University of Oxford, United Kingdom (England)
Period of Award
1st October 2007 – 30th September 2012
Defining the role of the Fanconi Anaemia tumour suppressor Pathway in DNA crosslink repair and replication fork
Fanconi Anemia (FA) is an inherited condition in which children develop a serious anaemia. The majority of patients with this condition go on to develop acute myeloid leukaemia during adulthood. FA is caused by a damaged version of one of the FANC genes, which the patients inherit from their parents. Previous research has discovered that these genes code for a group of proteins which are involved in repairing damage to DNA.
Cancer is caused by damage to certain genes that control cell division and multiplication. Genes are made from DNA and all cells have mechanisms to repair any damage to their DNA. This sort of damage can be caused by numerous factors – sunlight, chemicals, and even the normal process of cell metabolism. The FANC genes code for proteins that form the core of one of these mechanisms, which repairs a type of DNA damage called inter-strand crosslinks.
Dr Niedzwiedz’s fellowship project is aimed at investigating exactly how the FANC proteins carry out this type of DNA damage repair and what happens when they fail to work (as in Fanconi Anaemia) and why this leads on to cause leukaemia.
Watch a lab tour with Dr Niedzwiedz here.