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1. Amura CR, Brodsky KS, Gitomer B, McFann K, Lazennec G, Nichols MT, Jani A, Schrier RW, Doctor RB: CXCR2 agonists in ADPKD liver cyst fluids promote cell proliferation. Am J Physiol Cell Physiol; 2008 Mar;294(3):C786-96
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  • [Title] CXCR2 agonists in ADPKD liver cyst fluids promote cell proliferation.
  • Autosomal dominant polycystic kidney disease (ADPKD) is a highly prevalent genetic disease that results in cyst formation in kidney and liver.
  • Comparative analyses of human kidney and liver cyst fluids revealed disparate cytokine/growth factor profiles.
  • CXCR2 agonists, including IL-8, epithelial neutrophil-activating peptide (ENA-78), growth-related oncogene-alpha (GRO-alpha), are potent proliferative agents that were found at high levels in liver but not kidney cyst fluids.
  • Liver cysts are lined by epithelial cells derived from the intrahepatic bile duct (i.e., cholangiocytes).
  • In polarized pkd2(WS25/-) mouse liver cyst epithelial monolayers, CXCR2 agonists were released both apically and basally, indicating that they may act both on the endothelial and epithelial cells within or lining the cyst wall.
  • IL-8 and human liver cyst fluid induced cell proliferation of HMEC-1 cells, a human microvascular endothelial cell line, and Mz-ChA1 cells, a human cholangiocyte cell model.
  • Hypoxia and mechanical stretch, two likely stressors acting on the liver cyst epithelia, significantly increased IL-8 secretion and promoter activity.
  • These studies support the hypothesis that CXCR2 signaling promotes ADPKD liver cyst growth.


2. Mott JL, Bronk SF, Mesa RA, Kaufmann SH, Gores GJ: BH3-only protein mimetic obatoclax sensitizes cholangiocarcinoma cells to Apo2L/TRAIL-induced apoptosis. Mol Cancer Ther; 2008 Aug;7(8):2339-47
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  • The drug obatoclax (GX15-070) inhibits antiapoptotic members of the Bcl-2 family including Mcl-1.
  • Obatoclax induced minimal apoptosis alone; however, it increased apoptosis 3- to 13-fold in all three cancer cell lines when combined with Apo2L/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).
  • Obatoclax is a potentially promising adjunctive agent for the treatment of this cancer.

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  • (PMID = 18723481.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK079875-01; United States / NCI NIH HHS / CA / CA 69008; United States / NIDDK NIH HHS / DK / K01 DK079875-01; United States / NCI NIH HHS / CA / R01 CA069008-14; United States / NIDDK NIH HHS / DK / R01 DK063947; United States / NIDDK NIH HHS / DK / DK 79875; United States / NCI NIH HHS / CA / CA096780-05; United States / NCI NIH HHS / CA / K23 CA 96780; United States / NCI NIH HHS / CA / CA069008-14; United States / NIDDK NIH HHS / DK / DK 63947; United States / NIDDK NIH HHS / DK / K01 DK079875; United States / NIDDK NIH HHS / DK / R01 DK063947-06; United States / NCI NIH HHS / CA / R01 CA069008; United States / NCI NIH HHS / CA / K23 CA096780; United States / NCI NIH HHS / CA / K23 CA096780-05; United States / NIDDK NIH HHS / DK / DK063947-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pyrroles; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / obatoclax
  • [Other-IDs] NLM/ NIHMS66399; NLM/ PMC2562222
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3. Hisaka T, Yano H, Ogasawara S, Momosaki S, Nishida N, Takemoto Y, Kojiro S, Katafuchi Y, Kojiro M: Interferon-alphaCon1 suppresses proliferation of liver cancer cell lines in vitro and in vivo. J Hepatol; 2004 Nov;41(5):782-9
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  • [Title] Interferon-alphaCon1 suppresses proliferation of liver cancer cell lines in vitro and in vivo.
  • BACKGROUND/AIMS: We investigated the effects of consensus interferon (IFN-alphaCon1), a nonnaturally occurring type I interferon with higher specific activity than other type I IFNs, on the growth of human liver cancer cells.
  • METHODS: The effect of IFN-alphaCon1 on the proliferation of 13 liver cancer cell lines was investigated in vitro.
  • [MeSH-major] Antiviral Agents / pharmacology. Carcinoma, Hepatocellular / drug therapy. Interferon Type I / pharmacology. Liver Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Bile Duct Neoplasms / drug therapy. Bile Duct Neoplasms / pathology. Bile Ducts, Intrahepatic. Cell Division / drug effects. Cell Line, Tumor. Cholangiocarcinoma / drug therapy. Cholangiocarcinoma / pathology. Humans. In Vitro Techniques. Interferon-alpha. Mice. Mice, Inbred BALB C. Mice, Nude. Recombinant Proteins

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  • (PMID = 15519651.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antiviral Agents; 0 / Interferon Type I; 0 / Interferon-alpha; 0 / Recombinant Proteins; 118390-30-0 / interferon alfacon-1
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4. Price P: Cholangiocarcinoma and the role of radiation and chemotherapy. Hepatogastroenterology; 2001 Jan-Feb;48(37):51-2
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  • Many cases are localized while metastatic disease within the liver and abdomen do occur.
  • There is as yet no standard therapy for advanced bile duct tumors.
  • Advances may be made by: (i) The combined use of radiation and chemotherapy, (ii) High dose conformal radiotherapy, (iii) Novel chemotherapeutic agents.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bile Duct Neoplasms / therapy. Bile Ducts, Intrahepatic. Cholangiocarcinoma / therapy

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  • (PMID = 11268997.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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5. Seubwai W, Wongkham C, Puapairoj A, Okada S, Wongkham S: 22-oxa-1,25-dihydroxyvitamin D3 efficiently inhibits tumor growth in inoculated mice and primary histoculture of cholangiocarcinoma. Cancer; 2010 Dec 1;116(23):5535-43
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  • The current data encourage further investigation of 1,25(OH)2 D3 or its analogues as therapeutic agents in the treatment of patients with CCA.
  • [MeSH-major] Bile Duct Neoplasms / drug therapy. Bile Ducts, Intrahepatic. Calcitriol / analogs & derivatives. Cholangiocarcinoma / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Calcium / blood. Cell Cycle / drug effects. Cell Proliferation / drug effects. Humans. Mice. Tumor Cells, Cultured. Xenograft Model Antitumor Assays


6. Sato Y, Harada K, Furubo S, Kizawa K, Sanzen T, Yasoshima M, Ozaki S, Isse K, Sasaki M, Nakanuma Y: Inhibition of intrahepatic bile duct dilation of the polycystic kidney rat with a novel tyrosine kinase inhibitor gefitinib. Am J Pathol; 2006 Oct;169(4):1238-50
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  • [Title] Inhibition of intrahepatic bile duct dilation of the polycystic kidney rat with a novel tyrosine kinase inhibitor gefitinib.
  • The polycystic kidney (PCK) rat represents a liver and kidney cyst pathology corresponding to Caroli's disease with congenital hepatic fibrosis and autosomal recessive polycystic kidney disease.
  • In vivo, treatment with gefitinib significantly inhibited the cystic dilatation of the intrahepatic bile ducts of PCK rats, which was accompanied by improvement of liver fibrosis.
  • These results suggest that signaling pathways mediated by epidermal growth factor receptor are involved in biliary dysgenesis of the PCK rat, with the mechanisms of cyst progression being different between the liver and kidney.
  • [MeSH-major] Bile Ducts, Intrahepatic / drug effects. Polycystic Kidney Diseases / drug therapy. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Animals. Dilatation, Pathologic / drug therapy. Dilatation, Pathologic / enzymology. Disease Models, Animal. Liver / enzymology. Liver / pathology. Liver Diseases / drug therapy. Liver Diseases / enzymology. Liver Diseases / pathology. Mitogen-Activated Protein Kinase 3 / analysis. Mitogen-Activated Protein Kinase 3 / metabolism. Mitogen-Activated Protein Kinase 7 / analysis. Mitogen-Activated Protein Kinase 7 / metabolism. Rats

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  • (PMID = 17003482.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 7; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ PMC1698840
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7. Yun BR, Lee MJ, Kim JH, Kim IH, Yu GR, Kim DG: Enhancement of parthenolide-induced apoptosis by a PKC-alpha inhibition through heme oxygenase-1 blockage in cholangiocarcinoma cells. Exp Mol Med; 2010 Nov 30;42(11):787-97
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  • Cholangiocarcinoma (CC) is a chemoresistant intrahepatic bile duct carcinoma with a poor prognosis.
  • The combination of PTL and Ro efficiently improved tumor growth inhibition compared to treatment with either agent alone in an in vivo subcutaneous tumor model.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Nucleus / metabolism. Cholangiocarcinoma / metabolism. Heme Oxygenase-1 / metabolism. NF-E2-Related Factor 2 / metabolism. Sesquiterpenes / pharmacology
  • [MeSH-minor] Active Transport, Cell Nucleus / drug effects. Apoptosis / drug effects. Apoptosis / genetics. Cell Line, Tumor. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Enzyme Activation. Enzyme Inhibitors / pharmacology. Humans. Lactones / chemistry. Protein Kinase C-alpha / antagonists & inhibitors. RNA, Small Interfering / genetics. Signal Transduction / drug effects

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  • (PMID = 20938215.001).
  • [ISSN] 2092-6413
  • [Journal-full-title] Experimental & molecular medicine
  • [ISO-abbreviation] Exp. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Lactones; 0 / NF-E2-Related Factor 2; 0 / RNA, Small Interfering; 0 / Sesquiterpenes; 2RDB26I5ZB / parthenolide; EC 1.14.99.3 / HMOX1 protein, human; EC 1.14.99.3 / Heme Oxygenase-1; EC 2.7.11.13 / Protein Kinase C-alpha
  • [Other-IDs] NLM/ PMC2992858
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8. Yamada T, Arai T, Nagino M, Oda K, Shoda J, Suzuki H, Sugiyama Y, Nimura Y: Impaired expression of hepatic multidrug resistance protein 2 is associated with posthepatectomy hyperbilirubinemia in patients with biliary cancer. Langenbecks Arch Surg; 2005 Sep;390(5):421-9
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  • [Title] Impaired expression of hepatic multidrug resistance protein 2 is associated with posthepatectomy hyperbilirubinemia in patients with biliary cancer.
  • BACKGROUND AND AIMS: Hyperbilirubinemia is a critical complication following hepatectomy for biliary cancer.
  • MATERIALS AND METHODS: The MRP2 expression before hepatectomy was determined by immunostaining and Western blotting in patients with biliary cancer.
  • To directly determine the effect of chronic bile duct obstruction on the MRP2 expression, the expression levels were compared between the cholestatic and noncholestatic lobes in each of seven patients.
  • In another 39 patients, the correlation of the MRP2 expression of the anticipated remnant liver with the posthepatectomy severe hyperbilirubinemia, defined as a serum total bilirubin concentration>or=200 micromol/l, was evaluated.
  • Postoperative maximum bilirubin levels were significantly correlated with MRP2 expression of the anticipated remnant liver.
  • CONCLUSIONS: Decreased MRP2 expression, caused by biliary obstruction due to cancer, is a possible risk factor for posthepatectomy severe hyperbilirubinemia.
  • [MeSH-major] Biliary Tract Neoplasms / surgery. Hepatectomy / adverse effects. Hyperbilirubinemia / metabolism. Liver / metabolism. Membrane Transport Proteins / metabolism. Multidrug Resistance-Associated Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cholestasis, Intrahepatic / etiology. Cholestasis, Intrahepatic / metabolism. Cholestasis, Intrahepatic / surgery. Drug Resistance, Multiple. Female. Humans. Immunohistochemistry. Male. Middle Aged

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  • (PMID = 15965653.001).
  • [ISSN] 1435-2443
  • [Journal-full-title] Langenbeck's archives of surgery
  • [ISO-abbreviation] Langenbecks Arch Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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9. Francis H, Onori P, Gaudio E, Franchitto A, DeMorrow S, Venter J, Kopriva S, Carpino G, Mancinelli R, White M, Meng F, Vetuschi A, Sferra R, Alpini G: H3 histamine receptor-mediated activation of protein kinase Calpha inhibits the growth of cholangiocarcinoma in vitro and in vivo. Mol Cancer Res; 2009 Oct;7(10):1704-13
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  • Expression of HRH3 in intrahepatic and extrahepatic cell lines, normal cholangiocytes, and human tissue arrays was measured.

