Andrew Blackford is a group leader and Cancer Research UK fellow within the Cancer Research UK/MRC Oxford Institute for Radiation Oncology and Department of Oncology, based at the Weatherall Institute of Molecular Medicine. His group studies the signalling mechanisms cells use to respond to DNA damage and why defects in these pathways cause human diseases such as cancer.
He grew up in the Netherlands and Belgium, and did his undergraduate studies at the University of Durham. After obtaining his PhD in the School of Cancer Sciences at the University of Birmingham in 2008, he undertook postdoctoral positions with Wojciech Niedzwiedz at the University of Oxford in 2009 and Steve Jackson in the Wellcome Trust/CRUK Gurdon Institute at the University of Cambridge in 2012. He was awarded a Cancer Research UK Career Development Fellowship to start his own group and took up his current post in June 2016.
ATM, ATR, and DNA-PK: The Trinity at the Heart of the DNA Damage Response.
Blackford AN. and Jackson SP., (2017), Mol Cell, 66, 801 - 817
PGBD5 promotes site-specific oncogenic mutations in human tumors.
Henssen AG. et al, (2017), Nat Genet, 49, 1005 - 1014
Synthetic lethality between PAXX and XLF in mammalian development.
Balmus G. et al, (2016), Genes Dev, 30, 2152 - 2157
DNA repair. PAXX, a paralog of XRCC4 and XLF, interacts with Ku to promote DNA double-strand break repair.
Ochi T. et al, (2015), Science, 347, 185 - 188
TopBP1 interacts with BLM to maintain genome stability but is dispensable for preventing BLM degradation.
Blackford AN. et al, (2015), Mol Cell, 57, 1133 - 1141