Disease relevance of Cholangiocarcinoma

• LCA was without effect on the induction of either hepatocellular carcinomas or cholangiocarcinomas [1].
• Toxicity was assessable for 94 courses in 23 patients (12 patients with breast carcinoma, nine with hepatocellular carcinoma, and two with cholangiocarcinoma) [2].
• CONCLUSIONS: This study found no statistically significant beneficial effect of a higher dose of ursodeoxycholic acid than previously used on survival or prevention of cholangiocarcinoma in primary sclerosing cholangitis [3].
• The mean peak systolic frequency seen in hepatocellular carcinoma (1.2 kHz) was significantly greater than in cholangiocarcinoma (0.6 kHz), metastatic tumors (0.5 kHz), or hemangiomas (0.3 kHz) [4].
• Three ursodeoxycholic acid and 4 placebo patients died from cholangiocarcinoma, and 1 placebo patient died from liver failure [3].

High impact information on Cholangiocarcinoma

• Overexpression of human aspartyl(asparaginyl)beta-hydroxylase in hepatocellular carcinoma and cholangiocarcinoma [5].
• DCA enhanced the development of cholangiocarcinomas without influencing that of hepatocellular lesions [1].
• The gamma-secretase inhibitor N-[N-(3,5-Difluorophenacetyl-L-alanyl)-S-phenylglycine]-t-butyl ester, which blocks Notch signaling, enhanced tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in cholangiocarcinoma cells [6].
• CONCLUSIONS: These data implicate a direct link between the inflammatory mediator iNOS and Notch signaling, and have implications for the development and progression of cholangiocarcinoma [6].
• This induction of COX-2 may participate in the genesis and progression of cholangiocarcinomas [7].

Chemical compound and disease context of Cholangiocarcinoma

• BACKGROUND & AIMS: Successful treatment in nonresectable Bismuth type III and IV cholangiocarcinoma is seldom achieved [8].
• Because receptor tyrosine kinases and cyclooxygenase (COX)-2 have been implicated in carcinogenesis, we examined the hypothesis that bile acids modulate these enzymes in KMBC cells, a human cholangiocarcinoma cell line [7].
• Iridium-192 wire for hilar cholangiocarcinoma [9].
• Because ductular secretion also increases biliary HCO3-concentration, the purpose of this study was to evaluate whether UDC has direct effects on duct cells by measuring intracellular calcium concentration ([Ca2+]i) and membrane Cl- permeability in Mz-ChA-1 human cholangiocarcinoma cells [10].
• This study was designed to examine the direct effect of COX-2 and its inhibitor celecoxib on the growth of human intrahepatic cholangiocarcinoma cells [11].
• Receiver-operating characteristics curve analysis showed that serum trypsinogen-2 had the highest accuracy in differentiating between cholangiocarcinoma and PSC [12].

Biological context of Cholangiocarcinoma

• Hepatocytic phenotypes induced in sarcomatous cholangiocarcinoma cells treated with 5-azacytidine [13].
• In dominant-negative transfection studies, patch clamp analysis of Mz-ChA1 cholangiocarcinoma cells showed that expression of the PDZ1 domain of EBP50 selectively decreased the endogenous cAMP-mediated Cl secretory response [14].
• In common with pancreatic adenocarcinomas, in which 75 to 95% of cases contain a mutation in K-ras, cholangiocarcinomas show a very high frequency of ras gene mutation, but within a tumor only a fraction of cells contain a ras mutation [15].
• Little or no increase in expression of TGF alpha or the hepatocyte-specific prothrombin gene was detectable in the first 48 hours, whereas levels of the oncogene c-erb-B2 that is associated with cholangiocarcinoma were expressed from 48 to 96 hours.(ABSTRACT TRUNCATED AT 250 WORDS)[16]
• Cyclooxygenase-2 promotes human cholangiocarcinoma growth: evidence for cyclooxygenase-2-independent mechanism in celecoxib-mediated induction of p21waf1/cip1 and p27kip1 and cell cycle arrest [11].

Anatomical context of Cholangiocarcinoma

• These included four hepatocellular carcinomas, two cholangiocarcinomas, a spindle cell carcinoma of the bile duct, a hemangioendothelial sarcoma of the liver, and an osteogenic sarcoma of the tibia [17].
• Finally, genetic marking studies suggest that either hepatocytes or oval cells can develop into a hepatocellular carcinoma or cholangiocarcinoma if a sufficient number of genetic mutations accumulate [18].
• Sialyl-Tn antigen was detected on mucinous glycoprotein in four (80%) with cholangiocarcinoma, two (50%) with common bile duct carcinoma, and all pancreatic carcinoma samples [19].
• Expression of MUC1 and MUC2 mucin antigens in intrahepatic bile duct tumors: its relationship with a new morphological classification of cholangiocarcinoma [20].
• Since cholecystokinin (CCK) promotes growth of normal biliary tract, we sought to determine whether CCK affects the growth and metabolism of human cholangiocarcinoma line SLU 132 [21].

Gene context of Cholangiocarcinoma

• RESULTS: SSTR2 messenger RNA was expressed in all seven human cholangiocarcinoma specimens [22].
• In conclusion, these results show a novel p53-dependent mechanism in the PPARgamma ligand-mediated inhibition of cholangiocarcinoma growth and suggest a potential therapeutic role of PPARgamma ligands in the treatment of human cholangiocarcinoma [23].
• Thus, PGs alone can induce cholangiocarcinoma growth, and the HGF- and IL-6-induced proliferation is mediated, at least in part, by PGs [24].
• Thus, our aims were to determine the role of IL-6-mediated signaling mechanisms, and in particular the MAPK pathways, in the growth regulation of human cholangiocarcinoma [25].
• Expression of E-cadherin, alpha-catenin, beta-catenin, and CD44 (standard and variant isoforms) in human cholangiocarcinoma: an immunohistochemical study [26].

Analytical, diagnostic and therapeutic context of Cholangiocarcinoma

• Moreover, we detected by in situ hybridization strong expression of HGF/SF mRNA transcripts in the cancerous epithelial glands of cholangiocarcinoma developed in recipient rats after in vivo cell transplantation of C611B cells [27].
• The aim of this study was to evaluate FDG positron emission tomography (PET) for detection and staging of human cholangiocarcinoma (CC) [28].
• We suggest that the tumors produced as described here provide a good animal model of mucin-producing cholangiocarcinomas [29].
• CONCLUSION: This is the first study to demonstrate that functional antagonism of coexpressed Bcl-X(L) and Mcl-1 proteins using the mBzR antagonist Pk11195 can facilitate apoptosis in cholangiocarcinoma following chemotherapy and radiotherapy [30].
• METHODS: Using bioactive and enzyme-linked immunosorbent assays, serum level of IL-6 was measured in 35 healthy adults and in 60 patients presenting for definitive management of cholangiocarcinoma (CC) (15 patients), hepatocellular carcinoma (HCC) (14), metastatic colorectal cancer (MCRC) (26), and benign biliary disease (BBD) (5) [31].

References