Hepatic chemoembolization: clinical and experimental correlation

Chemoembolization has become the preferred treatment for patients with inoperable, hypervascular hepatic malignancies in the Far East, but controversial elsewhere. In vivo microscopy in addition to other experimental procedures are used in this presentation to better understand the mechanisms involved in chemoembolization. In chemoembolization Lipiodol acts as a contrast material, a vehicle for chemotherapy and an embolic agent. Although not optimal, Lipiodol injected into the hepatic artery, traverses the peribiliary plexus to the portal veins resulting in a dual embolization. Chemoembolization creates ischemia, slows arterial flow and increases the contact time between the infusate and the neoplasms, increasing the tumor cell kill. However, the vascular occlusion also produces infarction and fibrosis compounding the already existing cirrhosis frequently associated with hepatocellular carcinoma. Lipiodol/ethanol (3:1) injected into the segmental or lobar hepatic artery supplying the neoplasm also gains access to the associated portal venous branches causing focal ablation. This preoperative approach is easier to perform than direct portal vein occlusion, with less parenchymal damage and comparable hypertrophy of the remnant liver frequently necessary for adequate hepatic function following resection. Polymer-drug conjugates, e.g. PG-TXL, have considerable potential for intra-arterial delivery especially with the dramatic increase in concentration of the drug in the tumor and its efficacy. Using in vivo microscopy especially with green fluorescent protein (GFP) gene as an efficient and non-toxic tumor cell marker, the events leading to hepatic metastases can be documented which will serve to better evaluate these varied techniques of chemoembolization.