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"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.

But mutations in promoters sifted out of mountains of data by the team's novel mathematical formula, or algorithm, called GECCO, lay in genes never before implicated in pancreatic cancer.

(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 million from Silicon Valley VCs to pull it off Researchers looked at cells sampled from 308 people with pancreatic cancer, finding mutations in gene promoter regions that provide important clues about pathways perturbed in the illness and suggesting new targets for future treatments.

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.

But a new wave of research, exemplified by a study published in Nature Genetics by a team at Cold Spring Harbor Laboratory (CSHL), is significantly improving our ability to target cancer cells by studying "the other 98%" of DNA in human chromosomes, sometimes called the genome's "dark matter." Research led by Michael Feigin, Ph.

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