L1 elements can uproot themselves and move to new areas in the DNA, sometimes accidentally moving into genes that control the cell’s growth. This happened around 100X in each tumour sample, and in some tumours it happened 700X. Cambridge Uni scientists used cutting-edge technology that can read DNA to study the genes of 43 esophageal tumour and blood samples to discover how much these mobile genetic sequences travel.
If a jumping gene lands in or near an important gene that controls cell growth, it can wreak havoc, changing how the gene works so that it inadvertently tells the cell to grow and divide out of control – which could lead to cancer. “Research has shown that this might also happen in lung and bowel cancers. So it’s vital we find out more about how the cells do this in a bid to find ways to treat these cancers.”
The research is part of the International Cancer Genome Consortium (ICGC) — a global project using the latest gene sequencing technology to reveal the genetic changes behind cancer. “Esophageal cancer is one of the hardest cancers to treat, and we are committed to funding more research to find out its underlying causes.” http://www.cancerresearchuk.org/about-us/cancer-news/press-release/2015-07-10-jumping-genes-may-drive-oesophageal-cancer
Inserts produced by L1 activity and how they are treated by paired-end sequencing.
Mobile element inserts mimic multiple translocations. Circos plot of mobile element inserts detected by discordant read pairs in tumour 7409, which had the highest number detected. The genome is displayed as a circle, chromosomes 1 to Y, with curved lines representing the apparent rearrangements detected. For example, the many apparent junctions between chromosome 14 and other chromosomes (green), represent copies of a chromosome 14 sequence that have been transduced and inserted all over the genome
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