Experimental renal and hepatic artery embolization with a new embolic agent, atelocollagen, in a porcine model.

PURPOSE: We aimed to investigate the potentiality of atelocollagen, a new embolic agent which is collagen type I in a porcine experimental model. MATERIALS AND METHODS: Three pigs underwent transcatheter embolization of lower interlobular arteries of the renal artery (n=6) and one branch of the hepatic artery (n=3) with collagen type I. Angiography was performed prearterial, during, and postarterial embolization. After the procedure, samples from the embolized organs were evaluated by histological analysis. RESULTS: Six lower interlobular renal arteries and three hepatic arteries were successfully embolized by administration of 0.8±0.3 mL and 2.9±1.2 mL, respectively, of the collagen type I. Histological findings of the embolized kidney specimens showed that the collagenous materials filled the arterial lumen, whose size ranged from 2.02 to 839.82 µm and reached the level of afferent arteries of glomerular tufts. Although the area of occluded arteries of the liver was smaller than the kidney, histological findings of the liver specimens showed that the collagenous materials filled small arterial lumens from 2.81 to 187.86 µm in diameter. CONCLUSION: Atelocollagen, a collagen type I, has the potential to be used to embolize the distal vessels of both renal and hepatic arteries.

Precursor Lesions of Pancreatic Cancer

This review article describes morphological aspects, gene abnormalities, and mucin expression profiles in precursor lesions such as pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasm (IPMN), and mucinous cystic neoplasm (MCN) of the pancreas, as well as their relation to pancreatic ductal adenocarcinoma (PDAC). The gene abnormalities in precursors of PDAC are summarized as follows: (1) KRAS mutation and p16/CDKN2A inactivation are early events whose frequencies increase with the dysplasia grade in both PanIN and IPMN; (2) TP53 mutation and SMAD4/DPC4 inactivation are late events observed in PanIN3 or carcinomatous change of IPMN in both PanIN and IPMN, although the frequency of the TP53 mutation is lower in IPMN than in PDAC; and (3) also in MCN, KRAS mutation is an early event whose frequency increases with the dysplasia grade, whereas TP53 mutation and SMAD4/DPC4 inactivation are evident only in the carcinoma. The mucin expression profiles in precursors of PDAC are summarized as follows: (1) MUC1 expression increases with the PanIN grade, and is high in PDAC; (2) the expression pattern of MUC2 differs markedly between the major subtypes of IPMN with different malignancy potentials (i.e., IPMN-intestinal type with MUC2+ expression and IPMN-gastric type with MUC2- expression); (3) MUC2 is not expressed in any grade of PanINs, which is useful for differentiating PanIN from intestinal-type IPMN; (4) de novo expression of MUC4, which appears to increase with the dysplasia grade; and (5) high de novo expression of MUC5AC in all grades of PanINs, all types of IPMN, MCN, and PDAC.