Research appearing in Nature used gene silencing to study evaluate prostate cancer cell lines.

Researchers at the University of Michigan Comprehensive Cancer Center have identified a series of genes that become fused when their chromosomes trade places with each other.

“We defined a new class of mutations in prostate cancer,” says Arul Chinnaiyan, M.D., Ph.D., director of the Michigan Center for Translational Pathology. “ But we found other fusions as well, some of which were unique to individual patients. Our next step is to understand if these play a role in driving disease.”

These repeated gene fusions are thought to be the driving mechanism behind the formation of particular kinds of cancer and could serve as a marker for diagnosing those cancers or as a target for drug development.

Some fusions were seen in multiple cell lines studied, while other gene fusions appeared only once. The fusions were found only in cancer cells and not in normal cells.

The team was the first to identify rearrangements in chromosomes and fused genes in prostate cancer, though gene fusions had previously been known to play a role in blood cell cancers such as leukemia and lymphoma and in Ewing’s sarcoma.

The group had previously used microarray technology to identify gene fusions in prostate cancer. “We now have the ability to use next-generation sequencing technology. This will open up the field in cancer research,” says Dr. Chinnaiyan. This allows the team to find information about the fusion without knowing where to look in the first place. While the current study focused on prostate cancer, his team is also looking at gene fusions involved in breast cancer, lung cancer, and melanoma.

The article appears in the January 11 online edition of Nature.

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