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Scientists identify vital role of enzyme in survival of certain cancers

The results offer the foundations for a clinical trial evaluating the effects of POLQ inhibitors

Study

Scientists at the Francis Crick Institute (the Crick), in collaboration with UK and US-based biotech Artios, have identified how an enzyme involved in DNA repair becomes vital to the survival of certain cancers, if the usual method of DNA repair goes wrong.

The findings suggest that blocking the polymerase theta (POLQ) enzyme can prevent some cancer cells from repairing their DNA, ultimately leading to cancer cell death, and provides the foundations for Artios’ phase 1 clinical trial evaluating the effects of POLQ inhibitors.

Ondrej Belan, first author and postdoctoral researcher at the Crick, said, “While it is known that blocking POLQ and homologous recombination at the same time hinders DNA repair, our research now provides the scientific foundation to explain how.

“This mechanistic understanding of how POLQ inhibitors work will help us explore their full potential, including what other treatments they can be combined with and what cancers they are most effective against.”

When DNA is replicated, the two strands that make up the double helix are separated, and each strand is used as a template to synthesise a new double helix. However, this process can go wrong, and there are several types of mechanisms designed to repair these errors so that replication can continue normally.

In their research, published in Molecular Cell, the team studied how DNA gaps are repaired in human cancer cells using advanced imaging tools that monitor DNA replication in real time.

They found that POLQ fills in the gaps in DNA to allow replication in cancer cells unable to repair DNA gaps using a common method called homologous recombination. However, the DNA repair process by POLQ is prone to errors, which introduces variations in the DNA of cancer cells.

The researchers hope that drugs that block POLQ could limit mutation diversity and the impact it has on cancer evolution and the development of resistance to cancer treatments.

“The introduction of diversity into the genetic make-up of cancer cells makes it more likely that harmful characteristics will arise,” explained Simon Boulton, senior author, principal group leader at the Crick and scientific co-founder and vice president of scientific strategy at Artios.

“Being able to slow cancer mutation rates and cancer evolution, a process whereby tumours become more advanced and often harder to treat, can be a highly valuable tool for doctors treating patients with cancers,” he added.

Article by
Emily Kimber

1st December 2022

From: Research

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