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Scientists out cancer cells in permanent coma

Published on March 29, 2005 at 12:43 AM · No Comments

Scientists funded by Marie Curie Cancer Care and the Association for International Cancer Research have made an unexpected discovery that could point the way to a completely new approach to treating cancer.

Current treatments are based on cutting out or killing cancer cells. Now scientists based at the Marie Curie Research Institute, in Surrey, believe the work could lead to a third way of dealing with them. They have successfully put cancer cells into a permanent ‘coma’ by reactivating a natural self-defence mechanism which responds to dangerous mutations by putting the cell into a state called senescence – meaning that it cannot divide any more.

In cancers this safeguarding mechanism is bypassed, enabling cell division to run out of control. Scientists previously thought that in cancers it was damaged beyond repair.

This new work published on the 15th March 2005 [1] shows that they can switch back on the mechanism that triggers senescence in cells for the deadly skin cancer malignant melanoma. The cells stop dividing – and never divide again.

Dr Colin Goding, Head of the Signalling and Development Group, who led the research, explained: “When certain genes called oncogenes are activated by mutation, they cause cancer to develop. Many oncogenes control cell growth or cell division.

“When these are mutated, it’s like the accelerator in a car being jammed on – the cell is continuously getting instructions to divide: “In our lifetime of 70 years or so, we get mutations in these genes all the time, but may only get cancer once. That is partly because we are protected by the senescence mechanism.

“Normal cells sense that something is wrong – that the accelerator is jammed on – and they put on this brake on cell division called senescence, which means the cell will never divide again. It’s in a coma – permanently.

“We thought that when normal cells became melanomas, it wasn’t possible to switch on senescence – these are cancer cells, so by definition, they’ve overcome this braking mechanism.

“We were looking at a gene called Tbx2, which is too active in melanoma and other cancers, and wanted to know exactly what it did and how it did it. It turned out to be linked to a mechanism that repressed senescence.

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