PLEASE READ THE GCMAF IMMUNOTHERAPY BOOK HERE

GcMAF The Book

Immunotherapy

 

GCMAF, NAGALASE & IMMUNOTHERAPY

 

Written by Anna Chukova

 

Macrophage Activation Factor (GcMaf) (VDTP)

 

This is a handbook of further information regarding this remarkable molecule and its effectiveness, mobilising your body’s defence mechanism that protects us all against disease.

 

The Activation of Macrophages

This is a key mechanism for fighting off disease before it gains a foothold in your body.

 

About the author

 

Anna Chukova, was born 23rd October 1963. 

Anna’s father, Vasil Chukov, was a cell biologist (BSc) and prominent researcher in human disease and Anna showed great interest in her father’s work from an early age, which she continued into adulthood, going on to study in Sofia, Bulgaria where she received a PhD in immunology. Her studies and research led her to the work of Professor Yamamoto, assembling a library of information and published studies, whilst further expanding on his ground-breaking immunotherapy research. She soon became recognized for her work with hormone Vitamin D, its impact on the immune system and its particular effect on patients suffering from a compromised immune system. It was here that Anna discovered that the prevention of disease relies upon building the patient’s immune system, which in turn requires boosting their Vitamin D levels back up to the higher end of the recommended scale using a 25 hydroxy blood analysis to obtain the results, this test is repeated at 12 week intervals.

With over two decades of research Anna has also focused her attention on cancer immunotherapy and a lesser-known molecule called Vitamin D Transport Protein (VDTP), or Globulin component Macrophage Activating Factor (GcMaf) This is the focus of this book.

Anna puts her heart, soul, knowledge and skills into making a difference for people living with acute and chronic disease. Working within a team, she continues to research and further push the boundaries of immunotherapy, she blends the best of her talents to drive forward the development and innovation of immunology within current clinical conditions. She is hopeful for the future of Immunotherapy, as many of her discoveries break new ground in the field of disease prevention and in turn improving and reversing the ever-declining health of humanity.

Special thanks

Anna gives special thanks to her beloved friend and knowledgeable colleague, Maryjane Aria for the unwavering dedication, support, knowledge and research that she has collated and shared over the past 12 years. Without her, this book would not have been possible.  

 

Preface

 

Since its discovery in the early 1980’s, the role that Vitamin D Transport Protein (VDTP), or Globulin component Macrophage Activating Factor (GcMaf) plays in the immune system is becoming more understood. Since that discovery, unfortunately the research has been stalled, suppressed and in some cases unjustly discredited by powerful voices in both the media and the scientific community. This has not happened by accident, nor because it is a needless and fruitless academic enquiry. It can no longer be denied that GcMaf (VDTP) has a very real place in both the body and within scientific and medical research worldwide. For those working in this field it is the worst kept secret of all time.

 

Immuno-therapies have been developing at an alarming pace with billions of dollars being poured into the laboratories looking for new and novel ways to combat disease. Of course, the billions spent on this research do not come without the desire for results and a return on the investment. The feedback loop of investment leading to profit via patents and mandatory uptake of the products is the millstone around the necks of those wishing to produce a cure for disease instead of developing a product that merely performs as an ‘ill-health’ management option.

 

What should be alarming about this, within this industry, is the word ‘patent’. It is impossible to patent something that is naturally occurring in nature. Every single chemical in the medical and pharmaceutical industry that has been synthesized in a laboratory has at some time been patented. Once the patent expires, then generic drugs and products can be marketed at a vastly reduced price, but not before the medical manufacturers, the original patent holders, have made enormous profits.

 

GcMaf (VDTP) is a naturally occurring substance that every healthy human being produces. It cannot be patented. No single entity or corporation can own the rights to it. It is yours and you have every right to make it within yourself, use it and even if you donate blood, you are freely sharing it. Because it is bio-identical in every single human being, it comes completely without risk of harm or side effects. So why has it been so suppressed for so long? The simple answer is ‘because it works effectively’.

 

GcMaf (VDTP) is not the magic bullet for all illnesses. Neither should it be treated as such. If you drink too much alcohol it will not cure your hangover or repair your liver. If you smoke it will not fix the hardening of your arteries. It will not fix a broken arm or help you to lose weight or cure cataracts. It is however vital to your ability to defend yourself from infections and must always be considered as a key body systemic component that a healthy lifestyle supports.

 

This book seeks to explain the biochemical interactions and how it functions within the body and how it is vital to good health. If you continue your investigations into the subject of GcMaf (VDTP) and why it is so difficult to find either the genuine product or reliable reviews of it, you’ll discover the disturbing truth as to why none of the multinational pharmaceutical corporations are promoting it.  

 

Introduction

 

This booklet has been prepared to highlight and provide information on two exceptional proteins involved in the fight against cancer and infectious disease. GcMaf has the potential to all prevent medical conditions that will attack our immune system.

 

• GcMaf (Group Component Macrophage Activation Factor)
• Nagalase (α-N-acetylgalactosaminidase).

 

These two naturally occurring, bio-identical protein molecules (made by our own bodies using our own genes) have the potential to be used in the treatment of cancer and all infectious disease.

 

The precursor to GcMaf is part of the normal circulating protein mixture in the blood. It is part of the natural albumin family of proteins. The precursor to GcMaf is the albumin family protein GcGlobulin. It is also known as Vitamin D Binding Protein, or Vitamin D Transport Protein. GcMaf is maintained as a precursor to be converted when required. If it were present as the converted type, then all macrophages would be activated all the time, which the body does not want as it requires energy and a balance for wound healing and cell communication.

 

The precursor to GcMaf is called Vitamin D transport protein (VDTP) or Gc-Globulin. It acts as a transport binding protein for Vitamin D. It can bind actin, a breakdown product from muscles and tissues which need clearing and recycling. The protein can also bind oleic acid.

This is also why Vitamin D is so important for the immune system, as the higher levels of stored Vitamin D you have the more you will have readily available for your GcMaf to bind and stabilize to.

Nagalase is an enzyme generated by the body which can cleave galactose sugar from proteins when required. It is also produced by cancer cells and most viruses. In this book we will cover additional information regarding how these proteins are generated in the body.

 

Research data on GcMaf has been accumulating since the initial work of Prof. Nobuto Yamamoto. Many research groups (Inui et al, Saburi et al, Maryjayne Aria and myself) are now unlocking the capability of this protein and its ability to activate macrophages for combating cancer and infectious disease.

In conjunction with the increase in research of GcMaf the knowledge and role of Nagalase (N-Acetylgalactosaminidase) has also increased. This GcMaf protein present in the body is employed to promote healing from the invasion of external infectious agents.

Ultimately it is hoped that GcMaf and Nagalase can be used to:

 

• Identify the presence of cancer and to aid in its clearance from the body
• Detect and reverse early cancers long before imaging can identify them
• Determine whether a cancer treatment program is working or not

 

Nagalase screening, coupled with early treatment using GcMaf (VDTP), has the potential to become a front-line treatment in cancer therapy for everyone. You may consider this a bold statement; however, the data being generated through active research (as highlighted in this handbook), can provide the facts and reveal the science behind GcMaf (VDTP), Nagalase, and the molecular biology of macrophage activation that will demonstrate this statement to be true. These are real and large advancements in cancer therapy.

This booklet has three major objectives.

 

• To further the cause of making GcMaf available to all who need it
• To highlight the importance of GcMaf in novel cancer therapies
• To promote the establishment of Nagalase as a potential cancer screening marker for all high-risk patients

 

With Nagalase testing the technology is available to identify cancer when it is just a handful of cells which can then be easily reversed with a 3-month course of GcMaf injections. These possibilities will drive the capability for early-stage detection and the effective treatment in overcoming cancer.

 

•  Protein Production

• How Your Body Makes GcMaf

 

GcMaf (VDTP) and Nagalase are both proteins. A brief mention of protein synthesis is required. Proteins are composed of building blocks called amino acids. There are 20 amino acids that are available to be used to make proteins. Some are classed as essential. There are nine amino acids that we are unable to generate and so can only acquire from food. The others can be generated from the vast array of biochemical pathways that occur in every cell. There is a continuous breakdown of excess proteins and amino acids, to individual elements, that are then reconverted and used to generate new amino acids and new proteins.

 

Amino acids can undergo different reactions to join themselves together in chains called peptides or proteins. The sequence of the amino acids in the chains is directed by our genes in our DNA sequence. This is the so-called genetic code. The genes can hold the information for over 10 million proteins; all this with 4 DNA nucleotides and 20 amino acids!

 

The amino acids sequence is a linear item. To preserve space and provide extra binding areas, receptor areas, and different slight changes in charge, the sequence folds in on itself. Some proteins combine with others in a mixture to form a complex of subunits that are required for its function.

 

The basic concept is depicted below:

Proteins are therefore long chains of hundreds of amino acids that make up the “protein molecule”. The protein molecule may look like an indistinct ball of haphazardly placed clumps. However, for a protein the folding and combination of any other subunits is a specific formation of the three-dimensional structure. The final structure is a very precisely positioned set of amino acids. Even a slight positional change, or a missing amino acid that is then replaced by another will significantly alter the structure of the protein. It will even alter its activity, positional, or messenger function. It may even block a receptor site. In other words, it would be disastrous. The amino acids can attach to sugars on the outside of the protein complex. These sugars provide the messenger, communicating, or function activity of proteins. These proteins are termed glycoproteins, whilst most of the immune system’s “messenger molecules” are Homologous proteins.

 

• GcMaf Formation

 

Vitamin D-binding protein (VDTP) is the precursor protein from which our immune cells make GcMaf. DTP contains 458 amino acids, one of which is incredibly special and quite different from all the others. This is a threonine amino acid, the 420th amino acid in its chain.

Attached to this threonine is a group of three sugars. The presence of these sugars defines the purpose of the entire VDTP protein molecule. Now imagine (VDTP) as this large 3D complexed protein with three sugars attached. The first sugar is an α-N-acetylgalactosamine (GalNac) directly bound to the threonine amino acid. The second is a sialic acid (SA, also known as N-acetylneuraminic acid) sugar molecule and the third is a β-galactose (Gal) sugar.  All three are attached to one another, as shown in the diagram below, in an upside-down “Y”-shaped configuration. The lines (–) indicate the bonds formed by sugars which connect themselves to each other and to the protein.

The amino acid threonine at position 420 is on the surface of the 3D complex of VDTP making it ideally placed to be presented to cells on initial contact.

VDTP is converted into GcMaf by using two reactions. Treatment with the β-galactosidase enzyme which is embedded in the outer cell membrane of B-lymphocytes, and present in the lysosomal vesicles of most cells. The second reaction is to remove the Sialic acid sugar. This is performed by the enzyme Sialidase, which is in the outer membrane of T-lymphocyte cells and present in the lysosomes of most cells. With the cleavage of these two sugars, the Vitamin D-Binding Protein has been converted into GcMaf.

 

The GcMaf is converted and ready to seek out a macrophage where it will lock onto its receptor and then send the powerful activation message. This is where the macrophage now alters its type from M2 to M1. From, the wound healing and regulatory type, to the surveillance and invader seeking phagocytotic role. GcMaf is the most potent of macrophage stimulatory molecules that we know.

 

• The Initial Research

 

The initial research leads to a great understanding for the basic science of GcMaf (VDTP)which has been confirmed by the additional studies of other scientific groups. Insights gained in one study become the driving force for designing the next one. Yamamoto spent a quarter of a century examining the basic molecular biology and immunology of the action of cancer and GcMaf (VDTP). The work on Nagalase (α-N-acetylgalactosaminidase) and glycoprotein macrophage activating factor (GcMaf) was methodical, progressive, and fascinatingly revealing. The work involved an intricate set of hypothesis and path of experimental results that together formed a vast infrastructure of data on the cancer formation and treatment sides, upon which the final conclusions are based.

 

Yamamoto did not try out a new, unknown, and potentially toxic drug on a bunch of people. Yamamoto completed the science and research; exactly, precisely, down to the sub-molecular level, how cancer breaks our bodies, then resolved how to reverse it using the body’s own systems as the overriding therapeutic tool. The research results deserve to have these findings dispersed to be understood and taken with credibility, which as yet has not yet occurred.

 

• Cancer a Brief Insight

The idea of being diagnosed with Cancer is terrible and undoubtedly the disease that strikes most fear. It is many things to many people? From the point of view of the cancer patient, it may be seen as a fear-inducing, death sentence. From the perspective of a family member cancer is a stressful period of mourning, that requires constant support, negotiating the ever-changing emotional, financial and physical changes that occur from diagnosis and lasting for an undefined period of time, with the ending often being the loss of a loved one. For the doctor who must locate and treat the cancer to the best of their ability; cancer is both a laborious, sometimes unrewarding task, as well as an opportunity to provide exceptional, loving patient care.

The molecular biologist, however, views cancer as a vicious and protracted conflict directed between cancer cells and the immune supporting cells, it is a Nano-scale on-going battle that is happening in each of us, every moment of every day. We now know that we are all developing potential cancer cells all the time through the mismatched mutations that occur during our normal cell division and by the invasion of microorganisms and viruses. However, a healthy immune system overcomes them as fast as they are made. Anything that weakens the immune system can shift that delicate balance in favour of cancer, allowing it to gain a foothold and grow.

Cancer Research and prevention has had enormous resources applied to it over the years, with early detection and effective treatments beyond the classical, surgery, radiotherapy and chemotherapy needed to assist in the fight against this deadly disease.

 

The rise of the interest in immunotherapy has conveyed some hope, with antibodies like Herceptin (Trastuzumab for breast cancer), Erbitux (Cetuximab for bowel cancer) being increasingly used for treatments.

 

• How Cancer Begins

 

A cancer occurs when a cell’s genes mutate and is expressed or affects the expression of other essential control genes. Cells in the body are continuously replacing themselves by a process of mitosis: – or cell division. Mitosis generates a direct copy of the original cell if all the procedures and processes and cell requirements are present. During the cell division process there is the possibility that any cell’s genes can become mutated by various mismatches, or incomplete copying processes. Sometimes extra DNA can be inserted, or removed due to viral, bacterial, or fungal infections. This process can generate cells containing damaged genes. There are approximately 30 trillion cells in the body which can go through mitosis every single. A mutation rate of 6 mutations per 2 million mitotic divisions has been estimated. This would provide potentially 3 million mutations daily that is corrected by the body automatically in a normal healthy human. If there is a presence of any mutagens such as medications, cleaning agents, bacterial, fungal, or viral infections then the rate may be higher!

This provides many opportunities for potential cancerous mutations to occur. Cancerous cells are therefore made up of cells that carry damaged genes. Normal healthy cells have a special contact segregation mechanism to stop them getting too big or absorbing any other cells they touch.

Cancerous cells have lost the ability to cooperate with the rest of the cellular community and so grow uninhibited, randomly and out of control. These mutated cells grow, forming an isolated local community made up of malignant tumor cells. Tumors grow where they form and are able to grow new blood vessels. Cancer cells need a lot of energy and more nutrients for their fast growth. As we know processed sugar is a major contributor to cancer growth, so stopping sugar intake will help slow this growth.

Some tumor cells send out signals that tell the body to produce new blood vessels at the tumor site which proved not only a food and oxygen supply, but also an avenue for escape to a new part of the body, through these new blood vessels and into bloodstream. Cells that break away from the tumor begin to spread to surrounding tissues (via the bloodstream or lymphatic system) where they can start new tumors This is called metastasis when these escaping tumor cells go on to establish satellite communities at other locations in other organs.

 

The life of any cancer can be viewed as a continuous continuum: – starting with one cell (on the far-left side) and expanding in its tumor growth phase ending with the movement and progression to metastasis and ending (to the far-right side) as a unmolested massive complex of metastatic tumors comprised of many billions of cells, wide ranging self-generated intertwined blood vessels which occupying multiple locations in the body. This progression of the cancer life cycle ends with a cancer which had become large enough, to overwhelm and ultimately, kill its host.

Cancer specialists evaluate what “stage” the cancer is according to where the tumor complexity lies on this continuum.

