[en] We report a 9-year-old boy with a 6-h history of acute abdominal pain due to torsion of a pedunculated hepatic mesenchymal hamartoma. The lesion was seen, on US and CT, to connect to the liver through a pedicle. Mesenchymal hepatic hamartomas are unusual tumours that may be pedunculated, and this is a unique case complicated by torsion. The radiological and pathological findings, differential diagnosis, and clinical course are discussed. (orig.)

[en] Liver tumors in childhood are rare tumors. Approximately two thirds of all liver masses in children are malignant. Among children younger than 5 years, HB accounted for 91 %, whereas among those 15 to 19 years of age, HCC accounted for 87 % of cases.The causes of most liver tumors of childhood are unknown. HB occurs in association with several cancer genetic syndromes. HCC often occurs after the development of cirrhosis. The AFP is a tumor marker to assess response to therapy as well as to monitor for disease recurrence. Surgery is the mainstay of the treatment for liver tumors. The role of CHT is to improve resectability of the tumor. In the case of unresectable liver tumors the liver transplantation give the real hope for cure. (author)

[en] Settlement of colorectal cancer metastases in the liver is a typical example of the dynamic development of new techniques in oncology. Surgery, it is also currently irreplaceable in the treatment of liver metastases of colorectal cancer, where surgical treatment now steadily growing new therapeutic methods and thus give a chance for patients in whom resection is not possible. Advances in chemotherapy significantly affect the results of surgical treatment and treat this disease can be considered an example of an interdisciplinary approach to solving cancer. Increasingly sophisticated equipment along with ample experience in hepatobiliary surgery have significantly reduced the number of postoperative complications, leading to continuous improvement of survival results in patients with metastatic colorectal cancer in the liver. (author)

[en] To evaluate the additional value of inversion recovery (IR) single-shot turbo spin-echo (SSTSE) imaging with sensitivity encoding (SENSE) using the inversion time (TI) value of hepatic haemangioma as a supplement to conventional T2-weighted turbo spin-echo (TSE) imaging for the discrimination of hepatic haemangiomas and cysts. A total of 134 lesions (77 hepatic haemangiomas, 57 hepatic cysts) in 59 patients were evaluated. Three readers evaluated these images and used a five-point scale to evaluate the lesion status. A receiver operating characteristic (ROC) analysis and 2 x 2 table analysis were used. The ROC analysis for all the readers and all the cases revealed a significantly higher area under the curve (AUC) for the combination of moderately and heavily T2-weighted TSE with IR-SSTSE images (0.945) than for moderately and heavily T2-weighted TSE images alone (0.894) (P < 0.001). For the combination of T2-weighted TSE with IR-SSTSE versus T2-weighted TSE alone, the 2 x 2 table analysis revealed a higher true-positive rate; this difference was statistically significant (P < 0.0001). The introduction of IR-SSTSE with SENSE sequences significantly improves the diagnostic accuracy of the differentiation of hepatic haemangioma and cysts while increasing the time required for routine abdominal imaging by only 20 s. (orig.)

No abstract available

[en] An imbalance between proliferation and apoptosis is one of the main features of carcinogenesis. TRAIL (TNF-related apoptosis-inducing ligand) induces apoptosis upon binding to the TRAIL death receptors, TRAIL receptor 1 (TRAIL-R1) and TRAIL-R2, whereas binding to TRAIL-R3 and TRAIL-R4 might promote cell survival and proliferation. The anti-tumor activity of TRAIL-R1 and TRAIL-R2 agonists is currently investigated in clinical trials. To gain further insight into the regulation of apoptosis in hepatocellular carcinoma (HCC), we investigated the TRAIL pathway and the regulators of apoptosis caspase-8, Bcl-xL and Mcl-1 in patients with HCC regarding patient survival. We analyzed 157 hepatocellular carcinoma patients who underwent partial liver resection or orthotopic liver transplantation and healthy control liver tissue using immunohistochemistry on tissue microarrays for the expression of TRAIL-R1 to TRAIL-R4, caspase-8, Bcl-xL and Mcl-1. Immunohistochemical data were evaluated for potential associations with clinico-pathological parameters and survival. Whereas TRAIL-R1 was downregulated in HCC in comparison to normal liver tissue, TRAIL-R2 and –R4 were upregulated in HCC, especially in G2 and G3 tumors. TRAIL-R1 downregulation and upregulation of TRAIL-R2 and TRAIL-R4 correlated with tumor dedifferentiation (G2/G3). TRAIL-R3, Bcl-xL and Mcl-1 showed no differential expression in tumor tissue compared to normal tissue. The expression levels of TRAIL receptors did not correlate with patient survival after partial hepatectomy. Interestingly, in tumor tissue, but not in normal hepatocytes, caspase-8 showed a strong nuclear staining. Low cytosolic and high nuclear staining intensity of caspase-8 significantly correlated with impaired survival after partial hepatectomy, which, for cytosolic caspase-8, was independent from tumor grade. Assessment of TRAIL-receptor expression patterns may have therapeutic implications for the use of TRAIL receptor agonists in HCC therapy. Tumor-specific nuclear localisation of caspase-8 in HCC suggests an apoptosis-independent function of caspase-8 and correlates with patient survival

[en] Published in summary form only

No abstract available

[en] Short communication. 6 refs, 4 figs

[en] Metastasis is responsible for the rapid recurrence and poor survival of malignancies. Epithelial-mesenchymal transition (EMT) has a critical role in metastasis. Increasing evidence indicates that EMT can be regulated by microRNAs (miRNAs). The aim of this study was to investigate the role of miR-26b in modulating epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma (HCC), as well as to identify its underlying mechanism of action. The expression level of miR-26b was assessed in multiple HCC cell lines (HepG2, MHCC97H, Hep3B, MHCC97L, HCCC9810, BEL-7402, Huh7 and QGY-7703), as well as in liver tissue from patients with HCC. Follow-up studies examined the effects of a miR-26b mimic (increased expression) and a miR-26b inhibitor (decreased expression) on markers of EMT, wound healing and cell migration. The molecular target of miR-26b was also identified using a computer algorithm and confirmed experimentally. MiR-26b expression was decreased in HCC cell lines and was inversely correlated with the grade of HCC. Increased expression of miR-26b inhibited the migration and invasiveness of HCC cell lines, which was accompanied by decreased expression of the epithelial marker E-cadherin and increased expression of the mesenchymal marker vimentin, at both the mRNA and protein expression levels. A binding site for miR-26b was theoretically identified in the 3′UTR of USP9X. Further studies revealed that overexpression of miR-26b repressed the endogenous level of USP9X protein expression. Overexpression of miR-26b also repressed Smad4 expression, whereas its inhibition elevated Smad4 expression. Taken together, our results indicate that miR-26b were inhibited in HCC. In HCC cell lines, miR-26b targeted the 3′UTR of USP9X, which in turn affects EMT through Smad4 and the TGF-β signaling pathway. Our analysis of clinical HCC samples verifies that miR-26b also targets USP9X expression to inhibit the EMT of hepatocytes. Thus, miR-26b may have some effects on the EMT of HCC cells