Research Topics
| Mark MeuthSummaryAffiliation: University of Sheffield Country: UK Publications
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Detail Information
Publications
Chk1 suppressed cell deathMark Meuth
Institute for Cancer Studies, University of Sheffield, School of Medicine and Biomedical Sciences, Sheffield S10 2RX, UK
Cell Div 5:21. 2010..This review will consider these findings in the context of known pathways of Chk1 signalling and potential applications of therapies that target Chk1...- Differential expression of hMLH1 and hMSH2 is related to bladder cancer grade, stage and prognosis but not microsatellite instabilityJames W F Catto
Institute for Cancer Studies, Division of Genomic Medicine, University of Sheffield, Sheffield, United Kingdom
Int J Cancer 105:484-90. 2003..Our findings indicate that reduced expression of the MMR proteins may have an important contribution in the development of a subset of TCCs and suggest a potential role for MMR expression as prognostic indicators... - Multifocal urothelial cancers with the mutator phenotype are of monoclonal origin and require panurothelial treatment for tumor clearanceJames W F Catto
Academic Urology Unit, University of Sheffield, Sheffield, United Kingdom
J Urol 175:2323-30. 2006..Tumors with high MSI have numerous DNA mutations, of which many provide no selection benefit. While these tumors represent an ideal model for studying UC clonality, their low frequency has prevented their previous investigation... - Promoter hypermethylation is associated with tumor location, stage, and subsequent progression in transitional cell carcinomaJames W F Catto
Academic Urology Unit, K Floor, Royal Hallamshire Hospital, Glossop Rd, Sheffield, S10 2JF United Kingdom
J Clin Oncol 23:2903-10. 2005..Here we investigate the extent of promoter hypermethylation in TCC throughout the urinary tract... - Distinct patterns of microsatellite instability are seen in tumours of the urinary tractJames W F Catto
The Institute for Cancer Studies, University of Sheffield, UK
Oncogene 22:8699-706. 2003..In addition, we have confirmed that MSI and EMAST are discrete forms of MSI, and that the presence of EMAST does not affect tumour phenotype... - Promoter hypermethylation in circulating blood cells identifies prostate cancer progressionMorgan Roupret
Institute for Cancer Studies, University of Sheffield, Royal Hallamshire Hospital, Sheffield, United Kingdom
Int J Cancer 122:952-6. 2008..The extent of this hypermethylation increases during disease progression and can be used to identify the extent and duration of treatment response in prostate cancer... - A comparison of the performance of microsatellite and methylation urine analysis for predicting the recurrence of urothelial cell carcinoma, and definition of a set of markers by Bayesian network analysisMorgan Roupret
Institute for Cancer Studies and Academic Urology Unit, University of Sheffield, Royal Hallamshire Hospital, UK
BJU Int 101:1448-53. 2008.... - Molecular detection of localized prostate cancer using quantitative methylation-specific PCR on urinary cells obtained following prostate massageMorgan Roupret
Institute for Cancer Studies and Academic Urology Unit, University of Sheffield, Royal Hallamshire Hospital, Sheffield, UK
Clin Cancer Res 13:1720-5. 2007..Many patients require repeat prostate biopsies to diagnose the disease. We investigated whether aberrant promoter hypermethylation in prostatic fluid could reliably detect prostate cancer... - A mutant allele of MRE11 found in mismatch repair-deficient tumor cells suppresses the cellular response to DNA replication fork stress in a dominant negative mannerQin Wen
Institute for Cancer Studies, University of Sheffield, School of Medicine and Biomedical Sciences, Sheffield S10 2RX, United Kingdom
Mol Biol Cell 19:1693-705. 2008..Together, our results suggest that the mutant Mre11 suppresses the cellular response to replication stress by binding to ssDNA regions at disrupted forks and impeding replication restart in a dominant negative manner... - The ERCC1/XPF endonuclease is required for completion of homologous recombination at DNA replication forks stalled by inter-strand cross-linksAli Z Al-Minawi
The Institute for Cancer Studies, University of Sheffield, Medical School, Sheffield S10 2RX, UK
Nucleic Acids Res 37:6400-13. 2009..We also find no additional sensitivity to cisplatin by siRNA co-depletion of XRCC3 and ERCC1, showing that the two proteins act on the same pathway to promote survival... - ATR and Chk1 suppress a caspase-3-dependent apoptotic response following DNA replication stressKatie Myers
Institute for Cancer Studies, School of Medicine and Biomedical Sciences, University of Sheffield, Sheffield, United Kingdom
PLoS Genet 5:e1000324. 2009.... - Thymidine selectively enhances growth suppressive effects of camptothecin/irinotecan in MSI+ cells and tumors containing a mutation of MRE11Rene Rodriguez
Institute for Cancer Studies, University of Sheffield, School of Medicine and Biomedical Sciences, Sheffield, United Kingdom
Clin Cancer Res 14:5476-83. 2008..Here, we attempt to exploit the altered response of mismatch repair (MMR)-deficient colon cancer cells and tumors to camptothecin or irinotecan and thymidine by combining them to improve therapeutic response... - A tumour-derived mutant allele of XRCC2 preferentially suppresses homologous recombination at DNA replication forksAtul Mohindra
Institute for Cancer Studies, University of Sheffield, School of Medicine, Sheffield, UK
Hum Mol Genet 13:203-12. 2004..They further suggest a critical role for XRCC2 in HRR at replication forks, possibly in the loading of RAD51 onto gapped DNA... - Defects in homologous recombination repair in mismatch-repair-deficient tumour cell linesAtul Mohindra
Institute for Cancer Studies, University of Sheffield School of Medicine, Beech Hill Road, UK
Hum Mol Genet 11:2189-200. 2002..The increased thymidine sensitivity and the loss of an important pathway for the repair of DNA double-strand breaks create new opportunities for therapies directed specifically against this subset of tumours... - Reduced apoptotic response to camptothecin in CHO cells deficient in XRCC3John M Hinz
Institute for Cancer Studies, University of Sheffield School of Medicine, Beech Hill Road, Sheffield S10 2RX, UK
Carcinogenesis 24:249-53. 2003..These results suggest that XRCC3 activity may be necessary for efficient entry into apoptosis in response to DSBs... - ATM is required for the cellular response to thymidine induced replication fork stressEmma Bolderson
Institute for Cancer Studies, School of Medicine, University of Sheffield, UK
Hum Mol Genet 13:2937-45. 2004..Taken together, our results implicate ATM in the HRR-mediated rescue of replication forks impaired by thymidine treatment... - A naturally occurring mutation in an ATP-binding domain of the recombination repair gene XRCC3 ablates its function without causing cancer susceptibilitySaeed Rafii
Institute for Cancer Studies, Division of Genomic Medicine, University of Sheffield Medical School, Beech Hill Road, Sheffield, S10 2RX, UK
Hum Mol Genet 12:915-23. 2003..Thus we have no evidence that D213N increases the risk of cancer. We propose that not all components of the homologous recombination repair complex can act as cancer susceptibility genes... - A potential role for the XRCC2 R188H polymorphic site in DNA-damage repair and breast cancerSaeed Rafii
Institute for Cancer Studies, Division of Genomic Medicine, University of Sheffield Medical School, Sheffield, S10 2RX, UK
Hum Mol Genet 11:1433-8. 2002..9; 95% CI=(1.0, 3.8)]. These results support the hypothesis that subtle variation in DNA repair capacity may influence cancer susceptibility in the population...