sunnuntai 6. joulukuuta 2015

Dr. Bradstreet found dead in a river - Gc MAF treatment a highly effective macrophage activating therapy


Three days before Dr. Bradstreet was found dead in a river, U.S. govt. agents raided his research facility to seize a breakthrough cancer treatment called GcMAF

Dr Jeffrey Bradstreet, whose body was found floating in a North Carolina river on June 19, had successfully treated over 2,000 autistic children with GcMAF.
He believed that many of these children had been damaged by immunizations…he is also one of a number of doctors who have recently been found dead under suspicious circumstances.
On June 16, three days before his body was found, the FDA obtained a search and seizure order and agents raided his Georgia medical clinic to seize the breakthrough treatment. (See video below)
(NaturalNews) The history of the suppression of medical science in America is a long one, filled with true accounts of pioneering doctors and clinicians being threatened, intimidated and even assassinated in order to bury emerging cures and keep the "sick care" industry in control. (The American Medical Association, for example, has been found guilty by the U.S. federal courts of a conspiracy to destroy the chiropractic industry, by the way.)

Over the last few days, we've learned that before being found shot in the chest and floating in the river, pioneering medical researcher Dr. Bradstreet was working with a little-known molecule that occurs naturally in the human body. Called, "GcMAF", this molecule has the potential to be a universal cancer cure for many people. It has also been shown to reverse signs of autism in the vast majority of patients receiving the treatment.

While GcMAF is perfectly legal as a treatment in dozens of advanced nations around the world, the U.S. Food and Drug Administration has outlawed it, calling it an "unapproved drug." It is with this designation -- an effort to suppress the forward progress of medical science -- that the U.S. government conducted a raid on Dr. Bradstreet's clinic, specifically seeking to confiscate GcMAF in order to shut down his research and halt his treatment of patients. Meanwhile, Big Pharma gets special permission to unleash untested, experimental drugs on the public as long as those drugs earn sufficient profits.

In this article, I summarize the videos, articles and documents covering GcMAF and the mysterious death of Dr. Bradstreet. An exhaustive investigation needs to be pursued on this matter, possibly involving private investigators. The timing and manner of Dr. Bradstreet's death seems highly suspicious, especially in light of the many other holistic doctors who have recently been found dead under mysterious circumstances. (Dr. Nicholas Gonzalez died just days ago...)

Motive to murder medical researchers and suppress a promising cancer treatment breakthrough

Is there a motive for the murder of pioneering cancer researchers working on a possible universal cancer cure? Of course there is... it's the most common motive in the world: MONEY.

A universal cancer cure would destroy the profitability of the highly lucrative cancer industry and collapse the American Cancer Society, hospitals, oncology clinics and pharmaceutical companies that depend on chemotherapy revenues to stay profitable. Key to their profitability is the inescapable fact that conventional cancer treatments simply don't work most of the time, creating a reliable profit stream of repeat business from patients who are never cured (by design).

Would the cancer industry murder doctors to protect its profits? Of course it would. The industry kills patients as a routine part of its business operations! For example, an oncologist named Farid Fata was recently sentenced to 56 years in prison for falsely diagnosing patients with cancer so that he could sell them chemotherapy treatments they didn't need. See the article Cancer doctors 'fess up to making false diagnoses just to make more money.

Click here to search for "cancer false diagnosis" at, the search engine for truth seekers.

INVESTIGATION: Here's what we know so far

Video detailing the Dr. Bradstreet search warrant, served June 30, during which the U.S. government seized GcMAF from Dr. Bradstreet's research clinic:

HealthNutNews story that covers the apparent series of murders of holistic doctors, many of whom are working on advanced treatment protocols that render high-profit sectors of conventional medicine OBSOLETE:

Yet another doctor was just found murdered inside his home here on the East Coast of Florida. This makes six doctors to be found dead in the last month just from this region of the country alone. Four out of the six were found dead here in Florida. We lost the holistic Dr. Teresa Sievers, MD, who was found murdered in her Florida home just weeks ago. We've also lost the alternative Dr. Jeff Bradstreet, MD, who was found in a river with a gunshot to his chest. He'd recently moved to Georgia from Florida. We've also lost the Osteopath. Dr. Riley, who was found in Georgia at her home; just a few hours from the Florida border. She was found with a gunshot wound to her head.

Now we've lost Dr. Schwartz MD, who was found murdered in his home, on Sunday, July 19th, 2015. This was four weeks to the day after the death of the first physician: (Dr. Bradstreet MD) who I broke the story on a month ago. His family is still seeking answers as to what happened to him and they're some of the kindest people I know. The latest MD, Dr. Schwartz, in the picture above, lived just north of the fit, healthy, holistic Dr. Hedendal; who was the second doctor to be found dead this past Father's Day, in Boca Raton. This was the same day that Dr. Holt died at the age of 33. Both were fathers; and again, both men died here in Florida on June 21st, 2015. entry describing the extraordinary benefits of GcMAF in a published study:

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...

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.

In other words, the administration of GcMAF eradicated tumors and left patients cancer-free for 4+ years with no additional treatment!

Both U.S. and UK governments desperately seizing all supply, shutting down clinics, even as millions die from cancer every decade...

UK govt. admission that GcMAF was on track to being commercialized as a pioneering cancer treatmentso they had to confiscate it!

GcMAF (Globulin component Macrophage Activating Factor), a blood product, claims to treat a range of conditions including cancer, HIV and autism...

More than 10,000 vials were seized at this site and production of this unlicensed medicine has now ceased. These products were sold through various European websites and UK patients may have bought it from one of these websites. We are working with colleagues in other countries to alert them to the potential risks. Our investigations are ongoing and we have received no reports to date of side effects caused by this product.

Learn more:

GcMAF (Gc Protein derived Macrophage Activating Factor) - Gc MAF treatment is a highly effective macrophage activating therapy, used to stimulate the immune system and activate macrophages so that they can destroy cancer cells and other abnormal cells in the body.

