Abstract
BACKGROUND. pp32 is a differentiation-regulated nuclear phosphoprotein that is highly expressed in many cancers, but is restricted to self-renewing and long-lived normal cell populations. During murine embryogenesis, pp32 is expressed in primitive cell populations, diminishing as tissues terminally differentiate. Functionally, pp32 confers resistance to programmed cell death and, paradoxically, inhibits transformation mediated in vitro by a broad range of oncogenes, suggesting that pp32 is a multifunctional molecule with potentially complex activities in cancer. METHODS. We studied pp32 expression in prostatic adenocarcinomas and benign prostatic hyperplasia by in situ hybridization. RESULTS. In benign prostatic tissues, moderate pp32 expression occurs only in the basal cells. This study found elevated pp32 expression in 98% (54/55) of prostatic adenocarcinomas of Gleason score ≤5 (P < 0.0001). CONCLUSIONS. These results suggest that pp32 may be diagnostically useful and may contribute mechanistically to prostate tumor development. In comparison to other molecular alterations, increased pp32 expression is one of the most frequent events in primary prostate cancer.
Original language | English (US) |
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Pages (from-to) | 231-237 |
Number of pages | 7 |
Journal | Prostate |
Volume | 34 |
Issue number | 3 |
DOIs | |
State | Published - Feb 15 1998 |
Keywords
- In-situ hybridization
- Pp32
- Prostate cancer
ASJC Scopus subject areas
- Oncology
- Urology