Abstract
DNA lesions resulting from impaired progression of replication forks are implicated in genetic instability and tumorigenesis. Because the cellular response to these lesions poses an important tumorigenesis barrier, the responsible signalling and repair pathways are often mutated or inactive in tumours. Here, we discuss how such deficiencies can in turn be exploited for cancer therapy.
Original language | English |
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Pages (from-to) | 1352-4 |
Number of pages | 3 |
Journal | Biochemical Society Transactions |
Volume | 35 |
Issue number | Pt 5 |
DOIs | |
Publication status | Published - 2007 |