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  • (PMID = 19825989.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK062975-04; United States / NIDDK NIH HHS / DK / DK076898; United States / NIDDK NIH HHS / DK / DK062975-04; United States / NIDDK NIH HHS / DK / R01 DK062975; United States / NIDDK NIH HHS / DK / DK58411; United States / NIDDK NIH HHS / DK / R01 DK058411; United States / NIDDK NIH HHS / DK / R01 DK054811; United States / NIDDK NIH HHS / DK / DK054811-08; United States / NIDDK NIH HHS / DK / R01 DK076898-02; United States / NIDDK NIH HHS / DK / DK062975; United States / NIDDK NIH HHS / DK / K01 DK078532; United States / NIDDK NIH HHS / DK / R01 DK076898; United States / NIDDK NIH HHS / DK / DK076898-02; United States / NIDDK NIH HHS / DK / R01 DK054811-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Histamine Agonists; 0 / Methylhistamines; 0 / Receptors, Histamine H3; 0 / Vascular Endothelial Growth Factor A; 4QD397987E / Histidine; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 2.7.11.13 / Protein Kinase C-alpha; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  • [Other-IDs] NLM/ NIHMS160179; NLM/ PMC2788765
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10. Wu Y, Saiura A, Yamamoto J, Koga R, Asahara S, Kamei A, Takano K, Ikari T, Seki M, Yamaguchi T, Muto T: Locally advanced intrahepatic cholangiocarcinoma successfully resected after transcatheter arterial chemoembolization with degradable starch microspheres: report of a case. Hepatogastroenterology; 2007 Jul-Aug;54(77):1345-7
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  • [Title] Locally advanced intrahepatic cholangiocarcinoma successfully resected after transcatheter arterial chemoembolization with degradable starch microspheres: report of a case.
  • We describe a case of initially unresectable locally advanced intrahepatic cholangiocarcinoma that showed remarkable regression after transcatheter arterial chemoembolization with degradable starch microspheres, allowing for subsequent successful curative resection.
  • Computerized tomography examination showed a huge mass in the right liver extended partially to the left liver.
  • Intrahepatic cholangiocarcinoma was strongly suspected, but surgical resection was abandoned due to the local spread in the liver.
  • The anticancer agents, mitomycin C and epirubicin, combined with degradable starch microspheres were injected from the catheter for chemoembolization.
  • Then right trisegmentectomy together with extra-hepatic bile duct excision was performed.
  • Transcatheter arterial chemotherapy with degradable starch microspheres may be a treatment of choice with locally advanced intrahepatic cholangiocarcinoma.
  • [MeSH-major] Bile Duct Neoplasms / therapy. Bile Ducts, Intrahepatic. Chemoembolization, Therapeutic. Cholangiocarcinoma / therapy. Microspheres. Starch / administration & dosage

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  • (PMID = 17708251.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / degradable starch microspheres; 9005-25-8 / Starch
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11. Blechacz BR, Smoot RL, Bronk SF, Werneburg NW, Sirica AE, Gores GJ: Sorafenib inhibits signal transducer and activator of transcription-3 signaling in cholangiocarcinoma cells by activating the phosphatase shatterproof 2. Hepatology; 2009 Dec;50(6):1861-70
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  • In an orthotopic, syngeneic CCA model in rats, sorafenib displayed significant tumor suppression resulting in a survival benefit for treated animals.

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  • (PMID = 19821497.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA083650-10; United States / NCI NIH HHS / CA / R01 CA 39225; United States / NIDDK NIH HHS / DK / R01 DK059427-11; None / None / / R01 DK059427-11; United States / NCI NIH HHS / CA / R01 CA 83650; United States / NIDDK NIH HHS / DK / R01 DK059427; United States / NIDDK NIH HHS / DK / R56 DK059427; United States / NCI NIH HHS / CA / R01 CA083650; United States / NCI NIH HHS / CA / CA039225-24; United States / NIDDK NIH HHS / DK / DK84567; United States / NIDDK NIH HHS / DK / DK059427-06; United States / NIDDK NIH HHS / DK / R56 DK059427-06; United States / NCI NIH HHS / CA / R01 CA039225; United States / NIDDK NIH HHS / DK / DK59427; United States / NCI NIH HHS / CA / R01 CA039225-24; United States / NIDDK NIH HHS / DK / P30 DK084567
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 25X51I8RD4 / Niacinamide; 42HK56048U / Tyrosine; 9ZOQ3TZI87 / sorafenib; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
  • [Other-IDs] NLM/ NIHMS207481; NLM/ PMC2891152
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12. Treekitkarnmongkol W, Suthiphongchai T: High expression of ErbB2 contributes to cholangiocarcinoma cell invasion and proliferation through AKT/p70S6K. World J Gastroenterol; 2010 Aug 28;16(32):4047-54
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  • The ability of this drug to inhibit neoplastic properties (invasion, motility and proliferation) increased concomitantly with the level of ErbB2 expression.
  • [MeSH-major] Bile Duct Neoplasms. Bile Ducts, Intrahepatic. Cell Proliferation. Cholangiocarcinoma. Proto-Oncogene Proteins c-akt / metabolism. Receptor, ErbB-2 / metabolism. Ribosomal Protein S6 Kinases, 70-kDa / metabolism
  • [MeSH-minor] Benzothiazoles / metabolism. Cell Line, Tumor. Cell Movement. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Neoplasm Invasiveness. RNA, Small Interfering / metabolism. Tyrphostins / metabolism

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  • (PMID = 20731018.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Benzothiazoles; 0 / RNA, Small Interfering; 0 / Tyrphostins; 0 / tyrphostin AG825; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ PMC2928458
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13. Fava G, Demorrow S, Gaudio E, Franchitto A, Onori P, Carpino G, Glaser S, Francis H, Coufal M, Marucci L, Alvaro D, Marzioni M, Horst T, Mancinelli R, Benedetti A, Alpini G: Endothelin inhibits cholangiocarcinoma growth by a decrease in the vascular endothelial growth factor expression. Liver Int; 2009 Aug;29(7):1031-42
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  • BACKGROUND: Endothelins (ET-1, ET-2, ET-3) are peptides with vasoactive properties interacting with ET(A) and ET(B) receptors.
  • ET-1 inhibits secretin-stimulated ductal secretion (hallmark of cholangiocyte growth) of cholestatic rats by interaction with ET receptors.
  • AIM: The aims of the studies were to evaluate (i) the effect of ET-1 on cholangiocarcinoma growth in Mz-ChA-1 cells and nude mice and (ii) whether ET-1 regulation of cholangiocarcinoma growth is associated with changes in the expression of vascular endothelial growth factor-A (VEGF-A), VEGF-C, VEGF receptor-2 (VEGFR-2) and VEGFR-3.
  • METHODS: We determined the expression of ET(A) and ET(B) receptors on normal and malignant (Mz-ChA-1) cholangiocytes and human cholangiocarcinoma tissue and the effect of ET-1 on the proliferation and expression of VEGF-A, VEGF-C (regulators of tumour angiogenesis) and its receptors, VEGFR-2 and VEGFR-3, in Mz-ChA-1 cells.
  • In vivo, Mz-ChA-1 cells were injected into the flanks of athymic mice and injections of ET-1 or saline into the tumours were performed daily.
  • The effect of ET-1 on tumour size, cell proliferation, apoptosis, collagen quantity and the expression of VEGF-A and VEGF-C and VEGFR-2 and VEGFR-3 were measured after 73 days.
  • RESULTS: Higher expression of ET(A) and ET(B) was observed in malignant compared with normal cholangiocytes.
  • ET-1 inhibited proliferation and VEGF-A, VEGF-C, VEGFR-2 and VEGFR-3 expression of Mz-ChA-1 cells.
  • Chronic ET-1 treatment decreased tumour volume, tumour cell proliferation and VEGF-A and VEGF-C expression but increased apoptosis and collagen tissue deposition compared with controls.
  • CONCLUSIONS: Modulation of VEGF-A and VEGF-C (by ET-1) may be important for managing cholangiocarcinoma growth.

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  • (PMID = 19291182.001).
  • [ISSN] 1478-3231
  • [Journal-full-title] Liver international : official journal of the International Association for the Study of the Liver
  • [ISO-abbreviation] Liver Int.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK062975-04; United States / NIDDK NIH HHS / DK / DK062975-04; United States / NIDDK NIH HHS / DK / R01 DK062975; United States / NIDDK NIH HHS / DK / DK58411; United States / NIDDK NIH HHS / DK / R01 DK058411; United States / NIDDK NIH HHS / DK / R01 DK054811; United States / NIDDK NIH HHS / DK / DK062975; United States / NIDDK NIH HHS / DK / DK76898; United States / NIDDK NIH HHS / DK / R01 DK054811-07; United States / NIDDK NIH HHS / DK / K01 DK078532; United States / NIDDK NIH HHS / DK / R01 DK076898-01A2; United States / NIDDK NIH HHS / DK / R01 DK076898; United States / NIDDK NIH HHS / DK / KO1DK078532; United States / NIDDK NIH HHS / DK / DK054811-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endothelin-1; 0 / RNA, Messenger; 0 / Receptor, Endothelin A; 0 / Receptor, Endothelin B; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C; 9007-34-5 / Collagen; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-3
  • [Other-IDs] NLM/ NIHMS104417; NLM/ PMC2706939
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14. Elferink RO: Cholestasis. Gut; 2003 May;52 Suppl 2:ii42-8
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  • In contrast with urine formation, bile flow is not dependent on hydrostatic forces, but driven by osmotic pressure of solutes secreted across the apical membrane of hepatocytes and bile duct epithelial cells.
  • The most important solutes in bile are bile salts, lipids, electrolytes, and organic anions.
  • The direct consequence of the osmotic mechanism of bile formation is that impaired function of these pumps leads to impaired bile flow-that is, cholestasis.
  • Identification of the molecular defect in these diseases was not only important for diagnostic reasons but also emphasised that impaired transporter function has pathological consequences.
  • [MeSH-minor] Bile / secretion. Bile Acids and Salts / metabolism. Cholestasis, Intrahepatic / genetics. Cholestasis, Intrahepatic / metabolism. Female. Humans. Membrane Transport Proteins / genetics. Membrane Transport Proteins / metabolism. Mutation. Pregnancy. Pregnancy Complications / metabolism

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  • (PMID = 12651881.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / Membrane Transport Proteins
  • [Number-of-references] 108
  • [Other-IDs] NLM/ PMC1867745
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15. Xu L, Hausmann M, Dietmaier W, Kellermeier S, Pesch T, Stieber-Gunckel M, Lippert E, Klebl F, Rogler G: Expression of growth factor receptors and targeting of EGFR in cholangiocarcinoma cell lines. BMC Cancer; 2010;10:302
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  • BACKGROUND: Cholangiocarcinoma (CC) is a malignant neoplasm of the bile ducts or the gallbladder.
  • [MeSH-major] Bile Duct Neoplasms / metabolism. Bile Ducts, Intrahepatic / metabolism. Cholangiocarcinoma / metabolism. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal, Humanized. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cetuximab. Dose-Response Relationship, Drug. Gene Expression Regulation, Neoplastic. Humans. Mutation. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins c-met / metabolism. RNA, Messenger / metabolism. Receptors, Growth Factor / metabolism. Receptors, Somatomedin / metabolism. Receptors, Vascular Endothelial Growth Factor / metabolism. Time Factors. ras Proteins / genetics

