TL;DRAbstract
Since 1993, the incidence of clinical T3 prostate cancer has been reported to be 10% of all newly diagnosed cancers annually (1). However, prior to the era of PSA screening, clinical T3 cancers comprised nearly 20–30% of all newly diagnosed prostate cancers (2,3). In the pre-prostate-specific antigen (PSA) era, treatment outcomes of clinical T3 cancers frequently involved an initial monotherapy approach (either radical surgery or radiation therapy [RT]) with subsequent salvage of a monotherapy failure with a secondary therapy. Analysis of the results from this era using PSA as evidence for biochemical failure revealed unexpected high failure rates for monotherapy treatments. More recently, owing to detailed pathologic examination and the knowledge gained from using PSA to monitor outcomes, an appreciation of the limitations of the monotherapy approach has evolved. The recent momentum has encouraged the use of early, multimodality treatment in the treatment of locally invasive or clinic
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Since 1993, the incidence of clinical T3 prostate cancer has been reported to be 10% of all newly diagnosed cancers annually (1). However, prior to the era of PSA screening, clinical T3 cancers comprised nearly 20–30% of all newly diagnosed prostate cancers (2,3). In the pre-prostate-specific antigen (PSA) era, treatment outcomes of clinical T3 cancers frequently involved an initial monotherapy approach (either radical surgery or radiation therapy [RT]) with subsequent salvage of a monotherapy failure with a secondary therapy. Analysis of the results from this era using PSA as evidence for biochemical failure revealed unexpected high failure rates for monotherapy treatments. More recently, owing to detailed pathologic examination and the knowledge gained from using PSA to monitor outcomes, an appreciation of the limitations of the monotherapy approach has evolved. The recent momentum has encouraged the use of early, multimodality treatment in the treatment of locally invasive or clinic
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