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29. Liver transplantation in a 7-month-old girl with Caroli's disease.

Author

Kim, Robin D., Book, Linda, Haafiz, Allah, Schwartz, Jason J., Sorensen, John B., and Gonzalez-Peralta, Regino P.

Subjects
LIVER transplantation, BILE duct diseases, SURGICAL complications, HYPERTENSION, FIBROSIS, CIRRHOSIS of the liver, PEDIATRICS
Abstract

Abstract: Caroli''s disease (including Caroli''s syndrome) is a rare autosomal recessive disorder of the liver characterized by diffuse cystic dilatation of the intrahepatic bile ducts. The disease may present at any age and is characterized by recurrent episodes of biliary obstruction, cholangitis, hepaticolithiasis, and liver abscesses. Caroli''s syndrome is further associated with congenital hepatic fibrosis and portal hypertension. Patients with recurrent complications or cirrhosis may die because of recurrent infection, portal hypertension, liver failure, or cholangiocarcinoma. Liver transplantation is the treatment of choice for these complicated patients. Here we describe the youngest reported patient with Caroli''s syndrome treated successfully using liver transplantation and review the recent literature. [Copyright &y& Elsevier]

Published
2011
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32. Heat shock protein 90 inhibition abrogates hepatocellular cancer growth through cdc2-mediated G2/M cell cycle arrest and apoptosis.

Author

Watanabe, Go, Behrns, Kevin E., Jae-Sung Kim, and Kim, Robin D.

Subjects
HEAT shock proteins, LIVER cancer, CELL cycle, BIOLOGICAL rhythms, APOPTOSIS, CELL death
Abstract

17-(demethoxy), 17-allylamino geldanamycin (17-AAG) suppresses growth in some cancers by inhibiting Heat shock protein 90 (Hsp90). We examined the effects of 17-AAG-mediated Hsp90 inhibition on human hepatocellular carcinoma (HCC) growth in vitro and in vivo. Human HCC cell lines, Hep3B and HuH7, were exposed to 17-AAG and cell viabilities and apoptosis were determined. Cell cycle profiles were analyzed and the G2/M cell cycle checkpoint proteins cdc2 and cyclin B1 were examined. Studies were performed to determine whether 17-AAG-mediated cdc2 decrease was due to altered gene expression, transcription, or protein degradation. The effects of 17-AAG on Hep3B and HuH7 xenograft growth in athymic nude mice were also examined. Hep3B and HuH7 treated with 17-AAG versus untreated controls showed decreased cell viability and increased apoptosis. Cells treated with 17-AAG also showed an increased fraction in G2/M phase and an associated decrease in cdc2 through protein degradation rather than through other mechanisms. Hsp90 inhibition by 17-AAG also decreased HCC xenograft growth in association with decreased cdc2 expression. 17-AAG-mediated inhibition of Hsp90 abrogates human HCC cell growth in vitro and in vivo through cdc2 decrease, which in turn induces G2/M cell cycle arrest and apoptosis. Hsp90 is a mediator of HCC growth and survival and its inhibition may serve as a potential treatment. [ABSTRACT FROM AUTHOR]

Published
2009
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35. Portal Vein Resection for Hilar Cholangiocarcinoma.

Author

Hemming, Alan W., Kim, Robin D., Mekeel, Kristin L., Fujita, Shiro, Reed, Alan I., Foley, David P., and Howard, Richard J.

Subjects
*CHOLANGIOCARCINOMA, *PORTAL vein surgery, *SURGICAL excision, *SURGEONS, *TUMORS
Abstract

Hilar cholangiocarcinoma remains a difficult challenge for the surgeon. Achieving negative surgical margins when resecting this relatively uncommon tumor is technically demanding as a result of the close proximity of the bile duct bifurcation to the vascular inflow of the liver. A recent advance in surgical treatment is the addition of portal vein resection to the procedure. Resection of the portal vein increases the number of patients offered a potentially curative approach but is technically more difficult and may increase the risk of the procedure. This study reviews the results of portal vein resection for hilar cholangiocarcinoma. Between 1998 and 2005, 60 patients underwent potentially curative resections of hilar cholangiocarcinoma. Mean patient age was 64 ± 12 years (range, 24-85 years). Liver resections performed along with biliary resection included 49 trisegmentectomies (37 right, 12 left) and 10 lobectomies (8 left, 2 right). One patient had only the bile duct resected. Four patients also had simultaneous pancreaticoduodenectomy performed. Twenty-six patients required portal vein resection and reconstruction to achieve negative margins, 3 of which also required reconstruction of the hepatic artery. Operative mortality was 8 per cent with an overall complication rate of 40 per cent. Patients who underwent portal vein resection had an operative mortality of 4 per cent, which was not different from the 12 per cent mortality in patients who did not undergo portal vein resection (P = 0.39). There was no difference in actuarial patient survival between patients who underwent portal vein resection and those who did not (5-year survival 39 per cent vs. 41 per cent, P = not significant). Negative margins were achieved in 80 per cent of cases and were associated with improved survival (P ≤ 0.01). Five-year actuarial survival in patients undergoing resection with negative margins was 45 per cent. There was no difference in margin status or long-term survival between those patients who underwent portal vein resection and those who did not. Only negative margin status was associated with improved survival by multivariate analysis. Portal vein resection for hilar cholangiocarcinoma is safe and allows a chance for long-term survival in otherwise unresectable patients. [ABSTRACT FROM AUTHOR]

Published
2006
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