Regions in the chromosomes known as "fragile sites" are not unusual, as past studies have shown, but these gaps in the DNA structure of a newly-reproduced cell can easily be broken apart, hence increasing chances of cancer in humans.

Whenever a new cell replicates itself and a hitch occurs in the copying of the 46 chromosomes, a gap is developed, hence encourage a string of inevitable chromosomal rearrangements. Worse, it can serve as a breeding ground for cancer.

Through an extensive mapping of these fragile sites, scientists from the Duke University School of Medicine discovered that these sites are formed from where the DNA copying had supposedly slowed or stalled due to certain sequences of DNA or simply in their structural elements.

"Other studies have been limited to looking at fragile sites on specific genes or chromosomes," said Thomas D. Petes, Ph.D., a Minnie Geller professor of molecular genetics and microbiology at Duke. "Ours is the first to examine thousands of these sites across the entire genome and ask what they might have in common."

In their study, which was published recently in the journal  Proceedings of the National Academy of Sciences, the team discovered a potential method on how to fully understand the genetic abnormalities underlying many solid tumors.

Petes and his team dropped off levels of DNA polymerase in the yeast cells ten times lower than the usual number. With a state-of-the-art technology called "gene chip," the team began to map out the segments where a particular rearrangement occurred.

The process produced a huge number of data that had to be analyzed by looking for further studies that could support the themes that kept coming up in the regions they surveyed. The team came down to a conclusion that reversed duplication, as well as the replication or termination signals and the transfer of RNA genes prompted the stalling in the replication of DNA.

It was in the 1980s that "fragile sites" was first used to describe the gap in the chromosomes of mammalian cells. They were found to have been produced by a faulty copying of DNA. The yeast Saccharomyces cerevisiae, meanwhile, served as an ideal sample in determining how polymerase could affect the pacing of the copying of the chromosomes.