Two-port access versus four-port access laparoscopic ovarian cystectomy.

OBJECTIVE: This study was conducted to compare the surgical outcomes between two-port access and four-port access laparoscopic ovarian cystectomy. METHODS: Four hundred and eighty nine patients who had received two-port access laparoscopic ovarian cystectomy (n=175) and four-port access laparoscopic ovarian cystectomy (n=314) in Chungnam National University Hospital from January 2009 to August 2012 were analyzed retrospectively. The data were compared between the bilaterality of the cysts and cyst diameter of less than 6 cm and 6 cm or more. RESULTS: There were no significant differences in patient's age, parity, body weight, body mass index and history of previous surgery between the two-port and four-port access laparoscopy group. Bilaterality of ovarian cysts was more in fourport access laparoscopy group (13.7% vs. 32.5%, P=0.000). There were no significant differences in operation time, hemoglobin change, hospital stay, adhesiolysis, transfusion, and insertion of hemo-vac between the two-port and four-port access laparoscopy group for size matched compare. However additional analgesics were more in four-port access laparoscopy group for unilateral ovarian cystectomy. CONCLUSION: Two-port access laparoscopic surgery was feasible and safe for unilateral and bilateral ovarian cystectomy compare with four-port access laparoscopic surgery.

High-mobility group box 1 (HMGB1) protein regulates tumor-associated cell migration through the interaction with BTB domain.

High-mobility group box 1 (HMGB1) was shown to be strongly implicated in high incidences of metastasis and the poor clinical pathologic conditions found in various human tumors. In this study, we explored the possible mechanism of HMGB1 in tumor metastases in vitro, using a human carcinoma cell system. BTB, as a negative regulator of cell cycle progression, was identified as a HMGB1 interacting partner. The ectopic expression of HMGB1 activates cell growth by suppressing BTB-induced cell death, decreasing Bax and p53 expression, while enhancing Bcl-xL, Bcl-2, cyclin D1, and NF-κB expression. HMGB1 activates the FAK/PI3K/mTOR signaling cascade, and BTB prominently inhibits HMGB1-induced oncogenesis. The effect of HMGB1 on FAK/mTOR signaling was also confirmed through the silencing of HMGB1 expression. These insights provide evidence that HMGB1 enhances cell proliferation and suppresses apoptosis. Collectively, our results show an underlying mechanism for an HMGB1-associated promotion of carcinoma cells.

Cell-Specific Growth Inhibition of Human Cervical Cancer Cell by Recombinant Adenovirus p53 in vitro and in vivo.

PURPOSE: Despite the significance of the p53 adenoviral vector in cancer gene therapy, an advanced strategy for the development of preferential tumor cell-specific delivery and the long-term persistent gene expression control of p53 are required. In this study, the time-course expression patterns of p53 and E6, on cervical cancer cells, were investigated to obtain a molecular level understanding of the cell-dependent tumor growth suppression effects of a recombinant adenovirus expressing p53, both in vitro and in vivo. MATERIALS AND METHODS: The expressions of p53 and E6 in CaSki, SiHa, HeLa, HeLaS3, C33A and HT3 cervical cancer cell lines were examined. After infection with AdCMVp53, the cell growth inhibition was studied via cell count, MTT and Neutral red assays. After transfecting the AdCMVp53 and AdCMVLacZ into the cancer cells-xenografted nude mice, the anti-tumor effects were investigated for one month. RESULTS: The p53 protein levels were more notably expressed in the CaSki and HeLa than in the SiHa and HeLaS3 On day 6, the p53 was only detected in the HeLaS3. In contrast, the p53 expression was highly maintained in the C33A and HT3. The E6 mRNA levels gradually decreased in only the CaSki and HeLa. The growth suppression effects also showed cell-dependent patterns, which were consistent with the reciprocal expression patterns of p53 and E6. After transfection of the AdCMVp53, into the CaSki- and SiHa-xenografted nude mice, the tumor size was remarkably decreased in the SiHa cells as compared to that in the AdCMVLacZ transfected mice, indicating cell-specific growth inhibition patterns. CONCLUSION: The adenovirus-mediated p53 gene transfection was very effective both in vitro and in vivo. Also, the anti-tumor effects were accomplished via the differential role of p53-specific apoptotic cell death, which was dependent on the cervical cancer cell line.