News - November 18, 2011

Cancer cells 'steal' DNA from host

Cancer cells seem able to replicate missing hereditary material, say Wageningen researchers. Their observation is based on a recent study of a 10,000-year-old transmissible tumour found in dogs.

Such mitochondria are the energy suppliers of the cell. Some tumours seem to have the ability to steal them from their 'host'.
Cancer cells can divide extremely fast because crucial growth retardation genes have disappeared or are damaged. But this is not the only genetic material which cancer cells no longer have. Each cell consists of several cellular energy plants called mitochondria which have their own circular-shaped DNA molecules. During the course of one's life, parts of this DNA are depleted - especially in fast-splitting cancer cells. While this hinders energy production in the mitochondria, cancer cells do not seem to be any worse for it. Two Wageningen researchers attempt to explain why this is so in Trends in Genetics.
Ten thousand years
The researchers, Duur Aanen and Marc Maas from the Laboratory of Genetics, examined a seldom found transmissible form of cancer in a tumour about ten thousand years old which is, in a very exceptional way, sexually transmitted from dog to dog. The prevailing theory says that cells can survive the loss of mitochondrial DNA when it happens in one lifetime. 'But during sexual cell division when egg cells are produced, a clean-up occurs,' says Aanen. In this way, the next generation gets undamaged mitochondria again. But things ought to be different for a tumour. Too much damage has been accumulated over ten thousand years and this would form an enormous blockage to the cell. And yet, it seems that something has taken place in the dog tumour in this case.
Last January, a group of English researchers published a possible explanation in Science. They used DNA sequencing to show that the mitochondria in the dog tumour were 'borrowed' from the canine host.  This type of 'theft' is crucial for the survival of the cancer cell, says Aanen and Maas. 'We don't know the mechanism behind this, and it's difficult to explain how it happens,' says Aanen. But the fact remains that the tumour has done this at least twice in the last ten thousand years.
Cancer within a cancer
The reason for the disappearance of pieces of hereditary material from mitochondria can be traced to evolution, Aanen thinks. In each cell, mitochondria compete among themselves to replicate as fast as possible. If big chunks of DNA could be disposed of, the remaining DNA could replicate faster.
Ironically, the selection for quick replication takes place at the cost of the whole in this case, as it does in cancer. Just as the unrestrained division of cancer cells harms the organism, the selection of mitochondria which replicate faster but function less damages the cell. It is in fact like a cancer within a cancer. 'It was great thinking through this,' relates Aanen, 'because I am particularly interested in the levels of selection.