over 38 different types of cancer.
GcMAF is the body’s own internal medicine. ALL healthy people have it. GcMAF is the best treatment yet found for tumor cancers and 50 other diseases. It is a human protein, a human right, the king of immunotherapies and has no side effects.
Gc-protein is the precursor for the major macrophage-activating factor (MAF). Gc-protein carries one trisaccharide consisting of N-acetylgalactosamine with dibranched galactose and sialic acid termini.
Normally MAF is produced from Gc-protein by sequential removal of the galactose (by beta-galactosidase of inflammation-primed B lymphocytes) and sialic acid (sialidase of T lymphocytes) from this protein with N-acetylgalactosamine as the remaining sugar.
Macrophage-activation for phagocytosis and antigen presentation is the first step in the immune development cascade. Lost precursor activity leads to immunosuppression.
Gc-MAF call in the "big guns" by activateing macrophages (big eaters). Macrophages literally eat cancer cells, bacteria, viruses, etc.
GcMAF is the body’s own internal medicine. ALL healthy people have it. GcMAF is the best treatment yet found for tumor cancers and 50 other diseases. It is a human protein, a human right, the king of immunotherapies and has no side effects.
Gc-protein is the precursor for the major macrophage-activating factor (MAF). Gc-protein carries one trisaccharide consisting of N-acetylgalactosamine with dibranched galactose and sialic acid termini.
Normally MAF is produced from Gc-protein by sequential removal of the galactose (by beta-galactosidase of inflammation-primed B lymphocytes) and sialic acid (sialidase of T lymphocytes) from this protein with N-acetylgalactosamine as the remaining sugar.
Macrophage-activation for phagocytosis and antigen presentation is the first step in the immune development cascade. Lost precursor activity leads to immunosuppression.
Gc-MAF call in the "big guns" by activateing macrophages (big eaters). Macrophages literally eat cancer cells, bacteria, viruses, etc.
Macrophages (meaning “big eaters” in Greek) are an important type of white blood cell. They patrol the body, eating up foreign invaders and dead cells. They also help to alert other immune cells to the presence of infections.
Macrophages can be stirred into action by a small sugar-coated protein (glycoprotein) called Gc-MAF, short for Gc Macrophage Activating Factor, which is produced by the body. But it’s thought that the production of Gc-MAF is blocked by an enzyme called Nagalase (alpha-N-acetylgalactosaminidase), produced by many cancers. This is one of the mechanisms that helps tumors evade the immune system.
Macrophages can be stirred into action by a small sugar-coated protein (glycoprotein) called Gc-MAF, short for Gc Macrophage Activating Factor, which is produced by the body. But it’s thought that the production of Gc-MAF is blocked by an enzyme called Nagalase (alpha-N-acetylgalactosaminidase), produced by many cancers. This is one of the mechanisms that helps tumors evade the immune system.
What does GcMAF do?
In addition to rebuilding a depressed immune system, GcMAF acts as a “director” of your immune system:
GcMAF is a cell-signaling glycoprotein that talks to macrophages, enabling them to rapidly find, attack, and kill viruses and cancer cells. By activating macrophages, GcMAF triggers a cascade that activates the entire immune system.
80% of terminal stage four tumour cancers cases can be saved (40% if they’ve had chemo), but usually when they are closely monitored, which is why residential Treatment Centres are being run in Switzerland. If they have three months to live and have not had chemo, almost no one needs to be lost.
In stage 4 cancer, some doctors who use the full protocol, listed on “Treatment Strategies,” are saving every patient (if they have not had chemotherapy.) Success can be achieved with all tumor cancers including breast, lung, prostate, pancreatic and melanoma.
GcMAF can eradicate chronic inflammation and viral infections. It is better than antibiotics in many areas
25% successful with Autism
50% or more with Chronic Herpes, Chronic Acne, Chronic cirrhosis of the liver, Chronic kidney disease, Chronic depression, Colitis, Crohn’s, Fibromyalgia, Hepatitis, Herpes, LMBBS, ME/CFS, Osteoporosis, Periodontal disease, Psoriasis and various types of Immune dysfunction including allergies.
Halt deterioration in Parkinsons, multiple sclerosis (MS), dementia and ALS, and in its role of immune system regulator.
Reverse diseases that attack the immune system like Lupus and Arthritis.
Effective with wound healing.
- Inhibits angiogenesis – stops blood supply to tumours
- Activates macrophages – phagocytosis and destruction of cancer cells
- Apoptosis – suicide of cancer cells
- Reverts the cancer cell phenotype to normal (Turns cancer cells into healthy cells)
- Reduces the metastatic potential of human cancer cells in culture.
- Increases energy production at the mitochondrial level – ME/CFS
- Improves human neuronal metabolic activity through cAMP signaling – autism, ME/CFS, MS, ALS
- Counters toxic effects including cadmium – ME/CFS
- It abolishes neuropathic pain due to neuro-oxidative stress (stress due to the anti-cancer drug oxaliplatin) in the lab. (neurodegenerative diseases and autism that have oxidative stress as a pathogenetic mechanism)
- It increases neuronal connectivity by promoting differentiation and the formation of dendrites and neuritis (autism and ME/CFS, where there is a lack of connectivity between neurons).
GcMAF is a cell-signaling glycoprotein that talks to macrophages, enabling them to rapidly find, attack, and kill viruses and cancer cells. By activating macrophages, GcMAF triggers a cascade that activates the entire immune system.
80% of terminal stage four tumour cancers cases can be saved (40% if they’ve had chemo), but usually when they are closely monitored, which is why residential Treatment Centres are being run in Switzerland. If they have three months to live and have not had chemo, almost no one needs to be lost.
In stage 4 cancer, some doctors who use the full protocol, listed on “Treatment Strategies,” are saving every patient (if they have not had chemotherapy.) Success can be achieved with all tumor cancers including breast, lung, prostate, pancreatic and melanoma.
GcMAF can eradicate chronic inflammation and viral infections. It is better than antibiotics in many areas
25% successful with Autism
50% or more with Chronic Herpes, Chronic Acne, Chronic cirrhosis of the liver, Chronic kidney disease, Chronic depression, Colitis, Crohn’s, Fibromyalgia, Hepatitis, Herpes, LMBBS, ME/CFS, Osteoporosis, Periodontal disease, Psoriasis and various types of Immune dysfunction including allergies.
Halt deterioration in Parkinsons, multiple sclerosis (MS), dementia and ALS, and in its role of immune system regulator.
Reverse diseases that attack the immune system like Lupus and Arthritis.
Effective with wound healing.
What can damage or reduce GcMAF?
- Try to avoid anything that suppresses your immune system (or you may nullify the good effects of GcMAF:)
- LDN appears to stop the action of GcMAF, as do Tamoxifen and Letrozole.
- Externally administered heparin (used to stop blood clots) can completely block GcMAF.
- Aspartame -the well known sweetener – can negatively interact with your intestinal microflora and reduce your immune defences
- All kinds of Corticosteroids (Prednisolon, Prednisone, Betapred, Solu-Cortef, Solu-Medrol etc). So avoid Cortisone and steroids if possible.
- Anti- inflammatory drugs should be avoided. (NSAIDs like Ibuprofen, Diklofenalk. Celebrex Aspirin etc should be taken in moderation.)
- Cytotoxic medications or chemotherapy (Cyclophosphamide (Sendoxan) Etoposide (Vepesid) Metotrexat, Taxotere, Taxol, Navelbine etc etc) although there is some evidence GcMAF may reduce the side effects and the damage these poisons do.
- Radiation Therapy.
- Morphine analogs, (Morfin, Tramadole, kodeine, Fentanylplasters, Oxynorm, Oxycodon etc). Take buprenorphine instead.
- Dr Yamamoto also warns against beta blockers (seloken, Selo-Zok etc)
- Carrageenan (Chocomel) can block macrophage (gcMAF) activity. Also known as E407 or E407a.
- Remember, in men, high cortisol will cause a man to lose his testosterone down the road because cortisol will block testosterone from working at the cell receptor sites. A man will lose his sex drive and be 15 kgs overweight. He will frequently have high cholesterol and high triglycerides. It’s a perfect setup for a heart attack.
How is GcMAF made by the body?
Vitamin D3 binding protein (Gc-Protein) has three sugar molecules attached to it (D-glactose, N-AcetylGalactosamine and sialic acid). The immune system B-cells remove the D-galactose via the enzyme beta-galactosidase. The immune system T-cells then remove the sialic acid via the enzyme sialidase. The result is GcMAF.
What is nagalase?
Nagalase is a protein made by all cancer cells and viruses (HIV, hepatitis B, hepatitis C, influenza, herpes, Epstein-Barr virus, and others). Its formal, official chemical name is alpha-N-acetylgalactosaminidase.
As an extremely sensitive marker for all cancers, Nagalase provides a powerful system for early detection. Repeated testing of nagalase levels provides a reliable and accurate method for tracking the results of any therapeutic regimen for cancer, AIDS, or other chronic viral infection. A healthy level is below 0.65 nmol/min/mg. Increased nagalase activity has NOT been detected in the blood of healthy humans.
Nagalase (n-acetylgactosaminidase) is an enzyme that deglycosylates the Gc protein also known as vitamin D binding protein (VDBP).
Nagalase is an extracellular matrix-degrading enzyme that is secreted by cancerous cells in the process of tumor invasion. It also is an intrisic component of envelope protein of various virions, such as HIV and the influenza virus. It is also secreted from virus-infected cells. Nagalase is the intrinsic component of the envelope protein gp120 of HIV-virions and of the envelope protein hemagglutinin (HA) of influenza virus. Nagalase activity is the sum of enzyme activities carried by both HIV virions and unassembled envelope proteins.
Studies correlating nagalse levels with tumour burden suggest that the measurement of this enzyme can diagnose the presence of cancerous lesions below levels detectable by other diagnostic means. Increased activity of nagalase has been detected in the blood of patients with a wide variety of cancers, like cancer of the prostate, breast, colon, lung, oesophagus, stomach, liver, pancreas, kidney, bladder, testis, uterus and ovary, mesothelioma, melanoma, fibrosarcoma, glioblastoma, neuroblastoma and various leukemias. It seems likely that secretory capacity of individual tumor tissue varies among tumor types depending upon tumor size, staging, and the degree of malignancy or invasiveness. It has been established that the nagalase activity is directly proportional to viable tumour burden
If you have cancer or other diseases, then it is likely that you will have high levels of nagalase in the serum of your blood.
