How do checkpoints work at the molecular level, and 2) Are checkpoints required for the evolution of tumour cells during carcinogenesis and do they help them to survive exposure to radiation and genotoxic anti-cancer drugs?
Our aim is to identify rational strategies through which pharmacological inhibition of checkpoints can be exploited for therapeutic purposes. Zachos, G., Rainey, M., and Gillespie, DAF. (2003) Chk1-deficient vertebrate somatic cells are viable but exhibit multiple checkpoint and survival defects in response to ionising radiation and inhibition of DNA replication. EMBO J. 22:713-723. Zachos, G., Rainey, M.D., and Gillespie, D.A.F (2005). Chk1-dependent S-M checkpoint delay is linked to maintenance of viable replication structures. Mol. Cell. Biol. 25:563-74 Robinson, H., Jones, R., Walker, M., Zachos, G., Brown, R., Cassidy, J., and Gillespie, D.A. (2006) Chk1-dependent slowing of S-phase progression protects DT40 B-lymphoma cells against killing by the nucleoside analogue 5-Fluorouracil. Oncogene 25: 5359-5369. Zachos, G., Black, E.J., Walker, M., Scott, M.T., Vagnarelli, P., Earnshaw, W.C., and Gillespie, D.A.F. Chk1 Is Required for Spindle Checkpoint Function. (2007) Dev.
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