The GcMAF Book

Chapter 18

The Cancer continuum and the 'Point of no return'

Stages in the life of a cancer. How Dr. Yamamoto chose his patients had a lot to do with getting 100% cure rates. The optimum point in the cancer continuum for GcMAF therapy. The bigger a cancer gets the less likely GcMAF will work. Tracking effectiveness of all cancer therapies with Nagalase and AMAS. An expanding tumor sooner or later reaches a “point of no return.”

The Cancer Continuum

One could view the life of any cancer as a continuum starting with one cell (on the far left side) and continuing through growth and metastasis and finally (to the far right side) as a massive complex of metastatic tumors comprised of many billions of cells, occupying multiple locations in the body —a cancer that has become large enough to overwhelm and kill its host. Cancer specialists “stage” cancer according to where it lies on this continuum.

How cancer grows and spreads

Malignant tumors begin with one cancer cell. This cell multiplies by dividing to become an expanding tumor mass. At first, 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 and spill over into the local lymph channels (which try to contain them). Again, if unchecked, the cancer cells next manage to crash the barriers to the bloodstream, which, like enemy submarines, they silently navigate to far- flung regions of the body where they spawn new colonies. Up to this point the body’s cancer containment barriers have worked. By breaking out, the cancer has become the insidious, most feared, most deadly form: metastatic cancer.

Prior to metastasis, almost all cancers are considered curable. After metastasis, the odds of a cure plummet. But even now, at this, the metastatic stage, oncologists continue lobbing chemotherapeutic bombs and radiologists still blast away with particle beams. In the current system, these well-intended efforts are for the most part futile: metastatic cancer may be slowed but is rarely cured. But as you will see, the standard therapies that reduce tumor burden greatly improve the odds that GcMAF will be effective.

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Optimum treatment depends on the stage of the cancer

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 work best. This is true because natural therapies enhance the body’s own anti-cancer systems rather than damaging them. By the time 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 detection is the Holy Grail

The effectiveness of any therapy, including GcMAF, has everything to do with the point along this continuum at which treatment is initiated. Early detection has justifiably become the gospel of cancer therapy. The sooner a cancer is detected, regardless of type, the better the prognosis. Catching a cancer before it metastasizes is especially important. We want to move the point of detection as far to the left as we can. AMAS and Nagalase testing will do that.

Metastatic cancer

In “metastatic” disease the tumor has spread beyond the reach of surgery, and chemo and radiation have not succeeded at containment. Pandora’s Box is now wide open. These are the patients on whom Dr. Yamamoto chose to focus: the ones with demonstrable early metastatic disease (defined by the presence of Nagalase) but for whom the standard therapies had failed. Weekly intramuscular injections of 100 nanograms (100 billionths of a gram; you’d need a powerful microscope to be able to see it!) for 3-6 months cured every single one of these “incurable” patients.

Yamamoto’s work pushed the envelope in that he cured carefully chosen early stage metastatic cancers. As tumor size and metastases increase, the chance of success with GcMAF declines. With larger (greater than 2 cm.) metastatic tumors, GcMAF may not work or a longer duration of treatment may be required. The probability of success with GcMAF can be improved by reducing tumor burden via chemo, radiation, and surgery. Sooner or later, however, as a cancer continues to grow, even large numbers of highly activated macrophages won’t be enough to carry the day.

Choice of cancer stage had everything to do with Yamamoto’s success

Why did Dr. Yamamoto choose to treat patients at the point in the cancer continuum where conventional therapies had failed? Obviously, if conventional therapies had cured these cancers, there would be no further need for GcMAF or any other treatment. Yamamoto chose this group of patients because he knew that GcMAF would be most effective in patients with low tumor burden who had flunked the mainstream approach and still had cancer growing somewhere within them.

Elevated Nagalase levels told him that metastatic disease continued to lurk somewhere in these patients’ bodies. All cancer cells make Nagalase (and normal cells never make it), so the presence of Nagalase is synonymous with the presence of cancer.

