New drugs to utilise DNA damage response to kill cancer cells
pharmafile | July 26, 2016 | News story | Research and Development, Sales and Marketing | AstraZeneca, Cancer, Wellcome Trust, chemotherapy, dna damage response, university of sussex
The University of Sussex is set to produce a portfolio of new cancer drugs which exploit our DNA damage response (DDR) system in order to kill cancer cells as part of a £6 million project funded by the Wellcome Trust and in collaboration with AstraZeneca.
DNA in healthy cells is damaged thousands of times daily, but the impact is reduced by the DDR system 1 – a network of cellular pathways which identify and repair the damage. However, many cancers are known to have defects within these pathways – which enable cancerous cells to grow and divide.
The University of Sussex aims to utilise this knowledge to develop new precision drugs which can maximise DNA damage, or prevent its repair. AstraZeneca will have the first option to develop any compounds which are discovered. It is hoped that the products will trigger the death of cancer cells via unsustainable levels of DNA damage.
These new compounds are also theorised to produce fewer side effects than traditional chemotherapies, and could also be used in tandem to increase the effectiveness of chemo and radiotherapy, which work by causing DNA damage to the cells.
“Despite major advances in the treatment of cancer, there remains a substantial unmet need for highly specific drugs that selectively kill cancer cells,” explained Professor Simon Ward, director of the University of Sussex’s Drug Discovery Centre. “In order to create effective treatments for this disease – we must stop focusing on the cancer’s location and recognise the importance of targeting the genetic make-up of individual tumours,” he continued. “By designing drugs which exploit the defects in our DNA in order to kill cancer cells we can produce more effective treatments which have less side-effects for patients.”
Professor Tony Carr, director of Sussex University’s Genome Damage and Stability Centre, added: “The opportunities to develop new drugs and new treatment regimes dependent on the genetic composition of a specific tumour are immense. This new funding will be an important step forward in exploiting our basic knowledge of DNA damage response mechanisms and tumour genotypes to identify new molecules that can exploit the same paradigm of synthetic sensitivity that underpins the success of the DNA repair inhibitor Olaparib.”
Matt Fellows
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