[Metastatic gastrointestinal hepatoid adenocarcinoma of the liver: a high-grade carcinoma that is easily confused with primary hepatocellular carcinoma].

Objective: To investigate the clinicopathologic and immunophenotypic features of metastatic gastrointestinal hepatoid adenocarcinomas in the liver. Methods: Eight cases of hepatic metastatic gastrointestinal hepatoid adenocarcinoma diagnosed at the Affiliated Drum Tower Hospital, Nanjing University Medical School from January 2009 to January 2019 were retrospectively analyzed. The clinical data, histopathologic features and immunohistochemical (IHC) characteristics performed by EnVision method were analyzed. Results: There were five males and three females with a mean age of 66 years. The primary sites included one case each from the distal esophagus and the right colon, and the other six cases were from the stomach. Pre-treatment serum AFP levels were increased in four patients, normal in two, and was not known in two other patients. Liver metastases occurred in all eight patients at initial diagnosis. Microscopically, the primary tumor was composed of areas showing hepatic differentiation with or without typical adenocarcinoma component; and the areas with hepatic differentiation morphologically resembled hepatocellular carcinoma (HCC). IHC staining showed variable expression of HCC markers such as Glypican 3, AFP, SALL4 and HepPar-1, and gastrointestinal adenocarcinoma markers such as CK19, CDX-2 and Villin in both the primary and metastatic foci of hepatoid adenocarcinoma. Conclusions: Hepatoid adenocarcinoma in the digestive tract gives rise to only non-specific symptoms, and shows high propensity for invasion and metastasis. When liver metastasis is the presenting symptom, it is difficult to distinguish metastatic hepatoid adenocarcinoma from the primary HCC based on histopathologic characteristics alone. The accurate diagnosis of metastatic hepatoid adenocarcinoma in the liver requires combination of clinical, radiologic, histopathologic and IHC findings.

Long non-coding RNA BANCR indicates poor prognosis for breast cancer and promotes cell proliferation and invasion.

OBJECTIVE: We investigated the expression of human long non-coding ribonucleic acid (lncRNA), BRAF-activated non-coding RNA (BANCR) in breast cancer tissues and its effects on the in vitro proliferation, apoptosis, invasion and metastasis of breast cancer cells; also, we investigated its possible mechanism. PATIENTS AND METHODS: The expressions of BANCR in 65 pairs of breast cancer tissues and para-carcinoma normal breast tissues were detected by Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR). The expressions of BANCR in normal breast epithelial cells (MCF10A) and breast cancer cells (MCF-7, MDA-MB-231, SKBR3 and BT-20) were further detected. The knockdown efficiency of BANCR small interfering RNA (siRNA) in MCF-7 cells was detected by qRT-PCR. The effects of BANCR knockdown on proliferation, apoptosis, invasion and metastasis capacities of MCF-7 cells were explored via methyl thiazolyl tetrazolium (MTT) proliferation assay, cell colony formation assay, fluorescence-activated cell sorting (FACS) and transwell migration assay. Western blotting was used to detect the changes in expressions of apoptosis-related proteins, epithelial-mesenchymal transition (EMT)-related proteins and matrix metalloproteinases (MMPs) after knockdown of BANCR. RESULTS: The expression level of lncRNA BANCR in breast cancer tissues was significantly higher than that in para-carcinoma normal tissues. The prognosis of patients in low-expression BANCR group was significantly superior to that of patients in high-expression BANCR group. After BANCR knockdown in breast cancer MCF-7 cells, the cell proliferation and colony formation capacities were significantly inhibited. Further mechanism research showed that inhibiting BANCR could promote the apoptosis of MCF-7 cells. Results of Western blotting revealed that the expressions of B-cell lymphoma 2 associated X protein (BAX), cleaved-Caspase-3 and cleaved-poly adenosine diphosphate-ribose polymerase (PARP) in knockdown group were significantly up-regulated compared with those in control group. Both wound-healing assay and transwell migration assay showed that the down-regulation of lncRNA BANCR could inhibit the invasion and metastasis capacities of MCF-7 cells, whose mechanism was related to the inhibition of EMT process and down-regulation of MMP expressions in cells. CONCLUSIONS: LncRNA BANCR is highly expressed in breast cancer, which is significantly correlated with the prognosis of patients; moreover, it can promote the growth, invasion and metastasis of ovarian cancer cells. The down-regulation of BANCR can inhibit the proliferation, invasion and metastasis capacities of MCF-7 cells.

[Study on effect of emodin on TGF beta 1 expression in pancreatic tissue of rats suffering from acute pancreatitis].

OBJECTIVE: To investigate the effect and mechanism of emodin on pancreatic repairing and remodeling in treating acute pancreatitis by analyzing the change of cytokine transforming growth factor beta 1(TGF beta 1) gene expression, DNA synthesis and protein content in pancreatic tissue. METHODS: Acute pancreatitis was induced in rats by intraperitoneal infusion of caerulein, treated or untreated by emodin. The animals were sacrificed at 6, 24, 48, 72 or 96 hrs after treatment separately. The mRNA expression of TGF beta 1, DNA synthesis and total protein content in pancreatic tissue were tested by reverse transcription-polymerase chain reaction (RT-PCR), 3H-thymidin method and Lowry's method respectively. RESULTS: Serum amylase level was decreased significantly after emodin treatment. TGF beta 1 mRNA expression was undetectable in the intact pancreas or in 6 hrs after pancreatitis induction in the non-treated group, but revealed at 24 hrs after and reached the peak at 72 hrs later. However, in the emodin treated group, TGF beta 1 mRNA expression was detected at 6 hrs after treatment, with a higher level in 24 hrs and 48 hrs as compared with the non-treated group, and reaching the peak at 48 hrs after treatment. Moreover, the DNA synthesis and total protein content in pancreatic tissue decreased significantly at 72 hrs and 48 hrs after induction respectively, but both parameters increased significantly in the emodin treated group 96 hrs after treatment. CONCLUSION: The mechanism of emodin in treating acute pancreatitis might be by way of enhancing cytokine TGF beta 1 gene expression, regulating cell growth and differentiation, stimulating the formation of extracellular matrix components, increasing DNA synthesis and protein content, and to take part in pancreatic repairing and remodeling.

[Immunohistochemical analysis of HLA class I antigens of the hepatocyte membrane in hepatitis B virus carriers].

HLA class I antigens on hepatocyte membrane were studied in liver biopsies from 46 patients with chronic hepatitis B virus infection by using immunoenzyme technique. The results revealed that the density of HLA class I antigens displayed on hepatocyte membrane in HBeAg positive carriers with minor hepatic inflammatory activity (the high replicative phase) was lower than that in patients with chronic active liver diseases (the low replicative phase) (P less than 0.005), but higher than that in patients with anti-HBe positivity and minor hepatic inflammatory activity (the nonreplicative phase) (P less than 0.05). In a follow-up of 21 HBeAg positive chronic HBV carriers, we found that five of the seven cases with high-density HLA class I antigens showed display of antigens on hepatocyte membrane, whereas only one of the 14 cases with lowdensity antigens were seroconverted from HBe antigen to antibody within one year. These findings suggest that the display on HLA class I antigens on hepatocyte membrane is enhanced and the cytotoxic T lymphacytes can recognize and lyze the infected hepatocytes.