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  • (PMID = 20565817.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / KRAS protein, human; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Receptors, Growth Factor; 0 / Receptors, Somatomedin; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / MET protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 3.6.5.2 / ras Proteins; PQX0D8J21J / Cetuximab
  • [Other-IDs] NLM/ PMC2896958
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16. Pawar P, Ma L, Byon CH, Liu H, Ahn EY, Jhala N, Arnoletti JP, McDonald JM, Chen Y: Molecular mechanisms of tamoxifen therapy for cholangiocarcinoma: role of calmodulin. Clin Cancer Res; 2009 Feb 15;15(4):1288-96
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  • [MeSH-major] Bile Duct Neoplasms / drug therapy. Calmodulin / antagonists & inhibitors. Cholangiocarcinoma / drug therapy. Tamoxifen / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Bile Ducts, Intrahepatic. CASP8 and FADD-Like Apoptosis Regulating Protein / antagonists & inhibitors. CASP8 and FADD-Like Apoptosis Regulating Protein / physiology. Caspases / physiology. Cell Line, Tumor. Female. Humans. Male. Mice. Mice, Inbred BALB C. Phosphorylation. Proto-Oncogene Proteins c-akt / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 19228732.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / T32 HL007918; United States / NHLBI NIH HHS / HL / T32 HL007918-11
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / Calmodulin; 094ZI81Y45 / Tamoxifen; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ NIHMS209446; NLM/ PMC2905314
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17. Harder J, Blum HE: [Cholangiocarcinoma]. Praxis (Bern 1994); 2002 Aug 21;91(34):1352-6
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  • They are a heterogeneous group of neoplasias that include the most common perihilar or Klatskin tumor (60%), the intrahepatic (peripheral) CCC, the extrahepatic bile duct cancer, the gallbladder cancer and the cancer of the ampulla of Vater.
  • At the time of diagnosis only 20% of patients can be treated by surgery, that offers the only chance for cure.
  • Due to high recurrence rates liver transplantation is not indicated.
  • The most frequently used agents are 5-FU and Gemcitabine that can be combined with external or internal radiation.
  • Evidence Based Medicine studies are needed before treatment strategies can be recommended for clinical practice.
  • [MeSH-major] Bile Duct Neoplasms / diagnosis. Bile Ducts, Intrahepatic. Cholangiocarcinoma / diagnosis
  • [MeSH-minor] Gallbladder Neoplasms / diagnosis. Gallbladder Neoplasms / pathology. Hepatic Duct, Common / pathology. Humans. Klatskin Tumor / diagnosis. Klatskin Tumor / pathology. Neoplasm Staging. Prognosis

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  • (PMID = 12233266.001).
  • [ISSN] 1661-8157
  • [Journal-full-title] Praxis
  • [ISO-abbreviation] Praxis (Bern 1994)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 24
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18. Ustundag Y, Bronk SF, Gores GJ: Proteasome inhibition-induces endoplasmic reticulum dysfunction and cell death of human cholangiocarcinoma cells. World J Gastroenterol; 2007 Feb 14;13(6):851-7
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  • The protein synthesis inhibitor, cycloheximide, blocked apoptosis induced by proteasome inhibitor indicating that ER dysfunction was dependent upon the formation of new proteins.
  • Proteasome inhibitors warrant evaluation as anticancer agents for the treatment of human cholangiocarcinoma.

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  • (PMID = 17352013.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK063947; United States / NIDDK NIH HHS / DK / DK63947
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cysteine Proteinase Inhibitors; 0 / Leupeptins; 0 / NF-kappa B; 0 / Proteasome Inhibitors; 0 / Protein Synthesis Inhibitors; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 98600C0908 / Cycloheximide; EC 3.4.22.- / Caspases; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Other-IDs] NLM/ PMC4065919
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19. Morinaga S, Yamamoto Y, Sugano N, Wada H, Shiozawa M, Akaike M, Sugimasa Y: Long-term survival after multimodal therapy in a patient demonstrating intrahepatic cholangiocarcinoma with hilar invasion and intrahepatic metastases. Int J Clin Oncol; 2008 Aug;13(4):361-4
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  • [Title] Long-term survival after multimodal therapy in a patient demonstrating intrahepatic cholangiocarcinoma with hilar invasion and intrahepatic metastases.
  • Specifically, the patient achieved an extended complete response after combination chemotherapy with TS-1 (an orally administered drug that is a combination of tegafur, 5-chloro-2, 4-dihydroxypyridine [CDHP], and oteracil potassium [Oxo]) and cisplatin for recurrence.
  • [MeSH-major] Bile Duct Neoplasms / therapy. Bile Ducts, Intrahepatic. Cholangiocarcinoma / therapy. Liver Neoplasms / secondary
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Combined Modality Therapy. Disease-Free Survival. Drug Combinations. Humans. Lymphatic Metastasis. Male. Oxonic Acid / administration & dosage. Tegafur / administration & dosage

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  • (PMID = 18704639.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; Q20Q21Q62J / Cisplatin
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20. Alvaro D, Mancino MG, Onori P, Franchitto A, Alpini G, Francis H, Glaser S, Gaudio E: Estrogens and the pathophysiology of the biliary tree. World J Gastroenterol; 2006 Jun 14;12(22):3537-45
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  • Estrogens are not only essential for the female reproductive system, but they also control fundamental functions in other tissues including the cardiovascular system, bone, brain and liver.
  • Recently, estrogens have been shown to target the biliary tree, where they modulate the proliferative and secretory activities of cholangiocytes, the epithelial cells lining bile ducts.

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  • (PMID = 16773710.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK058411; United States / NIDDK NIH HHS / DK / R01 DK062975; United States / NIDDK NIH HHS / DK / DK062975; United States / NIDDK NIH HHS / DK / DK58411
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Estrogens; 0 / Growth Substances; 0 / Receptors, Estrogen
  • [Number-of-references] 99
  • [Other-IDs] NLM/ PMC4087569
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21. Dechakhamphu S, Pinlaor S, Sitthithaworn P, Nair J, Bartsch H, Yongvanit P: Lipid peroxidation and etheno DNA adducts in white blood cells of liver fluke-infected patients: protection by plasma alpha-tocopherol and praziquantel. Cancer Epidemiol Biomarkers Prev; 2010 Jan;19(1):310-8
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  • [Title] Lipid peroxidation and etheno DNA adducts in white blood cells of liver fluke-infected patients: protection by plasma alpha-tocopherol and praziquantel.
  • Chronic infection by the liver fluke Opisthorchis viverrini is a strong risk factor for cholangiocarcinoma.
  • Two months after a single dose to infected patients of the antiparasitic drug praziquantel, epsilondA and epsilondC levels in WBC were decreased to control level (P < 0.03); plasma 8-isoprostane, malondialdehyde, nitrate/nitrite, and alkaline phosphatase (ALP) were concomitantly lowered. epsilondA and epsilondC levels in WBC were positively correlated with plasma 8-isoprostane, malondialdehyde, and nitrate/nitrite levels and ALP activity, whereas plasma alpha-tocopherol levels showed inverse correlations.
  • We conclude that chronic O.viverrini infection induces an accumulation of lipid peroxidation-derived DNA damage through oxidative/nitrative stress, which is lowered by the plasma alpha-tocopherol and by antiparasitic drug therapy.
  • [MeSH-major] Anthelmintics / therapeutic use. DNA Adducts / blood. Lipid Peroxidation / drug effects. Opisthorchiasis / blood. Praziquantel / therapeutic use. alpha-Tocopherol / blood
  • [MeSH-minor] Animals. Bile Duct Neoplasms / blood. Bile Duct Neoplasms / parasitology. Bile Duct Neoplasms / prevention & control. Bile Ducts, Intrahepatic / metabolism. Bile Ducts, Intrahepatic / parasitology. Cholangiocarcinoma / blood. Cholangiocarcinoma / parasitology. Cholangiocarcinoma / prevention & control. Dinoprost / analogs & derivatives. Dinoprost / blood. Female. Humans. Leukocytes / drug effects. Male. Malondialdehyde / blood. Middle Aged. Nitrates / blood. Nitrites / blood. Opisthorchis. Oxidative Stress / drug effects. Oxidative Stress / physiology

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  • (PMID = 20056652.001).
  • [ISSN] 1538-7755
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthelmintics; 0 / DNA Adducts; 0 / Nitrates; 0 / Nitrites; 27415-26-5 / 8-epi-prostaglandin F2alpha; 4Y8F71G49Q / Malondialdehyde; 6490C9U457 / Praziquantel; B7IN85G1HY / Dinoprost; H4N855PNZ1 / alpha-Tocopherol
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22. Chaimuangraj S, Thamavit W, Tsuda H, Moore MA: Experimental investigation of opisthorchiasis-associated cholangiocarcinoma induction in the Syrian hamster - pointers for control of the human disease. Asian Pac J Cancer Prev; 2003 Apr-Jun;4(2):87-93
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  • In the North-east of Thailand exceptionally high levels of cholangiocellular carcinomas (CCCs) are encountered, related to infestation with Opisthorchis viverrini liver flukes.
  • While removal of the parasite with the antihelminthic drug Praziquantel can protect against carcinogenesis, this is dependent on the timing of the drug administration and the efficacy of application to the human situation remains to be confirmed.
  • The available information would suggest that interest needs to be concentrated on potential chemopreventive agents which could be administered to individuals at high risk.
  • [MeSH-major] Bile Duct Neoplasms / parasitology. Bile Ducts, Intrahepatic. Cholangiocarcinoma / parasitology. Disease Models, Animal. Mesocricetus. Opisthorchiasis / complications
  • [MeSH-minor] Animals. Cricetinae

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  • (PMID = 12875618.001).
  • [ISSN] 1513-7368
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Thailand
  • [Number-of-references] 57
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23. Smirnova OV, Ostroukhova TY, Bogorad RL: JAK-STAT pathway in carcinogenesis: is it relevant to cholangiocarcinoma progression? World J Gastroenterol; 2007 Dec 28;13(48):6478-91
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  • The features of JAK-STAT signaling in liver cells are discussed in the current review.
  • [MeSH-major] Bile Duct Neoplasms / physiopathology. Cholangiocarcinoma / physiopathology. Janus Kinases / physiology. STAT Transcription Factors / physiology
  • [MeSH-minor] Bile Ducts, Intrahepatic. Humans. Signal Transduction / physiology

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  • (PMID = 18161917.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / STAT Transcription Factors; EC 2.7.10.2 / Janus Kinases
  • [Number-of-references] 183
  • [Other-IDs] NLM/ PMC4611286
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24. Wongkham S, Junking M, Wongkham C, Sripa B, Chur-In S, Araki N: Suppression of galectin-3 expression enhances apoptosis and chemosensitivity in liver fluke-associated cholangiocarcinoma. Cancer Sci; 2009 Nov;100(11):2077-84
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  • [Title] Suppression of galectin-3 expression enhances apoptosis and chemosensitivity in liver fluke-associated cholangiocarcinoma.
  • Cholangiocarcinoma (CCA) is a fatal disease with high resistance to anticancer drugs.
  • Suppression of Gal-3 expression in CCA cells with siGal-3-K402 significantly enhanced apoptosis induced by cisplatin or 5-fluorouracil by approximately 10 times, whereas overexpression of Gal-3 led to an increased resistance to drugs.
  • Hence, Gal-3 expression level in cancer cells or tissues may be a marker for predicting chemotherapeutic response, and Gal-3 may be a specific gene-targeting therapy option for treating CCA.
  • [MeSH-major] Apoptosis. Bile Duct Neoplasms / drug therapy. Bile Ducts, Intrahepatic. Cholangiocarcinoma / drug therapy. Fascioliasis / complications. Galectin 3 / physiology