 

• Cancer Cell Growth

 

So, it can only take one mutated uncorrected gene to create a cancer cell. This cell multiplies by dividing to become an expanding tumor mass. Just like termites in your house, cancers persistently gnaw away, expanding and encroaching. They capture territory by spreading locally and pushing aside healthy tissues. Eventually they break through the barriers that keep them local spilling out and spreading around the body. If a tumor remains unchecked, the cancer cells seek to enter the bloodstream or lymphatic system and it at this stage that the body’s cancer containment barriers have finally been breached. Once this stage has been achieved the dangerous cancer has become the insidious, untreatable, most feared, and most deadly form of metastatic cancer. Prior to metastasis, almost all cancers can be considered treatable. After metastasis, the odds of a successful treatment fall dramatically to almost zero. Treatment at this metastatic stage by the oncologists continues to be chemotherapy, or any accepted and potentially new drugs that are in clinical trials, as well as the usual radiology, using sophisticated blasts and ionizing particle beams.

In the current system, these well-intended efforts are for the most part futile: metastatic cancer may be slowed but is rarely successfully treated.  However, these treatments and methods used in the standard therapies do reduce tumor burden which improves the odds that GcMaf (VDTP) will be effective.

 

• Features of Cancer Cells

 

• Normal cells stop replicating after they have doubled 50 or 60 times. Cancer cells do not stop reproducing and can be considered to have a type of “immortality”. A cancer cell will continue doubling until a tumor is formed that is made up of millions of copies of the original cancerous         cell.
• Cancer cells override normal cell signaling. This may be because the genes that coordinate the cell to stop reproducing on contact have been blocked. So, the cancer cell keeps on replicating, irrespective of the damage the tumor causes.
• Cancer cells can become detached, explaining how cancer cells spread (metastasis) to other parts of the body.
• Cancer cells stay immature and undifferentiated becoming increasingly primitive, with a tendency to reproduce ever more rapidly and haphazardly.

 

• Current Treatment Options Depend on the Stage of the Cancer

 

1. Optimum treatment strategies vary depending on the type and stage of the cancer. In the earliest stage, prior to detection on imaging (but positive on AMAS or Nagalase), ‘alternative’ treatment approaches are likely to ultimately work. This is true because natural therapies enhance the body’s own anti-cancer systems, rather than damaging them. Once a cancer has grown to the size where it can be seen on imaging, however, the “toxic triad” (surgery, radiation, and/or chemotherapy) have become necessary.

 

Early Cancer Detection is Key to Treatment Selection

 

• The effectiveness of any therapy, including GcMaf, has everything to do with the point along the life cycle when treatment is initiated. Early detection has justifiably become a crucial aspect in cancer therapy. The earlier a cancer is detected, almost regardless of type, the better the overall prognosis. Catching a cancer before it metastasizes is especially important.

      The desire is to move the point of detection as far to the beginning of the tumor life cycle as      possible. The use of AMAS and Nagalase testing enables the early detection and if used appropriately helps monitor the progress of treatments.

 

• Macrophages – the Main Defense Cells

 

• The body is a fabulous organism that has evolved over millennia to become the life-form we are now. Part of the old innate immune system is still present and provides the very basic and fundamental control mechanisms that prolongs life. Part of this old immune system is the curious, yet essential cell, the macrophage.
• First discovered in 1884 by the Russian zoologist Élie Metchnikoff. The macrophage is a specialist white blood cell that has unique properties. It “patrols” the body using the blood system as it’s very own road map. It also has specific associations with individual tissues and organs where their name changes, such as those in the central nervous system (Microglia), bone (Osteoclasts), liver (Kupffer cells), kidneys (Intraglomerular mesangial cells) etc.
• Macrophages are big white blood cells (three times larger than normal cells, see later!) that can chase, capture, engulf, and digest invading foreign bodies. This activity known as phagocytosis, gives the cells its name Macro meaning Big, and ‘phage’ meaning eater. It is a big eater cell!  
• They engulf dying cells, any general debris, any foreign invading cells, or anything that is different to the type of proteins specific to the body’s healthy cells, which they collect and then dispose of. Once a foreign body is detected it is immobilized using a “sticky” protein called Opsonin. The microbe, or cancer cell is ‘phagocytosed’ meaning it is encapsulated inside a an intracellular vesicle, which is also known as a“phagolysosome,” where it is then destroyed using an electron-driven free radical oxidative burst.
• The macrophage cells have a wide range of complex abilities such as being able to secrete cell messenger cytokines and take part in other cell interactions, which are covered further below.

 

• Macrophage activity can be simplified and split into two major functional modes termed

 

• M1 (classically activated macrophages)  
• At this stage they provide the active host-defense against pathogens using phagocytosis with the secretion of pro-inflammatory cytokines and micro-biocidal compounds.

 

                   M2 (alternatively activated macrophages) 

 

In this form they perform the functional role of regulatory activities such as healing and repairing damage to tissues and wounds.

 

Macrophages default to the M2 state, whilst the need for the active defense and inflammatory stage is triggered when needed. This controls the cell’s activities, reducing the overall energy burden. The most potent activation from M2 to an M1 state is performed by GcMaf. The enzymes necessary are held in small vesicles in cells which are released on the damage to cells caused by bacterial, viral, or physical contamination. This as you can imagine causes the M2 macrophages to be activated to M1 type, defending the contamination, and immediately helping with the healing process. The way it does this will be discussed later in the booklet.

Macrophages are large cells and are huge in comparison with red blood cells, normal white blood cells and any typical single cancer cell, which is around 7 microns (micrometres, or millionths of a meter) in diameter and have a volume of about 250 cubic microns. A macrophage cell in comparison is approximately 20 micrometres (20 millionths of a meter) in diameter, being about three times as wide as regular cells.

However, because of the relationship between size and volume macrophages have a volume of around 4000 cubic microns, about 16 times the volume of normal sized cells. If a cancer cell were the size of a dog, a macrophage would be about the size of an elephant!

Comprising various weaponry, they are packed full of a formidable array of sophisticated systems, all of which are programmed for a singular purpose: remove the enemy as quickly and efficiently as possible, a term known as “tumoricidal capacity.”

In the M2 mode, they are focused on wound healing and cell regulation, moving in the bloodstream and between cells in a casual movement, keeping everything in check and ensuring things are working correctly.  When activated they generate small appendages termed “pseudopodia” (false legs) which extend and effectively touch anything around them, checking that it is a “normal” acceptable part of the body. Activation occurs when they meet with an invading bacterium, virus, or any physical damage. Once activated they can effectively “walk” through tissues using these self-generated “legs”. They ramble around searching for cells or intruders that are “not self” or foreign. If the “enemy” is further away, or is trying to elude capture, the macrophage chases after it, extruding a cluster of these long thin sticky spaghetti-like tentacles that they wrap around the foreign body , in an unbreakable stranglehold.  

These pseudopodia legs secrete a “sticky” opsonin protein that confines the foreign body by engulfing it inside the macrophage cells cytoplasm, secreting a cocktail of corrosive free radicals and enzymes that rapidly digest its victim down into its original component parts (amino acids, nucleic acids, fatty acids, etc.).

The macrophage then spits out these pieces into the intercellular soup where the body quickly recycles them using these “spare parts” to build brand new healthy cells.

The macrophage can also take the foreign body, or parts of it, to the liver if required where the acquired (learned) immune system can then start the antibody immunity response, to fight off the disease of attack by the virus, bacteria, or cancer. It is a totally astonishing concept that this complex and truly combative scenario is a constant process, unfolding in every healthy person, every minute of every day.

 

• The Immune System: Cancer Conflict

 

This cancer conflict could be considered a direct war on the body. It is in effect a complex tactical sequence of cellular activities.  A series of deliberate actions, from all cellular types, highlights the range and sophistication of the attack and defense modes. Two cell types (cancer cells and macrophages) comprise the main forces of the opposing combatants in our immune system. Both have massive numbers of personnel and weaponry at their disposal and both have a strategy for success. For this is a war inside of us, the outcome of which will eventually determine whether about a third of us will live or die.  Hundreds of billions of cellular “warriors” fight for dominance over each other, whilst our lives depend on the outcome. A cellular battle to the death. Whilst Cancer cells appear to be programmed to survive and spread, on the other hand our immune system consists of enormous numbers of clever and cunning white blood cells doing their best to defend us against constant attack.

GcMaf treatment and Nagalase testing have the potential to dramatically change the outcome of the battle and ensure a continued advantage towards the immune system. A change in the approach of cancer treatment needs to occur. It has to occur in tandem with changes in the medical industry to give a real visible possibility of hope that cancer can be effectively treated and even eradicated. This has a vast effect on medical care delivery systems, including governments, Pharmaceutical giants, insurance companies, cancer care facilities and cancer specialists. For a multiplicity of reasons, not limited to money alone, these colossal barriers are resistant to change.

GcMaf and Nagalase are the two new elements that can make for vast and positive change if the medical industry were to accept them as part of cancer treatment. Ensuring that these new yet ancient elements are accepted into cancer treatment options and are made available to the general public, is a monumental challenge. Sadly though, people will continue to die because of the reluctance of modern medicine to embrace any kind of change, or new approach.

That said, if the screening of everyone for elevated Nagalase started today, alongside the administration of GcMaf to those with high results, then the possibility of eradicating almost all cancers could happen. Literally overnight.

 

The Body’s Immune Response to Cancer and Microbes

 

The guardians of our immune defense are composed of dozens of cell types, with many different functions. The macrophage cells are the body’s immune systems great defenders against the invading foreign bodies, such as cancer and infectious bacteria and viruses. Once the foreign invaders have entered the body, they try to establish a foothold and multiply manipulating the body’s system to their own advantage. Our immune system deploys these remarkable weapons in multiple wars on several fronts.

It was highlighted previously that macrophages are found throughout the body and are usually associated with specific organs. Our major organs are the first barriers exposed to all initial attacks. Within our skin, respiratory system, intestinal tract and bloodstream is where we sustain the largest exposure to external attack from foreign invading cells. And so it is here that we house the majority of our immune cells. Microbes in the form of bacteria, fungi, parasites and viruses, are ever present in the air we breathe, the food we ingest and on our skin. They tirelessly attack and try to invade us every waking minute and must be defeated on a continuous basis. Whilst unsurprisingly, our largest exposure to pathogens is in our gastrointestinal tract, otherwise known as our gut, which is our largest and most frequently breached barrier. Approximately 80% of our white-blood cells are embedded just beneath the intestinal mucosal surface. This is the reason the food we eat determines so much when it comes to our health. Eating processed GMO foods that are low in nutrition and high in additives is not only depleting the body of vital nutrients but is also a direct attack on our immune system and so the food you eat has a direct outcome on this ongoing battle.

Our immune cells deploy a fantastic and unimaginable array of war machinery, all coordinated by a sophisticated communications system. The active immune cells are capable of releasing an onslaught of chemical messages consisting of secreted proteins, glycoproteins, cytokines, inter cell-signaling molecules, neurotransmitters, etc. All of which help identify the foreign invaders, provide their location, estimate their numbers and coordinate the attack.

This immune response functions well when allowed, but there is a problem with the immune response when it comes to cancers and this is called Nagalase (α-N-acetylgalactosaminidase).

 

What is Nagalase?

 

Nagalase is expressed and generated by all cancer cells and viruses particularly the viruses that have an external envelope such as HIV, Hepatitis B, Hepatitis C, Influenza, Herpes simplex, Epstein-Barr virus, and others. In relatively simple terms Nagalase is an enzyme that removes a sugar from other proteins in a biochemical reaction, usually to provide the sugar N-acetylgalactosamine for additional biochemical reactions in the body. Nagalase can be a bit non-specific in its actions and can act as the N-acetylgalactosamine sugar biochemical bond, even if there are other sugars attached to it.

 

What makes this specific capability of Nagalase important?

 

Nagalase provides a method by which cancer cells and viruses can decrease the initial immune system of our bodies to enhance their foothold during early-stage infections. It allows the cancer cells to remain “undetected” until they reach a critical mass and move down the cancer life cycle to the untreatable metastasis stage.

Nagalase can block the formation blocks of normal natural GcMaf from the precursor VDTP (Vitamin D Transport Protein). Cancer cells and viruses appear to produce and secrete Nagalase on a continual basis, so as you approach a cancer cell, or tumor, the concentration of Nagalase naturally increases, so, at the point where activated M1 macrophages are needed most, the cancer cells have a mechanism to decrease their activation completely and prevent their detection.

The Following diagram (also presented earlier) shows how GcMaf is made, as well as the result of Nagalase.

The presence of Nagalase prevents normal natural GcMaf (VDTP) from being formed. Please also note that it cannot be converted to have all three sugars attached. Which means that it reverts to being a simple carrier protein, losing its capability to act as a messenger, or stimulatory protein. Of course, the closer a molecule of the precursor protein VDTP gets to a cancer tumor, the Nagalase concentration increases meaning that VDTP cannot be converted to GcMaf (VDTP)

This is a truly clever and effective tool to stop the body from defending itself. By blocking the normal natural GcMaf (VDTP) production, Nagalase stops the anti-cancer and anti-viral immune activity response, thus allowing cancer and infections to spread. and grow without restriction. Here macrophages remain in the “deactivated” M2 phase, leaving cancer to grow and take over, which alas will eventually kill the patient.  Nagalase is remarkably efficient, it is an enzyme. This means it is an effective catalyst able to remove the sugars from not just one DTP precursor but as many as it can come across. One Nagalase molecule can thus destroy a huge quantity of DTP precursor molecules.

Administering purified GcMaf overcomes this natural activation blockage, re-activating the macrophages.

It can also be understood that enough GcMaf has to be provided to reach a concentration higher than the Nagalase at the tumor sites. As well as circulate throughout the bloodstream to stimulate additional macrophages to become the activated M2 type. As already mentioned, GcMaf is a cell-signaling glycoprotein specific for macrophages. It stimulates macrophages to rapidly locate, attack and destroy cancer cells. By activating macrophages, GcMaf triggers a cascade that activates the entire immune system. As we have already determined viruses also make Nagalase and so the outcome is the same as that of cancer survival, as it is essential the macrophages be incapacitated, and the macrophages be activated into attack.

 

However, Nagalase has a very positive outcome with a secondary role that can be exploited by the medical profession, as it can be measured and therefore direct concentrations due to cancer, or tumor size can be indicated. It can become a sensitive marker for all cancers and viruses, meaning it could be a reliable system for early detection of tumors, or viral infections. It can also be used to monitor the effectiveness of any resulting treatment. Falling Nagalase levels would tend to indicate cancer remission, or viral decrease. And so Nagalase, that is so effective at hiding cancers and viruses from detection within the body, has become a highly effective detection tool for us when it comes to detecting the very presence of disease and monitoring treatment protocols.

 

• When GcMaf is Administered and Activates Macrophages

 

Once GcMaf (VDTP) presents its protruding last few amino acids, you should recall that the single sugar α-N-acetylgalactosamine is present. This portion of the protein complex, with its sugar presenting acts as a messenger molecule seeking the relevant receptor on the macrophage cell. Once the GcMaf (VDTP) protein complex attaches in position, this protruding part naturally fits into a cleft in the macrophage cell, causing a message to be conveyed that changes the biochemical profile inside the macrophage from its more sedate M2 type, to its surveillance, marauding, phagocytotic M1 type.

When GcMaf is injected at a level of 100ng a week, it does not sound much, so how can such a small amount do anything positive? This normal response highlights the control the body has on life. It shows that normal levels of GcMaf (VDTP) must be much lower than this.

Why? Well because the body needs something effective to create the response to fight off any disease. If the body required more grams of protein to be effective then that would take time, resources and energy to produce macrophage activation and the body risks becoming overrun. So it has developed a system where only a relatively small amount of activating agents is required. Usually this is produced at the place where a foreign invader (bacteria, virus, and fungi) has entered the body, ie: where it is immediately needed. Macrophages are activated at that point and rapidly seek out the invader.

Once activated, Macrophages have a positive feedback system of chemical messengers. Macrophages and other immune defense cells such as lymphocytes release these messenger molecules (cytokines, interferons, leukotrienes, and other small molecules) into the bloodstream, which takes over the immediate GcMaf (VDTP) activation message, activating macrophages in the immediate vicinity. All this happens almost instantaneously. Everything is extremely well-organized and perfectly coordinated. The invader is identified, and that message is sent to all macrophages. An inflammatory response is then started to protect and engulf the invader.