As an extremely sensitive marker for all cancers, Nagalase provides a powerful system for early detection. Repeated testing of nagalase levels provides a reliable and accurate method for tracking the results of any therapeutic regimen for cancer, AIDS, or other chronic viral infection. A healthy level is below 0.65 nmol/min/mg. Increased nagalase activity has NOT been detected in the blood of healthy humans.
Nagalase (n-acetylgactosaminidase) is an enzyme that deglycosylates the Gc protein also known as vitamin D binding protein (VDBP).
Nagalase is an extracellular matrix-degrading enzyme that is secreted by cancerous cells in the process of tumor invasion. It also is an intrisic component of envelope protein of various virions, such as HIV and the influenza virus. It is also secreted from virus-infected cells. Nagalase is the intrinsic component of the envelope protein gp120 of HIV-virions and of the envelope protein hemagglutinin (HA) of influenza virus. Nagalase activity is the sum of enzyme activities carried by both HIV virions and unassembled envelope proteins.
Studies correlating nagalse levels with tumour burden suggest that the measurement of this enzyme can diagnose the presence of cancerous lesions below levels detectable by other diagnostic means. Increased activity of nagalase has been detected in the blood of patients with a wide variety of cancers, like cancer of the prostate, breast, colon, lung, oesophagus, stomach, liver, pancreas, kidney, bladder, testis, uterus and ovary, mesothelioma, melanoma, fibrosarcoma, glioblastoma, neuroblastoma and various leukemias. It seems likely that secretory capacity of individual tumor tissue varies among tumor types depending upon tumor size, staging, and the degree of malignancy or invasiveness. It has been established that the nagalase activity is directly proportional to viable tumour burden
If you have cancer or other diseases, then it is likely that you will have high levels of nagalase in the serum of your blood.
What does nagalase do?
Nagalase causes immunodeficiency. Nagalase blocks production of GcMAF by removing a portion of the molecule. Also known as alpha-N-acetylgalactosaminidase, nagalase removes the N-acetylgalactosamine from the Gc-Protein. Once the N-acetylgalactosamine is removed, the Gc-Protein cannot function properly as Gc-MAF.
This prevents the immune system from doing its job. Without an active immune system, cancer and viral infections can grow unchecked.
Nagalase is known to deglycosylate the vitamin D3-binding protein VDBP (in humans better known as Gc-protein). Nagalase, emasculates the GcMAF precursor protein (DBP) by knocking off its three sugar molecules. The DBP protein that would have become a GcMAF is permanently disfigured and disabled. With one simple, swift maneuver, Nagalase has brought the entire immune system to its knees.
“Serum vitamin D3-binding protein (DBP) is the precursor for the principal macrophage activating factor (GcMAF). These patient's serum contained alpha-N-acetylgalactosaminidase (Nagalase) that deglycosylates (removes the sugars from) DBP. Deglycosylated DBP cannot be converted to GcMAF, leading to immunosuppression.”
(Microbes Infect. 2005 Apr;7(4):674-81. Epub 2005 Mar 22. Pathogenic significance of alpha-N-acetylgalactosaminidase activity found in the hemagglutinin of influenza virus. Yamamoto N, Urade M.)
Malignant cancer cells and viruses send out an enzyme called Nagalase that prevents production of your GcMAF. Nagalase stops its beneficial effects, and neutralizes your immune system. So diseases become chronic, and cancer cells grow unchecked.
Nagalase is known to inactivate Gc-MAF by deglycosylating its natural precursor Gc-protein. Nagalase completely removes the trisaccharide from the Gc-protein by deglycosylation. After it has been deglycosylated, the Gc protein is thereby rendered incapable of conversion into active GcMAF. Since Gc-protein cannot be converted to GcMAF, the activation of macrophages is prevented.
Nagalase is known to deglycosylate the vitamin D3-binding protein VDBP (in humans better known as Gc-protein). Nagalase, emasculates the GcMAF precursor protein (DBP) by knocking off its three sugar molecules. The DBP protein that would have become a GcMAF is permanently disfigured and disabled. With one simple, swift maneuver, Nagalase has brought the entire immune system to its knees.
“Serum vitamin D3-binding protein (DBP) is the precursor for the principal macrophage activating factor (GcMAF). These patient's serum contained alpha-N-acetylgalactosaminidase (Nagalase) that deglycosylates (removes the sugars from) DBP. Deglycosylated DBP cannot be converted to GcMAF, leading to immunosuppression.”
(Microbes Infect. 2005 Apr;7(4):674-81. Epub 2005 Mar 22. Pathogenic significance of alpha-N-acetylgalactosaminidase activity found in the hemagglutinin of influenza virus. Yamamoto N, Urade M.)
Malignant cancer cells and viruses send out an enzyme called Nagalase that prevents production of your GcMAF. Nagalase stops its beneficial effects, and neutralizes your immune system. So diseases become chronic, and cancer cells grow unchecked.
Nagalase is known to inactivate Gc-MAF by deglycosylating its natural precursor Gc-protein. Nagalase completely removes the trisaccharide from the Gc-protein by deglycosylation. After it has been deglycosylated, the Gc protein is thereby rendered incapable of conversion into active GcMAF. Since Gc-protein cannot be converted to GcMAF, the activation of macrophages is prevented.
Can nagalase levels be tested?
Yes.
The test measures the activity of alpha-N-acetylgalactosaminidase (nagalase) in blood. Normally present at only trace levels, Nagalase shows up in the blood when a cancer or virus appears. A healthy level is below 0.65 nmol/min/mg. Do not believe anyone who says that a healthy level is higher than that. If you stop GcMAF therapy at a nagalase level above 0.65, the nagalase will take over again within a few weeks and your immune system will collapse again. The ideal level is below 0.65.
The current method for diagnosing most cancers requires us to wait until a mass shows up on imaging (e.g., a mammogram, chest X-ray, or colonoscopy). Long before tumors can be found this way, a nagalase test can tell us that early stage cancer exists somewhere in the body. Nagalase appears in the blood stream when a nascent cancer is just a minute cluster of abnormal cells, long before conventional diagnostic methods can detect it. Through blood testing, we can find this red flag, even when present at exceedingly low levels. The old adage, “Where there’s smoke, there’s fire” applies here. This information provides a huge head-start for treatment and prevention.
Higher levels of nagalase are believed to be a marker of immuno-suppression and subsequently lowered levels are seen as an indicator of effectiveness for the Gc-MAF therapy. A drop in Nagalase levels shows you are a responder, and that the grip of the disease is being broken. Rising Nagalase levels indicate a cancer or virus is growing and spreading. Conversely, Nagalase levels will decrease if the cancer or infection is being effectively destroyed. Consecutive rising Nagalase levels are therefore a red flag, warning us it may be time to entertain new treatment options. Conversely, if levels are going down, stay the course: the cancer or virus is going away.
You need to find a local laboratory who will withdraw your blood into a syringe, spin it down in a centrifuge to extract the yellow serum, and pack the serum to keep it cool for dispatch.
So if you decide to test your nagalase levels, it is suggested that you do so just before commencing GcMAF therapy (don’t wait for the results) and repeat the test every 8 weeks throughout treatment.
European Laboratory of Nutrients (ELN)
If you use ELN in Holland and the USA, it has been taking 5 weeks to get results back, so its only useful after you’ve been on GcMAF for 8 weeks and compare the first and second results. And by then you are 8+5=13 weeks down the track. In long term diseases like stage 4 cancer, nagalase at 13 weeks may be the first definite indicator you get.
The cost of a nagalase blood test is 50 euros from European Laboratory of Nutrients (ELN) plus any additional costs from your Doctor or Clinic to extract and prepare the blood sample.
There is no problem to run the assays on samples from outside Belgium. FedEx is an reliable courier for transport of biological material. Please contact us for logistics-related questions.
http://www.hdri-usa.com/
Health Diagnostics and Research Institute
540 Bordentown Ave., Suite 2300
South Amboy, NJ 08879, USA
Tel 732-721-1234
Fax 732-525-3288
[email protected]
http://www.europeanlaboratory.nl/
Regulierenring 9
3981 LA Bunnik
The Netherlands
Phone: +31 30 2871492
Fax: +31 30 2802688
[email protected]
http://www.redlabs.be/naa
Redlabs in Belgium
R.E.D. Laboratories N.V./S.A.
Z.1 Researchpark 100
B-1731 Zellik
Belgium
+32-(0)2-481-5310
+32-(0)2-481-5311
+32-(0)2-481-5323
http://www.redlabs.be/contact
R.E.D. Laboratories Reno, Nevada
Attn: Craig Setter
University of Nevada, Reno
1664 N Virginia St. MS 0554
Reno, NV 89557, USA
775-682-8280
775-682-8290
http://www.redlabs.be/request-forms
Nagalase in blood is a sensitive test for monitoring the effect of therapy. Because of the short half-life of nagalase, the method is suitable for monitoring various types of therapy. The great sensitivity of the test may help the practitioner in obtaining a better understanding of the therapy and to fine-tune the treatment.
Note: The values may be affected by drugs used in the five days preceding the sampling. Drug use must be indicated on the questionnaire submitted with the blood test.
https://gcmaf.se/nagalase-blood-test/
The test measures the activity of alpha-N-acetylgalactosaminidase (nagalase) in blood. Normally present at only trace levels, Nagalase shows up in the blood when a cancer or virus appears. A healthy level is below 0.65 nmol/min/mg. Do not believe anyone who says that a healthy level is higher than that. If you stop GcMAF therapy at a nagalase level above 0.65, the nagalase will take over again within a few weeks and your immune system will collapse again. The ideal level is below 0.65.
The current method for diagnosing most cancers requires us to wait until a mass shows up on imaging (e.g., a mammogram, chest X-ray, or colonoscopy). Long before tumors can be found this way, a nagalase test can tell us that early stage cancer exists somewhere in the body. Nagalase appears in the blood stream when a nascent cancer is just a minute cluster of abnormal cells, long before conventional diagnostic methods can detect it. Through blood testing, we can find this red flag, even when present at exceedingly low levels. The old adage, “Where there’s smoke, there’s fire” applies here. This information provides a huge head-start for treatment and prevention.
Higher levels of nagalase are believed to be a marker of immuno-suppression and subsequently lowered levels are seen as an indicator of effectiveness for the Gc-MAF therapy. A drop in Nagalase levels shows you are a responder, and that the grip of the disease is being broken. Rising Nagalase levels indicate a cancer or virus is growing and spreading. Conversely, Nagalase levels will decrease if the cancer or infection is being effectively destroyed. Consecutive rising Nagalase levels are therefore a red flag, warning us it may be time to entertain new treatment options. Conversely, if levels are going down, stay the course: the cancer or virus is going away.
