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DNA Damage and Disease: Studying the signalling mechanisms cells use to respond to DNA damage and why defects in these pathways cause human diseases such as cancer.


Project Description

Studying the signalling mechanisms cells use to respond to DNA damage and why defects in these pathways cause human diseases such as cancer.

We study the signalling mechanisms cells use to respond to DNA damage and why defects in these pathways cause human diseases such as cancer. We are looking for a student with interest and experience in an area of cancer cell biology to join us.

Mutations caused by DNA damage enable a normal cell to become cancerous. This is highlighted by the fact that individuals with mutations in many genes involved in DNA damage recognition, signalling and repair are predisposed to cancer, and that somatically acquired defects in such genes can drive tumour formation. Furthermore, some of the most effective cancer treatments work in tumour cells by inducing DNA damage, particularly DNA double-strand breaks, which are especially toxic and difficult to repair accurately without introducing mutations. Exploiting knowledge of DNA double-strand break repair is therefore likely to lead to more effective and personalised cancer therapies and treatments for patients with DNA repair disorders in future.

The aim of our research is to gain a greater understanding of the signalling mechanisms cells use to coordinate DNA double-strand break recognition and repair with cell cycle checkpoint activation and apoptosis. In doing so, we hope to provide novel insights into carcinogenesis and how it is held at bay by the cell’s DNA damage response system. We also aim to translate our research to develop novel potential cancer treatments. In particular, we are interested in the potential utility of signalling events for use as biomarkers and to identify novel targets in the DNA damage response for anti-cancer drugs.

Multiple projects are currently available in the lab, so if you are interested in this area and in working in a young, dynamic and friendly academic environment, please contact Dr Andrew Blackford () for further information or find us on Instagram (www.instagram.com/blackfordlab).

Projects will involve training in standard molecular and cell biology techniques, as well as cutting edge CRISPR-Cas9 genome editing, super-resolution microscopy and proteomics. There will also be opportunities to gain experience in biochemistry, bioinformatics, structural biology and mouse models. Students will be encouraged to attend and present their work at national and international meetings, and to be involved in organizing and presenting at journal clubs.

As well as the specific training detailed above, students will have access to high-quality training in scientific and generic skills, as well as access to a wide-range of seminars and training opportunities through the many research institutes and centres based in Oxford.

All MRC WIMM graduate students are encouraged to participate in the successful mentoring scheme of the Radcliffe Department of Medicine, which is the host department of the MRC WIMM. This mentoring scheme provides an additional possible channel for personal and professional development outside the regular supervisory framework.

Funding Notes

Funding for this project is available through the WIMM Prize Studentship, which offers funding to outstanding candidates from any country. Successful candidates will have all tuition and college fees paid and will receive a stipend of £18,000 per annum.

Applications must be received, including all relevant supporting materials, by Friday 11th January 2019 at 12 noon (midday).

Please visit our website for more information on how to apply.

References

Ochi T et al. (2015) PAXX, a paralog of XRCC4 and XLF, interacts with Ku to promote DNA double-strand break repair. Science 347, 185–188.

Balmus G et al. (2016) Synthetic lethality between PAXX and XLF in mammalian development. Genes Dev. 30, 2152-2157.

Blackford AN & Jackson SP (2017) ATM, ATR, and DNA-PK: the trinity at the heart of the DNA damage response. Mol. Cell 66, 801-817.

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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