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  • (PMID = 19723119.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Galectin 3
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25. Zhong F, Zhang S, Shao C, Yang J, Wu X: Arsenic trioxide inhibits cholangiocarcinoma cell growth and induces apoptosis. Pathol Oncol Res; 2010 Sep;16(3):413-20
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  • Arsenic trioxide (As(2)O(3)), an ingredient in many traditional Chinese medicines, has drawn broad attention due to its therapeutic effects on a variety of cancers, including some solid tumors.
  • As(2)O(3)-induced apoptosis was partially inhibited by caspase inhibitor and accompanied by changes in the expression of Bcl-2 family proteins, decrease of mitochondrial membrane potential (MMP), release of cytochrome C from mitochondria, activation of caspase-3, caspase-9, and cleavage of poly (ADP-ribose) polymerase (PARP).
  • [MeSH-major] Apoptosis / drug effects. Arsenicals / pharmacology. Bile Duct Neoplasms / pathology. Bile Ducts, Intrahepatic / pathology. Cell Proliferation / drug effects. Cholangiocarcinoma / pathology. Oxides / pharmacology
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Cell Separation. Flow Cytometry. Humans. Signal Transduction / drug effects

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  • (PMID = 20012722.001).
  • [ISSN] 1532-2807
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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26. Socoteanu MP, Mott F, Alpini G, Frankel AE: c-Met targeted therapy of cholangiocarcinoma. World J Gastroenterol; 2008 May 21;14(19):2990-4
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  • We reviewed the current use and options for future development of c-Met agents to treat this disease.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bile Duct Neoplasms / drug therapy. Bile Ducts, Intrahepatic / drug effects. Cholangiocarcinoma / drug therapy. Proto-Oncogene Proteins c-met / antagonists & inhibitors. Signal Transduction / drug effects


27. Jarnagin WR, Schwartz LH, Gultekin DH, Gönen M, Haviland D, Shia J, D'Angelica M, Fong Y, Dematteo R, Tse A, Blumgart LH, Kemeny N: Regional chemotherapy for unresectable primary liver cancer: results of a phase II clinical trial and assessment of DCE-MRI as a biomarker of survival. Ann Oncol; 2009 Sep;20(9):1589-95
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  • [Title] Regional chemotherapy for unresectable primary liver cancer: results of a phase II clinical trial and assessment of DCE-MRI as a biomarker of survival.
  • BACKGROUND: This study reports the results of hepatic arterial infusion (HAI) with floxuridine (FUDR) and dexamethasone (dex) in patients with unresectable intrahepatic cholangiocarcinoma (ICC) or hepatocellular carcinoma (HCC) and investigates dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) assessment of tumor vascularity as a biomarker of outcome.
  • CONCLUSIONS: In patients with unresectable primary liver cancer, HAI therapy can be effective and safe.

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  • (PMID = 19491285.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21CA121553-01A1
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 039LU44I5M / Floxuridine; 7S5I7G3JQL / Dexamethasone
  • [Other-IDs] NLM/ PMC2731015
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28. Kristiansen TZ, Harsha HC, Grønborg M, Maitra A, Pandey A: Differential membrane proteomics using 18O-labeling to identify biomarkers for cholangiocarcinoma. J Proteome Res; 2008 Nov;7(11):4670-7
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  • Quantitative proteomic methodologies allow profiling of hundreds to thousands of proteins in a high-throughput fashion.
  • This approach is increasingly applied to cancer biomarker discovery to identify proteins that are differentially regulated in cancers.
  • We used a membrane protein enrichment strategy coupled with 18O labeling based quantitative proteomics to identify proteins that are highly expressed in cholangiocarcinomas.
  • In addition to identifying several proteins previously known to be overexpressed in cholangiocarcinoma, we discovered a number of molecules that were previously not associated with cholangiocarcinoma.
  • Using immunoblotting and immunohistochemical labeling of tissue microarrays, we validated Golgi membrane protein 1, Annexin IV and Epidermal growth factor receptor pathway substrate 8 (EPS8) as candidate biomarkers for cholangiocarcinomas.

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  • (PMID = 18839982.001).
  • [ISSN] 1535-3893
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / P50 CA62924
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Oxygen Isotopes; 0 / Proteome
  • [Other-IDs] NLM/ NIHMS91009; NLM/ PMC3204659
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29. Lin ZY, Chuang WL, Chuang YH, Yu ML, Hsieh MY, Wang LY, Tsai JF: Discordant influence of amphotericin B on epirubicin cytotoxicity in primary hepatic malignant cells collected by a new primary culture technique. J Gastroenterol Hepatol; 2006 Feb;21(2):398-405
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  • [Title] Discordant influence of amphotericin B on epirubicin cytotoxicity in primary hepatic malignant cells collected by a new primary culture technique.
  • BACKGROUND: The purpose of this prospective study was to investigate whether amphotericin B (AmB) had any potential role in the systemic chemotherapy of primary hepatic malignancy using cancer cells collected by the authors' method of primary culture.
  • Six patients with HCC and one patient with cholangiocarcinoma (7/16, 44%) had successful culture and the cancer cells at the 4th passage were continuously exposed to therapeutic ranges of epirubicin (0, 0.5, 1.0, 1.5, 2.0 microg/mL) with or without the combination of 2.5 microg/mL AmB for 24 h. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was applied to evaluate the effects of the drugs.
  • CONCLUSIONS: Amphotericin B has a discordant influence on epirubicin cytotoxicity in primary cultured hepatic malignant cells.
  • [MeSH-major] Amphotericin B / therapeutic use. Anti-Bacterial Agents / therapeutic use. Antibiotics, Antineoplastic / adverse effects. Epirubicin / adverse effects. Liver Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Bile Duct Neoplasms / drug therapy. Bile Duct Neoplasms / pathology. Bile Ducts, Intrahepatic. Biopsy, Fine-Needle. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / pathology. Cell Culture Techniques. Cell Proliferation / drug effects. Cholangiocarcinoma / drug therapy. Cholangiocarcinoma / pathology. Drug Interactions. Drug Therapy, Combination. Female. Follow-Up Studies. Humans. Male. Middle Aged. Prospective Studies. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 16509865.001).
  • [ISSN] 0815-9319
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antibiotics, Antineoplastic; 3Z8479ZZ5X / Epirubicin; 7XU7A7DROE / Amphotericin B
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30. Vickers SM, Jhala NC, Ahn EY, McDonald JM, Pan G, Bland KI: Tamoxifen (TMX)/Fas induced growth inhibition of human cholangiocarcinoma (HCC) by gamma interferon (IFN-gamma). Ann Surg; 2002 Jun;235(6):872-8
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  • SUMMARY BACKGROUND DATA: Cholangiocarcinoma remains one of the most difficult tumors to treat in clinical medicine.
  • Surgery offers the only opportunity for a cure, with the majority of patients failing to qualify for such treatment.
  • Mice received either no treatment or intra tumor IFN-gamma and/or intra peritoneal TMX.

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  • (PMID = 12035045.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K01 CA083767; United States / NCI NIH HHS / CA / K01 CA 83767-01-02
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD95; 0 / Antineoplastic Agents; 0 / BAK1 protein, human; 0 / Bak1 protein, mouse; 0 / Membrane Proteins; 0 / anti-Fas monoclonal antibody; 0 / bcl-2 Homologous Antagonist-Killer Protein; 094ZI81Y45 / Tamoxifen; 82115-62-6 / Interferon-gamma; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC1422518
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31. Hayashi N, Hasuike Y, Fukuchi N, Kida H, Tujie M, Yoshida T, Ebisui C, Sakita I, Koshino T, Izumiyama K, Koro T, Fujimoto T: [A case of unresectable cholangiocellular carcinoma treated with surgery followed by combination chemotherapy]. Gan To Kagaku Ryoho; 2005 Oct;32(11):1852-4
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  • The patient was a 44-year-old man, who was investigated for lateral abdominal pain and liver dysfunction, and subsequently referred to our department with a diagnosis of unresectable intrahepatic cholangiocellular carcinoma (CCC).
  • Radiological examinations revealed the huge mass in the right lobe of the liver with intrahepatic metastasis in the left lobe.
  • After 15 courses of home anti-cancer chemotherapy, abdominal CT revealed that the size of intrahepatic metastasis in the left lobe of the liver had not shown growth, whereas other metastitic sites popped up in the caudate lobe, which were free of chemical agent flow.
  • He died of liver failure 7 months after the operation.
  • [MeSH-major] Bile Duct Neoplasms / therapy. Bile Ducts, Intrahepatic. Cholangiocarcinoma / therapy
  • [MeSH-minor] Adult. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cisplatin / administration & dosage. Fluorouracil / administration & dosage. Hepatectomy. Humans. Infusions, Intra-Arterial. Liver Neoplasms / secondary. Lymph Node Excision. Male

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  • (PMID = 16315961.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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32. Demols A, Maréchal R, Devière J, Van Laethem JL: The multidisciplinary management of gastrointestinal cancer. Biliary tract cancers: from pathogenesis to endoscopic treatment. Best Pract Res Clin Gastroenterol; 2007;21(6):1015-29
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  • [Title] The multidisciplinary management of gastrointestinal cancer. Biliary tract cancers: from pathogenesis to endoscopic treatment.
  • Even if it is a rare tumour, its incidence is increasing over these last decades, probably due in part to a better knowledge of the disease and to an improvement of the diagnosis.
  • Accurate diagnosis and staging are key steps to determine the appropriate treatment.
  • The only curative treatment of this cancer is surgical resection.
  • Liver transplantation (with or without neoadjuvant treatment) can be an option for highly selected cases.
  • For most of these patients, palliative therapeutic options exist and are in further development, based on multimodal promising combinations including chemotherapy, targeted agents, radiation, endoscopic stenting and photodynamic treatment.
  • [MeSH-major] Bile Duct Neoplasms / therapy. Bile Ducts, Intrahepatic / surgery. Biliary Tract Surgical Procedures. Cholangiocarcinoma / therapy. Endoscopy. Liver Transplantation
  • [MeSH-minor] Chemotherapy, Adjuvant. Humans. Neoadjuvant Therapy. Neoplasm Staging. Radiotherapy, Adjuvant. Treatment Outcome


33. Jansen PL, Müller M, Kuipers F: [Bile formation and cholestasis]. Ned Tijdschr Geneeskd; 2000 Dec 9;144(50):2384-91
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  • [Title] [Bile formation and cholestasis].
  • [Transliterated title] Galvorming en cholestase.
  • Transport proteins in hepatocytes and bile duct epithelium mediate uptake and secretion of cholephilic compounds in the liver and are involved in bile formation.
  • Many of these proteins have recently been cloned and characterized and appear to belong to large gene families.
  • Apart from the liver these proteins are expressed in the blood-brain barrier, placenta, kidneys, lungs, intestine and seminiferous tubules.
  • Prokaryotes and yeasts contain similar proteins.
  • In cancer cells they are involved in multidrug resistance.
  • Some genetic cholestatic liver diseases, including progressive familial intrahepatic cholestasis, Dubin-Johnson syndrome, benign recurrent intrahepatic cholestasis and intrahepatic cholestasis of pregnancy result from mutations in transport protein genes.
  • These proteins also play a role in drug-induced liver disease and in primary biliary cirrhosis.
  • Cyclosporine and oestradiol (glucuronide) for instance inhibit bile salt export protein (BSEP).
  • [MeSH-major] Bile / secretion. Carrier Proteins / metabolism. Cholestasis, Intrahepatic / genetics. Liver / metabolism. Liver Cirrhosis / genetics
  • [MeSH-minor] Bile Acids and Salts / metabolism. Female. Gene Expression Regulation. Humans. Liver Cirrhosis, Biliary / genetics. Male. Mutation. Pregnancy

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  • (PMID = 11145092.001).
  • [ISSN] 0028-2162
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / Carrier Proteins
  • [Number-of-references] 46
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34. Francis H, Alpini G, DeMorrow S: Recent advances in the regulation of cholangiocarcinoma growth. Am J Physiol Gastrointest Liver Physiol; 2010 Jul;299(1):G1-9
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  • Cholangiocarcinomas arise after the neoplastic transformation of the cholangiocytes that line the intra- and extrahepatic biliary epithelium.
  • Symptoms usually do not present until late in the course of the disease, at which time they are relatively resistant to chemotherapeutic agents and as such are difficult to treat and display a poor prognosis.
  • However, the incidence of this devastating cancer is on the rise and renewed efforts to understand the pathogenesis of cholangiocarcinoma is needed to design novel therapeutic strategies to combat this disease.

