Friday, May 10, 2013

ONCE AGAIN FAILURE OF RECEPTORS PROVE TO BE THE REASON CANCER DEVELOPS.
WHILE IN TRIPLE NEGATIVE HEPARAN SULFATE ALTERATION OR LACK OF, SEEMS TO BE THE CULPRIT THAT WILL LEAD TO SECONDARY OVER-EXPRESSION OF TUMOR GROWTH FACTORS FOR BREAST CANCER, IN OVARIAN CANCER IT IS THE BETAGLYCAN WHICH APPEARS TO BE DEFICIENT AND TRIGGER A SECONDARY INCREASE OF ACTIVIN.  THE PROOF IS IN THE PUDDING,
IF YOU FIGHT ACTIVIN, YOU GO NOWHERE BUT IF YOU FIGHT BETAGLYCAN BY RESTORING ITS FUNCTION, THE RECEPTOR WORKS RELATIVELY AND YOU KIND OF STOP THE METASTASIS AND SPREAD OF THE DISEASE
NOBODY HAS SHOWN THIS YET BUT YOU WILL FIND A DROP OF ACTIVIN (HOW DIFFERENT IT IS FROM SURVIVIN? HELL DON'T LET ME CONFUSE YOU BY JUMPING FROM CAMELS TO RABBITS!)

THE GLYCAN ARE MORE IMPORTANT THAN YOU THINK
IT IS AN INTERESTING SPECULATION THAT HISTONE DEACETYLASE INHIBITOR WORK BECAUSE IN RESTORING THE GLYCAN OR IS IT CAUSATIVE OF THE ABNORMALITY.
ONE THING THAT IS WORRISOME IS THAT A SINGLE FRAME SHIFT AT THE m-ARNA COULD TRIGGER THESE EPIGENETIC EVENTS.

ALL IN ALL THIS AT THE RECEPTOR IS READ AS A CRISIS OR STRESS THE AKT IS OVEREXPRESSED AND CAUSE PTEN DEPRESSION, OR GSK DEPRESSION, AND AFFECT THE Wnt THROUGH CROSS TALK AND OVARIAN CANCER IS WELL ON ITS WAY EXACERBATED AT THIS POINT BY SECONDARY INCREASE OF TGF CALLED ACTIVIN!
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