A broad computational study of cancer genome sequences identifies telltale mutational signatures associated with smoking tobacco and demonstrates, for the first time, that smoking increases cancer risk by causing somatic mutations in tissues directly and indirectly exposed to tobacco smoke. The international study by scientists at Los Alamos National Laboratory, together with researchers at the UK's Wellcome Trust Sanger Institute and other collaborators, was published in the November 4, 2016 issue of Science. The open-access article is titled “Mutational Signatures Associated with Tobacco Smoking in Human Cancer.” "This study offers fresh insights into how tobacco smoke causes cancer," said Dr. Ludmil Alexandrov, Oppenheimer Fellow at Los Alamos National Laboratory and co-lead author of the study. "Our analysis demonstrates that tobacco smoking causes mutations that lead to cancer by multiple distinct mechanisms. Tobacco smoking damages DNA in organs directly exposed to smoke, as well as speeds up a mutational cellular clock in organs that are both directly and indirectly exposed to smoke." Tobacco smoke is a complex mixture containing more than 7,000 chemicals including over 70 known to cause cancer. Previous large-scale epidemiological studies have associated tobacco smoking with increased risk for 17 different types of cancer, including cancer in tissue not directly exposed to smoke. However, the mechanisms by which tobacco smoking causes cancer have previously remained elusive. This study demonstrates that smoking increases cancer risk by causing somatic mutations that both directly damage DNA and increase the speed of an endogenous molecular clock.
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