From the FAQ page of the treatment clinic:

What exactly is Second Generation GcMAF?
High Dose Second Generation Gc-MAF is produced using our new Patent Pending process which was developed here in Japan by Saisei Mirai in collaboration with Dr Hitoshi Hori and Dr Yoshihiro Uto at the University of Tokushima who have been studying GcMAF for over 20 years. Studies on GcMAF began at the University of Tokushima in 1992, after they were introduced to Dr Nobuto Yamamoto's work and a collaboration began...

Second Generation GcMAF is made using a new and improved 2nd generation method of Gc-MAF production which is 10-20 times more concentrated and is more active and stable than other GcMAF that is currently available. Importantly, this much higher concentration GcMAF has been clinically demonstrated to be largely free of any side effects in the great majority of patients and is much more stable because it is resistant to oxidation.

That same site describes Oral GcMAF as follows: "Oral GcMAF is a form of GcMAF produced from bovine colostrum by Saisei Mirai which was developed in collaboration with Tokushima University."

It also lists the following health conditions as being treatable with GcMAF, potentially a "universal cancer cure" substance:

Gc-MAF and/or oral Colostrum MAF macrophage activation therapy is indicated in the treatment of any diseases where there is immune dysfunction or where the immune system is compromised, such as:

  • Cancer
  • Autoimmune diseases
  • Epstein-Barr Virus (EBV)
  • Hepatitis B virus (HBV)
  • Herpes Simplex virus (HSV)
  • Cystitis
  • Hepatitis C virus (HCV)
  • Multiple sclerosis (MS)
  • Urinary tract infection (UTI)
  • Autism Spectrum Disorders (ASD)
  • Rheumatoid arthritis (RA)
  • Endometriosis
  • Chronic Fatigue Syndrome (CFS)
  • Lyme disease (Lyme borreliosis)
  • IgA deficiency disorder
  • Myalgic Encephalomyelitis (ME)
  • Mycobacteria infections
  • Parkinson's disease
  • Tuberculosis
  • Fibromyalgia
  • Human papillomavirus (HPV)
  • Lupus (Systemic lupus erythematosus, SLE)
  • Dengue fever
  • Pneumonia infection
  • Warts caused by viral infection
  • Norovirus
  • Malaria Influenza virus (flu)
  • Herpes simplex virus (HSV)
  • Q fever (Coxiella burnetii)
  • Polycystic ovary syndrome (PCOS)
  • Chicken pox (varicella zoster virus)
  • Psoriasis
  • Respiratory tract infections
  • Ulcerative colitis, Crohn's disease
  • Type 1 diabetes (T1DM), insulin-dependent diabetes (IDDM)
  • Type 1.5 diabetes, Latent autoimmune diabetes of adults (LADA)

Do you see yet why the medical establishment must SUPPRESS GcMAF and destroy all knowledge of its clinical applications? This one substance holds the potential to render numerous vaccines and pharmaceuticals utterly obsolete.

GcMAF protein described at

Researchers and practitioners have demonstrated that GcMAF can reverse diseases that attack the immune system such as: chronic inflammation, bacterial and viral infections, chronic herpes, chronic acne, Lyme disease, fibromyalgia osteoporosis, Hodgkin's, Lupus, MS, Parkinson's and remarkably – autism.

A clinical study out of Italy on 94 children with autism showed that 83 of them made considerable progress while on GcMAF. The most common reported improvements involve:

• Cognitive abilities including attention and focus, learning and understanding, receptiveness and awareness of the environment and both receptive and expressive language gains.

• Social Skills including willingness to interact and communicate with peers.

• Behavior including less hyperactivity, less stereotypical behaviors and improved cooperation and compliance.

In another study of 1500 children with autism, 85% had high levels of viruses and a compromised immune system. All 1500 received weekly GcMAF injections and 70% of the children responded to the treatment with reduced symptoms and another 15% made full recoveries. The other 15% did not respond.

It was stated that the reduction of autistic symptoms is permanent provided that GcMAF has been taken long enough for the body to produce its own GcMAF which typically takes 24 weeks.

The systematic suppression of medical science to protect the lucrative cancer treatment industry (chemotherapy, oncology, radiotherapy, etc.) covers the systematic suppression of advanced cancer treatments and cures:

Back in 1993, Nobuto Yamamoto, then working at Temple University School of Medicine in Philadelphia, PA, USA, first described a remarkable molecule. His paper reported the conversion of vitamin D3 binding protein (DBP, known in humans as Gc) into a potent macrophage-activating factor (MAF), known as Gc-MAF. Macrophages are a key part of the human immune system with two roles: to engulf and destroy pathogens and cellular debris, and to recruit other immune cells to respond to the pathogen.

Gc-MAF hasn't had the benefit of a single patent owner – as a natural molecule, it cannot be patented without being modified – with the will and resources to push it under the noses of the public and health authorities. Dr Yamamoto has run small human trials in breast, prostate and colorectal cancers, with promising results.

David Noakes might just be the person to bring Gc-MAF into the mainstream. He's the CEO of Immuno Biotech Ltd. and spokesperson for First Immune Gc-MAF, a project he describes as, "PhD and BSc biochemists and biomedical scientists... with external doctors, oncologists and scientists who kindly provide advice, committed to bringing some of the increasing number of published but relatively unused medical cures to as many people as we can." At the moment, Noakes and his colleagues are supplying Gc-MAF to 30 countries where it is legal, via a network of "around 300" doctors. Their Gc-MAF is made to extremely high standards, and is being used in ongoing clinical research by Noakes' collaborators and others. Their ultimate goal is to, "Build the case that GcMAF is effective for various illnesses, which will help to make it available to the public".

