New research suggests that Novartis’s leukaemia drug Gleevec might have wider applications in treating cancer than was previously thought.
The view is expressed by scientists at the Technical University of Munich, who have discovered additional anti-cancer properties in the antibody treatment and their findings are detailed in the latest edition of the Nature specialist journal Leukemia.
The German team has discovered evidence that Gleevec (imatinib) switches on a tumour killing pathway, called autophagy, not previously linked to the drug. Autophagy is a process by which proteins and organelles are degraded within a cell, leading to cell death.
The team, led by Dr Hermann Schätzl, has shown how treatment with Gleevec results in the production of ring-shaped structures in the cell fluid that indicate the formation of autophagosomes – the structures essential for autophagy. Importantly, these structures are detected in cell lines from different tissues, providing hope that imatinib may promote tumour regression in a variety of cancers, say the researchers.
The study has implications for the way cancer, and particularly chronic myeloid leukaemia is treated. They add that Gleevec used in combination with other autophagy-inducing drugs could potentially rapidly reduce the size of a tumour.
Until now, it had been assumed that Gleevec has its powerful effect against CML and gastrointestinal stromal tumours by neutralising enzymes called tyrosine kynases that that encourage the growth of cancer cells.
Dr Kat Arney, senior science information officer at Cancer Research UK, said: “Although we’re a long way from knowing if Gleevec could be used to treat other types of cancers, these interesting lab tests help us understand more about how the drug works.”
In September last year, new research from Stanford University suggested Gleevec might also have a role in treating rheumatoid arthritis. The researchers presented evidence that the drug dampened down key aspects of the immune system, including TNF-alpha release, macrophage and B-cell production, that are implicated in rheumatoid arthritis. By Michael Day
