Professor Mark Meuth
Director of the Institute for Cancer Studies
Institute for Cancer Studies
Department of Oncology
The Medical School
Beech Hill Road
Telephone: +44 (0)114 271 3288
Facsimile: +44 (0)114 271 1602
Purdue University, Lafayette, IN. BSc (with distinction) Biochemistry
Massachusetts Institute of Technology, Cambridge, MA. PhD Cell Biology
Karolinska Institute, Stockholm SWEDEN. Biochemistry
University of Toronto, Toronto CANADA. Medical Genetics
Positions and Employment
American Cancer Society Postdoctoral fellow, with Dr. Peter Reichard, Department of Biochemistry, Medical Nobel Institute, Karolinska Institute.
Postdoctoral fellow with Dr. Louis Siminovitch, Department of Medical Genetics, University of Toronto.
Research Assistant Professor/Laboratory Head, Institute de Recherches Cliniques de Montreal, and Department of Medicine, University of Montreal.
Visiting Fellow, Imperial Cancer Research Fund, Mill Hill Laboratories, London, U.K.
Research Scientist, Imperial Cancer Research Fund, Clare Hall Laboratories, South Mimms, U.K.
Senior Scientist, Imperial Cancer Research Fund, Clare Hall Laboratories.
Professor and Division Head, Department of Radiation Oncology, Division of Experimental Oncology, University of Utah, School of Medicine, Salt Lake City, UT.
Adjunct Professor of Biochemistry, University of Utah
Professor of Oncological Sciences, University of Utah
Professor of Cellular Genetics, University of Sheffield, School of Medicine
Head, Institute for Cancer Studies, University of Sheffield, School of Medicine
Head, Section of Oncology and Pathology, University of Sheffield, School of Medicine
1970-1973 National Science Foundation Predoctoral Fellow
1987 Fellow of the Foundation for the Promotion of Cancer Research, SaitamaCancer Center, Research Institute, Saitama-ken, Japan
Our major research goal over the past several years has been to understand the molecular mechanisms underlying the genomic instability apparent in tumor cells. Cells have elaborate mechanisms that repair DNA damage and prevent mutations, however it has become increasingly clear that DNA repair is closely linked with other types of DNA damage responses such as cell cycle checkpoints and the induction of cell death (apoptosis). Therefore current work is directed at understanding interactions between DNA repair pathways (in particular mismatch and homologous recombination repair) and cell cycle checkpoints and apoptosis. We are also investigating how these interactions become disrupted in tumor cells and the consequences of this disruption for the development and treatment of the disease. In collaboration with Angie Cox we are attempting to understand how inherited polymorphisms of key genes in these pathways may subtly affect function and contribute to increased risk of cancer or response to therapy. The overall goal of this effort is to identify individuals at risk and deliver the most appropriate therapy to cancer patients.
Gagou, M.E., Ganesh, A., Thompson, R., Phear, G., Sanders, C. and Meuth, M. (2011)
The human Pif1 helicase suppresses apoptosis in response to DNA replication inhibitors in tumor cells.
Cancer Res. In press.
Gagou, M.E., Zuazua-Villar, P. and Meuth, M. (2010)
Enhanced H2AX phosphorylation, DNA replication fork arrest and cell death in the absence of Chk1.
Mol. Biol. Cell, 21, 739-752.
Meuth, M. (2010)
Chk1 suppressed cell death (review).
Cell Division 5:21doi:10.1186/1747-1028-5-21
Myers, K., Gagou, M.E., Zuazua-Villar, P., Rodriguez, R., and Meuth M. (2009)
ATR and Chk1 suppress a Caspase-3 apoptotic response following DNA replication stress.
PLoS Genetics, 5(1):e1000324.
George, T., Wen, Q., Griffiths, R., Ganesh, A, Meuth, M. and Sanders, C.M (2009)
Human Pif1 helicase unwinds synthetic DNA structures resembling stalled DNA replication forks.
Nucleic Acids Res. 37, 6491-6502.
Al-Minawi, A., Lee, Y.-F., Hakkansson, D., Johansson, F., Lundin, C., Saleh-Gohari, N., Schultz, N., Jenssen, D., Bryant, H.E., Meuth, M., Hinz, J.M., Helleday, T. (2009)
The ERCC1/XPF endonuclease is required for completion of homologous recombination at DNA replication forks stalled by inter-strand crosslinks.
Nucleic Acids Res. 37,6400-6413.
T. Helleday and M. Meuth
Products useful in the treatment of MMR deficient tumours
Patent application submitted, June 2002.