GcMAF suppliers fighting for survival against a global medical monopoly that profits from disease

MUST-SEE website:

From the site:

The medical laws have been changed over the last 40 years so that all the brilliant breakthroughs in cancer are denied to the British public. Lord Maurice Saatchi had to watch his wife die, while his doctor told him the only thing he was allowed to prescribe her was chemotherapy, which would shorten her life. He hopes to bring the Medical Innovation Bill to Parliament, so instead of obeying a destructive government law, a doctor will be able to prescribe whatever treatment is best for the patient...

Bad law kills, and Britain has the worst medical laws in Europe. The 1939 Cancer Act makes it illegal to discuss the possibility cancer can be cured, which is partly why 160,000 people die unnecessarily of cancer in Britain every year. Science and treatments are decades ahead of where the medical industry is today. The MHRA's job is to get life saving treatments like GcMAF out to people as quickly as possible. Instead they block them to protect billion dollar Big Pharma monopolies, who also fund the MHRA. Over a hundred thousand lives could be saved every year if the 1939 Cancer Act were repealed, and the MHRA were closed down.

There are 142 eminent scientists who have published GcMAF research papers on the US National Library of Medicine alone.

From the how GcMAF works page:

Your GcMAF empowers your body to cure itself. In a healthy person your own GcMAF has 11 actions discovered so far, including two on cells, three excellent effects on the brain, and 6 on cancer. Amongst these it acts as a "director" of your immune system. But viruses and malignant cells like cancer send out an enzyme called Nagalase that prevents production of your GcMAF: that stops its 11 beneficial effects, and neutralises your immune system. So diseases become chronic, and cancer cells grow unchecked.

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 under "Treatment Protocol" on this website.

What is GcMAF?
It is a human protein. One week's GcMAF looks like a small raindrop. If properly produced it is perfectly sterile, and a most ethical course for doctors.

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.

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.) One GcMAF has been tested in universities, laboratories and clinics, where, as a result of the testing, consistent activity and sterility have always been found, and been the subject of 40 scientific research papers.

What does GcMAF do?
The GcMAF Conference 2013 showed GcMAF is a far more powerful molecule than thought, both in terms of the science, and doctors' results. 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 tumour cancers including breast, lung, prostate, pancreatic and melanoma.

GcMAF can eradicate chronic inflammation and viral infections. It is better than antibiotics in many areas, and 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. Research shows GcMAF can halt deterioration in Parkinsons, multiple sclerosis (MS), dementia and ALS, and in its role of immune system regulator, can reverse diseases that attack the immune system like Lupus and Arthritis. And is effective with wound healing. Its successful with tumour cancers, and some others.

In addition to rebuilding a depressed immune system, GcMAF:
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).

See the 31 research papers published, particularly Brescia, and the 60 published by others listed under "The science".

Learn more:

 Pharma & Healthcare
The Little Black Book of Billionaire Secrets

Here's Why Authorities Searched The Offices Of Controversial Autism Doctor Bradstreet

According to a federal government warrant, the offices of controversial autism doctor Jeff Bradstreet were the target in June of a search related to an experimental drug for autism.
The compound, globulin component macrophage-activating factor, known as GcMAF, is one that Bradstreet reportedly used in “over 2000 children” with autism.
Bradstreet, according to authorities in Rutherford County, NC, committed suicide there on June 19, after the search warrant was executed in late June.
According to the copy of the warrant provided to me by the United States Attorney’s Office of the Northern District of Georgia, the search warrant was executed at Bradstreet’s Buford, GA, ‘wellness center’ because authorities were seeking information related to “evidence of a crime and contraband, fruits of crime, or items illegally possessed” associated with violations of interstate commerce statutes covering food, drug, or other products that are “adulterated or misbranded” and with “frauds and swindles” by “wire, radio, or television.”

Punishments for those convicted of these crimes can include fines and up to 20 years in prison.
The warrant specifically references GcMAF and any records related to sale, shipping, billing, and delivery of GcMAF. It also covers Bradstreet’s financial records and Internet activities.
GcMAF is thought in some circles to modulate the immune system in ways that make it a treatment for everything from autism (which some believe is immune related) to cancer. Bradstreet was the focus of GcMAF and autism in online communities, with discussions centered around “doing the GcMAF through Bradstreet” in online forums.
One forum references a link to Bradstreet’s blog as having “several posts” related to GcMAF, but a search of the site in its current iteration turns up no GcMAF-related hits - (ETA: Those posts apparently were deleted, but you can read some of at these links herehereherehere, and here).
At least some users who discussed doing GcMAF treatments through Bradstreet appear to have been US based and discussed traveling to his offices for the shots. The shots appear to have cost about $50 each.
Bradstreet’s name and GcMAF for autism are closely linked in online searches. He also published a paper in a now-defunct journal on the subject, and a video of Bradstreet talking about using GcMAF for autism is available on YouTube.

Three studies related to GcMAF as a treatment for everything from autism to cancer have been retracted in the last year, and the UK government issued a warning about the manufacture of GcMAF after discovering that one factory producing the protein was using plasma marked, “not to be administered to humans or used in any blood products,” according to the research publication watchdog site Retraction Watch.
Bradstreet’s death has led to a swirl of online speculationabout a conspiracy to murder alternative medicine practitioners, fueled by reports of the murder of Florida doctor Teresa Sievers, who is described as being known for her work with transgender patients, and the death of another Florida doctor, Bruce Hedendal, 67, who was found dead in his car, reportedly of natural causes.
Hedendal reportedly served a prison term in the early 2000s for tax evasion. Bradstreet also had Florida ties.A Bradstreet family member has set up a GoFundMe campaign site “to find the answers to the many questions leading up to the death of Dr Bradstreet,” and I have reached out through the site to that family member for comment.
I am a journalist and biologist. My book, The Informed Parent, with co-author Tara Haelle, is available for pre-order. Read more about me here and find me (too often) onTwitter.

