Introduction

1. No. 026 Re-evaluating the Biological Significance of Seminal Vesicle Invasion in Locally Advanced Prostate Cancer N Sapre†, J Pedersen††, L Harewood†, J Peters†, A Costello†, C Hovens†, NM Corcoran† †Department of Urology and Surgery, Royal Melbourne Hospital, University of Melbourne †Australian Prostate Cancer Research Centre, Epworth Hospital, Victoria, Australia ††TissuPath Pty Ltd, Hawthorn, VIC, Australia Results From total 903 patients, 249 patients with pT3 disease were identified. Clinico-pathological characteristics of study cohort were categorised by presence or absence of SVI. SVI+ tumours were found to have significantly higher total and index tumour volume, gleason score were and associated with a higher pre-operative PSA. Routes of invasion: Of the 46 patients with SVI, the route of SVI was by direct extension in 40 (87%) and metastatic in 6 (13%) patients. Of patients who had direct extension 31/40 (77.5%) patients had direct extension exclusively through the base, 5 had multifocal extension and 3 patients exhibited involvement of the ejaculatory duct. Pre-operative PSA, pathological Gleason score, total and index tumour volumes were the only significant independent predictors on multivariable analysis. Introduction Seminal vesicle invasion (SVI) by prostate cancer is a pathological feature that has been known to be associated with poorer prognosis. The clinical association of SVI with the development of metastatic disease raises the possibility that the SVI either represents a privileged staging site for tumour cell dissemination or that SVI is a surrogate marker of large aggressive tumour, as a large tumour is more likely to encroach into central zone and invade seminal vesicles. Aim To differentiate between these two possibilities we conducted a detailed study of patients with locally advanced (pT3) disease to examine the impact of SVI on clinical outcome. b) a) Methods Patients with EPE and/or SVI were identified from a prospectively recorded and maintained prostate cancer database. Patients were categorized according to the presence of seminal vesicle invasion as determined by routine pathological assessment, with or without concomitant extraprostatic extension. Tumour volumes were measured routinely by computed planimetry at the time of histological assessment. Figure 1 a and b: SVI (marked as red) by direct extension (a) and as a metastatic deposit (b) on volumetric analysis by digital planimetry. Figure 2. Kaplan-Meier curve of significant biochemical recurrence with a PSA doubling time < 6 months stratified by the presence or absence of seminal vesicle invasion (SVI). Conclusions Our results suggest that SVI is a surrogate marker of larger and more aggressive, tumours with higher Gleason scores rather than a privileged site of tumour cell dissemination. These tumours due to their size and aggressiveness must gain the ability to breach the prostatic capsule and/or ejaculatory duct and invade the seminal vesicle muscular wall. In patients who have larger more aggressive tumours one would expect to have significantly earlier biochemical recurrence. Our findings that SVI may be an indirect marker of inherent biological aggressiveness and size of the tumour is mirrored by some series and contradicted by others. These differences may be attributable to varied methods of diagnosing SVI and calculating tumour volumes, which may not be standardized across all pathological laboratories. Table 2. Cox proportional hazards regression models of biochemical using PSA recurrence with a doubling time of < 6 months as the predicted event. Presence of SVI did not significantly predict biochemical recurrence on multi-variate analysis. Acknowledgements N Sapre is the recipient of the Cancer Council Victoria and Cybec Cancer Research Postgraduate Scholarships. Poster presentation sponsor