You need to find a local laboratory who will withdraw your blood into a syringe, spin it down in a centrifuge to extract the yellow serum, and pack the serum to keep it cool for dispatch.
So if you decide to test your nagalase levels, it is suggested that you do so just before commencing GcMAF therapy (don’t wait for the results) and repeat the test every 8 weeks throughout treatment.
European Laboratory of Nutrients (ELN)
If you use ELN in Holland and the USA, it has been taking 5 weeks to get results back, so its only useful after you’ve been on GcMAF for 8 weeks and compare the first and second results. And by then you are 8+5=13 weeks down the track. In long term diseases like stage 4 cancer, nagalase at 13 weeks may be the first definite indicator you get.
The cost of a nagalase blood test is 50 euros from European Laboratory of Nutrients (ELN) plus any additional costs from your Doctor or Clinic to extract and prepare the blood sample.
There is no problem to run the assays on samples from outside Belgium. FedEx is an reliable courier for transport of biological material. Please contact us for logistics-related questions.
http://www.hdri-usa.com/
Health Diagnostics and Research Institute
540 Bordentown Ave., Suite 2300
South Amboy, NJ 08879, USA
Tel 732-721-1234
Fax 732-525-3288
[email protected]
http://www.europeanlaboratory.nl/
Regulierenring 9
3981 LA Bunnik
The Netherlands
Phone: +31 30 2871492
Fax: +31 30 2802688
[email protected]
http://www.redlabs.be/naa
Redlabs in Belgium
R.E.D. Laboratories N.V./S.A.
Z.1 Researchpark 100
B-1731 Zellik
Belgium
+32-(0)2-481-5310
+32-(0)2-481-5311
+32-(0)2-481-5323
http://www.redlabs.be/contact
R.E.D. Laboratories Reno, Nevada
Attn: Craig Setter
University of Nevada, Reno
1664 N Virginia St. MS 0554
Reno, NV 89557, USA
775-682-8280
775-682-8290
http://www.redlabs.be/request-forms
Nagalase in blood is a sensitive test for monitoring the effect of therapy. Because of the short half-life of nagalase, the method is suitable for monitoring various types of therapy. The great sensitivity of the test may help the practitioner in obtaining a better understanding of the therapy and to fine-tune the treatment.
Note: The values may be affected by drugs used in the five days preceding the sampling. Drug use must be indicated on the questionnaire submitted with the blood test.
https://gcmaf.se/nagalase-blood-test/
What is the recommended protocol for using GcMAF?
Everyone responds differently. No one can accurately predict how you will respond.
It is proposed that patients could be treated with substitution therapy with Gc-MAF. GcMAF is therefore a replacement therapy for those who can’t make their own. Taking GcMAF replaces the missing part of the immune system, and also acts as the body’s own internal medicine.
The dosing varies from 0.03ml once a week up to 4ml per day. In ME/CFS, autism and Lyme, we recommend you start with a very low dose of 0.03ml. The maximum continuous dose is 2ml a day. The highest dose is 16 shots or 4ml a day, but only for 2 days as the body cannot remove the cancer debris fast enough. Do not stop GcMAF until after your nagalase gets below 0.65, when your own GcMAF will take over again.
Minutes after a receiving a dose, 10 of the body’s actions restart. In three weeks of two GcMAF 0.25ml doses a week, your immune system is rebuilt to above normal strength. You need two doses a week for typically 24 weeks for many diseases and early cancers, up to seven one ml doses a week and a year for stage 4 cancers. Your body then takes the disease down without side effects, and successfully in 80% of cases -depending upon how well you follow the protocol.
The life of GcMAF is only six days – you have to keep taking it until your disease has gone (ie your nagalase is under 0.65 nmol/min/mg) then a further 8 weeks, or the immune system gets shut down again.
If you have your blood taken for monocyte counts, vitamin D levels, and nagalase at the beginning, you should see on your next test after three weeks that your immune system is back to full strength, and after 8 weeks significantly falling nagalase will indicate the disease is losing its grip. Don’t stop the GcMAF until your nagalase gets below 0.65 nmol/min/mg, when it loses the ability to prevent your body producing your own GcMAF, and then you no longer need to supplement. Even better, get scans.
Under the UK GMC Good Prescription Guidelines paragraph 68 a doctor may use the treatment of his choice. You have a legal right to choose your medication – Declaration of Helsinki (1975). If you have a cancer...
Avoid the five main causes of cancer
1. Too much sugar
2. Lack of vitamin D3
2. Poor nutrition lacking in amino acids and trace metals,
4. Lack of oxygen and exercise,
5. Severe shock stress.
Avoid sugars
Stay away from: sugar, which feeds cancer, carbohydrates which turn into sugar; and grains beans and potatoes, which also contain cancer inducing lectins and poisons – wheat is the worst. Avoid soya milk which blocks the absorbance of trace metals.
Some sweeteners are damaging in other ways – asparthame lowers your immune system; even Splenda is a chlorocarbon like DDT – See http://www.wnho.net/splenda_chlorocarbon.htm
The best appears to be the natural plant sweetener Xylitol or Stevia, to which they add relatively harmless maltodextrin for supermarkets. Second best is saccharin.
Breast cancer
If you have a root canal, you are advised to have that tooth removed. (See article)
And ordinary milk contains estrogen, which is a growth factor for uterine cancer, and for breast cancer but less so.
For stage one:
1. A standard dose of 0.25ml GcMAF twice a week, for stage 2 three doses a week, stage 3 five doses a week, late stage 4 up to a full 1ml five times a week. You should expect no side effects with 1ml a day.
2. At least 10,000iu of vitamin D3 a day, 100mcg K2, 400mg of magnesium citrate.
3. No sugar or carbohydrates (so no cereals or bread etc) which feed cancer.
4. Eat vegetables, fish, and white meat.
5. If your weight drops below your perfect weight for your height, take Branch Chain Amino Acids (BCAA) from a vitamin shop, or better, Master Amino Acid Pattern.
If nebulising
the dose is 0.5ml to 1.0 ml a day in 5ml of saline.
If you add drugs to this, the more you add the more you will reduce your chances of success. More is less.
Don’t stop the GcMAF until 8 weeks after you have scans proving you are cancer free, or 8 weeks after your nagalase drops below 0.65.
GcMAF is usually successful with terminal stage four pancreatic cancer, but it takes doses of one ml a day initially. Chemotherapy can make blood and immune system counts so low treatment fails.
Dosage
From GcMAF’s discovery in 1990 until 2013, 0.25ml of GcMAF a week was recommended, because it was thought GcMAF only rebuilt the immune system and activated macrophages, where it has a half life of 6 days. In 2013 we carried out laboratory research and published research papers (See “the Science” here) in which we discovered four more attacks GcMAF has on cancer, three excellent results on the brain, and two on cells. These have a half life of 3 days. Coupled with feedback over four years, we’ve now re-adjusted the dosing. So for cancer we now suggest at least two 0.25 doses a week, which is enough for good responders. In our Treatment Centres our doctors give a maximum of 2ml, one vial a day for 2 days only, because the body cannot transport cancer debris away at that level. The most we give continually is 1ml a day.
If you are treating an infection or a cold, give one 0.25-0.5 shot only. It may be gone in 36 hours. If you take shots every day, the immune system will be kept high, producing mucous and maintaining the symptoms long after the cold should have left.
Stage 4 cancer
Late stage cancer, it takes a year to 18 months to become cancer free. GcMAF has six attacks on cancer; four direct, where its half life is three days. So most importantly increase the GcMAF dosage, and put into different parts of the body at least twice a week. As a macrophage activator its half life is 5 days (the half life of macrophages is 6 days). These 5 attacks start up in within minutes. You can see the increase in activity in the spleen on live scans. The sixth attack, the immune system, is fully rebuilt by GcMAF in 3 weeks. IV by a doctor is best.
There are out-patient Treatment Centres in Europe where doctors use ultrasonography to accurately measure your tumors, and to place the GcMAF in the right place every day for a week or more. Re-measure a week later and a 25% reduction in the first week is average.
If you can have surgery to reduce tumour mass, do so, but make sure you are on GcMAF for at least three weeks before the surgery and 8 weeks afterwards, so that your rebuilt immune system can prevent secondaries caused by cancer cells released by surgery settling elsewhere. And then keep the GcMAF up for 8 weeks after scans show your tumours are gone, or nagalase first drops below 0.65.
If you wish to speed your recovery you can:
1. GcMAF needs normal levels of vitamin D to function strongly (take 10,000iu a day). in low responders, larger doses are required. GcMAF needs normal levels of vitamin D (40ng/ml+) to fully function. Laboratory tests have shown GcMAF is 2.5 times more effective with normal levels of vitamin D. Sunbathe whenever you can. Take up to 10,000 IU (225 micrograms) of vitamin D3 a day. One day of sunbathing gives you 20,000 IU of Vitamin D. On a blood test, you want to aim for a vitamin D level of 60-80 ng/ml,which is about 150 nmol/l (multiply by 2.496). Participants who do well all have high vitamin D levels (and the rate of tumor mass reduction drops as winter approaches) 80 percent of cancer, CFS and HIV patients have low levels of vitamin D (under 30ng/ml).
2. Take plenty of exercise, preferably in the sunshine, and breathe deeply. This gets oxygen around, and disease cannot stand it.
3. Drink at least 4 pints or 2.5 litres of water during a day.
4. Proper nutrition is essential. Eat plenty of lipids, the food of your immune system.
5. Get your PINI score checked. Its a blood test, and its: Alpha 1 acid glycoprotein x C-reactive protein / albumin x prealbumin. It should be below one.
6. High dose vitamin C – 25,000 IU during a day. Better still, get your doctor to give it IV. There are synergistic effects with GcMAF Or up to 10 grams (10,000mg) ascorbic acid. (Side effects appear at 50 grams a day.)
7. Detoxing: Emulsified vitamin A, selenium and vitamin E. This is for the lymphatic system to carry away wastes, and is important. Non responders can respond if they take Chlorella with cod liver oil that has correct ratios of vitamins A to D. This binds to heavy metals and chelates them out and also offers absorption of missing minerals.