Macrophages can also multiply rapidly. When they find an area of high cancer cell or viral particle density, there isn’t time to wait for the reinforcing activated macrophages seeking out where the problem is and so they cleverly clone themselves on short notice. This multiplication process occurs only in activated macrophages. The whole event snowballs creating far improved chances for the immune system’s ability to regain the upper hand.

It only requires 1 molecule of GcMaf (VDTP) to activate 1 macrophage, again highlighting how effective the Nagalase from cancer cells is at blocking it. A single dose of 100ng of GcMaf provides almost 300 molecules for each current circulating macrophage. Thus, highlighting how such a small dose is so effective, as the chance meeting of GcMaf (VDTP) by each macrophage is increased. With late stage cancers 3000ng daily is required for the very best outcome.

The stimulation is extremely intense and provides an almost immediate response. The macrophage is stimulated to become the activated invader seeking and destroying defense cells of the body’s innate immune system.  There has been no other as potent an activator of macrophages as GcMaf (VDTP) which can instigate and restore the “tumoricidal capacity” of macrophages.

Above is an image of a GcMaf (VDTP) activated macrophage about to engulf and phagocytose a breast cancer cell. The cells are stained here for easier visualization in a laboratory culture. Please note the pseudopodia that are projecting from the macrophage that is typical of the activated M1 macrophage type.

Our macrophage cells can engulf and dismantle enemy invaders. They can make and use ionized particles that literally rip holes in the outer cell membranes of infectious microbes and cancer cells.

Macrophages release a selection of enzymes and chemical messengers that break down the cancer cell wall, reducing its integrity and allowing it to disintegrate. The cell contents spill out, and the cancer cell goes through a process of apoptosis. Macrophages surround the cancer cells and effectively digest it enabling the contents to be mopped up and recycled. These combative aspects are visualized in the pictures above. The activated macrophages “eat” into the cancer cells (breast carcinoma in this case) as seen by the “halo” around them. The cancer cell walls are broken down and their cell structure falls apart.

 

• Antigen Presentation

 

Of course, macrophages use phagocytosis as a front-line defense against any pathogen, or foreign body attack. Once macrophages have phagocytosed and destroyed the cancer cell, or foreign invader (bacteria or virus) they transport some of the cellular breakdown parts to start the learnt immune system. The first line of defense is the innate immune system. The next line of defense is the sophisticated antibody protection system that is the “learnt” immune system.

Macrophages can become antigen presenting cells once they phagocytose the cancer cells or invading foreign bodies. Macrophages therefore have an important role in the presentation of the antigens of phagocytosed infectious organisms, or cancer cell debris. Macrophages can express high levels of interferon-gamma stimulating T-Cell activation. This boosts the antigen presentation by macrophages resulting in the increased activation of T cells to generate antibodies. Macrophages also disperse chemical signals (chemokines, cytokines etc.) to increase the number of white blood cells (termed neutrophils and monocytes) which release a range of toxic agents designed to kill extracellular pathogens. The release of the chemical messengers increases the self-stimulation as well as recruiting and transferring the activation of macrophages to all other immune cells, for the destruction of the foreign cells or invading organisms.

 This cellular set of messages and the stimulation of the other immune cells results in a well-informed set of immune cells that know exactly what “foreign” cell or invading microorganism they are looking for. These cells spread the message and the immune system becomes the formidable sentinels of the body. The chemical messages now provide a complete method for the immune system to recognize the cancer cells which when they locate them aim to engulf and destroy them without hesitation. The innate immune surveillance system has been fully activated. We then wonder why cancer cells can progress to the stage of tumors if the immune cells are so good at protecting the body. And again, this is due to the protein that cancer cells and viruses express – namely Nagalase.

 

• Nagalase Creates Immunosuppression

 

As we have covered cancer cells tumors and viral infections secrete the enzyme that prevents GcMaf production called Nagalase (α-N-acetylgalactosaminidase) that prevent macrophages from becoming the M1 surveillance and attack minded phagocytosing macrophages that are so vital as soldiers, but also as messengers.

If macrophages do not become activated, then the vital antigen presenting activities simply do not happen. Which prevents the stimulation of additional immune cells such as the neutrophils and monocytes, which release toxic agents designed to kill extracellular pathogens. When these chemical messengers are released, they increase the self-stimulation effect of the overall immune system, recruiting and transferring the activation of macrophages to all other immune cells, which in turn helps build the rapid attack and destruction of problematic foreign cells and invading organisms.

And so, another catastrophic effect that Nagalase has when it prevents the precursor GcGlobulin being converted to GcMaf/VDTP, is that it has a catastrophic effect on the overall immune systems communication channels. It is like pulling the plug on the internet, it breaks the chain of communication. For it is Macrophages that start the entire immune system’s communication chain. Without this conversion and the subsequent cascade of chemical messengers and stimulation of additional immune cells the whole system grinds to a halt. Instead of being on red alert, the immune system’s emergency status remains on green and in low energy holiday mode.  it effectively switches off the whole system, like your computer when it goes into sleep mode if left unattended, this is called immunosuppression and is an environment in which cancers and viruses can grow and thrive without any interruption.

Without any antigen presentation the rest of the immune system remains lethargic and unresponsive. This GcMaf blocking event was precisely explained by Yamamoto in his paper on his prostate cancer studies. He summarized the lack of stimulation of macrophages succinctly, as:

 

“Macrophages are the major phagocytic and antigen-presenting cells. Because macrophage activation for phagocytosis and antigen presentation to B and T lymphocytes is the first (and) indispensable step in the development of both humoral and cellular immunity, lack of macrophage activation leads to immunosuppression.” (Immunotherapy of Prostate Cancer with GcMaf. Yamamoto et al., Translational Oncology Vol. 1, No. 2, 2008.)

 

Nagalase: -A Useful Indicator

 

As stated, above even when extremely low amounts of Nagalase are detected, the indication is that there is cancer, or a viral infection is present, as Nagalase is secreted by cancer cells and viruses. The malignant and viral entities that make Nagalase are not otherwise present. A positive Nagalase test therefore confirms that a cancer (or a nasty virus) is starting to grow within us.

With enough samples and study monitoring tumor sizes (tumor load), the Nagalase concentration could also be used to effectively determine overall tumor growth. Unfortunately, though, this Nagalase: Tumor ratio is currently only suitable for each patient, as determining a universal indicator for everybody would not be suitable, or possible to project, as each case is different. However, Nagalase can be useful as an indicator for all cancer sufferers once a base level for that patient has been set, after the first test for all subsequent tests to measure against. As a rising level could potentially indicate cancer tumor growth, whilst a falling level of Nagalase would indicate tumor regression.

 

However, a general base level could be set by studying and measuring Nagalase levels in people with no infection or cancer, as this could create a Universal general Nagalase base level. Whilst subsequent levels over a time period would be the indicator for every individual’s cancer progression, or regression.                                                  

This is a remarkable concept, when you consider the scale and research of the cancer industry, for here is a simple, safe blood test that can be used as a useful and accurate diagnostic tool to not only detect, but also monitor the effectiveness of any cancer treatment.

 

• Benefits of Early Cancer Detection

 

Alternative cancer treatments are the most effective when it comes to early, small cancers. Alternative treatments enhance the natural immune function to aid the removal of the source of the inflammation that is causing the cancer in the first place. The concept is to “catch it early” rather than waiting until the tumor is established and growth has become unwieldy and out of control. And is therefore harder to manage. Initial cancers with a small number of cells respond most effectively to natural therapies. Cancers that have become large enough to see on imaging pose a much more significant threat and so require far more drastic measures, such as surgery, chemotherapy and radiation treatment.

The current and typical method for diagnosing most cancers occurs only when a tumor mass can be imaged as a mammogram, chest X-ray, or in colonoscopy. This delayed approach requires time and allows the Nagalase concentration levels to be increased depressing the innate immune system further. Having routine blood samples specifically for Nagalase can detect early-stage cancer existing in the body even if not yet able to be observed. Earlier less invasive detection methods provide a treatment window with alternative treatments to be started much, much earlier.

 

•  Biomarker Testing

 

Current conventional cancer treatment therapy does not require early detection, it relies upon the cancer to achieve a stage that can be visualized on scans, X-rays or even physically. The biopsy most often simply confirms what everyone already knows and understands. The use of biomarkers seems to be acceptable in almost all other forms of medical identification except it seems in the field of cancer therapy.

 

.      Monitoring Cancer Treatments Using Nagalase

 

Using novel cancer biomarkers such as the Nagalase blood test would mean that biopsies can be avoided entirely, removing the need for sampling tumors. Biopsies break the tumor open causing the potentially catastrophic event of the once contained cancer cells, now let loose, spilling out and circulating around the body to metastasize in new locations.  Biomarker testing reduces this risk and leaves the cancer cells naturally contained.  

Measured levels of Nagalase in cancer patients also decrease after surgery, even with the partial removal of a tumor. Radiation treatment and chemotherapy have also been shown to provide a decrease in Nagalase levels. Any cancer treatment that is effective and therefore is capable of decreasing cancer tumor size or cancer cell load cell (or viral numbers) will show a decrease in corresponding Nagalase levels.

Administration with GcMaf (VDTP) also shows a decrease in corresponding Nagalase levels. Treatment and a decreasing Nagalase level do not mean the cancer has been totally removed. Continuous Nagalase measurements giving baseline Nagalase levels would indicate the tumor load has been eradicated.  

 

Will the medical profession accept early markers?

Biomarker assay analysis such as Nagalase however, are a cause for concern for the overall regimented and systematically conditioned medical profession. These novel biomarkers are out of the ordinary, whether they help, or not. Modern medical professionals need to adhere to the “norm.” and any thinking outside of the pathway, or outside the way they were trained in is difficult to accept. It is a major cause for concern as funding and investment into facilities that are alternative are fraught with issues of understanding and arguably a general lack of personal advancement of knowledge within the profession.

And so, a radical change in approach of both detection and treatment needs to occur to ensure the death rates fall. Changes will come, but slowly.  Early detection and early treatment approaches can combine techniques, with GcMaf and targeted antibodies working alongside the electron beam radiation treatments and effective chemotherapy treatments for example. And then hopefully, eventually this will become the norm when it comes to effectively treating cancer. But we recognize that this is a steep mountain to climb.

To highlight this issue of the uptake of new and innovative testing methods by the medical institutions; An anonymous Russian scientist has developed a novel technique that provides early indications of cancer using a small blood plasma sample and an Electron Spin Resonance (ESR) to Electron Paramagnetic Resonance (EPR) ratio. Comparing the blood of cancer free patients, they can pinpoint the changes in the ESR/EPR pattern to indicate a presence of early cancer. They have enough data on samples, from a pin prick using just a few drops of blood, filtered to remove the red blood cells, to gauge what cancer type is growing. This test is so sensitive they can even detect it as much as 2-3 years in advance before it can be visualized as a tumor.

When trying to have the system accepted as a routine blood analysis in Russia, all of the hospitals and cancer specialists rejected it. So they approached cancer specialists in the USA in the hope they may be more forward thinking and to discuss the development of the technique in order to help their cancer patients. The same answer came back almost every time. The method is too “novel and detects too early”!! Whilst “How can a few cells be treated when they cannot be visualized, or their location is not known.”

As if the location is vital. For this negates and systematically quashes the notion that something like this simple test could if used regularly, create early notice of cancerous cell presence that could then be treated. Yet it is preferred that the cancer grow to a size large enough for everyone to see it on a scanned image. As we know this is the metastasized stage when the immune system is overrun and become dormant and submissive to the cancer that is now so unwieldy and strong and the chances are drastically shortened.

The critical issue is that Nagalase testing once available will need to be thoroughly understood by the medical professionals adjusting and adopting new regimens for the successful treatment of early-stage cancers. Guidance in this process by a trained professional will be critical. For we can only hope that in the early days of GcMaf availability, until proper accreditation is established, finding a doctor who is experienced in the use of GcMaf and Nagalase testing will be challenging.

 

• Anti-Malignin Antibody Serum Assay (AMAS): Alternative Biomarker

 

There is another exciting biomarker test specific for cancer cells and malignant tumors that we would like to highlight. This is the Anti-Malignin Antibody Serum assay (AMAS). This assay measures and detects the anti-malignin antibody expressed in >99% of patients with tumors and is a very useful initial screening test and can also be used to monitor the effectiveness of any ongoing cancer therapies.

As described earlier Cancer cells are generated due to mutations and the presence of mutagens. These regular mutations provide a base level of the anti-malignin antibody. The levels are elevated when cancer is present and decreases to baseline levels when the cancer has been eradicated. The AMAS has accuracy greater than 99% when duplicate samples are assayed. If a treatment is effective and causes a reduction in a cancer load, the measured AMAS will be reduced. A decrease in measured AMAS will occur even if the effective treatment is surgically based on chemotherapy, radiation treatment or an alternative cancer therapy like GcMaf. If the cancer load falls the measured AMAS level also decreases. If the cancer remains, the measured AMAS will also remain positive.

The AMAS test simultaneously screens for all cancer types, unlike some other specific biomarkers such as prostate cancer (PSA measurement) and colorectal cancer (CEA).

Much like the Nagalase test,

The AMAS test can highlight the presence of cancers and to follow their regression. Yet, the anti-malignin antibody is not generated by viruses, so the AMAS assay cannot detect these sorts of infections. The Nagalase and AMAS tests should be part of the normal routine blood screening for all susceptible or at-risk people.

If Nagalase becomes a standard blood test it can be used in a powerful way with the standard AMAS to distinguish between cancers and severe viral infections. It was described earlier that all viruses and cancers express Nagalase. Thus, high Nagalase levels could be caused by a growing cancer or a viral infection. The anti-malignin antibody is expressed by cancer cells. Understanding the differences between the measured levels of these two biomarkers helps understand and determine the type of infection. If the levels of both Nagalase and AMAS are measured and are deemed to be higher than the average normal baselines, then cancer is the cause of the increase. If Nagalase is raised and a normal AMAS level is measured, then a viral infection is present.

 

• GcMaf (VDTP) Research Work

 

The first research papers on cancer treatment using GcMaf (VDTP) were published by Prof. Nobuto Yamamoto. The described work with GcMaf (VDTP) started in the 1990’s and continues into this current decade. The number of research groups has increased and yet a commercial preparation suitable for regular use as a cancer treatment has not yet been fulfilled. There needs to be a defined production and clinical trial plan to expedite GcMaf (VDTP) as a fully acceptable drug treatment.

The use of the GcMaf (VDTP) protein has been proven to remove cancer tumors in patients. The details in the papers have provided the information for the preparation of today’s GcMaf (VDTP). Yamamoto also detailed his strategy for treatment, whilst his research papers provide an impressive series of science masterpieces, laying the foundations for further progression.

All of Yamamoto’s patients had all received the prior treatments of surgery, chemotherapy, and radiation therapy. All of which still had metastatic disease. Their prognoses at this stage (due to the metastasized cancers) were that the secondary tumors were inoperable and untreatable. All of his patients were in the earliest phase of metastatic disease and received GcMaf (VDTP) shortly after the standard treatments had been completed.

After several weeks of treatment, it was shown that Yamamoto’s approach had fully eradicated any metastatic breast, prostate and colon cancers in all the treated patients. Conventional treatments are effective in reducing tumor load, however, they often spread loose cells that go on to form metastasized cancers elsewhere, rather than removing all remaining traces of cancer. He worked with patients who the medical oncologists had effectively washed their hands of, with palliative care as the only remaining option.

In standard modern medicines terms, cases of metastatic cancer being successfully treated and eradicated are a rare occurrence. This is despite government’s funding the cancer industry with billions of dollars over the last 50 years.

Please note that Yamamoto based his treatment plan on relatively low doses of GcMaf (100ng GcMaf once a week) compared to 3000ng what we now use today for the very best results.

The GcMaf (VDTP) patient data that Yamamoto presented showed cancer tumor clearance in a reasonably rapid time frame. The breast and prostate cancer patients showed tumor clearance in less than 6 months. The treatment regimen was weekly administration of GcMaf injections. The colorectal cancer patients in the study had a tumor clearance in approximately a year. Yamamoto diligently followed up these patients over a 5-7-year period and none of his treated patients had any recurrence. Using higher doses of 3000ng daily ensure more cancer fighters recover from Cancer than previously. 