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  • (PMID = 20430870.001).
  • [ISSN] 1522-1547
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK07698; United States / NIDDK NIH HHS / DK / DK58411; United States / NIDDK NIH HHS / DK / R01 DK054811; United States / NIDDK NIH HHS / DK / R03 DK088012; United States / NIDDK NIH HHS / DK / R01 DK076898; United States / NIDDK NIH HHS / DK / K01 DK078532
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gastrointestinal Hormones; 0 / Inflammation Mediators; 0 / Intercellular Signaling Peptides and Proteins; 0 / Nerve Tissue Proteins
  • [Number-of-references] 105
  • [Other-IDs] NLM/ PMC2904122
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35. Aldrighetti L, Arru M, Ronzoni M, Salvioni M, Villa E, Ferla G: Extrahepatic biliary stenoses after hepatic arterial infusion (HAI) of floxuridine (FUdR) for liver metastases from colorectal cancer. Hepatogastroenterology; 2001 Sep-Oct;48(41):1302-7
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  • [Title] Extrahepatic biliary stenoses after hepatic arterial infusion (HAI) of floxuridine (FUdR) for liver metastases from colorectal cancer.
  • Hepatic arterial infusion of floxuridine is an effective treatment for unresectable hepatic metastases from colorectal cancer.
  • Despite its pharmacological advantage of higher tumor drug concentration with minimal systemic toxicity, hepatic arterial infusion of floxuridine is characterized by regional toxicity, including hepatobiliary damage resembling idiopathic sclerosing cholangitis (5-29% of treated cases).
  • Unlike previous reports describing biliary damage of both intrahepatic and extrahepatic ducts, a case series of extrahepatic biliary stenosis after hepatic arterial infusion with floxuridine is herein described.
  • Five patients (9.2%) developed biliary toxicity with jaundice and cholangitis (3 cases), alterations of liver function tests and radiological features of biliary tract abnormalities.
  • They received from 9 to 19 cycles (mean 14.5 +/- 6.3 cycles) of floxuridine infusion with a total drug delivered dose ranging from 20.3 to 41.02 mg/kg (mean: 31.4 +/- 13.5 mg/kg).
  • Radiological findings included common hepatic duct complete obstruction in 1 case, common hepatic duct stenosis in 2 cases, common bile duct obstruction in 1 case, and intrahepatic bile ducts dilation without a well-recognized obstruction in 1 case.
  • The present series suggests that in some patients receiving hepatic arterial infusion of floxuridine extrahepatic biliary stenosis may represent the primary event leading to a secondary intrahepatic biliary damage that does not correlate with specific floxuridine toxicity but results from bile stasis and infection, recurrent cholangitis and eventually biliary sclerosis.
  • Aggressive research for extrahepatic biliary sclerosis is advised, since an early nonsurgical treatment of extrahepatic biliary stenosis may prevent an irreversible intrahepatic biliary sclerosis worsening the prognosis of metastatic liver disease.
  • [MeSH-major] Adenocarcinoma / secondary. Cholestasis, Extrahepatic / chemically induced. Colorectal Neoplasms / drug therapy. Floxuridine / adverse effects. Infusions, Intra-Arterial. Liver Neoplasms / secondary
  • [MeSH-minor] Aged. Cholangiography. Cholangitis, Sclerosing / chemically induced. Cholangitis, Sclerosing / diagnosis. Cholangitis, Sclerosing / therapy. Dose-Response Relationship, Drug. Female. Follow-Up Studies. Humans. Liver Function Tests. Male. Middle Aged. Stents


36. Tanida T, Tanemura M, Kobayashi S, Wada H, Marubashi S, Eguchi H, Takeda Y, Umeshita H, Mori M, Doki Y, Nagano H: [A case report--intrahepatic arterial infusion with CDDP and S-1 administration can elicit long-term survival for the patient with recurrenced intrahepatic cholangiocarcinoma after resection]. Gan To Kagaku Ryoho; 2010 Nov;37(12):2729-31
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  • [Title] [A case report--intrahepatic arterial infusion with CDDP and S-1 administration can elicit long-term survival for the patient with recurrenced intrahepatic cholangiocarcinoma after resection].
  • To cure intrahepatic cholangiocarcinoma (ICC), only a surgical resection is the potential treatment at present.
  • However, recurrence tumors in residual liver and/or distant organs even after curative surgery are commonly experienced in clinical course.
  • Here, we report the prolonged survival case with recurrent ICC after hepatic resection followed by combined therapy of intrahepatic arterial infusion with CDDP and S-1 administration.
  • After that, liver tumor of 30 mm in diameter was detected in S1/8 by abdominal CT examination.
  • Subsequently, caudate lobectomy and partial resection of Segment 8 were performed under the diagnosis of Hepatocellular carcinoma in Osaka university hospital.
  • The pathological stage was T2N0M0, Stage II with moderately differentiated intrahepatic cholangiocarcinoma.
  • As the recurrence tumor was found in Segment 4 of residual liver, we started a treatment with intrahepatic arterial infusion with CDDP and S-1 administration, immediately.
  • These combined therapy displayed beneficial effects and a recurrent liver tumor was well controlled.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Bile Duct Neoplasms / drug therapy. Bile Ducts, Intrahepatic. Cholangiocarcinoma / drug therapy
  • [MeSH-minor] Aged. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents / administration & dosage. Cisplatin / administration & dosage. Drug Combinations. Female. Hepatic Artery. Humans. Infusions, Intra-Arterial. Neoplasm Recurrence, Local. Oxonic Acid / administration & dosage. Tegafur / administration & dosage

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  • (PMID = 21224694.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; Q20Q21Q62J / Cisplatin
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37. Frampton G, Coufal M, Li H, Ramirez J, DeMorrow S: Opposing actions of endocannabinoids on cholangiocarcinoma growth is via the differential activation of Notch signaling. Exp Cell Res; 2010 May 15;316(9):1465-78
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  • Implicated in cancer, Notch signaling requires the gamma-secretase complex for activation.

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20347808.001).
  • [ISSN] 1090-2422
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK078532-03S1; United States / NIDDK NIH HHS / DK / K01 DK078532-03S1; United States / NIDDK NIH HHS / DK / DK078532-03; United States / NIDDK NIH HHS / DK / K01 DK078532-03; United States / NIDDK NIH HHS / DK / K01 DK078532
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arachidonic Acids; 0 / Cannabinoid Receptor Modulators; 0 / Endocannabinoids; 0 / Glycerides; 0 / Polyunsaturated Alkamides; 0 / Presenilin-1; 0 / Presenilin-2; 0 / RNA, Messenger; 0 / Receptor, Notch1; 0 / Receptor, Notch2; 53847-30-6 / 2-arachidonylglycerol; 94421-68-8 / anandamide; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ NIHMS192888; NLM/ PMC2872061
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38. Buranrat B, Prawan A, Sripa B, Kukongviriyapan V: Inflammatory cytokines suppress arylamine N-acetyltransferase 1 in cholangiocarcinoma cells. World J Gastroenterol; 2007 Dec 14;13(46):6219-25
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  • AIM: To evaluate the effect of inflammatory cytokines on arylamine N-acetyltransferase 1 (NAT1), which is a phase-II enzyme involved in the biotransformation of aromatic and heterocyclic amines found in food, drugs and the environment.
  • [MeSH-major] Arylamine N-Acetyltransferase / metabolism. Bile Duct Neoplasms / enzymology. Bile Ducts, Intrahepatic. Cholangiocarcinoma / enzymology. Interferon-gamma / physiology. Interleukin-1beta / physiology. Isoenzymes / metabolism. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Cell Line, Tumor. Epithelial Cells / drug effects. Epithelial Cells / enzymology. Epithelial Cells / pathology. Glutathione / metabolism. Humans. Nitric Oxide / metabolism. Nitric Oxide Donors / pharmacology. Oxidation-Reduction. Oxidative Stress. RNA, Messenger / metabolism. S-Nitrosoglutathione / pharmacology. Superoxides / metabolism

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  • (PMID = 18069763.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Interleukin-1beta; 0 / Isoenzymes; 0 / Nitric Oxide Donors; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 11062-77-4 / Superoxides; 31C4KY9ESH / Nitric Oxide; 57564-91-7 / S-Nitrosoglutathione; 82115-62-6 / Interferon-gamma; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / N-acetyltransferase 1; GAN16C9B8O / Glutathione
  • [Other-IDs] NLM/ PMC4171233
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39. Pusl T, Beuers U: Ursodeoxycholic acid treatment of vanishing bile duct syndromes. World J Gastroenterol; 2006 Jun 14;12(22):3487-95
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  • [Title] Ursodeoxycholic acid treatment of vanishing bile duct syndromes.
  • Vanishing bile duct syndromes (VBDS) are characterized by progressive loss of small intrahepatic ducts caused by a variety of different diseases leading to chronic cholestasis, cirrhosis, and premature death from liver failure.
  • Ursodeoxycholic acid (UDCA), a hydrophilic dihydroxy bile acid, is the only drug currently approved for the treatment of patients with PBC, and anticholestatic effects have been reported for several other cholestatic syndromes.
  • Several potential mechanisms of action of UDCA have been proposed including stimulation of hepatobiliary secretion, inhibition of apoptosis and protection of cholangiocytes against toxic effects of hydrophobic bile acids.
  • [MeSH-major] Bile Duct Diseases / drug therapy. Bile Ducts, Intrahepatic / pathology. Cholagogues and Choleretics / therapeutic use. Ursodeoxycholic Acid / therapeutic use
  • [MeSH-minor] Apoptosis / drug effects. Bile Acids and Salts / pharmacology. Cholestasis / physiopathology. Humans. Liver Cirrhosis / physiopathology. Liver Failure / etiology. Liver Failure / pathology. Liver Failure / physiopathology. Syndrome

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  • (PMID = 16773706.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / Cholagogues and Choleretics; 724L30Y2QR / Ursodeoxycholic Acid
  • [Number-of-references] 117
  • [Other-IDs] NLM/ PMC4087565
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40. Thelen A, Neuhaus P: Liver transplantation for hilar cholangiocarcinoma. J Hepatobiliary Pancreat Surg; 2007;14(5):469-75
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  • [Title] Liver transplantation for hilar cholangiocarcinoma.
  • Hilar cholangiocarcinoma was accepted as an indication for liver transplantation at the beginning of the transplantation era.
  • Owing to disappointing long-term results for this indication, and in parallel, encouraging results in patients with benign disease, hilar cholangiocarcinoma has generally not been accepted as an indication for liver transplantation in recent years.
  • To improve results, more aggressive approaches have been used: "abdominal organ cluster transplantation" and "extended bile duct resection", which lead to increased long-term survival rates.
  • However, with improving results after conventional extrahepatic bile duct resection in combination with partial hepatectomy, extended procedures in combination with liver transplantation never became a real option in the treatment of hilar cholangiocarcinoma.
  • However, new awareness of liver transplantation in the treatment of this cancer has been raised for patients with hilar cholangiocarcinoma in the context of underlying liver diseases such as primary sclerosing cholangitis, which preclude liver resection.
  • Patients with neoadjuvant radiochemotherapy show long-term results similar to those for liver transplantation for other indications.
  • Also, photodynamic therapy and the use of new antiproliferative immunosuppressive agents may be an approach for further improvement of the long-term results.
  • Currently, liver transplantation for the treatment of hilar cholangiocarcinoma should be restricted to centers with experience in the treatment of this cancer and should be taken into consideration in patients with contraindications to liver resection.
  • [MeSH-major] Bile Duct Neoplasms / surgery. Bile Ducts, Intrahepatic / surgery. Cholangiocarcinoma / surgery. Liver Transplantation
  • [MeSH-minor] Chemotherapy, Adjuvant. Humans. Liver Diseases / complications. Liver Diseases / surgery. Neoadjuvant Therapy / methods. Patient Selection. Radiotherapy, Adjuvant. Recurrence. Survival Rate. Treatment Outcome


