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By this end of May something must have happened, since the 0.4 million hits in Google for FRACTAL CANCER catapulted in six months more than twenty-fold, to over 10 million hits in Google in the USA - and even to 120 million hits in Google India (since over there all ancient temples were architected with the very compressed information needed for the parsimonious algorithm of self-similar repeats).

just like my - too early - original Google Tech Talk You Tube was recorded in 58 minutes 9 years ago in 2008. At the time of inception (2002, that is, 15 years ago) it was predicted at the outset that the breakthrough of reversing both mistaken axioms of Genomics (the Junk DNA and Central Dogma misnomers) would not be accepted very quickly - though the peer-reviewed science paper "Principle of Recursive Genome Function" appeared almost at the minute when the establishment admitted with ENCODE that "the community of scientists have to re-think long held beliefs".This is one of the reasons pancreas cancer is so painful." It's possible, Feigin says, that axon guidance signals -- and indeed cell adhesion signals -- "are actually being used by tumor cells" to gain advantages over healthy cells."Tumors, for example, can actually spread via nerves; this is called peri-neural invasion." A question naturally arises: if these and several other pathways were already implicated in pancreatic cancer, what is the advantage of the new knowledge about promoter mutations?Most prominent among these were promoters affecting genes involved in cell adhesion and axon guidance.Both pathways involve cascades of interactions among dozens or hundreds of proteins, each one encoded by a different gene.Therefore, promoters are "invisible" when only the exomes of cells are sequenced, as has been commonplace in cancer genetics research.

"Promoters are important in determining when specific genes are turned on and off," says Feigin, "and I became interested in figuring out whether mutations within promoters -- as opposed to within the genes they regulate -consistently affects the way cancers develop and sustain themselves." The team "looked all across the genome," Feigin says, "and, interestingly, while we did find mutations in promoters, we never found clusters of these mutations near any of the genes that prior research had already told us were typically mutated in pancreatic cancer." Genes called KRAS and p53 are mutated in the majority of pancreas cancer cells, for example.Leo Szilárd also suggested the first purchase of the less peaceful Manhattan Project.In an admirably cautious manner, the purchase was not fission- or fusion-material.The cell adhesion pathway affected by newly discovered mutations in gene promoter regions is important for obvious reasons in cancer: cancer cells want to grow and proliferate, a process that can culminate in their migration from their tissue of origin.Once they have broken free, they can travel via the bloodstream to other places in the body, a process called metastasis that is often responsible for cancer fatalities.When they did, nuclear technology emerged prompted by the fact that fission (or fusion) releases unheard amounts of energy. First, however, quantum physics had to be developed to understand and thus control the process.

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