AstraZeneca's DDR lunch event at WCSJ 2017
Every year, over 1,200 science journalists from around the world gather at The World Conference of Science Journalists to explore cutting-edge science and crucial issues at the interface of science and society.
This October in San Francisco, AstraZeneca will join the discussion at the conference by hosting a special lunch event to introduce and explain the significance of the DNA Damage Response (DDR) mechanism for the discovery of potential new cancer therapies.
What is DNA damage response and why is it important?
DNA Damage Response Inhibition is an innovative new anti-cancer platform which could revolutionise the treatment of cancer. It works by exploiting DNA Damage Response defects which are specific to cancer cells, and kills them whilst sparing normal cells.1
AstraZeneca is pioneering this new treatment paradigm. We believe it is a crucial step forward in our aim of one day eliminating cancer as a cause of death.
The science behind DNA Damage Response Inhibition
Every day, DNA in our cells is damaged thousands of times by natural causes and external factors. If not corrected, this DNA damage could eventually lead to cancer.1 The body has developed systems to protect the cells from DNA damage, called the DNA Damage Response or DDR.1
A faulty DNA Damage Response system helps cancer develop, as it allows mutations that promote uncontrolled cell growth.2 Cancer cells with a DNA Damage Response deficiency are heavily reliant on remaining ‘back up’ DNA Damage Response systems.1
DNA Damage Response Inhibition exploits these defects by blocking the remaining response systems cancer cells are relying on to survive, which in turn causes them to die. Healthy cells are not vulnerable to this type of treatment.1
What we're working on
AstraZeneca is committed to investigating the potential of DNA Damage Response Inhibition across a range of tumour types. We currently have five compounds being investigated in clinical trials. The mechanism of action of DNA Damage Response Inhibitors suggests that they can be combined with other DNA Damage Response Inhibitors, immuno-oncology agents and targeted therapies.
1. O’Connor M, ‘Targeting The DNA Damage Response In Cancer’ (2015) 60 Molecular Cell
2. Jackson S and Bartek J, ‘The DNA-Damage Response In Human Biology And Disease’ (2009) 461 Nature