8. Maintain an alkaline PH in your body. A teaspoon of bicarbonate of soda in water once a day or vegetables like pureed asparagus and broccoli. Broccoli sprouts are particularly good
9. GcMAF performs better in the presence of oleic acid. Its an Omega 9 oil, the best source is olive oil.
10. Drink green tea.
11. Curcumin, specifically turmeric, is helpful with melanoma and breast cancer. Its difficult to get into the body. Try it liposomal.
It is proposed that patients could be treated with substitution therapy with Gc-MAF. GcMAF is therefore a replacement therapy for those who can’t make their own. Taking GcMAF replaces the missing part of the immune system, and also acts as the body’s own internal medicine.
The dosing varies from 0.03ml once a week up to 4ml per day. In ME/CFS, autism and Lyme, we recommend you start with a very low dose of 0.03ml. The maximum continuous dose is 2ml a day. The highest dose is 16 shots or 4ml a day, but only for 2 days as the body cannot remove the cancer debris fast enough. Do not stop GcMAF until after your nagalase gets below 0.65, when your own GcMAF will take over again.
Minutes after a receiving a dose, 10 of the body’s actions restart. In three weeks of two GcMAF 0.25ml doses a week, your immune system is rebuilt to above normal strength. You need two doses a week for typically 24 weeks for many diseases and early cancers, up to seven one ml doses a week and a year for stage 4 cancers. Your body then takes the disease down without side effects, and successfully in 80% of cases -depending upon how well you follow the protocol.
The life of GcMAF is only six days – you have to keep taking it until your disease has gone (ie your nagalase is under 0.65 nmol/min/mg) then a further 8 weeks, or the immune system gets shut down again.
If you have your blood taken for monocyte counts, vitamin D levels, and nagalase at the beginning, you should see on your next test after three weeks that your immune system is back to full strength, and after 8 weeks significantly falling nagalase will indicate the disease is losing its grip. Don’t stop the GcMAF until your nagalase gets below 0.65 nmol/min/mg, when it loses the ability to prevent your body producing your own GcMAF, and then you no longer need to supplement. Even better, get scans.
Under the UK GMC Good Prescription Guidelines paragraph 68 a doctor may use the treatment of his choice. You have a legal right to choose your medication – Declaration of Helsinki (1975). If you have a cancer...
Avoid the five main causes of cancer
1. Too much sugar
2. Lack of vitamin D3
2. Poor nutrition lacking in amino acids and trace metals,
4. Lack of oxygen and exercise,
5. Severe shock stress.
Avoid sugars
Stay away from: sugar, which feeds cancer, carbohydrates which turn into sugar; and grains beans and potatoes, which also contain cancer inducing lectins and poisons – wheat is the worst. Avoid soya milk which blocks the absorbance of trace metals.
Some sweeteners are damaging in other ways – asparthame lowers your immune system; even Splenda is a chlorocarbon like DDT – See http://www.wnho.net/splenda_chlorocarbon.htm
The best appears to be the natural plant sweetener Xylitol or Stevia, to which they add relatively harmless maltodextrin for supermarkets. Second best is saccharin.
Breast cancer
If you have a root canal, you are advised to have that tooth removed. (See article)
And ordinary milk contains estrogen, which is a growth factor for uterine cancer, and for breast cancer but less so.
For stage one:
1. A standard dose of 0.25ml GcMAF twice a week, for stage 2 three doses a week, stage 3 five doses a week, late stage 4 up to a full 1ml five times a week. You should expect no side effects with 1ml a day.
2. At least 10,000iu of vitamin D3 a day, 100mcg K2, 400mg of magnesium citrate.
3. No sugar or carbohydrates (so no cereals or bread etc) which feed cancer.
4. Eat vegetables, fish, and white meat.
5. If your weight drops below your perfect weight for your height, take Branch Chain Amino Acids (BCAA) from a vitamin shop, or better, Master Amino Acid Pattern.
If nebulising
the dose is 0.5ml to 1.0 ml a day in 5ml of saline.
If you add drugs to this, the more you add the more you will reduce your chances of success. More is less.
Don’t stop the GcMAF until 8 weeks after you have scans proving you are cancer free, or 8 weeks after your nagalase drops below 0.65.
GcMAF is usually successful with terminal stage four pancreatic cancer, but it takes doses of one ml a day initially. Chemotherapy can make blood and immune system counts so low treatment fails.
Dosage
From GcMAF’s discovery in 1990 until 2013, 0.25ml of GcMAF a week was recommended, because it was thought GcMAF only rebuilt the immune system and activated macrophages, where it has a half life of 6 days. In 2013 we carried out laboratory research and published research papers (See “the Science” here) in which we discovered four more attacks GcMAF has on cancer, three excellent results on the brain, and two on cells. These have a half life of 3 days. Coupled with feedback over four years, we’ve now re-adjusted the dosing. So for cancer we now suggest at least two 0.25 doses a week, which is enough for good responders. In our Treatment Centres our doctors give a maximum of 2ml, one vial a day for 2 days only, because the body cannot transport cancer debris away at that level. The most we give continually is 1ml a day.
If you are treating an infection or a cold, give one 0.25-0.5 shot only. It may be gone in 36 hours. If you take shots every day, the immune system will be kept high, producing mucous and maintaining the symptoms long after the cold should have left.
Stage 4 cancer
Late stage cancer, it takes a year to 18 months to become cancer free. GcMAF has six attacks on cancer; four direct, where its half life is three days. So most importantly increase the GcMAF dosage, and put into different parts of the body at least twice a week. As a macrophage activator its half life is 5 days (the half life of macrophages is 6 days). These 5 attacks start up in within minutes. You can see the increase in activity in the spleen on live scans. The sixth attack, the immune system, is fully rebuilt by GcMAF in 3 weeks. IV by a doctor is best.
There are out-patient Treatment Centres in Europe where doctors use ultrasonography to accurately measure your tumors, and to place the GcMAF in the right place every day for a week or more. Re-measure a week later and a 25% reduction in the first week is average.
If you can have surgery to reduce tumour mass, do so, but make sure you are on GcMAF for at least three weeks before the surgery and 8 weeks afterwards, so that your rebuilt immune system can prevent secondaries caused by cancer cells released by surgery settling elsewhere. And then keep the GcMAF up for 8 weeks after scans show your tumours are gone, or nagalase first drops below 0.65.
If you wish to speed your recovery you can:
1. GcMAF needs normal levels of vitamin D to function strongly (take 10,000iu a day). in low responders, larger doses are required. GcMAF needs normal levels of vitamin D (40ng/ml+) to fully function. Laboratory tests have shown GcMAF is 2.5 times more effective with normal levels of vitamin D. Sunbathe whenever you can. Take up to 10,000 IU (225 micrograms) of vitamin D3 a day. One day of sunbathing gives you 20,000 IU of Vitamin D. On a blood test, you want to aim for a vitamin D level of 60-80 ng/ml,which is about 150 nmol/l (multiply by 2.496). Participants who do well all have high vitamin D levels (and the rate of tumor mass reduction drops as winter approaches) 80 percent of cancer, CFS and HIV patients have low levels of vitamin D (under 30ng/ml).
2. Take plenty of exercise, preferably in the sunshine, and breathe deeply. This gets oxygen around, and disease cannot stand it.
3. Drink at least 4 pints or 2.5 litres of water during a day.
4. Proper nutrition is essential. Eat plenty of lipids, the food of your immune system.
5. Get your PINI score checked. Its a blood test, and its: Alpha 1 acid glycoprotein x C-reactive protein / albumin x prealbumin. It should be below one.
6. High dose vitamin C – 25,000 IU during a day. Better still, get your doctor to give it IV. There are synergistic effects with GcMAF Or up to 10 grams (10,000mg) ascorbic acid. (Side effects appear at 50 grams a day.)
7. Detoxing: Emulsified vitamin A, selenium and vitamin E. This is for the lymphatic system to carry away wastes, and is important. Non responders can respond if they take Chlorella with cod liver oil that has correct ratios of vitamins A to D. This binds to heavy metals and chelates them out and also offers absorption of missing minerals.
8. Maintain an alkaline PH in your body. A teaspoon of bicarbonate of soda in water once a day or vegetables like pureed asparagus and broccoli. Broccoli sprouts are particularly good
9. GcMAF performs better in the presence of oleic acid. Its an Omega 9 oil, the best source is olive oil.
10. Drink green tea.
11. Curcumin, specifically turmeric, is helpful with melanoma and breast cancer. Its difficult to get into the body. Try it liposomal.
What tests are done on GcMAF to guarantee its potency?
GcMAF needs to be produced in highly professional sterile laboratories by GMP-trained scientists. Sterile, certified substrates with traceability should be used, with sterile, certified equipment. Without tests and assays, any product purporting to be GcMAF can be without activity and useless.
The molecules of GcMAF prepared should be identical to those made by the human body. GcMAF is extracted and isolated; its a 24 step process, and at the end it must have tests to prove its sterility and activity. (If it does not come with published tests, its probably not GcMAF.)
Activity assays are vital – GcMAF must be proven to exist, be sterile, and most importantly, be active, and activity assays can only be done with living cells.
The only way to test that GcMAF is active is with live macrophage and live cancer cell lines. You cannot prove GcMAF is active unless you carry out live cell tests. In the laboratory tests Immuno Biotec photographs through microscopes as newly activated macrophages eat cancer cells, and in the absence of macrophages, GcMAF turns the cancer cells back into healthy cells. These results guarantee that each batch of GcMAF is active.
The penultimate of the nine tests is to add macrophages to the MCF7 cancer cell line in vitro. Nothing happens. Then we add the GcMAF. In 72 hours the cancer cells have been eaten by the macrophages. The last is to add GcMAF to the cancer cells without macrophages. In 72 hours the GcMAF has reverted the cancer cells back into healthy cells.
Immuno Biotec puts live macrophages cells and MCF7 breast cancer cells together; nothing happens. Then they add GcMAF; in 72 hours the macrophages eat all the MCF7 breast cancer cells. Then GcMAF and MCF7 breast cancer cells are placed together, and the GcMAF turns the cancer cells back into healthy cells.
Contamination: A good laboratory should aim for a viral clearance of better than 10 to the power of 20.
Tests can include:
1. Sterility – to USP and Ph Eur sterility standards preferably performed externally.
2. Endotoxin test to confirm the absence of endotoxins in the sample. It should be 0.02 to 0.03, the bottom limit of detection. (10.0 is the max acceptable)
3. Protein Quantification using BCA Protein assay
4. Electrophoresis Silver Stained SDS Page for product identification;
5. Electrophoresis Western blot probed with biotin labelled Helix Pomatia Lectin (binding directly to the terminal N-acetylgalactosaminyl present in Gc MAF).
