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Received truth turned on end in cancer research

This release is also avaialable in Swedish.

It has long been the accepted view of cancer researchers that there is a difference between the mechanism behind the development of leukemias, on the one hand, and solid tumors like breast cancer, prostate cancer, gastrointestinal cancer, etc, on the other. A research team at the Section for Clinical Genetics at Lund University is now claiming just the opposite: the same mechanism gives rise to all non-hereditary forms of cancer. These findings are being published in Nature Genetics.

A well-known mechanism for the development of cancer is that the chromosomes in a cell break apart and then recombine in an incorrect way. At the points of fissure, gene fragments are exposed that can recombine with so-called fusion genes, yielding fusion proteins. Leukemias-blood cancer-normally develop from cells that contain such fusion proteins. It is not known how this occurs in detail, but in some way the fusion proteins prompt formerly normal cells to transform into cancer cells. On the other hand, solid tumors, which make up the majority of all cancer cases, have been seen as developing as a result of certain cells losing the inhibiting mechanism in the form of so-called tumor suppressor genes that keep tumors from arising.

"This is no doubt correct in regard to hereditary cancer. But hereditary cancer accounts for only 5-10 percent of all cancer cases. We now maintain that all of the others have the same developmental mechanisms. In non-hereditary cancer forms it is the occurrence of fusion genes and not the lack of tumor suppressor genes that is essential," says Professor Felix Mitelman.

Mitelman and his associates Bertil Johansson and Fredrik Mertens have gathered information about aberrant chromosomes in cancer for years. In 1997 Nature Genetics devoted an entire issue to the large material the Lund team had compiled, something that has
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Contact: Ingela Bjrck
ingela.bjorck@info.lu.se
46-46-222-7646
Swedish Research Council
6-Apr-2004


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