213P - Relationship of bone scan index and progression-free survival data for metastatic CRPC patients who received ODM-201

Date 28 September 2014
Event ESMO 2014
Session Poster Display session
Topics Cytotoxic agents
Prostate Cancer
Staging procedures (clinical staging)
Basic Principles in the Management and Treatment (of cancer)
Biological therapy
Presenter Robert Jones
Citation Annals of Oncology (2014) 25 (suppl_4): iv58-iv84. 10.1093/annonc/mdu326
Authors R. Jones1, M. Reza2, C. Massard3, J. Aspegren4, L. Mattila4, L. Edenbrandt5, A. Bjartell6, M. Mustonen4, K. Fizazi7
  • 1Cardiff University, Velindre Cancer Centre, CF10 3AX - Cardiff/GB
  • 2Dept Of Clinical Physiology And Nuclear Medicine, Clinical Science, Lund University, 205 02 - Malmö/SE
  • 3Sitep, Institute Gustave Roussy, FR-94805 - Villejuif/FR
  • 4Research And Development, Orion Corporation Orion Pharma, 02101 - Espoo/FI
  • 5Dept Of Clinical Physiology And Nuclear Medicine, Clinical Sciences, Lund University, 20502 - Malmö/SE
  • 6Dept. Of Urology, Clinical Sciences, Lund University, Malmö/SE
  • 7Department Of Cancer Medicine, Institut Gustave Roussy, University of Paris, Villejuif/FR



ODM-201 is an androgen receptor (AR) inhibitor with high nonclinical and clinical efficacy. Bone scan index (BSI) is an imaging biomarker that reflects the percent of skeletal mass affected by tumor.


We retrospectively studied a consecutive series of 47 metastatic CRPC (mCRPC) patients (pts), who received ODM-201 in ARADES trial. Total of 36/113 mCRPC pts (median age 68, range 55-82) with baseline and 12-week bone metastases were randomly selected to this evaluation. BSI data was obtained by using the automated quantification software EXINI boneBSI (EXINI Diagnostics AB, Lund, Sweden). Cox proportional-hazards regression models and Kaplan-Meier estimates of the survival function were used to investigate the association between changes in BSI and PSA from baseline to 12 weeks follow-up and progression data.


Using Pearson correlation, BSI change from baseline correlated with RECIST target lesion response (r = 0.50; p = 0.0418), and CTC change from baseline (r = 0.66; p < 0.0001). BSI %-change correlated with PSA %-change (r = 0.76; p < 0.0001), RECIST target lesion response (r = 0.51; p = 0.0384), CTC %-change (r = 0.62; p = 0.0011), and CTC conversion rate (r = 0.67; p < 0.0001). BSI %-change was also associated with time to radiographic progression (HR = 1.01; p = 0.0006) in univariate analysis, and it remained associated (HR = 1.01; p = 0.0004) in a multivariate analysis including subgroup. Pts with small (<20%) increase in BSI during 12 weeks had significantly longer time to PSA progression (median 74 vs. 25 weeks, HR = 5.8; p = 0.0444) in the chemo-/CYP17i-naïve population, and significantly longer time to radiographic progression (median not reached vs. 13 weeks, HR = 3.3; p = 0.0224) when analyzing all subgroups together. In an analysis including all subgroups and all 47 pts, pts with baseline BSI > 1 had significantly shorter median time to radiographic progression than pts with baseline BSI ≤ 1, 23 weeks and not reached, respectively (p = 0.0186).


The on-treatment change in BSI was related to progression-free survival (PFS) in pts with mCRPC and bone metastases, and increase in BSI was significantly associated with reduced PFS. BSI for quantification of bone metastases could be a valuable complement to the traditional methods for evaluation of treatment response in mCRPC pts.


C. Massard is a member of Orion Pharma advisory board; J. Aspegren is an employee of Orion Pharma; L. Mattila is an employee of Orion Pharma; L. Edenbrandt is employed and shareholder in EXINI Diagnostics AB (Lund, Sweden), which provides the software EXINIbonebsi used in this study; M. Mustonen is an employee of Orion Pharma; K. Fizazi is a member of Orion Pharma advisory board.All other authors have declared no conflicts of interest.