RESUMO
Objective To investigate the levels of 5-hydroxymethylcytosine (5-hmC) and teneleven-translocation proteins (TET1/2/3) in diagnosis and prognosis prediction of hepatocellular carcinoma (HCC).Methods The expression of 5-hmC in 130 cases of HCC tissues were detected by immunohistochemical staining.Kaplan-Meier test was used for survival analysis.TET family plays critical role in the conversion of 5-methylcytosine (5-mC) to 5-hmC.The TET levels were detected by using immunohistochemical staining and RT-PCR,the correlation between 5-hmC and TET was analyzed.Results The level of 5-hmC decreased in HCC tissues,as compared with non-tumor tissues,the expression of TET1 was downregulated in HCC.There was significant difference in the expression between low and high grades of HCC tissues (x2 =10.611,P =0.001).Kaplan-Meier survival analysis showed that there was significant difference between the 5-hmC expression level and the survival rate of HCC patients (x2 =4.412,P =0.036).Conclusions In HCC tissues the expression of 5-hmC was specifically downregulated.Low 5-hmC level is significantly correlated with poor differentiation of the tumor and worse overall survival.Decreased expression of TET1 is likely one of the mechanisms underlying 5-hmC loss in HCC.
RESUMO
<p><b>OBJECTIVE</b>To identify the type of iron deposition and describe its amount, distribution and associated lesions, in order to support an etiologic diagnosis for hemochromatosis.</p><p><b>METHODS</b>Hematoxylineosin (HE) stain, reticular fiber stain, Masson's stain and Perl's iron stain were used to assess liver biopsies from 31 patients with hemochromatosis. The Ishak scoring system and Deugnier scoring system were used to assess the histological change in liver and to semi-quantify the excess of hepatic iron. Genetic testing results were received from a portion of the patients and used in analysis.</p><p><b>RESULTS</b>One patient had hereditary (-HFE) hemochromatosis complicated with Gilbert's syndrome, for which the pattern of iron deposition was similar to that of the four patients with Gilbert's syndrome. Iron accumulation appeared as fine granules predominating at the biliary pole of cells and was distributed throughout the lobule with a decreasing gradient spanning from the periportal to centrolobular areas. Mild chronic inflammation was found to be commonly associated with low stage fibrosis.One patient had HFE hemochromatosis complicated with hepatitis B virus infection, and the pattern of iron deposition resembled that in the eight patients with viral hepatitis, wherein the deposition was mainly in the sinusoidal cells and/or portal macrophages. Histological grading and fibrosis staging differed among patients. The five patients with blood disordered showed iron accumulation mainly in the periportal hepatocytes, but mesenchymal iron deposits were also present. The grade of inflammation, as well as of fibrosis,was mild. The five patients with alcoholic disease and the five patients with drug-induced hepatitis showed hepatic iron deposition in swollen or ballooned hepatocytes. The two patients with excessive iron supply showed iron deposition localized within the parenchymal and mesenchymal cells.</p><p><b>CONCLUSION</b>Etiologic diagnosis of hemochromatosis relies on both the type of iron deposition and the nature of associated lesions. Liver biopsy is necessary for both diagnosis and prognosis.</p>