6. Electrophoresis Western Blot probed with Anti Vitamin D Binding Protein (specific to Gc Globulin and Gc MAF)
7. RAW 264.7 live macrophage cell based proliferation assay for activity, ie potency,
8. Breast carcinoma phagocytosis activity assay. Macrophages are added to live MCF7 breast cancer cells; nothing happens. GcMAF is added; withIn 72 hours the macrophages are observed to phagocytise (eat and destroy) the cancer cells.
9. Third activity assay: GcMAF is added to MCF7 cancer cells without macrophages. On addition of GcMAF a cell morphology change is observed In 72 hours where cancer cells adopt a normal cell morphology. (Experiment first performed by Professor Ruggiero’s team and published January 2012)
The molecules of GcMAF prepared should be identical to those made by the human body. GcMAF is extracted and isolated; its a 24 step process, and at the end it must have tests to prove its sterility and activity. (If it does not come with published tests, its probably not GcMAF.)
Activity assays are vital – GcMAF must be proven to exist, be sterile, and most importantly, be active, and activity assays can only be done with living cells.
The only way to test that GcMAF is active is with live macrophage and live cancer cell lines. You cannot prove GcMAF is active unless you carry out live cell tests. In the laboratory tests Immuno Biotec photographs through microscopes as newly activated macrophages eat cancer cells, and in the absence of macrophages, GcMAF turns the cancer cells back into healthy cells. These results guarantee that each batch of GcMAF is active.
The penultimate of the nine tests is to add macrophages to the MCF7 cancer cell line in vitro. Nothing happens. Then we add the GcMAF. In 72 hours the cancer cells have been eaten by the macrophages. The last is to add GcMAF to the cancer cells without macrophages. In 72 hours the GcMAF has reverted the cancer cells back into healthy cells.
Immuno Biotec puts live macrophages cells and MCF7 breast cancer cells together; nothing happens. Then they add GcMAF; in 72 hours the macrophages eat all the MCF7 breast cancer cells. Then GcMAF and MCF7 breast cancer cells are placed together, and the GcMAF turns the cancer cells back into healthy cells.
Contamination: A good laboratory should aim for a viral clearance of better than 10 to the power of 20.
Tests can include:
1. Sterility – to USP and Ph Eur sterility standards preferably performed externally.
2. Endotoxin test to confirm the absence of endotoxins in the sample. It should be 0.02 to 0.03, the bottom limit of detection. (10.0 is the max acceptable)
3. Protein Quantification using BCA Protein assay
4. Electrophoresis Silver Stained SDS Page for product identification;
5. Electrophoresis Western blot probed with biotin labelled Helix Pomatia Lectin (binding directly to the terminal N-acetylgalactosaminyl present in Gc MAF).
6. Electrophoresis Western Blot probed with Anti Vitamin D Binding Protein (specific to Gc Globulin and Gc MAF)
7. RAW 264.7 live macrophage cell based proliferation assay for activity, ie potency,
8. Breast carcinoma phagocytosis activity assay. Macrophages are added to live MCF7 breast cancer cells; nothing happens. GcMAF is added; withIn 72 hours the macrophages are observed to phagocytise (eat and destroy) the cancer cells.
9. Third activity assay: GcMAF is added to MCF7 cancer cells without macrophages. On addition of GcMAF a cell morphology change is observed In 72 hours where cancer cells adopt a normal cell morphology. (Experiment first performed by Professor Ruggiero’s team and published January 2012)
Where can someone get GcMAF?
Is Gc-MAF patented?
patent_6410269_preparation_of_potent_macrophage_activating_factors_derived_from_cloned_vitamin_d_binding_protein_and_its_domain_and_their_therapeutic_usage_for_cancer_hiv-infection_and_osteopetrosis.pdf |
What studies have been published?
1996_defective_lymphocyte_glycosidases_in_the_macrophage_activation_cascade_of_juvenile_osteopetrosis.pdf |
2003_vitamin_d_binding_protein-macrophage_activating_factor__dbp-maf___inhibits_angiogenesis_and_tumor_growth_in_mice1.pdf |
2008_immunotherapy_for_prostate_cancer_with_gc_protein_derived_macrophage_activating_factor.pdf |
2008_immunotherapy_of_metastatic_breast_cancer_patients_with_vitamin_d-binding_protein-derived_macrophage_activating_factor__gcmaf_.pdf |
2009_immunotherapy_of_hiv-infected_patients_with_gc_protein-derived_macrophage_activating_factor__gcmaf_.pdf |
2010_vitamin_d_binding_protein-macrophage_activating_factor_directly_inhibits_proliferation_migration_and_upar_expression_of_prostate_cancer_cells.pdf |
2013_effects_of_gc-macrophage_activating_factor_in_human_neurons__implications_for_treatment_of_chronic_fatigue_syndrome.pdf |
2013_gc_protein-derived_macrophage-activating_factor_decreases_α-n-acetylgalactosaminidase_levels_in_advanced_cancer_patients.pdf |
2013_therapeutic_effects_of_highly_purified_de-glycosylated_gcmaf_in_the_immunotherapy_of_patients_with_chronic_diseases.pdf |
2013_vitamin_d_binding_protein-derived_macrophage_activating_factor_induces_human_breast_cancer_cell_apoptosis_through_stimulation_of_macrophages.pdf |
2013_vitamin_d_binding_protein-derived_macrophage_activating_factor_stimulates_proliferation_and_signalling_in_a_human_neuronal_cell_line.pdf |
2014_clinical_experience_of_cancer_immunotherapy_integrated_with_oleic_acid_complexed_with_de-glycosylated_vitamin_d_binding_protein.pdf |
2014_focuss_ultra_brain_her2_pancreatic_gcmaf_antic_res_abs_greece.pdf |
2014_oleic_acid_deglycosylated_vitamin_d_binding_protein_nitric_oxide_a_molecular_triad_made_lethal_to_cancer.pdf |
2014_the_effect_of_gcmaf_complexed_with_oleic_acid_on_multiple_myeloma_cultures.pdf |
2015_effects_glyco_goleic_myeloma_hodgkins_cells.pdf |
More Published Studies
1: Hamilton G, Rath B, Klameth L, Hochmair MJ. Small cell lung cancer: Recruitment of macrophages by circulating tumor cells. Oncoimmunology. 2015 Oct 29;5(3):e1093277. eCollection 2016 Mar. PubMed PMID: 27141354; PubMed Central
PMCID: PMC4839345.
PMCID: PMC4839345.
2: Delanghe JR, Speeckaert R, Speeckaert MM. Behind the scenes of vitamin D binding protein: more than vitamin D binding. Best Pract Res Clin Endocrinol Metab. 2015 Oct;29(5):773-86. doi: 10.1016/j.beem.2015.06.006. Epub 2015 Jul 2.
Review. PubMed PMID: 26522461.
Review. PubMed PMID: 26522461.
3: Inui T, Kubo K, Kuchiike D, Uto Y, Nishikata T, Sakamoto N, Mette M. Oral Colostrum Macrophage-activating Factor for Serious Infection and Chronic Fatigue Syndrome: Three Case Reports. Anticancer Res. 2015 Aug;35(8):4545-9. PubMed
PMID: 26168499.
PMID: 26168499.
4: Uto Y, Kawai T, Sasaki T, Hamada K, Yamada H, Kuchiike D, Kubo K, Inui T, Mette M, Tokunaga K, Hayakawa A, Go A, Oosaki T. Degalactosylated/Desialylated Bovine Colostrum Induces Macrophage Phagocytic Activity Independently of Inflammatory Cytokine Production. Anticancer Res. 2015 Aug;35(8):4487-92. PubMed
PMID: 26168491.
PMID: 26168491.
5: Branca JJ, Morucci G, Malentacchi F, Gelmini S, Ruggiero M, Pacini S. Effects of oxaliplatin and oleic acid Gc-protein-derived macrophage-activating factor on murine and human microglia. J Neurosci Res. 2015 Sep;93(9):1364-77. doi:
10.1002/jnr.23588. Epub 2015 Mar 18. PubMed
PMID: 25782915.
10.1002/jnr.23588. Epub 2015 Mar 18. PubMed
PMID: 25782915.
6: Morucci G, Branca JJ, Gulisano M, Ruggiero M, Paternostro F, Pacini A, Di Cesare Mannelli L, Pacini S. Gc-protein-derived macrophage activating factor counteracts the neuronal damage induced by oxaliplatin. Anticancer Drugs. 2015
Feb;26(2):197-209. doi: 10.1097/CAD.0000000000000177.
PubMed PMID: 25304987.
Feb;26(2):197-209. doi: 10.1097/CAD.0000000000000177.
PubMed PMID: 25304987.
7: Immunotherapy of metastatic colorectal cancer with vitamin D-binding protein-derived macrophage-activating factor, GcMAF. Cancer Immunol Immunother. 2014 Dec;63(12):1349.
8: ‘Immunotherapy of metastatic breast cancer patients with vitamin D-binding protein-derived macrophage activating factor (GcMAF)’ by Yamamoto, N., Suyama, H., Yamamoto, N. and Ushijima, N. Int J Cancer. 2014 Sep 15;135(6):1509. PubMed
PMID: 25180398.
PMID: 25180398.
9: Inui T, Makita K, Miura H, Matsuda A, Kuchiike D, Kubo K, Mette M, Uto Y, Nishikata T, Hori H, Sakamoto N. Case report: A breast cancer patient treated with GcMAF, sonodynamic therapy and hormone therapy. Anticancer Res. 2014 Aug;34(8): 4589-93. Erratum in: Anticancer Res. 2015 Apr;35(4):2477. PubMed
PMID: 25075104.
PMID: 25075104.
10: Ishikawa M, Inoue T, Inui T, Kuchiike D, Kubo K, Uto Y, Nishikata T. A novel assay system for macrophage-activating factor activity using a human U937 cell line. Anticancer Res. 2014 Aug;34(8):4577-81. PubMed
PMID: 25075102.
PMID: 25075102.
11: Ruggiero M, Ward E, Smith R, Branca JJ, Noakes D, Morucci G, Taubmann M,
Thyer L, Pacini S. Oleic Acid, deglycosylated vitamin D-binding protein, nitric
oxide: a molecular triad made lethal to cancer. Anticancer Res. 2014
Jul;34(7):3569-78. PubMed PMID: 24982371.
