The Lethal Clone in Prostate Cancer: Redefining the Index

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The Lethal Clone in Prostate Cancer: Redefining the Index Christopher E. Barbieri, Francesca Demichelis, Mark A. Rubin  European Urology  Volume 66, Issue 3, Pages 395-397 (September 2014) DOI: 10.1016/j.eururo.2013.12.052 Copyright © 2013 European Association of Urology Terms and Conditions

Fig. 1 Speckle-type POZ protein (SPOP), phosphatase and tensin homolog (PTEN), and tumor protein 53 (TP53) abnormalities across the spectrum of early and advanced prostate cancer. SPOP mutations occur in 10–15% of prostate cancer, with relatively stable prevalence across stages of disease. Mutations and deletions in PTEN and TP53 increase in frequency with advanced disease (but do not always occur together). Co-occurrence of SPOP mutations and PTEN and TP53 lesions are uncommon in early prostate cancer, but begin to overlap with advanced disease. European Urology 2014 66, 395-397DOI: (10.1016/j.eururo.2013.12.052) Copyright © 2013 European Association of Urology Terms and Conditions