41. Onori P, DeMorrow S, Gaudio E, Franchitto A, Mancinelli R, Venter J, Kopriva S, Ueno Y, Alvaro D, Savage J, Alpini G, Francis H: Caffeic acid phenethyl ester decreases cholangiocarcinoma growth by inhibition of NF-kappaB and induction of apoptosis. Int J Cancer; 2009 Aug 1;125(3):565-76
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  • [Title] Caffeic acid phenethyl ester decreases cholangiocarcinoma growth by inhibition of NF-kappaB and induction of apoptosis.
  • Caffeic acid phenethyl ester (CAPE) inhibits the growth of tumor cells and is a known inhibitor of nuclear factor kappa beta (NF-kappaB), which is constitutively active in cholangiocarcinoma (CCH) cells.
  • We evaluated the effects of CAPE on CCH growth both in vitro and in vivo.
  • Inhibition of NF-kappaB DNA-binding activity was confirmed in nuclear extracts treated with CAPE at 50, 40 and 20 microM.
  • CAPE decreases the expression of NF-kappaB1 (p50) and RelA (p65).
  • CAPE decreased the growth of a number of CCH cells but not normal cholangiocytes.
  • Cell cycle decrease was seen by a decrease in PCNA protein expression and the number of BrdU-positive cells treated with CAPE at 20 microM compared to vehicle.
  • Inhibition of growth and increased cell cycle arrest of Mz-ChA-1 cells by CAPE were coupled with increased apoptosis.
  • Bax expression was increased, whereas Bcl-2 was decreased in cells treated with CAPE compared to vehicle.
  • In vivo studies were performed in BALB/c nude (nu/nu) mice implanted subcutaneously with Mz-ChA-1 cells and treated with daily IP injections of DMSO or CAPE (10 mg/kg body weight in DMSO) for 77 days.
  • Tumor growth was decreased and tumor latency was increased 2-fold in CAPE compared to vehicle-treated nude mice.
  • In tumor samples, decreased CCH growth by CAPE was coupled with increased apoptosis.
  • CAPE both in vivo and in vitro decreases the growth of CCH cells by increasing apoptosis.
  • These results demonstrate that CAPE might be an important therapeutic tool in the treatment of CCH.

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  • (PMID = 19358267.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK062975; United States / NIDDK NIH HHS / DK / R01 DK054811; United States / NIDDK NIH HHS / DK / DK062975; United States / NIDDK NIH HHS / DK / DK062975-01A2; United States / NIDDK NIH HHS / DK / DK76898; United States / NIDDK NIH HHS / DK / R01 DK054811-07; United States / NIDDK NIH HHS / DK / DK054811; United States / NIDDK NIH HHS / DK / K01 DK078532; United States / NIDDK NIH HHS / DK / R01 DK076898-01A2; United States / NIDDK NIH HHS / DK / R01 DK076898; United States / NIDDK NIH HHS / DK / DK054811-07; United States / NIDDK NIH HHS / DK / R01 DK062975-01A2; United States / NIDDK NIH HHS / DK / R01 DK054811-01A2; United States / NIDDK NIH HHS / DK / DK078532
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / Biomarkers, Tumor; 0 / Caffeic Acids; 0 / Cytotoxins; 0 / NF-kappa B; 0 / Proliferating Cell Nuclear Antigen; 0 / Transcription Factor RelA; 0 / bcl-2-Associated X Protein; 9007-49-2 / DNA; G960R9S5SK / caffeic acid phenethyl ester; ML9LGA7468 / Phenylethyl Alcohol; YOW8V9698H / Dimethyl Sulfoxide
  • [Other-IDs] NLM/ NIHMS98131; NLM/ PMC3051346
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42. Rizell M, Andersson M, Cahlin C, Hafström L, Olausson M, Lindnér P: Effects of the mTOR inhibitor sirolimus in patients with hepatocellular and cholangiocellular cancer. Int J Clin Oncol; 2008 Feb;13(1):66-70
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  • [Title] Effects of the mTOR inhibitor sirolimus in patients with hepatocellular and cholangiocellular cancer.
  • BACKGROUND: Hepatocellular cancer (HCC), as well as cholangiocellular cancer (CCC), has an extremely poor prognosis due to the extent of tumor at diagnosis and the underlying liver disease.
  • Sirolimus is used in the transplantation setting as an immunosuppressive agent, but it also possesses antiproliferative and antiangiogenic properties.
  • RESULTS: Of the patients with HCC, one had partial remission (PR) and fi ve patients had stable disease (SD) at 3 months.
  • This pilot study indicates that sirolimus might be a promising drug for this treatment, but further clinical studies elucidating the biological effects are advocated.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Bile Duct Neoplasms / drug therapy. Bile Ducts, Intrahepatic. Carcinoma, Hepatocellular / drug therapy. Cholangiocarcinoma / drug therapy. Liver Neoplasms / drug therapy. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Protein Kinases / metabolism. Sirolimus / therapeutic use

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  • (PMID = 18307022.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
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43. Xu Y, Zhu M, Zhang S, Liu H, Li T, Qin C: Expression and prognostic value of PRL-3 in human intrahepatic cholangiocarcinoma. Pathol Oncol Res; 2010 Jun;16(2):169-75
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  • [Title] Expression and prognostic value of PRL-3 in human intrahepatic cholangiocarcinoma.
  • Phosphatase of regenerating liver (PRL)-3 is involved in the metastasis of various tumors, but the expression of PRL-3 and its possible role in primary intrahepatic cholangiocarcinoma (ICC) has not been reported yet.
  • In this study, we assessed the expression levels of PRL-3 by immunohistochemistry in 102 primary ICC samples, 62 matched lymph node metastases (LNM) and 102 adjacent normal liver tissues.
  • Immunochemistry results suggested PRL-3 expression was negative or weak in non-neoplastic intrahepatic bile ducts of adjacent liver tissue.
  • [MeSH-major] Bile Duct Neoplasms / metabolism. Bile Ducts, Intrahepatic / metabolism. Biomarkers, Tumor / analysis. Cholangiocarcinoma / metabolism. Neoplasm Proteins / biosynthesis. Protein Tyrosine Phosphatases / biosynthesis

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  • (PMID = 19757198.001).
  • [ISSN] 1532-2807
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; EC 3.1.3.48 / PTP4A3 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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44. Averbach A, Stuart OA, Chang D, Sugarbaker PH: Lattice intrahepatic doxorubicin with and without in-flow occlusion: a pharmacokinetic study of direct liver injection. Eur J Surg Oncol; 2000 Feb;26(1):73-9
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  • [Title] Lattice intrahepatic doxorubicin with and without in-flow occlusion: a pharmacokinetic study of direct liver injection.
  • AIM: To assess possible improvements in drug delivery to unresectable liver tumours we investigated the pharmacokinetics of intrahepatic doxorubicin in the dog liver with and without inflow occlusion.
  • METHODS: Using a lattice template, doxorubicin was injected into 16 sites (over a 9 cm2 area) in each of three lobes of the liver for a total of 48 sites.
  • Dogs with intravenous and intra-arterial delivery of the same total doses of doxorubicin were used as controls.
  • Experiments using intrahepatic injection were performed with and without a 30 min occlusion of the hepatic artery, common bile duct and portal vein (inflow occlusion).
  • The studies with vascular stasis were performed to determine if drug clearance from the injection sites and their plasma levels were reduced.
  • Also, it was observed that blood and drug loss along the needle tract was reduced when inflow occlusion was used.
  • Plasma and liver samples were harvested over a 90-min period and analysed by high pressure liquid chromatography (HPLC).
  • RESULTS: In plasma mean peak levels and mean area under the curve (AUC) were significantly lower with intrahepatic doxorubicin (P<0.05) than with intravenous or intra-atrial delivery.
  • In the liver AUCintrahepatic/AUCintravenous ratios were 3.45 and 3.6 with 4.8 mg and 96 mg of doxorubicin respectively.
  • The liver extraction ratio (AUCliver/AUCplasma) after intravenous administration with 4.8 mg and 96 mg of doxorubicin was 31.9 with both doses of doxorubicin.
  • The corresponding extraction ratios were 107.6 and 51 for intra-arterial administration and 425.2 and 237.7 for intrahepatic administration for the two doses of doxorubicin.
  • Intrahepatic injection with inflow occlusion minimized the leakage back along the needle-tracts.
  • The liver visibly retained the injected drug more completely.
  • However, there was a decrease in systemic clearance resulting in a reduction of the pharmacological advantage.
  • CONCLUSION: These results indicate that lattice-intrahepatic administration of doxorubicin into the liver using a lattice template was associated with a significant increase in local and decrease in systemic exposure as compared to intravenous or intra-arterial administration of the same doses.
  • Simultaneous occlusion of arterial and portal venous inflow was not shown to improve regional drug delivery.
  • These pharmacokinetic studies may constitute a basis for palliative treatment of liver tumours by lattice intralesional injection when these cancers are found to be unresectable at the time of exploratory surgery.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacokinetics. Antibiotics, Antineoplastic / therapeutic use. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / metabolism. Doxorubicin / pharmacokinetics. Doxorubicin / therapeutic use. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism
  • [MeSH-minor] Animals. Area Under Curve. Chromatography, High Pressure Liquid. Colorectal Neoplasms / pathology. Dogs. Female. Infusions, Intra-Arterial. Infusions, Intravenous. Injections, Intralesional / methods. Male. Random Allocation. Time Factors

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  • (PMID = 10718184.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin
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45. Tan FL, Ooi A, Huang D, Wong JC, Qian CN, Chao C, Ooi L, Tan YM, Chung A, Cheow PC, Zhang Z, Petillo D, Yang XJ, Teh BT: p38delta/MAPK13 as a diagnostic marker for cholangiocarcinoma and its involvement in cell motility and invasion. Int J Cancer; 2010 May 15;126(10):2353-61
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  • [Title] p38delta/MAPK13 as a diagnostic marker for cholangiocarcinoma and its involvement in cell motility and invasion.
  • Cholangiocarcinoma (CC) and hepatocellularcarcinoma (HCC) are two main forms of liver malignancies, which exhibit differences in drug response and prognosis.
  • Immunohistotochemical staining for cytokeratin markers has been used to some success in the differential diagnosis of CC from HCC.
  • However, there remains a need for additional markers for increased sensitivity and specificity of diagnosis.
  • We performed microarray gene expression profiling on 17 cases of CC, 12 cases of adjacent normal liver tissue, and three case of normal bile duct tissue. p38delta was upregulated in 16 out of 17 cases of CC relative to normal tissue.
  • In summary, p38delta may serve as a novel diagnostic marker for CC and may also serve as a new target for molecular based therapy of this disease.
  • [MeSH-major] Bile Duct Neoplasms / diagnosis. Bile Ducts, Intrahepatic. Biomarkers, Tumor / metabolism. Cholangiocarcinoma / diagnosis. Mitogen-Activated Protein Kinase 13 / metabolism
  • [MeSH-minor] Antigens, Neoplasm / metabolism. Blotting, Western. Cell Movement. Collagen. Diagnosis, Differential. Drug Combinations. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. Immunohistochemistry. Immunoprecipitation. Laminin. Neoplasm Invasiveness. Predictive Value of Tests. Proteoglycans. Sensitivity and Specificity. Up-Regulation