12: Siniscalco D, Bradstreet JJ, Cirillo A, Antonucci N. The in vitro GcMAF
effects on endocannabinoid system transcriptionomics, receptor formation, and
cell activity of autism-derived macrophages. J Neuroinflammation. 2014 Apr
17;11:78. doi: 10.1186/1742-2094-11-78. PubMed PMID: 24739187; PubMed Central
PMCID: PMC3996516.
13: Ikeda T, Kasai M, Tatsukawa E, Kamitakahara M, Shibata Y, Yokoi T, Nemoto TK,
Ioku K. A bone substitute with high affinity for vitamin D-binding
protein–relationship with niche of osteoclasts. J Cell Mol Med. 2014
Jan;18(1):170-80. doi: 10.1111/jcmm.12180. Epub 2013 Nov 28. PubMed PMID:
24286277; PubMed Central PMCID: PMC3916128.
14: Thyer L, Ward E, Smith R, Branca JJ, Morucci G, Gulisano M, Noakes D,
Eslinger R, Pacini S. GC protein-derived macrophage-activating factor decreases
α-N-acetylgalactosaminidase levels in advanced cancer patients. Oncoimmunology.
2013 Aug 1;2(8):e25769. Epub 2013 Jul 29. PubMed PMID: 24179708; PubMed Central
PMCID: PMC3812199.
15: Sayegh L, Fuleihan Gel-H, Nassar AH. Vitamin D in endometriosis: a causative
or confounding factor? Metabolism. 2014 Jan;63(1):32-41. doi:
10.1016/j.metabol.2013.09.012. Epub 2013 Oct 14. Review. PubMed PMID: 24135500.
16: Thyer L, Ward E, Smith R, Fiore MG, Magherini S, Branca JJ, Morucci G,
Gulisano M, Ruggiero M, Pacini S. A novel role for a major component of the
vitamin D axis: vitamin D binding protein-derived macrophage activating factor
induces human breast cancer cell apoptosis through stimulation of macrophages.
Nutrients. 2013 Jul 8;5(7):2577-89. doi: 10.3390/nu5072577. PubMed PMID:
23857228; PubMed Central PMCID: PMC3738989.
17: Inui T, Kuchiike D, Kubo K, Mette M, Uto Y, Hori H, Sakamoto N. Clinical
experience of integrative cancer immunotherapy with GcMAF. Anticancer Res. 2013
Jul;33(7):2917-9. PubMed PMID: 23780980.
18: Hirota K, Nakagawa Y, Takeuchi R, Uto Y, Hori H, Onizuka S, Terada H.
Antitumor effect of degalactosylated gc-globulin on orthotopic grafted lung
cancer in mice. Anticancer Res. 2013 Jul;33(7):2911-5. PubMed PMID: 23780979.
19: Kuchiike D, Uto Y, Mukai H, Ishiyama N, Abe C, Tanaka D, Kawai T, Kubo K,
Mette M, Inui T, Endo Y, Hori H. Degalactosylated/desialylated human serum
containing GcMAF induces macrophage phagocytic activity and in vivo antitumor
activity. Anticancer Res. 2013 Jul;33(7):2881-5. PubMed PMID: 23780974.
20: Toyohara Y, Hashitani S, Kishimoto H, Noguchi K, Yamamoto N, Urade M.
Inhibitory effect of vitamin D-binding protein-derived macrophage activating
factor on DMBA-induced hamster cheek pouch carcinogenesis and its derived
carcinoma cell line. Oncol Lett. 2011 Jul;2(4):685-691. Epub 2011 May 13. PubMed
PMID: 22848250; PubMed Central PMCID: PMC3406437.
21: Bellone M, Rigamonti N. Vitamin D-binding protein-derived
macrophage-activating factor, GcMAF, and prostate cancer. Cancer Immunol
Immunother. 2012 Dec;61(12):2377-8. doi: 10.1007/s00262-012-1310-9. Epub 2012 Jun
28. PubMed PMID: 22740161.
22: Uto Y, Yamamoto S, Mukai H, Ishiyama N, Takeuchi R, Nakagawa Y, Hirota K,
Terada H, Onizuka S, Hori H. β-Galactosidase treatment is a common first-stage
modification of the three major subtypes of Gc protein to GcMAF. Anticancer Res.
2012 Jun;32(6):2359-64. PubMed PMID: 22641675.
23: Pacini S, Punzi T, Morucci G, Gulisano M, Ruggiero M. Effects of vitamin
D-binding protein-derived macrophage-activating factor on human breast cancer
cells. Anticancer Res. 2012 Jan;32(1):45-52. PubMed PMID: 22213287.
24: Pacini S, Morucci G, Punzi T, Gulisano M, Ruggiero M, Amato M, Aterini S.
Effect of paricalcitol and GcMAF on angiogenesis and human peripheral blood
mononuclear cell proliferation and signaling. J Nephrol. 2012
Jul-Aug;25(4):577-81. doi: 10.5301/jn.5000035. PubMed PMID: 21956771.
25: Uto Y, Yamamoto S, Takeuchi R, Nakagawa Y, Hirota K, Terada H, Onizuka S,
Nakata E, Hori H. Effect of the Gc-derived macrophage-activating factor precursor
(preGcMAF) on phagocytic activation of mouse peritoneal macrophages. Anticancer
Res. 2011 Jul;31(7):2489-92. PubMed PMID: 21873164.
26: Debruyne E, Speeckaert M, Weygaerde YV, Delanghe J. Phenotype of Gc-globulin
influences the macrophage activating factor (MAF) levels in serum. Clin Chem Lab
Med. 2011 Nov;49(11):1855-60. doi: 10.1515/CCLM.2011.676. Epub 2011 Aug 23.
PubMed PMID: 21859424.
27: Pacini S, Morucci G, Punzi T, Gulisano M, Ruggiero M. Gc protein-derived
macrophage-activating factor (GcMAF) stimulates cAMP formation in human
mononuclear cells and inhibits angiogenesis in chick embryo chorionallantoic
membrane assay. Cancer Immunol Immunother. 2011 Apr;60(4):479-85. doi:
10.1007/s00262-010-0953-7. Epub 2010 Dec 14. PubMed PMID: 21170647.
28: Faserl K, Golderer G, Kremser L, Lindner H, Sarg B, Wildt L, Seeber B.
Polymorphism in vitamin D-binding protein as a genetic risk factor in the
pathogenesis of endometriosis. J Clin Endocrinol Metab. 2011 Jan;96(1):E233-41.
doi: 10.1210/jc.2010-1532. Epub 2010 Oct 27. PubMed PMID: 20980430.
29: Gregory KJ, Zhao B, Bielenberg DR, Dridi S, Wu J, Jiang W, Huang B,
Pirie-Shepherd S, Fannon M. Vitamin D binding protein-macrophage activating
factor directly inhibits proliferation, migration, and uPAR expression of
prostate cancer cells. PLoS One. 2010 Oct 18;5(10):e13428. doi:
10.1371/journal.pone.0013428. PubMed PMID: 20976141; PubMed Central PMCID:
PMC2956649.
30: Nonaka K, Onizuka S, Ishibashi H, Uto Y, Hori H, Nakayama T, Matsuura N,
Kanematsu T, Fujioka H. Vitamin D binding protein-macrophage activating factor
inhibits HCC in SCID mice. J Surg Res. 2012 Jan;172(1):116-22. doi:
10.1016/j.jss.2010.07.057. Epub 2010 Sep 17. PubMed PMID: 20855083.
31: Ravnsborg T, Olsen DT, Thysen AH, Christiansen M, Houen G, Højrup P. The
glycosylation and characterization of the candidate Gc macrophage activating
factor. Biochim Biophys Acta. 2010 Apr;1804(4):909-17. doi:
10.1016/j.bbapap.2009.12.022. Epub 2010 Jan 13. PubMed PMID: 20079467.
32: Rehder DS, Nelson RW, Borges CR. Glycosylation status of vitamin D binding
protein in cancer patients. Protein Sci. 2009 Oct;18(10):2036-42. doi:
10.1002/pro.214. PubMed PMID: 19642159; PubMed Central PMCID: PMC2786967.
33: Fang Y, van Meurs JB, Arp P, van Leeuwen JP, Hofman A, Pols HA, Uitterlinden
AG. Vitamin D binding protein genotype and osteoporosis. Calcif Tissue Int. 2009
Aug;85(2):85-93. doi: 10.1007/s00223-009-9251-9. Epub 2009 Jun 2. PubMed PMID:
19488670; PubMed Central PMCID: PMC2729412.
34: Yamamoto N, Ushijima N, Koga Y. Immunotherapy of HIV-infected patients with
Gc protein-derived macrophage activating factor (GcMAF). J Med Virol. 2009
Jan;81(1):16-26. doi: 10.1002/jmv.21376.
35: Yamamoto N, Suyama H, Yamamoto N. Immunotherapy for Prostate Cancer with Gc
Protein-Derived Macrophage-Activating Factor, GcMAF. Transl Oncol. 2008
Jul;1(2):65-72. PubMed PMID: 18633461; PubMed Central PMCID: PMC2510818.
36: Spiriti J, Bogani F, van der Vaart A, Ghirlanda G. Modulation of protein
stability by O-glycosylation in a designed Gc-MAF analog. Biophys Chem. 2008
May;134(3):157-67. doi: 10.1016/j.bpc.2008.02.005. Epub 2008 Feb 21. PubMed PMID:
18329161.
37: Yamamoto N, Suyama H, Nakazato H, Yamamoto N, Koga Y. Immunotherapy of
metastatic colorectal cancer with vitamin D-binding protein-derived
macrophage-activating factor, GcMAF. Cancer Immunol Immunother. 2008
Jul;57(7):1007-16. Retraction in: Cancer Immunol Immunother. 2014
Dec;63(12):1349. PubMed PMID: 18058096.
38: Yamamoto N, Suyama H, Yamamoto N, Ushijima N. Immunotherapy of metastatic
breast cancer patients with vitamin D-binding protein-derived macrophage
activating factor (GcMAF). Int J Cancer. 2008 Jan 15;122(2):461-7. Retraction in:
Int J Cancer. 2014 Sep 15;135(6):1509. PubMed PMID: 17935130.
39: Meier U, Gressner O, Lammert F, Gressner AM. Gc-globulin: roles in response
to injury. Clin Chem. 2006 Jul;52(7):1247-53. Epub 2006 May 18. Review. PubMed
PMID: 16709624.
