ABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of triggering receptors expressed on myeloid cells-1 (TREM-1) in the oncogenesis and progression of hepatocellular carcinoma (HCC).</p><p><b>METHODS</b>The expression and localization of TREM-1 were detected by immunohistochemistry in 76 specimens of HCC, 33 specimens of liver cirrhosis, 30 specimens of hepatitis and 20 normal liver tissues. The association between TREM-1 expression and the clinicopathologic parameters of HCC was analyzed. Human normal hepatic cell line LO2 and HCC cell line SMMC-7721 were examined for TREM-1 expression pattern using RT-PCR and Western blotting.</p><p><b>RESULTS</b>All the normal liver samples showed negative expression of TREM-1 protein, which was significantly up-regulated in the other 3 tissues. The positivity rates of TREM-1 expression were not significantly different between hepatitis, cirrhosis and HCC tissues [20.00% (6/30), 24.24% (8/33), and 21.05% (16/76), respectively; Χ² =0.195, P=0.907]. Different from chronic hepatitis and liver cirrhosis tissues where TREM-1 expression was located mainly in the nucleus and occasionally in the cytoplasm of the hepatocytes, HCC tissues showed a cellular localization of TREM-1 protein almost exclusively in the cytoplasm. In HCC, TREM-1 expression was negatively correlated with the histological grade of the tumor (r=-0.261, P=0.023) but not related with the patients' age, gender, tumor size, clinical stage, pre-existing hepatitis and cirrhosis, lymph node metastasis, or intrahepatic vascular embolism (all P>0.05). In the in vitro experiments, low levels of TREM-1 mRNA and protein expressions were detected in LO2 cells line, but their expressions were markedly up-regulated in SMMC-7721 cells.</p><p><b>CONCLUSION</b>Aberrant enhancement of the expression and cytoplasmic accumulation of TREM-1 may correlate closely with the oncogenesis and progression of HCC.</p>
Subject(s)
Humans , Carcinogenesis , Carcinoma, Hepatocellular , Metabolism , Cell Line , Cell Line, Tumor , Cell Nucleus , Cytoplasm , Disease Progression , Gene Expression Regulation, Neoplastic , Hepatocytes , Metabolism , Immunohistochemistry , Liver Cirrhosis , Liver Neoplasms , Metabolism , Membrane Glycoproteins , Metabolism , Receptors, Immunologic , Metabolism , Triggering Receptor Expressed on Myeloid Cells-1 , Up-RegulationABSTRACT
Purpose To investigate clinicopathological features, diagnosis and differential diagnosis of non-sebaceous lymphadenoma of the parotid gland. Methods The histopathological morphology, immunohistochemical profiles and clinicopathological features were an-alyzed in two cases of NSL, along with review the related literatures. Results Two patients were female adults. Microscopically, The tumor was a well-circumscribed mass surrounded by a fibrous capsule of variable thickness and comprised a mixture of proliferating epi-thelium accompanied by a prominent lymphoid component, reactive lymphoid follicles were found in lymphoid stroma. The epithelial component took the form of anastomosing trabeculae, glands, solid basaloid islands or cyst formation. The cysts and glands were lined with luminal cells and abluminal cells, filled with eosinophilic secretions with occasional histiocytes. The epithelial cell was no seba-ceous differentiation, significant cytological atypia and mitotic activity. A fibrous capsule with subcapsular sinus was seen around the mass in one case. Immunohistochemically, the abluminal cells were positive for p63, CK34βE12 and CK5/6, while the epithelial cells were positive for CK(AE1/AE3) and CK7. Conclusion NSL is a very rare benign of salivary gland, which occuring in the lymph node lesions are less reported, knowledge of the wide histological spectrum of this rare tumor is important in order to avoid misdiagno-sis, particularly as malignant tumor.