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  • (PMID = 19816939.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 119978-18-6 / matrigel; 9007-34-5 / Collagen; EC 2.7.1.- / Mitogen-Activated Protein Kinase 13
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46. Chiorean MV, Guicciardi ME, Yoon JH, Bronk SF, Kaufmanns SH, Gores GJ: Imatinib mesylate induces apoptosis in human cholangiocarcinoma cells. Liver Int; 2004 Dec;24(6):687-95
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  • BACKGROUND: Cholangiocarcinoma is a highly malignant, usually fatal cancer with limited therapeutic options.
  • Receptor tyrosine kinases contribute to the development and progression of this cancer.
  • However, the ability of this drug to inhibit signal transduction and induce apoptosis in human cholangiocarcinoma cells is incompletely studied.
  • CONCLUSIONS: These results indicate that STI-571 induces caspase-dependent apoptosis in a human cholangiocarcinoma cell line and suggest that STI-571 might warrant further investigation as a possible agent for treatment of human cholangiocarcinoma.
  • [MeSH-major] Apoptosis / drug effects. Bile Duct Neoplasms / pathology. Bile Ducts, Intrahepatic. Caspases / drug effects. Cholangiocarcinoma / pathology. Piperazines / pharmacology. Pyrimidines / pharmacology
  • [MeSH-minor] Analysis of Variance. Benzamides. Epidermal Growth Factor / drug effects. Epidermal Growth Factor / metabolism. Female. Humans. Imatinib Mesylate. Immunoblotting. Male. Mitochondria / metabolism. Probability. Sensitivity and Specificity. Tumor Cells, Cultured

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  • (PMID = 15566522.001).
  • [ISSN] 1478-3223
  • [Journal-full-title] Liver international : official journal of the International Association for the Study of the Liver
  • [ISO-abbreviation] Liver Int.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA69008; United States / NIDDK NIH HHS / DK / DK59427
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 62229-50-9 / Epidermal Growth Factor; 8A1O1M485B / Imatinib Mesylate; EC 3.4.22.- / Caspases
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47. Cheon YK: The role of photodynamic therapy for hilar cholangiocarcinoma. Korean J Intern Med; 2010 Dec;25(4):345-52
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  • The prognosis for hilar cholangiocarcinoma is limited by tumor spread along the biliary tree leading to refractory obstructive cholestasis, cholangitis, and liver failure.
  • Palliation with biliary endoprostheses results in median survival times of 4-6 months for advanced bile duct cancer.
  • Photodynamic therapy (PDT) is a local photochemical tumor treatment consisting of a photosensitizing agent combined with laser irradiation of a distinct wavelength.
  • Optimum control of tumor spread along the bile ducts and control of cholestasis and cholangitis will prolong survival in one to two thirds of patients, and renders them suitable for other antitumor therapies.
  • [MeSH-major] Bile Duct Neoplasms / drug therapy. Bile Ducts, Intrahepatic. Cholangiocarcinoma / drug therapy. Photochemotherapy

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  • (PMID = 21179270.001).
  • [ISSN] 1226-3303
  • [Journal-full-title] The Korean journal of internal medicine
  • [ISO-abbreviation] Korean J. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2997961
  • [Keywords] NOTNLM ; Bile duct neoplasms / Cholangiocarcinoma / Photodynamic therapy / Photosensitizing agents
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48. Mancino A, Mancino MG, Glaser SS, Alpini G, Bolognese A, Izzo L, Francis H, Onori P, Franchitto A, Ginanni-Corradini S, Gaudio E, Alvaro D: Estrogens stimulate the proliferation of human cholangiocarcinoma by inducing the expression and secretion of vascular endothelial growth factor. Dig Liver Dis; 2009 Feb;41(2):156-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Seven biopsies of intra-hepatic cholangiocarcinoma and the HuH-28 cell lines were investigated.

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  • (PMID = 18395502.001).
  • [ISSN] 1878-3562
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK 58411; United States / NIDDK NIH HHS / DK / R01 DK058411; United States / NIDDK NIH HHS / DK / R01 DK054811; United States / NIDDK NIH HHS / DK / DK054811-04; United States / NIDDK NIH HHS / DK / R01 DK054811-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Estrogens; 0 / Vascular Endothelial Growth Factor A; 4TI98Z838E / Estradiol; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Other-IDs] NLM/ NIHMS52144; NLM/ PMC2626155
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49. Watanapa P, Watanapa WB: Liver fluke-associated cholangiocarcinoma. Br J Surg; 2002 Aug;89(8):962-70
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  • [Title] Liver fluke-associated cholangiocarcinoma.
  • BACKGROUND: Infection with liver flukes has been reported to be associated with bile duct malignancy.
  • Possible mechanisms of carcinogenesis include chronic irritation, nitric oxide formation, intrinsic nitrosation and activation of drug-metabolizing enzymes.
  • Early detection of bile duct malignancy is difficult and not clinically available at present, although cholangiocarcinoma-associated soluble antigen has been reported in an experimental study to be a useful early marker of cancer development.
  • Long-term survival after surgical treatment of liver fluke-associated cancer is similar to that reported in patients without liver fluke infestation.
  • CONCLUSION: Liver fluke-associated cholangiocarcinoma is still a health problem in developing countries.
  • [MeSH-major] Bile Duct Neoplasms / parasitology. Bile Ducts, Intrahepatic. Cholangiocarcinoma / parasitology. Liver Diseases, Parasitic / complications. Opisthorchiasis / complications. Opisthorchis. Phenanthrenes
  • [MeSH-minor] Animals. Cricetinae. Diterpenes / therapeutic use. Epoxy Compounds. Humans. Survival Analysis. Treatment Outcome

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  • (PMID = 12153620.001).
  • [ISSN] 0007-1323
  • [Journal-full-title] The British journal of surgery
  • [ISO-abbreviation] Br J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Diterpenes; 0 / Epoxy Compounds; 0 / Phenanthrenes; 19ALD1S53J / triptolide
  • [Number-of-references] 75
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50. Martin R, Jarnagin W: Intrahepatic cholangiocarcinoma. Current management. Minerva Chir; 2003 Aug;58(4):469-78
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  • [Title] Intrahepatic cholangiocarcinoma. Current management.
  • Peripheral/Intrahepatic Cholangiocarcinoma (IHC), a malignant epithelial tumor originating from the intrahepatic bile ducts, is the second most common primary liver cancer after hepatocellular carcinoma.
  • Unlike hepatocellular carcinoma, however, IHC is infrequently associated with chronic underlying liver disease.
  • Of the approximately 4000 patients seen at Memorial Sloan-Kettering Cancer Center with hepatic lesions since from 1995-2001, 7% had a diagnosis of cholangiocarcinoma and only 1% had IHC.
  • Single agent or combination chemotherapy and radiation therapy have not been shown to have a significant impact, either as primary treatment or as an adjuvant to resection.
  • [MeSH-major] Bile Duct Neoplasms / surgery. Bile Ducts, Intrahepatic / surgery. Cholangiocarcinoma / surgery
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chemotherapy, Adjuvant. Cholestasis, Intrahepatic / etiology. Comorbidity. Humans. Jaundice, Obstructive / etiology. Liver Diseases / epidemiology. Neoplasm Recurrence, Local. Prognosis. Radiotherapy, Adjuvant. Survival Analysis. Treatment Outcome

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  • (PMID = 14603159.001).
  • [ISSN] 0026-4733
  • [Journal-full-title] Minerva chirurgica
  • [ISO-abbreviation] Minerva Chir
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 29
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51. National Toxicology Program: NTP technical report on the toxicology and carcinogenesis studies of 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153) (CAS No. 35065-27-1) in female Harlan Sprague-Dawley rats (Gavage studies). Natl Toxicol Program Tech Rep Ser; 2006 May;(529):4-168
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  • Structurally related compounds that bind to the AhR and exhibit biological actions similar to TCDD are commonly referred to as "dioxin-like compounds" (DLCs).
  • The toxic equivalency of DLCs was nominated for evaluation because of the widespread human exposure to DLCs and the lack of data on the adequacy of the TEF methodology for predicting relative potency for cancer risk.
  • Manufacture and use of the chemical was stopped due to increased PCB residues in the environment, but it continues to be released into the environment through the use and disposal of products containing PCBs, as by-products during the manufacture of certain organic chemicals, and during the combustion and biodegradation of some waste materials.
  • PCB 153 was selected for study by the National Toxicology Program as a part of the dioxin TEF evaluation to assess the cancer risk posed by complex mixtures of polychlorinated dibenzodioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs).
  • PCB 153 was also included in a mixture study with PCB 126, since previous studies have demonstrated interactions between PCB 153 and DLCs on pharmacokinetic and biological effects.
  • In the liver of vehicle controls, no measurable concentrations of PCB 153 were observed at any time point.
  • In liver, lung, and blood of rats from the 3,000 microg/kg stop-exposure group, PCB 153 concentrations were slightly above or below the levels observed in the 1,000 microg/kg group.
  • Organ Weights: Absolute liver weights of 1,000 microg/kg rats and absolute and relative liver weights of 3,000 microg/kg rats were significantly greater than those of vehicle controls at week 14.
  • At week 31, relative liver weights of 1,000 microg/kg rats and absolute and relative liver weights of 3,000 microg/kg rats were significantly greater than those of vehicle controls.
  • At week 53, absolute and relative liver weights were significantly greater in rats administered 100 microg/kg or greater compared to vehicle controls.
  • The incidences of diffuse fatty change in the 300 microg/kg or greater groups and bile duct hyperplasia of the liver in 300 microg/kg and 3,000 microg/kg (core and stop-exposure) groups were significantly increased.
  • The incidences of oval cell hyperplasia and pigmentation of the liver were significantly increased in the 3,000 microg/kg core study group.
  • CONCLUSIONS: Under the conditions of this 2-year gavage study there was equivocal evidence of carcinogenic activity of PCB 153 in female Harlan Sprague-Dawley rats based on the occurrences of cholangioma of the liver.
  • PCB 153 administration caused increased incidences of nonneoplastic lesions of the liver, thyroid gland, ovary, oviduct, and uterus in female rats.
  • [MeSH-major] Bile Ducts, Intrahepatic / pathology. Carcinogens / toxicity. Polychlorinated Biphenyls / toxicity
  • [MeSH-minor] Adenoma, Bile Duct / chemically induced. Adenoma, Bile Duct / pathology. Administration, Oral. Animals. Bile Duct Neoplasms / chemically induced. Bile Duct Neoplasms / pathology. Cell Enlargement / drug effects. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Female. Hepatocytes / drug effects. Hepatocytes / pathology. Liver / drug effects. Liver / pathology. Organ Size / drug effects. Rats. Rats, Sprague-Dawley. Thyroid Hormones / blood. Toxicity Tests