Many other groups have now added to Yamamoto’s innovative work and have repeated tumor clearance in patients. The cancer curative rate observed by Yamamoto was reported to be “dependent on both the number of receptors for the particular antigen on macrophages and the number of antigens on each cell.” (Int. J. Cancer: 122, 461–467 (2008). Yamamoto describes the specifics in his breast cancer paper from 200 as:

“Thus, the macrophages activated by GcMaf developed an enormous variation of receptors that recognize a variety of microbial agents (e.g., bacteria and viruses) and abnormalities in malignant cell surfaces. The fundamental nature of macrophages to recognize cell surface abnormality is universal to all types of cancers.”

Yamamoto found that a weekly administration of 100ng GcMaf to cancer patients provided measured observable benefits of tumor regression on a wide range of cancers. With the administrative use of 3000ng we are seeing a high percentage of people having complete recovery.

Yamamoto highlighted this difference in the 2008 prostate cancer paper on the connection between cell surface abnormalities, degree of differentiation, and effectiveness of GcMaf: “Efficacy of GcMaf therapy and curative rates of various cancers by GcMaf therapy depend on the degree of (cancer) cell membrane abnormality, which corresponds to the grade of differentiation of the malignant cells.” (Translational Oncology. 2008 July; 1(2): 65–72).

 

 Example protocol of GcMaf (VDTP) 

 

For late-stage cancers (stage 3 and beyond) the recommended dose of GcMaf (VDTP) is 3000ng injected daily intramuscularly or Sub Q for a period of 90 days. This equates to 1ml from the 7500ng vial daily. Each vial contains 2.5ml. 36 vials would be needed for the 3 months course. The dose is injected sub–Q or intramscular. Earlier stage cancers would require 1500ng/0.5ml taken from the 7500ng daily for 3 months, this is 18 vials for the 3-month course for best results based on the years of collating research   This is in addition to maintaining sufficient vitamin D levels 90-100 is optimal as mentioned above and as part of the overall treatment plan. It goes without saying that there is no one size fits all. Should you require personal advice regarding dosing, please email [email protected]

 

A brief guide for using GcMaf/VDTP

ADULTS over 14 years

Stage 1 early-stage cancer VDTP/GcMaf  protocols

Administration is via Injecting I.M or Sub C using a small gauge needle and a 0.5ml or a 1ml syringe. 

Month 1

1ml of VDTP/GcMaf per day, from a 7500ng vial (3000ng a day) 

Total of 12 vials of 7500ng for the month.

Month 2 & 3

0.5ml of VDTP/GcMaf per day, from a 7500ng vial (1500ng a day) 

Total of 12 vials of 7500ng for two months (6 vials per month).

Over the 3-month course this is a total of 24 vials of the 7500ng vials.

 

Stage 2 through to Palliative care
Administration is via Injecting I.M or Sub C using a small gauge needle and a 1ml syringe. 

1ml of VDTP/GcMaf per day, from a 7500ng vial (3000ng per day)

12 vials are required a Month, so 36 vials are required for 3 months’ supply.

 

Lung cancer, we suggest nebulising1500ng 0.5ml daily and injecting 1500ng which is a total of 300ng/1ml daily from a 7500ng vial. 12 vials are required Monthly and 36 vials are required for 3 months’ supply.

Please note that each vial contains 2.50ml

 

Undifferentiated tumor cells appear to be more effectively destroyed than differentiated cells.

 

Cancers cells such as adenocarcinomas breast and prostate cancer are classed as undifferentiated. They are quickly engulfed and destroyed by activated macrophages. Cancers such as squamous cell carcinoma cells are attacked by the activated macrophages, but at a slower rate.

These cancers all express Nagalase so the administration of GcMaf helps overcome the deficiency allowing a macrophage stimulation to fight off the infection. The diseases that Yamamoto treated included: – Cancers, including prostate, breast, colon, stomach, liver, lung (including mesothelioma), kidney, bladder, uterus, ovarian, head/neck, brain cancers, melanoma, and fibrosarcoma.

Yamamoto also treated other infections and disease targets and viral infections such as Influenza, Hepatitis type B and Hepatitis type C, Human Immunodeficiency Virus (HIV) Herpes Type 1 and Type 2viruses. In fact, all enveloped viruses appear to be susceptible to activated macrophage destruction.

 

How GcMaf destroys HIV

 

HIV—like all viruses—makes Nagalase, the enzyme that blocks GcMaf production. Without GcMaf, macrophages become indolent and the anti-viral immune response shuts down. This allows the HIV infection to spread. To remedy this situation, Dr. Yamamoto simply gave these patients GcMaf. This reactivated the sleeping macrophages, which then proceeded to phagocytize all of the viruses.

 

The precise molecular biological pathways and mechanisms involved with HIV, Nagalase, and GcMAF are identical to those for cancer cells, and need not be repeated here.

 

In HIV studies they first showed that HIV patients had high Nagalase levels which correlated with their high HIV RNA levels (a way to measure the amount of HIV infection). Then, as he administered GcMAF (3000 ng. 3 x weekly for 12 weeks), all patients’ Nagalase levels gradually went down to control levels, and, in tandem with the Nagalase, viral load went down to zero. This data “suggests that these patients were free of both HIV virions and HIV-infected cells.”

 

Professor Yamamoto followed these patients for seven years, and their viral load (HIV-1 RNA), CD4 counts (helper cells, a type of lymphocyte used to evaluate immunocompetence), p24 antigen (HIV-specific antigen), viral culture, and Nagalase levels remained normal. All patients continued to be free of disease. (Note: anemic HIV patients were excluded from this study. Anemia is common in HIV patients. The effect of GcMAF on anemic HIV patients is thus unknown.)

 

GcMaf has showed positive results in mice

 

Work by Nonaka et al 2012; using a mouse model demonstrated that treatment with GcMaf (VDTP) at a level of 40ng/Kg/d caused an obvious decrease in tumor size.

Liver cell cancer is detailed as Hepatocellular Cancer (HCC). From the research work completed and detailed in the scientific paper referenced above; Nonaka and his co-workers provided the following conclusion.

 

“Conclusion: VDTP-maf has at least two novel functions, namely, an anti-angiogenic activity and tumor killing activity through the activation of macrophages. VDTP-maf may therefore represent a new strategy for the treatment of HCC.”

 

It can clearly be seen, the difference in tumor size from 6 cancer tumor experimental mice, three having been treated with GcMaf (VDTP).

 

Pivotal Breast Adenocarcinoma Paper

 

Following breakthroughs, the next key phase in the field of GcMaf research was  that of Ruggiero et al Anticancer Research 35: 5525-5532 (2015) on breast cancer, which was a pivotal paper. As here the blood monitoring and biomarker assay tests were performed and verified by an independent Italian hospital and so adding further credibility to their discoveries.

A 37-year-old patient presented with adenocarcinoma in her right breast in 1985. The breast cancer diagnosis was swiftly followed by partial resection surgery, with lymphadenectomy and post-surgical irradiation.  In 1999, at the age of 51 years, the adenocarcinoma had returned to haunt her and so she was diagnosed with breast cancer once more, only this time it was in her left breast. Since no testing had been done on the previous tumor, it is not known whether this was a metastasis of the original cancer, or a newer independent occurrence. So another partial resection mastectomy followed, with anti-estrogen receptor (ER) treatment for a further 6 years, as a preventative measure.

In March 2014, at the age of 66 years, following a routine mammography, an infiltrating adenocarcinoma was diagnosed in the remaining part of the right breast. In the proximity of the areola, (the superior external quadrant), an inhomogeneous lesion of 14×9.2×12 mm (1.545 mm3) with irregular margins was detected and confirmed by ultrasonography. Immediately after this diagnosis, the patient underwent ultrasound-guided fine-needle (14-gauge) biopsy, and four specimens from different areas of the lesion were examined, whilst Magnetic resonance imaging (MRI) was performed to assess the local extension of the tumor.*

Hence, we have a case of a woman diagnosed with recurrent breast cancer, but the breakthrough here is the self-administered supplementation diet that she followed for three weeks prior to the planned surgery. This diet being a ketogenic diet rich in olive oil and high doses of Vitamin D3 that led to unexpected positive changes in her tumor markers.

 

•  The Successful Remedy

 

  The time frame from diagnosis to surgery was only 3 weeks, during that time the patient stuck to a ketogenic diet and self-administered a commercial preparation of oleic acid associated with glycosylated Vitamin D Transport protein, she also enriched her diet with commercial olive oil and fermented milk products also rich in natural glycosylated Vitamin D Transport protein.

Following the surgery, the surgeon gave a verbal anecdotal response: “the tumor could have been removed using two spoons, as it was surrounded by white blood cells [that] almost act[ed] like a capsule.” The following Assays for Progesterone receptors demonstrated a switch from <1% to a more normal 20% and other assays indicated a complete switching off of the HER2 protein and gene, showing great success.

And so what this paper shows is that breast adenocarcinoma can be eradicated using GcMaf, whilst the best use and form of treatment is combination of therapies once tumor cells have become established.

 

• GcMaf Treatments

 

The GcMaf (VDTP) administered was a highly purified preparation and a human form of the macrophage stimulating molecule. This means that the 3-D structure and method of interaction is identical to the same molecules generated in the body. It is therefore a natural molecule in every function. There has never been any mentioned, or recorded adverse reactions, side effects, or toxic reactions to pure GcMaf (VDTP).  This includes Yamamoto’s work and from any other group using purified GcMaf (VDTP).

The administration of GcMaf is normally by intramuscular (IM) injections. This was the favored route by Yamamoto, and others, however advocated the use of subcutaneous and oral delivery. Oral delivery is used as a buccal delivery by holding the GcMaf (VDTP) in the buccal area mainly under the tongue, for uptake through the multiple arteries and veins in the sublingual cavity. The membranes are particularly thin on the lingual artery and lingual veins. The tonsillar branch of the facial artery and the pharyngeal artery are secondary supplies to the buccal cavity. The blood supply is full and accessible. Some of the GcMaf preparations that were used contained oleic acid and Vitamin D which aids the uptake into the blood vessels. Particularly good results in clearing dental cavities were also noted in his work although no direct research papers were generated.

They also injected preparations directly into the arteries supplying the pancreas, using ultrasound to follow the needle position. Using this technique, he had good success with treating pancreatic cancer and again he presented results at several meetings, but never generated peer reviewed research papers.

Yamamoto worked on early small tumors that had been de-bulked and reduced in size. The cancers were solid and had not metastasized. Yamamoto had a success rate that was close to 100% when using GcMaf (VDTP) therapy.

 

*The MRI, the surgery, and the analyses on estrogen receptor (ER), progesterone receptor (PgR), human epidermal growth factor receptor (HER2) and nuclear protein Ki67 (both on the preoperative biopsy and on the surgical specimens) were performed at the University Hospital (Italian Public Health Service) of Firenze, Italy.

Analyses were performed according to the European standards of quality (UNI EN ISO 9001:2008) and were examined and countersigned by four different medical professionals.

 

The pivotal paper was for advanced breast adenocarcinoma, alas other groups are reluctant to publish their findings on GcMaf (VDTP) treatments and any successes they have had for fear of reprisal. Whilst as many of you will know the wider pharmaceutical industry has curbed much of GcMaf ‘s (VDTP) untapped potential and often block the publishing of papers and cause many retractions.

Despite this, the slow increase of GcMaf (VDTP) treatments has driven the need for biomarker assays being used as a routine assay. Some work was being performed by the University Hospital of Groningen, but the wider field of oncologists and hematologists declined the use of this technology for the same reason as above. Early detection provides complex issues as it could not be seen on a screen and therefore, they couldn’t treat the patient. So yet again the patients must wait until the cancer has become established and a major issue for the patient. The need for Nagalase and AMAS as routine assays is becoming an important step in the cancer treatment process. Nagalase/AMAS can therefore be used to monitor the effectiveness of any cancer treatment, including both drug and alternative therapies, separately or in combination.

 

GcMaf (VDTP)Attributes

 

As you will now be aware, there are several major advantages that GcMaf have over a number of conditions and diseases. As the number of quiet researchers has increased so has the number of disease targets. There have been several relatively unknown innovative ways of using GcMaf in the laboratory to elucidate its modes of direct action.

For we have covered the stimulation of macrophages for fighting cancer and infectious disease. We have also mentioned that GcMaf is bound to Vitamin D as it is used to carry Vitamins D throughout the bloodstream. It can also bind (VDTP) oleic acid and actin. So as a messenger molecule it can switch on specific protein pathways as well as switch some pathways off. The number is unknown and further research is needed to determine exactly what is being switched on and off, as almost every cell has a Vitamin D receptor, the potential number of switches is immense.

The research is a continuous flow as the knowledge is being worked on every day and constantly updated and so will be reported when new information and clinical results become available.

 

• Inhibition of Angiogenesis

The effects of Gc protein-derived macrophage-activating factor (GcMaf) (VDTP)have been studied in cancer and other conditions where angiogenesis is deregulated. In this study, we demonstrate for the first time that the mitogenic response of human peripheral blood mononuclear cells (PBMCs) to GcMaf (VDTP) was associated with 3′-5′-cyclic adenosine monophosphate (cAMP) formation. The effect was dose dependent, and maximal stimulation was achieved using 0.1 ng/ml. Heparin inhibited the stimulatory effect of GcMaf on PBMCs. In addition, we demonstrate that GcMaf (VDTP) 1 ng/ml) inhibited prostaglandin E(1)- and human breast cancer cell-stimulated angiogenesis in chick embryo chorioallantoic membrane (CAM) assay. Finally, we tested different GcMaf preparations on CAM, and the assay proved to be a reliable, reproducible and inexpensive method to determine the relative potencies of different preparations and their stability; we observed that storage at room temperature for 15 days decreased GcMaf potency by about 50%. These data could prove useful for upcoming clinical trials on GcMaf.

 

Gc protein-derived macrophage-activating factor (GcMaf)/(VDTP) immunotherapy has been steadily advancing over the last two decades. Oral colostrum macrophage-activating factor (MAF) produced from bovine colostrum has shown high macrophage phagocytic activity. GcMaf(VDTP)-based immunotherapy has a wide application for use in treating many diseases via macrophage activation or for use as supportive therapy. Three case studies demonstrate that oral colostrum MAF can be used for serious infection and chronic fatigue syndrome (CFS) without adverse effects. We demonstrate that colostrum MAF shows promising clinical results in patients with infectious diseases and for symptoms of fatigue, which is common in many chronic diseases. Copyright© 2015 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.

 

As part of the actions that GcMaf (VDTP) has in stimulating macrophages it also has a direct effect on the cancer tumor itself. GcMaf directly reduces the ability of cancer tumors to generate their own blood supply. Cancer As stated earlier, cancer tumors secrete proteins that promote the generation of blood vessels, a process known as angiogenesis. Obviously, the greater the number of blood vessels, the greater the chance that cancer has to acquire nutrients and therefore grow more rapidly. If the number of blood vessels, or growth is restricted, then the tumor growth itself could be reduced. There is an assay to determine if agents can stop the angiogenesis using embryos in chicken eggs called the chorioallantoic membrane model (CAM). It allows a direct delivery of chemicals and medicines to be placed on the embryos to create a visual count of the blood vessels being formed.

Please see the images below that depict the assay results of the chorioallantoic membrane showing blood vessels that give an instant easy to read result. Usually a photo is taken and the blood vessels projecting from the fertilised egg are counted.

The assay used chick embryo chorioallantoic membrane treated with prostaglandin E1and human breast cancer cells causing the observed blood vessel formation. The angiogenesis caused by the prostaglandin E1 and human breast cancer cell was reversed when in the presence of 1ng/mL of GcMaf (VDTP).

 

The image on the left show’s angiogenesis caused by the prostaglandin E1

 

The image on the right shows human breast cancer cells reversed when in the presence of 1ng/mL of GcMaf.

The left column of B&W images (Photos A, C and E) has Prostaglandin E1

The left column of B&W images (Photo B, D and F) has been treated with 1ng/mL of GcMaf.

 

GcMaf was therefore shown to cause an inhibition of angiogenesis. The effect is observable at extremely low levels, highlighting the effectiveness of GcMaf and conversely how potent Nagalase is at stopping normal levels of GcMaf having the desired effect.

