Why premature cell division promotes cancers
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IMAGE: The replication (green) and transcription (brown) machineries are simultaneously active on the genes carrying a replication origin, resulting in collisions and DNA breaks. view more 

Credit: UNIGE

The accumulation of mutations in the human genome is at the origin of cancers, as well as the development of resistance to treatments. The Cyclin E and Myc genes are active in the control of cell division. When they are mutated, for example in response to a carcinogen, these genes induce cells to start replicating their DNA prematurely during the cell cycle. This abnormal cell division causes a tumor to develop. Why is this the case? Biologists from the University of Geneva (UNIGE), Switzerland, show that precocious entry of the genome into the replication phase leads to molecular collisions occurring on the DNA and induces new mutations. These results, published in the journal Nature, could be used to develop new therapeutic approaches.

When a cell divides into two daughter cells, it must replicate its entire genome and transcribe part of it to make new proteins. Cell division is notably regulated by specific genes, including the proto-oncogenes Cyclin E and Myc. Their overexpression or mutation into oncogenes, following exposure of cells to

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