The findings have longer-term implications at the level of therapy, as well as diagnosis, which, the scientists say, could lead to the development of gene inhibitors to create a more rational treatment of the cancer.
A similar discovery of gene rearrangement in chronic myeloid leukaemia led to development of Gleevec, a drug that's proven successful in treating that cancer.
A team at the University of Michigan found that prostate cancer samples revealed something only seen in blood-related cancers: a recombination of genes that turned cells malignant.
"We were looking for genes that we thought might be oncogenes (cancer-causing). We found these two genes, which inspired us to look further. Then we looked at the expression transcript and found a new gene, and then another," said Dr. Arul Chinnaiyan, a pathology professor at the university and lead author of the study.
The researchers found that combinations of other genes created these new genes. A prostate gene designated TMPRSS2 fused with two other genes, ETV1 and ERG. The combination caused the ETV1 and ERG genes to be unusually active, presumably driving the growth of the cancer cells, the experts commented.
Rearrangements of those genes have been implicated in the genesis of Ewing's sarcoma, a relatively rare bone cancer, and similar combinations caused by gene rearrangements have been found in leukaemias and lymphomas.
What makes this latest discovery in prostate cancer so remarkable is that this is an epithelial cancer: a malignancy of the tissue that lines organs. Breast cancer, colon cancer and lung cancer also are forms of epithelial cancer.
"It is likely that prostate cancer is not special in this regard," he said. "Breast cancer and colon cancer might have similar rearrangements that haven't been found as yet."
The hope is that scientists will be taking this approach and applying its thinking to identify similar gene arrangements in other cancers.
The findings are reported this month in the Oct. 28 issue of Science.