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BLACKFORD GROUP

DNA Damage & Disease

RESEARCH THEMES

DNA Damage & Repair

RESEARCH SUMMARY

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

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. To achieve this, we are using cutting-edge bioinformatics, proteomics, microscopy and CRISPR-Cas9 gene-editing techniques to answer specific questions related to DNA damage signalling. 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. 

VACANCIES

We are always looking for talented and ambitious individuals to join us, especially those with previous experience in areas including bioinformatics, biochemistry, animal models and super-resolution imaging. 

Informal enquiries welcome so please get in touch with your CV if you would like to join our team!

GROUP MEMBERS

 
Andrew Blackford, Associate Professor
Kaima Tsukada, Postdoctoral Researcher
Matthew Fawkes, DPhil Student
Robert Horsley, DPhil Student
Julius Bannister, DPhil Student

ALUMNI & NEXT DESTINATIONS

 
Sam left the lab to start a second postdoctoral position in KJ Patel's group here in Oxford.
 
Ann-Marie left the lab to take up a highly competitive place on the University of Oxford's graduate-entry/accelerated medicine course.
 
Tasaduq Hussain Wani, Postdoctoral Researcher (2020-2021)
Hussain left the lab to start a second postdoctoral position in the lab of Andrew Truman at the University of North Carolina at Charlotte.
 
Zoulikha completed her MRes degree before starting a job with Bio-Rad Laboratories.
 
Johanna left the lab to complete her undergraduate studies at Yale University, before starting as a business analyst at McKinsey & Company.
 
Roos returned to the Netherlands to complete her Masters degree at Radboud University. She has since started a PhD in the lab of Ana Ruiz Saenz at Erasmus University Medical Center in Rotterdam.
 
Sofiya returned to Italy to complete her Masters degree at the University of l’Aquila. She has since started a PhD in the lab of Frank Rösl at the DKFZ in Heidelberg.

Emily left to complete her final undergraduate year at the University of Birmingham. She has since started a PhD in the lab of Fumiko Esashi at the Dunn School of Pathology at the University of Oxford.

LATEST NEWS

New 'molecular fibres' may help cells repair DNA

Research by the Blackford lab has for the first time observed molecular structures that may hold together broken DNA ends during cell division.

Latest publications

Related research themes

DNA Damage & Repair
DNA Damage & Repair