Guest guest Posted December 29, 2006 Report Share Posted December 29, 2006 'Mutant genes' could treat cancer Chromosomes house genes The same genetic mechanism that drives tumour growth could also treat cancer, US scientists believe. Inheriting the wrong number of gene-rich chromosomes both caused and prevented cancers developing in mice, the California University team found. In the future, drugs that block the accurate delivery of the right number of chromosomes to new cells could destroy certain cancers, they hope. They explain their idea of " aneuploidy therapy " in Cancer Cell journal. Aneuploidy - too few or too many chromosomes - is known to be linked with cancer. But it is not clear whether aneuploidy is merely a consequence of mutations in tumour causing genes, or if it directly causes cancer by promoting mutations in these genes. Human cells ideally have 23 pairs of chromosomes, one set inherited from the mother and the other set passed on from the father. These chromosomes carry genes, which are made up of DNA - the code of life. The University of California, San Diego team looked at mice with highly variable numbers of chromosomes to see if this aneuploidy made the animals more cancer-prone. Indeed, the mice with the wrong number of chromosomes were more likely to develop tumours as they aged than other mice. When the scientists added other genetic errors to the cancer-prone mice, however, the cancer development slowed. The team also looked at mice that were missing a tumour suppressor gene, which is a gene that acts to prevent cell growth. Mice that lacked this gene were more susceptible to cancer, as expected. When the scientists created mice that lacked the tumour suppressor gene but also had a high rate of aneuploidy, tumour growth was again slowed. Lead researcher Beth Weaver said: " This study opens up a whole series of potential therapeutic targets for cancer. " By increasing the level of genetic damage, we can kill those tumour cells. " Quote Link to comment Share on other sites More sharing options...
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