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In this way these mutations are unlike those usually found in KRAS and p53, for example, which impair or otherwise alter the function of the proteins they encode.

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.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.Now, after nearly a decade, it is compressed by Dr. Self-similar repeats in the DNA are visible in the billions of A, C, T, G-s (it is hopeless to try not to repeat sequences if you can only use 4 letters to write a very long book) ...but it was 2009 when I had proven that the hand-coded prototype that repeats follow the Zipf-Mandelbrot-Fractal-Parabolic-Distribution-Curve.(Jul 04) [Independence Day] A 27-year-old who worked for Apple as a teenager wants to make a yearly blood test to diagnose cancer — and he just got $5.5 million from Silicon Valley VCs to pull it off (This portrait was taken a while ago ... What really counts is not when you explain for the first time something like Fracto Gene; "Fractal Genome Grows Fractal Organisms".

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".

The axon guidance pathway associated with promoter mutations has a less obvious but no less important role in pancreatic cancer.

"In pancreas cancer, nerves are often attracted to or get attracted to the tumor," explains Feigin, "and sometimes they grow right through the tumor.

Over the last decade, it has made good sense to study the genetic drivers of cancer by sequencing a tiny portion of the human genome called the exome -- the 2% of our three billion base pairs that "spell out" the 21,000 genes in our chromosomes.

If cancer is a disease precipitated by changes in genes, after all, we need to know lots about how and when different genes change in the many distinctive subtypes of cancer.

Even without much understanding of genome regulation a type of cancer became largely cured! Although we knew before, that "the genome is not forever" (e.g.