Abstract
Arising from: Tomlins et al. Nature 448, 595–599 (2007)10.1038/nature06024; Tomlins et al. reply
The first recurrent translocation event in prostate cancer has been recently described1; it results in the translocation of an ETS (E26 transformation specific) transcription factor (ERG or ETV1) to the TMPRSS2 promoter region, which contains androgen responsive elements1. The TMPRSS2:ERG genetic rearrangement has been reported to occur in approximately 40% of primary prostate tumours (ETV1 genetic rearrangements occur at a much lower frequency), and it results in the aberrant androgen-regulated expression of ERG1,2,3. Tomlins et al.4 concluded that ETS genetic rearrangements are sufficient to initiate prostate neoplasia. However, here we show that ETS genetic rearrangements may in fact represent progression events rather than initiation events in prostate tumorigenesis. To this end, we demonstrate that the prostate-specific overexpression of ERG does not initiate prostate tumorigenesis.
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References
Tomlins, S. A. et al. Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer. Science 310, 644–648 (2005)
Tu, J. J., Rohan, S., Kao, J., Kitabayashi, N., Mathew, S. & Chen, Y.T. Gene fusions between TMPRSS2 and ETS family genes in prostate cancer: frequency and transcript variant analysis by RT–PCR and FISH on paraffin-embedded tissues. Mod. Pathol. 20, 921–928 (2007)
Perner, S. et al. TMPRSS2-ERG fusion prostate cancer: an early molecular event associated with invasion. Am. J. Surg. Pathol. 31, 882–888 (2007)
Tomlins, S. A. et al. Distinct classes of chromosomal rearrangements create oncogenic ETS gene fusions in prostate cancer. Nature 448, 595–599 (2007)
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Carver, B., Tran, J., Chen, Z. et al. ETS rearrangements and prostate cancer initiation. Nature 457, E1 (2009). https://doi.org/10.1038/nature07738
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DOI: https://doi.org/10.1038/nature07738
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