作者: Nicholas C Popescu
DOI: 10.1016/S0304-3835(02)00596-7
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摘要: Abstract The organization and replication of DNA render fragile sites (FSs) prone to breakage, recombination as well becoming preferential targets for mutagens–carcinogens integration oncogenic viruses. For many years, attempts link FSs cancer generated mostly circumstantial evidence. discoveries that chromosome translocations, amplification proto-oncogenes, deletion tumor suppressor genes, viruses all result from the specific breakage genomic at FSs, however, have provided compelling support such a link, further suggesting causative role in cancer.