THE CURE FOR ALL ADVANCED CANCERS
and any missing bases replaced correctly before p53 will release
its hold.
I find p53 mutations also occur when tapeworm larvae are
present, even without vanadium. (Conversely I find p53 muta-
tions don’t occur in the presence of vanadium or tapeworm lar-
vae if good germanium is present!)
When the p53 gene has become mutated, multiplication is
allowed to go on and on, in spite of the gross mutations that are
now occurring and being passed along. If p53, also called the
“tumor suppresser gene”, is incapacitated, how long can the hy-
peractive little mass be controlled so a tumor does not develop?
Everything now depends on bcl-2 and bax. If this last mecha-
nism fails, you will have a tumor.
The Final Defense......................................................
More and more mutations, many of them translocations
(misplacement) of chromosome parts, are occurring now that
p53 is gone (mutated). Bits of chromosomes litter the cytoplasm
making it look like a war zone. The cells are completely dis-
abled as productive members of their community due to these
mutations. Yet they must multiply, because Clostridium is fill-
ing the cells with toxic amines, the brakes (pyruvic aldehyde)
are out, and the accelerator (thiourea) given full reign.
It is only a matter of time before the bcl-2 gene will also
mutate.^56 Its characteristic mutation is yet another translocation.
After this, the cells cannot self-destruct.
The Syncrometer detects overproduction of bcl-2 protein in
all growing tumors, whether benign or malignant. It should be
produced for thirty seconds only, out of each minute. Now it is
produced for forty seconds, leaving only twenty seconds for
bax.
(^56) Tsujimoto, Y., Bashir, M., Givol, I., Cossman, J., Jaffe, E., Croce., C., DNA
Rearrangements in Human Follicular Lymphoma Can Involve The 5’ or the 3’ region
of the bcl-2 Gene, Proc. Natl. Acad. Sci. USA, v. 84, Mar. 1987, pp. 1329-31.