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DNA repair fidelity, radiosensitivity and cancer.

Project Description

With almost half of all cancer patients receiving radiotherapy, tumour-specific radiosensitization remains an important goal for cancer research. Radiosensitivity is associated with failure to accurately repair DNA double-strand breaks (DSBs), thus leading to cell death. Using yeast and human model systems we have previously identified a number of genes required for efficient DSB repair, radioresistance and genome stability. Further, we have exploited a conserved synthetic lethal relationship to further target cancers deficient in one such gene, SETD2, which has recently entered clinical trials.

The aim of this project is to identify and characterize genes required for high fidelity DSB repair. Such genes will be examined to determine their role in suppressing mutagenic repair, radiation sensitivity, and immune responses. Findings will be exploited, using synthetic lethal pharmacological approaches, to enhance radiation targeting of specific cancers. Techniques will include cancer genetics, radiation biology, cell and molecular biology and biochemistry.

The DPhil project will provide an opportunity to join cutting-edge research lab addressing important basic research questions with clinical translational potential. The student will undertake an exciting novel project and learn/develop state of the art techniques in a variety of disciplines including mammalian genetics, radiobiology, cell and molecular biology, biochemistry and bioinformatics. Further transferrable skills (eg writing, presentational, organizational) will also be acquired. The Humphrey lab has extensive successful DPhil supervision experience, with students going on to successful careers in research, medicine and industry.

Pai, C-C., Deegan, R.S., Gal, C., Subramanian, L., Sarkar,S., Blaikley, E.J., Walker, C., Hulme, L., Bernhard, E., Codlin, S., Bähler, J., Allshire, R., Whitehall, S. Humphrey, T.C., (2014). A histone H3K36 chromatin switch coordinates DNA double-strand break repair pathway choice. Nature Communications (5):4091 10.1038/ncomms5091.

K. Jha, D.K., Pfister, S.X., Humphrey, T.C., Strahl, B.D. (2014) SET-ting the stage for DNA repair, Nat Struct Mol Biol, 21, 655-7.

Ahrabi S., Sarkar S., Pfister S.X., Pirovano G., Higgins G.S., Porter A.C.G., Humphrey T.C. (2016) A role for human homologous recombination factors in suppressing microhomology-mediated end joining. Nucleic Acids Res. 44, 5743-5757.

Funding Notes

All complete applications received by 12 noon (UK time) on Friday 10 January 2020 will automatically be considered for all relevant competitive University and funding opportunities, including the Clarendon Fund, Medical Research Council funding, and various College funds. Please refer to the Funding and Costs webpage (View Website) for this course for further details relating to funded scholarships and divisional funding opportunities.

Funded studentships are highly competitive and are awarded to the highest ranked applicant(s) based on the advertised entry requirements for each programme of study.


Whilst you must register three referees, the department may start the assessment of your application if two of the three references are submitted by the course deadline and your application is otherwise complete. Please note that you may still be required to ensure your third referee supplies a reference for consideration.

Academic references are strongly encouraged, though you may use up to one professional reference provided that it is relevant to the course.

How good is research at University of Oxford in Clinical Medicine?

FTE Category A staff submitted: 238.51

Research output data provided by the Research Excellence Framework (REF)

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