Tim Humphrey DPhil
- Cancer and Haematology
- Elizabeth Blaikley, DPhil Student
- Rachel Deegan, DPhil Student
- Lydia Hulme, Ph.D.
- Torben Kasparek, DPhil Student
- Chen-Chun Pai, DPhil
- Carol Walker, Lab Manager
- McFarlane R J and Humphrey T C (2010) A role for recombination in centromere function Trends Genet, 26(5):209-213.
- Moss J, Tinline-Purvis H, Walker C, Folkes L, Stratford M, Hayles J, Hoe K, Kim D, Park H, Kearsey S, Fleck O, Holmberg C, Nielsen O, and Humphrey T (2010) Break-induced ATR and Ddb1-Cul4Cdt2 ubiquitin ligase-dependent nucleotide synthesis promotes homologous recombination repair in fission yeast. Genes Dev, 24(23):2705-16.
- Tinline-Purvis Helen, Savory Andrew P, Cullen Jason K, Dave Anoushka, Moss Jennifer, Bridge Wendy L, Marguerat Samuel, Bahler Jurg, Ragoussis Jiannis, Mott Richard, Walker Carol A, and Humphrey Timothy C (2009) Failed gene conversion leads to extensive end processing and chromosomal rearrangements in fission yeast. EMBO J, 28(21):3400-12.
- Cullen Jason K, Hussey Sharon P, Walker Carol, Prudden John, Wee Boon-Yu, Dave Anoushka, Findlay James S, Savory Andrew P, and Humphrey Timothy C (2007) Break-induced loss of heterozygosity in fission yeast: dual roles for homologous recombination in promoting translocations and preventing de novo telomere addition. Mol Cell Biol, 27(21):7745-57.
- George Vinoj T, Brooks Gavin, and Humphrey Timothy C (2007) Regulation of cell cycle and stress responses to hydrostatic pressure in fission yeast. Mol Biol Cell, 18(10):4168-79.
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DNA double-strand breaks (DSBs) are highly genotoxic lesions, arising either through DNA metabolism or from exposure to DNA damaging agents such as ionizing radiation. In addition to causing cell death, such lesions can cause chromosomal rearrangements, a hallmark of cancer cells, which can lead to oncogene activation or to loss of heterozygosity. The objective of the laboratory is to understand how genome stability is maintained in response to DSB's. We are examining the mechanisms and determinants of DSB repair, including the role of tumour suppressor genes, in suppressing break-induced chromosomal rearrangements in normal cells. Further we are examining DSB misrepair and the fate of unrepaired broken chromosomes, to gain new insights into the mechanisms by which such lesions contribute to genome instability and tumorigenesis. We are using the genetically amenable fission yeast Schizosaccharomyces pombe as our primary model system in which DNA damage responses are evolutionarily conserved. Findings made in fission yeast are being analysed further in mammalian cells. research techniques employed include genetics, molecular biology and biochemistry.
2007 Senior Group Leader,
Radiation Oncology and Biology, Oxford University
2003-2007 Senior Group Leader,
MRC Radiation and Genome Stability Unit
1997-2003 Group Leader MRC,
Radiation and Genome Stability Unit
1997 Director of Graduate Studies
1993-1997 Post-Doctoral Research Fellow,
1991-1993 Post-Doctoral Research Fellow,
1985-1987 Research Assistant,
Awards Training and Qualifications
- 2003 MRC Career Appointment
- 1996- 1997 Charles A. King Trust Post-Doctoral Fellowship Award
- 1994- 1995 Human Frontiers Science Programme Fellowship Award
- 1993- 1994 European Molecular Biology Long-Term Fellowship
- 1991 D. Phil. Molecular Biology, Oxford University
- 1985 B.Sc. Hons. Brewing and Microbiology, Heriot-Watt University