The effects of laparoscopic liver resection (LLR) and open liver resection (OLR) on oncological outcomes for colorectal cancer liver metastases (CCLM) remain inconclusive. Major databases were searched from January 1992 to October 2016. Effects of LLR vs OLR were determined. The primary endpoints were oncological outcomes. In total, 32 eligible non-randomized studies with 4697 patients (LLR: 1809, OLR: 2888) were analyzed. There were higher rates of clear surgical margins (OR: 1.64, 95%CI: 1.32 to 2.05, p < 0.00001) in the LLR group, without significant differences in disease recurrence, 3- or 5-year overall survival(OS) and disease free survival(DFS) between the two approaches. LLR was associated with less intraoperative blood loss (WMD: −147.46 [−195.78 to −99.15] mL, P < 0.00001) and fewer blood transfusions (OR: 0.41 [0.30–0.58], P < 0.00001), but with longer operation time (WMD:14.44 [1.01 to 27.88] min, P < 0.00001) compared to OLR. Less overall morbidity (OR: 0.64 [0.55 to 0.75], p < 0.00001) and shorter postoperative hospital stay (WMD: −2.36 [−3.06 to −1.66] d, p < 0.00001) were observed for patients undergoing LLR, while there was no statistical difference in mortality. LLR appears to be a safe and feasible alternative to OLR in the treatment of CCLM in selected patients.

Background: High resistance to drug is taken as a characteristic of human tumors, which is usually mediated by multidrug resistance-associated genes. ABCC2, an ATP-binding cassette multidrug resistance transporter, is found to be expressed in a variety of human cancers. In this study the effect of a RNAi construct targeting ABCC2 on the chemosensitivity of NPC cell line CNE2 against cisplatin was investigated.

We found that tetrandrine (TET) can reverse the resistance of Candida albicans to fluconazole (FLC) and that this interaction is associated with the inhibition of drug efflux pumps. Mitochondrial aerobic respiration, which plays a major role in C. albicans metabolism, is the primary source of ATP for cellular processes, including the activation of efflux pumps. However, it was unclear if TET exerts its synergistic action against C. albicans via its impact on the mitochondrial aerobic respiratory metabolism. To investigate this mechanism, we examined the impact of FLC in the presence or absence of TET on two C. albicans strains obtained from a single parental source (FLC-sensitive strain CA-1 and FLC-resistant strain CA-16). We analysed key measures of energy generation and conversion, including the activity of respiration chain complexes I and III (CI and CIII), ATP synthase (CV) activity, and the generation of reactive oxygen species (ROS), and studied intracellular ATP levels and the mitochondrial membrane potential (DY m ), which has a critical impact on energy transport. Mitochondrial morphology was observed by confocal microscopy. Our functional analyses revealed that, compared with strains treated only with FLC, TET+FLC increased the ATP levels and decreased DY m in CA-1, but decreased ATP levels and increased DY m in CA-16 (P,0.05). Additionally, CI, CIII and CV activity decreased by 23-48 %. The production of ROS increased by two-to threefold and mitochondrial morphology was altered in both strains. Our data suggested that TET impacted mitochondrial aerobic respiratory metabolism by influencing the generation and transport of ATP, reducing the utilization of ATP, and resulting in the inhibition of drug efflux pump activity. This activity contributed to the synergistic action of TET on FLC against C. albicans.

Cisplatin (CDDP) is one of the most active drugs to treat nasopharyngeal carcinoma (NPC) patients. To further understand the mechanisms of CDDP-resistance in NPC, two CDDP-resistant sublines (CNE2-CDDP and CNE2-CDDP-5Fu) derived from parental NPC cell line CNE2 were established. It was found that at the IC50 level, the resistance of CNE2-CDDP and CNE2-CDDP-5Fu against CDDP was 2.63-fold and 5.35-fold stronger than that of parental CNE2, respectively. Of the four ABC transporters (ABCB1, ABCC1, ABCC2 and ABCG2) related to MDR, only ABCC2 was found to be elevated both in CDDP-resistant sublines, with ABCC2 located in nucleus of CNE2-CDDP-5Fu but not in CNE2-CDDP and parental CNE2. Further research showed that compared to untreated CNE2, the intracellular levels of CDDP were decreased by 2.03-fold in CNE2-CDDP and 2.78-fold in CNE2-CDDP-5Fu. After treatment with PSC833, a modulator of MDR associated transporters including ABCC2, the intracellular level of CDDP was increased in CDDP-resistant sublines, and the resistance to CDDP was partially reversed from 2.63-fold to 1.62-fold in CNE2-CDDP and from 5.35-fold to 4.62-fold in CNE2-CDDP-5Fu. These data indicate that ABCC2 may play an important role in NPC resistant to CDDP.