Cancer Biology
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New research provides hope for patients with hard to beat breast cancer

 

A team of scientists from The University of Nottingham and Oxford University, has found a new way to slow the growth of the most aggressive type of breast cancer, according to research published in the journal Oncogene today.

The Cancer Research UK (CRUK)-backed team found that using a drug called JQ1 can alter how cancer cells respond to hypoxia – or low oxygen – found in more than 50 per cent of breast tumours overall and most commonly in triple negative breast cancer, the form of the disease that is hardest to treat.

JQ1 works by stopping cancer cells adapting to the lack of oxygen. The study results showed that JQ1 slowed tumour growth and limited the number of blood vessels that were produced.

When a patient’s breast cancer is starved of oxygen it can be much more difficult to treat successfully. That’s because the way cancer cells adapt to low oxygen changes their biology and makes them resistant to standard therapies. When there are low levels of oxygen, tumour cells turn on specific genes which send signals for new blood vessels to supply them with fresh oxygen, giving cancer the nutrients it needs to grow and spread.

Dr Alan McIntyre, co-author of the study, at the University of Nottingham, said: “Triple negative breast cancer is a challenge. By tackling hypoxia that so often compromises the treatment of breast cancers, JQ1 could be an important key to helping women with aggressive breast tumours.”  

The study explains how the family of drugs to which JQ1 belongs works. Although this group of drugs - called bromodomain and extraterminal inhibitors or BETi - has been used to treat cancer before, this study sheds light on the role these drugs could play in hypoxia, which could prove vital for patients with hard-to-treat breast cancers.

Read more.

Publication reference:  The BET Inhibitor JQ1 Selectively Impairs Tumour Response to Hpoxia and Downrregulates CA9 and Angiogenesis in Triple Negative Breast Cancer

 

Posted on Wednesday 22nd June 2016

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