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  • (PMID = 16835634.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Thyroid Hormones; DFC2HB4I0K / Polychlorinated Biphenyls; ZRU0C9E32O / 2,4,5,2',4',5'-hexachlorobiphenyl
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52. Gusani NJ, Balaa FK, Steel JL, Geller DA, Marsh JW, Zajko AB, Carr BI, Gamblin TC: Treatment of unresectable cholangiocarcinoma with gemcitabine-based transcatheter arterial chemoembolization (TACE): a single-institution experience. J Gastrointest Surg; 2008 Jan;12(1):129-37
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  • We report our experience treating cholangiocarcinoma with TACE using chemotherapeutic regimens based on the well-tolerated drug gemcitabine.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Bile Duct Neoplasms / therapy. Bile Ducts, Intrahepatic. Chemoembolization, Therapeutic / methods. Cholangiocarcinoma / therapy. Deoxycytidine / analogs & derivatives. Hepatectomy / contraindications
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy. Cholangiopancreatography, Endoscopic Retrograde. Cisplatin / administration & dosage. Drug Therapy, Combination. Female. Follow-Up Studies. Hepatic Artery. Humans. Injections, Intra-Arterial. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Staging. Organoplatinum Compounds / administration & dosage. Retrospective Studies. Ribonucleotide Reductases / antagonists & inhibitors. Survival Rate. Time Factors. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 17851723.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / K12 HD049109
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Organoplatinum Compounds; 04ZR38536J / oxaliplatin; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 1.17.4.- / Ribonucleotide Reductases; Q20Q21Q62J / Cisplatin
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53. Malek NP, Greten T, Kubicka S: [Systemic treatment of liver and biliary tumors]. Internist (Berl); 2007 Jan;48(1):46-9
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  • [Title] [Systemic treatment of liver and biliary tumors].
  • [Transliterated title] Systemische Therapie von Leber- und Gallenwegstumoren.
  • This is primarily due to the reduced liver function of most patients and the low sensitivity of liver cancer cells to chemotherapy.
  • In addition to anti-angiogenic drugs, compounds which interfere with specific signal transduction cascades have shown promising results in smaller trials.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bile Duct Neoplasms / drug therapy. Bile Ducts, Intrahepatic. Carcinoma, Hepatocellular / drug therapy. Cholangiocarcinoma / drug therapy. Liver Neoplasms / drug therapy
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials, Phase III as Topic. Drug Delivery Systems. Drug Resistance, Neoplasm. Humans. Signal Transduction / drug effects

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  • (PMID = 17177032.001).
  • [ISSN] 0020-9554
  • [Journal-full-title] Der Internist
  • [ISO-abbreviation] Internist (Berl)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents
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54. Savier E, Azoulay D, Huguet E, Lokiec F, Gil-Delgado M, Bismuth H: Percutaneous isolated hepatic perfusion for chemotherapy: a phase 1 study. Arch Surg; 2003 Mar;138(3):325-32
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  • BACKGROUND: Increasing the drug concentration in tumors may produce massive tumoral response.
  • By using a variety of hepatic vascular isolation techniques, high concentrations of chemotherapeutic drugs may be achieved in the hepatic vascular bed.
  • PATIENTS: Ten patients with irresectable and chemoresistant hepatic tumors were eligible for study participation; 4 patients with hepatic metastases of breast cancer, gastric cancer, colorectal cancer, and cholangiocarcinoma were included.
  • Each course involved IHP of the liver for 15 to 30 minutes, without oxygenation, with 1 to 3 boluses of melphalan (15 mg).
  • One partial response was observed (hepatic metastases of breast cancer).
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Chemotherapy, Cancer, Regional Perfusion / methods. Liver Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / secondary. Bile Duct Neoplasms / secondary. Bile Ducts, Intrahepatic. Breast Neoplasms / pathology. Cholangiocarcinoma / secondary. Colorectal Neoplasms / secondary. Fatal Outcome. Female. Humans. Laparotomy. Male. Melphalan / blood. Middle Aged. Radiography, Interventional. Stomach Neoplasms / pathology

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  • (PMID = 12611582.001).
  • [ISSN] 0004-0010
  • [Journal-full-title] Archives of surgery (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; Q41OR9510P / Melphalan
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55. Zhang Z, Oyesanya RA, Campbell DJ, Almenara JA, Dewitt JL, Sirica AE: Preclinical assessment of simultaneous targeting of epidermal growth factor receptor (ErbB1) and ErbB2 as a strategy for cholangiocarcinoma therapy. Hepatology; 2010 Sep;52(3):975-86
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  • Overexpression of epidermal growth factor receptor (ErbB1) and/or ErbB2 has been implicated in the pathogenesis of cholangiocarcinoma, suggesting that combined ErbB1/ErbB2 targeting might serve as a target-based therapeutic strategy for this highly lethal cancer.
  • The efficacy of lapatinib to significantly suppress liver tumor growth was tested in an orthotopic, syngeneic rat model of intrahepatic cholangiocarcinoma progression.
  • Lapatinib treatment also produced a significant suppression of intrahepatic cholangiocarcinoma growth when administered early to rats, but was without effect in inhibiting liver tumor growth in rats with more advanced tumors.
  • CONCLUSION: Our findings suggest that simultaneous targeting of ErbB1 and ErbB2 could be a potentially selective strategy for cholangiocarcinoma therapy, but is likely to be ineffective by itself against advanced cancer.

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  • [CommentIn] Hepatology. 2011 Jan;53(1):375-6 [21254190.001]
  • [CommentIn] Nat Rev Gastroenterol Hepatol. 2010 Nov;7(11):591 [21069929.001]
  • (PMID = 20607690.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / K12 GM093857; United States / NCI NIH HHS / CA / R01 CA039225; United States / NCI NIH HHS / CA / R01 CA 39225; United States / NCI NIH HHS / CA / R01 CA 83650
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AG 1517; 0 / AG-879; 0 / Antineoplastic Agents; 0 / Erbb2 protein, rat; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / Tyrphostins; 0VUA21238F / lapatinib; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
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56. Buranrat B, Prawan A, Kukongviriyapan U, Kongpetch S, Kukongviriyapan V: Dicoumarol enhances gemcitabine-induced cytotoxicity in high NQO1-expressing cholangiocarcinoma cells. World J Gastroenterol; 2010 May 21;16(19):2362-70
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  • METHODS: Four human cell lines with different NQO1 activity were used; the human CCA cell lines, KKU-100, KKU-OCA17, KKU-M214, and Chang liver cells.
  • Western blotting analysis was performed to determine levels of survival related proteins.
  • CONCLUSION: NQO1 may be important in sensitizing cells to anticancer drugs and inhibition of NQO1 may be a strategy for the treatment of CCA.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Bile Duct Neoplasms / enzymology. Bile Ducts, Intrahepatic / drug effects. Cholangiocarcinoma / enzymology. NAD(P)H Dehydrogenase (Quinone) / antagonists & inhibitors
  • [MeSH-minor] Antimetabolites, Antineoplastic / pharmacology. Cell Line, Tumor. Cell Survival / drug effects. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Dicumarol / pharmacology. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Enzyme Inhibitors / pharmacology. Glutathione / metabolism. Humans. Membrane Potential, Mitochondrial / drug effects. NF-kappa B / metabolism. Oxidation-Reduction. Oxidative Stress / drug effects. RNA, Messenger / metabolism. Reactive Oxygen Species / metabolism. Tumor Suppressor Protein p53 / metabolism. bcl-X Protein / metabolism

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  • (PMID = 20480521.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / BCL2L1 protein, human; 0 / Enzyme Inhibitors; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / bcl-X Protein; 0W860991D6 / Deoxycytidine; 7QID3E7BG7 / Dicumarol; B76N6SBZ8R / gemcitabine; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; GAN16C9B8O / Glutathione
  • [Other-IDs] NLM/ PMC2874140
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57. Ieta K, Tanaka F, Utsunomiya T, Kuwano H, Mori M: CEACAM6 gene expression in intrahepatic cholangiocarcinoma. Br J Cancer; 2006 Aug 21;95(4):532-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CEACAM6 gene expression in intrahepatic cholangiocarcinoma.
  • The purpose of this study was to investigate the clinicopathological and biological significance of human carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) gene expression in human intrahepatic cholangiocarcinoma.
  • CEACAM6 expression status was determined and analysed with respect to various clinicopathological parameters in 23 intrahepatic cholangiocarcinomas.
  • CEACAM6 gene expression in cancer tissues was higher than in noncancerous tissues in 16 of the 23 cases; however, it was not statistically significant.
  • CEACAM6 is a potential prognostic indicator and potential chemoresistant marker to gemcitabine for patients with intrahepatic cholangiocarcinoma.
  • [MeSH-major] Antigens, CD / metabolism. Bile Duct Neoplasms / metabolism. Bile Ducts, Intrahepatic. Cell Adhesion Molecules / metabolism. Cholangiocarcinoma / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cell Division. Cell Line, Tumor. Drug Screening Assays, Antitumor. Humans. Prognosis. Transfection

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  • (PMID = 16868542.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / CD66 antigens; 0 / Cell Adhesion Molecules
  • [Other-IDs] NLM/ PMC2360665
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58. Utsunomiya T, Inoue H, Tanaka F, Yamaguchi H, Ohta M, Okamoto M, Mimori K, Mori M: Expression of cancer-testis antigen (CTA) genes in intrahepatic cholangiocarcinoma. Ann Surg Oncol; 2004 Oct;11(10):934-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of cancer-testis antigen (CTA) genes in intrahepatic cholangiocarcinoma.
  • BACKGROUND: Cancer-testis antigens (CTA), such as MAGE, are selectively expressed in various types of human neoplasms but not in normal tissues other than testis.
  • This characteristic feature of CTA makes them promising antigens for cancer-specific immunotherapy.
  • METHODS: We investigated the expression of five genes, including MAGE-1, MAGE-3, NY-ESO-1, SCP-1, and SSX-4, in 20 surgical samples of intrahepatic cholangiocarcinomas (IHCC) using reverse transcription-polymerase chain reaction.
  • To visualize the localization of MAGE proteins, we performed immunohistochemical studies.
  • Furthermore, the correlation between the CTA expression and DNA methylation status was studied in three bile duct cancer cell lines.
  • An immunohistochemical analysis of MAGE proteins demonstrated homogenous or focal distributions in cytoplasm of the IHCC.
  • Using a demethylating agent, MAGE-1, NY-ESO-1, SCP-1, and SSX-4 were induced in two of three cell lines, whereas MAGE-3 was not.
  • Some of the patients with IHCC, therefore, should be candidates for potentially useful cancer-specific immunotherapy.
  • [MeSH-major] Antigens, Neoplasm / analysis. Antigens, Neoplasm / biosynthesis. Bile Duct Neoplasms / genetics. Bile Duct Neoplasms / immunology. Cholangiocarcinoma / genetics. Cholangiocarcinoma / immunology. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Liver Neoplasms / genetics. Liver Neoplasms / immunology


59. Harisinghani MG, Hahn PF: Computed tomography and magnetic resonance imaging evaluation of liver cancer. Gastroenterol Clin North Am; 2002 Sep;31(3):759-76, vi
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  • [Title] Computed tomography and magnetic resonance imaging evaluation of liver cancer.
  • Focal liver lesions occur commonly and with varying histology, each requiring radically different management.
  • There are a multitude of imaging modalities currently being used for detecting and characterizing focal liver neoplasms.
  • CT and MRI have benefited from rapid technologic advances, and MRI, in particular, from the advent of new contrast agents.
  • [MeSH-major] Liver Neoplasms / diagnosis. Magnetic Resonance Imaging. Tomography, X-Ray Computed
  • [MeSH-minor] Adenoma, Liver Cell / diagnosis. Bile Duct Neoplasms / diagnosis. Bile Ducts, Intrahepatic / radiography. Carcinoma, Hepatocellular / diagnosis. Carcinoma, Hepatocellular / etiology. Cholangiocarcinoma / diagnosis. Contrast Media. Hemangioma / diagnosis. Humans. Lymphoma / diagnosis

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  • (PMID = 12481730.001).
  • [ISSN] 0889-8553
  • [Journal-full-title] Gastroenterology clinics of North America
  • [ISO-abbreviation] Gastroenterol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
  • [Number-of-references] 43
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60. Fingas CD, Blechacz BR, Smoot RL, Guicciardi ME, Mott J, Bronk SF, Werneburg NW, Sirica AE, Gores GJ: A smac mimetic reduces TNF related apoptosis inducing ligand (TRAIL)-induced invasion and metastasis of cholangiocarcinoma cells. Hepatology; 2010 Aug;52(2):550-61
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  • Second mitochondria-derived activator of caspase (smac) mimetics are promising cancer therapeutic agents that enhance proapoptotic death receptor signaling by causing cellular degradation of inhibitor of apoptosis (IAP) proteins.