Key result
Somatic mutations and genetic instability are hypothesized to contribute to the development of atherosclerosis, sharing pathological mechanisms with carcinogenesis.
Design
Review
Authors
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Hypothesis-generating for somatic mutations in atherosclerosis; leaves open any therapeutic targeting pending prospective studies.
This paper highlights the 'monoclonal' hypothesis of atherosclerosis, suggesting that somatic mutations and genetic instability may drive plaque formation similarly to carcinogenesis.
Andreassi et al. (2000) conducted a review in Atherosclerosis. Somatic mutations was evaluated. Somatic mutations and genetic instability are hypothesized to contribute to the development of atherosclerosis, sharing pathological mechanisms with carcinogenesis.
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