Logo of oncoimmun

Oncoimmunology. 2013 Aug 1; 2(8): e25769.
Published online 2013 Jul 29. doi:  10.4161/onci.25769
PMCID: PMC3812199

GC protein-derived macrophage-activating factor decreases α-N-acetylgalactosaminidase levels in advanced cancer patients



α-N-acetylgalactosaminidase (nagalase) is known to accumulate in the serum of cancer patients, where it mediates the deglycosylation of group-specific component (GC), best known as vitamin D-binding protein (VDBP), which is the precursor of GC protein-derived macrophage-activating factor (GcMAF).
Deglycosylated VDBP cannot be converted into GcMAF and decreased GcMAF levels reportedly promote immunodeficiency in individuals bearing advanced neoplasms. 

The increase in nagalase activity observed in cancer patients is mostly due to the fact that malignant cells release enzymatically active nagalase. 

Thus, serum nagalase activity reflects not only tumor burden and aggressiveness, but also the clinical progression of the disease.
- Nowadays, the assessment of serum nagalase activity is proposed as a reliable means to determine the clinical severity of multiple neoplasms.
In serum, nagalase acts as an endo- (but not as an exo-) enzyme, being unable to deglycosylate an N-acetylgalactosamine (GalNAc) residue of GcMAF. Thus, circulating nagalase cannot degrade exogenous GcMAF.- This observation suggested that patients with elevated nagalase activity may benefit from the exogenous provision of GcMAF. Alongside, GcMAF was observed to exert multiple anticancer effects in vivo and in vitro, both in experimental and in spontaneous tumor models. Given the impact of GcMAF on macrophages and their central role anticancer immune responses, GcMAF is widely considered as an immunotherapeutic agent.
However, in addition to stimulating tumor-infiltrating macrophages, GcMAF not only directly inhibits the proliferation of various human cancer cells in vitro,, but also reverts the malignant phenotype of human breast cancer cells.
Moreover, GcMAF reportedly
inhibits angiogenesis, thus depriving neoplastic lesions of the oxygen and nutrient supplies that are needed for tumor progression and metastasis.-
Recently, it has been proposed that the antineoplastic effects of GcMAF are
mediated by the vitamin D receptor (VDR), and it was demonstrated that GcMAF stimulates an intracellular signaling pathway impinging on cyclic AMP. This signal transduction cascade could actually be responsible for death of malignant cells exposed to GcMAF

Taken together, these in vitro and in vivo findings lend a rationale to the observation that GcMAF exert dramatic anticancer effects in (at least a fraction of) patients with advanced cancer.-
Of note, in the aforementioned studies, the anticancer effects of GcMAF were evaluated by measuring serum nagalase activity as a marker of tumor burden and progression.
The biological effects of GcMAF have been documented in a variety of experimental systems and make the subject of more than 50 peer-reviewed papers published during the past 20 y. 

Because of the solid scientific rationale underlying the compassionate use of GcMAF in advanced cancer patients, hundreds of physicians in all parts of the world have adopted this approach for a variety of indications in which it could prove useful.

Here, we present a series of clinical cases exemplifying the results that have been obtained with the administration of GcMAF to patients with diverse types of advanced cancers, with a particular focus on the effects of GcMAF on serum nagalase activity. We are well aware that these cases, because of their heterogeneity and reduced number, can be considered anecdotal. However, a very recent study on the evaluation of clinical practice strongly encourages the re-evaluation of individual cases such as those presented here. Thus, while some studies present large and impressive statistics obtained from large clinical cohorts, others may report a limited number of noteworthy cases, as we do here. According to this novel, authoritative, epistemological approach, “all of these stories become evidence of what works in medicine.”Therefore, we believe that the clinical cases reported below point to beneficial effects for the administration of GcMAF to advanced cancer patients, prompting further studies to formally address this possibility.


The mean pre-GcMAF treatment serum nagalase activity documented in our patient cohort was 2.84 ± 0.26 nM/min/mg, with a range of 1.00–5.60 nM/min/mg (Table 1). At the time of second testing (average interval = 112 d), the mean serum nagalase activity in the course of GcMAF treatment was 2.01 ± 0.22 nM/min/mg, with a range of 1.00–3.20 nM/min/mg. The difference between these values was statistically significant (p < 0.05). Of note, no patient of this cohort was initially observed to be within the laboratory reference range for serum nagalase activity (0.90–0.92 nM/min/mg). At the time of final testing (average interval = 263 d), the mean serum nagalase activity of the patient cohort was 1.59 ± 0.17 nM/min/mg, with a range of 0.60–2.80 nM/min/mg. The difference between this value and the serum nagalase activity recorded before the initiation of GcMAF treatment was also statistically significant (p < 0.01).
Table thumbnail
Table 1. Nagalase levels before and after GcMAF therapy*

