
Prof. Nicola Curtin
Professor of Experimental Therapeutics
- Email: n.j.curtin@ncl.ac.uk
- Telephone: +44 (0) 191 246 4415
- Fax: +44 (0) 191 246 4415
- Address: Northern Institute for Cancer Research
School of Clinical & Laboratory Sciences
Medical School
University of Newcastle upon Tyne
NE2 4HH
Professor of Experimental Cancer Therapeutics since 2006. Team leader for DNA damage signalling and repair projects within CR-UK Drug Development Programme
Selected Publications
- Bryant H; Helleday T; Schultz N; Thomas HD; Parker K; Flower D; Lopez E; Kyle S; Meuth M; Curtin NJ. Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase.
Nature 2005, 434(7035), 913-917.
- Calabrese C; Kyle S; Li J; Maegley K; Newell DR; Notarianni E; Stratford I; Skalitzky D; Thomas HD; Wang L; Webber S; Almassy R; William K; Curtin NJ; Barton S; Batey M; Calvert AH; Canan-Koch S; Durkacz B; Hostomsky Z; Kumpf R. Anticancer chemosensitization and radiosensitization by the novel poly(ADP-ribose) polymerase-1 inhibitor AG14361.
Journal of the National Cancer Institute 2004, 96(1), 56-67.
- Zhao Y; Curtin NJ; Thomas HD; Batey M; Cowell I; Richardson C; Griffin RJ; Calvert AH; Newell DR; Smith G. Preclinical evaluation of a potent novel DNA-dependent protein kinase inhibitor NU7441.
Cancer Research 2006, 66(10), 5354-5362.
- Hickson, I.; Smith, G.; Zhao, Y.; Richardson, C.; Green, S.; Martin, N.; Orr, A.; Reaper, P.; Jackson, S.; Curtin, N.J. Identification and characterization of a novel and specific inhibitor of the ataxia-telangiectasia mutated kinase ATM.
Cancer Research 2004, 64(24), 9152-9159.
- Curtin NJ; Hostomsky Z; Newell DR; Wang L; Yiakouvaki A; Kyle S; Arris C; Canan-Koch S; Webber S; Durkacz BW; Calvert AH. Novel Poly(ADP-ribose) Polymerase-1 Inhibitor, AG14361, Restores Sensitivity to Temozolomide in Mismatch Repair-Deficient Cells.
Clinical Cancer Research 2004, 10(3), 881-889.
- Smith, L.M.; Willmore, E.; Austin, C.; Curtin, N.J. The novel poly(ADP-ribose) polymerase inhibitor, AG14361 sensitizes cells to topoisomerase I poisons by increasing the persistence of DNA strand breaks.
Clinical Cancer Research 2005, 11(23), 8449-8457.
More Publications