Ichiro Murakami

An Immunohistochemical and Ultrastructural Study of Case of Small‐cell Neuroendocrine Carcinoma in the Ampullary Region of the Duodenum

One case of small‐cell neuroendocrine carcinoma in the ampullary region of the duodenum is reported. The histological appearance of the tumor was identical to pulmonary small‐cell carcinoma. Neuroendocrine differentiation was demonstrated immunohistochemically by positive immunoreaction for neuron specific enolase, Leu 7 and chromogranin, and ultrastructurally by the presence of scanty dense core neurosecretory type granules. Small‐cell neuroendocrine carcinoma in the ampulla of Vater is extremely rare. To our knowledge, this is the sixth reported case.

Lectin Binding Patterns in Normal Liver, Chronic Active Hepatitis, Liver Cirrhosis, and Hepatocellular Carcinoma An Immunohistochemical and Immunoelectron Microscopic Study

We studied the binding patterns of 14 lectins in human normal and cirrhotic liver (LC) tissues and hepatocellular carcinomas (HCC) using the ABC method. Lectins were divided into 4 groups according to their binding patterns in normal tissues: (A) PHA, MPA, LcH, RCA I, and WGA, which bound to hepatocytes and all three types of sinusoidal cells; (B) BPA, GS‐I, PNA, and SBA, which bound to Kupffer cells and endothelia of interlobular arteries and veins and bile duct epithelia in the portal tract, but not to hepatocytes; (C) UEA‐I, which bound only to endothelia of interlobular arteries and veins and bile duct epithelia in the portal tract; (D) LBA, Lotus, LPA, and SJA, which showed no binding. Thus group B lectins may be useful markers of Kupffer cells. Only electron microscopic examination revealed the precise binding sites of lectins in sinusoidal cells and hepatocytes. Hepatocyte cell surface polarities demonstrated by lectin binding in LC and HCC were different from those in the normal liver. The binding pattern of PHA to LC hepatocytes changed from a membranous to both a membranous and a cytoplasmic pattern, and that of LcH to HCC cells changed to dot‐like staining in the cytoplasm. These changes of polarities in LC and HCC might be caused by changes in the distribution of lectin binding carbohydrates or by the altered glycosylation of glycoconjugates. Acta Pathol Jpn 42: 566–572, 1992.

Abstract 1034: Upregulation of Ezh2 expression correlates with higher tumor proliferation and grade in non-Hodgkin's B- and T-cell lymphoma

Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, ILnnPolycomb group (PcG) proteins are involved in regulation of hematopoiesis, which include two main members Ezh2 and Bmi-1. Reports on their expression levels in different subtypes of malignant lymphoma and role in lymphomagensis and tumor progression are rather limited. To address this issue, we analyzed a total of 197 patient samples including 10 samples of Hodgkin lymphoma (HL), 109 of B-cell lymphoma (BCL) and 78 of T-cell lymphoma (TCL) by immunohistochemistry. The results showed overall expression in HL, BCL and TCL to be 90%, 56.9% and 84.6% for Ezh2 and 90%, 82.5% and 84.6% for Bmi-1 respectively. Among BCL, highest Ezh2 positivity was seen in Burkitts lymphoma (BL) followed by high-grade follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL). In TCL, Ezh2 expression was observed in all subtypes and seemed more homogenous. Difference in its expression between aggressive and indolent subtypes of BCL was statistically significant (p= 0.000∼0.010). On the other hand, Bmi-1 was rather more consistently expressed in both BCL and TCL up to 100% in 7 subtypes. Difference in its expression between aggressive and indolent subtypes was statistically insignificant. Ki67 showed strong positive correlation with Ezh2 in BCL (Correlation coefficient (Co) =0.983, p= 0.000) and moderate correlation in TCL (Co=0 .629, p= 0.000). This correlation could not be detected in case of Bmi1. These data suggest that out of the two Polycomb group (PcG) proteins, only Ezh2 correlates with tumor proliferation and signals a more aggressive nature.nnCitation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1034. doi:1538-7445.AM2012-1034