Press Release
Drug breakthrough could improve breast cancer survival rates
22 December 2010
Breakthrough Breast Cancer scientists have identified a new class of drug which could help Herceptin (trastuzumab) work much more effectively and may improve survival rates for women with an aggressive form of breast cancer.
This followed the discovery of the reason why Herceptin stops working in some breast cancer patients – representing a major leap forward in our understanding of this targeted therapy. The findings are published online in the journal PLoS Biology.
The Breakthrough Breast Cancer-funded team at the University of Oxford showed that combining Herceptin with pan-HER inhibitors kills cancer cells much more effectively than Herceptin on its own. The drug combination does this by knocking out the activity of HER2 and, crucially, its related proteins, too. These results were then confirmed in mouse models.
Dr Anthony Kong, the Breakthrough Breast Cancer clinician scientist who led the study, said: “It was incredible to see how much more potent Herceptin becomes when combined with a new type of drug. We think this could have a big impact in improving survival rates for patients with HER2 positive breast cancer.
“We are hoping to set up a clinical trial in the near future to test this treatment combination in patients.”
Herceptin is currently used in combination with chemotherapy to treat HER2 positive breast cancer. Around 9,000 women are diagnosed with this type of the disease in the UK each year. While Herceptin works well for some patients, for others it either doesn’t work or stops working over time. Survival rates for patients with HER2 positive breast cancer remain lower than for breast cancer overall.
The scientists discovered a key mechanism through which cancer cells develop resistance to Herceptin. They also confirmed earlier studies which showed that in some cases Herceptin is not hugely effective in killing cancer cells – it mostly delays their growth. They found that, counter to previous thinking, Herceptin does not decrease the activity of its target, the HER2 protein, and went on to find the reason behind this.
Dr Norman Freshney, Director of Research at Breakthrough Breast Cancer, said: “Since Herceptin became available, thousands of patients have benefited from this new way of targeting breast cancer. However, poor response or resistance to this drug remains a considerable problem for many patients and these results explain why this may happen.
“This work highlights the importance of understanding the biology of breast cancer and developing new ways of targeting the tumour’s defects to have maximum lifesaving impact.”
In recent years the work of Dr Anthony Kong has been significantly funded by a range of trusts including Mary Kinross Charitable Trust, The Holbeck Charitable Trust, Doris Field Charitable Trust and in part by The Tolkien Trust.
Article Comments
I was very excited to here on the news this morning & now read about your research into breast cancer.
I was recently diagnoised with HER2-Positive breast cancer with secondary tumours in my shoulder, spine and possibly my liver. I had my first treatments of Herceptin & Docetaxel over 2 days, which worked with out too many side effects. Whilst having my second treatment of both drugs on the same day, I suffered a rare and very frightening, allergic reation to the Docetaxel and am now not able to have it. I feel that the Herceptin is not working as well on its own. My Oncologist is Dr Sugden who I see at The Horton Hospital Banbury or the Churchill Hospital in Oxford. I would be interested to know if I could could put myself forward as a candidate for any drug trails for the above combination of Herceptine with pan-HER inhibitors in the hopes that the treatment would help kill my cancer cells much more effectively than Herceptin on its own.
Maggie Williams
22nd Dec 2010 at 5:21 pm
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