Abstract
Transarterial chemoembolization (TACE) induced tumor necrosis is thought to represent additive results of chemotherapeutic cytotoxic insults and embolic ischemic effects. The benefit of chemotherapy as a constituent of transarterial therapy has been questioned, however, based on studies showing no tumor response differences between bland embolization and TACE. An established relationship between drug delivery and cellular necrosis following TACE is presently unproven. This study aimed to define the incremental tumor necrosis afforded by doxorubicin (DOX) during drug-eluting bead (DEB) TACE. In this IRB-approved study, VX2 liver tumors in New Zealand white rabbits were treated with DOX-loaded 70-150 micron DEBs (LC Bead M1; BTG). Rabbits were divided into 5 treatment groups with varying DOX doses: sham (saline, no beads), 0 mg (bland beads), 12.5 mg, 25 mg, and 37.5 mg. 130,000 beads (10% vial) were administered per procedure. DEB-TACE was followed by sacrifice at 3 and 5 days. Histologic analysis of harvested tumors was used to quantify percent tumor necrosis using the NanoZoomer Digital Pathology System (Hamamatsu). Statistical comparison of quantitative tumor necrosis was performed using one-way ANOVA and the Student’s t-test. 35 VX2 tumors (mean diameter 1.3 cm) in 21 rabbits (mean weight 2.8 kg) were successfully treated with selective DEB-TACE. Treatment groups included 8, 7, 7, 5, and 8 tumors, respectively. Mean tumor size was similar between treatment groups (P=0.311). Tumors showed progressively higher mean percent necrosis across treatment groups with increasing DOX dose (sham: 55%, 0 mg: 55%, 12.5 mg: 64%, 25 mg: 67%, 37.5 mg: 69%). Differences between sham and 0, 12.5, and 25 mg groups were not statistically significant. However, the increase in percent necrosis afforded by 37.5 mg DOX-loaded DEBs achieved statistical significance compared to sham (P=0.041). Incremental increases in DOX dose result in higher percent necrosis of rabbit VX2 liver tumors after DEB-TACE. This result indicates an essential role for chemotherapy-induced cytotoxicity in TACE efficacy, and supports the use of chemotherapeutic drugs as a component of transarterial therapy.
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