40: Kalkunte S, Brard L, Granai CO, Swamy N. Inhibition of angiogenesis by
vitamin D-binding protein: characterization of anti-endothelial activity of
DBP-maf. Angiogenesis. 2005;8(4):349-60. Epub 2006 Jan 7. PubMed PMID: 16400520.
41: Yamamoto N, Urade M. Pathogenic significance of
alpha-N-acetylgalactosaminidase activity found in the hemagglutinin of influenza
virus. Microbes Infect. 2005 Apr;7(4):674-81. Epub 2005 Mar 22. PubMed PMID:
15848273.
42: Nagasawa H, Sasaki H, Uto Y, Kubo S, Hori H. Association of the macrophage
activating factor (MAF) precursor activity with polymorphism in vitamin D-binding
protein. Anticancer Res. 2004 Sep-Oct;24(5C):3361-6. PubMed PMID: 15515432.
43: Onizuka S, Kawakami S, Taniguchi K, Fujioka H, Miyashita K. Pancreatic
carcinogenesis: apoptosis and angiogenesis. Pancreas. 2004 Apr;28(3):317-9.
PubMed PMID: 15084979.
44: Matsuura T, Uematsu T, Yamaoka M, Furusawa K. Effect of salivary gland
adenocarcinoma cell-derived alpha-N-acetylgalactosaminidase on the bioactivity of
macrophage activating factor. Int J Oncol. 2004 Mar;24(3):521-8. PubMed PMID:
14767536.
45: Schneider GB, Grecco KJ, Safadi FF, Popoff SN. The anabolic effects of
vitamin D-binding protein-macrophage activating factor (DBP-MAF) and a novel
small peptide on bone. Crit Rev Eukaryot Gene Expr. 2003;13(2-4):277-84. PubMed
PMID: 14696974.
46: Mohamad SB, Nagasawa H, Sasaki H, Uto Y, Nakagawa Y, Kawashima K, Hori H. Gc
protein-derived macrophage activating factor (GcMAF): isoelectric focusing
pattern and tumoricidal activity. Anticancer Res. 2003 Nov-Dec;23(6a):4451-7.
PubMed PMID: 14666733.
47: Gumireddy K, Reddy CD, Swamy N. Mitogen-activated protein kinase pathway
mediates DBP-maf-induced apoptosis in RAW 264.7 macrophages. J Cell Biochem. 2003
Sep 1;90(1):87-96. PubMed PMID: 12938159.
48: Kisker O, Onizuka S, Becker CM, Fannon M, Flynn E, D’Amato R, Zetter B,
Folkman J, Ray R, Swamy N, Pirie-Shepherd S. Vitamin D binding protein-macrophage
activating factor (DBP-maf) inhibits angiogenesis and tumor growth in mice.
Neoplasia. 2003 Jan-Feb;5(1):32-40. PubMed PMID: 12659668; PubMed Central PMCID:
PMC1502120.
49: Mohamad SB, Nagasawa H, Uto Y, Hori H. Preparation of Gc protein-derived
macrophage activating factor (GcMAF) and its structural characterization and
biological activities. Anticancer Res. 2002 Nov-Dec;22(6C):4297-300. PubMed PMID:
12553073.
50: Kanda S, Mochizuki Y, Miyata Y, Kanetake H, Yamamoto N. Effects of vitamin
D(3)-binding protein-derived macrophage activating factor (GcMAF) on
angiogenesis. J Natl Cancer Inst. 2002 Sep 4;94(17):1311-9. PubMed PMID:
12208896.
51: Swamy N, Ghosh S, Schneider GB, Ray R. Baculovirus-expressed vitamin
D-binding protein-macrophage activating factor (DBP-maf) activates osteoclasts
and binding of 25-hydroxyvitamin D(3) does not influence this activity. J Cell
Biochem. 2001;81(3):535-46. PubMed PMID: 11255236.
52: Kanan RM, Cook DB, Datta HK. Lectin immunoassay for macrophage-activating
factor (Gc-MAF) produced by deglycosylation of Gc-globulin: evidence for
noninducible generation of Gc-MAF. Clin Chem. 2000 Mar;46(3):412-4. PubMed PMID:
10702530.
53: Odgren PR, Popoff SN, Safadi FF, MacKay CA, Mason-Savas A, Seifert MF, Marks
SC Jr. The toothless osteopetrotic rat has a normal vitamin D-binding
protein-macrophage activating factor (DBP-MAF) cascade and chondrodysplasia
resistant to treatments with colony stimulating factor-1 (CSF-1) and/or DBP-MAF.
Bone. 1999 Aug;25(2):175-81. PubMed PMID: 10456382.
54: Koga Y, Naraparaju VR, Yamamoto N. Antitumor effect of vitamin D-binding
protein-derived macrophage activating factor on Ehrlich ascites tumor-bearing
mice. Proc Soc Exp Biol Med. 1999 Jan;220(1):20-6. PubMed PMID: 9893164.
55: Adebanjo OA, Moonga BS, Haddad JG, Huang CL, Zaidi M. A possible new role for
vitamin D-binding protein in osteoclast control: inhibition of extracellular Ca2+
sensing at low physiological concentrations. Biochem Biophys Res Commun. 1998 Aug
28;249(3):668-71. PubMed PMID: 9731194.
56: Yamamoto N, Naraparaju VR. Structurally well-defined macrophage activating
factor derived from vitamin D3-binding protein has a potent adjuvant activity for
immunization. Immunol Cell Biol. 1998 Jun;76(3):237-44. PubMed PMID: 9682967.
57: Yamamoto N, Naraparaju VR. Immunotherapy of BALB/c mice bearing Ehrlich
ascites tumor with vitamin D-binding protein-derived macrophage activating
factor. Cancer Res. 1997 Jun 1;57(11):2187-92. PubMed PMID: 9187119.
58: Yamamoto N, Naraparaju VR, Moore M, Brent LH. Deglycosylation of serum
vitamin D3-binding protein by alpha-N-acetylgalactosaminidase detected in the
plasma of patients with systemic lupus erythematosus. Clin Immunol Immunopathol.
1997 Mar;82(3):290-8. PubMed PMID: 9073553.
59: Yamamoto N, Naraparaju VR, Urade M. Prognostic utility of serum
alpha-N-acetylgalactosaminidase and immunosuppression resulted from
deglycosylation of serum Gc protein in oral cancer patients. Cancer Res. 1997 Jan
15;57(2):295-9. PubMed PMID: 9000571.
60: Korbelik M, Naraparaju VR, Yamamoto N. Macrophage-directed immunotherapy as
adjuvant to photodynamic therapy of cancer. Br J Cancer. 1997;75(2):202-7. PubMed
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61: Benis KA, Schneider GB. The effects of vitamin D binding protein-macrophage
activating factor and colony-stimulating factor-1 on hematopoietic cells in
normal and osteopetrotic rats. Blood. 1996 Oct 15;88(8):2898-905. PubMed PMID:
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62: Yamamoto N. Structural definition of a potent macrophage activating factor
derived from vitamin D3-binding protein with adjuvant activity for antibody
production. Mol Immunol. 1996 Oct;33(15):1157-64. PubMed PMID: 9070663.
63: Yamamoto N, Naraparaju VR. Role of vitamin D3-binding protein in activation
of mouse macrophages. J Immunol. 1996 Aug 15;157(4):1744-9. PubMed PMID: 8759764.
64: Yamamoto N, Naraparaju VR, Orchard PJ. Defective lymphocyte glycosidases in
the macrophage activation cascade of juvenile osteopetrosis. Blood. 1996 Aug
15;88(4):1473-8. PubMed PMID: 8695868.
65: Yamamoto N, Naraparaju VR. A defect in inducible beta-galactosidase of B
lymphocytes in the osteopetrotic (mi/mi) mouse. Immunology. 1996
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66: Yamamoto N, Naraparaju VR, Asbell SO. Deglycosylation of serum vitamin
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1996 Jun 15;56(12):2827-31. PubMed PMID: 8665521.
67: Yamamoto N, Naraparaju VR. Vitamin D3-binding protein as a precursor for
macrophage activating factor in the inflammation-primed macrophage activation
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68: Yamamoto N, Naraparaju VR. A defect in beta-galactosidase of B lymphocytes in
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69: Yamamoto N, Naraparaju VR, Srinivasula SM. Structural modification of serum
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70: Schneider GB, Benis KA, Flay NW, Ireland RA, Popoff SN. Effects of vitamin D
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71: Naraparaju VR, Yamamoto N. Roles of beta-galactosidase of B lymphocytes and
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72: Yamamoto N, Willett NP, Lindsay DD. Participation of serum proteins in the
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73: Yamamoto N, Lindsay DD, Naraparaju VR, Ireland RA, Popoff SN. A defect in the
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74: Yamamoto N, Kumashiro R. Conversion of vitamin D3 binding protein
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action of beta-galactosidase of B cells and sialidase of T cells. J Immunol. 1993
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75: Homma S, Yamamoto M, Yamamoto N. Vitamin D-binding protein (group-specific
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1993 Aug;71 ( Pt 4):249-57. PubMed PMID: 8225394.
76: Yamamoto N, Homma S, Haddad JG, Kowalski MA. Vitamin D3 binding protein
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77: Yamamoto N, Homma S. Vitamin D3 binding protein (group-specific component) is
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78: Yamamoto N, Homma S, Millman I. Identification of the serum factor required
for in vitro activation of macrophages. Role of vitamin D3-binding protein (group
specific component, Gc) in lysophospholipid activation of mouse peritoneal
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12: Siniscalco D, Bradstreet JJ, Cirillo A, Antonucci N. The in vitro GcMAF
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13: Ikeda T, Kasai M, Tatsukawa E, Kamitakahara M, Shibata Y, Yokoi T, Nemoto TK,
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14: Thyer L, Ward E, Smith R, Branca JJ, Morucci G, Gulisano M, Noakes D,
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15: Sayegh L, Fuleihan Gel-H, Nassar AH. Vitamin D in endometriosis: a causative
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vitamin D axis: vitamin D binding protein-derived macrophage activating factor
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17: Inui T, Kuchiike D, Kubo K, Mette M, Uto Y, Hori H, Sakamoto N. Clinical
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18: Hirota K, Nakagawa Y, Takeuchi R, Uto Y, Hori H, Onizuka S, Terada H.
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19: Kuchiike D, Uto Y, Mukai H, Ishiyama N, Abe C, Tanaka D, Kawai T, Kubo K,
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containing GcMAF induces macrophage phagocytic activity and in vivo antitumor
activity. Anticancer Res. 2013 Jul;33(7):2881-5. PubMed PMID: 23780974.
