LONDON, March 8, 2007--Cancer Research UK scientists in Glasgow have devised a new method of attacking cancer cells. They report the findings in the Journal of Clinical Investigation* today (Thursday).
A team of scientists from the Beatson Institute for Cancer Research gave mice a chemical that caused cancer cells to commit suicide, significantly slowing the growth of the tumours they were carrying. The chemical kick started a gene called p73 that brings about cancer cell death.
This early research could pave the way for a new agent to stop tumours growing. The researchers suggest that sending the protein – called 37AA – directly into the bloodstream using a ‘nanoparticle’ delivery system could be a potential way to find and kill tumour cells that have spread as well as those in the primary tumour.
In further laboratory studies the research team found that the chemical could kill several types of cancer cells – including bowel, cervical and bone cells.
Lead researcher Dr Kevin Ryan, a Cancer Research UK senior research fellow and head of the Tumour Cell Death Laboratory at the Beatson Institute, said: “Our study has shown for the first time that the selective activation of a gene called p73 can cause cell death in tumours. We think this approach has the potential to be developed into an effective treatment for cancer.”
The gene p73 is related to p53 – one of the most important genes known to protect against the development of cancer. p53, known as the ‘guardian of the genome’, was first identified by Cancer Research UK scientists in London.
p53 is damaged in the vast majority of cancers so scientists across the globe are looking for ways to restore the gene as a way of treating the disease. However, in some cancers, p53 is damaged in such a way that its function cannot be restored. p73 is a promising alternativ e target because it is rarely defective in human cancers.
Dr Ryan added: “Previously we thought p73 was just a ‘sleeping partner’ of p53, so we’re really excited that we’ve found a way to harness its function to treat cancer. While our studies are still at a preliminary stage, the next phase of our work is going to focus on developing a drug that mimics the effect of the 37AA protein. We hope this strategy could then be more readily tested for its potential development in human tumours.”
Professor Jim Cassidy, Cancer Research UK’s chair of medical oncology in Scotland said: “This fascinating piece of basic research has resulted in an experimental treatment that can cause malignant tumours to stop growing. In laboratory tests it killed a range of different cancer cells. We look forward to seeing if switching on p73 can translate into a treatment for patients.”
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Notes to Editors:
*A novel p53-derived apoptotic peptide de-represses p73 to cause tumor regression in vivo. Helen S. Bell et al, 2007. Journal of Clinical Investigation.
This research was funded by Cancer Research UK with support from the Biotechnology and Biological Sciences Research Council (BBSRC) and the Ludwig Institute for Cancer Research.
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