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Sarah A. Martin
Researcher at Queen Mary University of London
Publications - Â 48
Citations - Â 2582
Sarah A. Martin is an academic researcher from Queen Mary University of London. The author has contributed to research in topics: DNA mismatch repair & DNA repair. The author has an hindex of 22, co-authored 42 publications receiving 2323 citations. Previous affiliations of Sarah A. Martin include Icahn School of Medicine at Mount Sinai & New York University.
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Journal ArticleDOI
Synthetic lethal targeting of PTEN mutant cells with PARP inhibitors
Ana M. Mendes-Pereira,Sarah A. Martin,Rachel Brough,Afshan McCarthy,Jessica R. Taylor,Jung-Sik Kim,Todd Waldman,Christopher J. Lord,Alan Ashworth +8 more
TL;DR: The data presented here now suggests that the clinical assessment of PARP inhibitors should be extended beyond those with BRCA mutations to a larger group of patients with PTEN mutant tumours.
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Mismatch repair deficient colorectal cancer in the era of personalized treatment
TL;DR: The MMR deficient phenotype is described and how a deficiency in this DNA repair process may impact on the management of CRC, including surgery, adjuvant chemotherapy and the choice of systemic agents for the palliation of advanced disease are discussed.
Journal ArticleDOI
DNA Polymerases as Potential Therapeutic Targets for Cancers Deficient in the DNA Mismatch Repair Proteins MSH2 or MLH1
Sarah A. Martin,Nuala McCabe,Michelle J Mullarkey,Robert Cummins,Darren J. Burgess,Yusaku Nakabeppu,Sugako Oka,Elaine W. Kay,Christopher J. Lord,Alan Ashworth +9 more
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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DNA repair deficiency as a therapeutic target in cancer.
TL;DR: Inhibitors of poly(ADP-ribose) polymerase (PARP) have been shown to be highly selective for tumor cells with defects in the repair of double-strand DNA breaks by homologous recombination, particularly in the context of BRCA1 or BRCa2 mutation.
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Methotrexate induces oxidative DNA damage and is selectively lethal to tumour cells with defects in the DNA mismatch repair gene MSH2
Sarah A. Martin,Afshan McCarthy,Louise J. Barber,Darren J. Burgess,Suzanne Parry,Christopher J. Lord,Alan Ashworth +6 more
TL;DR: The observations suggest that this drug may have particular utility for the treatment of a subset of patients with tumours characterized by MSH2 mutations, and addition of folic acid to culture media substantially rescued the lethal phenotype caused by methotrexate.