In low risk prostate cancer (Gleason 3+3, PSA < 10ng/L), patients are often managed by active surveillance [1]. This involves an initial biopsy and an mpMRI scan, the latter being repeated at annual or 2-yearly intervals determined by PSA rise. If it were possible to predict tumor growth rate or identify factors indicative of accelerated growth, it would be possible to tailor the frequency of the scanning schedule and plan a treatment strategy in advance. The purpose of this pilot study was to correlate tumor doubling time (calculated from change in tumor volume on MRI done at 3 time points at least 1 year apart) with ADC. The change in doubling time was also correlated with the change in ADC in order to interrogate the latter as a biomarker of accelerated growth.Twenty-eight patients aged 52 to 82y (mean 67 +/- 6.09) were scanned three times on a 3T Philips Achieva using an endorectal coil. T2-W images were obtained in 3 orthogonal planes to the prostate with the following parameters (FSE, TR 2500ms, TE 110ms, FOV 14 cm, slice thickness 2.2 – 2.5 mm, 0.1mm gap, matrix 220x184, extrapolated to 256x256. In addition a ZOOM-EPI sequence (single shot EPI, TR 3544ms, TE 51ms, FOV 100 cm, slice thickness 2.2 – 2.5mm, matrix 80x79, extrapolated to 128x128) was used to obtain transverse slices that matched the T2-W images. ADC maps were calculated using scanner software and a monoexponential fit to the data. T2-W and ADC maps at all time points (TP) were viewed together and the dominant intraprostatic lesion (DIL) identified on the third time-point images as the largest hypointense lesion on T2-W imaging with corresponding restricted diffusion and a Type 2 or 3 pattern of contrast uptake [2] in an octant biopsy positive for cancer. Regions-of-interest were drawn around the DIL on every slice of the T2-W images and on a single slice of the ADC map containing the largest lesion area at each time-point (Figure 1). Tumor volumes calculated at each time point (from total tumor area X slice thickness) were used to calculate doubling times (DT); log doubling times were correlated with ADC and a change in log doubling time with a change in ADC using a Pearson’s correlation coefficient.Six patients had no visible tumor on mpMRI and were excluded from the final analysis. In the other 22, tumor volume was 220 +/- 212 mm3 at baseline (TP1), 312 +/- 294 mm3 at TP2 (16.1+/-5.7 months later) and 462 +/- 499 mm3 at TP3 (17.3 +/- 5.8 months from TP2, Figure 2). Five of 22 tumors (22.7%) showed acceleration in growth after TP2. However, differences in DT and log DT between the first two and second two time-points for the cohort were not significant (p=0.32 and 0.94 respectively, paired t-test). ADC, PSA and their changes between TPs and DT’s are given in Table 1. Log tumor DT at each stage and overall did not significantly correlate with ADC (ADCTP1: r² = -0.11, ADCTP2: r² = 0.27, Figure 3) or with PSA (r²=-0.3). Although change in log DT overall (TP3-TP1) did not correlate with a change in ADC (r²=0.31, p<0.2, Figure 4), a threshold of a 10% decrease in ADC identified 3 of 4 tumors and missed 1 of 22 cases with a doubling time of <12 months.There is a wide variation of doubling time of tumors managed by active surveillance. A change in ADC was indicative of tumors with a shorter DT, with a threshold of a 10% reduction in ADC (which is greater that the repeatability of the measurement in multicentre studies, [3]) picking up 75% and missing 5% of cases with a DT of less than 12 months. Investigation of ADC as a biomarker of accelerated growth in prostate cancer warrants validation in a larger cohort of patients managed by active surveillance.