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Antonia Syrnioti,Evangelia Athanasiou,Prodromos Hytiroglou 대한병리학회 2022 Journal of Pathology and Translational Medicine Vol.56 No.4
Hepatic carcinoma expressing inhibin is a recently described neoplasm with varied architecture, including trabecular, pseudoglandular, follicular/microcystic, organoid, solid and tubular patterns of growth. We report a case of hepatic carcinoma expressing inhibin that occurred in a 47-year-old woman presenting with epigastric and back pain. The tumor was located in the left hepatic lobe and measured 12 cm in diameter. On immunohistochemical stains, the neoplastic cells were positive for inhibin, as well as cytokeratins 7, 8/18 and 19. There was mild focal expression of synaptophysin, and lack of expression of hepatocytic markers. The histogenesis of hepatic carcinoma expressing inhibin is presently uncertain. From a practical point of view, this neoplasm can potentially cause diagnostic pitfalls by simulating other primary or metastatic tumors, such as hepatocellular carcinoma, cholangiocarcinoma, neuroendocrine tumors, and follicular carcinoma of thyroid gland. Performing inhibin immunostain could assist in the differential diagnosis of liver tumors with unusual histologic features.
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Yoon, So‐,Mi,Gerasimidou, Domniki,Kuwahara, Reiichiro,Hytiroglou, Prodromos,Yoo, Jeong Eun,Park, Young Nyun,Theise, Neil D. Wiley Subscription Services, Inc., A Wiley Company 2011 Hepatology Vol.53 No.3
<P><B>Abstract</B></P><P>Epithelial cell adhesion molecule (EpCAM) is a surface marker on human hepatic stem/progenitor cells that is reported as absent on mature hepatocytes. However, it has also been noted that in cirrhotic livers of diverse causes, many hepatocytes have EpCAM surface expression; this may represent aberrant EpCAM expression in injured hepatocytes or, as we now hypothesize, persistence of EpCAM in hepatocytes that have recently derived from hepatobiliary progenitors. To evaluate this concept, we investigated patterns of EpCAM expression in hepatobiliary cell compartments of liver biopsy specimens from patients with all stages of chronic hepatitis B and C, studying proliferation, senescence and telomere lengths. We found that EpCAM(+) hepatocytes were rare in early stages of disease, became increasingly prominent in later stages in parallel with the emergence of ductular reactions, and were consistently arrayed around the periphery of cords of keratin 19(+) hepatobiliary cells of the ductular reaction, with which they shared EpCAM expression. Proliferating cell nuclear antigen (proliferation marker) and p21 (senescence marker) were both higher in hepatocytes in cirrhosis than in normal livers, but ductular reaction hepatobiliary cells had the highest proliferation rate, in keeping with being stem/progenitor cell–derived transit amplifying cells. Telomere lengths in EpCAM(+) hepatocytes in cirrhosis were higher than EpCAM(−) hepatocytes (<I>P</I> < 0.046), and relatively shorter than those in the corresponding ductular reaction hepatobiliary cells (<I>P</I> = 0.057). <I>Conclusion:</I> These morphologic, topographic, immunophenotypic, and molecular data support the concept that EpCAM(+) hepatocytes in chronic viral hepatitis are recent progeny of the hepatobiliary stem/progenitor cell compartment through intermediates of the transit amplifying, ductular reaction hepatobiliary cells. (H<SMALL>EPATOLOGY</SMALL> 2011)</P>
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