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Purpose To show that hepatic tumor volume and enhancement pattern measurements can be obtained in a time-efficient and reproducible manner on a voxel-by-voxel basis to provide a true three-dimensional (3D) volumetric assessment. Materials and Methods Magnetic resonance (MR) imaging data obtained from 20 patients recruited for a single-institution prospective study were retrospectively evaluated. All patients had a diagnosis of hepatocellular carcinoma (HCC) and underwent drug-eluting beads (DEB) transcatheter arterial chemoembolization for the first time. All patients had undergone contrast-enhanced MR imaging before and after DEB transcatheter arterial chemoembolization; poor image quality excluded 3 patients, resulting in a final count of 17 patients. Volumetric RECIST (vRECIST) and quantitative EASL (qEASL) were measured, and segmentation and processing times were recorded. Results There were 34 scans analyzed. The time for semiautomatic segmentation was 65 seconds±33 (range, 40–200 seconds). vRECIST and qEASL of each tumor were computed Conclusions Semiautomatic quantitative tumor enhancement (qEASL) and volume (vRECIST) assessment is feasible in a workflow-efficient time frame. Clinical correlation is necessary, but vRECIST and qEASL could become part of the assessment of intraarterial therapy for interventional radiologists.

between 2 groups were selected. Results: At D7, bland SAP did not cause necrosis and only 68 genes were deregulated. Among them, 10 genes related to angiogenesis. VEGF was not different vs control. Dox-SAP caused parenchyma necrosis at D7 (presence on 92% of the tissue sections), which was progressively resorbed between M1 (31%) and M3 (0%) and replaced by an inflammatory reaction and a fibrotic remodeling tissue after the microspheres emptied, finally resulting in regenerated liver. In parallel, the overall number of modulated genes and the number of angiogenesis-related genes decreased from D7 to M1 and M3 (resp. 770, 257 and 46 modulated genes by Dox-SAP; and among them 71, 34 and 6 modulated related to angiogenesis). VEGF decreased at D7 and M1. The angiogenesis related-genes did not included VEGF and HIF1A but were interleukins and chemokines which mark an inflammatory reaction, and collagen molecules, metallopeptidases, growth factors, and adhesion molecules which orchestrate the tissue remodeling. Conclusion: Angiogenesis following chemoembolization in normal liver, associated to the inflammatory response and tissue remodeling, participates to the healing phase replacing the necrosis induced by Dox. This repair angiogenesis must be distinguished from tumoral angiogenesis.