VASCULAR AND INTERVENTIONAL RADIOLOGYR adiofrequency ablation (RFA) guided by medical imaging is now commonly used to treat a wide range of focal primary and metastatic tumors in solid organs, primarily the liver (1,2). The growing adoption and clinical implementation of this technique can be attributed to its minimal invasiveness, low morbidity, and cost efficiency (3). Thus, hepatic RFA has been adopted in consensus guidelines as a first-line therapy for primary cancer (eg, hepatocellular carcinoma) (4) and as a second-line therapy for metastatic tumors such as colorectal cancer (5,6).Despite various advantages, treatment efficacy remains challenging in some patient populations. This includes achieving complete ablation of tumors larger than 3 cm (1,2), where studies have suggested that RFA may be associated with higher tumor recurrence rates (7), in part due to the difficulty in achieving a periablational margin of more than 5 mm, which is associated with better clinical outcomes (8,9). Moreover, there is a growing amount of laboratory data supporting the contention that thermal ablation of normal liver required to achieve sufficient margins can increase Results: RFA performed after tumor cell injection induced increased metastatic tumor number (103 6 45 vs 52 6 44 [CT26], P = .009 and 87 6 51 vs 39 6 20 [MC38], P = .007), cellular proliferation (P , .001 for both), and intratumoral neovascularization (P , .001 for both), compared with the sham procedure. Tumor cell injection performed 1 day and 3 days after RFA also increased these indexes (P , .05), while no difference was demonstrated for cell injection 7 days after RFA (P . .05). Adjuvant c-Met or STAT3 inhibition reduced intrahepatic metastatic parameters after RFA to baseline (P , .03), equivalent to the sham group (P . .05).
Conclusion:Radiofrequency ablation of normal liver promotes intrahepatic metastatic implantation and increased growth over a short-lived (1-3 days) temporal window in animal models. This phenomenon can be potentially neutralized with specific inhibition of pathways including hepatocyte growth factor/tyrosine-protein kinase Met and signal transducer and activator of transcription 3.