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IMAGE: When TRF1 is phosphorylated by AKT, telomeres are normal (top); in the cell lines where AKT doesn t modify TRF1, telomeres are shorter and have a lower potential to generate tumours. view more
Credit: PLOS Genetics
The Telomeres and Telomerase Group led by Maria A. Blasco at the Spanish National Cancer Research Centre (CNIO) continues to make progress in unravelling the role that telomeres -the ends of chromosomes that are responsible for cellular ageing as they shorten- play in cancer. The CNIO team was among the first to propose that shelterins, proteins that wrap around telomeres and act as a protective shield, might be therapeutic targets for cancer treatment. Subsequently, they found that eliminating one of these shelterins, TRF1, blocks the initiation and progression of lung cancer and glioblastoma in mouse models and prevents glioblastoma stem cells from forming secondary tumours. Now, in a study published in
Un equipo del CNIO descubre cómo se regula la participación de los telómeros en la generación de tumores
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