20: Toyohara Y, Hashitani S, Kishimoto H, Noguchi K, Yamamoto N, Urade M.
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21: Bellone M, Rigamonti N. Vitamin D-binding protein-derived
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22: Uto Y, Yamamoto S, Mukai H, Ishiyama N, Takeuchi R, Nakagawa Y, Hirota K,
Terada H, Onizuka S, Hori H. β-Galactosidase treatment is a common first-stage
modification of the three major subtypes of Gc protein to GcMAF. Anticancer Res.
2012 Jun;32(6):2359-64. PubMed PMID: 22641675.
23: Pacini S, Punzi T, Morucci G, Gulisano M, Ruggiero M. Effects of vitamin
D-binding protein-derived macrophage-activating factor on human breast cancer
cells. Anticancer Res. 2012 Jan;32(1):45-52. PubMed PMID: 22213287.
24: Pacini S, Morucci G, Punzi T, Gulisano M, Ruggiero M, Amato M, Aterini S.
Effect of paricalcitol and GcMAF on angiogenesis and human peripheral blood
mononuclear cell proliferation and signaling. J Nephrol. 2012
Jul-Aug;25(4):577-81. doi: 10.5301/jn.5000035. PubMed PMID: 21956771.
25: Uto Y, Yamamoto S, Takeuchi R, Nakagawa Y, Hirota K, Terada H, Onizuka S,
Nakata E, Hori H. Effect of the Gc-derived macrophage-activating factor precursor
(preGcMAF) on phagocytic activation of mouse peritoneal macrophages. Anticancer
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26: Debruyne E, Speeckaert M, Weygaerde YV, Delanghe J. Phenotype of Gc-globulin
influences the macrophage activating factor (MAF) levels in serum. Clin Chem Lab
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27: Pacini S, Morucci G, Punzi T, Gulisano M, Ruggiero M. Gc protein-derived
macrophage-activating factor (GcMAF) stimulates cAMP formation in human
mononuclear cells and inhibits angiogenesis in chick embryo chorionallantoic
membrane assay. Cancer Immunol Immunother. 2011 Apr;60(4):479-85. doi:
10.1007/s00262-010-0953-7. Epub 2010 Dec 14. PubMed PMID: 21170647.
28: Faserl K, Golderer G, Kremser L, Lindner H, Sarg B, Wildt L, Seeber B.
Polymorphism in vitamin D-binding protein as a genetic risk factor in the
pathogenesis of endometriosis. J Clin Endocrinol Metab. 2011 Jan;96(1):E233-41.
doi: 10.1210/jc.2010-1532. Epub 2010 Oct 27. PubMed PMID: 20980430.
29: Gregory KJ, Zhao B, Bielenberg DR, Dridi S, Wu J, Jiang W, Huang B,
Pirie-Shepherd S, Fannon M. Vitamin D binding protein-macrophage activating
factor directly inhibits proliferation, migration, and uPAR expression of
prostate cancer cells. PLoS One. 2010 Oct 18;5(10):e13428. doi:
10.1371/journal.pone.0013428. PubMed PMID: 20976141; PubMed Central PMCID:
PMC2956649.
30: Nonaka K, Onizuka S, Ishibashi H, Uto Y, Hori H, Nakayama T, Matsuura N,
Kanematsu T, Fujioka H. Vitamin D binding protein-macrophage activating factor
inhibits HCC in SCID mice. J Surg Res. 2012 Jan;172(1):116-22. doi:
10.1016/j.jss.2010.07.057. Epub 2010 Sep 17. PubMed PMID: 20855083.
31: Ravnsborg T, Olsen DT, Thysen AH, Christiansen M, Houen G, Højrup P. The
glycosylation and characterization of the candidate Gc macrophage activating
factor. Biochim Biophys Acta. 2010 Apr;1804(4):909-17. doi:
10.1016/j.bbapap.2009.12.022. Epub 2010 Jan 13. PubMed PMID: 20079467.
32: Rehder DS, Nelson RW, Borges CR. Glycosylation status of vitamin D binding
protein in cancer patients. Protein Sci. 2009 Oct;18(10):2036-42. doi:
10.1002/pro.214. PubMed PMID: 19642159; PubMed Central PMCID: PMC2786967.
33: Fang Y, van Meurs JB, Arp P, van Leeuwen JP, Hofman A, Pols HA, Uitterlinden
AG. Vitamin D binding protein genotype and osteoporosis. Calcif Tissue Int. 2009
Aug;85(2):85-93. doi: 10.1007/s00223-009-9251-9. Epub 2009 Jun 2. PubMed PMID:
19488670; PubMed Central PMCID: PMC2729412.
34: Yamamoto N, Ushijima N, Koga Y. Immunotherapy of HIV-infected patients with
Gc protein-derived macrophage activating factor (GcMAF). J Med Virol. 2009
Jan;81(1):16-26. doi: 10.1002/jmv.21376.
35: Yamamoto N, Suyama H, Yamamoto N. Immunotherapy for Prostate Cancer with Gc
Protein-Derived Macrophage-Activating Factor, GcMAF. Transl Oncol. 2008
Jul;1(2):65-72. PubMed PMID: 18633461; PubMed Central PMCID: PMC2510818.
36: Spiriti J, Bogani F, van der Vaart A, Ghirlanda G. Modulation of protein
stability by O-glycosylation in a designed Gc-MAF analog. Biophys Chem. 2008
May;134(3):157-67. doi: 10.1016/j.bpc.2008.02.005. Epub 2008 Feb 21. PubMed PMID:
18329161.
37: Yamamoto N, Suyama H, Nakazato H, Yamamoto N, Koga Y. Immunotherapy of
metastatic colorectal cancer with vitamin D-binding protein-derived
macrophage-activating factor, GcMAF. Cancer Immunol Immunother. 2008
Jul;57(7):1007-16. Retraction in: Cancer Immunol Immunother. 2014
Dec;63(12):1349. PubMed PMID: 18058096.
38: Yamamoto N, Suyama H, Yamamoto N, Ushijima N. Immunotherapy of metastatic
breast cancer patients with vitamin D-binding protein-derived macrophage
activating factor (GcMAF). Int J Cancer. 2008 Jan 15;122(2):461-7. Retraction in:
Int J Cancer. 2014 Sep 15;135(6):1509. PubMed PMID: 17935130.
39: Meier U, Gressner O, Lammert F, Gressner AM. Gc-globulin: roles in response
to injury. Clin Chem. 2006 Jul;52(7):1247-53. Epub 2006 May 18. Review. PubMed
PMID: 16709624.
40: Kalkunte S, Brard L, Granai CO, Swamy N. Inhibition of angiogenesis by
vitamin D-binding protein: characterization of anti-endothelial activity of
DBP-maf. Angiogenesis. 2005;8(4):349-60. Epub 2006 Jan 7. PubMed PMID: 16400520.
41: Yamamoto N, Urade M. Pathogenic significance of
alpha-N-acetylgalactosaminidase activity found in the hemagglutinin of influenza
virus. Microbes Infect. 2005 Apr;7(4):674-81. Epub 2005 Mar 22. PubMed PMID:
15848273.
42: Nagasawa H, Sasaki H, Uto Y, Kubo S, Hori H. Association of the macrophage
activating factor (MAF) precursor activity with polymorphism in vitamin D-binding
protein. Anticancer Res. 2004 Sep-Oct;24(5C):3361-6. PubMed PMID: 15515432.
43: Onizuka S, Kawakami S, Taniguchi K, Fujioka H, Miyashita K. Pancreatic
carcinogenesis: apoptosis and angiogenesis. Pancreas. 2004 Apr;28(3):317-9.
PubMed PMID: 15084979.
44: Matsuura T, Uematsu T, Yamaoka M, Furusawa K. Effect of salivary gland
adenocarcinoma cell-derived alpha-N-acetylgalactosaminidase on the bioactivity of
macrophage activating factor. Int J Oncol. 2004 Mar;24(3):521-8. PubMed PMID:
14767536.
45: Schneider GB, Grecco KJ, Safadi FF, Popoff SN. The anabolic effects of
vitamin D-binding protein-macrophage activating factor (DBP-MAF) and a novel
small peptide on bone. Crit Rev Eukaryot Gene Expr. 2003;13(2-4):277-84. PubMed
PMID: 14696974.
46: Mohamad SB, Nagasawa H, Sasaki H, Uto Y, Nakagawa Y, Kawashima K, Hori H. Gc
protein-derived macrophage activating factor (GcMAF): isoelectric focusing
pattern and tumoricidal activity. Anticancer Res. 2003 Nov-Dec;23(6a):4451-7.
PubMed PMID: 14666733.
47: Gumireddy K, Reddy CD, Swamy N. Mitogen-activated protein kinase pathway
mediates DBP-maf-induced apoptosis in RAW 264.7 macrophages. J Cell Biochem. 2003
Sep 1;90(1):87-96. PubMed PMID: 12938159.
48: Kisker O, Onizuka S, Becker CM, Fannon M, Flynn E, D’Amato R, Zetter B,
Folkman J, Ray R, Swamy N, Pirie-Shepherd S. Vitamin D binding protein-macrophage
activating factor (DBP-maf) inhibits angiogenesis and tumor growth in mice.
Neoplasia. 2003 Jan-Feb;5(1):32-40. PubMed PMID: 12659668; PubMed Central PMCID:
PMC1502120.
49: Mohamad SB, Nagasawa H, Uto Y, Hori H. Preparation of Gc protein-derived
macrophage activating factor (GcMAF) and its structural characterization and
biological activities. Anticancer Res. 2002 Nov-Dec;22(6C):4297-300. PubMed PMID:
12553073.
50: Kanda S, Mochizuki Y, Miyata Y, Kanetake H, Yamamoto N. Effects of vitamin
D(3)-binding protein-derived macrophage activating factor (GcMAF) on
angiogenesis. J Natl Cancer Inst. 2002 Sep 4;94(17):1311-9. PubMed PMID:
12208896.
51: Swamy N, Ghosh S, Schneider GB, Ray R. Baculovirus-expressed vitamin
D-binding protein-macrophage activating factor (DBP-maf) activates osteoclasts
and binding of 25-hydroxyvitamin D(3) does not influence this activity. J Cell
Biochem. 2001;81(3):535-46. PubMed PMID: 11255236.
52: Kanan RM, Cook DB, Datta HK. Lectin immunoassay for macrophage-activating
factor (Gc-MAF) produced by deglycosylation of Gc-globulin: evidence for
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10702530.
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