Antisoma telomere targeting agent stops tumour growth in prostate cancer model
05-Nov-2004
London UK. Cancer drug developer Antisoma presents new data showing that one of its telomere targeting agents (TTAs) rapidly blocks prostate tumour growth in a human xenograft model. While in untreated control animals tumours grew to lethal size within 10 days, animals given the TTA experienced a halt in tumour growth at around day 7 and survived to the experiment's end on day 25. These findings extend the range of cancers shown to be susceptible to Antisoma's TTAs and demonstrate that the drugs have profound effects on tumour growth even when used as a sole treatment.
The presentation will be given by Antisoma's Head of Research, Professor Lloyd Kelland, at the AACR Special Conference on The Role of telomeres and telomerase in Cancer in San Francisco. It comes as the Company, working with the Cancer Research UK Group led by Professor Stephen Neidle at the London School of Pharmacy, nears completion of work to select a lead candidate from the TTA programme for clinical trials.
Professor Kelland commented "What's really exciting about these TTAs is the speed of their anti-tumour effects. We're not having to wait for many rounds of cell division before the effects kick in, which was a major concern with earlier drugs that were pure telomerase inhibitors."
Telomeres are protective regions found at the ends of chromosomes. In normal cells, they shorten slightly with each round of cell division until they become critically short, causing the cell to enter the self-destruct programme of apoptosis. Most cancer cells make the Enzyme telomerase, which maintains the length of telomeres and allows the cells to avoid apoptosis. A number of drugs have been developed that inhibit telomerase. These are generally characterised by a slow onset of action because they require rounds of cell division to 'run down' the telomeres to the point where apoptosis ensues. TTAs by contrast act more rapidly, binding to the telomere itself and destabilising it. One clear effect is the uncapping of chromosome ends leading to lethal end-to-end chromosome fusions. The action of TTAs is believed to involve prevention of telomerase binding to the telomere. However, it must have other facets because the drugs show broad effectiveness against cancer cell lines, including the minority that use alternative, non-telomerase mechanisms to maintain their telomeres.
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