Delivering the right treatment to the right patient at the right time.
Our group objective is to identify novel pathways governing cell proliferation, which are altered in cancers, to provide insights into drug resistance and predict response to chemotherapy and ionizing radiation.
We design and synthesise chemically modified DNA for diagnostic and therapeutic applications.
The aim or our research is to understand how genome stability is maintained in response to DNA double-strand breaks.
We aim to understand how repair of damaged DNA is controlled during chromosome duplication, and why potentially dangerous changes in the behaviour of cells can occur when this process goes wrong.
Research in Nick La Thangue’s group focusses on the mechanisms that give rise to the abnormal proliferation characteristic of tumour cells.
Our research is focused on gaining a greater understanding of how homologous recombination (HR), the major DNA repair pathway in mammalian cells, helps to prevent genomic instability, the underlying mechanism of many cancers. In particular, we study how tumor cells lacking BRCA1 or BRCA2 gene function differ from normal cells in their responses to exogenous damage induced by ionizing radiation, as well as to cell-intrinsic challenges that arise during DNA replication.
We are interested in the role of the ubiquitin-proteasome system in DNA repair, ageing, cancer and radiotherapy.
The long-term goal of the Dianov Laboratory is to study the proteins and mechanisms involved in the coordination and regulation of Base Excision Repair
We are investigating DNA damage signalling and repair factors in bladder cancer to develop new radiotherapy-based treatments and to identify markers to select the most suitable treatments for individual patients.