A glitch in copying the 46 chromosomes every time a cell divides
can leave gaps or breaks, giving rise to chromosomal rearrangements at
“fragile sites” that could act as breeding ground for cancer, according
to a study.
The “fragile sites” appear in
specific areas of the genome where the DNA-copying machinery is slowed
or stalled, either by certain sequences of DNA or by structural
elements.
"The study is the first to examine
thousands of these (fragile) sites across the entire genome and ask what
they might have in common," said Thomas Petes, a professor of molecular
genetics and microbiology at Duke University School of Medicine in the
US.(http://www.daijiworld.com/news/news_disp.asp?n_id=233126)
"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.(http://www.techtimes.com/articles/6646/20140507/dna-copying-machinery-flaw-on-fragile-sites-make-individuals-more-prone-to-cancer.htm)original research references:
#above cited three pictures thankfully shared from:http://www.vcbio.science.ru.nl/en/virtuallessons/cellcycle/trans/
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