This reference details the work generated for the CAM assay: – Pacini S, et al, Gc protein-derived macrophage-activating factor (GcMaf) stimulates cAMP formation in human mononuclear cells and inhibits angiogenesis in chick embryo chorioallantoic membrane assay. Cancer Immunol Immunother. 2011; 60(4): 479-485.

Induces Apoptosis

 

The work of monitoring GcMaf (VDTP) capability of causing apoptosis has been limited and is not regarded as a main attribute of the molecule. GcMaf (VDTP) can bind oleic acid which has come under extreme interest as it is a molecule that instigates apoptosis. It is able to be delivered to cancer cells by the GcMaf (VDTP), cancer cells are faster growing than normal cells so the membranes of cancer cells are more fluid as they are constantly being stretched and split so oleic acid can enter the cells easily once GcMaf (VDTP) has attached to the appropriate receptor. However, the following paper highlights the apoptosis capability of GcMaf (VDTP).

Reference: – Thyer L, et al; 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.

 

Cancer Cell Phenotype

 

Whilst it has not been fully studied with direct research publications, but initial observations highlight yet another area of interest and that is the morphology of tumors as it has been recorded that cancer cells can revert back to being normal cells once they have been brought back under control, this is called morphology. Please see below for an observed visual morphological change. Further research to monitor the cell specific markers would be needed to confirm this function of GcMaf (VDTP). As yet the evidence is anecdotal.

 

Figure of MCF7 cell mass degrading to a “normal” monolayer cultured in 40ng/mL GcMaf.

 

The photograph clearly shows the growth on the left of MCF7 breast carcinoma cells in a monolayer mass growing on the surface. Whereas the image on the right-hand side shows the same mass in the presence of GcMaf (40ng/mL). The morphology has been altered and the cell mass is decreased.

 

Improves Metabolic Activity

 

The work presented below highlights neuronal (brain) cell activity and how the interactions between these cells are observed to be improved in the presence of GcMaf. Certain conditions that are known to decrease neuronal interactions have been shown to be alleviated by using GcMaf. Such as:

• Autism
• ME/CFS
• MS
• ALS

With research also showing an alleviatiation of neuronal pain in rat models, as shown in this reference.

The pictures below show the human SH-SY5Y neuronal cells cultured in the absence and presence of GcMaf (VDTP). It is clear to see that the cells cultured in the presence of 8pM of GcMaf (VDTP) have numerous cell interactions with neighboring cells and have an overall better cell membrane content. It is as if the cells are looking to make additional contact with other cells to increase the network capability.

         

A: Control, 24 h.

B: Control, 72 h.

C: GcMaf, 8pM, 24 h.

D: GcMaf, 8pM, 72 h

     

Imagery showing the effects of GcMaf on human neuronal morphology.

 

Human SH-SY5Y neuronal cells were stained with haematoxylin-eosin after 24 h or 72h incubation with saline containing 8 pM Gc-protein (control), or with 8 pM GcMaf (VDTP) .

 

The table below shows the monitored levels of cAMP of cells cultured in the presence and absence of GcMaf. It can be seen that in the presence of 80pM of GcMaf (VDTP) the levels of cAMP are almost double that of normal cultured cells.

 

Treatment	cAMP
Control	10.5±1.2
GcMaf 8 pM	12.0±1.1
GcMaf 80 pM	19.8±1.2

 

cAMP Concentration in Human Neuronal Cells Stimulated with GcMaf(VDTP) Treatment cAMP

 

Reference: Smith et al.  American Journal of Immunology 9 (4): 120-129, 2013

 

Counters Toxic Effects Including Cadmium

 

Often the toxic compounds in our society cause many illnesses. These can be from cancer to allergic reactions to conditions such as autism. A typical indicator of such toxic compounds is the treatment of cells with the heavy metal cadmium. Below is a picture of the results from a reference paper regarding how GcMaf has protective capabilities against the toxic cadmium metal and specifically on neuronal (brain) cells.

Please see the image below, the brain cells on the left are cultured in the presence of cadmium at 10µM, whilst the cultures on the right contain the same amount of cadmium, but are also in the presence of 800pM GcMaf (VDTP) with oleic acid.

 The following series of images (top to bottom) increase in magnification, so as to better assess the culture of brain cells studied. Notice the way they grow to make connections between each other.

 

In the presence of GcMaf (VDTP) there is good homogeneous cell growth with obvious network interactions, the cells look healthy and functioning, as compared to the cadmium cultured neuronal cells alone. Thus, indicating that even with 800pM of GcMaf (VDTP) there is obvious protection of neuronal cells occurring, even in the presence of a heavy metal toxin.

For more see the original research paper: Morucci et al; Treatment and Prevention of Cadmium-induced alterations on human neurons. Italian Journal of Anatomy and Embryology (2013) 118 (Suppl. 2): S144

 

• GcMaf Increases Neuronal Connectivity

 

As stated, conditions such as Autism, ME and CFS have poor interactions of neuronal networks. The problem with many medications is the difficulty of getting across the blood brain barrier. The following details of further laboratory work shows how brain cell networking is improved using GcMaf (VDTP). Furthermore, clinical research from Dr Nicola Antonucci published data on the use of GcMaf in a clinical scenario, which provides further encouraging results and especially in the field of autism which has been presented at specific meetings and the clinical data

 

For further details, please read the original research paper: Branca et al; Vitamin D binding protein-derived macrophage activating factor stimulates proliferation and signaling in a human neuronal cell line. Italian Journal of Anatomy and Embryology (2013) 118 (Suppl. 2): S143 (P28).

 

• GcMaf can Inhibit Tumor Cell Growth

 

It has been reported that GcMaf alone can stop the growth and indeed reduce the number of cancer cells. Whilst we can also see a comparison in levels of GcMaf (VDTP) effectiveness as has been reported in the following research, using MCF7 human breast carcinoma cells.

MCF7 cells were cultured and allowed to grow in both the presence and absence of various amounts of GcMaf (VDTP). In the graph below we see the results of culturing MCF7 breast cells in the presence of GcGlobulin. As also compared to low levels of GcMaf (VDTP) alone, a low level of Vitamin D, a higher dose of GcMaf, a higher level of Vitamin D and then high levels of GcMaf (VDTP) and Vitamin D combined in column 6 (please see below for the exact figures). Whereas Panel B (right hand graph) depicts the decrease in breast cancer cell growth with GcMaf alone and again after 72 hours.

                  

Panel A: Assessment of cell proliferation by methyl-thiazol-tetrazolium (MTT)-based assay.

Panel B: Effects of 72-hour treatment with Vitamin D-binding Protein-derived Macrophage-activating Factor (DBP-MAF) on MCF-7 cell proliferation.

 

Treatment columns

• Control (VDBP, 40 ng/ml)
• DBP-MAF, 0.4 ng/ml
• Vitamin D (1,25(OH)-2D-3), 100 nM
• DBP-MAF, 40 ng/ml
• 1,25(OH)-2D-3, 1 μM
• 1,25(OH)-2D-3, 1 μM + DBP-MAF, 40 ng/ml

 

Panel B: Assessment of cell proliferation by cell count. MCF-7 cells (2×105 cells per well) were seeded in 24-well plates and then manually counted again after 72 hours using a haemocytometer.

 

Treatment columns

1: Control.

2: DBP-MAF 0.4 ng/ml.

 

Reference: Pacini S et al; Anticancer Research January 2012 vol. 32 no. 1 45-52

 

Should GcMaf be the Choice of Treatment for Cancer

 

As seen above GcMaf (VDTP) has a range of potential benefits for several important disease targets. Cancer and the stimulation of the macrophages remains the foremost benefit and the most understood. Some cancer patients might think about just using GcMaf (VDTP) alone as the chosen remedy for the removal of any tumors they have. It may seem a preferable option over surgery, chemotherapy and radiation therapy. The original clinical data was all from patients who had their tumor load decreased using the traditional cancer treatment methods. We know that GcMaf (VDTP) can stimulate macrophages to clear and find the metastasized cancer cells very effectively. GcMaf (VDTP) would be a choice and perhaps some benefit on non-surgical tumors or after all treatments have been attempted. However, the most beneficial is combination therapy as first used in treating a breast adenocarcinoma patient (as stated above) who prior to surgery received GcMaf (VDTP) causing her macrophages to encapsulate and seal off the cancer avoiding its spread and further aiding the surgical excision.

The successes had with pancreatic patients whose prognosis was poor and had little chance of survival otherwise. His approach could be employed once a cancer can be identified and confirmed. Again, this is a question of uptake as such a clinical approach will take time for current medical professionals to understand and adopt this new and innovative treatment plan of incorporating GcMaf (VDTP) as part of their standardized approach. Whilst using the Nagalase biomarker test to measure the treatments effectiveness.

In the earliest stages of cancer, when the mass is still very small (<5mm), the “debulk first” cannot be performed. If a patient has an elevated Nagalase level indicating that a cancer is present somewhere and its mass cannot be seen using the typical procedures, as we have now learnt it can be confirmed by a panel of typical cancer biomarker assays. Obviously in an ideal world this would be the time to start GcMaf (VDTP) treatment, to be then monitored by Nagalase level testing. But if a tumor has grown to such a degree that it is large enough to be identified and visualized with imaging capability, then it is prudent to have a surgeon remove it. Whilst the ideal scenario would be to also administer a GcMaf (VDTP) treatment in advance of the surgery and continue during recovery. Clearing away any cells that may have broken off during the surgery preventing them from locating elsewhere as metastasized cancer. Not only, this but GcMaf would also aid wound healing and shorten recovery times.

 

• GcMaf Therapy

 

The precursor to GcMaf (VDTP) is the albumin family protein GcGlobulin. It is also known as Vitamin D binding protein, or Vitamin D transport protein, which highlights an issue in our overall health, in that most people are Vitamin D deficient due to lack of sun exposure and a ‘modern’ diet. Vitamin D deficiency is very common and affects over 70% of the American population, for example, dramatically increasing the risk of neoplasm. In order to have an adequate amount of GcGlobulin present then a good supply of Vitamin D is needed. Therefore, testing is needed to determine the levels of deficiency. Whereas Supplementation of 10,000 IU a day of Vitamin D3 would be a reasonable dose for someone who is deficient with subsequent further testing would be required to determine the individual’s optimum dose.

Poor levels of Vitamin D mean poor levels of Vitamin D transport protein, meaning poor levels of GcMaf in times of need. Once a cancer, or infection has begun then Nagalase will easily mop up low levels of Vitamin D transport protein and prevent its conversion to GcMaf (VDTP). Hence external GcMaf (VDTP) is required, to help rebalance the ratio and stimulate macrophages to move into action and fight off the cancer and infection.

For late-stage cancers (stage 4 and beyond) the recommended dose of GcMaf (VDTP) is 3000ng injected daily Sub Q for a period of 90 days. This is in addition to maintaining sufficient vitamin D levels as mentioned above and as part of the overall treatment plan.

 

For individual GcMaf dosage protocols please contact [email protected] for further advice on a personal protocol.

 

• Potential Reducers of GcMaf Effectiveness

 

Protease inhibitors: – HIV patients taking protease inhibitors may notice a reduced effect when taking external GcMaf (VDTP). Macrophages stimulated with GcMaf (VDTP) move to the M1 type and are active in engulfing and phagocytosing cancer cells and infected damaged cells. The macrophage phagolysosomes contain proteases that work to digest cancer cells and viruses. Therefore, Protease inhibition may interfere with phagolysosomal protease activity. There is no published data to indicate this but GcMaf (VDTP) may take slightly longer to readdress the balance and “get over the hill” to treat the infection when taking this specific medication.

 

Opiates: – According to Prof. Yamamoto, opiates derived medicines such as morphine, Demerol, opium, oxycodone, hydrocodone, Percodan, Percocet, Vicodin, and Norco may also block GcMaf (VDTP) macrophage activating effect. As yet, there are no further published studies on this.

 

Anemia: – A lack of sufficient red blood cells may also compromise GcMaf (VDTP) overall effectiveness. Anemic patients were excluded from all of the studies. This may be because of suitable recovery, or additional complications. Again, as yet there are no published studies on this aspect of GcMaf (VDTP) and anemia.

 

Insufficient macrophages: – If a person doesn’t have a large enough pool of macrophages, or monocytes (the precursor cells that become macrophages), they might not respond as briskly to GcMaf (VDTP), as a person with “normal” macrophage/monocyte levels. Patients with low white cell counts (or otherwise compromised immune functions) should try to boost their monocyte/macrophage levels by suitable. Supplementation. Hydrolyzed whey protein is known to encourage the bone marrow to produce white blood cells. Other supplements may also be available to help restore macrophage levels.

 

• Medical Monitoring Required

 

Medical supervision is always recommended for the administration of GcMaf, whilst the benefits need to be observed in conjunction with current cancer treatment approaches to avoid any complications.

 

• GcMaf (VDTP) effectiveness depends on optimum administration of conventional mainstream cancer therapies. Tumour debulking using surgery, chemotherapy, and/or radiation would help the effectiveness of macrophage stimulation and phagocytosis.

 

• Physicians are necessary to understand and diagnose any other additional medical conditions in order to ascertain the best approach.

 

• Whilst a trained physician is needed to check the biomarkers such as AMAS or Nagalase levels (when available) to determine whether or not the GcMaf (VDTP) treatment is working and where to adjust it where necessary.

 

• Cancer imaging, ordered and interpreted by physicians, provides crucial information about cancer progress.

 

Good intentions coupled with poor training can lead to disaster. Anyone who allows a novice to administer GcMaf (VDTP) is making a big mistake. GcMaf (VDTP) administration must always be monitored by a physician who is trained in its use.

Rather than a substitute for conventional cancer therapy, GcMaf (VDTP) is an adjunct to it. GcMaf (VDTP) effectiveness depends on optimum administration of conventional mainstream cancer therapies.

 

•  Acquiring the Best GcMaf

 

The GcMaf (VDTP) available from suppliers can range greatly in quality. The emergence of GcMaf (VDTP) therapy and Nagalase testing as viable methods for treating and preventing cancer will inevitably be accompanied by genuine concern and debate about how best to put these valuable tools to work.

There will always be the denigrators of GcMaf (VDTP) available based upon little knowledge. People tend to gravitate towards negative reviews and remain skeptical towards positive results. Therefore, the supplier must always be able to provide their own independent data on the results of the material they offer and be able to explain these results in detail. Any good supplier will be able to discuss GcMaf (VDTP) with understanding and knowledge, whilst those who offer ineffective imitations, or counterfeit products will appear to offer the best without any back-up information. These are the suppliers to avoid.

Because it is identical (ie., bio-identical) to what the body produces naturally, pure GcMaf should never cause any adverse symptoms of any kind. Administration does raise the temperature a little, not excessively, but that is normal. There should never be any rashes at the entry point, no coughing, or any other adverse reactions displayed. If any such symptoms do appear in an individual taking GcMaf then the cause is impurity, contamination, or both. Seek genuine case studies and reviews before approaching any supplier.

 

With the ongoing war on our health, doctors, nurses and scientists have come together to form Vigor Life. A company specializing in individually tailored therapies and treatment plans for patients that the medical establishment has failed. As a startup company, backed by decades of professional scientific and clinical expertise, new cutting-edge therapies are now available worldwide.

 

GcMaf (VDTP) has been proven to be safe and effective in the treatment of a variety of illnesses and diseases. The latest research findings are indicating it has many more benefits than originally believed. As it is a naturally occurring protein that is produced in the bodies of all healthy people, by default, it has no adverse side effects. In effect, it is the right jigsaw piece to fill the deficiency and completes the whole picture. It is not an additive to mask the hole in the way allopathic medicine is used.

 

Vigor Life in Bulgaria and Saisei Marai in Japan are the only companies producing genuine bioidentical GcMaf in the world that is pure, unadulterated and consistently ‘active’ leaving it as the most effective product of its kind. All other producers of GcMaf have either stopped production, halted export or altered their processes in some way to leave their finished product unavailable beyond their borders, diluted, inert or even potentially harmful.

 

Many proponents of GcMaf (VDTP) are hailing it as a ‘magic bullet’ for cancer and other diseases, however they are doing as much harm to people’s perception of it as are the detractors. Vigor Life uses GcMaf (VDTP) only as part of a treatment plan in conjunction to strict adherence to the prescribed protocol of their doctor. It is reckless to think that GcMaf (VDTP) on its own is a cure. This is why Vigor Life only distributes through certified and licensed medical practitioners that possess extensive knowledge and experience in immunotherapy. They offer full spectrum support and advice for everyone using or considering GcMaf as part of their health regime. 

