Preliminary experience in laparoscopic resection of hepatic hydatidectocyst with the Da Vinci Surgical System (DVSS): a case report.

BACKGROUND: At present, Da Vinci robotic assisted hepatectomy has been routinely carried out in conditional units. But there is no report concerning the use of Da Vinci robots for hepatic hydatid cystectomy and experience on this aspect is seldom mentioned before. This study was to summarize the preliminary experience in laparoscopic resection of hepatic hydatidectocyst with the Da Vinci Surgical System (DVSS). CASE PRESENTATION: A 29-year-old female diagnosed as hepatic hydatid in the right anterior lobe of liver was treated with laparoscopic resection by the DVSS under general anesthesia. Appropriate disposal of tumor cell in vascular system and disinfection of surgical field with hypertonic saline were conducted. The hepatic hydatidectocyst was resected completely with an operation time of 130 min, an intraoperative blood loss of 200 ml and a length of hospital stay for five days. The vital signs of patient were stable and no cyst fluid allergy occurred after operation. CONCLUSIONS: Our result showed that laparoscopic resection of hepatic hydatidectocyst by using the DVSS is safe and feasible on the basis of hospitals have rich experience in treatment of cystic echinococcosisliver, resection with DVSS and laparoscopic excision.

MicroRNA-9 exerts antitumor effects on hepatocellular carcinoma progression by targeting HMGA2.

Accumulating evidence has demonstrated that the aberrant expression of microRNAs (miRs or miRNAs) may contribute to the initiation and progression of various types of human cancer and may also constitute biomarkers for cancer diagnosis and therapy. However, the specific function of miR-9 in hepatocellular carcinoma (HCC) remains unclear, and the mechanisms that underlie HCC are incompletely understood. Here, we report that miR-9 expression was significantly decreased in clinical tumor tissue samples, as well as in a cohort of HCC cell lines. In addition, it was demonstrated that overexpression of miR-9 suppressed the proliferative and migratory capacity of HCC cells and impaired cell cycle progression. Furthermore, high mobility group AT-hook 2 (HMGA2) was verified as a downstream target gene of miR-9 using a luciferase reporter assay. Quantitative RT-PCR and western blotting implicated HMGA2 in the miR-9-mediated reduction of HCC cell growth. In vivo, transfection with miR-9 mimics down-regulated the expression of HMGA2, thus leading to a dramatic reduction in tumor growth in a mouse xenograft model. These results suggest that miR-9 may exert critical antitumor effects on HCC by directly targeting HMGA2, and the miR9/HMGA2 signaling pathway may be of use for the diagnosis and prognosis of patients with HCC.