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CRISPR-based deep mutagenesis for characterisation of functional domains in oncogenic signalling pathways

  • Full or part time
  • Application Deadline
    Monday, May 27, 2019
  • Funded PhD Project (European/UK Students Only)
    Funded PhD Project (European/UK Students Only)

About This PhD Project

Project Description

CRISPR/Cas and base editing (BE) for genome manipulation have been transformative for the generation of cellular models to interrogate gene function in healthy and disease states. Development of CRISPR and BE systems to introduce or correct a range of mutations in a gene/protein of interest will be key to the future impact of genome editing.

The PhD student will generate advanced genome editing tools utilizing a range of experimental methods including molecular biology techniques and bio-informatics. These tools will be used to study the RAF kinase family and the molecular mechanisms of their signalling in cell proliferation and transformation. To this end, the PhD student will learn advanced technologies of cell biology, viral and non-viral delivery methods, cellular assays, biochemistry, next generation sequencing and multi-omics as well as an exciting opportunity to gather knowledge in the latest genome editing strategies.

This project is a collaboration between Simon Cook’s lab at the Babraham Institute and Discovery Sciences in AstraZeneca. The PhD student will be based initially in the Precise Genome Editing team at AstraZeneca, in Cambridge UK, and successively in the Signalling Laboratory, at the Babraham Institute, in Cambridge UK.

The student will have the opportunity to work within both the global PhD and post-doctoral student communities in AstraZeneca and the Babraham Institute.

We will expect you to maintain an awareness of current developments in the literature and identify and pursue opportunities within this scientific field. You will develop as a scientist through experimentation, internal and external presentations and authorship in peer-reviewed publications.

We believe in the potential of people who share our passion for science. By thinking boldly and working collaboratively to pursue discoveries, you will develop further and faster than you thought possible. AstraZeneca and the Babraham Institute are equal opportunity employers.

Essential Requirements:

M.Sc. or 1st class or Upper 2nd Hons BSc in Biochemistry, Molecular or Cellular Biology. This studentship comes with a stipend supported by the BBSRC. Only UK and EU citizens who have been resident in the UK for 3 years are eligible.

Start date (planned): 1 October 2019

All applications for PhD Studentships at the Babraham Institute need to be made using the University of Cambridge Graduate Application Portal ( regardless of funding source.

Please see the “Applying for a PhD” pages on our website ( for further details of the application process.

The deadline for submission of applications via the Graduate Application Portal is Monday 27 May 2019.

If you would like more information, or have any questions not answered on our website or the University’s graduate application site, please contact us:
HR and Graduate Studies Assistant, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, or email .

The Babraham Institute is a Disability Confident Employer and has a positive approach to employing disabled people.

The Babraham Institute receives strategic funding from the Biotechnology and Biological Sciences Research Council and is an Equal Opportunities Employer.


Further reading:
This project builds on a long history of collaborations between AstraZeneca and the Cook lab. Relevant publications include:

Sale MJ et al. (2019) Withdrawal of MEK1/2 inhibitor reverses acquired resistance driven by BRAFV600E amplification but drives EMT and chemoresistance when KRASG13D is amplified. Nature Commun. In press
Prescott JA & Cook SJ (2018) Targeting IKKβ in cancer: challenges and opportunities for the therapeutic utilisation of IKKβ inhibitors. Cells 7:115 Special issue on ‘NF-kB in cancer’

Cook SJ et al. (2017) Control of cell death and mitochondrial fission by ERK1/2 MAP Kinase signaling. State-of-the-art review. FEBS Journal 284:4177-4195

Caunt CJ et al. (2015) MEK1 and MEK2 inhibitors and cancer therapy; the long and winding road. Nat Revs Cancer. 15:577-592.

Cope CL et al. (2014) Acquired resistance to mTOR kinase inhibitors by upregulation of eIF4E and maintenance of Cap-dependent translation. J Cell Sci. 127: 788-800

Chell V et al. (2013) Tumour cell responses to new Fibroblast Growth Factor Receptor tyrosine kinase inhibitors and identification of a gatekeeper mutation in FGFR3 as a mechanism of acquired resistance. Oncogene. 32: 3059-3070

Little AS et al. (2011) Amplification of the driving oncogene, KRAS or BRAF, underpins acquired resistance to MEK1/2 inhibitors in colorectal cancer cells. Science Signalling. 4 (166) ra17

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