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Study Shows Fused Genes Trigger Development of Prostate Cancer

Posted on: Friday, 28 October 2005, 09:00 CDT

Study shows fused genes trigger development of prostate cancer

LOS ANGELES, Oct. 27 (Xinhua)-- Scrambled chromosomes and abnormal genes may cause prostate cancer, scientists reported on Thursday.

In a paper published in the Oct. 28 issue of Science, the researchers at the University of Michigan indicated that chromosomal rearrangements induce specific genes to merge and fuse.

This phenomenon can be detected in most prostate cancer tissue samples, but in health prostate tissue there is no evidence of gene fusion, the researchers noted. "The data in our study provides tantalizing evidence that gene fusion is the causative agent in prostate cancer," said Arul Chinnaiyan, a professor at the University of Michigan who directed the study.

"It's what drives the aberrant over-expression of cancer- causing genes and is the first step in the progression of tissue changes leading to prostate cancer."

Because this gene fusion occurs only in prostate cancer, a blood or urine test to detect the fused genes or their protein products would be specific for prostate cancer, according to Chinnaiyan.

If scientists could find a way to block the gene, it could be the basis for a new, effective treatment for prostate cancer, he said.

"This finding is an important advance, because it suggests that similar mechanisms may be involved in other epithelial cancers, such as breast, lung and colon," said Jacob Kagan at US National Cancer Institute.

The abnormal gene fusion associated with prostate cancer occurs when one of two genes, ERG or ETV1, merges with a prostate- specific gene called TMPRSS2, according to the Science paper. ERG and ETV1 are also known to be involved in the development of a bone cancer called Ewing's sarcoma, and other types of cancer.

While rearrangements in chromosomes and fused genes have been detected in blood cell cancers like leukemia and lymphoma, this is the first time they have been found in a common solid tumor like prostate cancer, which develops in epithelial cells lining the prostate gland.

"This is a paradigm shift for all epithelial tumors - such as cancers of the lung, breast, colon, ovary, liver and prostate, which are the most common types of cancer and account for most deaths due to cancer," Chinnaiyan said.

"We knew gene rearrangements were involved in hematologic malignancies and sarcomas. But finding this recurrent chromosomal rearrangement in prostate cancer suggests that other common epithelial cancers have their own recurrent chromosomal rearrangements. We just haven't found them yet."

The researchers hope to identify small molecule inhibitors targeting the genes involved in prostate cancer, thus design novel drugs to block the cancer development in future study.

Prostate cancer is the second most common cause of cancer- related deaths in men. According to the American Cancer Society, 232,000 men in the United States will be diagnosed with prostate cancer and 30,350 men will die from the disease in 2005.

Source: Xinhua News Agency - CEIS

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