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pubmed:abstractText |
Cardiovascular disease (CVD) is the single greatest cause of death in the United States and in Western Europe. There is strong epidemiologic evidence for an interaction of environmental and genetic factors in the development of clinically significant episodes of CVD. However, the specific contributions of each of these components to the onset and development of CVD remain unclear. According to the monoclonal hypothesis, arteriosclerotic plaques, the principal lesions associated with CVD, are monoclonal in origin and can be considered benign smooth muscle cells tumors of the artery wall. It follows that somatic cell alterations, possibly brought about by chemical mutagens or viruses, may play critical roles in plaque formation. During the past decade, evidence has been presented from a number of laboratories, including ours, that in animal model systems, both viruses and chemical carcinogens can play a role in the appearance and development of arteriosclerotic plaques. We have recently provided evidence consistent with the view that somatic cell alterations are critical to plaque development in man: DNA from human arteriosclerotic plaques. transforms cells in vitro and injection of these transformed cells into nude mice results in tumor formation. Thus, plaque DNA behaves similarly to tumor DNA under defined assay conditions.
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