The variant makes the cell motor sputter and mutate, so cancer can arise, says Associate Professor Thomas Helleday, who leads the research team at the Department of Genetics, Microbiology, and Toxicology, Stockholm University.

Even though it is easy to identify the some 15 percent of the population who have the harmful gene, which is called XRCC3 T241M, it is not meaningful to examine them since there are also other unknown factors that influence if this variant increases risk of cancer.

On the other hand, we can possibly make use of the faulty variant to custom design new treatments in the future. And even if this doesn ™t happen, it ™s nevertheless important to understand the mechanisms that make certain individuals more susceptible to cancer than others, he says.

Normally our genes have to be divided into two perfectly identical copies when a cell divides. The unfortunate variant causes a defect in the division of the genetic material (mitosis), which means that a daughter cell may get too few or too many genes. If a daughter cell does not receive a gene that prevents cancer, a so-called tumour suppressor gene, then a cancer can grow. One defence mechanism against cancer is for a cell that gets faulty genes to commit suicide (apoptosis). The defect caused by the unfortunate variant when it divides the genes is so tiny that the suicide mechanism does not detect the fault, which allows the cell to continue its growth into a cancer.

The variant causes just a tiny defect that cannot be detected by the defence mechanisms against cancer. Just as in life, minute mistakes can lead to fatal consequences if they are not discovered, says Thomas Helleday.

The main financiers of this research are the Swedish Pain Relief Foundation and the Swedish Cancer Society, and the findings are published in the April issue of the journal Human Molecular Genetics.

su.se

The research group of Thomas Bosch at the Zoological Institute of Kiel University has been studying stem cells in the freshwater polyp Hydra for many years. The scientists expect that their studies of the cells in this phylogenetically old and uniquely simple animal will give insights into the mechanisms that regulate the behaviour of stem cells, and have led to the development of complex cell systems in the course of evolution.

This is a marvellous result, also for me personally, explains Bosch, because I began to work on this topic as long ago as 1985, as a young post-doc in the USA. This functionalisation of stem cells, with the ability to control them and use them as a research tool, will result in a great step forward. As Hydra possesses many of the genes that the human body also uses for development as well as pathogen defence, these new transgenic stem cells allow functional studies that cannot be carried out so easily in complex organisms and in humans. And last but not least, studies on the stem cells of lower life-forms do not present any ethical problems.

Bosch is also involved in the two proposals of Kiel University for setting up of centres of excellence. One proposal, on the theme of inflammation at interfaces, is concerned with the defence mechanisms of the immune system, and the work reported here now makes it possible to study the evolutionary origin of genes involved in inflammation. In the proposed centre of excellence on Future Ocean, transgenic hydra will be used for functional studies of regulatory genes of marine organism. Both centre proposals have already passed through the first stage of approval by the German Research Foundation (Deutsche Forschungsgemeinschaft, DFG). The full applications will go before the DFG in April 2006, and a decision is expected in October 2006.

uni-kiel.de