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Cancer Lett. 2003 Mar 20;192(1):1-17.

Genetic alterations in cancer as a result of breakage at fragile sites.

Author information

1
Molecular Cytogenetics Section, Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20814-4958, USA. popescum@dc37a.nci.nih.gov

Abstract

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

PMID:
12637148
DOI:
10.1016/s0304-3835(02)00596-7
[Indexed for MEDLINE]

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