Yamamoto also knew that larger tumors would be harder for GcMAF-activated macrophages to vanquish, so he chose patients in whom the bulk of the cancers had been removed and in whom there was great reason to believe that the “tumor burden”—though metastatic—was at its lowest possible point.

Yamamoto’s research patients had special advantages. First, they were in the earliest stage of metastatic disease. Second—because they had endured the appropriate conventional combination of therapies—their “total tumor burden” (the number of cancer cells remaining after surgery, radiation, and/or chemotherapy) was very low. As a consequence, GcMAF-activated macrophages were given a huge advantage. The ratio of activated macrophages to cancer cells was high, and so the macros had no trouble polishing off their cancer meal.

Yamamoto’s stroke of brilliance was this: he chose patients at the point on the cancer continuum where GcMAF would exert the greatest impact. This point—early metastatic disease with recently minimized tumor burden—thus provided GcMAF with a tremendous likelihood of a cure. And that’s exactly what happened—in every single case.

If he had treated earlier—before standard therapies had had their chance to succeed or fail—he would not have known for sure whether or not these patients even had metastatic disease. If he had waited longer to treat, he would given the shrunken tumors time to grow back (“re-bulk”), and thus would have risked losing some of the patients.

The “point of no return”

Individual cancers are difficult to categorize and impossible to quantify, so we are dealing with probabilities here. At some point, however, the cancer and/or its metastases will gain enough mass to be able to thwart the best efforts of debulking followed by GcMAF. This is where the cancer shrugs off the GcMAF effect because it has now grown to that size at which it is now adding new cells faster than the activated macrophages can devour them. The meal is just too big. I call this the “point of no return.” It’s a cancer cliff, so to speak, beyond which no amount of GcMAF could rescue the patient.

In some cases surgical removal, radiation and/or chemotherapy might debulk the tumor back down to a size where the GcMAF could be effective. These kinds of decisions would obviously have to be made by an oncologist experienced in GcMAF therapy.

Is GcMAF effective in early cancers too small to show up on imaging?

Success rates should approach 100% in these cases. (A good reason to implement Nagalase screening for the masses as soon as possible. For now, go get an AMAS cancer screening test.)

Is GcMAF effective in early small cancers large enough to show up on imaging?

We also don’t know how effective GcMAF would be in early disease, but there is excellent reason to believe—based on Dr. Yamamoto’s studies—that all, or almost all, early small tumors that have not yet metastasized would respond to standard therapies followed by GcMAF. Based on the outcomes reported in Dr. Yamamoto’s studies, effectiveness would approach 100% for cancers that have been recently debulked and are in the early stages of metastasis when GcMAF therapy has been begun.

Is GcMAF effective in advanced (large metastatic) cancers?

Dr. Nobuto Yamamoto’s human studies focused only on the early group. We have no research-derived data addressing the issue of GcMAF effectiveness in more advanced cancers. The studies have not yet done, and we don’t know how advanced a cancer might be and still respond to GcMAF. There may well be great variability from one patient to another.

Tracking effectiveness of all cancer therapies with Nagalase and AMAS

If cancer is present, Nagalase and/or AMAS will be positive.

Nagalase and AMAS are not only qualitative markers, however, they are also quantitative—by which I mean rising or falling levels tell us what the cancer is up to. Nagalase/AMAS can therefore be used to monitor the effectiveness of any cancer treatment, including both drug and alternative therapies, separately or in combination.

Nagalase, AMAS and the “point of no return”

Normally, with GcMAF treatment, serial Nagalase (or AMAS) levels will decrease over time. This tells us the treatment is working (i.e., a declining cancer cell population is making less Nagalase). If, however, the malignant tumor mass had achieved the “point of no return” before GcMAF therapy had been initiated, the Nagalase and AMAS levels might drop initially but eventually would continue rising, indicating the GcMAF-activated macrophages have not overcome the cancer, and that it continues to grow.

Copyright © 2010 Timothy J. Smith, M.D.