An inflammatory response due to radiation injury can lead to the activation of fibroblasts and their transformation into myofibroblasts that produce organized collagen layers. We term these organized collagen layers "acute fibrosis" (FA). Small animal imaging has shown that accumulation of fibrosis is accelerated at a higher radiation dose with later remodeling of type III collagen into densely packed type I collagen structures, which later transform into what we term "chronic fibrosis" (FC). In prostate cancer (PCa) patients treated with EBRT, we evaluated image derived FA (IDFA) and FC (IDFC) estimates using non-contrast and late gadolinium contrast enhanced (LGE) IR UTE, respectively. We hypothesized that fibrosis changes during RT are associated to tumor regression. Four PCa patients undergoing radiation and hormone suppression were included. 1.5T MR imaging was acquired at three time-points (TPs); pre-RT, on-RT (30-40 Gy), and post-RT (60-78 Gy). IDFA imaging: Stack of spirals dual echo (TE = 50, 2690µs, TI = 60ms) IR UTE research application. Subtracting the two echoes yielded short TE signal intensity (SI). IDFC imaging: stack of spirals dual echo IR UTE research application, TE = 50µs, TI = 200ms, acquired 15 minutes following Gadovist administration. Remnant tumor was contoured at each TP with T2, ADC, and DCE. Relative quantification; IDFA = IR UTE SI/Gluteal Muscle SI and IDFC = LGE IR UTE SI/Gluteal Muscle SI. The sum of normalized IDFA and IDFC SI within the remnant tumor at each TP was divided by the corresponding tumor volume yielding tumor intensity (TI) FA and FC accumulation estimates: TIFA and TIFC. Mean delivered dose within the treated volume to regions where post-RT IDFA and IDFC > 100% gluteal muscle SI was determined. Univariate relationships were evaluated using correlation coefficients (r). The coefficients of variation for TIFA = 10% and TIFC = 11%. IDFA and IDFC were observed pre-RT on the prostate gland periphery, and on RT and post RT within the prostate gland. IDFA and IDFC mean doses were 74% and 85% of prescription, respectively. Tumor regression was incomplete by post-RT. Initial tumor burden was inversely correlated with pre-RT TIFC (r = -0.98, p = .01). Tumor volume change post RT was inversely correlated with larger on-RT TIFA (r = -0.76) and post-RT TIFC (r = -0.78). In this small pilot study, results suggest that IDFA and IDFC may be associated with improved tumor regression. They also suggest higher delivered dose is related to regions of greater IDFC. Quantitative fibrosis may be an early marker of RT response. Caution must be taken when interpreting these results given the small sample size. Future work will include a larger cohort of patients and include post-RT imaging.