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The genetic tumult within cancerous tumors is more than matched by the disorder in one of the mechanisms for switching cells’ genes on and off, scientists at Dana-Farber Cancer Institute and the Ó³»­´«Ã½ of MIT and Harvard report in a new study. Their findings, published online today in the journal Cancer Cell, indicate that the disarray in the on-off mechanism – known as methylation – is one of the defining characteristics of cancer and helps tumors adapt to changing circumstances.

A team of investigators from the Ó³»­´«Ã½, Massachusetts General Hospital and other leading biomedical research institutions has pinpointed rare mutations in a gene called APOA5 that increase a person’s risk of having a heart attack early in life. These mutations disable the APOA5 gene and also raise the levels in the blood of triglyceride-rich lipoproteins, a type of fat. The researchers’ findings, together with other recent genetic discoveries — specifically, the identification of protective mutations in the APOC3 gene that lower triglyceride levels and the risk of heart attack — refocus attention on abnormal triglyceride metabolism as an important risk factor for heart attack at any age. The work — the largest exome sequencing study yet published for any disease — appears this week in the journal Nature.