She and her team developed the method Break - seq to test their hypothesis that
chromosome fragile sites result from collisions between drug - induced unstable DNA replication and untimely gene transcription.
Using a novel method they developed to map chromosome breaks in a model organism, the budding yeast, Wenyi Feng, Ph.D., of Upstate Medical University and her colleagues have discovered new information as to how and where
chromosome fragile sites can occur in human DNA.
Their findings offer a better understanding of the mechanisms of
chromosome fragile sites and could lead to a breakthrough in identifying new cancer - associated genes.
Chromosome fragile sites are regions of DNA double strand breaks on human chromosomes.
«We are now investigating
chromosome fragile site formation in various human cell lines, including the chronic myeloid leukemia and Fragile X cells,» said Feng.
Not exact matches
The study results indicate that patients who have abnormal levels of breaks at common
fragile sites (CFSs),
sites within the
chromosomes that are sensitive to DNA damage, are more likely to have their cancer to return — treatment failure.
Mapping of XMRV integration
sites has revealed a strong preference for structurally open transcription regulatory regions of
chromosomes that are associated with cancer breakpoints, common
fragile sites, microRNA and cancer - related genes [5].