The discovery of recurrent gene fusions in a majority of prostate
cancers has important clinical and biological implications in the study
of common epithelial tumours.

Gene fusion and chromosomal
rearrangements were previously thought to be primarily the oncogenic
mechanism of hematological malignancies and sarcomas.  The resulting gene fusions can
serve as specific therapeutic targets, as exemplified by the
development of imatinib (Gleevec), which specifically inhibits the
BCR-ABL gene fusion product that defines chronic myeloid leukemia.

Prostate cancer cells: from www.bu.edu        

Prostate-nano-enlarged
The prostate
cancer gene fusions that have been identified so far are
characterized by 5' genomic regulatory elements, most commonly
controlled by androgen, fused to members of the Ets family of
transcription factors
, leading to the overexpression of oncogenic
transcription factors.

The specificity of ETS gene fusions in prostate cancer suggest that
they may potentially have causal roles in prostate cancer and suggest utility in
prostate cancer detection, stratification and treatment. 

Time will tell.

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