 

Interest in GcMaf (VDTP) has exploded around the world which has resulted in many more avenues of research into the role it plays throughout the body. The scientists and doctors at Vigor Life are at the forefront of this push to discover more about this vital protein.

 

• Purity and GcMaf production

 

A “pure” protein contains only molecules of a single protein, and no other molecules of any kind. Impurities cause compromised effectiveness, adverse reactions, and symptoms of toxicity. Making “pure” GcMaf (VDTP) is not a simple undertaking. Several groups now generate GcMaf to high standards. The methods of Yamamoto have been refined and improved. Some can use your own blood (apparently) although it is best to use external GcMaf before sending your own blood, as is the case with the Saisei-Mirai group. They also now offer an oral version, based upon the yoghurt production of the Bravo system. They also have a high concentration Version 2 which they use in the same approach as the one Yamamoto prescribed.

The methodology of GcMaf (VDTP) production is not onerous to learn and a good laboratory can make GcMaf relatively easily. However, the skill set lies with the preparation and the assurance that no contamination is present and that the vial preparations are also stored appropriately.

The administration of impure, or non-bio-identical, or contaminated GcMaf (VDTP) carries a high potential for side effects and adverse reactions. It also might not stimulate macrophages appropriately. The importance of establishing a GcMaf c(VDTP) verifying authority cannot be overstated. This approach is being worked towards by groups such as Effram but as, yet no clinical data has been provided, discussed, or presented.

 

• Pro-Biotic Emulsion GcMaf

 

There has been a rise in production of the yoghurt GcMaf by Bravo and others. These preparations use many probiotic bacteria that can use the enzymes in the GcMaf (VDTP) preparation. The idea is that the probiotic bacteria use the milk sugars and proteins to grow and secrete the enzymes and convert the GcGlobulin in the milk, or colostrum to generate GcMaf. This GcMaf is in a bovine form, that is to say, from cows, as the milk used is likely to be cow’s milk. Bovine GcMaf can stimulate macrophages in lab cultures and so it is assumed that it can also do this in the human body. The issue here is that once a live culture is consumed it may or may not survive it’s journey through to the gut. However, it is likely that the buccal cavity would be the ideal absorption area for GcMaf (VDTP) probiotic. A lot of “variables” occur with the non-targeted yoghurt approach and there has not as yet been any concentration data of GcMaf (VDTP) in the probiotic preparations, nor any conversion rates provided. So further research is needed.

It is true that probiotics will aid your gut flora, but the “conversion” relies upon bacterial growth and there is no guarantee that in each batch, the bacteria will grow at exactly the same rate, meaning each batch (if it does contain GcMaf (VDTP)) will come in differing concentrations, if at all.

 

• Beware of Contamination

 

Contamination occurs when a foreign agent gets into the GcMaf product from the outside, or as part of the manufacturing process. Contaminants can cause symptoms similar to impurities, including fatigue, weakness, malaise, muscle and joint pain. Such contaminants can be airborne or carried into the (otherwise sterile) production lab environment by hapless humans. Entering a biotech production facility is like dressing for a walk-in outer space: cap, gloves, full body gown, mask, boots. Oxygen tanks are not required, but the air must be filtered to remove dust, toxic chemicals, and pathogenic microorganisms.

 

• Certification

 

It is therefore necessary to establish a consumer protection certification program as soon as possible, whereby the product generated will be subjected to industry standard rigorous testing and then certified for both purity and activity.

One of the preparations available has taken this approach extremely seriously and has had samples from batches subjected to a rigorous identification and purity study on a number of samples throughout the manufacturing process to assess the presence of any contamination and materials used in the preparation. Here we present some of these results that were presented for review.

One of the assay methods developed (along with the normal bioanalytical approach) is to use liquid chromatography, coupled with mass spectrometry (LC-MS). This analytical method is extremely robust and sensitive. It can separate proteins and identify them based upon their charge and mass. The data is presented and assessed against a large protein database. This is because all proteins respond differently and therefore can be distinguished as single precise entities. The results are presented as below tested from Vigorlife GcMaf in Bulgaria.

This Figure shows Total Ion Current (TIC) Chromatogram of the Sample, which shows only one effective peak, as corresponding to the GcMaf macrophage activation molecule with the missing galactose sugar of about 179 and sialic acid sugar residue of about 309 molecular weight, as seen after deconvolution of the mass spectrum behind the peak with a retention time of 10.05min)

 In essence what this shows is that the final preparation contains the correct mass of protein for GcMaf (VDTP). There is only one peak which also shows that the preparation is pure and there is only GcMaf (VDTP) present. There is no contamination of any other proteins, enzymes, or starting material. This tells us that the conversion of the precursor GcGlobulin is complete and 100% converted.

The protein is also cut up using specific enzymes that can cut proteins at specific points. It is this pattern that is unique for each protein, when it is measured on the mass spectrometry analysis of digested material. The second figure below, shows the mass spectrum of the peak at 10.05min from the sample above. This mass spectrum does not show the mass of the molecule directly, but the data must be reconstructed.  It consists of multiple charged ions, ranging from 40 to 25 positive charges, which is difficult to interpret, despite the high resolution of the mass analyzer. Isotopic peaks are not possible to be determined, since the huge mass of the molecule expected around 52900Da, so deconvolution was carried out which has a lower accuracy, based on different charged states and manual peak picking.

Figure: MS Spectrum of the Peak at 10.05min. (from Sample)

 

Several of the peaks from the spectrum generated above are further reconstructed using software to provide an accurate estimate of the molecular weight of the sample protein. This data indicates that the molecular weight of the GcMaf is assigned to 52900Da which is a mass that is expected for GcMaf (VDTP).

The molecular weights of the two enzymes used: Neuraminidase (approx. 95kDa) and Galactosidase (approx. 540kDa) were also monitored with the assay in samples through the process. They are shown here below for clarity and to highlight that the profile is easily observed to be different from GcMaf (VDTP).

Figure: Reconstructed Spectrum Showing Molecular Weight of the Protein Within 100 -200Da Accuracy.

 

The next figure illustrates the Total ion current chromatograms of samples in the process in the same order from top to bottom. A straight red line is drawn to show retention time shifts for each of the individual samples.

Figure: Chromatograms of the Neuraminidase (bottom) and Galactosidase (top) enzymes.

 

Figure 5. Chromatograms of Final and Process Samples Respectively

 

Please see the following figure below. The top chromatogram is of the end product GcMaf in the container.

The bottom chromatogram is of the end product GcMaf after processing, prior to being filled in the container. Notice that there has not been any difference in the profiles due to any storage issues.

The third chromatogram is of the starting material GcGlobulin. There is a slight expected difference in this sample, due to the presence of Sialic acid and galactoside hydrophilic sugar residues, which are still attached to the molecule.

The fourth chromatogram is of the GcGlobulin having been treated with the β-Galactosidase. Here you can see a slight change as one of the sugars is removed. You can see the profile for the GcGlobulin and the β-Galactosidase ie there are two peaks present.

The final bottom chromatogram is after the material has been treated with neuraminidase. You can see the profile for the GcGlobulin and the neuraminidase ie there are two peaks present

The Peak areas of the protein in the first 3 chromatograms proportionally correspond to its concentration (if there is a standard substance to compare it to).

These assay results from Vigorlife in Bulgaria prove a perfect, cheaper and faster way (30 min in total) for monitoring, quantitation and measuring the purity of GcMaf protein, in its intact form.

 

• Discussion and Conclusion

 

The experimental work of developing of an LC-hr MS method for qualitative and quantitative analysis of GcMaf (VDTP) proved that the intact protein could be successfully determined in samples with moderate to simple compositional weight, in concentrations starting from 0,1µg/ml to about 3 orders of higher magnitude, but with additional optimization of quantitative parameters.

 

In these presented sets of samples, the evaluation of the results demonstrates several facts:

• Sample 4 and 5 are clear of enzymes. The preparation is pure and completely converted.

 

• Converted protein can withstand low pH of about 2,2 and high temperature of about 70℃ for at least 10 minutes during chromatographic separation. This is important for a viral removal step.

 

• The approximate mass of the converted protein is similar to the theoretical expected mass of about 52963Da.

 

• There is partial proof of the existence of neuraminidase and Galactosidase in the samples. However, there is no evidence of the enzymes in the material in the end process, or in the final filled material.

 

• The developed procedure could complement and/or substitute all analytical procedures from the second stage of the conversion process protocol with a substantial saving of resources and consumption of about 10µl sample (20µl in vial) for 3 determinations.

 

This final produced GcMaf (VDTP) product could even be used as an analytical standard for future quantitative work and MS determinations. The fact that this product contains only one protein, permits the quantitation of total proteins, respectively attributing the total protein concentration to this one protein for exact determination of its quantity. These results have been completed and thus generate an analytical standard that can be further used in the future.

 

Given the emergence of the Covid-19 (sars2) virus, it is perhaps prudent to examine the data and research that is available (Dec/2020) at this time. There is now no doubt among the independent scientific community, particularly those involved in the research of this virus, that it has been subject to CRISPR (a gene editing technique) manipulation. DNA analysis of this virus is showing similarities to HIV sequences of RNA and DNA that appear to have been inserted into a naturally occurring coronavirus. It is important to understand that coronaviruses have been in existence for an exceedingly long time and are responsible for many, normally minor, infections. This gene editing characteristic is why it is labelled ‘novel’. Under no circumstances can such a mutation occur in nature, in a single leap, in such a short period of time.

 

The particular gene sequence, suspected to have been inserted, does not confer upon the virus a greater potency or virulence when it comes to the immediate symptoms. The ‘gain of function’ that is desired by those that developed this virus, is to have longevity of infection and by extension, the production of antibodies. These antibodies can remain in the person’s system for many months after eradicating the initial infection and indicate not just a prior infection, even if the host has had no symptoms or illness, but yet reveal a positive test result (via the flawed PCR) that demands quarantine. It is assumed the host is still sick and, more importantly, contagious.

 

However, the primary objective of most corona viruses (including CovID19) is to infect and multiply within the respiratory system. The lungs are where most of your macrophages reside and are the first line of defense against such infections. The lungs are the battleground and subsequently where we find the most severe symptoms associated with this type of infection.

 

As has been explained earlier, having a dormant or weak immune response towards this initial point of entry for viruses, is extremely dangerous and proves that macrophage activation to fight off these pathogens is vital to the elimination of infection. GCMAF (VDTP), when coupled with an immunity boosting protocol, will naturally eliminate the infection and confer the chemical memory upon the macrophages in such a way as to provide lifelong immunity for subsequent exposures.

 

Further research is needed to confirm this hypothesis and Vigor Life will be at the vanguard of this as well as other avenues of research related to this inquiry.  GcMaf (VDTP) has been proven to be safe and effective in the treatment of a variety of viral illnesses and other diseases. The latest research findings are indicating it has many more benefits than originally believed. As it is a naturally occurring protein that is produced in the bodies of all healthy people, by default, it has no adverse side effects. In effect, it is the right jigsaw piece to fill the deficiency and completes the whole picture. It is not a ‘symptom suppressor’ to mask the hole in the way allopathic medicine is used.

 

The mRNA vaccine that is being pushed through the FDA approval process (Dec/2020) is expected to permanently trigger the production of antibodies with the intention of conferring lifelong immunity. There are conflicting schools of thought on this approach, arguing that there are no successful clinical trials that prove this approach to be safe and effective. With the immune system in a constant state of elevated preparedness, the likelihood of over reaction to a similar or second viral infection is heightened and the symptoms of such worsened.

 

According to the ‘law of unintended consequences’ what also is unclear are the many side effects that are dismissed as ‘inconsequential’ or of low incidence. There is nothing in the scientific literature that proves or even supports this claim.

 

The role that GcMaf plays in both immune system activation and modulation, to maintain the appropriate response, demands further research.

 

As mentioned above, the side effects of vaccines disprove their safety and efficacy. They are neither. The explosion in autism cases, particularly in the United States of America, should not be unexpected when observed in the context of their childhood vaccination programme. It has been shown in some studies that GcMaf (VDTP) can help with the injury that has been proven to be caused by vaccinations. The adjuvants used in these vaccines contain a cocktail of toxins completely unrelated to the actual pathogen that the vaccine is supposed to immunize the recipient from. It is these toxic compounds that are responsible for the damage that is being done. Cellular regeneration is known to occur but is inhibited by the presence of these toxins. As we also know that GcMaf activates the ‘clean up’ cells within the immune system, if these cells then clear away the debris of dead cells, damaged cells and the toxins that caused the damage, would it not then follow that cell regeneration would be allowed to occur more efficiently in the absence of these toxins  ? Vigor Life is pursuing research along this line of enquiry.

 

The USA is the most heavily medicated and vaccinated nation on earth. The American people are experiencing a vast number of previously (before the mass vaccination programmes) low incidence illnesses, many of which are auto-immune related. Multiple sclerosis, lupus, rheumatism and arthritis, ME, CFS, Lyme disease to name just a few. All of these conditions can be traced back to some environmental factor that is suppressing the immune system or over triggering the immune system such that it attacks itself indiscriminately. If GcMaf (VDTP) does in fact act as an immune system modulator, then as part of a treatment protocol, would it not reduce the inflammation symptoms that sufferers of these illnesses experience and allow better recovery rates and outcomes as well as faster recovery rates?

 

Please email: [email protected]

For further information regarding ordering or contact Saisei-Mirai in Japan

 

 

• Final Thoughts

 

 Not every GcMaf is suitable, not all suppliers can offer enough information, or guidance. Not all can discuss the virtues and science of the way their product functions. Research is ongoing and big advancements have been made.

The clinical data research paper is a pivotal one and as yet mainstream cancer treatment has missed out on this opportunity, despite it being presented and discussed at various scientific and cancer meetings. This research provides hope for GcMaf (VDTP), so please consider the above supplier for you GcMaf needs.

 

We hope this book helps with the advancement of your knowledge and becomes a useful research resource.

 

• AMAS Test Summary Points

• 16.1 Major points on the AMAS test

 

• It Measures the level of the anti-malignin antibody, a natural antibody expressed by all cancers.
• The anti-malignin antibody is present at low levels in everyone’s serum.
• The test detects all types of cancer at a very early stage.
• The test provides greater than 95% accuracy. Repeat testing is more than 99% accurate.
• The anti-malignin antibody is the earliest anticancer antibody to be detected.
• Early detection of the anti-malignin antibody, dramatically increases the possibility of a   permanent cure
• The anti-malignin antibody decreases with successful cancer treatment
• Normal levels for the anti-malignin antibody in successfully treated cancer patients indicates absence of malignancy

 

• How to Order the AMAS Test

 

To order a free AMAS kit, call 1-800-922-8378 or order online at: http://www.oncolabinc.com.

AMAS is a product of Oncolab, Inc., 36 The Fenway, Boston, MA 02215. Phone: 617-536-0850.

 

• AMAS Addendum

 

Information from Oncolab: – The AMAS test “should be used in the context of good clinical judgment by a physician experienced in the treatment of cancer.”

 “A normal AMAS level can occur in non-cancer, in terminal cancer, and in successfully treated cancer in which there is no further evidence of disease; clinical status must be used to distinguish these states.”

“As in all clinical laboratory tests, the AMAS test is not by itself diagnostic of the presence or absence of disease, and its results can only be assessed as an aid to diagnosis, detection or monitoring of disease in relation to the history, medical signs and symptoms and the overall condition of the patient.”

 

• References

 

A Checklist for Suitability of Biomarkers as Surrogate Endpoints in Chemoprevention of Breast Cancer. J. Cell. Biochem 19:172-185,1994. (National Cancer Institute Symposium)

A New Era for Cancer Diagnosis and Treatment Based Upon Earlier, Asymptomatic, Detection. J. Adv. Med. 10:149-150,1997.

A Quantitative Immune Response in Human Cancer. Cancer Detection and Prevention 22(l):S-159,1998.

Aglyco Pathology of Viral Receptors in Dementias. In Functional Diversity of Interacting Receptors. New York Academy of Sciences 757:413-417,1995.

