Scientists discover mutation that causes PARP inhibitor resistance

by | 11th May 2018 | News

Scientists have made a major discovery having identified a mutation that gives cancer cells resistance to AstraZeneca’s Lynparza and other PARP inhibitors.

Scientists have made a major discovery having identified a mutation that gives cancer cells resistance to AstraZeneca’s Lynparza and other PARP inhibitors.

The findings could help predict which patients are likely to develop resistance to treatment with PARP inhibitors and thus allow doctors to tailor treatment at the earliest opportunity.

Using a gene editing technique a team at the Institute of Cancer Research, London, were able to identify a specific mutation in the PARP1 protein that stops PARP inhibitors from working.

The authors note that testing for this mutation could deepen personalisation to an already targeted treatment, not only helping to shape decisions on whether to initiate treatment with PARP inhibitors but also when to switch patients to alternative options.

“The evolution of cancers into drug resistant forms is a major challenge we face in getting cancer treatments to work,” noted study leader Professor Chris Lord, Professor of Cancer Genomics at The ICR.

“We hope our research will help doctors use the best drug right from the outset, respond quickly to early signs of resistance, and work out the best ways to combine treatments to overcome drug resistance.”

“This important finding could in future allow clinicians to determine who would benefit most from these drugs, or to track when they are becoming less effective and when a change of treatment might be appropriate,” said Baroness Delyth Morgan, chief executive at Breast Cancer Now.

“Studies like this, which build on the development of PARP inhibitors as a brand new treatment option for some women with breast cancer, could help take us a step closer to an even more personalised approach to treating the disease.”

The research was funded by Cancer Research UK and Breast Cancer Now, and published today in the journal Nature Communications.

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