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EPFL | Cancer cells hijack the 3D structure of DNA

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A novel algorithmic approach on cancer cells


Scientists at EPFL and UNIL have used a novel algorithmic approach on cancer cells to understand how changes in histone marks (H3K27ac) induce repositioning of chromatin regions in the cell nucleus, and described how modifications of local contacts between regulatory elements (enhancers and promoters) influence oncogene expression.


In cancer, a lot of biology goes awry: Genes mutate, molecular processes change dramatically, and cells proliferate uncontrollably to form entirely new tissues that we call tumors. Multiple things go wrong at different levels, and this complexity is partly what makes cancer so difficult to research and treat.

So it stands to reason that cancer researchers focus their attention where all cancers begin: the genome. If we can understand what happens at the level of DNA, then we can perhaps one day not just treat but even prevent cancers altogether.

This drive has led a team of researchers from EPFL and the University of Lausanne (UNIL) to make a breakthrough discovery concerning a critical genetic aberration that occurs in cancer. Working together, the groups of Elisa Oricchio (EPFL) and Giovanni Ciriello (UNIL) have used a novel algorithm-based method to study how cancer cells re-organize the 3D structure of their DNA in order to ramp up the activity of cancer-promoting genes called “oncogenes.” The work is published in two journals, Nature Genetics and Nature Communications.


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