Molecular Pathology of Liver Diseases by Allan Tsung, David A. Geller (auth.), Satdarshan P. S. Monga

By Allan Tsung, David A. Geller (auth.), Satdarshan P. S. Monga (eds.)

Molecular Pathology of Liver ailments integrates the normal wisdom of physiological and pathological methods within the liver with a balanced emphasis on primary suggestions; well timed advances in mobile and molecular mechanisms; and utilized pathology. The textbook is prepared into numerous sections, every one of inclusive of an array of chapters that gradually and cohesively complicated on pertinent liver biology and pathology. the 1st 3 sections talk about the mobile composition of the liver besides their really good services, and additional dissect the molecular foundation of the mobile strategies which are so specified to the liver. the following part examines the mechanisms which are normally implicated within the mobile and molecular foundation of a number of hepatic pathologies, ultimately via a piece each one on a large number of non-neoplastic and neoplastic ailments of the liver. Molecular Pathology of Liver ailments is a entire reference on liver pathobiology for simple, translational and scientific researchers and physicians The layout of the amount will function a prepared connection with correct subject matters within the liver, hence delivering a pragmatic disease-based integrative source at the molecular pathology of liver ailment. Satdarshan (Paul) Singh Monga, MD is Director: department of Experimental Pathology and affiliate Professor of Pathology and medication, college of Pittsburgh, Pittsburgh, PA

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Two routes of hepatocarcinogenesis have been described, based on analyses of tumor transcriptome profiles [20, 57, 58]. The first of these is linked to a high level of genomic instability, with frequent LOH and loss of p53 [59]. The second carcinogenic pathway defines a different type of tumor progression, with maintenance of a stable chromosome profile during HCC development. Tumors undergoing this second route of progression are enriched in b(beta)-catenin mutations, and are well-differentiated tumors with a predominant activation of PV gene transcription.

Andreu P, Colnot S, Godard C, et al. Crypt-restricted proliferation and commitment to the Paneth cell lineage following Apc loss in the mouse intestine. Development. 2005;132(6):1443–51. Sansom OJ, Reed KR, Hayes AJ, et al. Loss of Apc in vivo immediately perturbs Wnt signaling, differentiation, and migration. Genes Dev. 2004;18(12):1385–90. Apte U, Thompson MD, Cui S, Liu B, Cieply B, Monga SP. Wnt/ beta-catenin signaling mediates oval cell response in rodents. Hepatology. 2008;47(1):288–95.

Canalicular surfaces form the bile canalicular network that transports bile produced by hepatocytes to the bile ducts. Lateral plasma membranes fuse alongside bile canaliculi to form zonulae occludens (tight junctions) that occlude the apical domain from the basolateral surface, and thus from the blood-bile barrier. Intermediate junctions, desmosomes, and gap junctions, also on lateral domains provide cohesive strength and functional communication between hepatocytes [8]. S. 1007/978-1-4419-7107-4_3, © Springer Science+Business Media, LLC 2011 17 18 Ultrastructive An analysis of the fine structural features of hepatocytes and nonparenchymal cells has been undertaken using electron microscopic techniques.

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