Narrative description of some notable clinical cases from The Netherlands

The following reports were collected and communicated by Dr. Steven Hofman (CMC, Capelle aan den Ijssel; The Netherlands) and refer to the years 2011–2012. In addition to GcMAF, most patients were prescribed supplementation of vitamins D and A. Additional supplements are indicated when assumed. Most of the patients did not assume conventional anticancer chemotherapy along with GcMAF. However, several patients had been subjected to conventional anticancer therapies in the previous years, as indicated in individual reports. When patients assumed conventional therapeutics, such as hormones, in the course of GcMAF administration (e.g., patient #8), this is indicated in the individual report. When not indicated otherwise, patients received 100 ng GcMAF weekly, as a single intramuscular injection, in line the commonly accepted recommendations.- Original reports are in italics. Each case is referred to with progressive numbers, as in Table 1.
In Figure 1, the decrease of serum nagalase activity in the patient cohort is plotted in function of the consecutive testing. Of note, since this is a retrospective analysis and not a clinical trial, nagalase determinations were not performed at the same time point in each individual patient. The overall shape of the graph, however, is very similar if not completely superimposable to that of other graphs of the same type that have previously been reported.-,
figure onci-2-e25769-g1
Figure 1. Time course of GcMAF treatment in 7 cancer patients with serum nagalase activity as a prognostic index. Data correspond to the patients described in the section “Narrative description of some notable clinical cases from The Netherlands.” ...
2. Male, born 1950. Carcinoma of the urine-bladder since 2009, previously treated with chemo-solutions locally. Nagalase level at presentation on July 4, 2011: 3.10. February 10, 2012: 2.30. May 25, 2012: 1.80. October 26, 2012: 1.40. Treatment with GcMAF and acupuncture, later GcMAF only (later intravenous route). Bladder considered clean by urologist in summer 2012. GcMAF-treatment continued. In this case, the consistent decrease in serum nagalase activity was associated with a significant clinical improvement. The drop in nagalase activity was evident at the first post-treatment testing, about 7 mo after the initiation of GcMAF treatment, and persisted until the last available determination, i.e., about 15 mo thereafter. The difference in serum nagalase activity as recorded before at last determination and before the initiation of GcMAF therapy was -1.70 nM/min/mg.
3. Female, born 1944. Bladder carcinoma treated since 2011 by urologist with curettage and BCG. Nagalase level at presentation on May 9, 2011: 4.10. October 24, 2011: 2.30. April 3, 2012: 1.40. September 10, 2012: 1.00. December 4, 2012: 0.75. During the nagalase testing period the Patient was advised to inject intramuscular GcMAF weekly, but the Patient was not consistent. The bladder was considered in good condition on several occasions this period by the treating urologist. Also in this case, a consistent decrease in serum nagalase activity was associated with a significant clinical improvement. Such a decrease in nagalase activity was evident at the first post-treatment testing, about 5 mo after the initiation of GcMAF treatment, and persisted until the last available determination, i.e., about 19 mo thereafter. The difference in serum nagalase activity as recorded before at last determination and before the initiation of GcMAF therapy was -3.35 nM/min/mg. The last available value of serum nagalase activity, 0.75 nM/min/mg, was within the normal range.
8. Male, born 1937. Prostate carcinoma found by PSA in 2009, no specific complaints. Treated by hormone-injections, which gave complaints. Before and in the same year colon carcinoma was found, and operated after irradiation and chemotherapy (no untreated tumor/metastases probable). Nagalase level at presentation on April 6, 2011: 2.00. August 29, 2011: 1.20. January 5, 2012: 0.81. July 5, 2012: 0.67. December 6, 2012: 0.75. Treatment with acupuncture and GcMAF; after some time, the hormone treatment was discontinued and complaints, also non-specific, improved a lot. Stays on low-frequency surveillance.Again, serum nagalase activity returned to normal values (0.75 nM/min/mg) after about 20 mo of GcMAF treatment. A decrease in nagalase activity, however, was evident already at the first test, i.e., 4 mo after the initiation of GcMAF treatment. According to the literature, the normalization of serum nagalase levels in prostate cancer patients may represent an index of tumor eradication.
9. Male, born 1948. Prostate carcinoma in 2008; prostate extirpated in 2009 with good prognosis. However aspecific reportts fatigue and pain stayed. GcMAF treatment was started, together with a few acupuncture treatments. Nagalase level at presentation on October 21, 2011: 1.90. February 2, 2012: 1.70. October 19, 2012: 1.20. Complaints decreased gradually and the injections were performed intravenously later on. The treatment continues.
10. Female, born 1947. Carcinoma of left breast (found on survey), operated with sentinel nodes in 2010, chemotherapy 4 of 6 series, no specific complaints left. Still some malaise, fatigue and sleep-disorder. Nagalase level at presentation on August 9, 2011: 1.70. January 16, 2012: 1.00. March 12, 2012: 0.72. December 11, 2012: 0.60. GcMAF-treatment (predominantly intravenous route) combined with acupuncture. GcMAF discontinued in April 2012. Aspecific complaints diminished. Patient still seen every few months. A significant decrease in serum nagalase activity could be observed after 5 mo of GcMAF treatment. Such a decrease persisted even after the interruption of GcMAF, and serum nagalase activity was normalized about 16 mo after the initiation of therapy. According to the literature, the normalization of serum nagalase activity in breast carcinoma patients may represent an index of tumor eradication.
11. Female, born 1950. Carcinoma of left breast, specific complaints, metastases probable. After local operation, irradiation of thorax, combined with chemotherapy, Herceptin-therapy. Partly complaints in association with treatments. Nagalase level at presentation on May 11, 2011: 5.60. October 6, 2011: 2.90. February 21, 2012: 1.80. October 18, 2012: 1.10. Treated with intramuscular, later intravenous GcMAF, and a few acupuncture-treatments. No further complaints (subsided in 3–6 weeks), still in intravenous GcMAF regimen. A significant decrease in serum nagalase activity could be observed approximately 5 mo after the initiation of therapy. Approximately after 17 mo of GcMAF treatment, serum nagalase levels approached normal values.
16. Male, born 1941. Larynx-carcinoma found and treated with curettage and irradiation in 2010. Hemorrhagic-recto-colitis in anamnesis, few complaints after 2005. Bladder carcinoma found in 2011, treated by local curettage and several cycles of BCG-instillations. Complaints related to tumor growth and treatments, no chemotherapy. Treatment consisted of acupuncture and GcMAF intramuscular, and later intravenous injections on a weekly basis. Nagalase level at presentation on May 16, 2011: 4.70. October 4, 2011: 2.00. February 10, 2012: 1.20. June 15, 2012: 1.00. October 23, 2012: 0.88. December 20, 2012: 0.90. During the immunotherapy with GcMAF there were interesting developments. Insisting on bladder extirpation by the urologists, coped with one change of urologist, two second opinions by a specialized cancer clinic and later by an urologist of the operation team scheduled. From the Patients side there were several favorable adjustments in lifestyle, like discontinuation of smoking and adopting a daily intake of cod-liver-oil and salvia-leaf (his own initiative). In the face of the urologists opinion I decided to give the GcMAF twice weekly over a period of six weeks. The last opinion of the treating urologist was to postpone a more final decision to February, due to a much better impression of the bladder mucosa beginning in January 2013. There is optimism in the three named actors in the current situation. In this case, a significant decrease of in serum nagalase activation following the administration of GcMAF was associated with significant clinical benefits, consistent with previous reports.