Antimalignin Antibody (AMAS®) Elevation Detects Persistent or Recurrent Breast Cancer. Cancer Detection and Prevention 20(5):508-509,1996.

Anti-Malignin Antibody and Scantag. Protides Biol. Fluids 30:337-352, 1983. Antonucci N, P. S. (2019, Feb 22). Clinical Experience of Integrative Autism treatment with a Novel type of Immunotherapy. Madridge Journal of Vaccines, III(1), 71-76.

Astrocytin and malignin: Two Polypeptide Fragments (Recognins) Related to Brain Tumor. National Cancer Institute Mon. 46:133-137, 1977.

Bender BS, Frank MM, Lawley TJ, Smith WJ, Brickman CM, Quinn TC. 1985. Defective reticuloendothelial systems Fc-receptor function in patients with acquired immunodeficiency syndrome. J Infect Dis 152:409–412.

Boehm T, Folkman J, Browder T, and O’Reilly MS (1997). Antiangiogenic therapy of experimental cancer does not induce acquired drug resistance. Nature 390, 404-407.

Bradford MM. 1976. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein dye binding. Anal Biochem 72:248– 254.

Bradstreet JJ, Vogelaar E, Thyer L. Initial Observations of Elevated AlphaN-Acetylgalactosaminidase Activity Associated with Autism and Observed Reductions from GC Protein-Macrophage Activating Factor Injections. Autism Insights. 2012; 4: 31-38.

Bumet, F. M. The concept of immunological surveillance. Prog. Exp. Tumor Res., 13:1- 27,1970.

Bumet, M. Immunologic factors in the process of carcinogenesis. Br. Med. Bull., 20:154- 158,1964.

Bumet, M. Immunologic factors in the process of carcinogenesis. Br. Med. Bull., 20:154-158, 1964.

Cao R, Farnebo J, Kurimoto M, and Cao Y (1999). Interleukin-18 acts as an angiogenesis and tumor suppressor. FASEB J 13, 2,195-202.

Chung LW, Baseman A, Assikis V, Zhau HE. Molecular insights into prostate cancer progression: the missing link of tumor microenvironment. J Urol. 2005 Jan; 173 (1):10-20.

Comparison of Antimalignin With Other Markers for Early Detection and Surrogate Endpoint Use in Chemoprevention Trials for Breast, Colon, and Prostate Cancer. J. Cell Biochem. 19:61,1994 (National Cancer Institute Symposium)

Coppenhaver. D. H., Sllenne, N. P., and Bowman, B. H. Post-translational heterogeneity of the human vitamin D-binding protein (group-specific component). Arch. Biochem. Biophys., 226: 218-223,1983.

Dalgleish AG, Beverly PCL, Clapham PR, Crawford DH, Greaves WF, Weiss RA. 1984. The CD4 (T4) antigen is an essential component of receptor for the AIDS retrovirus. Nature (London) 312:763–767.

Determination of Anti-Malignin Antibody and Malignin in 1,026 Cancer Patients and Controls: Relation of Antibody to Survival. J. Medicine 13:49-69, 1982.

Disarmed anti-malignin antibody in human cancer. Lancet. 1979 May 5;1(8123):987.

Early Detection and Monitoring of Cancer with the Anti-Malignin Antibody Test. Detection and Prevention: 18(l):65-78,1994.

Elevated Levels of Anti-Malignin Antibody are Quantitatively Related to Longer Survival in Cancer Patients. Protides Biol. Fluids 31:739-747, 1984.

Estevez ME, Ballart IJ, Diez RA, Planes N, Scaglione C, Sen L. 1986. Early defect of phagocytic cell function in subjects at risk for acquired immunodeficiency syndrome. Scand J Immunol 24:215–221.

Fauci AS. 1984. Immunologic abnormalities in the acquired immunodeficiency syndrome (AIDS). Clin Res 32:491–499.

Fidler IJ, Poste G. Springer Semin. Macrophage-mediated destruction of malignant tumor cells and new strategies for the therapy of metastatic disease. Immunopathol. 1982;5 (2): 161-74. Review.

Fidler IJ. Critical determinants of cancer metastasis: rationale for therapy. Cancer Chemother Pharmacol. 1999;43 Suppl:S3-10.

Fidler IJ. Macrophage therapy of cancer metastasis. Ciba Found Symp. 1988;141:211-22.

Fidler IJ. Origin of cancer metastases and its implications for therapy. Isr J Med Sci. 1988 Sep-Oct;24(9-10):456-63.

Fidler IJ. Therapy of disseminated melanoma by liposome-activated macrophages. World J Surg. 1992 Mar-Apr;16(2):270-6.

Fidler IJ. Therapy of disseminated melanoma by liposome-activated macrophages. World J Surg. 1992 Mar-Apr;16(2):270-6.

Freedman, H., and Ceglowski, W. Immunosuppression in the etiology of cancer. In: H. Freedman and W. Ceglowski (eds.), Immunological Aspects of Neoplasia, pp. 253-291. Baltimore: Williams & Wilkins, 1975.

Gloeb DJ, Lai S, Efantis J, O’Sullivan MJ. 1992. Survival and disease progression in human immunodeficiency virus-infected women after an index delivery. Am J Obst Gyn 167:152– 157.

Gonzalez-Angulo AM, Morales-Vasquez F, Hortobagyi GN. Overview of resistance to systemic therapy in patients with breast cancer. Adv Exp Med Biol. 2007;608:1-22.

Gougeon M-L, Colizzi V, Dalgleish A, Montagnier L. 1993. New concept in AIDS pathogenesis. AIDS Res Hum Retroviruses 9:287–289.

Gross, L. Immunological defect in aged populations and its relationship to cancer. Cancer Res.18: 201-204,1965.

Gurachevsky A, Kazmierczak SC, Jörres A, Muravsky V. (2008) Application of spin label electron paramagnetic resonance in the diagnosis and prognosis of cancer and sepsis. Clin Chem Lab Med. 46(9): 1203-10.

Hancock, JT, Malyt, F, Owen T.G. JONES, S. Properties of the superoxide-generating oxidase of B-lymphocyte cell lines Biochem. J. (1989) 262, 373-375.

Harada S, Purtilo D, Koyanagi Y, Sonnabend J, Yamamoto N. 1986. Sensitive assay for neutralizing antibodies against AIDS-related viruses (HTLV-III/LAV). J Immnol Methods 92:177–181.

Hashida S, Ishikawa S, Hashinaka K, Nishikata I, Oka S, Ishikawa E. 2000. Earlier detection of human immunodeficiency virus type 1 p24 antigen and immunoglobulin G and M antibodies to p17 antigen in seroconversion serum panels by immune complex transfer enzyme immunoassays. Clinical Diagnostic Lab Immunol 7:872–881.

Hermanek, P., and Sabin, L. H. (eds.) Union Intemationale contre Ic Cancer: TNM of malignant tumors. Head and neck tumors. New York: Springer Verlag, 1987.

Homma S, Yamamoto N. 1990. Activation process of macrophages after in vitro treatment of mouse lymphocytes with dodecylglycerol. Clin Exp Immunol 79:307–313.

Homma, S., Yamamoto, M., and Yamamoto, N. Vitamin D binding protein (group specific component is the sole serum protein required for macrophage activation after treatment of peritoneal cells with lysophosphatidylcholine. Immunol. Cell Biol.,71: 249-257, 1993.

Houghton AN, Mintzer D, Cordon – Cardo C, Welt S, Fliegel B, Vadhan S, Carswell E, Melamed MR, Oettgen HF, and Old LJ (1985). Mouse monoclonal IgG3 antibody detecting GD3 ganglioside: a phase I trial in patients with malignant melanoma. Proc Natl Acad Sci USA 82, 1242 – 46.

In Vitro Production of the General Transformation Antibody Related to Survival in Human Cancer Patients: Anti-Malignin Antibody (AMA). Cancer Detection and Prevention 18:Number 5/6, 551, 1985.

In Vitro Production of the General Transformation Antibody Related to Survival in Human Cancer Patients: Antimalignin Antibody Cancer Detection and Prevention 12:313-320, 1988.

Increased Accuracy of Anti-Malignin Antibody Determination in Unstored Sera Permits Screening” Cancer Detection and Prevention. 11:Number 1/2, 85, 1987.

Inui T, Amitani H, Kubo K, et al. Case Report: A Non-small Cell Lung Cancer Patient Treated with GcMAF, Sonodynamic Therapy and Tumor Treating Fields. Anticancer Res. 2016; 36(7): 3767-3770.

Inui T, Makita K, Miura H, et al. Case report: A breast cancer patient treated with GcMAF, sonodynamic therapy and hormone therapy. Anticancer Res. 2014;34:4589–93.

Kanda S, Mochizuki Y, Miyata Y, Kanetake H, and Yamamoto N (2002). Effects of vitamin- D3-binding protein-derived macrophage activating factor (Yoghurt Protein AB) on angiogenesis. JNCI 94, 1311-19.

Kato, H., and Torigoe, T. Radioimmunoassay for tumor antigen of human cervical squamous cell carcinoma. Cancer (Phila.), 40: 1621-1628,1977.

Kazmierczak SC, Gurachevsky A, Matthes G, Muravsky V (2006) Electron spin resonance spectroscopy of serum albumin: a novel new test for cancer diagnosis and monitoring. Clin Chem 52: 2129-2134.

Key ME. Macrophages in cancer metastases and their relevance to metastatic growth. Cancer Metastasis Rev. 1983;2(1):75-88.

Killion JJ, Fidler IJ. Systemic targeting of liposome-encapsulated immunomodulators to macrophages for treatment of cancer metastasis. Immunomethods. 1994 Jun;4(3):273-9.

Killion JJ, Fidler IJ. Therapy of cancer metastasis by tumoricidal activation of tissue macrophages using liposome-encapsulated immunomodulators. Pharmacol Ther. 1998 Jun;78(3):141-54.

Kirsh R, Bugelski PJ, Poste G. Drug delivery to macrophages for the therapy of cancer and infectious diseases.  Ann N Y Acad Sci. 1987;507:141-54. Review.

Kleinerman ES.Biologic therapy for osteosarcoma using liposome-encapsulated muramyl tripeptide. Hematol Oncol Clin North Am. 1995 Aug;9(4):927-38.

Kodelja V, Muller C, Tenorio S, Schebesch C, Orfanos CE, and Goerdt S (1997). Differences in angiogenic potential of classically vs alternatively activated macrophages. Immunobiology 197, 478 – 93. Neoplasia . 5,1, 2003

Koga Y, Naraparaju VR, and Yamamoto N (1999). Antitumor effect of vitamin D- binding protein – derived macrophage activating factor on Ehrlich ascites tumor – bearing mice. Proc Soc Exp Biol M

Koga Y, Naraparaju VR, Yamamoto N. Antitumor effects of vitamin D3-binding protein-derived macrophage activating factor on Ehrlich tumor bearing mice. Proc Soc Exp Biol Med 220:20–26. 1999.

Koga, Y., Naraparaju, V. R., and Yamamoto, N. Antitumor effects of vitamin D3-binding protein-derived macrophage activating factor on Ehrlich tumor bearing mice. Cancer Research Proc., 37: 481, 1996.

Korbelik M, Naraparaju VR, and Yamamoto N (1997). Macrophage-directed immunotherapy as adjuvant to photodynamic therapy of cancer. Br J Cancer 75, 202 – 207.

Korbelik M, Naraparaju VR, and Yamamoto N (1997). Macrophage-directed immunotherapy as adjuvant to photodynamic therapy of cancer. Br J Cancer 75, 202 – 207.

Levine AM, Berhane K, Masri-Lavine L, Sanchez ML, Young M, AugenbraunM, Cohen M, Anastos K, Newman M, Gange SJ,Watts H. 2001. Prevalence and correlates of anemia in large cohort of HIV infected women: Women’s interagency HIV study. J Aquir Immune Defic Syndr 26:28–35.

Lindberg, R. Distribution of cervical lymph node metastases from squamous cell carcinoma of the upper respiratory and digestive tracts. Cancer (Phila.), 29: 1446-1449,1972.

Link RP, Perlman KL, Pierce EA, Schnoes HK, DeLuca HF. 1986. Purification of human serum vitamin D-binding protein by 25-hydroxyvitamin D3-Sepharose chromatography. Anal Biochem 157:262–269.

Malignin antibody and early malignancy. The Lancet 337:977,1991.

Malignin Antibody As Early Warning. Cancer Detection and Prevention 17(l): 229,1993.

Malignin Antibody Returns to Normal After Successful Treatment of Breast Cancer. Cancer Detection and Prevention 17(l):180,1993.

Matsui T, Nakashima H, Yoshiyama H, Kobayashi N, Yamamoto N. 1987. Plaque staining assay for non- or weakly cytotoxic human immunodeficiency virus. J Clin Microbiol 25:1305–1307.

McKeating JA, McKnight A, McIntosh K, Clapham PR, Mulder C, Weiss RS. 1989. Evaluation of human and simian immunodeficiency virus plague and nerutralization assays. J Gen Virol 70:3327–3333.

Memo, 0. R., Lindberg. R. D., and Fletcher, G. H. An analysis of distant metastasis from squamous cell carcinoma of upper respiratory and digestive tracts. Cancer (Phila.), 1977.

Moller F, Rollag H, Froland SS. 1990.Reduced oxidative burst response in monocytes and monocyte-derived macrophages from HIV infected subjects. Clin Exp Immunol 82:10–15.

Monoclonal Anti-Malignin Antibodies. The Lancet 2:141-142, 1981.

Morton D, Eilber FR, Malmgren RA, and Wood WC (1970). Immunological factors which influence response to immunotherapy in malignant melanoma. Surgery 68, 158–63.

Muravsky V, Gurachevskaya T, Berezenko S, Schnurr K, Gurachevsky A. (2009) Fatty acid binding sites of human and bovine albumins: Differences observed by spin probe ESR. Spectrochim Acta A Mol Biomol Spectrosc.

N. Yamamoto, V. Naraparaju, M. Moore and L. Brent. Deglycosylation of Serum Vitamin D3-Binding Protein by α-N Acetylgalactosaminidase Detected in the Plasma of Patients with Systemic Lupus Erythematosus. Clinical Immunology and Immunopathology Volume 82, Issue 3, March 1997, Pages 290-298.

Naraparaju VR, Yamamoto N. 1994. Roles of b-galactosidase of B lymphocytes and sialidase of T lymphocytes in inflammation primed activation of macrophages. Immunol Lett 43:143– 148.

Nguyen M, Shing Y, and Folkman J (1994). Quantitation of angiogenesis and antiangiogenesis in the chick embryo chorioallantoic membrane. Microvasc. Res. 47, 31-40.

Ngwenya, B. Z., and Yamamoto N. Effects of inflammation products on immune systems: lysophosphatidylcholine stimulates macrophages. Cancer Immunol. Immunother., 21: 1074- 1082, 1986.

Ngwenya, B. Z., and Yamamoto, N. Activation of peritoneal macrophages by lysophosphatidylcholine. Biochem.Biophys. Acts839:9-15,1985

Ngwenya, B. Z., and Yamamoto, N. Contribution of lysophosphatidylcholine-treated nonadherent cells to mechanism of macrophage activation. Proc. Soc. Exp. Biol. Med.,193:118-124, 1990.

Nicolson GL, Poste G. Tumor cell diversity and host responses in cancer metastasis—part II—host immune responses and therapy of metastases. Curr Probl Cancer. 1983 Jan;7(7):1-42. Review.

Nobuto Yamamoto and Masumi Ueda. Cancer cell-killing by macrophages treated with Gc protein-derived macrophage activating factor (GcMaf ) Proc Amer Assoc Cancer Res, Volume 45, 2004. Experimental and Molecular Therapeutics 11: Specific Immune Mechanisms and Cancer Vaccines: Clinical Studies Abstract #1255

Nobuto Yamamoto, Masahiro Urade, Yoshihiko Koga, Nobuyuki Yamamoto, Theodor Sery and Masumi Ueda. Macrophages Activated By GCMAF Develop Enormous Variation of Receptors That Recognize and Eradicate Adenocarcinomas. Clinical Immunology, Volume 119, Supplement 1, 2006, Page S96. FOCIS 2006 Abstract Supplement – 6th Annual Meeting.

