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Nuala McCabe

Researcher at The Breast Cancer Research Foundation

Publications -  9
Citations -  7452

Nuala McCabe is an academic researcher from The Breast Cancer Research Foundation. The author has contributed to research in topics: DNA repair & Cancer. The author has an hindex of 7, co-authored 8 publications receiving 6600 citations. Previous affiliations of Nuala McCabe include Institute of Cancer Research.

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Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy

TL;DR: BRCA1 or BRCA2 dysfunction unexpectedly and profoundly sensitizes cells to the inhibition of PARP enzymatic activity, resulting in chromosomal instability, cell cycle arrest and subsequent apoptosis, illustrating how different pathways cooperate to repair damage.
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Deficiency in the repair of DNA damage by homologous recombination and sensitivity to poly(ADP-ribose) polymerase inhibition.

TL;DR: The results indicate that PARP inhibition might be a useful therapeutic strategy not only for the treatment of BRCA mutation-associated tumors but also for a wider range of tumors bearing a variety of deficiencies in the HR pathway or displaying properties of 'BRCAness.
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DNA Polymerases as Potential Therapeutic Targets for Cancers Deficient in the DNA Mismatch Repair Proteins MSH2 or MLH1

TL;DR: Synthetic sickness/lethality can be exploited to develop therapeutic strategies for cancer and deficiency in MSH2 is SSL with inhibition of the DNA polymerase POLB, whereas deficiency in MLH1 isSSL with DNA polymerases POLG inhibition.
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Exploiting the DNA repair defect in BRCA mutant cells in the design of new therapeutic strategies for cancer.

TL;DR: These efforts are described, based on understanding the DNA repair defects in BRCAdeficient cells, to define the optimal existing treatment for cancers arising from BRCA mutation carriers and the development of novel therapeutic approaches.
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BRCA2-deficient CAPAN-1 cells are extremely sensitive to the inhibition of poly (ADP-ribose) polymerase: An issue of potency

TL;DR: It is shown that CAPAN-1 cells are in fact very sensitive to the potent PARP inhibitors KU0058684 (IC50 3.2nM) and K U0058948 (IC 50 3.4nM), and treatment with potent ParP inhibitors remains an exciting potential therapy for cancers involving BRCA1 or BRCa2 deficiency.