Narrative description of some notable clinical cases from the United States of America

The following reports were communicated by RE and refer to the years 2012–2013. In most patients, the weekly administration of 100 ng GcMAF i.m. was initiated in August 2012, and the first assessment of serum nagalase activity was performed immediately before the initiation of treatment. None of the patients assumed conventional anticancer chemotherapy during along with GcMAF. Here, we report only those cases for which as least two nagalase determinations were available.
1. Male, age 64. Bladder carcinoma. Nagalase level at first testing in October 2012: 2.90. In January 2013: 2.60. Improved. In this case, a decrease in serum nagalase activity could be documented in about 3 mo of GcMAF treatment and was associated with clinical improvement.
4. Female, age 60. Ovarian carcinoma. Nagalase level at first testing in June 2012: 3.30. November 2012: 2.80. CA-125 tumor marker in December 2012: 15.7. In February 2013: 19.1 Improved. The weekly administration of GcMAF resulted in a significant decrease of serum nagalase activity in about 3 mo. Such a decrease was associated with clinical benefits. These changes, however, were not (as yet) associated with a decrease in the circulating levels of cancer antigen 125 (CA-125), another tumor marker.
7. Male, age 67. Prostate carcinoma. Nagalase level at first testing in August 2012: 3.40. In December 2012: 2.80. Improved. In this case, clinical benefits were associated with a significant decrease in serum nagalase activity in about 4 mo from the initiation of GcMAF therapy. These results are consistent with the findings reported above as well as with previously described cases.
12. Male, age 63. Squamous cell carcinoma of the tongue. Nagalase level at first testing in July 2012: 3.00. In September 2012: 1.50. In December 2012: 1.00. Improved. Again, clinical improvement was associated with a significant decrease in serum nagalase activity, which approached the normal range in approximately 5 mo. To the best of our knowledge, this is the first case of a patient affected by squamous cell carcinoma of the tongue receiving GcMAF. Also patient n. Thirteen (Table 1) was treated with GcMAF for a squamous cell carcinoma of the tongue and showed a decrease in serum nagalase activity in about 3 mo.
14. Male, age 54. Colorectal cancer. Nagalase level at first testing in July 2012: 3.90. In October 2012: 2.00. Discontinued. In this case, a significant decrease of serum nagalase activity could be documented approximately 3 mo after the initiation of GcMAF therapy. We are not aware of the reasons that led to treatment discontinuation.
15. Female, age 58. Squamous cell carcinoma of the head and neck. Nagalase level at first testing in June 2012: 2.90. In July 2012: 2.70. In February 2013: 2.00. Improved. In this case, a minimal decrease in serum nagalase activity as observed after 1 mo of GcMAF administration was associated with clinical benefits.
17. Female, age 35. Squamous cell carcinoma. Nagalase level at first testing in June 2012: 1.50. In September 2012: 1.10. Discontinued. In this case, a decrease of serum nagalase activity was observed after 3 mo of GcMAF therapy. We are not aware of the reasons that led to treatment discontinuation.
18. Female, age 69. Follicular lymphoma. Nagalase level at first testing in June 2012: 1.00. In August 2012: 1.30. In January 2013: 1.20. Improved. In this case, no association between serum nagalase activity, GcMAF treatment and clinical conditions could be revealed.
19. Female, age 66. Lymphoma. Nagalase level at first testing in August 2012: 2.20. In November 2012: 1.90. Improved. In this case, a clinical improvement was associated with a significant decrease in serum nagalase activity in about 3 mo after the initiation of GcMAF treatment.


GcMAF has been shown to inhibit multiple aspects of neoplastic transformation in vitro, in a variety of tumor models.- 
The clinical cases reported here are heterogeneous and refer to patients with different types of neoplasms and at different stages of malignant progression.
These cases include cancer patients in whom the effects of GcMAF had not been described before, such as subjects bearing various types of head and neck carcinoma (including tumors of the larynx and tongue), lymphoma, oligodendrocytoma and ovarian carcinoma. In some instances, patients were simultaneously affected by multiple types of tumors, as reported in the narrative description.

In many cases, patients received GcMAF along with other complementary treatments, such as acupuncture or administration of nutritional supplements. In all cases, GcMAF therapy was initiated at late stages of tumor progression, as conventional therapies were obviously preferred at less advanced stages. Thus, most of the cases described here fall under the category of compassionate treatment.

In fact, most of these patients had undergone conventional anticancer therapy in the previous years and had referred to GcMAF treatment when conventional chemo- or radiotherapy had proven ineffective or intolerable, as described in the individual reports.
Since this is an open-label, non-controlled, retrospective analysis, caution must be employed in drawing a cause-effect relationship between treatment and clinical outcome.

However, the response to GcMAF was often relatively robust and certain trends stand out.

Trends from Dutch cases

1. All patients presented with serum nagalase activity well above the normal value, that is about 0.95 nM/min/mg.
2. All patients showed a significant decrease in serum nagalase activity following GcMAF injections.
3. In all cases, serum nagalase activity was reduced at the second assessment, and such a decrease persisted in the following determinations.
4. In 4/7 cases, serum nagalase activity returned to normal levels by the last assessment.

