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Suzanne Kyle

Researcher at Newcastle University

Publications -  14
Citations -  5460

Suzanne Kyle is an academic researcher from Newcastle University. The author has contributed to research in topics: DNA repair & PARP inhibitor. The author has an hindex of 13, co-authored 14 publications receiving 4794 citations.

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Journal ArticleDOI

Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase

TL;DR: It is proposed that, in the absence of PARP1, spontaneous single-strand breaks collapse replication forks and trigger homologous recombination for repair and exploited in order to kill BRCA2-deficient tumours by PARP inhibition alone.
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Development of a Functional Assay for Homologous Recombination Status in Primary Cultures of Epithelial Ovarian Tumor and Correlation with Sensitivity to Poly(ADP-Ribose) Polymerase Inhibitors

TL;DR: HR status can be determined in primary cancer samples by Rad51 focus formation, and this correlates with in vitro response to PARP inhibition, and use of this assay as a biomarker now needs testing in the setting of a clinical trial.
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Identification and evaluation of a potent novel ATR inhibitor, NU6027, in breast and ovarian cancer cell lines

TL;DR: NU6027 inhibits ATR, impairing G2/M arrest and homologous recombination thus increasing sensitivity to DNA-damaging agents and PARP inhibitors and provides proof of concept data for clinical development of ATR inhibitors.
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Preclinical evaluation of a novel ATM inhibitor, KU59403, in vitro and in vivo in p53 functional and dysfunctional models of human cancer

TL;DR: KU59403 provides the first proof-of-principle preclinical data to support the future clinical development of ATM inhibitors, being the first compound to show good tissue distribution and significant chemosensitization in in vivo models of human cancer, without major toxicity.
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Wortmannin is a potent inhibitor of DNA double strand break but not single strand break repair in Chinese hamster ovary cells.

TL;DR: There was an excellent correlation between the concentration-dependence and exposure time of wortmannin required to enhance IR cytotoxicity and inhibit DSB repair, which implicate inhibition of DNA-dependent protein kinase, and the consequent inhibition of D SB repair, as the mechanism whereby wortmanin potentiates the cytot toxicity of IR.