Genetic weakness points to potential drug target

In collaboration with the Press Association
Breast cancer cell

US scientists have identified a molecule inside cells that, if targeted with drugs, could help slow the growth of tumour cells carrying certain genetic faults.

“This is certainly a very interesting development that highlights how DNA repair is crucial for cell function" - Professor Steve Jackson, Cancer Research UK

If confirmed in follow-up studies, the research could lead to a new class of treatment to target cancer cells carrying the BRCA1 and BRCA2 gene faults

The study, published in the journal Nature, focused on the molecular machinery used by cells to repair damage to their DNA. 

Researchers from New York University Medical Centre focussed on a protein called PolQ, which plays an important role in a particular process of DNA repair. The enzyme has also been shown to be active in breast and ovarian tumour samples.

The team found that the growth of tumour cells carrying faults in the BRCA1 gene were slowed when PolQ was switched off. Faults in the BRCA1 and BRCA2 genes are linked with some breast and ovarian cancers.

And experts believe these news findings could point to promising avenues of further drug research.

Professor Steve Jackson, a Cancer Research UK genetics expert from The Gurdon Institute at the University of Cambridge, said: “This new work suggests that drugs targeting PolQ, if they can be successfully developed, might selectively kill some cancer cells, especially those with associated BRCA1 or BRCA2 mutations." 

Dr Agnel Sfeir, lead author on the study, hopes the discovery, made during experiments carried out in mice and human cells could lead to new therapies for breast, ovarian and other cancers in future.

Professor Jackson cautioned that there was still more work to be done following this study, but he added that the early stage findings were promising.

“This is certainly a very interesting development that highlights how DNA repair is crucial for cell function and how many cancer cells are particularly reliant on certain cellular DNA repair mechanisms,” he said. 


  • Mateos-Gomez, P., et al. (2015). Mammalian polymerase θ promotes alternative NHEJ and suppresses recombination Nature DOI: 10.1038/nature14157