Trends from American cases

1. All patients, but one, presented with serum nagalase activity well above the normal value. Patient #18, indeed, presented with a serum nagalase activity that was very close to normal.
2. In most patients, a significant decrease in serum nagalase activity was observed upon the administration of GcMAF. In patient #18, such a decrease was not associated with clinical benefits, even though her serum nagalase activity was always on the low side. This lack of a strict inverse relationship between serum nagalase activity and clinical responses has been recently observed in a study describing the effects of GcMAF in autistic children. Most of these patients showed indeed a decrease in serum nagalase activity as well as a significant improvement of symptoms, but the two phenomena were not strictly correlated with each other.
A significant point that emerges from the analysis of the cases described above is the apparent absence of GcMAF-related side effects. This point, which has previously been documented in autistic children, is of great importance when GcMAF is considered for the compassionate treatment of patients with advanced or incurable diseases. As a matter of fact, in many countries, the complete absence of side effects is a prerequisite for the compassionate administration of substances that have not yet been approved by local sanitary authorities.
Obviously, these preliminary observations require a prolonged follow-up period to determine the best indications for the compassionate administration of GcMAF. As of today, GcMAF has been used (always as a compassionate therapy) with encouraging results in patients affected by virtually all types of cancers and at all stages of disease progression. However, it is tempting to hypothesize that patients bearing specific types and/or stages of malignancy might obtain consistent clinical benefits from the administration of GcMAF. Also the genetic background of patients, in particular in terms of VDR polymorphisms, might influence the individual response to GcMAF. In fact, we have recently demonstrated that the degree of response of human monocytes to GcMAF is associated with individual VDR genotypes. It can therefore be hypothesized that the antineoplastic effects of GcMAF may also be influenced by such polymorphisms.

Moreover, it should be kept in mind that the prognosis of patients affected by all types of cancers is dependent upon their nutritional and inflammatory status, which can be monitored by the Prognostic Inflammatory and Nutritional Index (PINI). The PINI score might therefore become part of the laboratory assessments performed in the course of GcMAF therapy, and - together with the assessment of serum nagalase activity testing and VDRpolymorphisms - it may assist physicians in monitoring the response of individual patient to GcMAF and adjusting doses and schedules in the course of treatment, if required. Studies investigating the impact of GCpolymorphisms on the response of cancer patients to GcMAF therapy as well as the contribution of distinct GC variants to the relative amounts of “non-inducible,” inactive GcMAF species will also be instrumental in determining the most correct approach to GcMAF administration.
The results reported here are consistent with previous results- as well as with a recent publication by Inui et al., who described three clinical cases successfully treated with combinatorial therapeutic regimens including subcutaneous or intramuscular injections of GcMAF-containing human serum. At variance with this latter study, the results presented here were obtained with highly purified GcMAF, ruling out the effects of other serum proteins that might have acted as confounding factors.
In conclusion, the clinical cases presented here reinforce the hypothesis that GcMAF could become part of anticancer immunotherapeutic regimens.

Materials and Methods

GcMAF production

Physicians obtained GcMAF from Immuno Biotech Ltd (Guernsey, UK). GcMAF was highly purified according to previously described procedures. Briefly, VDBP was isolated from purified human serum obtained from the American Red Cross, using either 25-hydroxyvitamin D3-sepharose high affinity chromatography or actin-agarose affinity chromatography. Bound material was eluted and further processed by incubation with three immobilized enzymes. The resulting GcMAF was filter sterilized. Protein content and concentration of the GcMAF solution were assayed using standard Bradford protein assay methods.At the end of the production process, GcMAF was checked for sterility in-house as well as externally, by independent laboratories. The safety and biological activity of GcMAF were tested on human monocytes,human breast cancer cells, and chick embryo chorionallantoic membranes.

Data collection

A retrospective chart review for the analysis of nagalase testing was accomplished on the initial cohort of patients seen by the clinicians (RE and Dr. Steven Hofman, CMC, Capelle aan den Ijssel; The Netherlands). All records were reviewed by physicians for confirmation of serum nagalase activity values, diagnoses, time intervals between testing, GcMAF dosing and clinical responses. The diagnosis of cancer was confirmed by other treating physicians.

GcMAF administration

The administration of GcMAF to individual patients was performed exclusively by their physicians (RE and Dr. Steven Hofman, CMC, Capelle aan den Ijssel; The Netherlands), according to the national rules and regulations. Original clinical records are conserved by the physicians, in their respective locations, as indicated. In the Results section, clinical cases are reported as close as possible to the originals notes of physicians, with minimal grammar and spelling corrections. Since each physicians used described the condition of individual patients in a different fashion, some heterogeneity in these notes has to be expected. The notes are purposely presented as they had been written so that each reader can draw her/his conclusions.

Serum nagalase activity determinations

Serum nagalase testing was performed at ELN Laboratories (Bunnik, The Netherlands) following the procedure published by Yamamoto et al. In particular, serum nagalase activity was determined by using an endpoint enzymatic assay based on a chromogenic substrate. ELN Laboratories established a reference range of 0.32–0.95 nM/min/mg of substrate based on serum samples collected from healthy volunteers, a range slightly higher than that previously reported, which was of 0.35–0.65 nM/min/mg. Further studies on elevated numbers of subjects will establish the most appropriate reference range. Irrespective of this issue, since all determinations were performed in the same laboratory, a relative decrease of in serum nagalase activity following GcMAF administration was used as an index of therapeutic efficacy.

Statistical methods

Statistical comparisons between the serum nagalase activity observed before and after (at two distinct time points) the administration of GcMAF were performed by Student’s t-tests.


The Authors wish to thank Dr. Steven Hofman, CMC, Capelle aan den Ijssel, The Netherlands, for providing the data concerning the patients he treated as well as for critical review of this study.

Disclosure of Potential Conflicts of Interest

DN is the CEO of Immuno Biotech Ltd (the company isolating and purifying the GcMAF protein). However, DN had no knowledge of the therapies being used nor of the names of any patients whose data were being analyzed. Neither he, nor any employee of Immuno Biotech Ltd, had any knowledge of the nagalase or other test results or the patient names used in this study.

