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Tracy Hampton, PhD

JAMA. 2005;294:2832.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

While chromosomal translocations resulting in fused genes have been found in various types of leukemias, lymphomas, and sarcomas, few have been documented in most types of solid cancers. But now a chromosomal rearrangement has been implicated as a potential cause of some prostate cancers, a finding that could lead to new diagnostic and therapeutic strategies (Tomlins et al. Science. 2005;310:644-648).

The findings come through the use of a research tool called Oncomine, a collection of data from numerous cancer studies across the globe, studies that use devices called microarrays to simultaneously screen the activity of thousands of genes (Hampton. JAMA. 2004;292:2073). The collection integrates 132 gene expression data sets representing 10 486 microarray experiments.

By surveying Oncomine for genes that are overactive in prostate tumors, Arul Chinnaiyan, MD, PhD, of the University of Michigan in Ann Arbor, and his team found two candidate genes—ERG and ETV1. . . [Full Text of this Article]