903P - Improved survival in patients with metastatic castration resistant prostate cancer (mCRPC) treated on clinical trials

Date 29 September 2012
Event ESMO Congress 2012
Session Poster presentation I
Topics Prostate Cancer
Presenter Carmel Pezaro
Authors C. Pezaro1, A.G. Omlin1, D. Mukherji2, S. Sandhu1, D. Bianchini1, A. Mulick Cassidy1, G. Maier1, D. Olmos Hidalgo1, G. Attard1, J.S. De Bono3
  • 1Prostate Targeted Therapy Group, The Royal Marsden NHS Foundation Trust and Institute of Cancer Research ICR, SM25PT - Sutton/UK
  • 2Department Of Hematology Oncology Po Box: 11-0236, The Royal Marsden NHS Foundation Trust and Institute of Cancer Research ICR, SM25PT - Sutton/UK
  • 3The Royal Marsden NHS Foundation Trust and Institute of Cancer Research ICR, SM25PT - Sutton/UK

Abstract

Background

Median overall survival (mOS) in patients (pts) with mCRPC was 13-16 months (m) in the pre-docetaxel era. These data, obtained from clinical trials, were used to construct currently available prognostic nomograms. We hypothesise that these models no longer reflect survival. Pts and physicians urgently require updated prognostic data on which to base management decisions.

Methods

Pts with mCRPC treated on Phase I-III and expanded access trials at our institution were identified and data retrospectively collected. Predicted survival by Halabi and Smaletz nomograms were compared to calculated survival using Kaplan-Maier analysis. Cox model multivariate (MV) analysis used variables at referral, including performance status (PS), Gleason (GS), prostate specific antigen (PSA), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), hemoglobin (Hb), visceral disease and albumin.

Results

Between 2003 and 2011, 442 CRPC pts were treated on clinical trials. At diagnosis median age was 62 years (y; 41.8 – 82.7) and 243 (55.0%) had metastatic disease. Median interval from diagnosis to CRPC was 2.8y (0.2 – 21.7). At referral 259 pts (58.6%) were chemotherapy-naïve. Halabi and Smaletz models predicted mOS from referral in chemo-naïve pts of 21m and 17m respectively, however the observed mOS was 32m (95%CI 29– 38). Survival from CRPC was 43m (CI 37 – 46) and 39m (CI 35 - 44) in pre- and post-chemo pts, respectively. In our MV model using data from 225 evaluable pre-chemo patients, ALP (HR 2.65, p = 0.001), LDH (HR 2.66, p = 0.018), albumin (HR 0.92, p = 0.002) and PSA (HR 1.31, p = 0.046) were each prognostic after controlling for other variables, whereas Hb, PS, GS and visceral disease did not show a statistically significant effect.

Conclusion

Our pts lived significantly longer than predicted by current nomograms. This is likely due to development of effective new treatments. MV analysis confirmed the importance of several previously identified prognostic factors. Survival data from this large cohort of CRPC pts should encourage men considering clinical trial participation. Previously developed nomograms no longer accurately predict survival.

Disclosure

C. Pezaro: Author is an ICR employee. The ICR has a commercial interest in Abiraterone and PI3K and AKT inhibitors.

D. Mukherji: Author is an ICR employee. The ICR has a commercial interest in Abiraterone and PI3K and AKT inhibitors.

S. Sandhu: Author is an ICR employee. The ICR has a commercial interest in Abiraterone and PI3K and AKT inhibitors.

A. Mulick Cassidy: Author is an ICR employee. The ICR has a commercial interest in Abiraterone and PI3K and AKT inhibitors.

G. Maier: Author is an ICR employee. The ICR has a commercial interest in Abiraterone and PI3K and AKT inhibitors.

D. Olmos: Author is an ICR employee. The ICR has a commercial interest in Abiraterone and PI3K and AKT inhibitors.

G. Attard: Author is an ICR employee. The ICR has a commercial interest in Abiraterone and PI3K and AKT inhibitors.

J.S. de Bono: Author is an ICR employee. The ICR has a commercial interest in Abiraterone and PI3K and AKT inhibitors.

All other authors have declared no conflicts of interest.