DNA Damage Response has recently emerged as an area of “hot” cancer science and one in which Cancer Research UK is a world leader, with an established and substantial portfolio of biological research.
CRT has begun to select new drug targets from this research to prove the importance of these proteins as potential therapeutic targets. The validated targets will go through the early stages of drug discovery at CRT’s Discovery Laboratories.
The research will build upon understanding how cells repair DNA damage caused by daily ‘wear and tear’ in the environment – including ultraviolet rays and tobacco - to identify possible points of therapeutic intervention for cancer patients.
Potential new drugs - that block the repair of gene faults - could destroy cancer cells by preventing their ability to grow, divide and survive.
Related Publications:
Our Cancer Research UK funded Scientists have published a wealth of papers in the area of DNA Damage Response:
Data explains how ubiquitination of FANCD2 promotes DNA repair.
Inhibition of DNA polymerase B selectively kills MSH2-deficient tumour cells, Inhibition of DNA polymerase G selectively kills MLH1-deficient tumour cells. These results suggest mechanism-based approaches to therapy.
Results define ALC1 as a DNA damage–response protein.
Identifies molecular roles for PARP-3 and APLF and by-pass mechanisms.
Clinical study indicating synergy between gemcitabine and carboplatin leading to further clinical studies
Ubiquitination of PCNA after DNA damage facilitates DNA damage bypass by dictating which polymerase is recruited to the fork.
© Cancer Research Technology 2012