Nobuto Yamamoto, Masahiro Urade. Microbes and infection. Institut Pasteur 7 , 4: 674-81, Apr 2005

Nobuto Yamamoto, Naofumi, Ushijima, and Yoshihiko Koga. Immunotherapy of HIV- infected patients with Gc protein-derived macrophage activating factor (GcMaf ). Serum Gc protein (known as vitamin D3-binding protein) is the precursor. J Med Virol. Jan; 81(1):16- 26. 2009.

Nobuto Yamamoto, Venkateswara R. Naraparaju and Masahiro Urade. Prognostic Utility of Serum a-N-Acetylgalactosaminidase and Immunosuppression Resulted from Deglycosylation of Serum Gc Protein in Oral Cancer Patients. Cancer Research 57, 295-299, January 15, 1997.

O’Reilly MS, Holmgren L, Chen C, and Folkman J (1996). Angiostatin induces and sustains dormancy of human primary tumors in mice. Nat Med 2, 689-92.

Ono M, Torisu H, Fukushi J, Nishie A, and Kuwano M (1999). Biological implications of macrophage infiltration in human tumor angiogenesis. Cancer Chemother Pharmacol 43(Suppl), 69 – 71.

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(4): 479-485.

Pak CC, Fidler IJ. Biotherapy.1991;3(1):55-64 Liposomal delivery of biological response modifiers to macrophages.

Pos O, Stevenhagen OPA, Meenhorst PL, Kroon FP, VanFurth R. 1992. Impaired phagocytosis of Staphylococcus aureus by granulocytes and monocytes of AIDS patients. Exp Immunol 88:23–28.

Poste G. Pathogenesis of metastatic disease: implications for current therapy and for the development of new therapeutic strategies. Cancer Treat Rep. 1986 Jan;70(1):183-99. Review.

Probert, J. C., Thompson, R. W., and Bagshow, M. A. Pattems of spread of distant metastases in head and neck cancer. Cancer (Phila.), 33: 127-133,1974.

Production of a Synthetic General Cancer Vaccine Which Augments the Concentration of Antimalignin Antibody In Vivo. Cancer Detection and Prevention 22(l):S-227,1998.

Rajiv J, Kerstin S, Rajeshwar M, Sambit S et al. (2009) Alterations in the functional capacity of albumin in patients with decompensated cirrhosis is associated with increased mortality. Hepatology 50: 555-564.

Ray, R. Molecular recognition in vitamin D- binding protein. Proc Soc Exp Biol Med 212, 305–312, 1996.

Return of Elevated Antimalignin Antibody to Normal Indicates Remission of Breast Cancer. American Association for Cancer Research 37:486,1996.

Roux-Lombard P, Aladjem D, Balavoine J-F, ChofflonM, Despont J-P, Hirschel B, JeannetM, Kapanci Y, Lang R, Toccanier M-F, Voinier B, Wilhelm A, Dayer JM, Cruchaud A. 1986. Altered functions of peripheral blood monocytes in homosexual males and intravenous drug with persistent generalized lymphadenopathy. Eur.J Clin Invest 16:262-270.

Ruggiero M, Branca J, Gulisano M, Morucci G, Thyer L, and Pacini S. Oleic acid/deglycosylated Vitamin D binding protein suppresses HER2 oncogene expression in human breast cancer. Anticancer Res. 34(10): 5845-5847, 2014S. Kazmierczak, A. Gurachevsky, G. Matthes, V. Muravsky; Electron spin resonance spectroscopy of serum albumin: a novel new test for cancer diagnosis and monitoring. Value in Health 18: (2015) A335–A766.

Saburi E, Saburi A, Ghanei M.Caspian Promising role for Gc-MAF in cancer immunotherapy: from bench to bedside. J. Intern. Med. 2017 Fall;8(4):228-238.

Sassykova A, Gurtskaya G, Kulkhan T1, Senshin S; Innovative Methods for Early Diagnostic Of Cancer; Value in Health 18: (2015) A335–A766.

Sato M, Tanaka H, Yamada T, Yamamoto N. 1977. Persistent infection of BHK/WI-2 cells with rubella virus and characterization rubella variants. Arch Virol 54:333–343.

Schnittman SM, Psallidopoulos MC, Lane HC, Thompson L, Basler M, Massari F, Fox CH, Salzman NP, Fauci AS. 1989. The reservoir for HIV-1 in human peripheral blood is a T cell that maintains expression of CD4. Science 245:305–308.

Seidel P, Gurachevsky A, Muravsky V, Schnurr K, Seibt G, et al. (2005) Recognition of malignant processes with neural nets from ESR spectra of serum albumin. Z Med Phys 15: 265-272.

Shafer, W. G., Hine, M. K., and Levy, B. M. A textbook of oral pathology, 4th Ed. Philadelphia: B. W. Saunders, 1983.

Shigeru Kanda, Yasushi Mochizuki, Yasuyoshi Miyata, Hiroshi Kanetake, Nobuto Yamamoto. Effects of Vitamin D3-Binding Protein-Derived Macrophage Activating Factor (GcMaf ) on Angiogenesis. Journal of the National Cancer Institute, Vol. 94, No. 17, 1311- 1319, September 4, 2002.

Spiro, R. H., Alfonso, A., Fan, H. W., and Strong, E. M. Cervical node metastasis from epidermoid carcinoma of oral cavity and oropharynx. Am. J. Surg., 128:562-567, 1974. 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. Journal of Neuroinflammation 2014, 11:78

Stein M,O’Sullivan P,Wachtel T, Fisher A, Mikolich D, Sepe S, Fort G, Carpenter C, Skowron G,MayerK. 1992. Causes of death in persons with human immunodeficiency virus infection. Am J Med 93:387–390.

Swamy N, Roy A, Chang R, Brisson M, and Ray R (1995). Affinity purification of human plasma vitamin D-binding protein. Protein Expr Purif 6, 185-88.

Thyer L, Ward E, Smith R, et al. GC protein-derived macrophage-activating factor decreases α-N-acetylgalactosaminidase levels in advanced cancer patients. Oncoimmunology. 2013; 2(8): e25769.

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.

Thyer et al ; Therapeutic effects of highly purified de-glycosylated GcMAF in the immunotherapy of patients with chronic diseases. American Journal of Immunology. Volume 9, Issue 3. Pages 78-84.. Viau, M., Constans, J., Debray, H., and Motreuil, J. Isolation and characterization of the O- glycan chain of the human vitamin-D binding protein. Biochem. Biophys. Res. Commun., 117: 324-331, 1983.

Voest EE, Kenyon BM, O’Reilly MS, Truitt G, D’Amato RJ, and Folkman J (1995). Inhibition of angiogenesis in vivo by interleukin 12. J Natl Cancer Inst 87, 581–86.

Weiner LM, Moldofsky PJ, Gatenby RA, O’Dwyer J, O’Brien J, Litwin S, and Comis RL (1980). Antibody delivery and effector cell activation in a phase II trial of recombinant gamma – interferon and the murine monoclonal antibody CO17- 1A in advanced colorectal carcinoma. Cancer Res 48, 2568–73.

Wendler I, Bienzle U, Hunsmann G. 1987. Neutralizing antibodies and the course of HIV- induced disease. AIDS Res Human Retroviruses 3:157–163.

Whitworth PW, Pak CC, Esgro J, Kleinerman ES, Fidler IJ. Macrophages and cancer. Cancer Metastasis Rev. 1990 Feb;8(4):319-51.

Withers HR, Lee SP. Semin. Modeling growth kinetics and statistical distribution of oligometastases. Radiat Oncol. 2006 Apr;16(2):111-9.

Xie K, Dong Z, Fidler IJ. Activation of nitric oxide synthase gene for inhibition of cancer metastasis. J Leukoc Biol. 1996 Jun;59(6):797-803.

Xie K, Fidler IJ. Therapy of cancer metastasis by activation of the inducible nitric oxide synthase. Cancer Metastasis Rev. 1998 Mar;17(1):55-75.

Yamamoto N, and Homma S (1991). Vitamin D3 binding protein (group-specific component) is a precursor for the macrophage-activating signal factor from lysophosphatidylcholine- treated lymphocytes. Proc Natl Acad Sci USA 88, 8539 – 43.

Yamamoto N, and Naraparaju VR. Immunotherapy of BALB/c mice bearing Ehrlich ascites tumor with vitamin D- binding protein -derived macrophage activating factor. Cancer Res 57, 2187–92, 1997.

Yamamoto N, Homma S, Millman I. 1991. 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 macrophages. J Immunol 147:273–280.

Yamamoto N, Homma S. 1991. Vitamin D3 binding protein (group specific component, Gc) is a precursor for the macrophage activating signal factor from lysophosphatidylcholine-treated lymphocytes. Proc Natl Acad Sci USA 88:539–543.

Yamamoto N, Hoober JK, Yamamoto N, and Yamamoto S (1992). Tumoricidal capacities of macrophages photodynamically activated with hematoporphoryin derivative. Photochem Photobiol 56, 245 – 50.

Yamamoto N, Kumashiro R.. Conversion of vitamin D3 binding protein (Group! specific component) to a macrophage activating factor by the stepwise action of b-galactosidase of B cells and sialidase of T cells. J Immunol 151:2794–2802, 1993.

Yamamoto N, Lindsay DD, Naraparaju VR, Ireland RA, and Popoff SN (1994). A defect in the inflammation-primed macrophage-activation cascade in osteopetrotic rats. J Immunol 152, 5100-07.

Yamamoto N, Naraparaju VR, and Srinivasula SM (1995). Structural modification of serum vitamin -D3 binding protein and immunosuppression in HIV – infected patients. AIDS Res Hum Retroviruses 11, 1373-78.

Yamamoto N, Naraparaju VR, Urade M, Prognostic utility of serumα-N- acetylgalactosaminidase and immunosuppression resulted from deglycosylation of serum Gc protein in oral cancer patients. Cancer Res 57:295–299. 1997.

Yamamoto N, Naraparaju VR. 1998. Structurally well-defined macrophage activating factor derived from vitamin D3-binding protein has a potent adjuvant activity for immunization. Immunol Cell Biol 76:237–244.

Yamamoto N, Naraparaju VR. Immunotherapy of BALB/c mice bearing Ehrlich ascites tumor with vitamin D3-binding protein derived macrophage activating factor. Cancer Res 57:2187–2192. 1997.

Yamamoto N, St., Claire DA, Homma S, Ngwenya BZ. 1988. Activation of mouse macrophages by alkylglycerols, inflammation products of cancerous tissues. Cancer Res 48:6044–6049.

Yamamoto N, Suyama H, Nakazato H, Yamamoto N-Y, Koga Y. 2008c. Immunotherapy of metastatic colorectal cancer with vitamin D binding protein-derived macrophage-activating factor, GcMaf . Cancer Immunol Immunother 57:1007–1016.

Yamamoto N, Suyama H, Yamamoto N-Y, 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.

Yamamoto N, Suyama H, Yamamoto N-Y. 2008b. Immunotherapy of prostate cancer with Gc protein-derived macrophage-activating factor, GcMaf . Translational Oncol 1:65–72.

Yamamoto N, Ueda M, Benson CE. 2007. Treatment of HIV-infected patients with Gc protein-derived macrophage activating factor (GcMaf ) eradicates HIV-infection. Proc 13th Int Cong Immunol. Italy: Medimond, Bologna. pp. 35–38.

Yamamoto N, Ueda M. 2004a. Therapeutic efficacy of vitamin D binding protein (Gc protein)-derived macrophage activating factor (GcMaf ) for prostate and breast cancers. Immunology. Italy: Medmond, Bologna. pp. 201–204.

Yamamoto N, Ueda M. 2004b. Eradication of HIV by treatment of HIV infected/AIDS patients with vitamin D-binding protein (Gc protein)-derived macrophage activating factor (GcMaf ). Immunology. Italy: Medmond, Bologna. pp. 197–200.

Yamamoto N, Urade M, Ueda M. 2005. Potent tumoricidal capacity of macrophages activated by Gc protein-derived macrophage activating factor (GcMaf) and its therapeutic efficacy for prostate, breast, and colorectal cancers. J Immunother 28:642.

Yamamoto N, Urade M. 2005. Pathogenic significance of a-Nacetylgalactosaminidase found in the hemagglutinin of influenza virus. Microbes Infect 7:674–681.

Yamamoto N. 1993. In vitro enzymatic conversion of glycosylated human vitamin D binding protein to a potent macrophage activating factor. U.S. Patent Number: 5,177,002.

Yamamoto N. 1996. Structural definition of a potent macrophage activating factor derived from vitamin D3 binding protein with adjuvant activity for antibody production. Mol Immunol 33:1157–1164.

Yamamoto N. 1997. Diagnostic and prognostic indices for cancer and AIDS. U.S. Patent Number: 5,620,846.

Yamamoto N. 1998a. Vitamin D and the immune system. In: Encyclopedia of Immunology. 2nd edition. Delves PJ, Roitt I, editors. Academic Press Ltd. London: pp. 2494–2499.

Yamamoto N. 1998b. Diagnostic and prognostic ELISA assays of serum or plasma a-N- acetylgalactosaminidase for cancer. U.S. Patent Number: 5,712,104.

Yamamoto N. 2002. Preparation of potent macrophage activating factor derived from cloned vitamin D binding protein and its domain and their therapeutic usage for cancer, HIV- infection and osteoporosis. U.S. Patent Number: 6,410,269.

Yamamoto N. Diagnostic and prognostic ELISA assays of serum α-N- acetylgalactosaminidase for AIDS. U.S. Patent Number: 5,985,545. 1999.

Yamamoto N. Pathogenic significance of a-N-acetylgalactosaminidase found in the envelope glycoprotein gp160 of human immunodeficiency virus type 1. AIDS Res Human Retroviruses 22:262–271, 2006.

Yamamoto, Masahiro Urade, Yoshihiko Koga, Nobuyuki Yamamoto, Theodor Sery and Masumi Ueda. Macrophages Activated By GCMAF Develop Enormous Variation of Receptors That Recognize and Eradicate Adenocarcinomas. Nobuto 2006.

Yamamoto, N., and Homma, S. Vitamin D3 binding protein (group-specific component, Gc) is a precursor for the macrophage activating signal factor from lysophosphatidylcholine- treated lymphocytes. Proc. NatI. Acad. Sci. USA, 88: 8539-8543, 1991.

Yamamoto, N., and Naraparaju, V. R. Role of mouse vitamin D3-binding protein in activation of macrophages. J. Immunol.,157: 1744-1751,1996.

Yamamoto, N., and Ngwenya, B. Z. Activation of macrophages by lysophospholipids and ether derivatives of neutral lipids and phospholipids. Cancer Res., 47: 2008-2013,1987.

Yamamoto, N., Kumashiro, R., Yamamoto, M., Willett, N. P., and Lindsay, D. D. Regulation of inflammation-primed activation of macrophages by two serum factors, vitamin D3-binding protein and albumin. Inf. Imm., 61: 5388-5391, 1993.

Yamamoto, N., Naraparaju, V. R., and Asbell, S. Deglycosylation of serum vitamin D3- binding protein leads to immunosuppression in cancer patients. Cancer Res.,56:2827- 2831,1996.

Yamamoto, N., Naraparaju, V. R., and Srinivasula, S. M. Structural modification of serum vitamin D1-binding protein and immunosuppression in AIDS patients. AIDS Ret. Hum. Retroviruses, 11: 1373-1378,1995.

Yamamoto, N., Ngwenya, B. Z., Sery, 1. W., and Pieringer R. A. Activation of macrophages by ether analogues of lysophospholipids. Cancer Immunol. Immunother. 2,5: 185-192, 1987.

Yamamoto, Nabuto; Naraparaju, Venka Tenkateswara, R. Structurally well-defined macrophage activating factor derived from vitamin D3-binding protein has a potent adjuvant activity for immunization. Special Feature. Immunology & Cell Biology. 76(3):237-244, June 1998.

Yamamoto. N., Willen, N. P., and Lindsay, D. D. Participation of serum proteins in the inflammation-primed activation of macrophages. Inflammation, 8: 311-322, 1994.

Yang F, Bergeron JM, Linehan LA, Lalley PA, Sakaguchi AY, and Bowman BH (1990). Mapping and conservation of the group-specific component gene in mouse. Genomics 7, 509-16.