Replication stress is an inherent source of DNA damage that living organisms suffer throughout their lives every time a cell divides. Our laboratory has previously contributed to this field by showing that replication stress can trigger ageing in mammals, and by showing that inhibition of the replication stress reponse kinase has potential anticancer activiy. In this context, the thesis of Maria has been focused on two independent questions. The first one was, can we make a mammalian model that limits the toxicity of replication stress? The second one was, can we identify tumors that have high levels of replication stress, and therefore wil be sensitive to ATR inhibitors?
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