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lie adjacent to, but not within, the sequences of the genes that they regulate.

Therefore, promoters are "invisible" when only the exomes of cells are sequenced, as has been commonplace in cancer genetics research.

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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.

D., a postdoctoral researcher in the laboratory of CSHL Professor David Tuveson, M. D., looked closely at cells sampled from 308 people with pancreatic cancer, one of the most lethal malignancies, with a 5-year survival rate of only 8%. This enabled Feigin and colleagues including computational biologist Tyler Garvin, Ph.

D., formerly of Adjunct Associate Professor Michael Schatz's lab, to focus narrowly on genome segments called gene promoters.

(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.