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| 1 | Cholangiocarcinoma, gone without the Wnt?显示文摘Cholangiocarcinoma(CCA) is a relatively rare malignancy of the intra- or extra-hepatic bile ducts that is classified according to its anatomical localization as intrahepatic, perihilar or distal. Overall, CCA has a dismal prognosis due to typical presentation at an advanced irresectable stage, lack of effective non-surgical treatments, and a high rate of disease recurrence. CCA frequently arises on a background of chronic liver inflammation and cholestasis. Chronic inflammation is accompanied by enhanced cell turnover with generation of additional inflammatory stimuli, and a microenvironment rich in pro-inflammatory mediators and proliferative factors that enable accumulation of mutations, transformation and expansion of mutated cells. A recent study by Boulter et al implicates the Wnt signaling cascade in cholangiocarcinogenesis. Wnt ligands Wnt7 B and Wnt10 A were found to be highly overexpressed in human CCA tissue. Wnt7 B protein was present throughout the tumor stroma, and often co-localized with a subset of CD68+ macrophages. To address in a direct manner whether Wnt signaling is engaged in development of CCA, Boulter et al explored the Wnt signaling pathway in an experimental model that recapitulates the multi-stage progression of human CCA.Wnt ligands found to be elevated in human CCA were also upregulated during the course of CCA development following thioacetamide treatment. Wnt10 a increased during the(pre-cancerous) regenerative phase, while Wnt7 b induction paralleled tumor growth. Along with upregulation of target genes, the findings demonstrate that the canonical Wnt pathway is progressively activated during cholangio-carcinogenesis. Macrophage depletion,eliminating a major source of Wnt7 b, prevented activation of the canonical Wnt cascade, and resulted in reduced number and volume of tumors in this model. Moreover,specific inhibitors of the canonical Wnt pathway(ICG-001 and C-59) caused reduction of tumor area and number,in xenograft and thioacetamide models of CCA. The aggregated findings show that experimental, and presumably human CCA, is a Wnt-driven tumor. Modulation of Wnt signaling, alone or in combination with surgicalor chemotherapy approaches, holds promise in the management of this fatal malignancy. | Anne T R Noll Thorsten Cramer Steven W M Olde Damink Frank G Schaap | 2016 | World Journal of Hepatology2016，8，26： | 3 |
| 2 | HIF-1 alpha is essential for myeloid cell-mediated inflammation显示文摘 | Cramer T Yamanishi Y Clansen B E | 2003 | Cell2003，112，5： | 2 |
| 3 | Hepatocytes as a sourceof collagen type ⅩⅧ endostatin显示文摘 | Schuppan D Cramer T Bauer M | 1998 | Lancet1998，352，9131： | 2 |
| 4 | Hepatocytes as a source of collagen type ⅩⅧ endostatin显示文摘 | Schuppan D Cramer T Bauer M | | 0，，： | 2 |
| 5 | HIF-lalpha is essential for myeloid cell-mediated inflammation 显示文摘 | Cramer T Yamanishi Y Clausen BE | 2003 | Cell2003，113，3： | 1 |
| 6 | Transfomling growth factor beta 1 stimulates vascular endothelial growth factor gene transcription in human cholangiocellular carcinomacells显示文摘 | Benckert C Jonas S Cramer T | 2003 | Cancer Res2003，163，： | 1 |
| 7 | A novel role for the hypoxia inducible transcription factor HlF-lalpha: critical regulation of inflammatory cell function显示文摘 | Cramer T Johnson RS | 2003 | Cell Cycle2003，2，3： | 1 |
| 8 | Transforming growth factor beta 1 stimulates vascular endothelial growth factor gene transcription in human cholangiocellular carcinoma cells显示文摘 | Benckert C Jonas S Cramer T | 2003 | Cancer Res2003，63，5： | 1 |
| 9 | The Madin darbycanine Kidney ( MDCK) epithelial cell monolayer as a model cel-lular transport barrier显示文摘 | Cho M J Thompson D P Cramer C T | 1989 | Pharm Res1989，6，1： | 1 |
| 10 | Dual mechanism of vascular endothelial growth factor upregulation by hypoxia in human hepatocellular carcinoma显示文摘 | Von Marschall Z Cramer T Hocker M | 2001 | Gut2001，48，1： | 1 |
| 11 | Actin-based cell motility and cell locomotion显示文摘 | Cramer L P | 1996 | Cell1996，84，： | 1 |
| 12 | HIF-1 is essential for myeloid eell-mediated inflammation 显示文摘 | Cramer T Yamanishi Y Clausen BE | 2003 | Cell2003，112，5： | 1 |
| 13 | Protein structure perturbations on chromatographic surfaces显示文摘 | Sane S U Cramer S M Przybycien T M | 1999 | Journal of Chromatography A1999，849，1： | 1 |
| 14 | Hepatocytes as asource of collagen type X Ⅷ endostatin显示文摘 | Cramer T Bauer M | 1998 | Lancet1998，352，9131： | 1 |
| 15 | Hepatocytes as a source of collagen type ⅩⅧ endostatin显示文摘 | Schuppan D Cramer T Bauer M | 1998 | Lancet1998，352，9131： | 1 |
| 16 | De novo expression of vascular endothelial growth factor in human pancreatic cancer:evidence for an autocrine mitogenic loop显示文摘 | Marschall Z V Cramer T Hcker M | 2000 | Gastroenterology2000，119，5： | 1 |
| 17 | Dual mechanism of vascular endothelial growth factorupregulation by hypoxia in human hypatocellular carcinoma显示文摘 | Marschall Z Cramer T Hocker M | 2001 | Gut2001，48，： | 1 |
| 18 | De novo expression of vascular endothelial growth factor in human pancreatic cancer: evidence for an autocrine mitogenic loop显示文摘 | yon Marschall Z Cramer T Hocker M | 2000 | Gastroenterology2000，119，5： | 1 |
| 19 | Mechanism and modeling of a thiol-ene photopolymerization显示文摘 | CRAMER N B DAVIES T BOWMAN CN | 2003 | Macromolecules2003，36，： | 1 |
| 20 | Hepatoctye growth factor and c-Met expression in rat and human liver fibrosis显示文摘 | Cramer T Schuppan D Bauer M | 2004 | Liver Int2004，24，4： | 1 |
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