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Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
Published on: December 30, 2025
DNA damage, p53, apoptosis and vascular disease
John Mercer1, Melli Mahmoudi, Martin Bennett
1Division of Cardiovascular Medicine, University of Cambridge, P.O. Box 110, Addenbrooke's Hospital, Cambridge CB2 2QQ, United Kingdom.
Abstract:
Atherosclerosis is the commonest cause of death in the Western world. The atherosclerotic plaque shows evidence of DNA damage, activation of damage repair pathways, p53 expression and apoptosis, involving a variety of different cell types. This review summarises the evidence for DNA damage in atherosclerosis, the likely stimuli inducing damage, and the increasing role of p53 in mediating apoptosis and its consequences in atherosclerosis.
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Nucleotide Excision Repair
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Nucleotide Excision Repair