See Also - katso myös: 
  1. Elevated enzyme found in most cancer patients, could GcMAF be the cure?
  2. How GcMAF Works - Pre-clinical trials & what we have learnt
  4. GcMAF immunotherapy: It's all about activating macrophages to do their work
  5. GcMAF macrophage activation therapy FAQ
  6. Goleic protein - vitamin supplement therapy
  7. GcMAF: The Latest Discovery in Natural Cancer Treatments
  8. GOLEIC the vitamin D binding protein destroying cancer at any stage and many other diseases



BCGbacillus Calmette-Guérin
CA-125cancer antigen 125
GcMAFGC protein-derived macrophage-activating factor
PINIprognostic inflammatory and nutritional index
PSAprostate-specific antigen
VDBPvitamin D-binding protein
VDRvitamin D receptor



1. 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;82:290–8. doi: 10.1006/clin.1996.4320. [PubMed][Cross Ref]
2. Mohamad SB, Nagasawa H, Uto Y, Hori H. Tumor cell alpha-N-acetylgalactosaminidase activity and its involvement in GcMAF-related macrophage activation. Comp Biochem Physiol A Mol Integr Physiol.2002;132:1–8. doi: 10.1016/S1095-6433(01)00522-0. [PubMed] [Cross Ref]
3. Greco M, Mitri MD, Chiriacò F, Leo G, Brienza E, Maffia M. Serum proteomic profile of cutaneous malignant melanoma and relation to cancer progression: association to tumor derived alpha-N-acetylgalactosaminidase activity. Cancer Lett. 2009;283:222–9. doi: 10.1016/j.canlet.2009.04.001. [PubMed][Cross Ref]
4. Reddi AL, Sankaranarayanan K, Arulraj HS, Devaraj N, Devaraj H. Serum alpha-N-acetylgalactosaminidase is associated with diagnosis/prognosis of patients with squamous cell carcinoma of the uterine cervix. Cancer Lett. 2000;158:61–4. doi: 10.1016/S0304-3835(00)00502-4. [PubMed][Cross Ref]
5. 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;122:461–7. doi: 10.1002/ijc.23107. [PubMed] [Cross Ref]
6. 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;57:1007–16. doi: 10.1007/s00262-007-0431-z. [PubMed] [Cross Ref]
7. Yamamoto N, Suyama H, Yamamoto N. Immunotherapy for Prostate Cancer with Gc Protein-Derived Macrophage-Activating Factor, GcMAF. Transl Oncol. 2008;1:65–72. [PMC free article] [PubMed]
8. Nonaka K, Onizuka S, Ishibashi H, Uto Y, Hori H, Nakayama T, et al. Vitamin D binding protein-macrophage activating factor inhibits HCC in SCID mice. J Surg Res. 2012;172:116–22. doi: 10.1016/j.jss.2010.07.057. [PubMed] [Cross Ref]
9. Gregory KJ, Zhao B, Bielenberg DR, Dridi S, Wu J, Jiang W, et al. Vitamin D binding protein-macrophage activating factor directly inhibits proliferation, migration, and uPAR expression of prostate cancer cells. PLoS One. 2010;5:e13428. doi: 10.1371/journal.pone.0013428. [PMC free article] [PubMed][Cross Ref]
10. 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;32:45–52. [PubMed]
11. 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;8:349–60. doi: 10.1007/s10456-005-9024-7. [PubMed] [Cross Ref]
12. 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;60:479–85. doi: 10.1007/s00262-010-0953-7. [PubMed] [Cross Ref]
13. Pacini S, Morucci G, Punzi T, Gulisano M, Ruggiero M, Amato M, et al. Effect of paricalcitol and GcMAF on angiogenesis and human peripheral blood mononuclear cell proliferation and signaling. J Nephrol. 2012;25:577–81. doi: 10.5301/jn.5000035. [PubMed] [Cross Ref]
14. 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;57:295–9. [PubMed]
15. Yamamoto N, Lindsay DD, Naraparaju VR, Ireland RA, Popoff SN. A defect in the inflammation-primed macrophage-activation cascade in osteopetrotic rats. J Immunol. 1994;152:5100–7. [PubMed]
16. Nunn R. Mere anecdote: evidence and stories in medicine. J Eval Clin Pract. 2011;17:920–6. doi: 10.1111/j.1365-2753.2011.01727.x. [PubMed] [Cross Ref]
17. Yamamoto N, Ushijima N, Koga Y. Immunotherapy of HIV-infected patients with Gc protein-derived macrophage activating factor (GcMAF) J Med Virol. 2009;81:16–26. doi: 10.1002/jmv.21376. [PubMed][Cross Ref]
18. Bradstreet JJ, Vogelaar E, Thyer L. Initial observations of elevated alpha-N-acetylgalactosaminidase activity associated with autism and observed reductions from GC protein-macrophage activating factor injections. Autism Insights. 2012;4:31–8. doi: 10.4137/AUI.S10485. [Cross Ref]
19. Fabris A, Biagioni P, Punzi T, Morucci G, Gulisano M, Pacini S, et al. Role of angiotensin-converting enzyme and vitamin D receptor gene polymorphisms in cancer anorexia-cachexia syndrome. Am J Immunol.2012;8:65–70.
20. Rehder DS, Nelson RW, Borges CR. Glycosylation status of vitamin D binding protein in cancer patients. Protein Sci. 2009;18:2036–42. doi: 10.1002/pro.214. [PMC free article] [PubMed] [Cross Ref]
21. Inui T, Kuchiike D, Kubo K, Mette M, Uto Y, Hori H, et al. Clinical Experience of Integrative Cancer Immunotherapy with GcMAF. Anticancer Res. 2013;33:2917–9. [PubMed
22. Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem. 1976;72:248–54. doi: 10.1016/0003-2697(76)90527-3. [PubMed] [Cross Ref]

Articles from Oncoimmunology are provided here courtesy of Landes Bioscience

Ei kommentteja:

Lähetä kommentti

You are welcome to show your opinion here!