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Denise Zwanziger Department of Endocrinology and Metabolism and Division of Laboratory Research, University Hospital Essen, Essen, Germany

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Helena Rakov Department of Endocrinology and Metabolism and Division of Laboratory Research, University Hospital Essen, Essen, Germany

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Kathrin Engels Department of Endocrinology and Metabolism and Division of Laboratory Research, University Hospital Essen, Essen, Germany

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Lars C. Moeller Department of Endocrinology and Metabolism and Division of Laboratory Research, University Hospital Essen, Essen, Germany

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Dagmar Führer Department of Endocrinology and Metabolism and Division of Laboratory Research, University Hospital Essen, Essen, Germany

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of the bile duct [ 10 ]. Biliary diseases in humans can be associated with altered claudin-1 expression or mutations. For instance, in the neonatal ichthyosis-sclerosing cholangitis syndrome, claudin-1 gene mutations may lead to increased paracellular

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Marta Di Stefano Division of Endocrine and Metabolic Diseases, IRCCS Istituto Auxologico Italiano, Milan, Italy

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Carla Colombo Division of Endocrine and Metabolic Diseases, IRCCS Istituto Auxologico Italiano, Milan, Italy
Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy

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Simone De Leo Division of Endocrine and Metabolic Diseases, IRCCS Istituto Auxologico Italiano, Milan, Italy

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Michela Perrino Division of Endocrine and Metabolic Diseases, IRCCS Istituto Auxologico Italiano, Milan, Italy

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Mauro Viganò Division of Hepatology, San Giuseppe Hospital Multimedica IRCCS, Milan, Italy

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Luca Persani Division of Endocrine and Metabolic Diseases, IRCCS Istituto Auxologico Italiano, Milan, Italy
Department of Clinical Sciences and Community Health, Milan, Italy

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Laura Fugazzola Division of Endocrine and Metabolic Diseases, IRCCS Istituto Auxologico Italiano, Milan, Italy
Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy

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role in inducing their proliferation in response to cholestasis [ 19 ], drugs inhibiting VEGF-R are predicted to cause biliary diseases. The antiangiogenic activity of TKIs at the epithelium and muscularis layers of the gallbladder may also contribute

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