909P - Predictive and prognostic roles of body mass index (BMI) in docetaxel(D)-treated castrate-resistant prostate cancer (CRPC)

Date 29 September 2012
Event ESMO Congress 2012
Session Poster presentation I
Topics Anti-Cancer Agents & Biologic Therapy
Prostate Cancer
Cancer Aetiology, Epidemiology, Prevention
Presenter Nataliya Rozumna-Martynyuk
Authors N. Rozumna-Martynyuk1, M.Y. Teo2, M.S.N. Mohd Sharial3, M. Doherty3, F. McDonnell4, S. O'Reilly5, D.G. Power6, R. McDermott7
  • 1Medical Oncology Unit, AMNCH Adelaide and Meath Hospital, 24 - Dublin/IE
  • 2Dept. Of Medical Oncology, AMNCH Adelaide and Meath Hospital, 24 - Dublin/IE
  • 3Medical Oncology, AMNCH Adelaide and Meath Hospital, 24 - Dublin/IE
  • 4Department Of Medical Oncology, Adelaide & Meath Hospital incorporating National Children's Hospital, Dublin/IE
  • 5Department Of Medical Oncology, Mercy University Hospital, Cork/IE
  • 6Medical Oncology, Mercy University Hospital, Cork/IE
  • 7Dept. Of Medical Oncology, Adelaide & Meath Hospital incorporating National Children's Hospital, Dublin/IE

Abstract

Introduction

Studies have suggested that overweight and obese patients with early stage prostate cancer present with lower PSA, higher grade disease and have poorer outcomes. Data remains limited on the influence of BMI on CRPC receiving D. We previously reported lower pretreatment PSA and rate of PSA response in obese pts (Teo et al, ASCO GU 2011). With an expanded cohort, we sought to examine the influence of BMI on PSA kinetics and CRPC survival.

Methods

Two institutional databases were analysed to identify pts who received D for CRPC. Demographics and serial PSA levels were extracted. Pts were divided into Group A, B and C, based on BMI range of ≤25.0, 25.1-29.9 and ≥30 kg/m respectively. PSA responses and half life were calculated using PCWG2 guidelines. Results were compared with Mann-Whitney and Fisher's exact tests. Time to PSA progression (TPP) and overall survival (OS) were estimated with Kaplan Meier and logrank methods.

Results

78 pts were identified, with median age of 66 yrs (44-80), median cycles of D of 7 (1-26), and median BMI of 28.5. Gleason score was evaluable in 75%, with a median score of 8. The number of pts in each BMI group was 21, 24 and 33, respectively. Pts in Gp C had significantly lower baseline PSA (table). More pts in Gp C were PSA non-responders compared to Gp A and B (p = .004). PSA nadir and rates of PSA reduction >30%, >50% and >90% at 3months were comparable in all groups. MMMMMedian TPP was 4.2 months in Gp A, 5.2 months in Gp B, and 4.4 months in Gp C (logrank p = .49). The longest median OS was observed in Gp A at 20 months, followed by Gp B at 19 months and Gp C at 15 months; these differences were not statistically significant (p = 0.38). Of 45 pts with treatment details, 24% had dose reduction and 44% had ≥1 infusion delays. Rates were similar across Gps A to C.

Conclusions

Obese CRPC pts have lower pre-D PSA levels and higher rate of non-responsive disease. However, BMI does not appear to influence PSA kinetics, tolerability of D and survival.

BMI (kg/m2) p
≤25 25.1 - 29.9 ≥30
n 21 24 33 NS
Baseline PSA, median ng/mL 131.0 236.6 81.6 0.007
PSA Reduction at 12wks, median % 34.4 47.2 41.4 NS
PSA Nadir as % of Baseline, median 51.1 41.6 39.6 NS
PSA Flare, % 9.5 25.0 14.8 NS
PSA Non-Responders, % 0.0 4.2 25.9 0.004
>30% PSA Reduction at 12wks, % 66.7 79.2 70.4 NS
>50% PSA Reduction at 12wks, % 47.6 62.5 59.3 NS
>90% PSA Reduction at 12wks, % 9.5 29.2 14.8 NS
PSA Half-life, days, median 51.1 41.6 39.6 NS

Disclosure

All authors have declared no conflicts of interest.